Manning (Executor of the Estate of Jane Louise Manning Deceased) v King's College Hospital NHS Trust

This is by any standards a tragic case. In late 1993 Mrs Jane Manning, who was then aged 35 and had two young children, was diagnosed at Kings College Hospital (“Kings”) with squamous cell carcinoma, (“SQC”) a rare form of tongue cancer. In January and February 1994 it was treated at the Royal Marsden Hospital (“The Marsden”) by external radiotherapy (“RT”) and brachytherapy (“BT”), the insertion of iridium wires to the tongue. On 11 September 2001 a biopsy of part of Mrs Manning’s tongue carried out by Professor Langdon at Kings was diagnosed by Dr Harrison, one of the two consultant oral pathologists at Kings, as a post-irradiation malignant fibrous histiocytoma. Following review the same day by Dr Fisher, a renowned specialist in sarcomas at The Marsden, who considered that the tumour was more likely to be a recurrent carcinoma presenting as a spindle-cell or sarcomatoid carcinoma than a post-irradiation sarcoma, Dr Harrison revised his diagnosis to that of a recurrent spindle-cell or sarcomatoid carcinoma. When Mrs Manning was seen a few weeks later in October 2001 by Mr Bridger,a surgeon in Devon where she was by then living, and two other maxillofacial consultants, it was unanimously agreed that this was one of the worst oral cavity cancers they had ever seen. The tongue had been almost totally destroyed. It was by then in Mr Bridger’s view totally inoperable. Mrs Manning who by now was in a hospice was in agony and unable to eat or drink. In February 2002 she was still in excruciating pain and a third surgeon, Mr Rhys Evans at the Marsden, expressed the view that the tumour was still at that late stage resectable with a reasonable chance of long term palliation and cure and that surgery would greatly improve her quality of life. Mrs Manning jumped at the chance, however remote, of a cure notwithstanding that the operation involved the complete removal of the tongue. The operation was performed on the 28^th February 2002 and succeeded in greatly alleviating her pain. It did not however succeed in curing the cancer and on 13 May 2002 Mrs Manning died in the Marsden. Her son Henry was then eleven years old and her daughter Lucy was ten years old.

The claims in this case were brought by Mrs Manning’s husband, Gary Manning, a dentist, suing both as the personal representative of Mrs Manning’s estate and on behalf of himself and their two children Henry and Lucy as dependents. By the time of the trial which began in October 2007 Mr Manning was himself suffering from the advanced stages of terminal cancer. Despite his illness and evident physical suffering he gave evidence at the trial and attended court throughout the trial with great dignity and courage. Sadly on 18^th January 2008, Mr Manning also died. His children have good cause to take great pride in his bravery and commitment to maintaining this action at a time when his own death was imminent and his health was rapidly deteriorating.

This case turns on the conduct of Mrs Manning’s medical care between the radiation treatment in early 1994 following the first diagnosis of SQC in late 1993 and the diagnosis of recurrent spindle-cell or sarcomatoid carcinoma in September 2001. Between those dates she was reviewed on a large number of occasions both at the Marsden and at Kings by Professor Langdon who was based at Kings and Dr Henk, an oncologist based at The Marsden, who ran a joint practice from both hospitals supervising the care of cancer patients. In that period of nearly eight years seven biopsies were performed on her tongue by Professor Langdon, which were the subject of biopsy reports prepared in one instance by Professor Johnson, then the head of the Oral Pathology Department at Kings and in all the others by Dr Harrison. The principal purpose of the biopsies was to investigate whether there had been a recurrence of the original SQC. They were performed on 6 May 1994, 28 July 1995, 14 September 1995, 2 December 1996, 26 February 2001, 19 June 2001 and 7 August 2001.The latter was reported by Professor Johnson, the others by Dr Harrison. All the biopsy reports were negative. In fact, as was admitted by the Defendants who are the Trust responsible for the clinical staff at Kings, the three biopsies performed in February, June and August 2001 contained evidence of Spindle Cell Carcinoma (“SPCC”), which is a well known variant of SQC and Dr Harrison was negligent in failing to diagnose it as such in the February and June 2001 reports and Professor Johnson was negligent in failing to diagnose it as such in the August 2001 report.

The allegations of negligence in this case fall into three categories:

allegations that Dr Harrison and Professor Johnson negligently failed to diagnose malignant SPCC in their reports on the February, June and August 2001 biopsies.

allegations that Dr Harrison was negligent in his reporting of the September 1995 and December 1996 biopsies; and

allegations that Professor Langdon was negligent (a) in December 1996 in failing to take a biopsy of “sufficient depth/and or from the posterior tongue”, failing to carry out further imaging by means of MRI scans or otherwise and failing to refer Mrs Manning to a pathologist sufficiently experienced and specialist in head and neck cancers, (b) in January and February 2001 in failing to have any sufficient regard to his clinical suspicion of recurrence and to Mrs Manning’s complaint of pain to her ear and failing to carry out an examination under anaesthesia (EUA) as recommended by Dr Henk and (c) in May 2001 in failing to perform a further biopsy but instead referring her for hyperbaric oxygen treatment when he knew or ought too have known that such treatment was likely to oxygenate and increase the growth of any tumour.

By far the most time at trial was taken up with an examination of the second set of allegations. The reasons can be shortly stated.

As to the third category, the allegations against Professor Langdon, although not formally abandoned these were not pressed by Mr Grace Q.C. who appeared on behalf of the Claimant, with any great vigour. Since it was Mr Manning’s case that the biopsy reports submitted by Dr Harrison and Professor Johnson were fundamentally flawed and conveyed a misleading and false sense of the absence of any features suspicious of malignancy, Mr Grace QC accepted in opening that it was hard not to have a certain sympathy with Professor Langdon in being guided by those reports.

As to the first category, the admitted negligent misreporting of the three biopsies in February, June and August 2001, any claim for substantial damages was faced with the insuperable obstacle of the decision of the House of Lords in Gregg v Scott [2005] Lloyd’s Law Reports HL 130. In that case the House of Lords held that it is not possible in a clinical negligence case to recover damages for a percentage reduction in the prospects of survival caused by the defendant’s negligence if those prospects had never been more than 50%. The reason in short is that in such circumstances the claimant cannot discharge the burden of proving that on the balance of probabilities the losses consequent on the death of the victim of the negligence were caused by the negligence and would not have occurred but for that negligence. As a result it dismissed an appeal against a dismissal by the Court of Appeal of an appeal against the dismissal by the trial judge of a claim for damages by reason of the reduction from 42% to 25% in the chances of the Claimant’s survival caused by a nine month delay in diagnosing cancer due to the defendant doctor’s negligent misdiagnosis. In this case it was accepted by Mr Manning that if his wife’s SPCC had been properly diagnosed in February 2001,as the defendants accepted it should have been, instead of September 2001 her chances of survival would have been less than 50%. Mr. Brown, the expert surgeon who gave evidence for Mr Manning, put the chances at around 35%.It was thus accepted by Mr Grace QC that the case falls squarely within the ratio of Greg v Scott with the result that the damages recoverable as a result of the admitted negligence in 2001 are confined principally to damages for pain and suffering. As appears below that pain and suffering, both physical and mental, was quite appalling and Mrs Manning was, as the Defendants accept, entitled to be compensated for it. But such is the law in this area that the scale of those damages is but a fraction of what she (or technically Mr Manning on behalf of her estate and her dependents) would be able to recover if it could be proved that but for a delay in diagnosis caused by a negligent biopsy report she would on the balance of probabilities have survived.

It was for that reason that in order to recover substantial damages it would be necessary for Mr Manning to make good the second category of allegations in relation to the 1995 and/or 1996 biopsy reports and prove on the balance of probabilities both that Dr Harrison was negligent in his reporting of the biopsies and that but for his negligence the cancer which was diagnosed in 2001 would have been diagnosed in 1995 or 1996 and successfully removed by surgery with the result that Mrs Manning would have survived.

When the trial opened the Defendants’ position in relation to the September 1995 and December 1996 biopsy reports was that even if (a) Mrs Manning did have cancer in September 1995 and/or December 1996 and (b) that cancer would have been revealed at the time but for Dr Harrison’s alleged negligence(both of which hypotheses were vehemently denied) the salvage surgery which the parties agreed she would in such circumstances have undergone would not, on the balance of probabilities, have led to her survival. This position was maintained right up until a very late stage of the trial, at which point it was finally conceded by Ms Mishcon, who appeared on behalf of the Defendants, that on the balance of probabilities Mrs Manning would have survived if she had undergone salvage surgery in September 1995 or December 1996 ,always assuming, which was still vehemently denied, that cancer was present on either or both of those dates.

As a result by the end of the trial the central dispute between the parties on liability concentrated on the second set of allegations and in particular on two main issues : (1) Was there a breach of duty of care on the part of Dr Harrison in relation to the 1995 and/or 1996 biopsies and (2) if there had been no breach of duty of care would Mrs Manning have survived? In the light of the Defendants’ concession referred to in the previous paragraph, this second question of causation turned on two subsidiary questions (i) Would a proper exercise of care by Dr Harrison in September 1995 and/or December 1996 have led to a further biopsy and (ii) if so would such a biopsy have disclosed cancer? In short was the cancer which it is admitted was visible in the 2001 biopsies already present, albeit undetected by Dr Harrison, in 1995 and/or 1996?

Both these issues were hotly contested and an enormous volume of evidence and submissions was devoted to them on both sides. The first issue involved an examination and assessment of the relevant standards applicable to the preparation of biopsy histopathology reports in 1995 and 1996 and whether Dr Harrison did or not fall short of them. This in turn involved both general questions as to the minimum standards which would have been met by a reasonably competent oral pathologist in those years and immensely detailed discussion as to the contents of the slides taken from the biopsies both at the time and subsequently for the purposes of this trial. That discussion was complemented by expert evidence from three consultant pathologists, two for the Claimant and one for the Defendants, which included their assessment of photographs prepared by two of them of particular fields within not only the September 1995 and December 1996 biopsies but also by way of comparison the 2001 and 2002 biopsies.

On the second issue, which was a causation issue, the answer to the first question, namely would a proper exercise of care by Dr Harrison in September 1995 and/or December 1996 have led to a further biopsy is integrally bound up with the detail of the respects in which, if any, Dr Harrison was negligent as will become apparent from a review of the evidence and submissions on the issue of negligence. The answer to the second question was approached by both parties from two distinct vantage points. First there was again an enormous volume of evidence and submissions as to what, with the benefit of hindsight (a tool which of necessity could not be deployed in answering the question of whether Dr Harrison was negligent) can be deduced from an examination of the biopsies, the slides and the photographs. Second there was a theoretical analysis as a matter of oncology and clinical observation of Mrs Manning’s symptoms over an eight year period of the inherent probabilities or improbabilities of cancer having been present in September 1995 and/or 1996. On this front a fundamental difference between the parties and their experts lay in their answer to the question whether the admitted tumour which was present and visible in all four of the 2001 biopsies was a new radiogenic primary cancer, as contended by the Defendants, or a recurrence or persistence (albeit this time in the form of SPCC) of the original SQC which had been treated by radiation in 1994,as contended by Mr Manning. The significance of this debate lay in the fact that if the Defendants are right and there was no cancer present in 1995 and/or 1996 it appeared to be common ground that the 2001 SPCC must have been a new primary. Conversely and arguing backwards from 2001 if the 2001 cancer was a new radiogenic primary that argues strongly against there having been cancer present in 1995 and/or 1996.If on the other hand the 2001 SPCC was not a new primary but rather a recurrence or persistence of the original 1993 cancer that would support the conclusion that the 2001 cancer was a recurrence or persistence of the original 1993 SQC which was present but undetected by Dr Harrison in December 1996 and/or September 1995.

I was told that there are some 22 consultant oral pathologists practising in England and Wales, of whom no fewer than 5 gave evidence at the trial. In addition to Dr Harrison and Professor Johnson who gave factual evidence about their involvement in the biopsy reports there were three pathology experts, one for the Defendants and two for Mr Manning, who gave expert evidence on both main liability issues namely (i) what should a reasonably competent pathologist in the position of Dr Harrison have done in September 1995 and December 2006 and (ii) on the balance of probabilities was there cancer present on either or both those occasions? On the latter issue there was a remarkable degree of divergence between the experts for the two sides. The experts for Mr Manning, Professor Sloan and Dr Woolgar, were adamant, notwithstanding prolonged and hostile cross examination that it was very likely that there was cancer present on both occasions.

For the Defendants Professor Speight was adamant that it was very unlikely that cancer was present. To this stark division of expert opinion there was added a barely less strongly held opposition of views formed by the two oral surgery experts called by the parties, Mr Brown for Mr Manning and Mr Watt Smith for the Defendants and the two oncology experts, Dr Plowman for Mr Manning and Dr Barley for the Defendants. Although the surgeons were called principally to deal with the issue of whether Mrs Manning had a greater than 50% chance of surviving salvage surgery in 1995 and/or 1996 if it had been undertaken(the issue on which as mentioned above the Defendants conceded near the end of the trial that she did) they also gave evidence on whether in their view there was cancer present in 1995 and/or 1996, Mr Brown being strongly of the view that there was and Mr Watt Smith strongly of the view that there was not. More importantly the oncologists were equally divided, Dr Plowman being strongly of the view that there was and Dr Barley strongly of the view that there was not.

It is necessary in order to see the allegations of negligence and causation in context first to set the scene by setting out a factual narrative of the development of Mrs Manning’s symptoms and her medical treatment between the first diagnosis of her SQC in December 1993 and her death in May 2002. In 1993 Mrs Manning developed an ulcer on the left side of her tongue which did not heal for some six months. She was seen Mr Brian O’Riordan, a consultant maxillofacial surgeon who performed a biopsy which revealed, according to the pathology report prepared by Dr Geoffrey Farrer-Brown at the Harley Street Clinic, “a moderately to poorly differentiated squamous cell carcinoma..” The report stated: “There is focal ulceration and tumour is invading deeply into muscle. There is moderate chronic inflammation with occasional foreign body giant cells adjacent.”

SQC of the tongue is a comparatively rare form of cancer and according to Dr Woolgar it is exceptional and highly unusual for someone under the age of 40 to develop any kind of tongue cancer. Mr O’Riordan referred Mrs Manning to Professor Langdon because of his special interest in head and neck cancer. Professor Langdon saw Mrs Manning on 9 December 1993. In evidence Professor Langdon said : “I saw Mrs Manning for the first time on 9 December 1993, when she gave a six month history of a non-healing ulcer on the left side of her tongue. She had no obvious risk factors – smoking or excessive alcohol consumption. Her medical history revealed that she was being treated at the Royal Brompton Hospital for severe sarcoid that had first manifested itself as a loss of visual acuity. She had experienced two retinal detachments as a result of this. She had also received a number of courses of steroids for her sarcoid during the preceding three years. On examination , she had an ulcer on the left lateral border of her tongue measuring 2.5 x 1.0 centimetres. Clinically there were no enlarged lymph nodes in her neck. I arranged for Mrs Manning to have an urgent CT scan and to see Dr JM Henk as an emergency at the Royal Marsden Hospital. In 1993 all my head and neck patients were being seen in joint clinics with Dr Henk, Consultant Clinical Oncologist, at the Royal Marsden Hospital. We held regular joint clinics together either at the Royal Marsden Hospital or at King’s College Hospital.”

Dr Henk saw Mrs Manning in his clinic on 21 December 1993. On examination he saw an ulcerated lesion on the left lateral border of the tongue which measured 3.5 cms by 1 cm. In evidence he described it as a T2NO carcinoma. (This is corroborated by the reference in Dr Harrison’s biopsy report dated 6 May 1994(as to which see below) under the heading clinical: “T2 squamous cell carcinoma”). The tongue was fully mobile and there was no extension to the floor of the mouth .The neck was clinically clear.

In conjunction with Professor Langdon Dr Henk decided to treat Mrs Manning’s SQC by radiotherapy, according to Professor Langdon because of her age (she was then 35) and according to Dr Henk because their experience at the time at The Marsden and Kings was that radiotherapy (“RT”) had the same cure rate as surgery but caused less disability. The radiation treatment took the form of external beam radiotherapy to her tongue and left side of her neck in January 1994 followed by brachytherapy (“BT”) by means of the implantation of iridium wires in her tongue in February 1994. This was carried out at the Marsden by Dr Henk to whom she had been referred by Professor Langdon. The evidence at trial was that subsequent experience of the adverse effects of radiation treatment, particularly the high dose involved in brachytherapy, has resulted in it being largely discontinued and replaced by surgery as the preferred treatment for SQC with the consequence that the pool of data on the effects of radiation and brachytherapy and the patterns of recurrence and subsequent clinical history is even more limited than would in any event have been the case given the comparative rareness of this particular form of cancer.

On 10 March 1994 she was seen with Professor Langdon by Dr Henk who recorded in his notes: “Tongue well healed but still complaining bitterly of a tender spot, which she says is in the left side of her throat. In fact the base of tongue just behind the volate papillae on the left side is very tender.” On 7 April 1994 she was seen by Dr Henk’s team. The notes included the observations: “ Feeling much better. Tongue only slightly sore. On examination there is still an area of about 1 cm in diameter which is not quite fully epithelialised. No lymph nodes palpable. See in one month.”

According to Dr Henk Mrs Manning had a more severe than normal reaction to RT and continued to complain of pain in the tongue for several months afterwards. According to Professor Langdon she continued to improve until 5 May 1994 when she presented with an indurated ulcer at the site of the original cancer. On that day Mrs Manning was seen by Dr Henk. The notes record: “ Says the tongue has been a little sore for the past week. On examination there is a yellowish looking ulcer just under a centimetre in diameter right in the middle of the high dose volume. The edge all round is quite indurated and I am suspicious that there is a recurrence here. I have indicated to Mrs Manning that there is a little unhealed area about which I am not completely happy and advise a biopsy. Letter.” (Emphasis added.). In the letter to Professor Langdon referred to in the notes Dr Henk set out his findings and wrote: “I am not particularly happy about this and think that she ought to have a biopsy at this stage to exclude recurrence. I would be grateful if you would see her again before the next joint clinic.”(emphasis added). Professor Langdon saw her the following day at Kings where he performed the first of the biopsies he was to carry out over the ensuing 7 years. His notes record: “indolent non-healing ulcer. L[eft] lat[eral] tongue.10 x 5 mm, Neck clear. ?indurated margin; performs biopsy of ulcer and margin”.

In his report dated 9 May 1994, the first of the pathology reports prepared by Dr Harrison on those biopsies, under the heading “Clinical” Dr Harrison referred to the history of “ T2 SQC lateral border of tongue. Radiotherapy” and then included the expression: “? Residual unhealing ulcer-indurated margin.? Residual squamous cell carcinoma”. The latter expression was what was described in evidence as a differential diagnosis, which was explained to mean an indication given by the surgeon requesting the pathology report to the pathologist preparing it that the patient had had SQC and that one of the possibilities which the surgeon was asking the pathologist to consider, investigate and if appropriate exclude was a recurrence of the SQC. The former referred to the alternative possibility identified by Professor Langdon that the clinical symptoms were the manifestation of a residual ulcer which was not healing. It is pertinent to observe that these two possibilities and the question in each case which was right lay at the heart of all the subsequent biopsies and pathology reports which give rise to the allegations of negligence against Dr Harrison and Professor Johnson. Under Macro Dr Harrison recorded the biopsy sample as being: “Wedge of pale grey mucosa of greatest dimension 0.8cm” and under Micro (in effect his conclusions) he reported : “ Sections show part of an inflamed chronic non-specific ulcer and adjacent mucosa without evidence of neoplasia.”

On 8 June 1994 Mrs Manning was seen by Dr Henk in his clinic. His notes record inter alia : “The biopsy was negative. The tongue is much better today than when I last saw it, with only a small shallow clean ulcer, less indurated and much more palpable.”

Despite the allaying of Dr Henk’s suspicion of recurrence by the May biopsy report and no doubt because of the established risk of recurrence of SQC in the tongue following RT and BT( Dr Plowman, the expert oncologist called on behalf of Mr Manning, said that there is a 15-20% chance that not all the cancerous cells will be killed by the RT and BT and Professor Langdon said in evidence that “something like a quarter of all mouth cancers recur after treatment”) ,Mrs Manning continued to be reviewed regularly approximately once a month as an outpatient by Professor Langdon and Dr Henk at their joint clinics at The Marsden. Thus Dr Henk’s notes record on 20 July 1994: “no evidence of local recurrence”, on 10 August 1994 No palpable tumour. The rest of the oral cavity is normal. No lymph nodes palpable.” , on 21 September 1994 : “ no sign of recurrence”, on 2 November 1994 : “She is extremely well. No nodes palpable. There are radiation changes over lateral aspect of the left tongue. No evidence of recurrence” and on 14 December 1994. “Well. There is no sign of recurrence, no nodes palpable. See in 3 months time.” (Emphasis in each case added). On the same date there is another entry in the notes of Dr Henk’s clinic: “Seen in the joint clinic with Professor Langdon. Jane is well, she is getting some soreness of the tongue which Professor Langdon thinks is probably due to her wisdom tooth rubbing…..On examination there is telangiectasia over the treated area consistent with radiation changes, no other abnormalities and nothing to feel on palpation. There are no neck nodes palpable. Review in 3 months time.”

In June 1994 Mrs Manning had complained of a feeling of electric shocks in the bottom of her back when she bent her neck forward. These were referred to as L’Hermitte phenomenon in the December 1994 clinical notes and recorded as still troubling Mrs Manning. She was referred to Dr Moore for an MRI scan which was performed on 21 January 1995. This was reported as “ essentially normal…. no mass can be seen within the tongue and there is no pathological nodal enlargement”.

On 23 February 1995 Mrs Manning was reviewed by Dr Henk whose locum registrar referred to the MRI scan (in a letter dated 23 February 1995 copied to Professor Langdon) and reported that Dr Henk “reassured [her] that we see no connection between her tongue cancer and this abnormal region in the right parotid. We feel that it is more likely to be related to her old sarcoidosis. For follow up clinic as arranged.”

On 28 July 1995 Mrs Manning was seen as an emergency by Professor Langdon at Kings. In a letter to Dr Henk dated 2 August 1995 Professor Langdon reported that she had “had a period of ten days discomfort on the left side of her mouth, with severe pain and a bad taste for three days. Clinically the oral mucosa on the left side of her tongue left lower alveolus and left buccal mucosa was red and atrophic; but worryingly there was a 10 mm exophytic ulcer on the lateral border of her tongue, at the site of the original primary. The base was necrotic and the surrounding area was indurated.I performed an immediate incisional biopsy ….Although I had little doubt clinically that this represented local recurrence, the pathology report has shown that it is a simple trophic ulcer with no evidence of any malignancy. When I saw Jane yesterday the area was already improved and she will be seeing us at the next clinic at The Royal Marsden in September.” (emphasis added).

The pathology report referred to in Professor Langdon’s letter was requested by him in a Request for Laboratory Examination dated 28 July 1995 .Under clinical details including site size and duration of lesion he entered : “Exophytic indurated ulcer at site of previous1 [which I take to be shorthand for primary or original] SCC [which I take to be shorthand for squamous cell carcinoma]-treated with iridium implants.” Under differential diagnosis he entered: “Rec[i.e recurrent] SCC [i.e squamous cell carcinoma]/trophic ulcer.” Professor Langdon confirmed in evidence in chief that this meant that he considered either to be a possibility. The reason he considered SQC to be a possibility was that the clinical features on this occasion were somewhat different to those of the previous biopsy in May 1994, in particular because the ulcer was elevated and the margins were raised up which he said can be a classical sign of a cancerous ulcer and the ulcer was indurated on palpation which is one of the clinical indications of cancer.- The Request recorded that the date of her next appointment was 1 August-i.e four days later.

The report itself was prepared by Professor Johnson and dated 31 July 1995.Under clinical the report recorded: “exophytic, indurated ulcer at site of previous 1 squamous cell carcinoma-treated with iridium implants. Non-smoker. Non-drinker. Differential diagnosis: Recurrent squamous cell carcinoma/trophic ulcer.” (Emphasis added). Under Macro it recorded: “As yet unfixed. For overnight fixation on machine. Thick wedge of mucosa 9x5x4mm deep. Divided in long axis. Embed both halves together on cut surface.” Under micro it recorded : “Thick strip of tongue, substantially normal over much of its length, but with a large non-specific ulcer at one end. There is a substantial thickness of chronically inflamed granulation tissue and a fibrino-purulent membrane on the surface.

On 1^st August Professor Langdon saw Mrs Manning and reassured her that the biopsy was negative for tumour recurrence with the result of the biopsy report and recorded that she was reassured.

On 30 August 1995 he saw her again and recorded: “3 weeks of severe pain in left tongue; “burst” 2 weeks ago; now more comfortable. exophytic necrotic tissue at [original] site”. Professor Langdon in his witness statement(which he adopted as part of his evidence in chief) said he interpreted this as having been a superficial infection following the biopsy of 28^th July 1995 which had discharged spontaneously.

On 13 September 1995 Professor Langdon saw Mrs Manning again and a junior doctor in his team Dr Taylor recorded in his notes: “Seen by Professor Langdon: tongue still painful ++;o[n]e[xamination] exophytic mass at left lateral tongue, related to lower left 7 tooth ;fibrionous surface. neck clear. T[o] C[ome] I[n} tomorrow for excision biopsy of exophytic mass … bite guard to keep tongue away from lower left tooth. Refer to Dr Henk 20/9/95”.In his witness statement Professor Langdon said of this consultation: “The biopsy site remained unhealed and when I saw Mrs Manning on 13 September 1995 I noted an exophytic mass at the same site related to the lower left second molar tooth and clinically I was concerned that she might have recurrent cancer. Following discussion with Mrs Manning and her husband I performed a wide excision of the area and impressions were taken for the construction of a bite guard to protect the area from irritation by the molar tooth. The biopsy was reported as “radiation ulcer. Evidence of malignancy is not seen.” I discussed with Professor Johnson the possibility that the exophytic lesion might be a manifestation of her sarcoid.” In his witness statement, adopted by him as part of his evidence in chief, Dr Henk said of this consultation: “ In late 1995 Mrs Manning developed a very odd looking soft cauliflower-like mass on the left side of her tongue at the site of the original carcinoma. I saw her at one of the joint clinics at King’s College Hospital. I can still recall seeing the mass on the tongue, in view of its unusual appearance. I thought that it did not have the typical features of recurrent carcinoma and could be some sort of granulomatous reaction, perhaps related to her sarcoidosis. Professor Langdon excised the lump and histology showed no evidence of tumour. Subsequently her tongue healed.”

“I saw Mrs Manning regularly over the following five years. In December 1996 Professor Langdon excised a small fibrous nodule, which showed no evidence of malignancy. Otherwise during this period her tongue remained healed with no sign of any abnormality other than the expected slight radiation telangectasia and scarring. I refer to Attachment A”.

In fact it appears that the biopsy was performed not by Professor Langdon but by Mr Taylor, a junior member of his surgical team, on 14 September. The Request for Laboratory Examination recorded under Clinical Details: “Exophytic Lesion. Left Lateral border of tongue present since mid July.Local Recurrence? H[istory of] SCC 1994. Radiotherapy.” (Emphasis added).The operation sheet recording the biopsy described it as an “Excision biopsy. Exophytic mass. Lesion L[eft] lateral border of tongue”.

On 19 September 1995 Dr Harrison wrote his pathology report on the biopsy taken on 13 September. It is the first of the pathology reports which are the subject of the second category of negligence allegations. It reads as follows:

The next day on 20^th September 1995 Mrs Manning was seen by Professor Langdon and Dr Henk at the Marsden clinic. This was a week after the biopsy. Professor Langdon’s notes record: “Path[ology]report-no malignancy. O[n] e[xamination] Healing painful.?? Sarcoid in tongue-discuss with NWJ[Professor Johnson].Review[in 1 month]”. In a letter to Mrs Manning’s GP the same day Professor Langdon reported on his review of Mrs Manning that day as follows: “Mrs Manning [sic] an aggressive-looking exophytic ulcer on the left side of her tongue at the original site of the primary carcinoma that we treated in December 1993. An excision biopsy of this ulcer shows only the effects of the previous radiation, with absolutely no evidence of malignancy whatsoever. We have reassured Mrs Manning accordingly, but of course will keep a very close eye on her in the ensuing months.”(emphasis added).

On 17 (or possibly 18) October 1995 Mrs Manning was reviewed by Professor Langdon. His notes record: “Tongue healed!…neck clear.” And in a letter to her GP of the same date he wrote: “We reviewed Mrs Manning on the head and neck clinic today. We were all very relieved to see that the ulcer on the left side of Jane’s tongue has now completely healed. There is no sign of any recurrence of her carcinoma, either in her mouth or in her neck. We will continue to monitor her closely at monthly intervals.”

In a letter to Professor Johnson also of 18 October 1995 Professor Langdon asked him to review Mrs Manning’s histology. He wrote: “….Jane’s medical history is very interesting in that she has had an aggressive sarcoid for some years, particularly involving her eyes, and she is now visually impaired as a result of this. Since her original treatment she has had a number of false alarms with exophytic ulcers arising in the site of the primary tumour. On each occasion, these have been diagnosis[sic]as non-specific ulcers(path reports 324/94.363/95,457/95).Neither Mike Henk or I have ever seen such florid, malignant-looking ulcers following iridium implants. There has been some suggestion that patients with sarcoid reactivating at the same site where they subsequently develop carcinomas. In view of the very strange appearance of these tongue lesions, I wonder if you would review the sections to see whether there is any possibility of such an association in this case. When we saw Jane yesterday, we were all very relieved to see that the latest ulcer had completely healed.”

In his witness statement Professor Langdon referred to Mrs Manning having been seen at the joint clinic at King’s College Hospital on 8 October 1995, when the area had completely healed, but this appears to be incorrect as appears from the references to ‘today’ and ‘yesterday’ in the documents quoted in the previous paragraphs. At trial it appeared that the explanation for the error may lie in the obliteration of the ‘1’ before the ‘8’ in ‘18 October’ in Professor Langdon’s clinical notes referred to in paragraph 30 above. As appears below the identity of the date is potentially relevant to the issue of causation on one of the particulars of negligence and in particular to the question whether Professor Langdon would have carried out a second biopsy if Dr Harrison had recommended that one should be done if the lesion did not heal.

In his witness statement, which he adopted as part of his evidence in chief Mr Manning, who was a practising dentist, gave a description of the lesion which was the subject of the 13 September 1995 biopsy in the course of summarising his wife’s condition between the initial RT and BT. He described it as a cauliflower-like florid, exophytic growth: “After the radiotherapy in 1994 Jane was in severe pain. She had lots of mucous and a distressing cough. She could not look after the children on her own and we had to engage a nanny. By May 1994, Jane had developed an ulcer in the same area of her tongue as the original tumour. It was excised and biopsied but the area remained very painful. From the middle of 1994 until early 1997, Jane suffered repeated recurrences of the ulcer in the same place. I think that on each occasion before the ulcer became obvious, she would sense that something was not right. I remember clearly that we went to America at some time between the two biopsies in July and September 1995. I was attending a dental course and Jane accompanied me. I remember that at that time she had a cauliflower-like growth on her tongue in the area of the July biopsy. It did not concern me particularly because we had been told that the biopsy was completely clear. I thought the growth must be the result of aberrant healing of radiated tissue. When we returned to England from that dental course in America, Jane had to go back to the hospital. There was no question about this, she could not leave her tongue as it was. Whilst the other ulcers that developed on Jane’s tongue could be described as indurated – which I take to mean like an indentation – this one was actually a florid, exophytic growth. The other ulcers she had were not visible if you looked casually into Jane’s mouth. This one was patently obvious. Jane was admitted to King’s College Hospital, the growth was removed and again we were reassured that the biopsy showed nothing to worry about. Jane’s tongue was always extremely painful after it had been biopsied. At some times the ulcers were also extremely painful; at other times they were more of a discomfort. They were always very distressing.”

By a letter dated 6^th November 1995 Professor Johnson reported to Professor Langdon on the results of the review which he had been asked to carry out. Referring to Doctor Harrison’s biopsy report of 19 September 1995, he said: “Several pieces of tissue were submitted in the same container from a biopsy taken on 14^th September. Again, on reviewing these, there is little to add. The area of ulceration is larger than before with a more extensive but feeble granulation tissue response and a widespread mixed acute chronic inflammatory infiltrate. Radiation-damaged fibroblasts are apparent as is endarteritis obliterans and the epithelium at the margins of the ulcer is somewhat atrophic. There is there no granulomatous or sarcoid reaction….I cannot comment on local irritating factors but the underlying pathogenesis would seem to involve radiation damage and reduce healing potential. I am not familiar with the reported association with sarcoid- of which there is no evidence here- but would be happy to read around the subject if you would like that.”

Professor Johnson commented on Doctor Harrison’s biopsy report of 9 May 1994: “ I concur with John Harrison’s report on 324/94. Given the subsequent clinical history I doubt if much would be gained by cutting serial sections or levels throughout the block. There is certainly no evidence of malignancy here. There is mild dysplasia of the adjacent epithelium explicable on the basis of the chronic inflammation associated with the ulcer…. There is considerable disruption of superficial striated muscle fibres and their replacement with fibrous tissue and considerable intimal thickening of mucosal blood vessels consistent with radiation change. There are no giant cell granulomata suggestive of sarcoid.” Referring to his own biopsy report dated 31 July 1995 (363/95) Professor Johnson wrote “I have little to add on reviewing the slides. There is a component of acute inflammation throughout the laminapropria, not surprising in view of the size of the ulcer and the continued acute insult. Radiation changes less marked than the previous biopsy. Once again there is no suggestion of sarcoid change.” (Emphasis added). No allegations of negligence are made against Professor Johnson in the Amended Particulars of Claim arising out of this letter.

In his witness statement which he adopted as part of his evidence in chief Professor Johnson said of this letter: “ I judged there to be no recurrent malignancy. I also did not believe that there was any need to request a deeper biopsy and/or repeat biopsy.”

On 22^nd November 1995 Mrs Manning was seen at Kings. The notes record L[eft] tongue healing well. One millimetre white patch… anterior to biopsy site at lower left 3 region. Query healing traumatic ulcer.

On 22^nd November 1995 Mrs Manning was seen by Professor Langdon. The notes record: “ Tongue soft and mobile. Neck clear. Small lesion breaking out to area of original cancer. In his witness statement Professor Langdon said that Mrs Manning developed another small ulcer on 22 November 1995 but this healed spontaneously.

On 17^th April 1996 Mrs Manning was seen at King’s. The notes record: “ No problems. On examination no sign of recurrence”. A letter to her GP reported: “ She denies any problems at the moment and I am pleased to report that there is no sign of local recurrence and her neck is clear.” On 8^th May 1996 she was seen at the Marsden by Professor Langdon and Doctor Henk who reported to her GP that “There is no sign of recurrence of the carcinoma of the tongue and we will review her again in the autumn.” On 9^th October 1996 she was seen at the Marsden by Doctor Henk who reported her GP that “That she remains well with no signs of recurrence of her carcinoma of the tongue and the neck is clear.”

On 19^th November 1996 Mrs Manning was seen at King’s as an emergency by Professor Langdon. The notes record: “ Worried re. lesion on tongue. Severe cold. Mouth breathing. L[eft] tongue sore. On examination fibrous nodule L[eft] ventral tongue at anterior margin of previous scar. 5 mm diameter. Neck clear. Looks innocent. In view of previous “ulcer” review at Marsden 11^th December.” In a letter on 25 November 1996 to Doctor Henk, Professor Langdon wrote: “Jane came to see me at King’s last week as an emergency. She had recently had a severe head cold and was mouth breathing. She also noted an area of soreness on the left side of her tongue. Clinically I detected a fibrous nodule 5mm in diameter on the left ventral aspect of her tongue at the anterior margin of the previous scar. The lesion was not ulcerated and was covered by a pale mucosa. It looked fairly innocent to me and in the light of our previous experience with Jane’s tongue I suggested that we watched it for a brief period and have asked her to come to our clinic at the Royal Marsden on 11 December.

On 2^nd December 1996 Professor Langdon saw Mrs Manning again. The notes record: “ Anxious ++. On examination no change-fibrous nodule at anterior margin of previous excision. Not ulcerated. Neck clear. L[ocal] A[anaesthetic] excision biopsy.” Professor Langdon then performed another excision biopsy.

The request for laboratory examination referred to the three previous biopsies of May 1994, July 1995 and September 1995. Under clinical details including site, size and duration of lesion it recorded: “SCC left lateral tongue. December 1993. Iridium wire implant. ?Rec [urrence] July 95: excised: radiation ulcer. Now three weeks tender nodule seven millimetres diameter at site of primary.

On 10^th December 1996 Doctor Harrison wrote his pathology report on Professor Langdon’s biopsy. It read as follows:

In his witness statement Professor Langdon said this about November 1996 and December 1996: “I saw Mrs Manning as an emergency at King’s College Hospital on 19 November 1996. She had found a small (5 mm) nodule on the left side of her tongue. Clinically, this looked entirely innocent and in view of her previous negative biopsies I advised a “watch and wait” policy but when I saw her again on 2 December 1996, there was no change. She was clearly worried and I performed another excision biopsy. Again I queried whether the lesion was a recurrent lesion or a sarcoid lesion. The biopsy was an excision biopsy which means that I excised the entire nodule with a small cuff of adjacent tissue. As the nodule was only 5mm in diameter, the biopsy specimen itself was small. As there was no induration (thickening of the underlying tissues) I did not incise deeply into the underlying muscle as I did not want to risk precipitating further radiation necrosis in the tongue. I did not biopsy any other areas of her tongue because her tongue had not changed over a period of time and clinically there were no abnormalities to suggest the presence of a cancer. Unnecessary surgery in previously irradiated tissue should be avoided as there is always the risk of delayed healing. This biopsy was again reported as “no evidence of malignancy”. After this appointment her follow-up reverted back to the clinics at the Royal Marsden Hospital.”

On 16^th January 1997 Mrs Manning was seen by Professor Langdon and Dr Henk at the Marsden in a letter to Mrs Manning’s GP Dr Henk wrote: “ There is no sign of recurrence of the carcinoma of the tongue and the neck remains clear. She will be reviewed again in three months time.”

Mrs Manning was then seen at the Marsden on 22^nd April 1997, 22^nd July 1997, and 29^th January 1998. On each occasion it was recorded that there was no sign of recurrence of the carcinoma of the tongue and her neck was normal to palpation/there were no lymph nodes palpable. In a letter dated 29 January 1998 to her GP from Dr Henk’s clinic, it was reported: “ She will be reviewed again in the combined clinic with Professor Langdon in 5 to 6 months time. She knows to come back earlier if problems arise.”

In July 1998 Mrs Manning was seen by Dr Mitchell at the Brompton who reported that she had a worsening lung function due to sarcoidosis for which he recommended treatment by steroids.

On 16 September 1998 she was seen by Professor Langdon at King’s. He reported to her GP: “From our point of view her tongue looks very healthy and there is no sign of any recurrence of the squamous cell carcinoma. Sadly as you know Jane’s sarcoid has recently undergone an exacerbation and she is being seen regularly at the Brompton Hospital regarding this. Her concern was that the doctors at the Brompton wanted to start her on systemic steroids and she was worried that this would increase the risk of her tongue cancer recurring. We have reassured her that this is not so and that it is more important for her sarcoid to be treated. We will see her again ourselves in 6 months time.” Mrs Manning was then treated for her sarcoidosis with steroids until November 2000.

On 2^nd July 1999 Mrs Manning was seen by Dr Henk at the Marsden. Dr Henk reported to Professor Langdon: “ Jane turned up to see me today. She said her appointments had got out of synch and she didn’t have an appointment made for either you or me. She told me that she’s moving to Devon tomorrow but her husband is keeping on his London practice so she can come up to London for continued follow-up. She is still under Dr Mitchell at the Brompton because her sarcoidosis is still active. On examination there is no sign of recurrence. There are no lymph nodes palpable. I have given her an appointment for my clinic in 6 months time so that she doesn’t get lost but if you would prefer it please get in touch with her and ask her to come to the joint clinic.”

On 17 December 1999 Dr Henk saw Mrs Manning at the Marsden and reported to her GP: “ She is keeping very well except that she is still on steroids for her sarcoidosis. There is no sign of recurrence of her carcinoma of the tongue and there are no lymph nodes palpable. I will see her again in 6 months time.”

On 15 June 2000 she was reviewed at Dr Henk’s clinic. It was reported to her GP: “ She remains well. There is no sign of recurrent carcinoma of the tongue and she had no cervical lymphadenopathy. She will be reviewed in clinic in 6 months time.”

On 15^th January 2001 Mrs Manning was seen at King’s by Professor Langdon at her request. The clinical notes record: “ Seen at request of patient. November 2000 following a long aircraft flight sore throughout site of RT left mouth.- speech affected. Partially settled after 3 weeks. Currently better but intermittently uncomfortable – sudden pain radiating to left ear. Occurs most days. Not related to eating. On examination scarring left lateral tongue ++. Tethered and indurated, no ulceration, telangiectasia ++ neck clear. Discuss with Mike Henk. Query review.”

In his witness statement Professor Langdon said of this consultation: “ She told me that during a long-haul flight in November 2000 her entire mouth on the left side became sore and this had affected her speech. The symptoms settled after 3 weeks but her tongue remained intermittently uncomfortable and she had sudden bouts of pain radiating to her left ear. On examination her tongue looked unchanged but as a precaution I asked Dr Henk to see her the following day at the Royal Marsden Hospital.”

She was seen the next day on 16^th January 2001 by Dr Henk at the Marsden. He reported to Professor Langdon: “ The appearance of the tongue is very much as I remember it from last year. The left lateral border is scarred and in particular there is some fibrosis extending into the floor of the mouth in the middle third. The tongue did not appear particularly tender and I could not elicit any ear pain from pressure in the scarred area. On mirror examination the larynx and hypopharynx looked completely normal. Jane says that the symptoms are actually getting better so I do not think that we need to intervene now. Obviously if the pain gets worse again she will need an examination under anaesthetic.”

On 22^nd January 2001 Mrs Manning wrote to Professor Langdon: “ I went to see Dr Henk and he was satisfied that there was nothing pathologically wrong which was very reassuring. He mentioned that there may be a link between my finishing a long course of steroids and my sore mouth. The pain I get has been quite debilitating but it comes and goes. Most times I have pain and I have found that Nurofen Plus is the only analgesic that helps. Any help on what may be the cause of the pain and how I should best cope with it would be gratefully received.”

Professor Langdon replied on 29^th January 2001: “ I had indeed spoken to Mike Henk who has since written to me formally. As you know we are both content that there is nothing in your tongue at the present time to cause us any concern regarding recurrence of your cancer. With regards to the pain you are experiencing this is essentially due to scarring around the nerve that supplies to the tongue and it is not uncommon for the pain to be referred to the ear. There is no magic treatment for this and if Nurofen is not entirely satisfactory there are a number of other treatments that we can try to see if it helps. I could either liaise with your medical practitioner in Devon or alternatively perhaps we should make an appointment for you to come up to one of my clinics at King’s and we can talk about possible treatments and start you off on some different tablets. In the long term I think you should let me see you once or twice a year on a formal basis. As you know Mike Henk retires some time this year and I think it is important that you should be seen on a regular basis. I will wait to hear from you to see what you think.”

On 13^th February 2001 Professor Langdon wrote to Mrs Manning’s new GP in Devon where she had by then moved. He wrote: “ …she has remained tumour free since [the beginning of 1994] although she has developed a number of ulcers at the primary site. We have of course biopsied these whenever they have occurred, but they have all proved to be trophic ulcers following her radiation with no evidence of malignant disease. Jane came to see me at her own request on 15 January this year as she was concerned that in recent weeks the primary site on her tongue had become painful once again. Apart from general soreness and burning at the site of the previous treatment she was also experiencing stabbing pains in her left ear. Clinically I could find nothing to be concerned about. There is certainly extensive scarring in the left side of her tongue, but there is no ulceration or other evidence of tumour recurrence. Her neck is also clinically clear of disease. I took the precaution of asking my colleague Dr Henk at the Marsden who had treated her original tumour to have a look at her and to confirm that there was nothing indicating an obvious recurrence. Clearly with Jane now living in Devon it’s difficult to organise regular follow ups. Jane would however like us to help with the pain, particularly the stabbing pains in her left ear. My treatment strategy would be to start her on a low dose of Tegretol, perhaps 200mg daily in total. Sometimes the lingual nerve does get incorporated into the scar tissue and produces stabbing pain referred to the ear. .. I would of course be happy to see Jane myself at any time when she wishes to come up to London but in the mean time I should be grateful if you would start her off with some medication.” (Emphasis added).

On 26^th February 2001 by arrangement Mrs Manning was reviewed by Professor Langdon at King’s. Professor Langdon’s notes record: “ Following discussion with GP Dr Steggles patient has been on Amitriptyline for 2 weeks – pain less severe – continue for further 4 weeks and reassess. If pain well controlled stay on Amitriptyline. On examination well localised nodule left lateral tongue adjacent to lower left [tooth]. No ulceration, discussion with patient and husband – for excision biopsy… wedge excision.”

A later entry in the notes apparently for the same day recorded: “ Pathology report – no evidence of malignancy. Patient informed. Review 6 months at King’s – patient will contact me re. convenient date.” In a letter dated 5^th March 2001 Professor Langdon wrote to Dr Steggles: “ As you know I arranged to see Jane again on 26^th January [an error for February]. The pain in her tongue was severe since starting a course of Amitriptyline which you kindly prescribed. Once again on clinical examination there was a well localised firm nodule in the left lateral margin of her tongue adjacent to the retained lower molar tooth on that side. There was no associated ulceration. However following a long discussion with herself and her husband I decided that excision biopsy of this nodule would be the only way to satisfy everybody’s worries. I performed the biopsy under local anaesthesia on 26^th January. I am pleased to report that as expected by Mike Henk and myself the pathology report on the nodule is of dense fibrous tissue representing post radiation fibrosis. There is no evidence of any tumour. I telephoned Jane at the end of last week and have arranged to see her in the summer for routine review. P.S. As her pain appears to be responding to Amitriptyline I would suggest that she continues with this for at least 6 months.”

The request for laboratory examination of the biopsy performed by Professor Langdon on 26^th February 2001 referred to the May 1994 and the two 1995 biopsies but not the 1996 biopsy. Under clinical details it recorded: “SCC left lateral tongue 1993. Treated iridium wires and external beam RT. Firm non-ulcerated nodule at site of [primary].” Under relevant habits it recorded: “ Sarcoid and intermittently on steroids.” The differential diagnosis was: “ Fibrosis, recurrence.”

Doctor Harrison’s pathology report on Professor Langdon’s biopsy dated 27^th February 2001 was in the following terms:”

On 30^th March 2001 Mrs Manning’s new GP in Devon, Dr Steggles, referred her to Mr Bridger a consultant ENT surgeon in Plymouth after reciting her medical history. He wrote: “ The additional problem started on Tuesday this week when she had a sudden quite significant bleed and when I cleaned away the remaining clot I discovered that there was 4mm diameter hole with some fairly foul necrotic material emanating from it. …her mouth is today looking very much better and cleaner and she certainly feels better. I have as you know discussed this at length with John Langdon and he has asked if she could be seen locally now that she is living here on a more permanent basis. As I shall be retiring today I am most grateful to you for continuing her care and perhaps as you did mention taking her on to the joint clinic.”

On 2^nd April 2001 Mrs Manning was seen by Mr Bridger. His notes record: “ December 1993 – squamous carcinoma left side tongue – given 80% chance cure. 7 years – no real problem – a bit dry. Oct 2000 left tongue sore – small lump – locally removed by John Langdon 26.1.01 histology = benign fibrous tissue. – hasn’t healed. Pain +++ - had 2 bleeds… On examination [diagram] induration hole into body of tongue. Nodes. Needs 1 MRI, 2 hyperbaric, 3 multidisciplinary appointment 4 get records 5 pain clinic.”

In a witness statement which was adduced by Mr Manning as evidence agreed by the defendants Mr Bridger stated: “ On presentation, Mrs Manning’s symptoms were highly suspicious. This development of pain, persistent and deteriorating, at the site of a previous cancer is not something that would, in my opinion, happen in somebody who is free of disease or getting better.

On 4^th April 2001 Mrs Manning was admitted to Plymouth Hospital for pain control. On 11^th April 2001 Mrs Manning was seen by Professor Langdon following a phone call from Dr Steggles. The notes record: “Acute bleed three weeks ago, seen by Plymouth head and neck clinic, told that there was massive tumour! Very distressed since. On examination necrotic cavity 1cm diameter at site of biopsy 26^th January [mistake for February] similar delayed healing…following previous biopsies. PAIN ++..pain not fully controlled…query hyperbaric O2”.

On the same day Professor Langdon wrote to Mr Bridger in these terms: “ I understand that Jane was recently referred to you by her GP Dr Steggles. She came to see me today somewhat distressed by your suggestion that she had active tongue cancer. I can fully appreciate you thinking this on examining her tongue for the first time. I thought that it might be useful for you to have a summary of her previous treatment….[referring to the biopsies in May 1994, July 1995 and September 1995]. Dr Henk and myself were very concerned at the florid appearance of these ulcers which on each occasion looked malignant. The pathology was reviewed independently and confirmed that no malignancy was present. In November 1996 she developed a fibrous nodule on the left ventral aspect of the tongue at the anterior margin of the previous excisions. In view of the previous experiences we elected to watch this area which remained static. .. In January this year Jane came to see me complaining of severe pain radiating to her left ear. This had started in November 2000. Clinically the appearance of her tongue had not changed remaining scarred and indurated with the nodule first noted in 1996 still present. Both Dr Henk and myself were content that she was tumour free and we felt that her pain was due to involvement of the lingual nerve in the scar tissue. However she was clearly very worried and on 26^th January I performed a very wide excision of the fibrous nodule. The pathology yet again was post radiation fibrosis with no evidence of recurrence. Unfortunately the biopsy site became infected and resulted in a secondary haemorrhage. The area has failed to heal to date and she now has severe local pain together with lingual nerve neuralgia…despite the appearance of her tongue, Dr Henk and I are happy that she is in fact tumour free. I have today referred her to Dr Philip Bryson for consideration of hyperbaric oxygen and to Dr Adrian Dashfield for the pain clinic.”

Mr Bridger in his witness statement said of this letter: “ I subsequently received, what I can only describe as an extremely patronising letter from Professor Langdon dated 11 April 2001, which read “She came to see me today somewhat distressed by your suggestion that she had active tongue cancer. I can fully appreciate you thinking this on examining her tongue for the first time. I thought that it might be useful for you to have a summary of her previous treatment.”… "despite the appearance of her tongue Dr Henk and I are happy that she is in fact tumour free." I was, in truth, completely astonished by the total arrogance of the letter. If I had received a letter from another specialist along the lines of the one which I wrote following Mrs Manning's visit to me, I would have thought ‘maybe I am missing something here and I had better look at this more carefully’. I thought that Professor Langdon’s suggestion that “Both Dr Henk and myself were content that she was tumour free and we felt that her pain was due to the involvement of the lingual nerve in the scar tissue” was absurd. I have had a special interest in cancer of the head and neck for 25 years and in all this time I have never known the development of severe pain due to the late involvement of the lingual nerve in benign scar tissue – I do not believe such a clinical picture exists. I felt Professor Langdon’s letter did not take my concerns seriously and that he would continue treating Mrs Manning in the same way that he had done in the past and ultimately Mrs Manning would suffer. I was certain he was wrong.”

On 12^th April 2001 Mrs Manning was seen at a pain clinic in Plymouth. Mr Taylor the Consultant in pain management wrote to Dr Steggles: “On examination she was obviously in some pain, I could find no external lymphadenopathy, tenderness or deformity. Her tongue is quite coated and she had some specks of candida on the right. There was deformity and a sinus hole at the base of the left side of the tongue with some slough. I do not know if this was the site of the biopsy and generally her pain is more posterior. I could find no abnormal neurological signs although she does feel the left side of her tongue has been numb following the initial radiotherapy treatment. Although there may be some neuropathic component to her pain I think she must have some recurrence of infection following the biopsy or recurrent disease…she intends to continue seeing Professor Langdon but I am not sure this is realistic if she continues to live in Devon and I am sure an assessment as proposed by Mr Bridger would be helpful together with an MRI scan. ..”

On 19^th April 2001 Mrs Manning was admitted as an in-patient to King’s by Professor Langdon. In a letter dated 2^nd May 2001 by Mr Heliotis a specialist registrar at King’s to the Department of Maxillofacial Surgery in Plymouth, Mr Heliotis wrote: “ …the primary reason for admission under Professor Langdon’s care this time was primarily to carry out some special investigations of the head and neck as she was getting pain from the ventral surface of the tongue radiating to the left ear hence causing some concern that there may still be tumour which for some bizarre reason we cannot diagnose histopathologically. In addition she needed her pain placed under control. This has been done by the pain team and you should get a copy of the medication we have discharged her on from the discharge letter. Unfortunately the MRI imaging of the neck and the PET scanning were not as helpful as we would have wished for. I personally spoke to Dr Kane, Consultant Radiologist who did the MRI and without the previous clinical history and the background to this patient by simply looking at the MRI scans she would have thought that the lesion in the tongue was indeed a tumour. However knowing that this was recently excised in February and also knowing that the area has received a considerable amount of radiotherapy and refuses to heal, this could also be a low grade inflammatory process as a result of the necrotic material around the tongue which is not healing and therefore causing the oedema which has picked up on the MRI. Also on the MRI scans there was no lymphadenopathy on the left side of her neck. There were two lymph nodes on the contra lateral side at round about the level 4 site. This could of course be as a result of the sarcoidosis. The PET scanning was after discussion with Dr Buxton a disappointment. As a result of the previous sarcoid the PET scan showed a massive uptake of isotope which is very diffused and Dr Buxton ruled this out as any chance of metastasis He was concerned about some mediastinal lymph node uptake which he could not be certain as to what the cause of that is, but again sarcoid could not be excluded. I discussed the results with Professor Langdon and following a very long discussion we decided that as the histopathology revealed no evidence of cancer and the MRI and PET scans were far from helpful, this lady would best be suitable in your hands for hyperbaric therapy. As I discussed with you on the phone and with Professor Langdon it would be suitable probably for several doses of hyperbaric oxygen therapy after which she could come back to us and if the necrotic area is well demarcated we could excise this and then she could undergo further treatment with hyperbaric oxygen. Speaking to her today on 1 May as she was not quite happy leaving because the pain is still not under control…I had spoken to Dr Mitchell her physician at the Brompton. I discussed the treatment option of hyper baric therapy and what complications it may have for her sarcoidosis but he quite adamantly said that there is no previous evidence that it can exacerbate the condition and in his opinion we should certainly go ahead with this treatment.” (Emphasis added).

In his witness statement Professor Langdon stated: “ The scans were initially reported as showing extensive tumour in the tongue and also pulmonary metastases, but this view changed after I discussed the clinical background with Dr Kane, Consultant Radiologist and Dr Buxton-Thomas, Consultant in Nuclear Medicine.”

On 24 April 2001 the report of a PET scan recorded that there was “Intense tracer uptake in the tongue and in the mid-zones of both lungs posteriorly. The conclusion was: “ The intense uptake in the tongue is consistent with the known lesion. The uptake in the lungs is suggestive of tumour metastases, with possible lymph nodes in the mediastinum…”

On 26^th April 2001 an MRI scan report stated: “…there is relatively well-defined increased signal intensity in the region of the known glossal ulcer. This abnormal signal extends to the floor of the mouth and indicates the presence of oedema within this region. .. I understand the patient has had a negative biopsy and PET scan. In view of these factors it is unlikely that the demonstrated oedema represents tumour and could represent ongoing inflammation related to radiation necrosis.” According to Dr Lewis-Jones, the Claimant’s expert consultant radiologist, the tumour as he described it shown on the MRI scan measured approximately 2.0 x 2.8 cms in diameter. The subsequent scan on 22^nd January 2002 showed the tumour to have increased in size to measure 6.5 x 5.0 cms in diameter. On that basis Dr Lewis-Jones estimated the volume of tumour to have almost quadrupled between those dates.

In his witness statement Professor Langdon stated: “ I recall going to the radiology department to speak to Dr Kane following receipt of the scans. We reviewed all the scans. Dr Kane’s initial view was that the MRI scan showed tumour but when I explained the clinical background it was decided that as there were no enlarged lymph nodes on the left side of the neck, the changes were compatible with the post-radiation changes and recent biopsies. That is, the changes resulted from inflammation and scarring rather than tumour recurrence. I also recall going to personally speak to Dr Buxton-Thomas to review all the scans. She felt that the previous extensive sarcoid accounted for the pulmonary changes on the PET scan and that the changes noted did not represent pulmonary metastases. She was convinced that the uptake was due to sarcoid. PET scan is not specific for malignancies. Many inflammatory lesions can be responsible for the increased uptake of the radioactive marker. In conjunction with the other findings it was thought that the uptake was due to infection and inflammation in the tongue and sarcoid deposits in the chest.

I also had a number of telephone discussions during 2001 with Dr Henk. These generally occurred at home in the evenings. I had worked with Dr Henk since 1977 and would often telephone him at home to discuss patients. I cannot recall the exact dates of the discussions, nor would I have made any notes. The discussions were based on the fact that as 2001 progressed the necrotic ulcer was getting bigger and my gut feeling was that it was a cancer. I asked Dr Henk during one discussion whether it was possible that the iridium wire transplant treatment could have caused that much change in the blood vessels to lead to the spreading of ischaemic necrosis. We also discussed future treatment options. During April 2001 I had heard from Dr Bryson who agreed that a course of hyperbaric oxygen treatment might be helpful and Mrs Manning underwent the treatment from 9 May 2001 to 11 June 2001. The referral for hyperbaric oxygen therapy was on the basis that all the evidence suggested that we were dealing with a necrotic non-healing ulcer resulting from severe post-radiation changes. Multiple biopsies had not only excluded the presence of malignancy, but had been reported as showing post-radiation changes. It was hoped that by increasing oxygenation of the tissues healing would be promoted.”

Between the 5^th and 15^th of May 2001 Mrs Manning was admitted to Plymouth Hospital for pain control. On 8^th May she began hyperbaric oxygen treatment in Plymouth. From 18^th May 2001 to 11^th June 2001 she continued daily hyperbaric oxygen treatment involving some 30 dives in all.

On 18^th June 2001 Professor Langdon arranged to admit Mrs Manning as an in-patient at King’s to reassess her tongue under a general anaesthetic before she was to undergo a further course of post-operative hyperbaric oxygen therapy. His findings were recorded as: “ Extensive… necrotic ulcer left tongue and floor of mouth. Induration.. of tongue extending well across midline to within 1 centimetre of right lateral border… No masses left and right neck.” In his witness statement Professor Langdon stated:” There was an extensive necrotic ulcer on the left side of the tongue with overhanging margins. There was extensive induration in her tongue which extended across the midline. Clinically her neck was free of masses. I was convinced that she had tumour recurrence and performed a further three biopsies from various sites around the margins of the ulcer. Once again the pathology report stated: “ Radiation ulceration without evidence of neoplasia or sarcoid.” During Mrs Manning’s admission she had a high ESR of 130 and also other changes suggesting a possible autoimmune disorder. I therefore arranged for a rheumatology opinion and carried out further investigations including blood cultures.”

The request for laboratory examination referred to three incisional biopsies. The previous biopsies referred to were those of May 1994, July 1995, September 1995 and February 2001. Again there was no reference to the December 1996 biopsy. Under clinical details it was recorded: “ SCC Granuloma/Arteritis/Sarcoid left lateral tongue December 1993. Treated by interstitial....and external beam radiotherapy. Now has chronic indurated non-healing ulcer. Clinically looks like recurrence. Sarcoid. The entry under other relevant habits was previous pulmonary and retinal sarcoid. The differential diagnosis was: “ Rec [urrent] SCC; granul(oma) : sarcoid.” At the bottom of the page the words ‘Urgent please’ were written in capital letters. (Emphasis added).

On 20^th June 2001 Dr Harrison presented his pathology report on the three incisional biopsies taken by Professor Langdon. The report was in the following terms:

On 28^th June 2001 Professor Langdon wrote to Dr Henk: “ I continue to be extremely worried about Jane Manning. You will recall that when we spoke 6 to 8 weeks ago I explained that following a further biopsy at the end of February this year the left lateral border of her tongue had necrosed quite extensively. I have arranged for her to have a course of hyperbaric oxygen therapy down at Derriford Hospital under the care of Philip Bryson. He gave her a preliminary course of 30 dives and then by agreement she came up to King’s to see me initially with a view that I would resect all the necrotic tissue on the lateral surface of her tongue. She was admitted last week and I was shocked to see that despite her hyperbaric oxygen treatment the necrosis had extended not only across to the midline of the tongue but deeply in the floor of her mouth. Under general anaesthetic I did a thorough EUA and undertook multiple geographical biopsies. The EUA showed an entirely soft neck with no lymphadenopathy whatsoever. Intra orally she now has a necrotic area on the left side of the tongue, this ulcer is undermined and it extends to the midline. The induration extends across the midline towards the right lateral margin. The necrotic ulcer also involves the floor of the mouth on the left and extends down to the maler hyoid muscle. All the geographical biopsies were once again negative and reported as showing radiation ulceration without evidence of neoplasia or sarcoid. When she was in hospital last week we noted that her ESR was 130 and undertook further additional investigations…. clearly she has some chronic inflammatory condition and I asked for a rheumatology opinion to see if perhaps she had an auto immune condition such as a vasculitis to account for the necrotic tissue. They felt that this was unlikely. Jane has now returned to Derriford for completion of her hyperbaric oxygen treatment with another 20 dives. I really am at a complete loss to know what to do with her. She has severe unremitting pain, for which she takes…Can you think of any explanation for what it going on? I am sure if you felt it would be helpful Jane would come up to London and see you once again.” (Emphasis added).

In his witness statement Professor Langdon stated: “ I also spoke on the telephone to Dr Mitchell and Professor DeBois at the Brompton who had treated Mrs Manning over the years for her sarcoid. They suggested that we should try treating her with a course of high-dose steroids in an attempt to suppress the fibrosis and necrosis in her tongue. At this time Mrs Manning was undergoing her post-operative hyperbaric treatment in Plymouth and I wrote to Dr Bryson asking him to start her steroid therapy.”

Between 3^rd of July and 3^rd August 2001 Mrs Manning had further daily hyperbaric oxygen treatment again amounting to some 30 dives.

On 16^th July 2001 she started on high-dose steroids.

On 20^th July 2001 Professor Johnson reported to Professor Langdon on the result of a review that Professor Langdon had asked him to carry out of the histopathology from 1993 to date. The review included the biopsies of May 1994, July 1995, September 1995, February 2001 and June 2001, but again apparently, not December 1996. Professor Johnson found no evidence of malignancy.

On 6^th August 2001 Mrs Langdon was readmitted to King’s. On the same day Professor Johnson circulated amongst an international group of oral pathologists particulars of Mrs Manning’s condition anonymously to try and obtain further expert opinion on the best treatment for Mrs Manning. His email stated: “ John Langdon has asked my advice on a patient of his- a young woman (born 1958) who had a squamous cell carcinoma of the tongue diagnosed in 1993 and treated by iridium implants and external beam to the upper neck. There has been no recurrence but the tongue has been almost continuously ulcerated since, and several biopsies performed. These all show non-specific features: no sign of neoplasm; there is endarteritis obliterans, radiation damage to fibroblasts and minimal wound healing. The angiogenesis is minimal and the inflammatory response beneath the ulcer non-specific. No vasculitis as such. No giant cells. A course of hyperbaric oxygen has not helped. Are either of you aware of any experimental treatments to promote wound healing (of soft connective tissues) by any cocktail of growth factors/cytokines? Do you know who I might approach to enquire further? There is the theoretical risk of activating latent neoplastic epithelium, but as she is a decade on I guess that is minimal. Needless to say her condition is very distressing and she is the wife of a dentist! Any thoughts would be welcome”.

Among the responses was one dated 22^nd August 2001 from Professor Mark Ferguson who suggested trying Recombinant Platelet Derived Growth Factor which was marketed as Regranex. The aim was to attempt to stimulate cells for healing. Professor Johnson provided this information to Professor Langdon who on 5^th September 2001 sought approval for use of Growth Factors in a letter to Dr Costello the Chairman of the King’s Drug and Therapeutics Committee. In the letter he referred to the BT and RT: “ Jane showed a good response to this treatment and the primary tumour resolved. However intermittently over the ensuing years Jane has represented with an indolent area of ulceration on the left lateral border of the tongue at the site of the primary tumour. Inevitably my first thought has always been that of tumour recurrence and she has undergone repeated biopsies over the years, all of which have been reported as radiation fibrosis, non-specific ulceration with no evidence of neoplasia. In March this year she presented with a florid exophytic ulcer again at the site of the primary carcinoma. Further biopsy again showed radiation fibrosis with no evidence of tumour. Notwithstanding this on the basis of the clinical appearance I admitted her to hospital for wide local excision of this ulcer. The definitive pathology report confirmed the incisional biopsy- radiation fibrosis with no evidence of neoplasia. Following this local excision Jane has developed a very nasty deep ulcer undermining the tongue, crossing the midline and extending down into the floor of the mouth. This ulcer is now 3cm x 2cm. Following intensive discussions with colleagues at the Brompton and at the Marsden we tried Jane first on high-dose systemic steroids with no effect and then we treated her with a concentrated course of hyperbaric oxygen 2 dives a day at 2.1 atmospheres. Again this manoeuvre was totally without benefit and indeed biopsy half way through the hyperbaric oxygen showed no evidence of neoangiogenesis! As you can imagine Jane has become very depressed and run-down. She has lost considerable weight and is now frankly cachectic. She has considerable pain and has had a period in a hospice in an attempt to obtain adequate pain control.” Professor Langdon then referred to the exchange about Regranex with Professor Ferguson: “ Following our helpful conversation yesterday I have since spoken to Brendan O’Sullivan and he is obtaining supplies for me to use on Jane as a named patient next week”. (Emphasis added).

On 7^th August Professor Langdon carried out an examination under anaesthetic. The operation sheet findings entry was: “ 1) Extensive ulcer destroying left lateral tongue and floor of mouth. Has now extended coronally across midline to divide anterior two-thirds of right tongue from posterior third. 2) Ulcer crater relatively clean (compared with previous examination under anaesthetic 19 June 2001) also ulcer is granulating and haemorrhaging….”.

On the same day Professor Langdon carried out a further biopsy. The request for laboratory examination referred to the June 2001 previous biopsy and the entry under clinical details was: “ Previous.. SCC tongue plus sarcoidosis. Non-healing ulcer left side of tongue. Several years (more than 5 years) last examination under anaesthetic on 19^th June. Previous biopsies show no recurrence. The differential diagnosis was:

On 9^th August 2001 Professor Johnson wrote a pathology report on Professor Langdon’s biopsy. It was in the following terms:

In his witness statement Professor Johnson stated: “ A biopsy for Mrs Manning fell to my duty roster on 9 August 2001. This was biopsy 500/01. I did not regard it as showing malignancy and saw no need to use immunostains or to discuss my opinion with Dr Harrison. Nothing had changed from the previous biopsies. It appeared to me that the changes continued to be due to radiation.”

On 11^th September 2001 Professor Langdon readmitted Mrs Manning to King’s for the first application of Regranex. In his witness statement he said that the ulcer looked cleaner and healthier than noted on 7^th August 2001. “As a routine precaution I took yet another biopsy of the area.” The request for laboratory examination referred to “Multiple biopsies since 1992. WWJ[ohnson] has reviewed recently.” The entry under clinical details was: “Chronic non-healing ulcer of left lateral tongue at site of previous T2 SCC treated by RT including implants of iridium wire following diagnosis in December 1993. Differential diagnosis was chronic non-healing ulcer: ? radiation induced; has had 60 days HBO; ? any evidence of neovascularisation.”

On 17^th September 2001 Dr Harrison sent the biopsy to Dr Fisher, a renowned Consultant Pathologist at the Marsden. His covering letter stated: “ I enclose a copy of my provisional report in which the essential history is stated and to which I can only add that the previous post-operative histology did not give any indication of malignancy.”

On 1^st October 2001 Dr Fisher reported to Dr Harrison on his review of Professor Langdon’s biopsies: “ This shows a sub-epithelial infiltrate of pleomorphic spindle and polygonal cells with frequent mitoses. Our immunohisto chemistry shows diffuse positivity for CAM 5.2 but not for other cytokeratins (MNF 116 and high molecular weight) or for SMA, desmin, calponin, caldesmon, CD 34 on S100 protein except for a sprinkling of possible inflammatory cells around the periphery. I think the cytokeratin positivity albeit with only one antibody, implies that this is more likely to represent recurrent spindle-cell (sarcomatoid) carcinoma than a post irradiation sarcoma.”

Based on Dr Fisher’s view, Dr Harrison issued an amended “definitive” biopsy report on 3^rd October 2001 in these terms:” Dr C Fisher of the Marsden has examined this case and using a wide range of immunohisto chemical markers has demonstrated one cytokeratin (CAM 5.2) in the tumour. He considers that this implies that the tumour is more likely to be a recurrent carcinoma present as a spindle-cell or sarcomatoid carcinoma rather than a post-irradiation sarcoma.

On 26^th October 2001 Mrs Manning was seen by Mr Bridger in Plymouth. In a letter dated 26^th October 2001 to Dr Eggleton, Mrs Manning’s new GP in Tavistock, he wrote: “ … to cut a long story short, Mrs Manning has been up to our clinic this morning and I examined her myself as did my two maxillofacial consultant colleagues. There was unanimous agreement that this was one of the worse oral cavity cancers we have ever seen. The tongue is almost totally destroyed and the tumour is involving the medial surface of the mandible and the tongue base as far as the epiglottis, along with the lateral wall of the pharynx. Although in theory surgery can almost always be carried out, there is little place for palliative surgery in this sort of thing and the morbidity of a total glossectomy, partial mandibulectomy etc, along with the negligible chance of a cure, make surgery not a realistic option for her. Mrs Manning did not want to hear the full implications of major surgery of this type, but they certainly would include worse speech than she has at present, chronic laryngeal aspiration almost certainly requiring tracheostomy and possibly even a laryngectomy along with percutaneous tube feeding. This might be worth it as a desperate measure if there was a chance of cure, but our unanimous feeling was that a cure was unlikely and therefore this sort of morbidity was unacceptable. Mrs Manning is fully informed about this and she has been reassured that all the resources of palliative care to control symptoms and maintain the best possible quality of life will be made available to her. As it happens this news did not come as a complete surprise to her and she and her husband accepted it very stoically.”

In his witness statement Mr Bridger said: “ I next examined Mrs Manning in clinic on 25 October 2001, along with two of my maxillofacial consultant colleagues after the diagnosis of cancer had been made in London. The drawing I made in my notes, when I first examined Mrs Manning in April, would suggest that approximately just under half of her tongue was involved. By the time she came back to me her entire tongue was infiltrated by cancer. In my view the tongue went from serious but operable in April to totally inoperable in October. In my mind’s eye I can actually picture it and remember how it looked. It was terrible. When I examined Mrs Manning in April she was in severe pain, she was lisping and had difficulty eating and drinking and was generally down. By October her tongue was almost totally destroyed and the tumour involved the medial surface of the mandible and the base of her tongue as far as the epiglottis, along with the lateral wall of the pharynx. In my opinion, by October she had no useful tongue at all. She could not talk properly, she could not eat or drink and she was in as much pain as anybody ever could be from this type of thing. She was in a terrible state, really bad. Her oral cancer was, and remains, one of the worst I have ever seen.”

Between 21^st September and 11^th November 2001 Mrs Manning was admitted St. Luke’s Hospice in Plymouth. The discharge notes recorded that: “ During the admission she was seen by Mr Bridger and diagnosed with advanced, recurrent carcinoma of the tongue which is inoperable. She has also been seen by Dr Hughes and diagnosed with chronic aspiration pneumonia and ongoing sarcoid. Major symptoms are pain, swallowing problems, speech problems and cough due to aspiration. She has a PEG in situ which was reinserted on 9^th November 2001. She has PEG feeding overnight and most of her fluids and medications are via the PEG. She manages the PEG herself. Pain is controlled but is likely to be an ongoing issue.”

On 27^th November 2001 Professor Langdon wrote to Mrs Manning: “… with regards to the biopsy results we did re-stain all tissues including all the biopsies that I undertook during the years since your tongue cancer was first treated by Dr Henk. All the biopsies were negative until the first one in February this year, which showed very very minimal staining with the new cytokeratin antibody. The biopsies subsequent to that, where as you know I was becoming increasingly suspicious, did themselves show increasing staining….”

On 22^nd January 2002 an MRI scan was carried out. In his report Dr Lewis-Jones said: “ The scan now shows evidence of a very large tongue tumour almost filling the oral cavity. There is evidence of extensive alteration and deformity on its left side with the normal tongue contour being replaced by a nodular mass. The sagittal images show that the tumour has virtually replaced all normal tongue tissue. On the left side the base of the tongue is sufficiently involved that the tumour has extended posteriorly into the area of the lateral pharyngeal wall. It has extended superiorly from this level and has gained access to the anatomical site of the pterygo-mandibular raphe. The soft tissues therefore of the pterygoid muscles and the adjacent para-pharyngeal space show evidence of early infiltration. There is still no pathological lymphadenopathy. The coronal images show inferior extension of tumour through the muscles of the floor of the mouth with a right digastric muscle still just being visible and the left digastric muscle showing evidence of invasion. The appearances are those of an extensive T4 tumour with invasion of the subcutaneous fat layers in relation to the chin and posterior extension through the tongue base into the lower part of the infra-temporal fossa. These are all features associated with the poor prognosis and with a low likelihood of total surgical resection.”

Dr Lewis said of a CT scan of the head, neck and mediastinum dated 22^nd January 2002:“ The CT scan shows similar features with a large mass replacing the tongue. No new information is provided.” … Conclusion-making a direct comparison of the MR scan performed pre-operatively on 22.01.02 with the examination performed on 26.04.01 reveals that there has been a marked increase in size of the tumour. The initial tumour measured approximately 2.0 x 2.8 cms in diameter on 26.04.01 and the subsequent scan of 22.01.02 shows this now to have increased in size to measure 6.5 x 5.0 cms in diameter. I estimate the volume of the tumour to have almost quadrupled in this interval review period. There has also been extensive ulceration and fissuring of the left side of the tongue. Initial scan showed that the left base of tongue was involved and the subsequent scan now shows extension into the tongue base bilaterally and also into the inferior part of the left infra-temporal fossa – a particularly poor prognostic sign. The tumour has also extended through the floor of the mouth.” (Emphasis added).

On 31^st January 2002 Mr Rhys-Evans, a surgeon at the Marsden, performed an examination under anaesthetic and biopsy of Mr Manning’s tongue. In the Head and Neck Unit operation note the entry under indication (pre-operative diagnosis) was: “ Rec[urrent] SCC tongue.” The entry under findings was:” Massive rec[urrent] left tongue base extending on to left lateral orophanrygeal wall invading whole of tongue and left floor of mouth, left tonsillar fossa up to superior pole. Right glossoalveolar sulcus free. Tumour removed to be able to visualise vallecula which is free. Epiglottis free larynx free.” Under post-operative diagnosis the entry was: “ Comments. The tumour is resectable with laryngeal preservation – needs total glossectomy….”

On 13^th February 2002 Dr Healey and Professor Fisher at the Marsden prepared a histopathology report on Mr Rhys-Evans’ biopsies. The report was in these terms: “T4 tumour tongue and base of tongue…

Tumour right lateral border of tongue.

Left tongue base.

All embedded levels.

Mid-tongue base

All embedded levels

On 12^th February 2002 Mr Rhys-Evans wrote to Mr Searle, a Plastic Surgeon at the Marsden as follows: “ Under summary… September 2001 – recurrence confirmed” “This patient was seen in the combined Head and Neck Clinic at the Royal Marsden Hospital on 24 January with massive recurrence of her squamous carcinoma which had caused increasing pain and ulceration over the past year. She has also developed chronic aspiration with episodes of pneumonia and a lung abscess. Her speech is virtually impossible and she has been fed through a gastrostomy. She has lost a great deal of weight and is in excruciating pain requiring a high dose of analgesia. Her airway at the moment is not affected unduly. Fortunately she has had no cervical lymphadenopathy. The recent scans have shown involvement of the whole of the tongue mainly on the left side encroaching on the left wall of the oropharynx and the floor of the mouth. It also abuts against the mandible on the left side and extends anterioally to the mandibular arch. Inferiorly there is tumour around the hyoid bone and it appears to be extending just into the pre-epiglottic space. She was admitted for pharyngoscopy, laryngoscopy and assessment of the tumour. The tumour appears to have grown from the original site on the left side involving the whole of the tongue and left floor of mouth. … There is no obvious cervical lymphadenopathy although tumour is palpable in the left sub-mandibular triangle and it is difficult to determine whether this is direct spread or level 1 involvement. This unfortunate lady has a very poor quality of life because of excruciating pain, inability to eat and virtually no speech. In my opinion the tumour is still at this late stage resectable with a reasonable chance of long-term palliation and indeed cure. It would also greatly improve her quality of life. Surgery would involve total glossectomy and resection of at least the mandibular ramus. … she will need a covering temporary tracheostomy but I hope we will be able to restore reasonable function safely without the need for total laryngectomy. Mr Adam Searle and I will be discussing these options with Jane and her husband but they have indicated that they would like to proceed with surgery as soon as possible.” In manuscript apparently in Mr Rhys-Evans’ handwriting there is then written “P.S. histology has confirmed spindle-cell carcinoma query radiation induced.” The letter was copied to Professor Langdon.

On 21 February 2002 Professor Langdon replied to Mr Rhys-Evans giving a summary history of Mrs Manning’s treatment. The letter included the following: “…at the end of February 2001 she presented yet again, this time with a firm non-ulcerated nodule again at the site of the original primary carcinoma. Biopsy of this lesion in February last year was again reported as post-radiation fibrosis. Following this biopsy once again the area did not heal and of course my suspicions were yet again aroused and in June 2001 I performed 3 geographical biopsies again all reported as radiation ulceration with no evidence of neoplasia. The ulcer became indolent and necrotic with no evidence of healing and again I repeated the biopsy in early August 2001 with again the diagnosis of radiation ulcer. Following discussion with Mike Henk we felt that this was probably chronic ulceration due to post-radiation ischaemia and I referred Jane to Philip Bryson at Plymouth for hyperbaric oxygen. Despite 60 dives the ulcer showed no evidence of healing or neovascularisation…. among others Dr Fisher at the Marsden reviewed the tissue [biopsied by Professor Langdon on 11 September 2001] and indeed the previous biopsies taken throughout 2001 and using monoclonal antibody markers he found that there was positive staining for one cytokeratin (CAM 5.2). On the basis of this he considered that the tumour was more likely to be a recurrent carcinoma rather than post-irradiation sarcoma. The final diagnosis was sarcomatoid carcinoma.” At this stage quite understandably Jane and her husband Gary had lost confidence in our management and as the family home was in Devon she transferred to Derriford Hospital under the care of Mike Bridger, Consultant ENT Surgeon. Prior to transferring her to Derriford I had spent considerable time counselling her. Thorough investigation failed to show any evidence of neck or pulmonary metastases despite a suspicious lesion in her lung fields for which she underwent a bronchoscopy and needle biopsy here at King’s. I suggested to her that a total glossectomy with laryngeal suspension could be considered as a salvage procedure which would certainly make her pain free. However following a review of the multi-disciplinary meeting at Derriford there was unanimous agreement that this would be little more than palliative surgery with minimal chance of cure. The decision was made at that stage to refer her to Dr Mary Nugent of St Luke’s Hospital for Palliative Care.” (Emphasis added).

On 28^th February 2002 Mr Hall a member of Mr Rhys-Evans’ Head and Neck Unit at the Marsden wrote to Dr Vickerage, Mrs Manning’s GP in Tavistock:

On 8^th March 2002 Dr J Seet and Professor Fisher prepared a histopathology report arising out of the operation. It was headed “Recurrent SCC tongue”. In the histology section there appeared the following: “ E5 to 24 and 30 to 32 tongue tumour. Sections show extensive involvement of both sides of the tongue by tumour. The tumour cells have spindle-cell morphology in areas and epithelioid morphology in other areas, all regarded as poorly differentiated carcinoma. Tumour invades into muscle, fat, salivary gland and is present with the marrow of the mandible. It is present in 18 out of the 20 slices into which the specimen was divided. There is perineurial venous and lymphatic invasion. Thrombosed vessels are seen within the tumour and there are areas of necrosis. Tumour is present at the right, left deep and posterior margins in several places. The adjacent tissue shows extensive fibrosis consistent with previous therapy. Two of the four lymph nodes identified within the specimen contain metastatic carcinoma.”

On the 13^th of May 2002 Mrs Manning died in the Marsden. In his witness statement adopted by him as part of his evidence in chief Mr Manning said: “ In November 2001 we were told that Jane was likely to survive that Christmas but not the next. Jane was referred to the Royal Marsden. Contrary to what Mr Bridger said they felt that the cancer was operable. In February 2002 Jane underwent extensive surgery at the Royal Marsden. She underwent a total glossectomy and partial pharyngectomy with reconstruction. Whilst this did not save her it did reduce the pain she was in and she died relatively pain free in May 2002.”

The allegations of negligence were set out in Paragraph 34 of the Amended Particulars of Claim as follows:

by Dr Harrison on 19^th September 1995 when reporting the biopsy taken by Professor Langdon on 14^th September 1995

failing to request or recommend a deeper biopsy;

failing to recommend a repeat or further biopsy if Professor Langdon was clinically suspicious of malignancy;

failing to recognise and describe cells suspicious of carcinoma;

failing to advise that carcinoma could not be excluded and instead advising that there was no evidence of malignancy;

failing to cut and examine further levels;

failing to have immunostains performed;

failing to discuss the case with another experienced tumour pathologist;

by Professor Langdon when he was suspicious of malignancy and believed that clinically there was evidence of recurrence

failing to carry out further imaging by means of MRI scan or otherwise;

failing to refer the case then or at any stage to a pathologist sufficiently experienced and specialist in head and neck cancers;

by Dr Harrison on 10^th December 1996 when reporting the biopsy taken by Professor Langdon on 2^nd December 1996:

failing to have pancytokeratin immunostains and/or a larger panel of epithelial/cytokeratin markers performed;

failing to discuss the case with any other consultant pathologist;

failing to recognise and report that the biopsy taken by Professor Langdon on 2^nd December 1996 was suggestive of malignancy or did not exclude malignancy;

failing to consider the possibility of malignancy, when the same was more likely than a post radiation effect nearly 3 years after radiation treatment;

wrongly concluding that evidence of malignancy was not seen;

failing to request or recommend a deeper biopsy;

failing to recommend a repeat or further biopsy if Professor Langdon was clinically suspicious of malignancy;

by Professor Langdon in January and February 2001:

failing to have any sufficient regard to his clinical suspicion of recurrence;

failing to have any sufficient regard to the deceased’s complaint of pain referred to her ear, which is “suggestive of carcinoma” (Langdon and Henk, Malignant Tumours of the Mouth, Jaws, and Salivary Glands, 2^nd edition, 1995, p 115);

failing to carry out an examination under anaesthesia as suggested by Dr Henk in his letter of 17^th January 2001;

by Dr Harrison on 28^th February 2001 when reporting the biopsy taken by Professor Langdon on 26^th February 2001

failing to request immunostains;

failing to discuss the case with any other consultant pathologist;

wrongly concluding that the abnormalities in the said biopsy were due to post radiation fibrosis, when the same was unlikely seven years after radiotherapy;

failing to recognise that the abnormalities were indicative of malignancy and diagnostic of spindle cell carcinoma or that malignancy could not be excluded;

failing to recognise that the increased uptake shown on the PET scan

failing to recognise the tumour mass shown in the MRI scan performed on 26^th April 2001;

by Professor Langdon in May 2001 failing to perform any further biopsy to the deceased’s tongue but instead referring her for hyperbaric oxygen treatment when he knew or ought to have known that such treatment was liable to oxygenate and increase the growth of any tumour;

by Dr Harrison on 20^th June 2001 when reporting the biopsies taken by

failing to request immunostains;

failing to discuss the case with any other consultant pathologist;

wrongly concluding that the said biopsies supported a diagnosis of radiation ulceration with no evidence of neoplasia;

failing to recognise or report that the said biopsies contained evidence of malignancy and were consistent with spindle cell carcinoma;

by Professor Johnson on 8^th August 2001 in reporting the biopsy taken by Professor Langdon on 7^th August 2001:

failing to request immunostains;

failing to discuss the case with any other consultant pathologist;

wrongly concluding that the said biopsy showed radiation ulceration;

failing to recognise and report that it showed a malignant spindle cell

The allegations in Paragraph 34 (1) (c)-(g) in relation to Dr Harrison’s September 1995 biopsy report were added by way of amendment on 10 October 1997 on the third day of the trial on an uncontested application for permission to amend.

In the Defence the following admissions were made in relation to the allegations of negligence against Dr Harrison and Professor Johnson in relation to the biopsy reports of February 2001,June2001 and August 2001:

For the purposes of this action only, it is admitted that there was a delay in diagnosing the cancer that was recognised in September 2001 and that this should have been diagnosed in February 2001, following the biopsy taken on 26 February 2001.

By way of mitigation, it is averred that the deceased’s case was difficult and complex, with a long history of ulceration that appeared to mimic carcinoma clinically but that had been shown histologically to be post radiation change and had healed after 1996. The histological distinction between malignancy and non malignant reactive change secondary to radiation is often, as in this case, subtle.

It is, however, denied that the delay of 7 months made any difference to the treatment the deceased received and/or to the outcome. The deceased would still have needed salvage surgery (partial glossectomy and selective neck dissection) and could not have received post operative radiotherapy. The tumour was of a highly malignant type. On the balance of probabilities earlier diagnosis and surgery would not have effected a cure or ensured that the deceased lived any longer…..

It is admitted that Dr Harrison on 28 February 2001 when reporting the biopsy taken on 26 February 2001 as benign post radiation fibrosis and not sarcoma should have been prompted by the presence of suspicious cells to examine further sections and apply immunocytochemical stains. For the purposes of this action only breach of duty in this respect is admitted.

It is admitted that Dr Harrison on 20 June 2001 when reporting the biopsy taken on 19 June 2001 should have recognised evidence consistent with a possible diagnosis of spindle cell carcinoma and accordingly examined further sections and/or undertaken extra stains. For the purposes of this action only breach of duty in this respect is admitted.

It is admitted that Professor Johnson on 9 August 2001 when reporting the biopsy taken on 7 August 2001 should have recognised a possible spindle cell carcinoma. For the purposes of this action only breach of duty in this respect is admitted.

As mentioned above it was accepted by Mr Manning that if the cancer which was admitted by the Defendants to have been present in 2001 had been diagnosed in February of that year rather than September it would not on the balance of probabilities have led to a successful cure. As a result it was accepted that the allegation that Mrs Manning’s death was caused by the negligence of the Defendants their servants or agents by reason of the biopsy reports of February, June and August 2001 could not succeed and that the damages recoverable by reason of the admitted negligence on those three occasions was limited principally to damages for pain and suffering.

The 2001 biopsies and the factual and expert evidence as to their contents are relevant to the causation issue as to whether, as Mr Manning submitted, they demonstrated a recurrence of a cancer that was already present in 1995 and/or 1996 or, as the defendants submitted, they constituted a new radiogenic primary cancer caused by the long term effect of the 1994 RT and BT. In the context however of the issue of negligence, the admissions set out above mean that it is not necessary to examine here the evidence and allegations of the negligence of Dr Harrison and Professor Johnson in relation to the 2001 biopsies in any great detail.

It is however pertinent to observe that the general admission in paragraph 34 of the Defence that the cancer should have been diagnosed in February 2001 goes considerably further and wider than the limited admissions made in relation to Dr Harrison’s February and June 2001 investigations, namely that in February he should have been prompted by the presence of suspicious cells to examine further sections and apply immunocytochemical stains and that in June he should have recognised evidence consistent with the possible diagnosis of spindle cell carcinoma and accordingly examined further the sections and/or undertaken extra stains.

It is also pertinent to observe that the evidence of all three expert pathologists, including not least that of Professor Speight who was called by the defendants, did not support the averments made by way of mitigation in paragraph 34.2 of the defence.

On the contrary Professor Sloan and Dr Woolgar on behalf of Mr Manning were of the opinion that the evidence of malignancy in all three of the February, June and August 2001 biopsies was to use a phrase that gained some currency in the trial “barn door obvious.” For his part Professor Speight, while of the view that the February 2001 biopsy was quite subtle and difficult, a tricky biopsy, nonetheless thought that it was clearly a malignant tumour in 2001. In relation to the February 2001 biopsy he said there were relatively few atypical cells in the deep aspect which were very suspicious in respect of which he was not able to allay his suspicions and which he thought were malignant. The June and August 2001 biopsies he accepted were “barn door obvious” (with the proviso that he did not like that word) and were obvious to any reasonably competent pathologist. He agreed that a malignant diagnosis should have been made in February 2001 by a reasonably competent pathologist and accepted that in relation to the June and August 2001 biopsies although the precise nature of the malignancy was not easy on the H and E slides, the fact that there was malignancy was quite straightforward and not difficult.

Professor Speight accepted that it is rather remarkable that two senior pathologists should have made what he accepted were bad mistakes. He said it was surprising that Professor Johnson in his 2001 review of the previous biopsies missed the malignancy. It is striking that even in the September 2001 biopsy report when Dr Harrison finally diagnosed malignancy, he expressed the view that it had arisen since the June 2001 biopsy, thereby demonstrating that even with the benefit of hindsight having again reviewed the February and June 2001 biopsies, he still missed the evidence of malignancy in those biopsies. Professor Speight found that surprising and was of the view that it implies that Dr Harrison for some reason was in a false sense of security misinterpreting the features in those biopsies. He described it as an aberration which he could not explain. When it was suggested to him by Mr Grace QC that Dr Harrison was just stuck in a mindset: “This is Mrs Manning, it must be radiation ulceration again”, Professor Speight’s answer was: “ I suspect that is correct. Having seen radiation ulcers previously he was lulled into a false sense of security that this was a continuation of the previous disease.” There followed this exchange: “ Q - But based on his actions and his failings in 2001, with the things we have just been discussing, if he was one of your students you would put him to the bottom of the class would you not – in metaphorical terms? A - In metaphorical terms I would not be very pleased with him.” In two long days of evidence in the witness box Professor Speight came across as a cautious and naturally fair-minded witness not given to over statement. While, as appears below, he did not accept Mr Grace QC’s suggestion that Dr Harrison’s mistakes in 2001 evidenced a reckless or arrogant approach on his part, it is perhaps a measure of the magnitude of the diagnostic errors made by Dr Harrison and Professor Johnson in 2001 that Professor Speight was prepared to express himself in such terms.

When it was put to Professor Langdon in cross-examination that it was disappointing from his point of view as a clinician that both Professor Johnson and Dr Harrison should fail to recognise carcinoma in 2001 he said it was “Absolutely horrifying”.

All three of the pathology experts commented on the February, June and August 2001 biopsies and the reports thereon by Dr Harrison and Professor Johnson. There is a broad measure of agreement between them on the presence of spindle cell carcinoma in the biopsies and the misdiagnoses in the biopsy reports.

Professor Sloan’s comments included the following:

Slides 126/01, Kings College Hospital, received February 27^th 2001 and reported 29^th February 2001.

Slides 391/01, parts 1, 2 and 3, Kings College Hospital, received June 19^th 2001 and reported June 20^th 2001.

Slides 500/01, Kings College Hospital, received August 8^th 2001 and reported August 9^th 2001.

Later appearances. From my review, I believe that there is clear evidence of spindle cell carcinoma in all four biopsies taken in 2001. The original cytokeratin immunostained sections provided by Dr Harrison demonstrate the features of spindle cell carcinoma……

The delay in diagnosis of recurrent cancer between January and September 2001

I agree that the changes were unlikely to be due solely to radiation change. As recorded in Section 9, I believe the changes were consistent with a spindle cell malignancy.

I agree that in examination of this biopsy there was a failure to recognise that the abnormalities were indicative of malignancy.(emphasis added)

I believe that the histological changes in this biopsy were sufficiently suspicious to warrant the application of immunostains and examination of further sections. This was not done. Therefore the allegation is found to be correct.

It is not known from the material provided, whether or not Dr Harrison discussed the case with a colleague. (see 3,c

I agree the conclusion of the report of 20 June 2001 was partly wrong. Although there was evidence of scarring and fibrosis, consistent with radiation damage, there were other features, of a hypercellular proliferation, which would not be consistent with this change.

I agree that there was a failure to recognise the presence of a malignant tumour. In my opinion there was evidence in this biopsy of a malignant spindle cell tumour, consistent with a carcinoma.

I believe that the histological changes in this biopsy were sufficiently suspicious to warrant the application of immunostains and examination of further sections. This was not done. Therefore the allegation is found to be correct.

It is not known from the material provided, whether or not Prof Johnson discussed the case with a colleague. (see 3,c)

I agree that the conclusion of the report of 9 August 2001 was wrong. Although there was evidence of radiation damage, there was also a hypercellular spindle cell proliferation consistent with malignancy (described in section 11)

I agree that there was a failure to recognise and report a malignancy in this biopsy” (emphasis added).”

It will be seen that in relation to each of the February, June and August 2001 biopsies Professor Speight was of the view that the histological changes in the biopsy were sufficiently suspicious to warrant the application of immuno stains and examination of further sections, and that the failure by respectively Dr Harrison and Professor Johnson to do either was negligent. In relation to the June and August biopsies he was of the view that Dr Harrison and Professor Johnson respectively failed to recognise the presence of a malignancy and in respect of the February 2001 biopsy that Dr Harrison failed to recognise that the abnormalities were indicative of malignancy. In cross examination he said that in essence his criticism of Dr Harrison and the respects in which he fell below a proper standard in February 2001, were that he failed to take deeper sections, failed to carry out immuno stains, thought he could rely on H and E staining alone and failed to recognise on the H and E sections the stigmata of malignancy. In his view a reasonably competent pathologist could not have missed the malignant cells and should have recognised stigmata of malignancy on the H and E slides alone.

In relation to June 2001 in cross examination Professor Speight added that there was a misinterpretation by Dr Harrison of the cytological features and “ the pattern of the lesion, in particular the pattern of hypercellularity, in other words interlacing bands fascicles or sheets which was quite striking in June and thereafter.” He referred to big swathes of cells streaming through the biopsy in particular interlacing bands in the superficial aspect and sheets of atypical polygonal cells which were continuously overlying epithelium so that the pattern was really quite striking. Professor Speight accepted that Dr Harrison’s fundamental mistake in June 2001 was to diagnose a radiation ulcer in the face of these highly suspicious features. His assumption that the proliferating cells were due to a healing radiation ulcer was a failure of interpretation on his part. However Professor Speight did not accept that Dr Harrison was guilty of an over confident reliance on his ability to make a diagnosis on the H and E slide alone, or that he was in some way recklessly arrogant. In his view the H and E stained section is the fundamental piece of evidence that a pathologist uses to make the diagnosis so that you can never over rely on the H and E stained sections. That is a fundamental tool for making a diagnosis. It is what pathologists use. However he did accept that Dr Harrison over relied on the H and E slide to the exclusion of other diagnostic tools that were available and that no reasonably competent pathologist could have excluded the diagnosis in June 2001 of carcinoma merely on the H and E slide alone. Professor Speight believed that Dr Harrison went through the deductive process of looking very carefully at the specimen and recording his findings but misinterpreted them in 2001.

Importantly Professor Speight did not accept that the mistakes Dr Harrison made in his intellectual process of eliminating malignancy in 2001, namely a failure of recognition and a failure to have sufficiently high index of suspicion involved exactly the same mistakes as he made in 1995 and 1996. In Professor Speight’s opinion “ after extensive and very careful examination of the 95 and 96 biopsies, I believe that his interpretation was correct.” In saying that he made it clear that he was talking not with the benefit of hindsight but referring to his own unaided interpretation of the same slides as were seen by Dr Harrison in September 1995 and December 1996.

In relation to the August 2001 biopsy Professor Speight confirmed in cross examination that in his view Professor Johnson was essentially making the same mistakes as Dr Harrison had made and that he agreed with all the allegations of negligence in relation to August 2001 and that malignancy was certainly diagnosable on H and E alone in June and August.

In posing the question this way I am of course conscious that I am conflating the two distinct issues of a) whether there was a breach or breaches of duty and b) if so whether but for such breach Professor Langdon would have conducted a further biopsy. The latter question is of course a part but only a part of the necessary element of causation which would have to be established for the claim to succeed. It is right that the breaches alleged include failing to take a further section and failing to discuss the biopsy with a colleague. However there is no evidence that if either of those steps had been taken by Dr Harrison either in September 1995 or December 1996 that would ipso facto have led to a diagnosis of carcinoma. In relation to taking further sections, the way it was put by Professor Sloan and Dr Woolgar was that Dr Harrison should have taken further sections because he should have realised that, in view of the suspicious features in the biopsies, either further sections would have revealed malignancy or if they did not then it would have been necessary to take further steps to seek to exclude malignancy. Similarly it was not suggested that a colleague to whom the biopsies was referred would necessarily have reached a diagnosis of malignancy. On the contrary, and this is a very important point, neither Professor Sloan nor Dr Woolgar suggested that the only proper diagnosis which a reasonably competent pathologist in the position of Dr Harrison in September 1995 or December 1996 could have made was one of malignancy. Again the suggestion was that a colleague would have expressed the view that it was not possible to exclude malignancy without taking further steps. The allegation that it was negligent to exclude malignancy on the basis of H and E slide alone applied only to the September 1995 biopsy because in December 1996 Dr Harrison did in fact carry out immuno staining. In relation to the failure to take immuno staining in September 1995, Professor Sloan and Dr Woolgar did not suggest that if Dr Harrison had performed an immuno stain that would have conclusively confirmed a diagnosis of malignancy. Rather the suggestion was that even a negative result on immuno staining would not have been sufficient to lead to a safe diagnosis of innocence because of the known existence of a significant false negative rate on immuno staining.

Equally it was not suggested that in the absence of a positive diagnosis of malignancy Professor Langdon would or should have embarked on major salvage surgery. Indeed Professor Langdon gave convincing evidence to the effect that he would not have contemplated such a course in the absence of a positive diagnosis. The only circumstances in which such a positive diagnosis would have been made would have been if Professor Langdon had performed a further biopsy which confirmed the presence of cancer. It follows in my judgment that the claim could not succeed unless it could be established that there was a breach or breaches of duty but for which Professor Langdon would have conducted a biopsy. Of course if that could be proved that is not the end of the story. It would still be necessary for Mr Manning to prove that if Professor Langdon had performed a further biopsy such a biopsy would have revealed malignancy. That raises the second main factual issue to which I have referred at the outset, namely whether there was or was not carcinoma present in 1995 and/or 1996, which I address later in this judgment.

The pathology experts addressed the 1995 and 1996 reports first in their individual reports and then in a joint report following a joint meeting in Sheffield in Professor Speight’s laboratory when they reviewed the biopsies together microscopically.

Professor Sloan’s report included the following comments:

Slides 457/95, parts 1 and 2, Kings College Hospital, received September 15^th 1995 and reported September 19^th 1995.

Slides 642/96, Kings College Hospital, received December 4^th 1996 and reported December l0th^t" 1996.

Time of recurrence of spindle cell carcinoma

First appearance. In my opinion, the first appearance of the spindle cell carcinoma is seen in 1995 (Slides 457/95, parts 1 and 2, Kings College Hospital, received September 15th 1995 and reported September 19th 1995), where there are bands of lozenge-shaped spindle cells. The diagnosis would have been difficult. The malignant cells are few in number and are in cords on the deeper aspect of the biopsy. The presence of radiation induced scar tissue tends to distract and contrasts with the typical straightforward diagnosis of carcinoma where the malignant cells tend to form abnormal sheets. It should be recognised that it is easier with hindsight, knowing the morphological features of the spindle cell carcinoma in later specimens. Nevertheless a competent oral pathologist should be concerned about even small islands or cords of cells in a post radiation ulcer. In this situation the possibility of recurrent carcinoma should be raised in the pathology report and deeper biopsies should be requested.

Second appearance. It is my opinion that spindle cell carcinoma was present in 1996 (Slides 642/96, Kings College Hospital, received December 4^th 1996 and reported December 10^th 1996). This opinion is based on the staining performed by Dr Woolgar and Professor MacDonald as well as on the morphological features. The biopsy was superficial and cytokeratin staining was negative as far as can be assessed from the original slides and reports. The report does not convey a strong sense of suspicion of recurrent cancer. I think that insufficient attention was given to the presence of atypical mitotic figures in the spindle cells which should have caused concern. An experienced oral pathologist should have sought an expert opinion from a specialist at a cancer centre when faced with these worrying bands of cells in a post irradiation setting, and would have alerted the surgeon to the possibility of malignancy in the differential diagnosis……

Mrs Manning's management between 1994 and early 2001 ……

Professor Langdon's statement

Dr Woolgar’s report included the following comments:

Professor Speight’s report included the following comments:

Microscopic Examination

Comment and Conclusion

Case number 642/96

Comment and Conclusion

Conclusions and opinion

There is no evidence in the report that a deeper biopsy was requested. However it is common practice for pathologists to discuss directly with senior consultants the need for further examination. It is not normal to give clinical advice to senior colleagues in the body of a written pathology report, which should remain objective and report the histopathological findings. I note from his witness statement that Dr Harrison regarded the biopsy as adequate and that he had sampled it in an appropriate manner. In my opinion, this specimen was sampled and examined appropriately.

It is not possible to know whether or not Dr Harrison made any recommendation to Professor Langdon for a repeat or further biopsy. In my opinion however, if the clinician is suspicious of malignancy, even in the face of a negative pathology report, then it is the clinician's responsibility to initiate further special tests including, where appropriate, a repeat biopsy. The pathology report is only one part of the overall case and only the clinician can interpret all the findings in the context of the clinical signs and symptoms. I regard the pathology report as satisfactory.

There is no evidence in the report that multiple levels were examined and levels were not included in the material supplied to me. Normally, faced with suspicious features in a biopsy, a pathologist would prepare deeper levels so as to examine more tissue. There is evidence in the report that Dr Harrison was suspicious and may not have prepared levels.

This allegation is unfounded, since the report shows that Dr Harrison did perform immunocytochemical stains for cytokeratins.

It is not known from the material provided, whether or not Dr Harrison discussed the case with a colleague. There is no evidence that he did not. It is common practice for pathologists to show and discuss cases with colleagues within the department, but this is not usually recorded.

There is evidence in the report that Dr Harrison did consider malignancy and undertook steps to exclude it. There was no reason why his thought processes, rather than his final conclusion, should have been reported to Professor Langdon.

There is evidence in the report that Dr Harrison did consider the possibility of malignancy. He carried out immunocytochemical stains to exclude the possibility that the noted atypical cells were epithelial.

The evidence from the staining at the time and in a retrospective examination of the material suggests that that there was no evidence of malignancy at the time. Therefore his conclusion was not wrong. In my opinion, having reviewed the whole case, it is extremely unlikely that there was malignancy at the site in 1996. The histology in 1996 is quite consistent with post-radiation change and the scattered spindle cells although pleomorphic are loosely arranged in an organising granulation tissue. This is quite different from the appearances seen in 2001 where the spindle cells are arranged in sheets and more discrete cellular masses towards the deep aspect of the specimen.

The response to this allegation is given in section 1a)

The response to this allegation is given in section 1 b)”

The three pathology experts dealt with the September 1995 and December 1996 biopsies in the Joint Report following their joint meeting as follows:

Doctor Harrison was at all material times a Consultant Oral Pathologist and as such he owed a duty of care to Mrs Manning. That duty required him to exercise reasonable skill and care. In order to identify the content of that duty the starting point is to identify the requisite standard of skill and care. The classic formulation in the context of a medical practitioner is that adopted by Mc Nair J in his direction to the jury in Bolam v Friern Hospital Management Committee [1957] 1 WLR 582, 586: “But where you get a situation which involves the use of some special skill or competence, then the test as to whether there has been negligence or not is not the test of the man on the top of a Clapham Omnibus, because he has not got this special skill. The test is the standard of the ordinary skilled man exercising and professing to have that special skill. A man need not possess the highest expert skill; it is well established law that it is sufficient if he exercises the ordinary skill of an ordinary competent man exercising that particular art”. In Whitehouse v Jordan [1981] 1 WLR 246 the House of Lords held that the Bolam test was applicable to medical treatment and in Maynard v West Midlands Health Authority [1984] 1 WLR 63 the House of Lords held that it was applicable to diagnosis. In Sidaway v Governors of Bethlem Royal Hospital [1985] AC 871 Lord Diplock said: “ My Lords, no convincing reason has in my view been advanced before your lordships that would justify treating the Bolam test as doing anything less than laying down a principle of English law that is comprehensive and applicable to every aspect of the duty of care owed by a doctor to his patient in the exercise of his healing functions as respects that patient.”

There is a helpful summary of the law and its particular application in the context of the requisite standard of care required of cytoscreeners operating under the National Cervical Screening Programme in the decision of the Court of Appeal in Penney, Palmer and Cannon v East Kent Health Authority [2000] Lloyds Law Reports (Medical) 41 at 45,46. That was a case in which the Court of Appeal upheld findings of negligence against cytoscreeners who had reported as negative cervical smears obtained from the Claimants, each of whom went on to develop cancer. At the trial the evidence before the judge included the relevant slides, the report made on each slide by the examining cytoscreener and the written and oral expert testimony of 5 eminent pathologists, 3 of whom were called by the defendant. As appears from the head note the Defendant appealed contending inter alia that: “…(iii) the judge was wrong to hold that the Bolam test did not apply and (iv) the supportive evidence of the three expert pathologists called by the defendant constituted a respectable and responsible body of opinion providing the defendant with good defence to the claims on a proper application of the Bolam test.”

The reasons of the Court of Appeal for dismissing the appeal, as summarised in the head note, included the following:”…. (3) as to the application of the Bolam test:

It was generally applicable as the cytoscreeners were exercising skill and judgment in determining what report they should make; but (b) It applied subject to the qualification that expert evidence that the Defendants’ conduct accorded with sound medical practice had to be capable of withstanding logical analysis; and ….(c) It did not apply to questions of fact which included the question of what was to be seen on the individual slides

On the facts of the case:

The approach was to determine:

In areas of conflict the judge was entitled to prefer the evidence of the Claimant’s experts on the question of what the slides showed;

All the experts endorsed the “absolute confidence” test, under which if there was any doubt in the mind of the cytoscreener as to whether the slide was normal he or she should not classify it as negative: to the extent that the Defendant’s experts were saying, in relation to an individual slide, that the cytoscreener could not say whether the features were or were not pre-cancerous but nevertheless it was acceptable to classify the slide as negative, their opinion did not withstand logical analysis…”

Lord Woolf, who delivered the judgment of the court, dealt with the law in the following passage: “In his judgment, the judge having set out the background facts with admirable clarity, including a detailed account of the task of the cytoscreeners, turned his attention to the law. He began by indicating that both parties agreed that :
"The standard which I have to apply is that of a reasonably competent screener exercising reasonable care at the time when the screening took place. I must ignore any advances in screening practice which have occurred since the relevant events. I must also put out of my mind when considering the extent of the screeners' duty of care the fact that all three [claimants] subsequently developed carcinoma.
Equally importantly I must bear constantly in mind that in cases where an exercise of judgment is called for, the fact that with the benefit of hindsight that judgment was exercised wrongly is not itself proof of negligence."

Medical and expert opinion is deeply divided on the issue. The question has to be determined on all the evidence in the case, which is primarily the oral evidence of the witnesses tested in cross examination. The court cannot simply accept the opinion or belief of a witness, however eminent, that such is or is not the case. The basis for the opinion must be examined, tested against other evidence, for consistency and logic and the validity of the reasoning.

The question is not answered by showing that there is a respectable and responsible body of medical opinion that the vaccine can, albeit rarely, cause permanent brain damage, or that this view may be more widely held than the contrary. The opinion of others not called to give evidence is not admissible to prove the truth of the opinion. The works of learned and qualified authors form part of the general corpus of medical and scientific learning on the subject and can be relied upon and adopted by suitably qualified experts. These experts may have their opinions tested in the light of the literature."

All five pathology experts in Penney had endorsed “the absolute confidence” test, under which if there was any doubt in the mind of the cytoscreener as to whether the slide was normal, he or she should not classify it as negative. One of the bases on which the trial judge had rejected the evidence of the pathologists called by the Defendant was that: “ …I do not consider that the evidence of Doctors Hudson and Boon stands up to the logical analysis as that phrase was used by Lord Brown-Wilkinson in Bolitho at page 1160 c to d. This is not to disparage the evidence of either. It is rather that in my judgment their opinions cannot stand with the “absolute confidence” test which Dr Hudson herself propounded with the agreement of the other experts. Here were admitted abnormalities which, to put it most favourably to the cytoscreener, he could not possibly have said were not pre-cancerous. Neither Dr Hudson nor Dr Boon had suggested that the cytoscreener had the ability to draw any such distinction, still less how they should apply it. It seems to me therefore that having regard for the potentially disastrous consequences of a mistaken classification a reasonably competent cytoscreener should have classified the smear as borderline even though that classification might have caused the patient short-term distress and perhaps the discomfort and embarrassment of a further smear. I cannot believe that any woman would not be prepared to put up with both if the alternative was an undiagnosed potential carcinoma.

The Court of Appeal approved of the judge’s application of the Bolitho test. “However this does not matter because the judge also in the alternative, applied the Bolitho test. The judge’s reasoning was that if the cytoscreener could not say with a reasonable degree of confidence that the abnormalities were not pre-cancerous, then it was inconsistent with what Dr Hudson and Dr Boon were agreed was the right approach to report her slide as negative”. The Court of Appeal rejected criticism of the judge’s reasoning made by counsel for the Defendants: “ He describes it as simplistic. He submits it amounted to no more than saying that if a slide contains features which might be abnormal then a negative classification should not be given. In relation to Mrs Penney’s slide, we do not consider this criticism is appropriate. The judge was basing himself on the difficulty of interpreting that particular slide. We do not regard the reasoning of the judge as inconsistent with the statistics which show that false negative rate would not be less than 5% to 15%. The judge’s reliance on the absolute confidence test is understandable.” (ibid paras 39-40).

In endorsing the absolute confidence test the Court of Appeal explained the rationale for the rule:

In the present case there were a number of statements by witnesses which broadly corresponded to the absolute confidence test. In cross-examination Professor Speight accepted that when a patient with a history of carcinoma is being dealt with and the surgeon asks the pathologist on the form “Query- recurrent carcinoma” the primary duty of the pathologist is to exclude carcinoma as close to 100% as he/she can: “Q In legal terms we might put it “beyond reasonable doubt”, do you understand what is meant by that? A- I do. It can never be 100%, but as close as we can get, yes I agree. Q- But 90% is not good enough because you have a 1 in 10 chance of missing it, have you not? A- That is probably right. Q- That would not be acceptable? A- No Q- You agree? A- I would like to be 99% if that were possible. Q- But 90% would not be enough because of the 1 in 10 chance? A- Yes Q- That is not good enough, you agree? A- There may be provisos to that but in general I would agree. …Q- Because the primary duty of the pathologist is to ensure that the patient is safe? A- Correct, and properly treated. Q- And properly treated? A- Appropriately treated. Q- Appropriately treated and recurrent cancer is not missed? A- Correct.”

Later in his evidence Professor Speight confirmed that he agreed that any reasonably competent pathologist looking to exclude carcinoma could not safely exclude carcinoma unless he was sure beyond reasonable doubt that it was not there. “ Q- In other words if you have got a reasonable doubt after doing all your intellectual reiterative processes then a reasonably competent pathologist cannot say this is not malignant? A-That’s correct.

I will return to Professor Speight’s application of that test to the 1995 biopsy.

Professor Sloan described the function of the pathologist in the context of the cancer case as being to do the best for the patient and to leave no stone unturned to get the right diagnosis for the surgical team and the oncology team: “ I see it as a skill really- something that you learn from training and experience. It’s about recognising the pattern, the architecture of the tissue and the cells in the tissue and being able to classify that as a particular diagnostic entity and recognise that in the current world literature.”

Dr Woolgar said that pathologists work on the basis of “100% or as near to 100% as you can be”. Speaking in the context of the 1995 biopsy she said that her view was that unless following further stains and levels and discussions with colleagues the consensus was that malignancy could be excluded 100% or as close as possible, no reasonably competent pathologist could allay their suspicions or fail to ask for further biopsy.

Professor Langdon said in cross examination that it is the pathologist’s job to advise the surgeon either that he is concerned about the diagnosis or cannot eliminate cancer. Again in the context of the 1995 biopsy he was asked whether, if he had been aware that the pathologist had seen suspicious cells, he would expect the pathologist to do special staining or immunohistochemistry. His answer was: “ I would have expected the pathologist to do whatever in their judgment was necessary either to warn me about the suspicious cells or exclude them as being evidence of the cancer.” Dr Harrison himself accepted in cross examination that when a surgeon asks a pathologist to prepare a pathology report after a biopsy the surgeon is asking the pathologist: “can you confidently exclude malignancy?” and that that is how he would see his task. In the context of a patient who has had a carcinoma where there is a concern that that there may be a further carcinoma at the same site he accepted that both the clinician and the pathologist have to have a high index of suspicion. Professor Langdon gave evidence to similar effect. If a patient with a history of carcinoma which has been treated, whether by surgery or radiotherapy, then presents with a lesion at the site of the original carcinoma he said the surgeon would need to have a high index of suspicion that it might be a recurrence. In those circumstances the surgeon would have to do all he could to exclude recurrence and he would expect the pathologist to do that as well. Implicitly if not explicitly the question being asked of the pathologist by the surgeon is: “Can you confidently exclude carcinoma in this case?”. If he had been aware in 1995 that the pathologist had seen suspicious cells he would have expected him to do whatever in his judgment was necessary either to warn him about the suspicious cells or exclude them as being evidence of cancer. In Professor Langdon’s view if the pathologist cannot eliminate recurrent SQC it is his job to advise the surgeon that he is concerned about the diagnosis or cannot eliminate cancer.

It can be readily appreciated why the test is such a high one. A pathologist presented with a biopsy of a patient with a history of carcinoma and a differential diagnosis of possible carcinoma is taken to understand that the purpose of the request for a histopathology report is to seek to confirm or exclude the recurrence of the carcinoma. A negative biopsy report is liable to result in the surgeon deciding not to take any further clinical steps to investigate further or to seek to remove any carcinoma that may be present. The foreseeable consequence of a negative report in a case where in fact carcinoma is present is that the carcinoma may be allowed to remain and grow undetected with adverse and potentially fatal consequences that might have been avoided if such further steps had been taken.

Before turning to the evidence in relation to the 1995 and 1996 biopsies it is necessary to say a word about the three pathology experts. As mentioned above all three are Consultant Oral Pathologists. All three also combine active medical practice with senior academic positions. Voluminous CVs were attached to each of their reports and elaborated in oral evidence. It would be neither practical nor necessary to recite them here in full.

At the time of giving evidence Dr Woolgar was senior lecturer in oral pathology at the University of Liverpool and an Honorary Consultant in oral pathology at the Royal Liverpool and Broad Green University Hospitals NHS Trust, a position she has held since 1994. She divides her working week spending three days a week as a reporting pathologist and two days a week in university teaching research and administration. For two years in 2000 and 2001 she temporarily ran the Department of Pathology at the University of Glasgow. Since 1996 she has organised and developed the Head and Neck Histopathology External Quality Assurance Scheme. She is or has been a member of the editorial board of Oral Oncology, the British Journal of Oral and Maxillofacial Surgery and the International Journal of Oral and Maxillofacial Surgery. She has published widely both books and papers including papers on “The survival and patterns of recurrence in 200 oral cancer patients treated by radical surgery and neck dissection, cervical lymph nodes metastasis in oral cancer and the influence of the pattern of mandibular invasion on recurrence and survival in oral squamous cell carcinoma.” During her time in Glasgow she had limited experience of BT which was routinely used during the years she was there and often got specimens from patients who had had BT to the tongue.

Professor Sloan when he gave evidence was between jobs. Between 1985 and September 2007 he had been an Honorary Consultant in Oral Pathology and Oral Medicine at the Central Manchester and Manchester Children’s University Healthcare Trust. From 1992 to 2007 he had also been Professor of Experimental Oral Pathology at the University of Manchester. He had been due to take up an appointment as Consultant Histopathologist at the Royal Victoria Infirmary at Newcastle upon Tyne and Honorary Professor in the School of Dental Science at the University of Newcastle upon Tyne on 1^st October 2007. However as a result of his commitment to this trial he deferred taking up these new appointments for several weeks. While in Manchester he spent 24 hours a week working as a practising pathologist. His pathology workload was between 2,500 and 3,000 cases a year including many tertiary referrals from around the north-west region. He has contributed to some nine books inter-alia on aspects of oral cancer, co-written two books including Oral and Maxillofacial Surgery, Radiology Pathology and Oral Medicine and written jointly or alone some 100 papers including several on squamous cell carcinoma of the oral cavity and one case report on spindle-cell carcinoma. He has been active in oral cancer research contributing inter-alia to the elucidation of the genetic basis of malignant transformation in the oral mucosa and has a clinical interest in screening for oral cancer. From 2003 to 2007 he was on the editorial board of the British Dental Journal and the British Journal of Oral and Maxillofacial Surgery and is currently on the editorial board of the Journal of Dental Research. Since 1990 he has been organiser of oral pathology audit within his department and the Northern Universities Group. While in Manchester he attended weekly head and neck multi-disciplinary team meetings at the Christy Hospital which is a specialist cancer hospital with radiotherapy facilities similar to the Royal Marsden. For the last 15 years his predominant area of interest and sub-specialisation has been mainly oral cancer mostly in relation to the molecular biology of oral cancer and the diagnostic aspects of oral cancer. His PHD was on fibroblasts and the periodontal ligaments, that is to say the structure that attaches teeth to the jawbone.

When he gave evidence at the trial, Professor Speight was an Honorary Consultant Pathologist at the Sheffield Teaching Hospitals NHS Trust, Professor of Oral Pathology at the School of Clinical Dentistry at the University of Sheffield and Dean of the School of Clinical Dentistry at the University of Sheffield. From 1990 to 2003 he was Honorary Consultant in Oral Pathology at University College London Hospitals NHS Trust and Head of Department of Oral and Maxillofacial Pathology at the Eastman Dental Institute and Hospital. From 1997 to 2003 he was Professor of Oral Pathology at the Eastman Dental Institute, from 1998 to 2003 he was Associate Dean for Research at that institute and from 2002 to 2003 he was Head of Cellular Pathology (histopathology, cytopathology, neuropathology, oral pathology and motuaries at University College London Hospitals NHS Trust. He has been specialty adviser in oral pathology to the Royal College of Surgeons from 2001 and to the Royal College of Pathologists from 2002. From 2006 he has been President of the International Association of Oral Pathologists, of which he was secretary from 1996 to 2004. In 2004 and 2005 he was on the organising committee of the International Congress of the International Association of Oral Pathologists. Since 1997 he has been on the editorial board of Oral Oncology, since 1999 he has been on the editorial board of Oral Pathology and Medicine and since 2002 he has been editor in chief of the Archives of Oral Biology. He has been awarded many research prizes inter-alia for research related to oral squamous carcinoma. He has contributed chapters to 12 books including on disorders of the oral cavity and the use of machine learning in screening for oral cancer. He has co-authored two books, one on the pathology of tumours of the oral tissues, the other on cysts of the oral and maxillofacial regions. He has written or co-written 122 papers including a systematic review of test performance in screening for oral cancer, and published 37 case reports and items of clinical research. He has also published 166 abstracts of research presentations many related to various aspects of oral cancer including, for example cell proliferation markers in oral squamous cell carcinomas and evaluation of performance in identifying oral cancer and associated pre-cancerous lesions.

As appears from the above summaries, each of the three expert pathology witnesses had enormous clinical and research expertise in oral pathology. Professor Speight and Professor Sloan, perhaps in that order, are plainly eminent in their field. At one point in his cross-examination Professor Speight said that Dr Woolgar and Professor Sloan on the one hand and he on the other were almost diametrically opposed in virtually everything as far as he could tell. This was both an exaggeration and an over-simplification. As appears below, on key aspects of a question of what was the requisite standard of care and whether there was a breach of that standard by Dr Harrison there was significant broad agreement between the three experts. By contrast on the separate and distinct factual question whether there was in fact carcinoma present in Mrs Manning in 1995 and/or 1996 and the related question whether the admitted SPCC in 2001 was a recurrence or a new primary, there was indeed a very marked difference of opinion between Dr Woolgar and Professor Sloan on the one hand and Professor Speight on the other which has contributed very greatly to the difficulty of the task I am required to perform of making a finding of fact on that crucial issue.

At various points in the trial attacks were made by Ms Mishcon and Mr Grace QC on the bona fides of Dr Woolgar, Professor Sloan and Professor Speight respectively. In my judgment those attacks were all misconceived and I have not the slightest hesitation in rejecting all of them.

The most serious attack was made by Ms Mishcon on Professor Sloan whom she accused of deliberately lying when he told the court that he had seen highly suspicious cells on the deep aspect of the 1996 biopsy which were not shown on the photographs produced in court. The allegation when made came as a surprise to me because it seemed to me obvious throughout Professor Sloan’s evidence in the witness box that he was a transparently honest witness who conscientiously did his best to consider all the evidence and all the countervailing arguments. Indeed a point taken against him by Ms Mishcon when inviting me to prefer the evidence of Professor Speight as more reliable was that on two potentially important aspects Professor Sloan openly conceded that he had changed his mind, in one case explicitly as a result of being persuaded by Professor Speight that his original view was wrong. In the event, at my invitation, Professor Sloan, at no small inconvenience to himself, given that he was between jobs, re-examined the 1996 biopsy slides, one weekend and took additional photographs of particular fields. Although the interpretation of what they showed remained in contention between the parties, it was plain that one at least of those photographs contained what Professor Sloan regarded as suspicious cells of the kind to which he had referred. Thereafter Ms Mishcon retracted the accusation of deliberate untruthfulness against Professor Sloan on her feet and repeated the retraction in her written reply submissions.

In addition Ms Mishcon commenced her cross-examination of Professor Sloan by comparing similarly worded extracts of his and Dr Woolgar’s reports and putting it to him that they evidenced collusion between the two of them. This allegation was strongly denied by Professor Sloan and again I have no hesitation in rejecting it. It is true that there are similarities between sections in the two reports and Professor Sloan accepted that he thought that he had read Dr Woolgar’s report before writing his own. However he said that the language and phraseology in his report was taken from the literature and that both reports had described key features in the biopsies. Having made that point Professor Sloan said “ All I can say is that I looked at the material and I reached my conclusions independently.” I unhesitatingly accept the truthfulness of that response.

Mr Grace QC for his part in his closing written submissions submitted that the Defendant’s expert witnesses including Professor Speight appeared at times to be acting as advocates for and arguing the Defendant’s case rather than demonstrating the impartiality required of them. While I accept that there was some force in that submission so far as Mr Watt-Smith and to a lesser extent Dr Barley were concerned, again I reject it so far as Professor Speight was concerned. Mr Grace QC made two specific criticisms of Professor Speight. The first was that his “Attempts to explain away all suspicious features by a “sectioning effect” … were altogether facile and unnecessarily favoured the Defendant’s position, since there is no reason why the random effect of sectioning should always favour the innocent explanation rather than malignancy…. The court should therefore be alive to the real prospect that Professor Speight’s evidence has at the very least been coloured by sympathy for, or a sense of loyalty towards, Dr Harrison.” (paragraph 10 (3) of the Claimants’ closing submission on liability). The second was that: “ There is no logical distinction to be made between Professor Speight’s view that the appearances of the February 2001 biopsy (hyper-cellularity) as well as “on the deep aspect an area suspicion for a spindle-cell malignancy” … were such as to require further levels and immunostains, and the view of Professor Sloan and Dr Woolgar that the same appearances in 1996 required further action to be taken to exclude carcinoma. If such action was required in 2001 then it was also required in 1996. The only explanation for this discrepancy is Professor Speight’s desire to exculpate Dr Harrison in relation to 1996.”

Again I reject both these criticisms. In relation to the first point, there was indeed a difference of opinion between the experts as to whether particular features visible in the biopsies were evidence of malignancy or could be explained innocently by being attributed to the effect of sectioning in the preparation of the biopsy. These differences of view go to the heart of the divergent views of Professor Sloan and Dr Woolgar on the one hand and Professor Speight on the other as to whether there was malignancy in 1995 and in particular 1996 or not. However in my judgment while there is some force in the point that Professor Speight’s approach on sectioning was to an extent speculative, these are examples of genuine differences of opinion and there is no warrant for the suggestion that Professor Speight’s expressed opinions did not genuinely reflect his professional view.

Similarly in relation to the second criticism I do not accept that Professor Speight was motivated by a desire to exculpate Dr Harrison in relation to 1996. Just as Professor Sloan was prepared to concede that he had changed his opinion on two matters, so Professor Speight was not only ready to criticise Dr Harrison where he thought it appropriate, but in fact, as appears below, expressed opinions in relation to issues of breach of duty which were unfavourable to Dr Harrison, particularly in relation to the 1995 biopsy. In addition Professor Speight on a number of occasions volunteered possible scenarios which would be contrary to the Defendants’ case on whether there was malignancy in 1995 and/or 1996.

It was undoubtedly the case that Professor Sloan strongly believed that Mrs Manning had cancer in 1995 and 1996 and that Professor Speight strongly believed that she did not. It is also the case that each of them advanced arguments in support of their views in emphatic terms. However I am perfectly satisfied that this represented a genuine difference of opinion between two distinguished pathologists in a very difficult case. I have absolutely no doubt that each of them, while strongly believing in the correctness of their opinions, was genuinely doing his best honestly to assist the court in the difficult exercise of trying to come to the right answer, although, as I have occasion to say below, I found Professor Speight to be less open-minded on occasion than Professor Sloan. I also found him on occasion a little slow to accept what appeared to be logical propositions which did not coincide with his own views.

Standing back from the detailed allegations of negligence it seemed to me having read Professor Sloan’s and Dr Woolgar’s reports and heard their oral evidence that their central conclusion which underlay all their detailed criticisms of Dr Harrison’s approach was that no reasonably competent pathologist in the position of Dr Harrison either in September 1995 or December 1996 could safely have excluded the possibility of carcinoma.

It of course by no means follows that it was their opinion that no reasonably competent pathologist could have failed to make a diagnosis of carcinoma. On the contrary, as mentioned above, in relation to both biopsies neither Professor Sloan nor Dr Woolgar would themselves, without the benefit of hindsight, have felt able to make a positive diagnosis of carcinoma or SPCC. In neither biopsy was there evidence of either dysplasia of the epithelium or foci of squamous cell carcinoma. Professor Sloan accepted that, consistent with the literature, in the absence of epithelial dysplasia one would have to find squamous cell carcinoma in order to make a positive diagnosis of SPCC. These two features, epithelial dysplasia and foci of squamous-cell carcinoma, neither of which was visible in either the September 1995 or December 1996 biopsies, came to be referred to in the trial as the two smoking guns of SPCC. Professor Sloan was recalled at one stage to comment on supplemental photographs taken by Professor Speight during the trial of particular fields in the 1996 biopsy. Commenting on abnormal appearances in three of those photographs (photographs 4 to 6) Professor Sloan said that his interpretation was that it was an SPCC and his explanation was that the proliferation was a neoplastic one which, not merely as a matter of probability but definitely, could not be explicable as a reaction to ulceration since it seemed to be away from the area of ulceration. Asked why, in those circumstances, he said that in 1996 (i.e without the benefit of hindsight) it would only be merely highly suspicious and not definitely SPCC, Professor Sloan’s answer was:

Professor Sloan went further. In his report he said of the September 1995 biopsy that: “Interlacing bands of plump spindle-cells were present in the granulation tissue. Lozenge-shaped cells with prominent nuclei were present within the bands and scattered in the loose connective tissue. The interlacing bands were highly cellular and unusual for a purely reactive feature. I would have been suspicious of recurrent carcinoma and would have requested immunocyto chemical stains for cytokeratins and mesenchymal markers together with deeper levels. I believe that an experienced oral pathologist should have been suspicious of recurrent carcinoma.” However in oral evidence he accepted that although he would have done deeper levels to look for dysplasia or foci of conventional squamous carcinoma because you need one or the other to make a definite diagnosis of SPCC, when asked what he thought those deeper levels would have shown if they had been performed, he accepted that: “We know that deeper levels were looked at because the experts have prepared some and we know that there is no evidence of dysplasia or squamous carcinoma in the sections. So Dr Harrison could not have made a diagnosis of spindle-cell carcinoma on this material because there was no dysplasia and no conventional squamous cell carcinoma….. This is something that the experts agreed on, that there was no unequivocal evidence of malignancy. Q- Therefore you could not have made the diagnosis of spindle-cell carcinoma? A- No. But he should have been suspicious; he should have indicated that suspicion to Professor Langdon. Q- What should he have indicated?... A- That suspicion, the fact that there was suspicious spindle-cells and levels had been taken, cytokeratins had been taken; nothing had been found… but say that deeper levels and cytokeratins had not revealed conventional squamous cell carcinoma or dysplasia; that the biopsy was suspicious. Q- What you are saying is that if you look with the microscope and you find the presence of these spindle-cells and the density, that makes you suspicious of spindle-cell carcinoma? A- Yes

Both in his September 1995 report and his December 1996 report, Dr Harrison made a firm diagnosis of innocence and explicitly excluded malignancy. In the former his conclusion was: “ The features are compatible with those of radiation ulcer. Evidence of malignancy is not seen” in the latter his conclusion was: “ Evidence of malignancy and sarcoidosis is not seen. The features suggest that this is an ulcer caused by trauma to tissue with a poor response because of the radiotherapy. Candidosis is present, possibly because of a similar aetiology.” In essence Professor Sloan’s and Dr Woolgar’s view was that those conclusions were misleadingly and unjustifiably reassuring to Professor Langdon and failed to reflect and alert Professor Langdon, as they should have done, to the fact that in neither case was it possible definitively to exclude the possibility of carcinoma or to allay suspicions as to the possible presence of carcinoma created by the presence in the biopsies of features which they regarded as suspicious, and indeed in the case of the 1996 biopsy highly suspicious, of carcinoma.

Both experts went on to criticize Dr Harrison with varying degrees of emphasis for spending too little time examining the biopsy slides ,(not in fact a specifically pleaded allegation of negligence), failing to take further levels from the biopsy, failing (in the case of the September 1995 biopsy) to perform immunostaining, failing to discuss the case with another pathologist, failing in the 1995 report to recognise and describe cells suspicious of carcinoma and failing to recommend a further biopsy.

Professor Speight did not agree with all those criticisms. However, although it is necessary briefly to address each of them individually, the scope of the difference of views in these areas between Professor Sloan and Dr Woolgar on the one hand and Professor Speight on the other was in my judgment overshadowed by the fact that on Professor Sloan’s and Dr Woolgar’s central criticism there was a significant measure of agreement by Professor Speight.

In relation to the September 1995 biopsy, Professor Speight’s report indicated that in his view there were features revealed on the H and E slides which were “ suspicious for recurrent squamous cell carcinoma.” In oral evidence he said that on the H and E alone, he was no more than 90% sure that there was no malignancy present. In his view in those circumstances Dr Harrison should have gone on to do immunostaining. Given that he did not do so, Professor Speight’s view was that he should have described the suspicious cells on the H and E in his report to Professor Langdon, and further, and critically, alerted Professor Langdon to the fact that he had a lingering suspicion. There was much debate in cross-examination as to what form such a communication of lingering suspicion should have taken. But in my view, given the evidence that Professor Langdon was at this time himself sure on the basis of clinical observation that Mrs Manning was suffering a recurrence of carcinoma, the precise wording that should have appeared in Dr Harrison’s report is only of secondary importance. The critical point is that Professor Speight accepted that “the essence of it is that you would consider it part of the duty of the pathologist to let the surgeon know explicitly or implicitly that you had got a lingering suspicion”.

It follows that on this vital aspect Professor Speight agreed with Dr Woolgar and Professor Sloan that the absence in Dr Harrison’s September 1995 report of any indication of a lingering suspicion fell below the standard required of a reasonably competent pathologist. In my view the duty of care owed by Dr Harrison to Mrs Manning in September 1995 required him to alert Professor Langdon to the fact that it was not possible on the basis of the September 1995 biopsy to eliminate the possibility of the presence of carcinoma and that it was not possible completely to allay the lingering suspicions as to the possible presence of malignancy which should have been created in his mind by the suspicious cells in the biopsy. His failure to alert Professor Langdon constituted a breach of his duty of care.

As explained below in my view if Dr Harrison had communicated such suspicion in his report it is obvious that Professor Langdon would have carried out a further biopsy. It is at the very least likely on the balance of probabilities that he would have done so.

In her written closing submissions Ms Mishcon submitted that even if there was a breach of duty in this regard it had no causative effect for two reasons. The first is that in one of his answers Professor Speight said that a reasonably competent pathologist would either have carried out immunostaining in 1995 or would have added a rider to his report stating that careful review was necessary with a further biopsy being performed if the biopsy did not heal within a reasonable time. Ms Mishcon pointed out that for the purposes of this litigation four different pancytokeratin stains were applied to the 1995 biopsy specimen by Dr Woolgar and/or Professor McDonald (the expert originally instructed by Mr Manning) and there was no keratin positive staining of any suspicious cells. Therefore she submitted immunostaining would have supported Dr Harrison’s diagnosis of a chronic ulcer. Her second point was that the 1995 biopsy was observed to be healing a week after the biopsy had been taken and had completely healed when Mrs Manning was reviewed two and a half weeks later. There would therefore have been no need for a further biopsy. Thus she argued if it is found that Dr Harrison should have carried out immunostaining or added a rider to his report advising careful review, his failure to do so had no causative effect in that (I infer her argument to run), Professor Langdon would not then have carried out a further biopsy.

In my view there are two answers to Ms Mishcon’s first point. The first is this. Doctor Harrison elected not to do immunostaining. In those circumstances Professor Speight’s view was that since it was not possible safely to exclude the possibility of carcinoma on the basis of the H and E slide, any report to Professor Langdon would be misleading if it omitted to alert him to lingering doubts as to whether there was carcinoma present or not. Even if, which for reasons explained below I do not accept, it would have been possible safely to exclude the possibility of carcinoma on the basis of immunostaining had Dr Harrison carried it out, it does not follow that Dr Harrison’s breach of duty in writing a definitive report based on the H and E slide giving a definitively innocent diagnosis without alerting Professor Langdon to lingering suspicions did not lead to Professor Langdon failing to carry out a biopsy which he would have carried out had he been so alerted. In other words, given that Dr Harrison’s breach of duty consisted in writing a misleading report and failing to alert Professor Langdon to lingering doubts which a reasonably competent pathologist who had not done immunostaining should have had, the causative effect of the breach is to be tested by reference to what would have happened if he had alerted Professor Langdon to the doubts, not by reference to what would have happened if he had not written the report at all at that stage.

The second answer is this. The agreed evidence was that, as was known at the time, immunostaining was subject to significant levels of false negative rates.

Professor Sloan when asked about this table and the Lewis Olsen paper, first of all stated his belief that the latter was relevant even though it related to SPCC in the larynx. Although in the larynx the SPCC has a better clinical outcome than in the mouth, it is in his view the same tumour. The 35% false negative rate in the Lewis Olsen series was therefore in his view significant. The Lewis and Olsen paper “tells us that it is not safe to exclude the diagnosis of spindle-cell carcinoma if the immunohistochemistry for keratin is negative on the suspicious spindle-cells.” The Lewis and Olsen paper referring to positive keratin expression rates of 50% to 75% in the previous studies stated: “ Our finding of 65% is in place for these results and this rate is roughly equivalent to that reported in a recent and larger series of malignant mixed… tumours…” It concluded that: “ The fact that not all SPCCs show detectable epithelial differentiation is not viewed as a contraindication to the diagnosis of SPCC carcinoma. Possible explanations for the lack of such features include (1) Sampling errors (2) Insufficient sensitivity of detection methods including fixation and processing variables and (3) Progressive loss of identifiable epithelial markers.” Professor Sloan agreed with those possible explanations for the false negative rates. In relation to the latter he pointed out that in SPCC there is a conversion from a carcinoma that was tied to sarcoma at this time and as the tumour progresses the percentage of cells which express cytokeratin become less and there may be no expression at all. He further said that the sort of false negative rate of 42% reflected in the average 58% positive figure in the table in the Lewis and Olsen paper was one which he would expect to have been known in the mid 1990s and was one which a reasonably competent pathologist should have known before the 1995 and 1996 biopsies. By 1995 he said that immunohistochemical markers were in routine practice and he would have expected a competent pathologist to have known about these figures. His conclusion was that a reasonably competent pathologist in 1995 and 1996 would have known that negative lack of staining could not safely exclude the diagnosis of SPCC.

On this basis Professor Sloan expressed the view that in 1995 a reasonably competent pathologist could not safely have excluded malignancy on looking at the material available to Dr Harrison. A reasonably competent pathologist in his view should have recognised the suspicious cells and having undertaken cytokeratin staining on further levels, if they were negative (as with the benefit of hindsight and the Woolgar/McDonald immunostaining we know they would have been) should have asked for a further biopsy. In other words the purpose of performing immunostaining would have been to see if malignancy could be confirmed, but not to enable a positive diagnosis of innocence to be made.

If Professor Sloan’s view is right, it follows that if Dr Harrison had performed immunostaining on the September 1995 biopsy, although it might, and in Professor Speight’s view would, have “supported” Dr Harrison’s diagnosis of a chronic ulcer it would not have enabled him safely to exclude the possibility that that diagnosis was incorrect and that in fact the explanation for the suspicious cells was carcinoma. On this point Dr Woolgar agreed with Professor Sloan. What of Professor Speight?

Professor Speight’s evidence on this point was not altogether consistent. The starting point is that, as mentioned above, he accepted that any reasonably competent pathologist looking to exclude carcinoma could not safely do so unless he was sure beyond reasonable doubt that it was not there. His understanding of “beyond reasonable doubt” was: “ It can never be 100%, but as close as we can get…I would like to be 99% if that were possible.” Ninety percent would not be good enough because of the 1 in 10 chance of missing a carcinoma. Applying that conclusion to the September 1995 biopsy Professor Speight confirmed his view that because Dr Harrison did not do an immunostaining he ought to have had a 10% residual doubt and therefore ought to have alerted the surgeon to the continuing existence of that doubt. He also said that a reasonably competent pathologist with a 10% residual doubt must take whatever steps he reasonably can to try and eliminate that residual doubt. Such steps might include asking the surgeon for another biopsy, might be taking further levels, might be doing immunostaining, might be discussing the case with a colleague.

Initially in evidence in chief Professor Speight said that having had 90% confidence that the September 1995 biopsy was explicable as a chronic ulcer on the basis of his examination of the H and E slide, after he had examined Dr Woolgar’s immunocytochemistry he was 99% sure that it was a chronic ulcer. His residual 10% doubt, on the H and E slides was based on the atypia of the epithelium adjacent to the ulcer which could either have a sinister explanation in the form of malignant cells invading the connective tissue or an innocent explanation in the form of proliferating epithelium or alternatively be explicable innocently by the cross-cutting effect of a biopsy which can make an innocent retepeg of migrating epithelium appear to be a small isolated and therefore possibly malignant island of epithelium in the connective tissue. Professor Speight’s evidence in chief was that the immunocytochemistry performed by Professor McDonald/Dr Woolgar “confirmed to me” that there were no epithelial cells invading the connective tissue from the epithelium adjacent to the ulcer. Thus he said that although there were highly suspicious features in the September 1995 biopsy such that a pathologist should immediately have been on high alert or have had a very high index of suspicion because in a spindle-cell carcinoma one sees the atypical epithelium or carcinoma overlying the lesion and the spindle-cells tend to proliferate or invade away from that epithelium into the connective tissue, his 90% confidence that the September 1995 biopsy was innocent based on the H and E increased to 99% based on the immunostaining, however elsewhere in his evidence in chief Professor Speight accepted that if he had even one percent doubt that there was a cell on the deep aspect which might be malignant he would alert the surgeon and that any reasonably competent pathologist would have to alert the surgeon if he could not allay his suspicion and was at all uncertain as to whether there was malignancy.

On its face there appeared to be an inconsistency between Professor Speight’s view that a 99% level of confidence based on the combination of the H and E and the immuno “confirmed” his innocent diagnosis on the one hand and on the other hand his evidence that a 1% doubt as to malignancy was sufficient to impose on a reasonably competent pathologist a duty to alert and would in fact have made Professor Speight alert the surgeon to the fact that it was not or had not been possible to exclude malignancy. The inconsistency re-emerged in cross-examination when Professor Speight said at one point that the immunostaining allayed his suspicions completely. Elsewhere Professor Speight had referred to what he described as the black swan phenomenon, a metaphor he used to describe the fact that in science it is never possible with 100% confidence to exclude any possibility. Thus although nobody has ever seen a black swan and all swans ever seen have been white, it is not possible for a scientist definitively to say with 100% certainty all swans are white, it not being possible in the absence of a comprehensive world-wide search to eliminate the theoretical possibility of a black swan. I understood the implication of Professor Speight’s reference to the black swan phenomenon to be that where the only thing that prevents a pathologist from giving a positive diagnosis is the inability to exclude the black swan, it is legitimate for a reasonably competent pathologist to make a positive diagnosis. It would appear therefore that when Professor Speight expressed the view that a reasonably competent pathologist would have to alert the surgeon if he had a 1% doubt, that by a 1% doubt he had in mind something more substantive than the inability to exclude the hypothetical black swan.

In relation to false negative rates on immunostaining, Professor Speight was critical of the overall 58% cytokeratin positivity (i.e. 42% false negative) which appeared in the table in the Lewis and Olsen paper. He pointed out that one of the studies quoted in the table as showing a 50% positive rate in fact in the body of the text was recorded as showing an 88% positive rate. In addition the paper did not include the results of a paper by Leonardi which, albeit on a small sample of 8 tumours, showed a 100% positive rate which would have made a difference to the average. Accordingly he said that the paper was flawed and he did not trust it. He did however accept that the false negative rate might be as high as 25%. Despite accepting that 25% false negative rate, Professor Speight said (in the context of the December 1996 biopsy, but the point is of equal application to the September 1995 biopsy) that the fact that the immunostaining was cytokeratin negative made the difference between 90% certainty in the H and E slides that the biopsy was innocent and “as absolute certainty as we can be” that the biopsy was innocent based on the immunostaining. Professor Speight said that it would only be if he was at least 60% suspicious that there was malignancy on the H and E slide that his suspicions would not be allayed by a negative cytokeratin on an immunostaining. He cited by was of example that if the 2001 biopsy had been negative for cytokeratin that would not have allayed his fears and would not have prevented him concluding that it was probably a carcinoma.

It was put to Professor Speight by Mr Grace QC, rightly in my view, that there was a logical flaw in this aspect of his evidence. As Professor Sloan pointed out the reason for performing immunostaining in a case where the pathologist has a 10% residual doubt as to whether there is malignancy is to see whether that doubt can be confirmed. If the immunostaining identifies an epithelial cell in the connective tissue that confirmation would be provided. However the reverse proposition does not follow. Given a 25% false negative rate, in any individual case in which the immunostaining is negative the pathologist has no way of telling whether it is one of the 25% false negatives or one of the 75% true negatives. Where the result is negative the immunostaining therefore logically takes matters no further, bearing in mind the overriding need to exclude carcinoma, since the pathologist in order to be safe would be bound to assume that it might be one of the 25%.

There was the following exchange between Mr Grace QC and Professor Speight: “… at that point in time you do not know whether it is going to be one that is in the 25% false negative group or one that is in the 75% positive group do you? Prospectively you do not know…. A- No no of course you don’t. Q- …which it is going to be? A- No but from the cytological features one could deduce whether you expected it to be positive or negative, based on the cytomorphometry. Q- Well if that is the case then there’s not much point in ever doing immunostains? A- That’s not correct I said “one can deduce, but one would not rely on deduction alone in that case…” (emphasis added). In that exchange Professor Speight appeared to accept the logic of the point being put to him by Mr Grace QC. The exchange continued: “ All I am suggesting Professor is that you cannot simply say: ‘This is cytokeratin negative, therefore it cannot be malignant’ because you don’t know whether it one of the 25% group or not? A- No, but if it is … Q- You cannot simply say: ‘It increases me from 90% to 97.5%’ could you? A- Well if it is cytokeratin negative, that is very strong evidence that the cells are not epithelial, so it suggests they are not epithelial. Q- Unless it is one of the 25% false negative categories? A- Yes, but in conjunction with all the other features, which we have seen through, it makes it very highly unlikely that the cells are epithelial because an epithelial cell in the connective tissue would be malignant and these cells did not show evidence of malignancy. Q- Well this becomes rather circular, does it not, because you are going back there to rely upon your assessment on the H and E stains? A- Which is vitally important, absolutely. Q- Well really to the exclusion of all else in your mind? A- Not to the exclusion of all else; in all the features taken together. Knowledge, experience, judgment, the context of the cells, their cytomorphometry, where they find themselves, their relationship to their partners, and the immunocytochemistry.”

Although in this latter exchange Professor Speight seemed somewhat resistant to the logic of Mr Grace QC’s point, the logic of it is in my view unanswerable. While a cytokeratin negative might indeed be very strong evidence that the cells are not epithelial, it would be over simplistic to suggest that a 90% level of confidence could be increased to a 97.5% level of confidence by virtue of the 75% positive rate on immunostaining. Indeed Professor Speight did not appear to suggest such an approach. Moreover and in any event even if such an approach were legitimate, one would be left with a 2 ½% possibility of carcinoma. Applying the very high test to which I have referred earlier in this judgment and indeed applying Professor Speight’s own approach, a pathologist who was left with a 2 ½% doubt as to malignancy could not safely exclude the possibility of malignancy.

Taking Professor Speight’s evidence in the round, it did not seem to me that he was expressing the view that a reasonably competent pathologist who had, as he said should have been the case, no more than a 90% level of confidence that the biopsies in September 1995 and December 1996 were innocent, could safely have excluded the possibility of carcinoma by virtue of the negative cytokeratin on the two immunostainings done by Professor McDonald in September 1995 and by Dr Harrison in December 1996. Even if my understanding of Professor Speight’s evidence is incorrect in this respect, it does not affect my view that in such circumstances no reasonably competent pathologist could safely have excluded carcinoma in respect of either biopsy. In reaching that conclusion I am of course mindful of the so called Bolam test. In his summing up to the jury in that case to which I have referred earlier McNair J said: “ He is not guilty of negligence if he has acted in accordance with the practice accepted as proper by a responsible body of medical men skilled in that particular art… putting it another way round, a man is not negligent if he is acting in accordance with such a practice merely because there is a body of opinion that would take a contrary view.” The Bolam test was reformulated by Lord Scarman in Sidaway v Governors of Bethlem Royal Hospital [1985] AC 871,881 F: “ A doctor is not negligent if he acts in accordance with a practice accepted at the time as proper by a responsible body of medical opinion even though other doctors adopt a different practice.”

However it is not a complete answer to a claim of negligence against a doctor that evidence has been adduced from an expert that the act or omission complained of was approved by a responsible body of medical opinion or indeed that the expert, being himself a reasonably competent practitioner, would have acted in the same way as the defendant. As mentioned above, in Bolitho v City and Hackney HA [1998] AC 232 Hl, the House of Lords held that the Bolam test is subject to the proviso that the court must be persuaded of the logical force of the expert evidence in question.

The matter is addressed by the learned editors of Jackson and Powell on Professional Liability 6^th edition 2007 at paragraph 13-024 in these terms:

In my respectful view the conclusion of the learned editors of Jackson and Powell in the latter statement is correct.

Applying the approach prescribed by Lord Browne-Wilkinson in Bolitho to Professor Speight’s evidence, it seems to me that if and to the extent that he was suggesting that a pathologist who ought to have had no higher than a 90% level of confidence that there was no carcinoma present in the September 1995 biopsy could nonetheless safely have excluded carcinoma on the basis of a negative cytokeratin on immunostaining, that view is inconsistent with the requirement of a very high level of confidence on the part of a pathologist before he can safely exclude carcinoma which was

explicitly and implicitly approved by the Court of Appeal in Penney and

explicitly endorsed by Professor Speight in the extracts of his own evidence cited above.

It follows that in my view a reasonably competent pathologist, who should have had no higher than a 90% level of confidence that there was no carcinoma present in the September 1995 biopsy based on the H and E slide alone could not safely have excluded that possibility by reason only of a cytokeratin negative immunostaining. Thus, even if, instead of writing the pathology report which he in fact did in September 1995, Dr Harrison had gone on to perform immunostaining, he would still have been bound to alert Professor Langdon to the existence of lingering doubts as to the possibility of carcinoma. As a result if, as in my view is the case, Professor Langdon would in those circumstances have carried out a further biopsy, Ms Mishcon’s submission that had Dr Harrison performed immunostaining in September 1995 there would have been no further biopsy is in my view incorrect.

The answer to Ms Mishcon’s second point, namely that the 1995 biopsy was observed to be healing a week after the biopsy had been taken and had completely healed when Mrs Manning was reviewed two and a half weeks later, so that there would have been no need for a further biopsy is as follows. Ms Mishcon’s argument is based on one answer given by Professor Speight where he said that in the absence of immunostaining a reasonably competent pathologist in September 1995 would have added a rider to his report stating that careful review was necessary with a further biopsy being performed if the biopsy did not heal within a reasonable time. Professor Speight expanded on that answer. He said that 14 days is the guide for waiting for a lesion to heal. If it hasn’t healed in 14 days then the surgeon has to use his judgment as to whether or not to take another biopsy.

Thus where the pathologist recommends a further biopsy if the lesion does not heal, he would expect the surgeon to understand the pathologist to mean if it does not heal within 14 days. Thus the risk of allowing undiagnosed cancer would continue for a maximum of 14 days which he regarded as a negligible and extremely small increased risk in terms of the impact on ultimate prognosis should there turn out in fact to be malignancy. On the chronology in this case the biopsy was performed on 14 September, the pathology report was written on 19 September, on 20 September Mrs Manning was seen by Professor Langdon and Dr Henk at the Marsden Clinic and Professor Langdon’s notes record on examination “healing- painful??” and on 17 or 18 October Mrs Manning was reviewed by Professor Langdon whose notes record: “Tongue healed!...”. Because Mrs Manning was not seen between 20^th September and 17th or 18^th October we do not know how soon, if at all, before 17^th or 18^th October her tongue healed and in particular whether it healed within 14 days. That is probably because, Dr Harrison’s actual pathology report having been negative, there was no urgent review of Mrs Manning, Professor Langdon’s notes concluding on 20^th September that they “will keep a very close eye on her in the ensuing months.” No doubt had a report been written in the terms contemplated by Professor Speight in the answer to which I have just referred, Mrs Manning would have been reviewed within a week or two of the biopsy report to see if the lesion had in fact healed. What such a review would have revealed we cannot know. What we do know is that after one week it was healing but had not yet healed. If the only issue bearing on a decision whether to perform a further biopsy was whether the lesion was healing and how long it was taking to heal I am inclined to believe that even if it had not completely healed within 2 weeks the fact that it was in the process of healing might have been sufficient to persuade Professor Langdon to hold back, with the result that given that it did heal no later than 17^th or 18^th October no biopsy would have been performed. However in my judgment it is unrealistic to suppose that the issue of the healing of the lesion would have been the only issue bearing on that decision.

It is impossible to ignore two further vital factors. The first is that the answer of Professor Speight relied on by Ms Mishcon was only one of the ways in which he expressed his views on this topic. Of greater importance in my view was his confirmation that the essential point which a reasonably competent pathologist would have been obliged to communicate to Professor Langdon was the existence of lingering doubts based on the H and E slides. The precise language was he accepted less important than the essential importance of the obligation to communicate the existence of lingering doubts. That is to say doubts as to whether there might be carcinoma present. There was some debate between the three pathology experts as to whether the obligation when communicating the lingering doubts was confined to referring to the existence of suspicious cells or extended to an explicit mention of the suspicion of possible carcinoma. It seemed to me that such differences of view as there were on this point were of marginal relevance. Even if all that was required was reference to the existence of suspicious cells in circumstances where the suspicion could not be allayed, the necessary implication as it seems to me of the reference to suspicious cells or suspicion would be a suspicion on the part of the pathologist that they might be malignant. In what other sense could they be suspicious and of what else could the pathologist be communicating his suspicion other than the possible presence, albeit unidentified and undetected, of malignancy of some kind?

As mentioned above, in his report in the descriptive section in relation to the September 1995 biopsy under microscopic examination Professor Speight wrote: “…in addition however the adjacent epithelium shows mild atypia and scattered throughout the ulcer there are prominent plump polygonal and spindle cells with large open nuclei with prominent nucleoli. In one area adjacent to the ulcer there are two islands of squamous epithelium in the superficial corium showing some evidence of atypia and with prominent enlarged nuclei. In another area in the centre of the ulcer there are two small islands of epithelium showing cytological atypia and one large prominent abnormal mitotic figure. The features are those of widespread ulceration consistent with radiation damage. In addition there are features suspicious for recurrent squamous cell carcinoma (emphasis added). … The features are consistent with ulceration associated with radiation induced damage. In addition there are scattered suspicious pleomorphic cells within the tissue.” (emphasis added). In his comment and conclusion section he wrote…these features are characteristic of radiation induced damage and thus far I agree with the interpretation of Dr Harrison in his report. In addition however there are many plump and pleomorphic cells within the connective tissue. In places these form small sheets of spindle cells. These are quite consistent with atypical fibroblasts as a consequence of radiation damage (“radiation fibroblasts”). There are also one or two small suspicious islands of epithelial cells. These are suspicious for recurrent carcinoma but may be proliferative for regenerative epithelium at the margin of the ulcer. (emphasis added). I would add that in evidence at trial Professor Speight accepted that aspects of the September 1995 biopsy were not merely suspicious but highly suspicious.

Further in the joint report of all three pathologists Professor Speight agreed that: “There are some features that should have been noticed that were not recorded in Dr Harrison’s report on 19^th September 1995…. while we accept the probability that the 1995 report of “chronic ulcer” is correct we agreed a more descriptive report recording the presence of suspicious cells should have been issued.” When that passage of the joint report was put to him in cross examination Professor Speight accepted that “one way or another, and it does not matter perhaps what form of words is adopted, suspicion should have been conveyed to the surgeon”. (emphasis added). He accepted that that is implicit in that passage of the joint report and was what all three pathologists agreed.

In this respect Professor Speight changed his position in the course of giving evidence. Early on in his evidence he said that Dr Harrison did not in his view fall below an acceptable standard of practice in not doing immunostaining in September 1995 because it was quite reasonable for him to have reached the diagnosis he did following careful examination of the H and E sections. A majority of pathologists at the time in his view would not have done immunocytochemistry in 1995. He also said that while he would have said that there is some evidence of atypia in the epithelium that was not something that a reasonably competent pathologist in his view was bound to do. It would have been good practice but failure to do it would not have indicated incompetence. Later in cross examination he repeated that although he was critical of Dr Harrison for not having done immunocytochemistry he did not think that his failure to do so indicated incompetence. He also said that although he himself could not go beyond 90% confidence of innocence on the H and E slides alone he could not say that Dr Harrison ought also to have had that level of uncertainty on the H and E slides in 1995 because he might be more confident than Professor Speight. He was known to be a very assiduous pathologist, would have spent time looking at every cell and in his mind might have been 99% sure based on his histological examination. However later in his cross examination in the passages just cited Professor Speight accepted that Dr Harrison should have written a more descriptive report recording the presence of suspicious cells and conveyed suspicion to the surgeon and that in September 1995 Dr Harrison should have taken immunostaining and that if, he failed to do so he should have alerted the surgeon to lingering doubt. That is because he accepted that based on the H and E slide there was a 10% lingering doubt in respect of the September 1995 biopsy and no reasonably competent pathologist could fail to alert the surgeon to such doubt. Professor Speight again explicitly confirmed that in September 1995 because Dr Harrison did not do an immunostaining he ought to have had a 10% residual doubt and therefore ought to have alerted the surgeon to the continuing existence of that doubt explicitly or by implication.

I have described this part of Professor Speight’s evidence in some detail because it seems to me of great importance. In its central conclusions that Dr Harrison should have described the suspicious cells in the September 1995 biopsy and alerted Professor Langdon to his lingering doubts Professor Speight was in agreement with Professor Sloan and Dr Woolgar who reached those conclusions with less equivocation in their minds. To them it was very clear. In the case of Professor Speight, although his view that Dr Harrison should have described the suspicious cells was present in his original report, the view that he should have alerted Professor Langdon to lingering doubts as to the possible existence of malignancy was something which he came to accept as being the logical conclusion of (a) his view that it is the duty of a pathologist to alert the surgeon to lingering doubts unless he has excluded such doubts beyond reasonable doubt and (b) his belief that the nature of the suspicious cells in the H and E slides was such that it was not possible by an intellectual process of observation and analysis to get beyond a 90% level of confidence that there was no malignancy.

The question to which these conclusions of the expert pathologists gives rise is what would Professor Langdon have done if he had received a report from Dr Harrison on 19^th September 1995 which, instead of excluding malignancy had alerted him to lingering doubts as to the possible existence of malignancy and described the existence of the suspicious cells identified by the three expert pathologists in some such terms as those used in Professor Speight’s report? To be specific, would Professor Langdon have performed a further biopsy? In my view the answer to that question is clearly yes. The evidence is overwhelming that at the time he commissioned the September 1995 biopsy report Professor Langdon was sure as a matter of clinical observation that Mrs Manning had suffered a local recurrence of carcinoma. Indeed he had had little doubt that that was the case before the earlier July 1995 biopsy. The evidence of Professor Langdon’s state of mind in the period leading up to the September 1995 biopsy is set out in the narrative chronology earlier in this judgment. A clear picture emerges. Thus in his letter dated 2nd August 1995 to Dr Henk he referred to Mrs Manning having come to see him on the 28^th of July as an emergency and referred to the fact that “worryingly there was 10mm exophytic ulcer on the lateral border of her tongue at the site of the original primary….. clinically I had little doubt that this represented local recurrence. …”

In his witness statement he said that when he saw Mrs Manning on 13^th September the site of the biopsy which he had performed on the 28^th of July 1995 remained unhealed, that he noted an exophytic mass at the same site related to the lower left second molar tooth and that “clinically I was concerned that she might have recurrent cancer.”

The reference to the same site is important because of the evidence to which I refer below in more detail that recurrences of SQC normally occur at the same site as the original carcinoma. More generally Professor Langdon’s concerns that what he was seeing might be manifestations of a recurrence of the original carcinoma reflected the facts that (a) there is a high rate of recurrence of mouth cancer and (b) statistically the largest number of recurrences of SQC occur in the first two years. As to (a) in evidence in chief Professor Langdon said : “We know that cancers occurring in the mouth have a propensity to recur. Something like a quarter of all mouth cancers recur after treatment, and they recur in one of two ways. It is called loco-regional recurrence. The loco refers to local, in other words, the cancer recurs at the site where the original cancer was, and the regional bit of loco-regional applies to the head and neck region, and that is because the sort of cancer we are talking about, squamous cell carcinoma, has a propensity for invading cells to enter lymphatic channels, and the lymphatic channels drain into what we call the regional lymph nodes, the lymph nodes in the neck. So whenever you are following up a patient who has a history of mouth cancer above all else the two things you examine is the local site for evidence of local recurrence, and the region for evidence of lymph node metastases.” As to (b) “In cross examination when asked whether throughout the time of follow up of Mrs. Manning there had to be a high index of suspicion for recurrence he confirmed that to be the case but emphasised that this was particularly so during the first two years because recurrence is at its highest, in the first two to three years. He also said, speaking generally of his approach while in practice that if a patient with a history of carcinoma which has been treated, whether by surgery or by radiotherapy, then presents with a lesion at the site of the original carcinoma you would need to have a high index of suspicion that this might be a recurrence.

Specifically in relation to Mrs Manning he confirmed as a fair summary of how things were between Dr Harrison and himself over the years, although not in relation to any particular moment in time, Dr Harrison’s evidence that : “I can recall I had a few discussions with Professor Langdon about Mrs. Manning’s pathology. Generally, it would be if we were passing each other on the stairs or at meetings. We did not have any formal discussions. The nature of the discussions would be that Professor Langdon would say it was a strange case and he was sure there was a carcinoma. I would discuss how all the samples appeared to be post-radiation necrosis as the tissue had altered and weakened, and that there was no indication of malignancy.”(emphasis added).

When asked what his state of mind was in 1995 and 1996 he said that, whereas in December 1996 he did not think that it was a carcinoma because the lesion looked innocent and was not suspicious of recurrent cancer, by contrast in 1995 he was sure it was cancer because Mrs Manning was presenting with recurrent ulcers. When Professor Langdon was asked why that made him sure it was a carcinoma there was the following exchange : “ A  Because recurrence very often – not invariably but very often – presents as ulceration of an area, particularly if the ulcer has features of cancer, thickened margins, underlying induration. Q And were those present in 1995? A.  Not typically, but it was sufficiently unusual for my first thought to be is this recurrent cancer. Q That the ulcer was sufficiently unusual? A.  Yes. Q Can I just ask, so that it’s clear, Mr. Harrison says that you would say it’s a strange case and you were sure there was a carcinoma, and you said that is what you felt in 1995? A.  Yes.(emphasis added). And did you feel that to be the case? A.  We had a number of scares with Mrs. Manning’s tongue from the moment that she was treated at the Royal Marsden, certainly for the first two years. She would return, she would have an ulcer, we would do a biopsy, it would be negative, and this was the pattern of events certainly for the first two years. Q That is 1993 to 1995? A.  Yes, my Lord.”

Thus the background to the commissioning and receipt of the September 1995 biopsy report was that Professor Langdon had been on the lookout for recurrence for some time, had commissioned two biopsy reports in May 1994 and July 1995 each of which cited recurrent squamous cell carcinoma as a differential diagnosis, had little doubt that the exophytic ulcer which he had seen and biopsied in July 1995 was local recurrence, specifically considered that the July 1995 ulcer might be malignant because it was different from the previous biopsy in May 1994 with raised margins which he said can be a classical sign of a cancerous ulcer and because the ulcer was indurated on palpation which he said was one of the clinical indications of cancer and finally noted when he saw her on 13^th September 1995 that the July 1995 biopsy site remained unhealed and that the exophytic mass observed on that day was on the same site. In short Mrs Manning was a source of ongoing concern to Professor Langdon and the negative biopsy report of July 1995 had been unexpected by him. In those circumstances it stands to reason in my view as a matter of common sense that if in his September 1995 biopsy report Dr Harrison had recorded the presence of suspicious cells and alerted Professor Langdon in one way or another to the fact that he had lingering doubts as to whether there might be malignancy present, Professor Langdon would not have been prepared to sit back and await events but on the contrary would have performed a further biopsy in order to seek to resolve what at its lowest would have amounted to a very worrying inability on the basis of the September 1995 biopsy to exclude malignancy. Apart from anything else it was accepted by all the experts that it is possible, albeit unlikely, for a wound to heal over even if cancer cells are present. Indeed Professor Sloan had personal experience of that happening.

At one point in his evidence Professor Langdon said that if he had been told that the September 1995 biopsy contained features suspicious for recurrent carcinoma, although he would not have sat on his hands and would certainly have wanted to keep a very close eye on Mrs Manning, nonetheless because it was an excision biopsy in which he had removed the entire area that was abnormal and it healed up post-operatively he would not have done another biopsy but would have watched it exceedingly carefully to see if it remained healed and if anything changed. When Mr Grace QC challenged this evidence and put to Professor Langdon the passages in Professor Speight’s report referring to evidence of atypia and features suspicious for recurrent spindle-cell carcinoma and suggested that if he had been told that there were those features as described and that they were suspicious for recurrent SCC then given that he was convinced clinically that Mrs Manning was suffering from a recurrence, he would not just have waited and watched, Professor Langdon said: “No. If the pathology report had said suspicious of squamous cell carcinoma of course I would not. I would have repeated the biopsy. But if a pathology report showed mild atypia that is normal in many patients with mouth cancer….”

It appeared at one stage that Professor Langdon was drawing a distinction between a report which referred to the existence of suspicious cells and a report which referred to suspicion of carcinoma and explicitly used the word carcinoma: “Q- … if you had been told of those features, suspicious for recurrent squamous cell carcinoma, you would have carried out a further biopsy? A- Yes indeed, if the pathologist is so concerned that they write in the report, “this is suspicious of recurrent squamous cell carcinoma” or “ I cannot eliminate recurrent squamous cell carcinoma”, then, yes…Q- If the pathologist is so concerned? A- That he actually writes in the report “this is suspicious of cancer” or “ I cannot eliminate cancer” then yes I would repeat the biopsy.”

Professor Langdon returned to this distinction later in his evidence:” I think if the pathologist actually uses the word “carcinoma” in the report, suggesting that there is that possibility, however remote, I would have been prompted to do a further biopsy. It is the use of the word “carcinoma” that outweighs everything else in the report….If a pathologist is willing to add their signature to a report that mentions the possibility of a carcinoma I think, whatever my clinical instinct, I would have probably been obliged or would have been obliged to do another biopsy, as much in a defensive way as in a clinical way really…. there is a big difference between a pathologist talking about suspicious cells and a pathologist committing themselves and using the word carcinoma or cancer. There are always suspicious looking cells in any biopsy of any tissue that has been heavily irradiated. It is because the radiotherapy causes damage fairly unselectively to normal cells as well as cancerous cells so inevitably there will be suspicious cells in such a biopsy. If a pathologist uses the word carcinoma or cancer then that has gone several steps further in their thought process so that is one part of it.”

It was in this way that Professor Langdon sought to square his answer that if Dr Harrison had reported that he had seen suspicious cells and recommended that Professor Langdon should do a biopsy if he had clinical concerns he would not have done a repeat biopsy because it was a generous one and his answer that if a pathologist refers to the possibility or suspicion of carcinoma that is something that would cause him to do a further biopsy. On its face this evidence seemed at first glance somewhat perplexing. Why should a report referring to cells suspicious of carcinoma lead to a further biopsy whereas a report referring merely to suspicious cells should not?

In the latter case the reference to suspicious cells would surely be intended and understood as a shorthand for cells suspicious of carcinoma. Of what else would they be suspicious and if they were not suspicious of carcinoma what would be the point of referring to them being suspicious? The explanation for this apparent inconsistency was I think that the real distinction Professor Langdon was making was not between a report that explicitly used the word carcinoma and one that did not but rather a report which explicitly or implicitly indicated that although there were suspicious cells the pathologist had allayed his suspicions and a report in which the pathologist had been unable to eliminate his suspicions such that he retained lingering doubts. Given the potentially fatal consequences of not doing a further biopsy in circumstances where the pathologist had been unable to eliminate the possibility of carcinoma, it would be most surprising if the surgeon’s decision as to whether or not to perform a biopsy turned on a point of semantics rather than a point of substance. It would be one thing for the surgeon to decide not to do a further biopsy when faced with a report which indicated that although the pathologist had seen suspicious cells he had allayed his suspicions. It would be quite another for the surgeon to decide not to do a further biopsy in circumstances where he was faced with a report in which the pathologist not only drew attention to the existence of suspicious cells but indicated to the surgeon that he retained lingering doubts as to whether there might in fact be carcinoma present as Professor Speight accepted that Dr Harrison should have done..

It is for this reason that in my view the crucial part of Professor Speight’s evidence was his confirmation that in his view a reasonably competent pathologist based on the September 1995 H and E slides would have been bound to alert the surgeon to the fact that he had lingering doubts as to whether there might be carcinoma present and that the precise language was less important than the communication of those lingering doubts. Professor Speight was making it clear that this was a point not of semantics or the precise language used in the report but a point of real substance. Professor Langdon confirmed that this was the correct approach in a passage in his evidence in which he was dealing with what his reaction would have been if in December 1996 he had been told by Dr Harrison that there were cells that were highly suspicious for recurrent carcinoma. Having said that if it had been put in those term he would have re-biopsied, he said this: “ …I wouldn’t have wanted to subject [Mrs Manning] to a delay. Once you have raised the possibility that a biopsy hasn’t ruled out the presence of cancer I would go for the quickest way of getting the information and reassuring her, or if it was positive telling her of the recurrence rather than waiting for a week or ten days to get the [MRI] scan first and then doing a biopsy and then waiting for the report. Q- Because a biopsy is quicker? A- Yes.”

In that passage Professor Langdon was confirming that the trigger for performing a further biopsy would be the raising by the pathologist of the possibility that the biopsy had not ruled out the presence of cancer. There was another passage, this time in the context of September 1995, which gives further support to the conclusion that Professor Langdon’s decision whether to perform a further biopsy would not have been dictated by the semantics of whether the word carcinoma was actually used in the report.: “Q- …Dr Harrison never reported the suspicious cells to you, but what I am asking you about is what you would have done had you had the report of suspicious cells from Dr Harrison, or from whoever the pathologist was. Add to that your own clinical conviction that this was a recurrence, you would not have had any difficulty in getting an MRI scan would you? A- I still wouldn’t have ordered an MRI scan, I would have repeated the biopsy…. Q- But you were sure that this was a recurrence as I understood it… you were sure in 1995 that there was a recurrence. If you had received pathological support for that in the form of a report of suspicious cells then surely you would have wanted to do one and you could exclude recurrence couldn’t you? A- Indeed and that would have been a repeat and wider biopsy.”

It is notable that in that passage in which Professor Langdon confirmed he would have done a further biopsy, the hypothesis made no reference to the word carcinoma but merely to suspicious cells. I would add in passing that at one point Professor Langdon confirmed that if a second biopsy had shown positive that would have led to salvage surgery. On this there was no dispute between the parties with the result that it was common ground that if a further biopsy had revealed evidence of malignancy either in September 1995 or December 1996 Professor Langdon would have carried out salvage surgery. As mentioned above by the end of the trial it was also common ground that the result of such salvage surgery would have been that Mrs Manning would have survived. Thus the critical question in the event of a finding that either in September 1995 or December 1996 that Professor Langdon would have carried out a further biopsy is whether or not such a biopsy would have revealed cancer.

It is also worth pointing out that, as was put to Professor Langdon in cross examination, in 2001 his clinical belief that Mrs Manning was suffering from recurrent cancer was such that neither the fact of a prior negative biopsy nor the adverse aspects of performing yet another biopsy deterred him from performing a further biopsy in June. The significance of this is that there was some suggestion that a further biopsy would or might have involved a partial glossectomy and that a surgeon would not have embarked on such a course lightly. While that consideration was undoubtedly a reason for avoiding an unnecessary further biopsy it would not in my judgment on the evidence have deterred Professor Langdon from carrying out a further biopsy in September 1995 or December 1996 if faced with a report from Dr Harrison which indicated that it had not been possible to eliminate the possibility of carcinoma as to which there remained lingering doubts.

In relation to the December 1996 biopsy, all three pathology experts agreed that it contained features which were highly suspicious of carcinoma. As we have seen Professor Speight in his report under the heading ‘microscopic examination’ stated: “ In addition however there are prominent pleomorphic spindle-cells in the superficial corium and throughout the ulcer. Occasional plump polygonal pleomorphic cells are also noted. The features are those of ulceration consistent with radiation induced damage. In addition there are atypical cells within the connective tissues suspicious for a recurrent spindle-cell carcinoma.” (emphasis added)

In his report Professor Sloan wrote of his microscopic examination of the 1996 biopsy: “… there are interlacing bands of spindle cells and kite-shaped cells most prominent towards the deep aspect of the biopsy. These cells do not have the features of radiation damaged fibroblasts and represent a spindle-cell proliferation. I would have been highly suspicious of spindle-cell carcinoma… in my opinion the features are those of a spindle-cell carcinoma.” (emphasis added)

In her report Dr Woolgar wrote of the 1996 biopsy: “ 2 mm … I agree that the surface epithelium shows proliferation and mild cytological atypia. The spindle and kite-shaped cells described as “ large fibroblasts” are quite striking and in view of the long delay since radiation treatment, they cannot be easily explained as a benign reactive fibroblast proliferation. Furthermore the spindle and kite-shaped cells are more frequent towards the base of the biopsy specimen where some appear to be arranged in small islands and short chords. This cellular arrangement visible on routinely stained sections makes me suspicious that these are epithelial cells- representing a spindle-cell carcinoma…. the immunostained sections provided by Dr Harrison show most of the spindle/kite-shaped cells stained positively with vimentin and on low-power assessment they show no obvious positive staining with CK and CK19. CK has stained the surface epithelium and high-power examination shows weak positive staining of a few cells around the edge of the ulcer. …I requested two immunostains- AE/1 – AE/3 and MNF/116 which I find more reliable markers of oral epithelial cells. Both stains show positive staining for the small islands and scattered individual kite-shaped and spindle-cells within the granulation tissue. The AE/1 – AE/3 staining is strong and. in my opinion, this stain, together with the distribution of the atypical cells, confirms the presence of spindle-cell carcinoma. … given the appearances in the routinely stained sections, I would have expected a competent and experienced pathologist (general and oral) to continue to suspect a spindle-cell carcinoma even though the immunostains were negative. In her summary and opinion Dr Woolgar wrote: “ …the diagnosis is not easy. The specimen was small and superficial. Nevertheless I believe there were sufficient features in the routinely stained sections to make the average pathologist consider the possibility of malignancy.” (emphasis added)

In their joint report the three expert pathologists wrote: “ We all agree that [the December 1996] biopsy shows an ulcerated oral mucosa containing cells that are highly suspicious of spindle-cell carcinoma.” (emphasis added)

In oral evidence Dr Woolgar confirmed her view that the 1996 biopsy was very suspicious of squamous cell carcinoma or spindle/squamous cell carcinoma. When asked what it was that made the 1996 biopsy highly suspicious as distinct from the 1995 biopsy being merely suspicious Dr Woolgar said first that the numbers of spindle-cells were more striking in 1996 and struck you much more easily as soon as you put the slide under the microscope. The degree of suspicion increased because the same features were there but were more obvious than in 1995. In addition the possibility of these features being explicable as a reaction to the previous biopsy which in December 1996 had been some 15 months earlier in September 1995 could be excluded. Similarly a reaction explained by radiotherapy seemed less likely because it was a further 15 months since the original radiotherapy. Finally the biopsy was not something that was obviously infected, ulcerated or painful. It had only been removed at Mrs Manning’s request and not because it looked obviously inflamed or ulcerated which Dr Woolgar interpreted as implying that the changes could not be explained as due to florid ongoing infection ulceration or irritation. Theoretically the irritation could be the result of a sharp tooth biting the tongue on tender tissues but in her view the picture presented in the December 1996 biopsy of plump cells tending to form bands, pleomorphism, the big nuclei, the busyness of the tissue were not something one is faced with every day when looking at a slide from a non-healing ulcer.

In oral evidence Professor Sloan said that the December 1996 biopsy had a greater cell density and was more hypercellular than the September 1995 biopsy and was for that reason highly suspicious. A comparison between the two biopsies, a procedure he described as routine particularly if the pathologist recognises highly suspicious features in the later biopsy, would have led him to think that the December 1996 lesion was a bit more cellular and a bit more worrying than in September 1995. Such a comparison would also have flagged up to the pathologist that there had been a suspicious lesion in September 1995 followed by a second lesion in December 1996 which would automatically lead the pathologist to ask the question: Is this a recurrence of the first lesion, which in itself would increase the degree of suspicion. Professor Sloan said that in his view it was relatively easy to be highly suspicious of the December 1996 biopsy. It was “ not difficult in the sense that some of the spindle-cell tumours that one rarely encounters have a range of bizarre features that makes it really difficult to actually put the diagnosis on. I think in this case we were looking at the sarcomatoid part of the spindle-cell carcinoma and I think it was relatively easy if you like to be highly suspicious of the 1996 biopsy. The difficulty was really more in relation to not having a bigger biopsy to establish a diagnosis.”

Later in his evidence he said that when he received all the case material he was convinced that he was looking at spindle-cell carcinoma in late 1995 and 1996.

Professor Speight in oral evidence confirmed that in his view both the September 1995 and December 1996 biopsies were highly suspicious. In one way the 1996 biopsy was less suspicious in that the adjacent epithelium did not show atypia but was just very typically reactive. On the other hand in his view the hypercellularity was more suspicious in December 1996 than in September 1995 as was the fact that in December 1996 there were more bands and suspicious arrangements of cells including at, but not confined to, the deep margin. In Professor Speight’s view the same amount of very high vigilance was necessary in December 1996 as in September 1995 to seek to exclude carcinoma.

Professor Sloan and Dr Woolgar on the one hand and Professor Speight on the other differed markedly in their conclusions as to the impact of the suspicious features in the December 1996 biopsy on the appropriate diagnosis. In his report Professor Sloan said that he would have requested cytokeratin markers, multiple levels and sought the opinion of an experienced colleague with expertise in spindle-cell tumour diagnosis.

In his view any other experienced oral pathologist would have been highly suspicious and would have requested cytokeratin markers, studied multiple levels and discussed the case with a specialist diagnostic pathologist. In Professor Sloan’s opinion the features were those of a spindle-cell carcinoma. He would have expected an experienced oral pathologist to have raised this possibility as a differential diagnosis in the report and to have prepared multiple levels, performed a panel of immunostains and discussed the case with an expert on spindle-cell tumours.

Later in his report Professor Sloan wrote: “ It is my opinion that spindle-cell carcinoma was present in 1996… this opinion is based on the staining performed by Dr Woolgar and Professor McDonald as well as on the morphological features. The biopsy was superficial and cytokeratin staining was negative as far as can be assessed from the original slides and reports. The report does not convey a strong sense of suspicion of recurrent cancer. I think that insufficient attention was given to the presence of atypical mitotic figures in the spindle-cells which should have caused concerns. An experienced oral pathologist should have sought an expert opinion from a specialist at a cancer centre when faced with these worrying bands of cells in a post-irradiation setting and would have alerted the surgeon to the possibility of malignancy in the differential diagnosis.”

In oral evidence Professor Sloan acknowledged that following discussion with Professor Speight at the joint experts meeting he had revised his view as to the presence of atypical mitotic figures in the spindle-cells and accepted that there were none. However his diagnosis and conclusions remained as set out in his report.

Doctor Woolgar in her report wrote: “ I would have examined multiple levels through the tissue block and I would have requested a range of cytokeratin markers. I think a competent experienced pathologist (general and oral) would have undertaken similar action- they should have noticed the atypical cells and their appearance and arrangement and actively sought to characterise them. The immunostained sections provided by Dr Harrison show most of the spindle/kite-shaped cells stained positively with vimentin and on low-power assessment, they show no obvious positive staining with CK and CK19. CK has stained the surface epithelium and high-power examination shows weak positive staining of a few cells around the edge of the ulcer. The reporting pathologist Dr Harrison concluded that the atypical cells within the exuberant granulation tissue were fibroblasts and that there was no evidence of malignancy. I requested two immunostains- AE/1-AE/3 and MNF/116 which I find more reliable markers of oral epithelial cells. Both stains show positive staining for the small islands and scattered individual kite-shaped and spindle-cells within the granulation tissue. The AE/1-AE/3 staining is strong and in my opinion this stain together with the distribution of the atypical cells confirms the presence of spindle-cell carcinoma. The choice of immunostains depends on both the laboratory and the individual pathologist. Most laboratories and individual pathologists tend to try out a range of immunostains and select the ones that seem most reliable in their hands. The stains may be referred to by different names, by different suppliers and laboratories and I am uncertain of the precise staining profile the CK and CK19. Nevertheless it is likely that CDK and CK19 were the stains that were used by Dr Harrison at that time and that he considered that they were reliable. Nevertheless given the appearances in the routinely stained sections, I would have expected a competent experienced pathologist (general and oral) to continue to suspect a spindle-cell carcinoma even though the immunostains were negative. In such cases the pathologist would normally request a further, deeper biopsy specimen which I believe would have led to the correct diagnosis of spindle-cell carcinoma.”

In her summary and opinion Dr Woolgar wrote: “ In my opinion additional staining has confirmed the presence of spindle-cell carcinoma in [December 1996]. The diagnosis is not easy. The specimen was small and superficial. Nevertheless I believe there were sufficient features in the routinely-stained sections to make the average pathologist consider the possibility of malignancy. The reporting pathologist noticed these features and requested two immunostains CK and Vimentin. I assumed that Dr Harrison routinely relied on these two immunostains and considered them reliable. However in my opinion, an experienced oral pathologist with a declared interest in oral cancer (such as Dr Harrison) should have put more weight on the morphological characteristics including the presence of atypical mitotic figures. I believe such features would seriously concern any experienced pathologist. I think most pathologists (both general and oral) would have requested a larger panel of immunostains including AE/1-AE/3 and MNF/116.

Doctor Harrison’s use of words and phrases such as “suggest” and “appear to represent” in the pathology report does convey a sense of uncertainty but the report fails to stress the small, superficial nature of the specimen and it does not recommend a further biopsy if there is ongoing clinical concern or suspicion of recurrence. I would expect an experienced pathologist to clearly point out the uncertainties and the need for a further biopsy unless the clinical lesion healed completely and the clinician was confident that the possibility of malignancy had been excluded.”

Later in her report Dr Woolgar wrote: “ It is unfortunate that specimen 5 (642/96) was the shallowest specimen- only 2mm thick. A larger biopsy at this stage may well have made the correct diagnosis more obvious. I would have expected an experienced pathologist (general and oral) who felt unable to make a firm diagnosis of malignancy on such a small superficial specimen but was suspicious to request a larger/deeper biopsy as soon as possible since the risk of misdiagnosing cancer far outweighs the discomfort and potentially damaging effects of a redone biopsy procedure.” Doctor Woolgar, like Professor Sloan, accepted in evidence that she had been wrong about the presence of the atypical mitotic figures but nonetheless maintained her overall conclusions.

Professor Speight in his report wrote of the December 1996 biopsy: “ Examination of immunocytochemical stained sections shows that the tissues are negative for cytokeratin 19. The section labelled CK shows positive staining for the overlying epithelium and occasional small positive cells within the ulcer slough. This is consistent with regenerative epithelium within an ulcer. The suspicious spindle-cells in the superficial corium are negative for cytokeratin. The section labelled Vim (presumed Vimentin) shows that the spindle-cells are positive, consistent with them being fibroblasts. Comment and conclusion; the report issued from King’s Health Care dated 10^th December 1996 signed by Dr J D Harrison describes an ulcer and changes consistent with radiation damage. The report notes the suspicious cells and records immunocytochemical stains for cytokeratin. The report concludes that the lesion is an ulcer caused by trauma associated with radiotherapy. It also notes the presence of candidal infection. This case has been reported and stained appropriately and I agree with the interpretation and diagnosis. These features are consistent with radiation induced damage to the mucosa and the atypical cells being radiation fibroblasts.” In his comment on the pleaded allegations in relation to the December 1996 biopsy, Professor Speight wrote inter alia:” Allegation 3… (d) there is evidence in the report that Dr Harrison did consider malignancy and undertook steps to exclude it. There was no reason why his thought processes, rather than his final conclusion, should have been reported to Professor Langdon. (e) There is evidence in the report that Dr Harrison did consider the possibility of malignancy. He carried out immunocytochemical stains to exclude the possibility that the noted atypical cells were epithelial. (f) The evidence from the staining at the time and in a retrospective examination of the material suggests that there was no evidence of malignancy at the time.

Therefore his conclusion was not wrong. In my opinion, having reviewed the whole case, it is extremely unlikely that there was malignancy at the site in 1996. The histology in 1996 is quite consistent with post-radiation change and the scattered spindle-cells although pleomorphic are loosely arranged in an organising granulation tissue. This is quite different from the appearance as seen in 2001 where the spindle-cells are arranged in sheets and more discreet cellular masses towards the deep aspect of the specimens.”

In oral evidence, although Professor Speight maintained his agreement with Dr Harrison’s benign diagnosis of the December 1996 biopsy, he accepted that on the H and E section alone, just as with the September 1995 biopsy, he was unable to reach a higher level than about 90% confidence that there was no malignancy. He would thus have had a roughly 10% residual doubt as to the possible existence of carcinoma. Before being asked questions about it in the witness box he said that he had not thought about putting a figure on his level of confidence and his residual doubts, but, asked to do so, having said initially that his confidence would have been perhaps a bit more than 90% he confirmed that he was happy with 90:10, his overall conclusion being that the evidence was consistent with a healing chronic ulcer. When asked if there were any stigmata of malignancy on the H and E section of the December 1996 biopsy, Professor Speight said that there was pleomorphism of the cells which he satisfied himself was due to sectioning through randomly orientated fibroblasts rather than what he called true pleomorphism. In addition there were atypical cells which showed odd shapes with some hyperchromatism which were much fewer in number and which he regarded as being radiation fibroblasts, which he described as true pleomorphism which could not be explained away by a sectioning effect. In his view the plump cells although some were present on the deep aspect were distributed fairly evenly throughout the lesion as one would expect in a healing ulcer.

This contrasted with the position in 2001 where they were focused on the deep aspect. There were also atypical cells within the connective tissue which were suspicious for recurrent spindle-cell carcinoma. Further there were cells which could have been mitotic (although one of which he considered to be apoptotic and therefore innocent) but they were so few that he did not record them in his report.

Professor Speight said that in his opinion an experienced consultant oral pathologist looking at the December 1996 section should be able to use a deductive process and come to the conclusion that this was a chronic ulcer. However based on the H and E slide alone, he would have to have a 10% doubt and thus could not have sufficient confidence on the H and E slide alone confidently to exclude malignancy definitively. For that reason in his view a reasonably competent pathologist would have had to go on to do immunostaining.

In relation to the effect of immunostaining on the diagnosis, Professor Speight’s evidence was similar to his evidence on the September 1995 biopsy. That is to say initially he said that with immunostaining “that brings it up to as certain as one can be, I suppose the 99% … it is the lingering doubt about the possibility that the black swan is still there which the immunocytochemistry helps allay that final doubt.”

This was consistent with the fact that when it was put to Professor Speight that contrary to Dr Harrison’s evidence that he did not regard immuno as being necessary because he had excluded malignancy to his own satisfaction on the H and E slide, he could not have done so to more than 90%. Professor Speight’s answer was: “ I don’t know what was in his mind but I know he did the immuno and I know it was negative. … I can’t say to what degree of confidence he eliminated it before he did his immunocytochemistry, but he must have had a lingering need to reassure himself or otherwise he would not have done any immunocytochemistry.”

However as set out above, Professor Speight accepted in cross examination that immunostaining was subject to a 25% false negative rate and thus had no answer to Mr Grace QCs point that the immunostaining in 1996 could not totally allay the residual 10% lingering doubts left on the H and E slide. Professor Speight had earlier accepted that any reasonably competent pathologist seeking to exclude carcinoma could not safely do so unless he was sure beyond reasonable doubt that it was not there, that if you have a reasonable doubt after doing all your intellectual reiterative processes then a reasonably competent pathologist cannot say a biopsy is not malignant and that if a pathologist has a 10% residual doubt on a biopsy which he thinks is very likely to be innocent and he cannot rule out the lingering doubt he has to alert the surgeon to the existence of the lingering doubt. Although of course in September 1995 the position is much clearer in that Dr Harrison did not carry out immunostaining and thus could not reasonably have reached more than a 90% level of confidence that there was no malignancy, the logic in my view is the same in both cases.

I have already expressed my view that even if Dr Harrison had performed immunostaining in September 1995 (as Professor McDonald/Dr Woolgar did) the well known phenomenon of false negative rates meant that even a negative staining of the suspicious cells would not have been sufficient to allay the 10% lingering doubt with which he should have been left after examining the H and E slide and thus would not have relieved a reasonably competent pathologist in the position of Dr Harrison of the duty to alert Professor Langdon to the lingering doubts as to the possibility of the presence of carcinoma. Even though in December 1996 Dr Harrison did in fact perform a degree of immunostaining which showed negative, for precisely the same reasons as would have applied if he had done immunostaining in September 1995, in my view the false negative phenomenon meant that a reasonably competent pathologist in his position could not have sufficiently allayed his lingering doubts and suspicions to the point where he was relieved of the duty to alert Professor Langdon to them. I would add, although my finding is not dependant on this, that in the immunostaining which was done for the purpose of the trial the so called archipelago stained positive. Whatever the correct interpretation of the archipelago is, in my view it is clear that it created a level of doubt which at the lowest would have required Dr Harrison to alert Professor Langdon to lingering doubts if he had performed such an additional immunostaining.

For these reasons in my view, the duty of care owed by Dr Harrison to Mrs Manning in December 1996 required him to alert Professor Langdon to the fact that it was not possible on the basis of the December 1996 biopsy to eliminate the possibility of the presence of carcinoma and that it was not possible completely to allay the suspicions created by the highly suspicious features which, unlike in the case of the September 1995 biopsy report, Dr Harrison did to some extent identify in the descriptive part of his December 1996 biopsy report. Doctor Harrison’s failure to so alert Professor Langdon constituted a breach of his duty of care.

As with the September 1995 biopsy, this gives rise to the question whether Professor Langdon, had he been so alerted by Dr Harrison, would have performed a further biopsy. Although the answer is not as clear cut in my view as in the case of September 1995, on the balance of probabilities I believe that he would have done so. It is clear from the evidence both documentary and oral that Professor Langdon’s state of mind in December 1996 was quite different from what it had been in September 1995. In September 1995 he had been sure clinically that Mrs Manning was suffering recurrent carcinoma before he carried out the biopsy and the initiative for carrying out a biopsy was that of Professor Langdon who wanted to see if it would confirm his clinical suspicion. He had been in little doubt clinically that the lesion seen in July 1995 represented local recurrence, both that lesion and the September 1995 lesion had been on the same site as the December 1993 original carcinoma, the July 1995 biopsy site remained unhealed when he reviewed Mrs Manning on 13^th September 1995 and clinically the September 1995 lesion had features which he described as characteristic of cancer and September 1995 was well within the expected period for a recurrence.

By contrast in December 1996 Professor Langdon performed the biopsy not to allay his own suspicions but rather to allay Mrs Manning’s anxieties. When he had seen her on 19^th November 1996 at King’s he had found a fibrous nodule at the anterior margin of the previous scar 5 millimetres in diameter. His notes record that his view was that it looked innocent. Although she had been seen on 19^th November at King’s as an emergency, Professor Langdon had suggested that it should be watched for a brief period and asked her to come to the joint Henk Langdon clinic at the Marsden on 11^th December 1996. In oral evidence Professor Langdon said that on 19^th November 1996 he had told Mrs Manning that he was not worried about the small nodule on her tongue and that it did not look like a recurrence. In the 12 months since she had been seen by Professor Langdon on 22^nd November 1995, she had been reviewed three times, on 17^th April 1996 when the notes recorded that there was no sign of recurrence, on 8^th May 1996 when she was seen at the Marsden by Professor Langdon and Dr Henk who again reported that there was no sign of recurrence and that she would be reviewed again in the autumn, and on 9^th October 1996 when she had been seen again by Dr Henk who reported to her GP that she remained well with no signs of recurrence.

However Professor Langdon’s differential diagnosis in the request for laboratory examination of the December 1996 biopsy was: “Query recurrent SCC”. In the event Dr Harrison’s report of 10^th December 1996 concluded: “ Evidence of malignancy… is not seen” and in oral evidence Professor Langdon said he had quite a vivid memory of a discussion about this biopsy report with Dr Harrison who: “pointed out these odd looking cells and explained that they could be fibroblasts, they could be epithelial cells, but with the staining he had undertaken, specialist staining, he told us that he was happy that they were fibroblasts in connective tissue and not cancerous epithelial cells.” (In his closing written submissions Mr Grace QC invited the court to “ dismiss the attempt by Dr Harrison to suggest that the 1996 or any slides were discussed in early 1997 at a monthly meeting and to conclude that the only discussion was in the autumn of 2001”. This was on the basis of references in paragraphs 24 and 25 of Dr Harrison’s witness statement, and a chain of pre-litigation correspondence which it was submitted established that the only relevant meetings were in 2001 and 2002. I have considered those references and also a statement by Professor Johnson in paragraph 20 of his witness statement, that he recalled discussing Mrs Manning’s case at a Clinico Pathology Conference which involved the maxillofacial surgeons based at Kings College Hospital, the oral pathologists and junior staff, of which no formal records were kept and his oral evidence that that meeting would have been in the autumn of 2001. However, it does not seem to me that there is anything in any of those references which would justify me in rejecting Professor Langdon’s clear evidence of a vivid recollection of a conversation with Dr Harrison in the terms I have set out (shortly after the December 1996 biopsy report.) )

I note in passing that the comments attributed by Professor Langdon to Dr Harrison in that conversation are consistent with Professor Speight’s comment that the fact that Dr Harrison carried out immuno staining in December 1996 suggested that he had not been able to allay his suspicions on the H and E slide alone and are inconsistent with Dr Harrison’s evidence in chief that by the time he had finished his half hour examination of the H and E slide in December 1996 he had no doubts about the suspicious cells which he had observed on the H and E, that he was convinced that immuno staining was not going to change anything and did not consider it to be essential but was only performing it because there had been so many biopsies on the patient, it was unusual for so many biopsies to be taken and he wanted there to be “absolutely no doubt that nothing could have been missed histologically.”

For present purposes the significance of Professor Langdon’s recollection of his conversation with Dr Harrison after the December 1996 biopsy report is that it shows that in that conversation Dr Harrison reinforced the clear impression in the report itself that there was nothing to worry about in the biopsy. Before that meeting, according to Dr Harrison’s evidence, Professor Langdon had been saying that Mrs Manning’s was a strange case and the effect of what Dr Harrison said at the meeting was that “I would have allayed everybody suspicions about this case and… the matter would have seemed to have been settled.” Indeed, later in his evidence Dr Harrison confirmed that he was not trying in either the September 1995 or the December 1996 biopsy report to convey the suspicion that there might be malignancy:

It is equally clear from Professor Langdon’s evidence that he did not interpret Dr Harrison’s December 1996 report as intending to convey any suspicion. On the contrary he understood it as intended to be reassuring. When asked to explain why he saw no need to ask Professor Johnson to review the December 1996 slide in the way that he had asked him to do in 1995, Professor Langdon said: “… because clinically I wasn’t in the least bit suspicious that she had had a recurrence at this time because we had discussed the biopsy at our clinico pathological interview and because the biopsy site healed entirely uneventfully and the tongue looked quite healthy thereafter.”

Later in his evidence Professor Langdon explicitly acknowledged that on reading Dr Harrison’s report in December 1996 he did not think that Dr Harrison was expressing suspicion of a recurrent spindle cell carcinoma or carcinoma of any sort. He also confirmed that if he had thought that Dr Harrison was expressing such a suspicion he would have done something about it. There was then the following exchange:

This latter exchange is significant in that it shows that if Dr Harrison had referred in the September 1995 report to the existence of cells suspicious of recurrent carcinoma, then even if, contrary to my conclusions set out above, that had not caused Professor Langdon to do a further biopsy in September 1995, it would have served to increase very considerably Professor Langdon’s index of suspicion on receipt of the December 1996 report.

In a later passage in Professor Langdon’s evidence there was the following exchange:

In re-examination Ms Mishcon read the following extract from the joint pathology experts report:

She asked Professor Langdon whether if he had received such a report he would have done a repeat biopsy, his answer was:

Although the passage from the joint experts report put to Professor Langdon was based on the views of Dr Woolgar and Professor Sloan rather than Professor Speight, it will be recalled that it was also Professor Speight’s evidence in the context of the September 1995 report, that a reasonably competent pathologist who was left with a 10% residual doubt (as he said should have been the case absent immuno staining) should have alerted the surgeon to those lingering doubts and called for careful review and a further biopsy if the lesion did not heal. The logic of Professor Speight’s evidence that a reasonably competent pathologist should also have had a 10% residual doubt on the December 1996 H and E slide coupled with his acceptance of the 25% false negative on immuno staining suggests, in my view, that a reasonably competent pathologist should have acted in the same way following the immuno staining in December 1996. It is notable that in the answers just cited, Professor Langdon made it clear that he would have conducted a further biopsy even without the added element of a recommendation from the pathologist to do a repeat biopsy if the surgeon had on-going clinical concern. An indication that the pathologist could not be certain that suspicious cells did not in fact represent carcinoma would have been enough to cause Professor Langdon to carry out a further biopsy. Given the background of Professor Langdon’s certainty in 1995 there was recurrent carcinoma and the fact that December 1996 was also within the time in which recurrence would not be unusual, this is not surprising. The purpose of requesting the 1996 biopsy was after all to check whether carcinoma was present.

Taken together with Professor Langdon’s evidence, summarised earlier, as to how he would have reacted to a report in September 1995 alerting him to lingering doubts, in my judgment Professor Langdon would probably have performed a further biopsy in December 1996 if in Dr Harrison’s report he had indicated that it was not possible definitively to exclude the possibility of carcinoma and that he had lingering suspicion which he was not able completely to allay.

Turning now to the detailed particulars of negligence in paragraph 34 of the Amended Particulars of Claim, it follows from what I have said thus far that in my judgment the allegation in paragraph 34(1)(d) that Dr Harrison was negligent on 19 September 1995 when reporting the biopsy taken by Professor Langdon on 14 September 1995 in failing to advise that carcinoma could not be excluded has been proved. I also find that if instead Dr Harrison had reported that the biopsy did not exclude malignancy Professor Langdon would probably have performed a further biopsy.

The allegation that he was negligent in “instead advising that there was no evidence of malignancy” is ambiguous. On one view it could be taken as meaning that there was on the September 1995 biopsy evidence of malignancy in the sense that as a matter of objective fact there was carcinoma present and that any reasonably competent pathologist should have reported that the suspicious features on the biopsy were evidence of the presence of such carcinoma. If that were intended to be the allegation in my judgment it would fail. As mentioned above, neither Professor Sloan nor Dr Woolgar was of the view that Dr Harrison had any positive obligation to diagnose the existence of malignancy. Nor, as I read their evidence did they consider that a reasonably competent pathologist would positively have reported that the suspicious features which they identified were evidence of malignancy. Their evidence and that of Professor Speight was not that the suspicious features were evidence of malignancy but rather that they gave rise to a suspicion that malignancy might be present, which suspicion a reasonably competent pathologist could not allay on the basis of the H and E slide.

If the allegation was intended to mean that Dr Harrison was negligent in that by advising that there was no evidence of malignancy without qualification he gave the false and misleading impression that there were no features suspicious of malignancy or at any rate no features in respect of which suspicion had not, and could not reasonably have been allayed, then in my view it would succeed. It would in effect be the positive flipside of the first half of the allegation in that sub-paragraph, namely negligently failing to advise that it was not possible to exclude carcinoma. It is in that sense that I have assumed the allegation to be intended to be meant and in that sense I find it has been proved. Given the finding which I make that if Dr Harrison in his report had advised as he should have done that it was not possible to exclude carcinoma Professor Langdon would probably have performed a further biopsy, the allegation in the second part of that paragraph does not in my view add anything material to the outcome of the case. If Dr Harrison had not advised Professor Langdon that there was no evidence of malignancy I also find that Professor Langdon would probably have performed a further biopsy.

It also follows from what I have said so far that the allegation in paragraph 34(3)(d) that Dr Harrison was negligent on 10 December 1996 when reporting the biopsy taken by Professor Langdon on 2 December 1996 by failing to report that the biopsy taken by Professor Langdon on 2 December 1996 did not exclude malignancy has been proved. Mr Grace Q.C. submitted that “ it is clear from the evidence of both Professor Langdon and Dr Harrison that the December 1996 report did not, and was not intended to, convey any sense of suspicion. It clearly should have done so, as is inherent in Professor Speight’s [incorrect in my judgment] view in his report that “an element of suspicion is implicit within the report.” and as is the opinion of Dr Woolgar and Professor Sloan. The reason why the report did not convey any sense of suspicion was because Dr Harrison had again by his “intellectual exercise” convinced himself, on the H&E slides alone, that this was no more than an ulcer. His CK staining was merely “ belt and braces” .The CK staining did not … provide him with the sufficient degree of confidence to allow him to exclude recurrent carcinoma”. I accept that submission.

Although it adds little to the previous finding I also find that the allegation that Dr Harrison negligently failed to recognise that the biopsy did not exclude malignancy has been proved. Dr Harrison was both candid and unapologetic in his confirmation in evidence that he did not and indeed still does not consider that there was any possibility of the existence of malignancy by the time he had concluded his “intellectual “investigation.

I also find that if instead Dr Harrison had reported that the biopsy did not exclude malignancy Professor Langdon would probably have performed a further biopsy. For what it is worth I also find that if Dr Harrison had recognised that the biopsy did not exclude malignancy Professor Langdon would probably have performed a further biopsy on the basis that if Dr Harrison had recognised it he would probably have reported it to Professor Langdon with the same consequences as I find in the previous sentence.

The additional allegation in paragraph 34(3)(d) that Dr Harrison was negligent in failing in his report of 10 December 1996 to recognise and report that the biopsy was “suggestive” of malignancy must in my view fail. In my view the word suggestive overstates the effect of the expert evidence. Again neither Professor Sloan nor Dr Woolgar went so far as to suggest that a reasonably competent pathologist would have been bound to make a positive diagnosis of malignancy in respect of the December 1996 biopsy. Professor Speight actually considered that Dr Harrison’s interpretation of the biopsy was correct, his ultimate criticism, if that is the right word, of Dr Harrison being confined to his view that a reasonably competent pathologist would have had a lingering doubt of the order of 10% as to whether there might be carcinoma present in the biopsy on the basis of the H and E slides alone, which could not have been removed beyond reasonable doubt by reference to the immunostaining.

The allegation in paragraph 34(3)(f) that Dr Harrison was negligent in wrongly concluding that evidence of malignancy was not seen is proved in my judgment. I repeat my comments as to the ambiguity of the wording which I made in the context of the allegation in paragraph 34(1)(d). It is clear that at the end of his “intellectual” exercise Dr Harrison did conclude that there were no features in respect of which suspicion had not been allayed. For the reasons already given in my view that was not a conclusion which a reasonably competent pathologist would have come to. I further find that if Dr Harrison had not come to that conclusion, Professor Langdon would probably have performed a further biopsy because in those circumstances Dr Harrison would have alerted him to the fact that he had not been able to allay his suspicions in relation to those features which were suspicious of malignancy.

In my judgment the allegation in paragraph 34(3)(e) that Dr Harrison was negligent on 10 December 1996 when reporting the biopsy taken by Professor Langdon on 2 December 1996 in failing to consider the possibility of malignancy, when the same was more likely than a post-radiation effect nearly three years after radiation treatment fails. It is quite clear from Dr Harrison’s evidence that he did consider the possibility of malignancy. His error, as I find it to be, was in failing to conclude and failing to advise Professor Langdon that that possibility could not safely be excluded.

The allegation in paragraph 34(1)(c) is that Dr Harrison on 19^th September 1995 when reporting the biopsy taken by Professor Langdon on 14^th September 1995 negligently failed to recognise and describe cells suspicious of carcinoma. In my judgment that allegation has been proved to the extent that Dr Harrison negligently failed in his report to describe cells suspicious of carcinoma.

I am not, however, satisfied that it has been proved on the balance of probabilities that he failed to recognise such cells.

In the joint experts reports the three pathology experts wrote: “While we accept the probability that the 1995 report of “chronic ulcer” is correct, we agreed a more descriptive report recording the presence of suspicious cells should have been issued.” They had previously written: “We agree that these slides show an ulcerated oral mucosa which focally contains fascicles of pleomorphic cells and areas of suspicious cells which warrant careful high-power examination. We agree that the practice of individual pathologists in the examination of tissues and the preparation of reports varies. We agree that there are some features that should have been noticed that were not recorded in Dr Harrison’s report of 19^th September 1995. We cannot know whether Dr Harrison saw these and/or communicated them verbally with colleagues or not.”

Professor Speight’s description in his report of what he saw in the H and E slide on the September 1995 biopsy included the following: “… in addition however the adjacent epithelium shows mild atypia and scattered throughout the ulcer there are prominent plump polygonal and spindle-cells with large open nuclei with prominent nucleoli. In one area adjacent to the ulcer there are two islands of squamous epithelium in the superficial corium showing some evidence of atypia and with prominent enlarged nuclei. In another area in the centre of the ulcer there are two small islands of epithelium showing cytological atypia and one large prominent abnormal mitotic figure. The features are those of widespread ulceration consistent with radiation damage. In addition there are features suspicious for recurrent squamous cell carcinoma…. throughout the biopsy there are scattered plump pleomorphic spindle-cells. The features are consistent with ulceration associated with radiation induced damage. In addition there are scattered suspicious pleomorphic cells within the tissue.”

In the comment and conclusion section Professor Speight wrote: “ These H and E stained sections show evidence of radiation induced ulceration and chronic radiation damage to the mucosa and sub-mucosa, including telangiectasia, acute inflammation and scarring of superficial muscle. These features are characteristic of radiation induced damage and thus far I agree with the interpretation of Dr Harrison in his report. In addition however there are many plump and pleomorphic cells within the connective tissue. In places these form small sheets of spindle-cells. These are quite consistent with atypical fibroblasts as a consequence of radiation damage (“radiation fibroblasts”). There are also one or two small suspicious islands of epithelial cells. These are suspicious for recurrent carcinoma, but may be proliferative or regenerative epithelium at the margin of the ulcer.”

Professor Sloan in his report wrote in his description of the H and E slides: “ …the oral epithelium at the ulcer margin showed irregular proliferation. Islands of squamous epithelium and elongated processes of squamous cells extending from the oral epithelium into the underlying connective tissue were seen. Interlacing bands of plump spindle-cells were present in the granulation tissue. Lozenge-shaped cells with prominent nuclei were present within the bands and scattered in the loose connective tissue. The interlacing bands were highly cellular and unusual for a purely reactive feature. I would have been suspicious of recurrent carcinoma….”.

Dr Woolgar’s description of the September 1995 H and E slides included the following: “This biopsy shows much “busier” tissue than specimens 2 and 3 [the May 1994 and July 1995 slides]… The surface epithelium at the edge of the ulcer shows marked proliferation with long irregular processes and at one side of the ulcer the epithelial processes appear to be detached from the surface and almost blend with the granulation tissue. The granulation tissue includes interlacing bands of plump spindle-cells which largely account for the busyness of the tissue at low magnification. The epithelial proliferation and the cellularity of the granulation tissue are worrisome… In my opinion an increase in cellularity and the busy appearances of the tissues compared to the previous biopsies is not expected given the long delay since the radiation treatment. The increase in cellularity due to reactive benign fibroblast proliferation usually occurs soon after radiotherapy and hence I would be uneasy in explaining this late increased cellularity as an innocent reaction to radiotherapy. I would have issued a report that clearly indicated the presence of worrisome features and my uncertainty in distinguishing reactive post-radiation features from possible neoplastic features and I would have recommended a repeat biopsy if there was ongoing clinical concern or continued suspicion of malignancy. In addition I would have discussed the slides with experienced colleagues. In my opinion a competent experienced pathologist general and oral would have taken a similar course - I would have expected them to notice and be concerned by the worrisome features; to examine multiple sections and express their concerns in the pathology report and also to advise a repeat biopsy if there was ongoing clinical concerns.”

It will be recalled that Dr Harrison’s report on the September 1995 biopsy contained a very brief description of what he saw in the H and E slides under the heading micro:

As to whether Dr Harrison failed to recognise cells suspicious of carcinoma, in his evidence in chief he said that he did recognise suspicious cells, that he investigated them and became confident that he could explain any suspiciousness as part of a particular process. He said that the suspicious cells which he observed “were part of the inflamed granulation tissue and the suspicious cells related to the presence of previous radiation. These cells could be called radiation fibroblasts.” He said there were other features in the slides which were also indicative of radiation damage namely fibrosis, atrophy of skeletal muscle and endarteritis obliterans. “So by the time I had made these observations and finished making the observations, the cells were no longer suspicious.”

It appears from these answers that Dr Harrison did recognise some at least of the suspicious cells referred to by the pathology experts and that the reason he did not describe them in his report was not that he had not seen them but rather that he had, upon investigation, reached the conclusion that they so clearly had an innocent explanation that they no longer remained suspicious at the end of his examination of the H and E slide. That of course is a conclusion with which the three experts disagreed. Although Professor Speight did agree that Dr Harrison’s innocent diagnosis was very likely correct, he agreed with Professor Sloan and Dr Woolgar that because of a residual 10% doubt in his mind on the H and E slide it was not possible on the H and E slide alone to allay the initial suspicions created by the cells. Doctor Harrison’s error was not a failure of observation but rather a failure of interpretation, or at any rate, an error in making a more definitive interpretation than in the opinion of the experts was warranted. Thus his failure to describe the suspicious cells resulted not from a negligent failure to observe them but from a negligent failure to appreciate that while there might be, and indeed probably was on the evidence of the H and E slides alone, an innocent explanation for the suspicious cells, it was not safe to exclude the possibility that there might be a malignant explanation for them.

Doctor Harrison made the point in his own defence that it is not infrequent for pathologists to observe suspicious cells in respect of which it is possible after investigation to reach a definitive view that they are in fact innocent. In such circumstances he said it would or might be misleading to the surgeon for the pathologist to refer to such cells in his report. The impression I got from the experts was that this may well be a question of degree so that there may be occasions where even if the pathologist can allay his suspicions on investigation he ought nonetheless if the features in question are particularly suspicious to describe them as well as giving his reasons as to why his suspicions were allayed. Be that as it may, Dr Harrison’s point, as it seems to me, was based on the premise that it is possible for the pathologist to allay his suspicions. In this case, where the expert pathologists are agreed that no reasonably competent pathologist could have allayed his suspicions on the H and E slide, the defence put forward by Dr Harrison does not in my view avail him.

I have already found that Dr Harrison ought to have alerted Professor Langdon to the fact that it was not possible to exclude carcinoma. Had he done so and also described the suspicious cells I have no doubt that Professor Langdon would probably have carried out a further biopsy. In case I am wrong to find that Dr Harrison should have alerted Professor Langdon to the fact that it was not possible safely to exclude carcinoma I should record that in my view even if Dr Harrison had not explicitly alerted Professor Langdon to that possibility but had nonetheless, as in my judgment he should have done, described the suspicious cells in his report, Professor Langdon would still probably have carried out a further biopsy. I do not, as I have said, accept that the actual use of the word carcinoma would in such circumstances have been decisive. Reference to and description of suspicious cells would, it seems to me, as a matter of necessary logic have carried the implication that they were suspicious of malignancy. It is in any event significant that Professor Speight himself in his own report does actually use the word carcinoma in his description of the H and E slide: “In addition there are features suspicious for recurrent squamous cell carcinoma.” Even if Dr Harrison had not used the word carcinoma but had described the suspicious cells described by the three experts, in my view it is, if Dr Harrison had been acting as a reasonably competent oral pathologist, probable that Professor Langdon would upon receipt of the report have discussed it with Dr Harrison and that in the course of such a discussion it would have been revealed that, as ought to have been the case, it was not possible for Dr Harrison completely or safely to eliminate the possibility of carcinoma. Again in such circumstances in my view Professor Langdon would probably have carried out a further biopsy.

I should add that my findings in relation to this allegation would have been the same even if Dr Harrison had done immunostaining. For the reasons given earlier in this judgment a reasonably competent pathologist would still have been unable to eliminate the possibility of carcinoma following immunostaining on the September 1995 biopsy and as a result Dr Harrison should still have described the suspicious cells in his report.

The allegation in paragraph 34(1)(e) of the Amended Particulars of Claim is that Dr Harrison was negligent on 19^th September 1995 when reporting the biopsy taken by Professor Langdon on 14^th September 1995 in failing to cut and examine further levels. In my judgment this allegation has not been proved.

Doctor Harrison in his evidence in chief said that he cut the September 1995 biopsy specimen into three pieces which he considered gave a good representation of the original specimen. He therefore did not consider it necessary to cut further levels. In the joint report the three pathology experts wrote: “We all agreed that in our contemporary practice we would cut levels in such a case and do immunocytochemistry before issuing a report. However the slide 94/457/1 contains three large profiles of tissue and we would not be unduly critical of a pathologist who had a different sampling strategy and reported on this one slide.” At trial it emerged that Professor Sloan and Professor Speight had intended to use the word contemporary in different senses. Professor Speight had intended to mean as at the time of the joint experts meeting in 2007. Professor Sloan had intended to mean as at the time of Dr Harrison’s biopsy report in September 1995.

In her report Dr Woolgar wrote: “The epithelial proliferation and the cellularity of the granulation tissue are worrisome and I would have cut further levels and requested immunohistochemistry for cytokeratins. I think it is important to cut further levels when there is a clinical suspicion of recurrent carcinoma since tumour may only involve part of the biopsy sample….. it has been well-known for many years that biopsies of irradiated tissues can be difficult to interpret due to reactive changes related to radiation damage and in my experience it is usual for pathologists (both general and oral) to exercise prudence and request additional sections and special stains before issuing the pathology reports in cases such as this one. Such procedures would have been routine in 1995…. I would have expected [a competent experienced pathologist (general and oral)] to notice and be concerned by the worrisome features, to examine multiple sections and express their concerns in the pathology report…”

However in cross examination Dr Woolgar accepted that as a matter of inference and reconstruction it appears that when she examined the September 1995 slides she did not think that she would benefit from looking at further levels of the biopsies.

Professor Sloan in his report wrote: “I would have been suspicious of recurrent carcinoma and would have requested immunocytochemical stains for cytokeratins and mesenchymal markers together with deeper levels.” Although in his report he said that any experienced oral pathologist should have asked for the slides to be reviewed by a histopathology colleague experienced in tumour diagnosis and to have been suspicious of recurrent carcinoma, he did not say that he believed that any experienced oral pathologist should have requested deeper levels.

In evidence in chief Professor Sloan said it is the duty of the pathologist to ask for the requisite number of levels that are needed to make a proper diagnosis. In the mid 1990s practice varied between different hospitals. Many laboratories took a single H and E section and then the pathologist requested further levels if he or she thought that they were needed. Other laboratories would have requested multiple levels from the outset in selected cases. Either practice was perfectly acceptable. In a laboratory operating the former practice, he said that in a case of suspected cancer or where the pathologist was being asked to exclude cancer it would be the pathologists’ duty to do extra levels to search for islands of cancer cells if the first H and E section showed no significant abnormality. It would be unsafe just to rely on the first level because one might miss islands of cells. In such circumstances his own practice if he found nothing on the first section would be to sample the whole tissue and take the block through to extinction until there was no tissue left. In the case of the December 1996 biopsy because it showed highly suspicious spindle-cells Professor Sloan would certainly have cut levels to look for foci of conventional squamous cell carcinomas, because the diagnosis could be clinched by finding a small focus of conventional squamous cell carcinoma. If the pathologist finds something highly suspicious in the first section it would absolutely not be safe to rely solely on that first section without going further. If there was real suspicion he could not imagine any competent pathologist considering it safe to rely on the first section. When examining a 7 millimetre long piece of tissue where the pathologist was highly suspicious on the first level Professor Sloan would certainly ask for levels right through the block so that all the tissue was examined. If a pathologist was highly suspicious of cells seen on the first level, if he were to form a view just on that first level and come to a conclusion that the cells were not malignant he would be running the risk of missing a cancer.

In cross examination Professor Sloan was asked about the passage in the joint report where the experts agreed that they would not be unduly critical of a pathologist in respect of the September 1995 biopsy who had a different sampling strategy and reported on one slide. He accepted that that meant that the experts were agreeing that it would not fall below an acceptable standard of practice to report on that one slide alone even though it was something that he would not have himself done. He was then asked whether he had changed his view since the joint report. His first answer was that he had not and that he remained of the view that it would not fall below an acceptable level to report on just one slide. However very shortly thereafter Professor Sloan said that he wished to resile from his first answer and from what he had agreed in the joint experts report and that he was of the view that the fact that Dr Harrison did not carry out further levels on the September 1995 biopsy did fall below an acceptable standard of practice. He repeated what he had said in chief namely that if the pathologist found suspicious spindle-cells and had the diagnosis of spindle-cell carcinoma in mind it would have been mandatory to go on and look for the other two elements that help make the diagnosis i.e. dysplasia or carcinoma.

In his evidence Professor Speight said that there had been a change of practice since the mid 1990s. In his current practice if the clinician is suspicious of malignancy or it is known that the patient has had malignancy or if for any other reason it is thought that the biopsy might be suspicious, in Professor Speight’s laboratory the pathologist will now ask the laboratory technician to cut more levels at the outset. By contrast in 1995 pathologists according to Professor Speight would look at the first section before deciding whether or not to ask the laboratory technician to cut further levels. He confirmed that all three pathologists at the joint meeting had agreed that the September 1995 biopsy tissue had been sampled in such a way that it was not unreasonable to report on that one slide. The reason, he said, was that it was evident that Dr Harrison had trisected the specimen not bisected it and there were three profiles on the slide each of which was very large. Normally one would bisect it. Professor Speight said you have to give credit to the judgment of the pathologist in sampling the tissue when he saw it, which the experts did not have the opportunity to do. They felt that by trisecting the tissue Dr Harrison’s sampling was representative and therefore that one slide was adequate. He specifically said that he did not agree that a reasonably competent pathologist in 1995 could not have excluded malignancy without cutting further levels and that he regarded Dr Harrison’s sampling as adequate.

In cross examination Professor Speight’s evidence was somewhat contradictory and not entirely easy to follow. Mr Grace QC put to Professor Speight what he had said in his report commenting on the allegation in the Particulars of Claim that in December 1996 (not September 1995) Dr Harrison was negligent in failing to take further levels. Professor Speight’s report stated: “Normally faced with suspicious features in a biopsy, a pathologist would prepare deeper levels so as to examine more tissue. There is no evidence in the report that multiple levels were examined and levels were not included in the materials supplied to me.” When it was put to him that he was there saying that the proper standard in circumstances where there are suspicious features is to prepare deeper levels so as to examine more tissue Professor Speight initially said: “It could be interpreted that way, yes… I’m saying that normally faced with suspicious features in a biopsy a pathologist would prepare deeper levels and I think most pathologists would, but whether or not it falls short of a proper standard, because one can satisfy oneself on the specimen whether or not it is representative. Of course Dr Harrison actually saw the specimen in real life, we didn’t, and he was the person who sampled it…..so his judgment as to whether or not it was representative, to some extent we have to respect that judgment. In my opinion the tissue is representative, the sections we saw on the slide were representative.”

He went on to say that it will depend on a judgment on looking at the specimen as to whether or not the pathologist feels it is representative. Professor Speight then resiled from his comment on allegation 3(a) by saying that it is not normal faced with suspicious features in a biopsy to examine or prepare deeper levels. He said that some pathologists take lots of levels and some take no levels at all. “Some people hardly ever do levels. They say that they have seen the specimen, they have taken the sample, and they believe their sample is representative and based on their experience taking levels makes no difference so it is a costly exercise that makes no difference and to be truthful it very rarely does make a difference. We do levels quite often now and it very rarely makes a difference to the diagnosis.” He accepted that failing to take further levels risks missing other features in the biopsy, either innocent or malignant, that would assist the pathologist in either excluding or confirming a diagnosis of carcinoma but said that he could not quantify the risk. He then said that while taking further levels would be good practice he was not sure it would be normal practice and said that he has two colleagues who virtually never take levels even when suspicious. He confirmed what he said in his report in relation to the allegation in the Particulars of Claim that Dr Harrison had been negligent in failing to take further levels in respect of the February 2001 biopsy where he wrote: “I believe that the histological changes in this biopsy were sufficiently suspicious to warrant the application of immunostains and examination of further sections. This was not done. Therefore the allegation is found to be correct.” His explanation for that was that in the February 2001 biopsy there was a collection of suspicious cells on the deep aspect which he thought were malignant which he looked at carefully and could not allay his suspicions in respect of and formed the opinion that levels would help to determine the extent of the proliferation and help to put it in context.

He distinguished the position in February 2001 from that in September 1995 and December 1996. In the former Dr Harrison he felt fell below the appropriate standard before he failed to take more levels and failed to ask for immunostaining because he should already have realised from the H and E stain itself that there was malignancy. In that situation the reason for doing further levels would have been to appreciate the context of the proliferation. Professor Speight’s view was that that did not apply in September 1995 or December 1996 where the circumstances were quite different. In both those cases the biopsies were in his opinion quite representative of all the tissues one would expect to see with clear evidence of a chronic ulcer. In February 2001 the only reason for taking further levels would be to find out what kind of malignancy there was but not whether there was a malignancy, something which in Professor Speight’s view should have been apparent from the H and E slides.

Coming back to the December 1996 biopsy Professor Speight said he would be prepared to accept that Dr Harrison had before him a biopsy which was representative of the tissues and could allay his suspicions without the need for further levels. He said that he himself thought that the tissue biopsy was representative and there was representative tissue to examine without the need for further levels in December 1996. He pointed out that when he wrote his own report on his examination of the December 1996 slide he did not record the need for further levels in his contemporaneous examination of the specimen whereas he would have done so had he thought that they were necessary as he did in his contemporaneous notes of the 2001 specimen. Finally Professor Speight confirmed that he did not think that Dr Harrison necessarily fell below the appropriate standard by failing to take further levels in September 1995 and December 1996.

I confess to having found considerable difficulty in penetrating the thicket of expert evidence on this issue in the search for a guiding principle by reference to which the appropriate standard of care is to be identified. One suggestion appeared to be that the decisive question is whether the pathologist can reasonably conclude that the existing section is a sufficiently representative sample of the entire biopsy tissue to make it unnecessary to cut further levels.

If that is the relevant criterion, in my judgment the expert evidence and Dr Harrison’s evidence do not show on the balance of probabilities that the September 1995 section examined by Dr Harrison was insufficiently representative. On the contrary Professor Speight explicitly said that it was, Dr Woolgar’s failure to pursue further levels herself suggests that she took the same view when she was examining the September 1995 biopsy and she confirmed in evidence that that is the logical inference. That is also the obvious inference from the joint report.

An alternative candidate for the relevant guiding principle would be that in a case where cancer is suspected and/or the pathologist is asked to investigate/seek to exclude carcinoma by the clinician a pathologist should cut further levels if there are no abnormal cells on the first section. Some support for that as the relevant test is provided by one of the answers given by Professor Speight referred to above. If that is the correct test, again in my view the allegation is not proved because it is accepted by all the pathologists that there were suspicious cells on the section examined by Dr Harrison.

A third candidate for the guiding principle would be that a pathologist should always ask for further levels where there are suspicious cells in the first section so as to seek to eliminate or confirm the presence of malignancy. Some support for this approach is to be found in the evidence of Professor Sloan and Professor Speight. However it is hard if not impossible to reconcile with (a) the fact that all three experts said in their joint report that they would not be unduly critical of Dr Harrison for failing to ask for further levels despite the fact that all three are agreed that there were suspicious indeed highly suspicious cells on the section examined by him, (b) the fact that neither Dr Woolgar nor Professor Speight themselves sought to take further levels when doing their own examination of the September 1995 biopsy and (c) the fact that according to Professor Speight he has colleagues whose practice is not to seek further levels even when confronted with suspicious cells. This latter point is not of itself determinative because, as explained above, the Bolam defence is subject to the Bolitho requirement of demonstrating that if a defendant relies on a practice adopted by a body of reasonable and responsible practitioners it must withstand the test of logic.

My impression is that if this were the relevant criterion it would be subject to the qualification that there is no duty to request further levels if the pathologist has, on reasonable grounds, satisfied himself that he can allay any suspicions arising from the existence of suspicious cells. It appeared to be common ground that there are very many biopsies which contain cells that are prima facie suspicious but where the suspicion can almost instantly be reasonably allayed on examination of the H and E slide. The matter in this case is complicated by the fact that although Dr Harrison undoubtedly did allay his suspicions on examining the H and E slide, all three experts agreed that it was not reasonable for him to do so to the extent of being able safely to exclude completely the possibility of carcinoma being present. Mr Grace QC submitted (in respect of the December 1996 biopsy, but the point is logically of equal application to the September 1995 biopsy) that since Dr Harrison could not reasonably have allayed his suspicions he was under a duty, applying this criterion to call for further levels.

One can see the logical force in that submission, although if it is right it would on analysis add little in practice to the submission, which I have accepted, that Dr Harrison was negligent in failing to appreciate and report to Professor Langdon that it was not possible safely to eliminate the possibility of carcinoma since, as I have also found, Professor Langdon would on that hypothesis have carried out a further biopsy. However one is left, in considering whether this is the appropriate criterion, with the undoubted fact that neither Dr Woolgar nor Professor Speight apparently felt it necessary to request further levels despite the fact that they could not completely eliminate the possibility of carcinoma on the H and E slide. This tends to suggest that the relevant criterion is the first of the three candidates, namely whether the pathologist can reasonably take the view that the section under examination is a sufficiently representative sample of the whole biopsy tissue. On that approach, even in a case such as this where, as I have found, a reasonably competent pathologist could not on examining the H and E slide alone have safely eliminated the possibility of carcinoma, and was thus under a duty to take such reasonable steps as were available to him to seek further to eliminate or confirm the possibility of malignancy and failing that to alert the surgeon to the existence of residual doubt, the solution to the problem would appear to be that whereas performing immunostaining would have been a step that a reasonably competent pathologist should have taken, requesting further samples would not have been.

While all three experts were in agreement that the inability completely to allay suspicions on the H and E slide in September 1995 carried with it a duty to go on to do immunostaining, I am not satisfied that, having regard to the evidence as to the representative nature of the original section there was in addition a duty on Dr Harrison to request further samples.

It will be apparent from the foregoing that I have not found this an easy issue. In reaching the conclusion I do, I draw some comfort from the reflection that if I am wrong it would not seem to me to have any impact on the outcome of this case. That is because there was no evidence to suggest that if further levels had been requested such levels would have confirmed the existence or probability of malignancy such as to have caused Professor Langdon for that reason to perform a second biopsy. Indeed Professor Sloan as mentioned above said in oral evidence: “We know that deeper levels were looked at because the experts have prepared some and we know that there is no evidence of dysplasia and no conventional squamous cell carcinoma.” Further and in any event even if it would have done, I have already found that if, as I have found he had a duty to do, Dr Harrison had alerted Professor Langdon to the fact that it was not possible to allay lingering doubts or to eliminate the possibility of the presence of carcinoma instead of advising him that there was no evidence of malignancy which he should not have done, Professor Langdon would probably have performed a second biopsy. Thus even if Dr Harrison was negligent in this additional respect, it would add nothing to Mr Manning’s ability to prove causation and thus to the establishment of a cause of action in negligence.

It is convenient to deal next with the allegation in paragraph 34(3)(a) of the Amended Particulars of Claim that Dr Harrison was negligent on 10 December 1996 when reporting the biopsy taken by Professor Langdon on 2 December 1996 in failing to examine multiple levels through the tissue block.

In evidence in chief Dr Harrison rejected the allegation that he should have taken multiple levels through the tissue block for the December 1996 biopsy on the ground that the tissue, which was 0.7 cm long and which he bisected longitudinally, was relatively thin and the two sections from the specimen were a reasonable sample. He said that the area viewed in the section was large compared with the whole volume of the specimen. He said that he felt that he had a good representative section that allowed him to see the relationship between the epithelium and the connective tissue and every other structure that he needed to see. He did not believe that cutting any further levels would have given him any better representation than the one he already had. He added that because it was a thin piece of tissue there was a risk that deeper sections would be more tangential because the surface was curved and would be of no benefit. In cross-examination when asked if he agreed with the proposition that if the pathologist is suspicious he should take further levels Dr Harrison’s answer was that taking levels was not the only possibility. A pathologist could show the histology to a colleague before undertaking further levels. It was not in his opinion an automatic reaction that if a pathologist is unsure he takes further levels.

He did however agree in general terms with the proposition that if the pathologist is suspicious then to allay his suspicion he needs to take further steps such as discussing it with a colleague and asking him or her to look down the microscope at the slide and getting his or her view or taking further levels. He accepted that he did neither of these things in any of September 1995, December 1996, February 2001 and June 2001. As to 2001 Dr Harrison accepted that he made a mistake in thinking that there was no malignancy and that nothing would be gained by taking deeper levels. However he said he was convinced that he was not mistaken in 1995 and 1996 and indeed that the deeper levels subsequently cut by others (presumably a reference to the levels cut by Professor McDonald and/Dr Woolgar) show that he was correct and that nothing was gained by further levels.

As to February 2001 in hindsight he accepted that he should have shown the existing sections to a colleague which he regarded as more important than cutting deeper levels or doing immunostaining. He said that the appropriate time to have taken deeper levels would have been if having showed it to a colleague he and the colleague remained unsure. The serious error he thought in hindsight that he had made in 2001 was not showing it to a colleague. Specifically in relation to December 1996 Dr Harrison repeated that in his view there was no need to cut deeper into the block particularly as it was a thin piece “What deeper levels do is to expand the area of the specimen that is being investigated. We still come down to an interpretation of the appearance in the deeper levels. I was, and am, of the opinion that a reasonable area of the specimens was being examined by me in the slides…. there is nothing magical about a deeper level that is going to give an answer in most cases. …we are trying to deal with a representative sample of the specimen. The specimens in 1995 and 1996 that we are discussing had good, substantial areas prepared for slides.”

There was then the following exchange: “ Q – But do you accept the logic of taking further levels, doctor? A – Yes I do. Q - .. but the logic is this is it not: that if you find suspicious cells in one part of the specimen, then you want to see if those suspicious cells are elsewhere in the specimen, and indeed whether they are more numerous, less numerous and so on? A – Yes that’s right. Q – That’s right isn’t it? A – That’s one reason, but one can also see that in a section, because a section – if it is the large representative part of the specimen – will show if there is variation between one part and another. A deeper level also does this. So if one is unsure about the relation of the tissues in a section, then one can have deeper sections cut. Q – If one is looking at an excision biopsy you want to see whether or not any suspicious cells are at the margins or how close to the margins they come. A – Yes that is correct.

In his report Professor Sloan wrote in relation to the December 1996 biopsy: “ …on reviewing the slides I found that there were three section profiles of two small pieces of tissue. Microscopically the biopsy was superficial and no more than 2millimetres in depth. There was surface oral epithelium, granulation tissue, slough and scar tissue. Muscle was not included. There are interlacing bands of spindle cells and kite-shaped cells, most prominent towards the deep aspect of the biopsy. These cells do not have the features of radiation damaged fibroblasts and represent a spindle cell proliferation. I would have been highly suspicious of spindle-cell carcinoma and would have requested cytokeratin markers, multiple levels and sought the opinion of an experienced colleague with expertise in spindle-cell tumour diagnosis. I believe that any other experienced oral pathologist would have been highly suspicious and would have requested cytokeratin markers, studied multiple levels and discussed the case with a specialist diagnostic pathologist. .. The original immunohistochemical slides provided by Dr Harrison were pale and the spindle cells showed weak vimentin positivity and no convincing CK or CK19 staining. The freshly immunostained sections show that the spindle-cells stained strongly for the epithelial cell marker AE/1 – AE/3. The spindle-cells also stained convincingly but less strongly with MFN116. In my opinion the features are those of a spindle-cell carcinoma. I would have expected an experienced oral pathologist to have raised this possibility as a differential diagnosis in the report and to have prepared multiple levels, performed a panel of immunostains and discussed the case with an expert on spindle tumours.

Dr. Woolgar wrote in relation to the December 1996 biopsy: “……… the H and the HE-stained slide shows three profiles of two small pieces of tissue. The thickness of the biopsy tissue appears to be around 2mm. My assessment confirms that the biopsy specimen is superficial consisting of ulcerated surface epithelium lined by exuberant granulation tissue and supported by scar tissue. No muscle is included. I agree that the surface epithelium shows proliferation and mild cytological atypia. The spindle and kite-shaped cells described as “large fibroblasts” are quite striking and in view of the long delay since radiation treatment, they cannot easily be explained as a benign reactive fibroblast proliferation. Furthermore the spindle and kite shaped cells are more frequent towards the base of biopsy specimen where some appear to be arranged in small islands and short cords. This cellular arrangement visible on routinely stained sections makes me suspicious that these are epithelial cells-representing a spindle cell carcinoma. I would have examined multiple levels through the tissue block and I would have requested a range of cytokeratin markers. I think a competent experienced pathologist (general and oral) would have undertaken similar actions – they should have noticed the atypical cells and their appearance and arrangements and actively sought to characterise them. …..

In my opinion, additional staining has confirmed the presence of spindle cell carcinoma in specimen 5.. the diagnosis is not easy. The specimen was small and superficial. Nevertheless I believe there were sufficient features in the routinely-stained sections to make the average pathologist consider the possibility of malignancy. …..”

I have already referred to what Professor Speight said in his report and in evidence on this topic.

Again, I have not found this easy. To a layman there would appear to be obvious common sense in the proposition that where a pathologist has ought reasonably to have suspicions as to the possibility of cancer which he cannot reasonably allay by an examination of the slides in front of him, in the normal course one of the steps which he ought to take in discharging his duty to take all reasonable steps to seek to confirm or allay his suspicions would be taking further levels. That would appear to be implicit in Professor Speight’s comment on the allegation of negligence in this regard against Dr. Harrison in December 1996. It would also appear to be implicit in Dr. Harrison’s acceptance in general terms of the proposition that if a pathologist is suspicious then to allay his suspicion he needs to take further steps such as discussing it with a colleague and asking him or her to look down the microscope at the slide and getting his or her view or taking further levels.

I have already referred to Dr. Harrison’s evidence that he felt that he had a good representative section that allowed him to see the relationship between the epithelium and the connective tissue and every other structure that he needed to see and that he did not believe that cutting any further levels would have given him any better representation than the one he already had. It is of course necessary to treat Dr. Harrison’s evidence with some caution on this because his evidence was that he managed to allay his suspicions on the H and E slide alone and thus did not consider it necessary to take any further steps to confirm or allay those suspicions. That evidence is inconsistent with the views of all three experts, who were of the view that it was not possible to allay suspicions on the H and E slides alone. Nor was I convinced by Dr. Harrison’s defence that because it was a thin piece of tissue there was a risk that deeper sections would be more tangential because the surface was curved and would therefore be of no benefit. It does not seem to me a satisfactory reason for not taking a step which might confirm or allay a continuing suspicion that it might not do so. Nor was I convinced by his defence that if you want to see whether or not any suspicious cells are at the margins or how close to the margins they come, you can assess the presence or absence of malignant cells at the margin in a section without necessarily cutting deeper levels. That does not strike me as of itself a reason not to take further levels as a belt and braces approach.

I was also impressed by the evidence of Dr. Woolgar and Professor Sloan on this issue. However, as I have recorded, Professor Speight said that he would be prepared to accept that Dr. Harrison had before him in December 1996 a biopsy which was representative of the tissues and that he himself thought that the biopsy tissue was representative and that there was representative tissue to examine without the need for further levels in December 1996. To my mind the factor which tips the scales against a finding of negligence on this issue is the fact that Professor Speight himself when he wrote his own report on his examination of the December 1996 slide did not record the need for further levels in his contemporaneous examination of the specimen, which he said he would have done had he thought that necessary, as he did in his contemporaneous notes of the 2001 specimen. Professor Speight struck me as a cautious and thoroughly competent pathologist and I would be reluctant to find Dr. Harrison negligent for failing to take a step which Professor Speight did not himself consider necessary unless convinced that Professor Speight’s reasoning was logically flawed. Accordingly I find this allegation not proved.

I should add that if I am wrong in this finding then, just as in the case of the September 1995 biopsy, it does not seem to me to have any impact on the outcome of the case. Again, that is because there was no evidence to suggest that if further levels had been requested and taken in December 1996 they would have confirmed the existence or probability of malignancy such as to have caused Professor Langdon for that reason to perform a second biopsy. Again, as in the case of September 1995, since I have already found that Dr. Harrison was negligent in another respect and that if he had not been so negligent Professor Langdon would probably have performed another biopsy, even if, contrary to my finding, Dr. Harrison was negligent in this additional respect it would add nothing to Mr. Manning’s ability to prove causation and thus to the establishment of a cause of action in negligence.

I deal next with the allegations in paragraphs 34 (1) (g) and 34 (3) (c) of the Amended Particulars of Claim respectively that Dr. Harrison was negligent on 19^th September 1995 when reporting the biopsy taken by Professor Langdon on 14^th September 1995 in failing to discuss the case with another experienced tumour pathologist and that he was negligent on 10^th December 1996 when reporting the biopsy taken by Professor Langdon on 2^nd December 1996 in failing to discuss the case with any other consultant pathologist.

Dr. Woolgar in her report said in relation to the September 1995 biopsy: “I would have issued a report that clearly indicated the presence of worrisome features and my uncertainty in distinguishing reactive post radiation features from possible neoplastic features, and I would have recommended a repeat biopsy if there was ongoing clinical concern or continued suspicion of malignancy. In addition I would have discussed the slides with experienced colleagues. In my opinion, a competent experienced pathologist (general and oral) would have taken a similar course. – I would have expected them to notice and be concerned by the worrisome features; to examine multiple sections and express their concerns in the pathology report, and also, to advise a repeat biopsy if there was ongoing clinical concerns.”(emphasis added) She did not refer to the need to discuss the biopsy with a colleague in relation to the December 1996 biopsy in her reports. She did however say that the cellular arrangement visible on routinely stained sections in the December 1996 biopsy made her suspicious that these were epithelial cells representing a spindle cell carcinoma. She added that she would have expected a competent experienced pathologist (general and oral) to continue to suspect a spindle cell carcinoma even though the immunostains were negative. In such cases the pathologist would normally request a further deeper biopsy specimen which she believed would have led to the correct diagnosis of SPCC.

In his report Professor Sloan said in relation to the September 1995 biopsy: “I believe that an experienced oral pathologist should have been suspicious of recurrent carcinoma. …..I would expect an experienced oral pathologist to have issued a report describing the presence of suspicious features and suggesting a repeat biopsy if the clinical suspicion of a recurrence existed. I would have asked for the slides to be reviewed by a histopathology colleague experienced in tumour diagnosis. I believe that any experienced oral pathologist should have done so.” In relation to the December 1996 report Professor Sloan wrote: “I would have been highly suspicious of spindle cell carcinoma and would have requested cytokeratin markers, multiple levels and sought the opinion of an experienced colleague with expertise in spindle cell tumour diagnosis. I believe that any other experienced oral pathologist would have been highly suspicious and would have requested cytokeratin markers, studied multiple levels and discussed the case with a specialist diagnostic pathologist.”(emphasis added)

In his report Professor Speight, commenting on the December 1996 allegation, stated: “It is not known from the material provided whether or not Dr. Harrison discussed the case with a colleague. There is no evidence that he did not. It is common practice for pathologists to show and discuss cases with colleagues within the department, but this is not usually recorded.”

Dr. Harrison accepted that in relation to the February 2001 biopsy, where he accepted that he was wrong not to recognise the suspicious signs of malignancy, with hindsight he should have shown the slides to a pathology colleague. He described his failure to do so as the serious error he made in 2001. By contrast he said he could see no reason to show the December 1996 to a colleague to reinforce a diagnosis because the biopsy was already explicable by the diagnosis he had himself reached. When Professor Speight’s statement in the report referred to above was put to him he accepted that it has always been common practice to discuss difficult cases where the pathologist has a suspicion or ought to have a suspicion. In relation to both the September 1995 and December 1996 biopsies Dr. Harrison remained “convinced I was not mistaken” .The inference appeared to be that he accepted the principle that where a pathologist ought reasonably to have suspicions which he cannot or ought not reasonably to be able to allay then he is under a duty to discuss the case with a colleague. Since I have found that, contrary to Dr. Harrison’s view, it was not reasonable for him to have allayed his suspicions in respect of either the September 1995 or December 1996 biopsy, it would seem to follow that, applying Dr. Harrison’s own approach, he ought to have discussed both biopsies with a colleague.

In his evidence in chief Professor Sloan said that any pathologist who did not discuss a suspicious case with a colleague was falling below an acceptable standard. He also said that no reasonably competent pathologist could exclude malignancy without getting a second opinion. In her evidence in chief Dr. Woolgar said that if the pathologist had allayed his suspicions and was confident of a benign diagnosis, it was not mandatory to discuss the biopsy with a colleague. However it seems to me that this answer needs to be seen in context. In my view Dr. Woolgar was referring to a situation in which the pathologist has allayed his suspicions on reasonable grounds and has reasonable grounds to be confident of a benign diagnosis. Thus Ms Mishcon’s submission in her written closing submissions that given that Dr. Harrison was confident of a diagnosis of a chronic ulcer it was perfectly reasonable not to discuss the 1995 biopsy with a colleague ignores the question whether it was reasonable for him to have such confidence. I have found, based on the expert evidence, that it was not. On the afternoon between the second and third days on which Dr. Harrison gave evidence, he reviewed the September 1995 and December 1996 biopsy slides. His report the next day on what he had seen was remarkable: “When I looked at the sections I saw cells that were suspicious of malignancy on a superficial glance, but a detailed appraisal convinced me beyond any doubt that the cells are not malignant or suspicious of malignancy – no longer suspicious.” He added that if the slides had appeared in his laboratory the previous day sent by a surgeon and he had been on call he would not have taken further levels and would not have discussed them with another pathologist. That is despite the fact that he had said the previous day in evidence that possibly because of a change in approach over the years he and his colleagues now routinely look at each other’s cases.

It thus appeared that despite everything that happened in relation to Mrs. Manning and all the expert evidence in this case, Dr. Harrison remained not only entirely convinced in the rightness of his initial view that it was possible to allay his suspicions but also that he would still see no need to take a second opinion. This episode seemed to me to illustrate graphically precisely why it is important for a pathologist to take a second opinion in a case such as this. It is a notorious feature of the working life of histopathologists that there is an inherent danger arising from the isolated nature of their function. It is precisely for that reason that the evidence in the trial showed that in recent years the profession has taken steps to increase cross-fertilisation between pathologists. Anybody in any profession can make an honest mistake. But where the consequences of mistakes can be a matter of life and death it is plainly of the utmost importance that all reasonable steps should be taken to guard against them and to minimise any adverse consequences.

The fact that Dr. Harrison candidly admitted that he would still not have consulted a colleague seems to me to show why the duty to consult a colleague and seek a second opinion cannot depend on the subjective confidence of a pathologist in the rightness of his diagnosis. There is no necessary correlation between the degree of a pathologist’s confidence that he has got it right and the objective question whether he has in fact got it right. It would be surprising and in my view afford inadequate protection to the patient if, in a case where no reasonably competent pathologist could allay his suspicions as to malignancy, a duty to seek a second opinion would only arise if the pathologist had in fact not allayed his suspicions.

There is no evidence that Dr. Harrison took a second opinion from another pathologist in relation to either the September 1995 or December 1996 biopsies. In relation to the latter although he said that he discussed Mrs. Manning’s case at one of the clinico-pathological meetings, he said that he was usually the only oral pathologist present and that those meetings were more of a training exercise for the junior surgeons and had no real advantage from the pathology side. Dr. Harrison said in evidence that he did not remember discussing the 1996 biopsy with Professor Johnson and he was sure that he did not show him the biopsy slides and that he did not go over them with Professor Johnson. Nor did he remember if he was present at the clinico pathology conference when the 1996 biopsy was discussed. As he candidly said, in his view “the 1996 case was explicable by the diagnosis I had made and I could see no reason to show this to a colleague to reinforce the diagnosis which I had made.” This is to be contrasted with his admission in relation to the February 2001 biopsy that if he had been more suspicious he would have shown it to another colleague who was likely to have been Professor Johnson and if he had not been available he would have taken it to histo-pathology.

In these circumstances in my judgment on the facts of this case the allegations that Dr. Harrison was negligent in failing to consult another pathologist in relation to each of the September 1995 and December 1996 biopsies are proved. I have already found that no reasonably competent pathologist could have allayed the doubts which he should have had as to the possible existence of carcinoma on both biopsies. In my judgment, in those circumstances a reasonably competent pathologist would have and Dr. Harrison should have consulted a second pathologist. He should certainly have done so before advising Professor Langdon as he did that there was no evidence of malignancy.

That raises the question whether if Dr. Harrison had consulted a colleague that would in itself have led to Professor Langdon performing a further biopsy. For these purposes it seems to me necessary to ignore the fact that as I have found Professor Johnson in August 2001 was himself negligent in his biopsy report. The relevant question seems to me what would a reasonably competent pathologist who had been consulted by Dr. Harrison have done. I do not by that comment mean to suggest that Professor Johnson was not generally a reasonably competent pathologist but rather to indicate that in my view if Professor Johnson had made the same mistake on such a consultation in September 1995 or December 1996 as he did in August 2001 that could not avail the defendants.

Taking all the evidence in this case in the round and having regard to the findings which I have made and make in the later parts of this judgment, in my view it is not possible to say on the balance of probabilities that a reasonably competent pathologist consulted by Dr. Harrison would on either occasion have advised that there was probably carcinoma present. He or she, unlike Professor Sloan and the other pathology experts in this case would not have had the benefit of hindsight. I do on the other hand believe and so find that on the balance of probabilities such a reasonably competent pathologist would have advised Dr. Harrison on both occasions that it was not possible safely to exclude the possibility of carcinoma. That being so in my view Dr. Harrison would have been under a duty to do what I have in any event held he was under a duty to do on each occasion, namely to alert Professor Langdon to the existence of lingering doubts as to the possibility of carcinoma which it had not been possible to allay. In those circumstances for all the reasons I have given I believe on the balance of probabilities that on both occasions Professor Langdon would for that reason alone have performed a further biopsy. Indeed the addition of a second opinion added to the weight of Dr. Harrison expressing the view that it was not possible to exclude the possibility of carcinoma would have reinforced the likelihood of such a further biopsy being performed.

I turn next to the allegations in paragraphs 34 (1) (f) and 34 (3) (b) respectively that Dr. Harrison was negligent on 19^th September 1995 when reporting the biopsy taken by Professor Langdon on 14^th September 1995 in failing to have immunostains performed and on 10^th December 1996 when reporting the biopsy taken by Professor Langdon on 2^nd December 1996 in failing to have pancytokeratin immunostains and/or a larger panel of epithelial/cytokeratin markers performed.

Dr. Woolgar in her report stated in relation to the September 1995 biopsy: “Immunohistochemistry may aid assessment of the nature and depth of the epithelial proliferation by highlighting irregular epithelial processes/islands. It has been well known for many years that biopsies of irradiated tissue can be difficult to interpret due to the active changes related to radiation damage and in my experience it is usual for pathologists (both general and oral) to exercise prudence and request additional sections and special stains before issuing the pathology report in cases such as this one. Such procedures would have been routine in 1995.”

Professor Sloan in his report wrote in relation to the September 1995 biopsy: “I would have been suspicious of recurrent carcinoma and would have requested immunocytochemical stains for cytokeratins and mesenchymal markers together with deeper levels. I believe that an experienced oral pathologist should have been suspicious of recurrent carcinoma.”

In evidence in chief when the allegation was put to Dr. Harrison his response was as follows: “I do not see what advantage immunostaining would have been because there is no evidence of malignancy in the section. We apply immunostaining to answer a question. I had no question to pose, to be answered by immunostaining.” He added: “Immunostaining is very intensive on labour. We have to choose - there has to be a good reason for asking for immunostaining. There was no good reason in this case.” It thus appears that Dr. Harrison’s reason for not doing immunostaining was the same as his reason for not consulting a colleague, namely that he did not have any doubts as to the possible existence of malignancy on the H and E slides after he had considered them. By contrast, Professor Speight in evidence said that he was left with a 10% residual doubt as to the possible presence of malignancy on the H and E slides alone in September 1995, that he would himself have done an immunostaining and that in his view Dr. Harrison should have done so. He said that his failure to do immunostaining or alert Professor Langdon to the existence of lingering doubts as to the possible existence of carcinoma fell below a proper standard. This is consistent with Professor Speight’s conclusion in his report: “In the sections I have examined there are cells and histological changes suspicious for recurrent carcinoma from September 1995 onwards. In these circumstances immunocytochemical staining to confirm that atypical cells are indeed “radiation fibroblasts” is indicated.” This was in contrast to his earlier evidence to the effect that the majority of pathologists at the time would not do immunostaining and that papers and textbooks emphasised that it was the histological features and not cytokeratin staining which was important in the diagnosis.

In my judgment in the light of my finding that a reasonably competent pathologist would not have and Dr. Harrison should not have allayed his suspicions in respect of the September 1995 biopsy on the H and E slides alone, Dr. Harrison was negligent in failing to do immunostaining on the September 1995 biopsy. That finding is in addition to and independent of my finding that he was also negligent in failing to alert Professor Langdon to the existence of lingering doubts and the inability safely to exclude the presence of malignancy in the September 1995 biopsy.

However I do not believe that Dr. Harrison’s failure to carry out immunostaining caused Professor Langdon to fail to perform a further biopsy which he would have performed if Dr. Harrison had done such an immunostaining. As already mentioned, both Dr. Woolgar and Professor Sloan accepted that even in the light of the immunostaining which was done for the purposes of the trial, no positive diagnosis of malignancy could reasonably have been made at the time. Thus immunostaining would not have increased the level of suspicion that should have been present in Dr. Harrison’s mind at the conclusion of his examination of the H and E slides. In my judgment the question whether Professor Langdon would probably have done a further biopsy is unaffected by Dr. Harrison’s failure to do immunostaining. For the reasons which I have given in my view Professor Langdon would probably have performed a further biopsy if Dr. Harrison had not been negligent in the other respects which I have found.

In relation to December 1996, Professor Sloan stated: “I would have been highly suspicious of spindle cell carcinoma and would have requested cytokeratin markers…. I believe that any other experienced oral pathologist would have been highly suspicious and would have requested cytokeratin markers….. The original immunohistochemical slides provided by Dr. Harrison were pale and the spindle cells showed weak vimentin positivity and no convincing CK or CK19 staining. The freshly immunostained sections show that the spindle cells stain strongly for the epithelial cell marker AE1 to AE3. The spindle cells also stained convincingly but less strongly with MFN116.”

Dr. Woolgar in her report wrote in relation to December 1996: “Furthermore the spindle and kite shaped cells are more frequent towards the base of the biopsy specimen where some appear to be arranged in small islands and short cords. This cellular arrangement visible on routinely stained sections makes me suspicious that these are epithelial cells – representing a spindle cell carcinoma. I would have examined multiple levels through the tissue block and I would have requested a range of cytokeratin markers. I think a competent experienced pathologist (general and oral) would have undertaken similar actions – they should have noticed the atypical cells and their appearance and arrangement and actively sought to characterise them.

The immunostained sections provided by Dr. Harrison show most of the spindle-kite shaped cells stained positively with vimentin and on low-power assessment they show no positive staining with CK and CK19. CK has stained the surface epithelium and high-power examination shows weak positive staining of a few cells around the edge of the ulcer. The reporting pathologist, Dr. Harrison, concluded that the atypical cells within the exuberant granulation tissue were fibroblasts and that there was no evidence of malignancies.

I requested two immunostains –AE1 to AE3 and MNF116 which I find more reliable markers of oral epithelial cells. Both stains show positive staining for the small islands and scattered individual kite shaped and spindle cells within the granulation tissue. The AE1 to AE3 staining is strong and in my opinion this stain together with the distribution of the atypical cells confirms the presence of spindle cell carcinoma. The choice of immunostains depends on both the laboratory and the individual pathologists. Most laboratories and individual pathologists tend to try out a range of immunostains and select the ones that seem most reliable in their hands. The stains may be referred to by different names by different suppliers and laboratories and I am uncertain of the precise staining profile of CK and CK19. Nevertheless it is likely that CK and CK19 were the stains that were used routinely by Dr. Harrison at that time and he considered they were reliable. Nevertheless given the appearances in the routinely stained sections I would have expected a competent experienced pathologist (general and oral) to continue to suspect a spindle cell carcinoma even though the immunostains were negative. In such cases, the pathologist would normally request a further, deeper biopsy specimen which I believe would have led to the correct diagnosis of spindle cell carcinoma.”

Professor Sloan in his report on December 1996 wrote: “There are interlacing bands of spindle cells and kite-shaped cells, most prominent towards the deep aspect of the biopsy. These cells do not have the features of radiation damaged fibroblasts and represent a spindle cell proliferation. I would have been highly suspicious of spindle cell carcinoma and would have requested cytokeratin markers….. I believe that any other experienced oral pathologist would have been highly suspicious and would have requested cytokeratin markers…. The original immunohistochemical slides provided by Dr. Harrison were pale and the spindle cells showed weak vimentin positivity and no convincing CK or CK19 staining. The freshly immunostained sections show that the spindle cells stained strongly for the epithelial marker AE1 to AE3. The spindle cells also stained convincingly but less strongly with MFN116. In my opinion the features are those of a spindle cell carcinoma.”

In the joint experts’ report the experts wrote: “We all agree that this biopsy shows an ulcerated oral mucosa containing cells that are highly suspicious of spindle cell carcinoma. We agree that Dr. Harrison must have recognised these suspicious cells and carried out appropriate immunocytochemical staining. In the original sections we agree that the spindle cells were negative for CK and CK19 and that the surface epithelial was not dysplastic. Professor Speight felt that Dr. Harrison carried out appropriate staining and that the results indicate that the lesion was a chronic ulcer. …”

Dr. Harrison as can be seen did in fact carry out immunocytochemical staining. However it was a subsequent and different form of immunostaining carried out for the purpose of the trial which revealed the famous archipelago of islands which stained positive and were regarded by the experts as suspicious. Thus the question is not whether Dr. Harrison was negligent for failing to do immunostaining in December 1996 but rather whether he was negligent for failing to carry out adequate staining.

As appears in the extract quoted above the experts agreed in the joint statement that he had carried out appropriate immunostaining. Professor Sloan in his evidence in chief said that in 1995 it was usual to use only one immunostain. In fact Dr. Harrison used a total of three cytokeratin stains. Moreover the CK used by Dr. Harrison was a clone for MMF116, a pancytokeratin used by Dr. Woolgar when she re-stained the specimen after having cut further levels.

Dr. Harrison in his evidence said that the reason he carried out immunostaining was because there had been so many biopsies that he wanted to carry out an additional stain so that there would be absolutely no doubt that nothing could have been missed histologically, even though he did not consider that that investigation was essential. For reasons which appear above, it is implicit in the views of the three experts that, contrary to Dr. Harrison’s view, immunostaining was essential. However, that notwithstanding, it does not seem to me that, judged by the standards applicable in 1996, Dr. Harrison was negligent in confining his immunostaining to the stains which he used. Accordingly I find this allegation is not proved.

As already mentioned, by the end of the trial this was the sole remaining contentious issue on causation. It was common ground by that stage of the proceedings that if (i) Dr Harrison was negligent in relation to the 1995 and/or 1996 biopsies and (ii) but for such negligence Professor Langdon would have carried out a further biopsy/biopsies, then if cancer had been present and revealed in such biopsy/biopsies, salvage surgery would have been performed and would have been successful so that Mrs Manning would have survived. I have found that Dr Harrison was negligent both in 1995 and 1996. I have also found that but for his negligence in September 1995, Professor Langdon would have performed a further biopsy and that if I am wrong about either or both of my findings that Dr Harrison was negligent in September 1995 and but for that negligence Professor Langdon would have performed a further biopsy in September 1995, then but for Dr Harrison’s negligence in December 1996, Professor Langdon would have carried out a further biopsy then. Thus the key question is whether cancer was actually present in Mrs Manning in September 1995 and/or December 1996. If it was, I did not understand it to be an issue that it would have been revealed in a further biopsy. Indeed such was the unchallenged evidence of three of the experts called on behalf of Mr Manning, namely Professor Sloan, Dr Woolgar and Dr Plowman.

This question gives rise to an altogether different enquiry from that involved in deciding whether Dr Harrison was negligent. In the latter enquiry hindsight is impermissible because the question revolves around what a reasonably competent pathologist in Dr Harrison’s position in 1995 and 1996 would and or ought to have done. By contrast, the question whether cancer was present in September 1995 and/or December 1996 involves the Court making a finding of fact on the balance of probabilities as to what was in fact the case. In reaching that decision the Court is both entitled and bound to have regard to all relevant evidence both factual and expert including in particular opinions of the experts informed by the benefit of hindsight.

I confess to having found this a formidably difficult task for at least four principal reasons. First and foremost both parties were able to point to unusual aspects of the other side’s case which meant that if true the case would be highly unusual. Thus it is inescapable that both if there was cancer present and if there was not cancer present certain events or phenomena must have occurred which would not normally be expected. Second, on a number of technical issues there were differences of opinion between experts, the resolution of which by the Court could not easily be achieved by reference to objectively ascertainable facts or criteria. This was particularly the case with the expert pathologists, the differences between whom in no small measure was agreed to lie in a difference of interpretation of what they saw in the biopsies. Since such subjective interpretation is based on years of training practice experience and expertise on the part of the pathologists, the Court is not well equipped to resolve such differences. Third, the underlying issue of whether there was cancer present in 1995 and/or 1996 was approached by both sides by reference to more than one area of medical expertise. In particular there was expert evidence from pathologists as to what was visible on the two biopsies and what inferences could be drawn therefrom. In addition, there was evidence from the oncologists as to the inherent probabilities as to whether the 2001 cancer was a new radiogenic primary cancer or a recurrent or persistent cancer and the inherent probabilities of whether there was a recurrent or persistent cancer present in 1995 and/or 1996.

The matter was further complicated by the fact that there was some degree of overlap between both sets of issues in two senses: first in varying degrees some of the experts in one discipline, in informing their opinions relied on what they had read and/or heard of the evidence of experts in the other discipline. Second insofar as within each area of expertise either party was able to point to unusual features of the other side’s case, the task of reaching an overall conclusion on whether on the balance of probabilities cancer was present in 1995 and/or 1996 was rendered even more complicated. The analogy of playing several games of chess at the same time springs to mind. Fourth, SPCC of the tongue is a rare form of cancer. As a result a feature of the literature is that studies and papers tend to be based on comparatively small populations so that caution needs to be exercised in considering whether statistically reliable propositions can be safely extrapolated from them. A further consequence was that none of the experts had a great deal of personal experience of observing and treating SPCC of the tongue. Added to this is the further complication that BT as a treatment for tongue cancer has apparently fallen largely out of fashion since it was used on Mrs Manning in 1994, with the result again that both literature on and individual experience on the part of the experts with the consequences of BT is necessarily limited.

Faced with these formidable difficulties, the responsibility of the Court, as it seems to me, is to absorb itself in the detailed evidence, both oral and written, to attempt to understand and evaluate the competing arguments as to the improbabilities of aspects of both sides cases, to seek to weigh the various probabilities and improbabilities on different aspects of the case and to stand back from the detail and consider the probabilities and improbabilities of each sides case in the round. Finally, while of course bearing in mind that the burden of proof falls on the claimant, the Court must eschew the temptation to avoid the discipline of seeking to explore the complex strands of argument and evidence and deciding difficult questions of fact by throwing up its hand and deciding that the very difficulties of the case dictate the inevitable conclusion that the Court cannot be satisfied on the balance of probabilities that the Claimant’s case has been proved. Such a conclusion, if justified, should be arrived at only after, rather than instead of, the undoubtedly difficult task of seeking to resolve the various issues with which the Court is confronted.

The most time consuming part of the trial was the evidence of the oral pathologists. In his written closing submissions Mr Grace QC submitted that the outcome of the case depends very substantially upon the Courts impression of the expert witnesses. In reply Ms Mishcon agreed with that submission adding: “Given that the whole case turns upon the evidence of the expert pathologists, it is the impression which they gave which is important.”

I have already made some reference to aspects of the impressions made by the three oral pathology expert witnesses on the Court and shall return to that aspect below. However, although there were significant differences of view between the pathology experts not only on issues related to negligence but also on whether on the balance of probabilities there actually was cancer present in September 1995 and/or December 1996, on Mr Grace QC’s primary case there is a preliminary issue which is largely independent of an assessment of what the biopsies showed and which, if decided in Mr Manning’s favour, leads to the inevitable conclusion that there was indeed cancer in both September 1995 and December 1996.

That issue is whether the cancer which, by the time of the trial, all the expert pathologists on both sides as well as both parties agreed was present in 2001 was, as the Defendants submitted, a new radiogenic primary or, as Mr Manning submitted, a recurrence or persistence of the original cancer which had been diagnosed in 1993, albeit that it had by 2001 transformed into SPCC from SQC.

In his written closing submissions Mr Grace QC presented the issue as in this way: “The only alternative aetiological theories before the Court are as follows:

The Defendants’ case that 2001 was a radiogenic new primary or

The Claimants case that 2001 was a recurrent (or rather, persistent) carcinoma from 1993, originating from tumour cells that survived the RT, and which either:

recurred, undiagnosed in 1995 and/or 1996 (i.e. within the most common timescale for recurrence); or

were coincidentally sampled, without clinical signs of recurrence, when the lesions were biopsied in 1995 and 1996, but then became manifest in 2000/2001: or

The claimants alternative case that September 1995 and/or December 1996 were the manifestations of a new tumour rather than recurrence. .. this is possible but largely immaterial.

The hypothesis described by Mr Grace QC as the Claimant’s alternative case in (3) above was not further elaborated or advanced at trials. It was based on a single speculative reference by Dr Woolgar in her report.

Its site

The pathology (intact epithelium in 2001 and morphological similarity of 2001 cells to 1996 cells)

The pathologists’ and clinicians’ contemporaneously expressed

If it was not a radiogenic new primary, the only alternative (no other alternative being advanced by the Defendant) is that it was a recurrent (or, rather, persistent) carcinoma from 1993. On the strong balance of probabilities, this is the case.

showed stigmata of malignancy (at least until the intellectual exercise determined that they were “consistent with” an innocent explanation) and

were at the least suspicious, or highly suspicious of a very bad carcinoma and

contained cells with similar morphological features to the 2001 tumour are wholly unrelated to the very same very rare carcinoma, SPCC that was belatedly diagnosed in 2001. If one adds to the above the strong opinion of Professor Sloan and Dr Woolgar that the 2001 cells were identical to the 1996 cells, it is overwhelmingly probable that there was a continuum between 1995/6 and 2001.

Put another way, it is “a coincidence too far” that the very same rare disease, the suspicion of which was excluded by the “intellectual exercise” in 1995 and 1996, should reappear in the same patient in 2001. Occam’s Razor (“entia non sunt multiplicanda praeter necessitatem”) – i.e. all unnecessary facts or constituents in the subject being analysed are to be eliminated, or, to translate from 14^th Century Latin to 21^st Century vernacular: “keep it simple, stupid” should be applied.

It will be seen that of Mr Grace QC’s seven headline points, only one, number (4) relies on the contents of the September 1995 and December 1996 biopsies and even point 4 is not wholly dependent on a finding as to whether Professor Sloan and Dr Woolgar’s opinion that the 2001 cells were strikingly similar to the 1996 cells is to be preferred to that of Professor Speight, which was that they were merely similar.

The evidence that the 2001 tumour was in the same site as the 1993 original SQC tumour is overwhelming. So is the evidence that the September 1995 and December 1996 lesions were in the same site as the 1993 primary tumour.

As to September 1995, Professor Langdon in his witness statement said that he noted an exophytic mass at the same site as the biopsy performed on the July 1995 ulcer related to the lower left second molar tooth and added “clinically I was concerned that she might have recurrent cancer.” The significance of the latter remark in the current context, is that, as appears below, there was powerful expert evidence to the effect that where a carcinoma appears on the same site as a previous cancer it is at the least very likely to be a recurrence of the original cancer rather than a new primary cancer. Thus the inference is that the exophytic mass was in the same site as the 1993 SQC. Indeed the site of the July 1995 ulcer referred to by Professor Langdon was itself referred to by him in his witness statement as being “at the site of the original cancer”. The clinical notes of Professor Langdon’ examination of Mrs Manning on 13^th September 1995 referred to an exophytic mass at the left lateral tongue related to lower left 7 tooth.

Professor Langdon’s notes of his examination of Mrs Manning on 30^th August 1995 also referred to an exophytic necrotic tissue at the original site (emphasis added). The request for laboratory examination for the September 1995 biopsy again referred to an exophytic lesion at the left lateral border of the tongue which was also marked pictorially and this description was repeated in Dr Harrison’s biopsy report of 15^th September 1995. Dr Henk in his witness statement referred to the lump excised by Professor Langdon in September 1995 as “a very odd looking soft cauliflower like mass on the left side of her tongue at the site of her original carcinoma.

The operation sheet also referred to an excision biopsy of an exophytic mass on the left lateral border of the tongue.

The note of the examination on 2^nd December 1996 repeats a reference to “fibrous nodule at anterior margin of previous excision.” The entry under clinical details including site. on the request for laboratory examination in relation to the December 1996 biopsy was:

As to the site of the 2001 cancer, the notes of Professor Langdon’s examination of 15^th January 2001 recorded:

On 16^th January Mrs Manning had been seen by Dr Henk who reported to Professor Langdon:

The entry under Clinical Details including site, size and duration of lesion in the request for laboratory examination dated 27^th February 2001 for the biopsy performed by Professor Langdon on 26^th February 2001 referred to SCC left lateral tongue 1993. Treated iridium wires and external beam RT firm non-ulcerated nodule at site of [primary]. (emphasis added) This description was repeated by Dr Harrison in his biopsy report dated 27^th February 2001. The biopsy itself was described by Dr Harrison as being 10 x 9 x 6mm.

On 11^th April 2001, the notes of Professor Langdon’s examination of Mrs Manning recorded:

On 18^th June 2001, Professor Langdon’s findings were recorded as:

In a letter to Dr Henk dated 28^th June 2001, Professor Langdon wrote:

On 5^th September 2001 Professor Langdon wrote to Dr Costello:

In a letter dated 21^st February 2002, to Mr Rhys Evans at the Marsden, Professor Langdon wrote:

“At the end of February 2001 she presented yet again, this time with a firm non-ulcerated nodule again at the site of the original primary carcinoma. Biopsy of this lesion in February last year was again reported as post-radiation fibrosis. Following this biopsy once again the area did not heal and of course my suspicions were yet again aroused and in June 2001 I performed three geographical biopsies, again all reported as radiation ulceration with no evidence of neoplasia (emphasis added).

Explaining why he gave a differential diagnosis in the request for the December 1996 biopsy of query recurrent squamous cell carcinoma, Professor Langdon said:

In relation to 2001, Professor Langdon in evidence confirmed that when he saw Mrs Manning at the beginning of 2001 she presented with severe pain radiating to her ear on the side of the original cancer. Clinically at that stage the appearance of her tongue had not changed since the previous review 6 months previously.

At one stage Dr Barley, the oncology expert called by the Defendants asserted that the 2001 carcinoma was not in the same site as the 1993 carcinoma. Indeed in some of the answers he gave to the questions in the agenda for the joint meeting between him and Dr Plowman, the oncologist called by Mr Manning, Dr Barley cited the fact that the 2001 carcinoma was not in the same site as the 1993 carcinoma as a reason supporting his view that the 2001 carcinoma was more likely to have been a new primary than a recurrence. At the trial, initially Dr Barley maintained this assertion. However in cross-examination, having accepted that it was based in part on an error on his part in interpreting one of the clinical records in 2001, he changed his position. He was shown Professor Langdon’s note of 26^th February 2001 which recorded the nodule as being on the left lateral tongue adjacent to lower left 7 tooth i.e. the site of the original 1993 tumour, and accepted that, on the assumption that what was subsequently excised in February 2001 was as there described, it was in the site of the original. Having previously agreed that second primary cancers carcinomas tend to occur in the penumbra rather than the same site of the original carcinoma, he accepted that the February 2001 carcinoma was not in the penumbra. Dr Barley was then shown Professor Langdon’s request for biopsy in February 2001 which referred to a “firm non-ulcerated nodule at the site of the primary” and accepted that Professor Langdon would be not just the best person to know where the February 2001 carcinoma was, but the only person on the basis that he alone was there. Having thus accepted that Professor Langdon’s view was preferable to his own in this respect, Dr Barley thus went on to accept that it is likely that Professor Langdon is right and that the 2001 tumour was in the same site as the 1993 tumour and that on the balance of probabilities that is where it was. He went on to accept that not only the 2001 admitted carcinoma but also the September 1995 and December 1996 ulcers (which he did not accept were carcinomas) were at the same site as the original 1993 carcinoma.

In her closing written submissions, Ms Mishcon did not seek to resurrect or rely on Dr Barley’s initial assertion that the 2001 carcinoma was not at the same site as the 1993 carcinoma and did not seek to rely on his initial evidence to that effect which was effectively abandoned .

In these circumstances I have no hesitation in finding, not only on the balance of probabilities but on the overwhelming weight of evidence, that the 2001 carcinoma was on the same site as the 1993 carcinoma.

Both Mr Brown, the expert surgeon called by Mr Manning, and Dr Plowman gave evidence that the fact that the 2001 carcinoma was in the same site as the original 1993 carcinoma made it much more likely that the 2001 carcinoma was a recurrence of the original carcinoma rather than a new radiogenic primary.

In his expert report Mr Brown cited the fact that the 2001 carcinoma was in the same site as one of the five reasons for his conclusion that it was probably a recurrent rather than new primary carcinoma.

At the trial Mr Brown was asked whether having seen the Defendants’ expert reports he had changed his view as to whether it was a new primary or a recurrence. His answer was:

In their joint experts report, in answer to the question whether if a tumour of the tongue occurred after several years on the same site as a previous tumour it is inevitably a recurrence of the original tumour, Mr Watt-Smith and Mr Brown agreed that: “if the new tumour is of similar pathological type and occurring at the same site of the former cancer, then it is likely to be a recurrence.”

They also agreed in their report that spindle-cell carcinoma is a known variant of squamous cell carcinoma. In evidence Mr Brown confirmed that so far as he was concerned there is no doubt that the tumour in 2001 was at the same site as the original carcinoma of 1993. In evidence Mr Watt-Smith did not seek to argue otherwise.

However on the question of whether, assuming that the 2001 tumour was on the same site, that makes it more likely that it was a recurrence rather than a primary, Mr Watt-Smith’s evidence at trial was unsatisfactory. In evidence in chief he was referred to Mr Brown’s evidence that one of the three factors which he said supported his view that it was a recurrence, was that it was at the same site. Asked if the fact that it was at the same site only supports recurrent cancer or whether it could also support primary cancer, Mr Watt-Smith answered that it supports both theories. He said that a new primary after RT will not usually occur at the centre where the lethal dose of radiation was but at the edge of the penumbra. This answer was not altogether clear in that he did not explicitly state whether by the edge of the penumbra he meant a different site from the original carcinoma or the same site. The implication of his answer that a second primary in the same site supports both theories was that he regarded the edge of the penumbra as the same site. However, he did not in terms seek to resile from his agreement, to which I have referred, in the joint report, that if the new tumour is of similar pathological type and occurring at the same site of the former cancer it is likely to be a recurrence.

Nor, if it was his intention to resile from that agreement did he make any attempt to explain how his new evidence was reconcilable with that agreement or what had caused him to depart from it. When it was put to him in cross-examination that expert evidence for Mr Manning had been that you would not expect to find a new primary on the same site as the original tumour, Mr Watt-Smith answered that if it is radiation induced it would be within the field of the radiation. He then said that if it was the case that the 2001 carcinoma was found on the same site as the 1993 one, it was his evidence that that could just as well be a new primary as a recurrence of the original. Again on its face this appeared to resile from the proposition with which he had agreed in the joint experts’ report.

Dr Plowman’s evidence was then put to him to the effect that a radiotherapy induced primary would not be precisely at the original site but would be elsewhere because a very much wider field is irradiated than the original carcinoma and thus would be somewhere in the target area. Mr Watt-Smith’s response was that a new primary can occur anywhere within the volume of original radiation but less likely at the centre and more likely towards the side. There was then the following exchange:

In his expert report Dr Plowman expressed the view that Mrs Manning’s 2001 tumour was a persistent one and not a new one, although it is fair to point out that this appeared to be based in large part on the assumption that Dr Woolgar’s and Dr Sloan’s conclusions in their expert reports that Mrs Manning had SPPC in December 1996 were correct.

In the joint oncology expert report Dr Plowman said that he could not contemplate any circumstance in his clinical practice where he would diagnose a carcinoma arising in the same site as that which he had treated for carcinoma either two, three, four or five years earlier as a ‘new primary’. At trial he expanded on those answers. In evidence in chief he said that he believed that the 2001 cancer was a recurrence in a less well differentiated form of the original carcinoma because it was in the same place. Referring to his answer in the joint report he said that recurrences of earlier tumours are located within 2 cm of the originally mapped tumour. They might not be in the epicentre of where the original tumour was but if they occurred slightly away from the centre it would only be insignificantly away. In the case of Mrs Manning he believed that the 2001 tumour was within 2 cm of the 1993 tumour. Shown the reference in Professor Langdon’s biopsy request form of 27 February 2001 to “? a non-ulcerative nodule at site of primary” Dr Plowman said: “If he says that, then it was the site of the primary.”

Dr Plowman was recalled and cross-examined about the fact that the 1996 biopsy did not stain positive for carcinoma in the immuno-staining. In the course of that cross-examination he accepted that, although the absence might be explicable by sampling errors, one would have expected to find some CK positive cells in the 1995 and 1996 biopsies. However in re-examination he confirmed that this did not change his view that on the balance of probabilities there was cancer present in 1995 and 1996. The first two reasons he gave were the fact that the 2001 carcinoma was in the same site as the original and the fact that in 2001 it presented as a carcinoma rather than a sarcoma. (I refer to this latter point below.) He repeated his opinion that second radiogenic primaries occur in the penumbra outside the high dose radiation zone and not within 2 cm of the original primary tumour. He said he strongly disagreed with the suggestion that there is no difference in terms of anatomical location between recurrent and new radiotherapy induced primary cancer. Recurrent carcinomas would occur within 2 cm of the irradiated original primary whereas new radiogenic primary carcinomas would occur in the penumbra of the irradiated zone and not within 2 cm. With Mrs Manning, the carcinoma in 2001 as well as those in 1995 and 1996 (if, as he believed, that is what they were) were consistent with recurrent carcinomas because they were in the same site as the original 1993 primary. This was the case in his view even though by the latter stages of the 2001 recurrence the tumour subsequently spread more widely.

In her written closing reply submissions and in cross-examination, Ms Mishcon relied on a paper by Laurent Schwartz and Others entitled “Synchronous and Metachronous Head and Neck Carcinomas”. This was a study of the incidence of metachronous carcinomas in a population of 851 patients who had had initial squamous cell carcinoma of the larynx, tongue, sinus, oral cavity, mobile tongue or base of tongue.

Dr Barley relied on this paper in a different context, referred to below, namely the issue of the percentage risk to Mrs Manning of suffering a second primary cancer. In the present context of relevance were:

The fact that for the purposes of the study the authors defined a second primary as one which had to be separated from the first by at least 2 cm of normal epithelium or had to occur at least three years after the first diagnosis and

As to (b) Dr Plowman was no less emphatic. Quite apart from the fact that Mrs Manning did not have the five principal risk factors identified in the Schwartz paper (elderly, smoker, alcohol consumer, male and site of first primary in the base of the tongue) and the fact that the paper was not dealing with radiogenic second carcinomas, even in the context of metachronous carcinomas Dr Plowman strongly disagreed that the Schwartz paper supported the proposition that second spontaneous (as distinct from recurring) carcinomas occur in the same site as the first carcinoma. He did not agree that metachronous tumours tend to occur in the same site as the original primary and did not consider that the Schwartz paper proved that they do. He said that he was sure that the table relied on by Ms Mishcon in the Schwartz paper did not as a matter of inference show that the second primaries referred to therein were occurring in exactly the same site as the original cancer. As he pointed out, the site of the second cancers in that table were loosely and generally defined as oral cavity, head and neck and oral cavity and oropharynx.

Dr Plowman had earlier said that he did not agree that metachronous tumours tend to occur in the same site as the original primary and that he did not believe that the Schwartz data backed up Ms Mishcon’s contention that they do. He said that the Schwartz table did not at all show that second metachronous tumours occurred at the same site as the original. In relation to radiogenic second primaries Dr Plowman said this: “… when the invasion was irradiated by Dr Henk there would have been a portal coming in from the left side of the face and a portal coming in from the front of the left side of the face. The portal which is coming in on the left side of the face does not stop when it reaches the tongue; it goes on exiting through the right side of the face; the one at the front exits at the back. It is not uncommon for the second cancer to arise, if it arises, in the lower dosed zone, say the other cheek or something. Q. Are you talking about a recurrence or a new primary? A. A new primary. Q. You have also got the brachytherapy pins, of course, in the left. A. Yes, but that, funnily enough, reduces the chance of getting a second cancer there. It is more common to get the second cancers in the lower dose surrounding area than in the very high dose. There is a sort of overkill there. …..”.

It is of note that elsewhere in Dr Barley’s evidence he accepted and agreed with Dr Plowman that a recurrence, as distinct from a second radiogenic primary, is likely to occur at the site of the original tumour. Indeed he accepted that no fewer than 90% of recurrences post RT occur within 2 cm of the original tumour, whereas a new radiogenic primary will tend to occur at the penumbra, which is outside that zone. Indeed he accepted that it would be very unusual for a new radiogenic primary to be at the site of the original and that all other things being equal, if you find a spindle-cell carcinoma in the same site and previous squamous cell carcinoma, other things being equal it is more likely to be a recurrence than a new primary.

Further he said that his interpretation of the diagrams in the medical records led him to conclude that the lesions in 1995 and 1996 were within the middle of the high dose RT region, in other words right where the original tumour had been and not in the penumbra. Thus, although, for different reasons, he did not believe that there was cancer present in 1995 and/or 1996, he accepted that if there was a tumour in 1995 and 1996 it was more likely to have been a recurrence than a new primary just based on the location. This was a significant concession, as it seemed to me, because in the light of the overwhelming evidence that the site of the 2001 carcinoma was the same as the September 1995 and December 1996 lesions, by parity of reasoning, the logic of this part of Dr Barley’s evidence is that, based on location, the 2001 carcinoma was more likely to have been a recurrence than a new radiogenic primary.

In answer to Mr Grace QC’s submissions on the inference to be drawn from the 2001 carcinoma being on the same site as the 1993 carcinoma, Ms Mishcon relied on two matters. The first was evidence given by Professor Speight in cross-examination on what he described as the biological principle of the shifting penumbra Ms Mishcon’s submission was that Professor Speight “explained that RT would create a crater in the tongue and that the cells at the margins of the crater would give rise to new epithelium which would migrate across the whole as part of the healing process. If the cells at the margin had been damaged by radiation, those damaged cells would end up at the exact site of the original tumour.” Professor Speight described the principle as follows:

As is apparent from that extract of Professor Speight’s evidence this theoretical explanation as to how a carcinoma appearing in the same site as a previous carcinoma could be radiogenic was just that, namely theoretical and speculative. Professor Speight did not suggest that he had any first hand experience of such a phenomenon. Doctor Barley said that he too had never seen such a case. Nor was it within his area of expertise. In my judgment, ignoring for the moment all the other factors relating to the issue whether Mrs Manning’s 2001 carcinoma was recurrent or a new primary, Professor Speight’s evidence on the shifting penumbra went little further than establishing that it is not a scientific impossibility for a second primary to appear on the same site as an earlier carcinoma. However, when applied to the facts of Mrs Manning’s case, there is a part of the evidence which renders this theoretical possibility largely academic.

Professor Speight accepted that in a case where a second primary appears in the same site as an earlier carcinoma by reason of radiation damaged cells migrating from the edge of the crater to the site you would not have an intact epithelium because you would have by definition a carcinoma arising from the epithelium. As discussed below, another of the principal reasons given by both Mr Brown and Dr Plowman for their conclusion that the 2001 carcinoma was more probably a recurrence than a second primary is the conclusion that in early 2001 Mrs Manning’s epithelium was intact. If that is right, the shifting penumbra argument would appear to fall away completely as an answer to Mr Brown’s and Dr Plowman’s first reason for concluding that the 2001 carcinoma was not a second radiogenic primary.

The second matter relied on by Ms Mishcon on the issue of site of the 2001 carcinoma was the fact that in re-examination Professor Sloan accepted that it was biologically possible for a second primary to occur at the same site due to field change. The evidence relied on by Ms Mishcon was a single isolated sentence. Asked how likely it was that there would be a new primary at the same site as the tumour which Mrs Manning suffered in 1993 Professor Sloan answered:

Professor Sloan did not elaborate on this evidence and in fact there had been discussion elsewhere of field changes leading to metastases in different sites in the same general region as a first carcinoma. The first part of his answer explicitly stated that if the tumour occurs at the same site it is a recurrence (as distinct from a second primary) and it may well be that in the second half of his answer Professor Sloan was not seeking to suggest that it is possible to have a second primary in the same site, in the technical and very specific and limited sense in which Mr Brown, Dr Plowman and Dr Barley were using it. Indeed he did not in terms say that it is a biological possibility that a second primary tumour could occur in the same site. In fact Professor Sloan went on to say that he thought that it was more likely that the 2001 carcinoma was a continuum or recurrence than a new primary, having regard to what would otherwise be the two coincidences that in 1995 and 1996 Mrs Manning had two lesions which each had cells which were highly suspicious for spindle cell carcinoma and then went on in 2001 to develop a second primary carcinoma which just happened to be a spindle cell carcinoma. For present purposes what matters is that it does not seem to me that Professor Sloan’s evidence advances Mishcon’s argument on the issue of the site to any material extent.

Mr Grace QC’s second point was that if the 2001 tumour were a radiogenic new primary it would be unusual for it to be a carcinoma and not a sarcoma. This was supported by the evidence of Mr Manning’s oncology expert and the defendants’ surgical expert. Dr Plowman said that if the 2001 tumour was a radiogenic second primary then on balance he would have expected it to be a sarcoma rather than a carcinoma. Radiation induced second cancers he said are more commonly, although not always, sarcomas. It would be unusual to have a second primary carcinoma induced by radiation. Mr Watt-Smith in cross-examination volunteered the opinion that the vast majority, 90% odd, of radiation induced primary cancers are sarcomas. Doctor Barley in cross-examination said that he agreed with Mr Watt-Smith and added that a radiation induced SPCC of the tongue would be a very rare event. Plainly, although by no means determinative, this is a factor pointing strongly against the probability of the 2001 carcinoma having been a new radiogenic primary.

Ms Mishcon did not suggest that there was any expert evidence to contradict the views of Dr Plowman and Mr Watt-Smith on this topic. In her written reply submissions her response on this point was to refer to the fact that all 59 of the cases in the Ellis and Corio study, 13 of which had had prior irradiation and all 20 of the cases in the Leventon study, 6 of which had had prior irradiation, were SPCC and not sarcomas. She submitted that there is no evidence in those papers that they were dealing with recurrences. This raises an issue which is of considerable importance in the context of the important question of the timescale in which recurrences and new primary carcinomas occur. On that issue, as we shall see, both sides placed great reliance on the statistical findings in the Ellis and Corio paper. For reasons which I shall explain when dealing with that issue I accept Dr Plowman’s interpretation of the statistics in that paper relating to the time lag in the case of post-radiation spindle cell carcinomas between the date of irradiation and the date of diagnosis. That interpretation is that those cases were in fact cases in which the patient had already suffered a prior carcinoma for which he or she was being treated by radiotherapy. Thus the carcinomas whose dates of diagnosis were recorded in the Ellis and Corio paper were probably recurrent carcinomas and not new primary carcinomas. It follows from that finding that in the current context the Ellis and Corio statistics do not assist Ms Mishcon. I do not consider that the Leventon paper provides a basis upon which to reject the clear evidence of Mr Watt-Smith for the defendants and Mr Brown for Mr Manning who agreed with each other on this topic. It was in any event not suggested to Mr Brown in cross-examination that his evidence on this point must be wrong by reason of either the Ellis and Corio or the Leventon paper.

The first main reason given by Mr Brown in his expert report for concluding that the 2001 carcinoma was a true recurrence of the December 1993 carcinoma was the appearance of the mass in the April 2001 MRI scan which he said shows a tumour arising in the depth of the tongue rather than the mucosal surface. In an agreed report on Mrs Manning’s MRI scans of January 1995, April 2001 and January 2002 Dr Lewis-Jones, an expert consultant radiologist, interpreted the 26 April 2001 MRI scan as showing an intermediate to low signal mass extending up to the mid line involving the anterior and middle of the tongue and concluded that it showed a tumour measuring approximately 2 x 2.8 centimetres in diameter. In evidence in chief Mr Brown said that the MRI scan led him to interpret the 2001 carcinoma as a recurrent disease because it showed a mass which had arisen deep to the mucosa whereas because all squamous cell and spindle cell carcinomas are mucosa diseases you would generally expect a new disease to arise in the mucosa. He said that in the 2001 scans there is clearly a mass which most people would interpret as recurrent disease both because the tumour was a mass deep in the tissues and not actually visible and because there was intact mucosa in the mouth. If it had been a new primary you would see an abnormality in the mucosa, an ulcer, an exophytic growth or cancer. He would expect there to be a visible ulcer affecting the mucosa. By contrast a mass measured 2.8 centimetres by Dr Lewis-Jones, which Mr Brown described as quite thick, which you cannot see clinically, must be deep in the tissue and therefore likely to be a recurrence.

Dr Lewis-Jones in his report said that the MRI appearances on 26 April 2001 show evidence of a mass lesion and expressed the opinion that recurrence of tumour would be the most likely cause based on those appearances alone. He also said that the MRI alone shows a mass in the left side of the tongue which he felt should have been regarded as due to recurrence until proved otherwise by biopsy.

In evidence in chief Mr Watt-Smith was asked to comment on the fact that one of the reasons given by Mr Brown as supporting his theory of recurrence rather than a new radiogenic primary was that there was a 2.8 centimetre mass seen on the MRI scan which must be deep in the tissue and therefore likely to be a recurrence. He first said that he agreed with Mr Brown, adding that the majority of surgeons would say, based on its location, that the tumour probably developed deep as a recurrence. But he then went on to volunteer the suggestion that an alternative explanation for the clinical evidence which would be consistent with it being a new primary rather than recurrent was that it could be budding off epithelium or migration of epithelium. However it was clear from what he said that he was basing this on evidence he had heard in court from Professor Sloan and when asked if he was in a position to say how likely it is that the large mass which Mr Brown said must be deep in the tissue and therefore likely to be a recurrence was caused by migrating epithelium and whether that fell within his expertise, he answered: “probably not.” This was, regrettably not the only occasion when Mr Watt-Smith appeared to advance arguments supportive of the Defendants’ case in respect of matters actually or apparently outside his field of expertise. I do not believe that it was put to Mr Brown that he was wrong to rely on the MRI appearance as a reason for concluding that the 2001 carcinoma was probably a recurrence by reference to Mr Watt-Smith’s suggestion of “budding epithelium” as an explanation for it.

In cross-examination Mr Watt-Smith confirmed that he had never seen the MRI scans. He said that for that reason he did not challenge Mr Brown’s evidence that the MRI pictures look like a deep recurrence and he repeated his agreement that the majority of surgeons would regard the MRI as showing a deep recurrence:-

In her written reply submissions Ms Mishcon quoted an extract from the report of the April 2001 MRI scan which said: “there is relatively well-defined increased signal intensity in the region of the known glossal ulcer.” She submitted that “Mr Watt-Smith said towards the end of his cross-examination that his interpretation of the April 2001 MRI report was that there was a well-defined increased signal which related to the tumour in the region of the ulcer and that therefore it must have been extremely close to the ulcer and his guess was that it was near the surface.” The evidence referred to by Ms Mishcon came in response to Mr Watt-Smith being shown, apparently for the first time, the extract of the MRI report referred to above. However Mr Watt-Smith went on to comment that because the tumour was 2.8 centimetres “the other side of this coin, or the other end of the diameter, does put it in the deep aspect, it is nearly 3 centimetres away.” This referred to a passage in the MRI report which said that the abnormal signal extended to the floor of the mouth. Mr Watt-Smith also accepted that in January and February there was no ulceration and the mucosa was intact (a point to which I refer below). Critically after both bits of evidence to which I have referred it was again put to Mr Watt-Smith that it would appear to the majority of surgeons and in particular to Mr Brown that this looks like a deep recurrence on the MRI and Mr Watt-Smith again confirmed that he did not challenge Mr Brown’s view on that and that he agreed with Mr Brown’s interpretation that this looks like a recurrence. Thus his earlier answer about the tumour being close to the ulcer was plainly taken into account by Mr Watt-Smith and did not affect his agreement with Mr Brown’s interpretation.

Mr Grace QC’s submission was that the presence of intact epithelium with no ulceration in February 2001 makes it highly improbable that the tumour in 2001 was a new primary, and indicates that this was a deeper recurrence. This submission raises two questions:

Was the mucosa intact? and

If so, does that make it highly improbable that the tumour in 2001 was a new primary?

As to i) it is clear both from the contemporary medical records and the evidence of Professor Langdon and Dr Henk that when Mrs Manning was examined in January 2001 by both of them complaining of pain caused by what is now known to have been a carcinoma the mucosa was intact. The clinical notes of Professor Langdon’s examination on 15 January 2001 record that there was no ulceration and Dr Henk’s letter to Professor Langdon reporting on his examination of Mrs Manning the following day reported that: “the appearance of the tongue is very much as I remember it from last year.” Neither document refers expressly or by implication to any sign of a breached mucosa. On the contrary both are inconsistent with any such signs. Dr Henk’s reference to the appearance of the tongue being very much as he remembered it from the previous year is a reference to his review of Mrs Manning on 16 June 2000 which is recorded in his letter to Dr Harrop-Griffiths on the same day: “She remains well. There is no sign of recurrent carcinoma of the tongue and she has no cervical lymphadenopathy.” It was accepted in the course of the trial by Ms Mishcon on behalf of the defendants that the carcinoma was present in January 2001 and she did not seek to argue that the mucosa was not intact at that time.

As to ii) the expert evidence was overwhelmingly in support of Mr Grace QC’s submission. Asked in evidence in chief what conclusions could be drawn from the fact that when Mrs Manning was examined by Professor Langdon and Dr Henk in January 2001 there was no ulceration and the mucosa was intact, Dr Plowman answered: “Carcinomas arise from mucosa. They cannot arise ab initio from the underlying muscle or connective tissue. Therefore the simple conclusion from that should be that it could not be a carcinoma …Carcinomas arise from the surface. Therefore, if you get a new cancer you would not expect a surface that is intact. I think that is the case in January 2001….. In January 2001 Dr Henk’s note states that the surface of the tongue was intact or words to that effect. Q. And, as I think he remembered it, six months or so before he had last seen her, that is the effect. A. Certainly he has issued a report in January saying that. Q. So does that help you as to whether this was a recurrence in 2001 or a wholly new one? A. I think it is most unlikely that it was a new primary; and I think something had been grumbling deep all that time.” (emphasis added).

It was at this stage that Ms Mishcon confirmed that it is common ground that the tumour was present by November 2000. Dr Plowman supported this by saying that extrapolating back from the dimensions of the tumour in April 2001 as shown by the MRI scan, the tumour was too big to have arisen in January 2001 which he said would have been impossible. Dr Plowman continued:

In cross-examination Dr Plowman confirmed the strength of his view:

In his expert report Mr Brown gave as his second reason for concluding that the 2001 carcinoma was a true recurrence. Dr Henk’s comments on 16 January 2001 in which he reported the tongue as unchanged from the year before:

In examination in chief he confirmed that this was one of the reasons why he believed that the 2001 carcinoma was a recurrence. Together with the fact that it arose in the same site as the 1993 carcinoma he regarded it as an important point. He described it as the same point as his conclusion from the MRI scan that the carcinoma was not arising from the mucosa.:

In cross-examination Mr Brown again linked the appearance of the mass of the tumour in April 2001 with the intact mucosa point.:

In cross-examination Mr Watt-Smith agreed that if the 2001 carcinoma was a new primary it would be very unusual and highly unlikely for the epithelium to be intact with no ulceration in January and February 2001. Later he agreed that in January and February 2001 there was no ulceration and the mucosa were intact and the ulceration did not commence until after the biopsy in late February 2001 with the tumour finding its way up into the ulcer by the time of the April 2001 scan. Thus in January and February 2001 the mucosa was intact and the epithelium was intact.

In his report Professor Sloan referred to the comment by Dr Henk in his witness statement that in hindsight the first symptom of the spindle cell carcinoma was almost certainly the pain of which Mrs Manning complained towards the end of 2000 and that the tumour appears to have been sub-mucosal therefore giving rise to no visible abnormality in the early stages. Professor Sloan expressed the opinion that “the fact that the tumour was growing beneath intact mucosa (‘sub-mucosal’) is against the spindle cell carcinoma being a new primary tumour growing from clinically abnormal surface epithelium. The features described by Dr Henk are consistent with the view that a slowly growing recurrent carcinoma was present in the deeper tissues. The pain experienced by Mrs Manning is likely to be due to the carcinoma extending to infiltrate nerves.”

He added that the scientific literature available at the time when Mrs Manning was being treated recognised the phenomenon of late recurrence after radiotherapy. Professor Sloan added:

In re-examination at trial Professor Sloan was asked whether the fact that in January and February 2001 there was no ulceration and the mucosa were intact despite the presence of a tumour helped him judge whether it was a new primary or a recurrence. His answer was:

He pointed out that Mrs Manning’s mucosa was being inspected carefully from 1996 through to 2001 and beyond by experts to look for change and there was no surface lesion identified. Professor Sloan explained that:

Professor Sloan was then asked if this could be the result of a new primary. He said that it was a possibility because one could imagine spindle cell carcinoma budding away from the under-surface of a dysplastic epithelium and not leaving a visible surface lesion that was detectable. However he said he thought it was highly unlikely that it could produce no surface lesion whereas an intact mucosa was not highly unlikely if it was a few original cells that got left behind in 1995/1996 and which then burrowed inwards, the tumour developing inside the tongue. Indeed he said that seemed to fit with the descriptions he had read and the clinical features of the case.

This seems to me an important part of Professor Speight’s evidence in that without it the defendants are left with no substantive answer either on the same site point or on the intact mucosa point. It seems to me that there are two significant problems with it. First it assumes that when what we now know to be the tumour was biopsied at the end of February 2001 it was an early biopsy, whereas it was common ground between the parties that the tumour was present from at least November 2000 when Mrs Manning complained of severe pain in her ear. Indeed Professor Speight himself did not suggest that in February 2001 the tumour was early and was unable when asked when he thought the tumour started to do more than give a “guesstimate” of somewhere round about September/ October 2000, which would have made the tumour 5-6 months old by the time it was biopsied in February 2001 with the mucosa still intact. Professor Langdon accepted that pain radiating to the ear is suggestive of a carcinoma invading the lingual nerve which was one of the reasons for him repeating biopsies in 2001. If, as seems not unreasonable on all the evidence, notwithstanding Dr Barley’s suggestion to the contrary, the extreme pain experienced by Mrs Manning in November 2000 was indeed caused by the tumour invading the lingual nerve, that in turn would suggest that it may very well (even on the hypothesis that it was a new primary) have been present growing in the connective tissue for some time before invading the lingual nerve.

Professor Speight said that if in February 2001 the tumour was T1 or less by definition it would be early but there was, so far as I am aware, no evidence that in February 2001 it was T1 or less. Mr Brown in his evidence on the April 2001 MRI scan said that when the tumour presented in 2001 it was T4. Indeed one of the reasons he gave for concluding that the tumour was recurrent was that a T4 that had developed as a new primary would have almost certainly been ulcerated and he had never seen a T4 of that size in the tongue without an ulcer that was not recurrent. A T4 in the tongue arising as a new primary cancer would normally have extensive ulcerations. By contrast where a tumour arises as a primary rather than a recurrent one normally sees more of the tumour than the scan shows. Tumours that become ulcerated do not necessarily show up very obviously on a scan and a T1 will often be reported as a normal scan because it is very much on the surface.

By contrast where there is a highly positive scan such as that of Mrs Manning with a large mass, that is very classical of recurrence with the tumour arising deep in the tissues and growing in that area. I have already referred to Dr Plowman’s evidence that, quite apart from the defendant’s concession that the tumour was already present in January 2001 and indeed in November 2000, his reason for concluding that it was present in January 2001 was that the April 2001 MRI scan showed a definite abnormality which was too large to have arisen between January 2001 and April 2001. Indeed he said given the size of the tumour in April 2001 (2.0 x 2.8 cm) it would have been impossible with a tumour of that size for it not to have been present in January 2001.

In short there was no solid evidential platform to satisfy the first condition of Professor Speight’s hypothetical scenario in which the 2001 carcinoma was a primary notwithstanding its presentation with intact mucosa, namely that it presented early.

The second problem with Professor Speight’s scenario is that it does not fit with the clinical presentation of Mrs Manning in January and February 2001. Professor Speight’s scenario assumes that for a certain length of time before the carcinoma ulcerates it grows down from the bottom of the epithelium into the underlying connective tissue and that for some time it may have spread laterally underneath the epithelium. The proposition that as the carcinoma gets bigger the epithelium begins to lift to produce a nodule again presupposes that both at the time that it lifts to produce a nodule and for some time before that it has been present underneath the epithelium, since otherwise it would not be pushing the epithelium up. Not only was there no evidential support for such a proposition in Mrs Manning’s case, on the contrary it was contradicted by all the evidence to which I have referred, in particular Mr Brown’s evidence based on the MRI scan that the tumour was growing deep in the tissue and the evidence of all the pathologists including Professor Speight that at the time of the biopsy at the end of February 2001, when there was indeed a small nodule there was no connection between the epithelium and the tumour. When this point was put in terms by Mr Grace QC to Professor Speight he accepted explicitly that there was no connection between the epithelium and the top of the tumour that was evident deep on that biopsy.

This led Professor Speight to make a further point. He said that in the February 2001 biopsy the overlying epithelium was dysplastic and that the pathological interpretation of that was that the tumour had risen from the dysplastic epithelium but at a site away from that section, that is to say elsewhere in the biopsy or possibly elsewhere in the patient. This was a reference to the following paragraph in Professor Speight’s expert report in which he was describing what he found on microscopic examination of the February 2001 biopsy:

Mr Grace QC’s response to that evidence was twofold. First he rightly pointed out that neither Professor Sloan nor Dr Woolgar in their expert reports made any reference when describing their microscopic examination of the February 2001 biopsy to any dysplastic epithelium. Coupled with the fact that Professor Speight only described the dysplastic epithelium as moderate and the fact that neither Dr Harrison nor Professor Johnson found epithelial dysplasia in 2001 and indeed in August 2001 Professor Johnson expressly stated that there was no epithelial dysplasia, he invited the court on the basis of that evidence to find insofar as it is necessary to make a decision on the point that there was no, or no significant, epithelial dysplasia in February 2001. His second point was that both Dr Plowman and Mr Brown convincingly refuted any suggestion that the allegedly dysplastic epithelium demonstrated an epithelial origin to the tumour on the basis that dysplasia can be wholly innocent and is not malignancy and was not related or connected to the 2001 tumour, dysplasia being a reversible phenomenon.

On Mr Grace QC’s second point Dr Plowman in cross-examination said that it was not possible that the fact [it was put to him as a fact, although as we have seen that was in dispute] that the epithelium was dysplastic meant that the 2001 carcinoma was a primary cancer. Nor did he accept that the dysplasia [if there was any] was related to the cancer. Dysplasia he said is not the same as cancer: it is a reversible phenomenon. As he put it it has not crossed the Rubicon to cancer and may never cross the Rubicon to be cancer. He said that dysplasia is not uncommon post radiation in a situation where it does not progress to a new primary. Commenting on the paragraph in Professor Speight’s report referring to moderate dysplasia he said that he believed that there was a disconnect between the dysplasia referred to by Professor Speight and the area in the deep aspect suspicious for spindle cell malignancy.

Mr Brown was even more emphatic. Like Dr Plowman he was at pains to point out that epithelial dysplasia is not malignant:

When Mr Brown was referred to the reference to moderate epithelial dysplasia in Professor Speight’s report and asked whether that does not show that there was something happening with the epithelium even if the mucosa was still intact Mr Brown’s response was:

A. A new tumour.

Q. And you cannot infer from the fact that there was a dysplastic change in the epithelium that it was a new cancer. Is that what you are saying?

A.

Yes that is very unlikely that that is a contributing factor to the decision of whether it is a recurrence or not…. What I am saying is that the fact that the pathologist has found some dysplastic change in the surface epithelium I don’t think comes into the discussion or argument about primary or secondary. The presence of dysplasia is not the issue; it is where the invasive cancer is. That is much more associated with where it arose from. The presence of dysplasia, I think, is often reported in relation to invasive squamous cell carcinoma but it has, in my view, very little relevance.” (emphasis added).

Mr Brown went on to make the point referred to above that his main reason for concluding that the 2001 carcinoma was recurrent rather than a new primary notwithstanding the alleged presence of epithelial dysplasia was because the MRI scan was so classical of recurrent cancer.

In relation to Mr Grace QC’s second point it is true that Dr Harrison did not refer to any epithelial dysplasia in his report of the February 2001 biopsy and that Professor Johnson explicitly reported in respect of the August 2001 biopsy that there was no dysplasia. I am not particularly impressed by that evidence both because it is common ground between the parties that Dr Harrison and Professor Johnson were negligent in resect of their February, June and August 2001 biopsies and because in relation to what Professor Johnson wrote about the August 2001 biopsy it is pertinent to note that Professor Sloan refers to “partially ulcerated surface epithelium” in his examination of that biopsy and in any event he records in relation to the June 2001 biopsy that one of the slides showed a completely ulcerated surface. By definition the June 2001 biopsy preceded the August one. As to the difference between the reports of Professor Sloan and Dr Woolgar one the one hand and Professor Speight on the other, unlike the minute attention to detail in their respective cross-examinations on the 1995 and 1996 slides, this was not a matter which attracted much if any attention in their cross-examinations. The court has thus little to go on in forming a judgment as to which view is correct. However it does not seem to me that it is necessary for Mr Grace QC’s purpose that there should be a positive finding that there was no epithelial dysplasia in February 2001.

I accept the evidence of Dr Plowman and Mr Brown in relation to point one that even if there was moderate epithelial dysplasia on the February 2001 biopsy it is highly unlikely that for that reason the correct interpretation of the 2001 carcinoma should be taken to be a new primary rather than a recurrent carcinoma. Their opinions on this point were clearly very strongly held and I found their evidence persuasive. By contrast Professor Speight’s evidence on this point was largely theoretical. It was not supported by the evidence in relation to how Mrs Manning presented in January and February 2001 and as an explanation for why there was intact mucosa if this was a second primary it was inconsistent with the evidence of the MRI scan and Mr Brown’s interpretation of that. While, of course, never forgetting that the overall burden of proving that there was cancer present in 1995 and/or 1996 lay on Mr Manning as Claimant, the reality of the position on this particular aspect of Professor Speight’s evidence as it seems to me is that if, as I find below, the presence of intact mucosa is prima facie inconsistent with and makes it highly unlikely that there could be a new primary carcinoma, one would need compelling evidence before concluding that such an unlikely event occurred in this case by reference to a theoretical argument.

That being so, if one puts to one side the epithelial dysplasia argument in my judgment Professor Speight’s other hypothetical explanation for the intact mucosa, namely the carcinoma arising from the bottom of the epithelium possibly spreading laterally underneath it and still in an early stage when Mrs Manning presented in February 2001, carries little or no weight against the mountain of expert evidence, embracing the Defendant’s own expert surgeon, that the presence of intact mucosa made it highly unlikely that the 2001 carcinoma was a new primary. It is also on its face inconsistent with the fact, accepted by Professor Speight, that in February 2001 there was no connection between the epithelium and the malignancy in the deeper aspect. This “early carcinoma” theory was raised by Professor Speight for the first time in re-examination and was thus not put to Dr Plowman or Mr Brown. It is to be inferred from the emphatic nature of their evidence on the intact mucosa point that it is a theory which they either assumed could have no application in this case or with which they did not agree.

This finding has in turn a knock-on effect on Professor Speight’s shifting penumbra theory as a theoretical explanation of how a new primary carcinoma could be present on the same site as the original 1993 carcinoma. It will be recalled that Professor Speight accepted that in order for it to be possible for there to be a new primary carcinoma on the same site by reason of the shifting epithelium there would have to be a breach in the mucosa because one would have by definition a carcinoma arising from the epithelium. There was no such breach, the mucosa being intact and it would seem to follow that if the “early carcinoma” theory is disregarded Professor Speight’s shifting epithelium explanation for the carcinoma being present on the same site must likewise fall away.

The cumulative effect of my findings in relation to Professor Speight’s theories of (a) the sifting epithelium, (b) the “early carcinoma “ and (c) the epithelial dysplasia is to leave the Defendants’ submissions in response to Mr Grace QC’s arguments based on the same site and the intact mucosa looking distinctly threadbare.

It is convenient at this point before looking at the other arguments raised by Mr Grace QC and Ms Mishcon on the primary versus recurrence issue to take stock of the evidence on that issue thus far.

This is therefore a convenient point at which to record my impressions of these four expert witnesses. They can be succinctly stated. I found both Dr Plowman and Mr Brown to be authoritative, careful and straightforward in their evidence, very persuasive and generally very impressive as expert witnesses. I have already referred to the impression that Mr Watt-Smith gave of being ready to volunteer opinions in areas outside his actual or apparent area of expertise. Mr Grace QC suggested that his trawling of the Internet in search of material to support the Defendant’s case both supported that impression and suggested a tendency, no doubt unwitting, to stray into the territory of advocate rather than expert witness. It was certainly noticeable that, unlike Professor Speight for example, Mr Watt-Smith often seemed reluctant to accept propositions which he was ultimately forced to accept of which in my view were correct and/or when accepting such points often to volunteer by way of addition, answers to questions which he had not been asked which appeared to support the Defendants’ case. Doctor Barley was a careful and meticulous witness who I have no doubt was doing his best to assist the court. I was however left with the impression that perhaps because he believed in the Defendants’ case, he was somewhat inflexible in his answers and reluctant to concede points which on their merits were persuasive.

Doctor Plowman has been a consultant in haematology and oncology at Great Ormond Street and a consultant in the Department of Radiotherapy at St. Bartholomew’s since 1982. From 1989 to 1994 he was Head of Radiotherapy and Clinical Oncology at St. Bartholomew’s, from 1994 to 1997 he was Head of the Joint Department of Radiotherapy and Clinical Oncology at both St. Bartholomew’s and the Royal London Hospital, a position he has held also from 2000 to date. He has published prodigiously both in the form of papers and books. Until eight to ten years ago most of his work was in oral cancer. At present most of his attention is directed towards the brain and spinal cord. In response to a suggestion by Ms Mishcon that he might not have experience in the area with which this case is concerned, Dr Plowman said that he has probably done 30 to 40 hairpin BT implants which is probably more than any of his colleagues, that in relation to the BT technique used on Mrs Manning he has probably had more experience than anyone in the east side of London and that he had a breadth of experience in oral cancer. He now sees six to ten cases of oral cancer a year but sits in the multi-disciplinary team meeting which discusses more such cases and sees 100 a year. I had no doubt that in relation to the matters on which he differed from Dr Barley he had sufficient experience to enable the court to have confidence in his views as an expert witness.

Mr Brown has since 1992 been consultant in oral and maxillofacial surgery at the University Hospital Liverpool. He is on the boards of the British Journal of Oral and Maxillofacial Surgery, the Journal of Craniomaxillofacial Surgery and the International Journal of Oral and Maxillofacial Surgery where he is the editor in relation to the oncology section, and also Head and Neck Surgery. He specialises in head and neck surgery and management of cancer within mouth, face and jaws. His key areas of interest are tumour invasion of the mandible and the management of oral cancer. He has developed a head and neck cancer database. Since 2005 he has been Hunterian professor at Liverpool University. As with Dr Plowman I had no doubt that his experience and expertise are such as to enable the court to place great confidence in his views.

If I do not summarise the CVs of Dr Barley and Mr Watt-Smith it is not because I considered that either of them lacked the necessary experience or expertise. Rather in relation to Mr Watt-Smith, it is because Ms Mishcon placed very little reliance on his evidence in her closing submissions and in relation to Dr Barley it is partly for that reason and partly because my lack of confidence in him as an expert witness derived not from any doubts as to his expertise but rather from the content of his evidence and the clear views which I formed as to his reliability and persuasiveness as a witness in the witness box and in his written reports.

In the event, as Mr Grace QC pointed out in his written closing submissions, Ms Mishcon in her written closing submissions placed little reliance on the evidence of Dr Barley and Mr Watt-Smith. Insofar as it is necessary to do so for the purpose of resolving differences between them, I have no hesitation in recording the fact that I found Dr Plowman and Mr Brown to be more reliable and impressive expert witnesses than respectively Mr Watt-Smith and Dr Barley and I prefer the evidence of the former to that of the latter.

In his report Mr Brown gave five main reasons for his conclusion that the 2001 carcinoma was probably a recurrence. They were (1) the appearance of the mass in the MRI scan (April 2001) which shows a tumour arising in the depth of the tongue rather than the mucosal surface. (2) The comments on 16^th January 2001 in which the tongue is reported as unchanged from the year before. This confirms that the tumour did not arise in the mucosa essential for a new primary disease. (3) The similarity of the pathology specimens from 1995 until the recurrence was finally resected. (4) The fact that a spindle-cell carcinoma is a variant of squamous cell carcinoma often associated with previous radiotherapy treatment. (5) The literature reported by Professor Sloan giving the incidence of late recurrence of oral cancer following the radiotherapy treatment. As was pointed out to him in cross-examination, the third reason was based on Mr Manning’s pathology experts Professor Sloan and Dr Woolgar. At the time he wrote the report he had of course not yet read Professor Speight’s reports. In re-examination he confirmed that his first and second reasons did not depend on the opinions of the pathology experts. Even leaving out of account their views, it remained Mr Brown’s view that: “Basically the appearance on the scan, the fact that it did not breach the mucosa, the fact that it is arising deep in the tissues would indicate that it is a recurrence, and the same site would indicate it is a recurrence… Q – So based on mass in the MRI scan, intact mucosa, and same site alone your view remains that on the balance of probabilities it is more likely to be recurrence than a new primary? A – Yes I think so.”

For his part Dr Plowman had said in the joint oncologist’s report that the chance of a second primary carcinoma occurring in the same site of the tongue in 2001 and constituted of cancer cells that were so similar to those seen in 1996 (and called carcinoma cells at that time in their retrospective review) by two expert pathologists would be exceedingly small. When asked in evidence how it would affect his view of the probabilities as between recurrent and a new primary if it is the case that all three pathology experts are of the view that there were cells highly suspicious of SPCC but Professor Speight stopped short of saying in retrospect that they were, he confirmed: “It does not make it quite as clear cut, but it does not change my overall conclusion.” Like Mr Brown it will be recalled that he was emphatic when expressing the view that it was “most unlikely” that the mucosa would not be breached if it was a new primary and that if the epithelium is intact and you have got cancer going on down below which is what he said it was, it argues very strongly that this was not a new primary. Particularly striking was his evidence that if tumour was present in January 2001 when the epithelium was intact it would be difficult to think of a mechanism as to how it could happen that that was a new primary.

I have dealt with the evidence and my conclusions on this part of the case at some length because of its central importance to the ultimate issue of whether there was cancer present in 1995 and/or 1996. Given the strength of Mr Manning’s case on this prior question thus far and in particular given that it is based in large part on the scientific improbability of there having been a new primary in 2001 I approach the remaining arguments on this question on the basis that it would require an even greater scientific improbability if not impossibility in the opposite direction to compel the conclusion that in fact the 2001 carcinoma was a new radiogenic primary or at least to lean to the conclusion that it cannot be said on the balance of probabilities that it was a recurrence..

Coming 7 years after the December 1993 carcinoma, Mr Grace QC’s submission is that the 2001 tumour was on balance too early to be new radiogenic primary. Doctor Plowman in cross examination expressed the view that the 2001 carcinoma was far more likely to be a recurrence than a new radiogenic primary because it was too soon to be the latter. Based on the incidence of radiogenic second primaries in data drawn from Nagasaki, Hiroshima and Chernobyl he said that solid radiogenic tumours start to occur after 6 or 7 years, usually more than 10 years. This was, if anything, more favourable to the Defendants than the evidence of Mr Watt-Smith who said that the generally accepted time for radiation induced sarcomas, which he teaches medical students, would be closer to 10 years after radiation so that 7 years would be unusually early for a radiogenic sarcoma. Although he suggested that carcinomas and sarcomas behaved differently he did not elaborate on what if any implications he considered that to have on the relevance of his 10 year figure. In her written closing submissions Ms Mishcon submitted that if there were no SPCC between 1994 and 2001 the SPCC which should have diagnosed in February 2001 would almost exactly match the mean interval of 6.9 years from irradiation to diagnosis identified in the Ellis and Corio paper which she submitted makes it more likely that it was a new primary.

The Ellis and Corio paper was a study in December 1980 of spindle-cell carcinoma of the oral cavity at the U.S. Armed Forces Institute of Pathology and Veteran’s Administration Dental Training Centre in Washington D.C. It involved a clinico-pathological assessment of 59 cases. The paper contains the following paragraph: “Thirteen patients had a history of prior therapeutic irradiation to the region where a spindle-cell tumour subsequently developed. The time interval from irradiation to diagnosis of spindle-cell carcinoma ranged from 1.5 to 10 years, with a mean of 6.9 years.” The paper added: “No significant findings as to personal habits, such as smoking, alcohol intake or occupation, of the patients could be gained from the available information.” Although 13 patients is not a very large sample, the mean figure of 6.9 years bears a striking similarity to the 7 years between Mrs Manning’s first carcinoma in December 1993 and the carcinoma that should have been diagnosed in February 2001. On its face, therefore, if the carcinomas suffered by these 13 patients were first time radiogenic carcinomas, the 6.9 year figure would strongly support the inference that Mrs Manning’s February 2001 carcinoma was a new radiogenic primary and not a recurrence.

However when these figures were put to Dr Plowman, his response was that the Ellis and Corio figures supported his conclusion, namely that the February 2001 carcinoma was a recurrence rather than a primary. His reasoning was that the 1.5 year figure at the bottom of the Ellis and Corio spectrum argued strongly against the carcinomas of the 13 patients referred to in that part of the study being new spindle-cell carcinomas. That is because whereas 1.5 years falls squarely within the 2 year period after an original carcinoma in which the large majority of recurrent carcinomas occur, it is massively below the usual 10 years+ to be expected for radiogenic primaries. Further the inference that these 13 carcinomas were in fact recurrences was strongly supported by the fact that Dr Plowman could think of no other reason why they should have had radiation treatment to their mouth in the first place unless it was to treat an existing cancer.

In my judgment Dr Plowman’s reasoning is compelling. The fact that the 1.5 year figure is very unlikely to have been a new radiogenic carcinoma suggests at the very least that some of the 13 carcinomas must have been recurrent. It follows that, again at the very least, the 6.9 year mean figure is very unlikely to represent the mean for new radiogenic primaries. The additional inferred fact that all 13 of the patients are likely to have had a previous carcinoma coupled with the fact that 1.5 years falls within the classic period in which recurrences are to be expected suggests that if any reliable inference is to be drawn from the 13 patients it is that they were all examples of recurrent carcinomas in respect of which the mean period between the first carcinoma (which is likely to have occurred shortly before the irradiation) and the second recurrent carcinoma was 6.9 years. That inference would of course strongly support the argument that Mrs Manning’s February 2001 carcinoma was probably a recurrent rather than a new primary one.

Doctor Plowman’s evidence was supported by that of Professor Sloan who said in his report:

On this evidence I find that, ignoring all other factors, it was inherently unlikely that Mrs Manning would develop a new radiogenic primary carcinoma as soon as 7 years after the radiation treatment in January 1994.

Mrs Manning was at low risk of suffering a second primary. Reference has already been made to the Schwartz study of 851 patients with initial squamous cell carcinoma of various parts of the head and neck. The study found that a 22% incidence of second metachronous cancers in 5 years. However, a univariate analysis of different factors influencing metachronous cancer incidence revealed that in respect of each of the 5 factors analysed Mrs Manning had a considerably lower risk than average. Thus the risk of developing a second cancer measured by site of the first primary ranged from 45.5% for the base of the tongue to as low as 9.5% for the mobile tongue where, where Mrs Manning’s 1993 carcinoma was diagnosed. The risk for females was 15.6% as against 29% for males. The risk for those under 40 was 20.3% and against 26.8% for 40 to 50 year olds, 38.2% for 50 to 60 year olds and 17.8% for over 60s. The figures in respect of non-smokers and non-drinkers are particularly striking. Thus the risk for non-smokers was 2.8% compared to 25.9% for those smoking up to 20 packs a year, 41.8% for those smoking 20 to 40 packs a year and 29.8% for those smoking more than 40 packs a year. The risk for non-drinkers was 4.6% compared to 30% for drinkers. It is of interest that the background to the study was a desire to improve the survival of head and neck cancer patients by devising an effective programme of screening for second malignancies. The authors of the study concluded that “ only the mall sub-set of non-smokers and non-drinkers should be excluded from such trials.”

Based on the Schwartz study Dr Barley in his report said that about 20% of patients who have been successfully treated for head and neck cancer will develop another primary cancer, about 30 of these cancers occurring in the head and neck region. In the draft joint oncologists’ report following the meeting between Dr Plowman and Dr Barley, Dr Barley repeated what he had said in his report adding his opinion that, having had one head and neck cancer, Mrs Manning had a significantly increased risk of developing a second primary cancer of the head and neck. Doctor Plowman in their draft statement noted that Mrs Manning was a non-smoking wife of a dentist by which he inferred good oral hygiene and did not think that she had the risk factors for metachronous carcinomas of the head and neck- particularly as she was in her late 30s- that are represented by the population studied in the Schwartz paper.

He concluded that she was therefore at a low risk of developing a second primary. In cross-examination Dr Plowman elaborated. He pointed out that the patients studied in the Schwartz paper had been the usual type of squamous cell carcinoma head and neck carcinoma patients where there is a preponderance of smoking, drinking, poor oral hygiene and usual advance stage and actually statistically male sex too. Since Mrs Manning had none of those characteristics Dr Plowman said that she was not in as high a risk bracket by a long way as those quoted in the Schwartz paper. When asked to put a figure on it he said it would be at most 1 to 2%. Doctor Barley in re-examination accepted that when you take into account Mrs Manning’s particulars she had a lower percentage risk of developing a second primary than the overall 20% figure for patients who have suffered an initial head and neck cancer revealed in the Schwartz paper.

In my view Dr Plowman’s estimate, based on his analysis of the Schwartz paper and his experience is the best evidence on this aspect of the case. In fact it does not appear to be materially at odds with the logical implications of Dr Barley’s evidence, since added to the 6% chance of Mrs Manning developing a second primary cancer in the head and neck (which I take to be the implication of his report). He accepted that her particular characteristics meant that she had a lower risk than the 22% average in the Schwartz paper.

Mr Grace QC relied heavily on the submission that it is highly improbable that the biopsies which in 1995 and 1996 by common consent (1) showed stigmata of malignancy (at least until the intellectual exercise determined that they were consistent with an innocent explanation), (2) were at least suspicious or highly suspicious of a very rare carcinoma, SPCC, and (3) contained cells with similar morphological features to the 2001 tumour are wholly unrelated to the very same very rare carcinoma, SPCC that was belatedly diagnosed in 2001. I have already referred to the fact that both Mr Brown and Dr Plowman made clear that their opinions that the February 2001 carcinoma was probably a recurrence rather than a new radiogenic primary were not dependant on the views of the expert pathologists on the correct interpretation of the various biopsies. Their very strongly expressed opinions on this critical matter were thus free-standing.

It is, however, the case that they both cited the similarity of the pathology specimens as an additional factor giving further support to their conclusions. Thus Mr Brown gave as his third main reason for concluding that the September 2001 disease was a true recurrence of the original tumour treated in 1994 “the similarity of the pathology specimens from 1995 until the recurrence was finally resected.” Doctor Plowman in his report wrote: “The persisting tongue ulceration was due to persistent cancer (although now changed to a more spindle shaped carcinoma histologically)- I believe that with expert histological opinion confirming cancer in the biopsies since 1996, that the tumour is a persistent one and not a new one.” One of the questions in the combined agenda for the joint meeting of pathology experts was: “ Does the biopsy of 11^th September 2001 (slides 578/01) which was diagnosed as showing spindle-cell carcinoma show scattered atypical lozenge or kite-shaped cells (tumour cells) with identical, or at least similar, morphological features to those in the biopsies of 1995 (slides 457/95) and 1996 (slides 642/96) ? The answer in the joint expert’s report was:

In considering this aspect of the case, it is important to guard against the risk of a circular or bootstraps argument. Neither Professor Sloan nor Dr Woolgar in their reports suggested that it was possible on the basis of the September 1995 or December 1996 biopsy to make a positive diagnosis of carcinoma. In evidence at trial they both accepted that it was not possible to make such a positive diagnosis on the basis of the biopsies taken in isolation. Their very strong ex post facto conclusions that carcinoma was present on both occasions was thus dependent in no small measure on the benefit of hindsight and in particular the inferences to be drawn from what was revealed in the 2001 biopsies. Whereas looking at the September 1995 and December 1996 biopsies on their own, they were unable to go further that saying that they were highly suspicious of carcinoma, in their view it was possible to harden mere suspicion, albeit a high level of suspicion, into a positive conclusion that cancer was present by reason of (a) a pattern of increasing busyness cellularity as between the three biopsies and (b) the similarity of certain features in the three biopsies and the unlikelihood of such similarities being merely the result of coincidence, especially given the very rare nature of SPCC.

Of course if Professor Sloan and Dr Woolgar are right and there was definitely cancer present in September 1995 and/or December 1996, that would be a powerful if not determinative reason to conclude that the 2001 carcinoma was recurrent rather than a new primary. But to the extent that their opinion on cancer being present in 1995 and 1996 is based on the coincidence factor, it would be over simplistic to cite their conclusion as a free-standing ground for concluding that the 2001 carcinoma was recurrent. That would be to beg the question whether their conclusion that cancer was present in September 1995 and/or December 1996 is correct or whether Professor Speight’s conclusion that it was not is correct.

However, if one were to conclude that the pathological evidence is insufficient on its own to support Professor Sloan’s and Dr Woolgar’s conclusion that carcinoma was on the balance of probabilities present in September 1995 and/or December 1996 but that it is also insufficient to support Professor Speight’s conclusion that carcinoma was very probably not present, so that the matter remains uncertain on the pathological evidence alone, it does seem to me that the fact that all three expert pathologists agreed that the cells in all three biopsies show similar morphological features does provide strong support for the conclusion that the 2001 carcinoma was not a new radiogenic primary. Taken on its own this factor would go no further than raising a serious question and demanding the closest of scrutiny of the other available evidence. However taken together with all the other factors which quite independently point strongly against the possibility of a new radiogenic primary in 2001 as being inherently highly unlikely if not scientifically impossible, the consideration that if it was indeed a wholly new cancer it would be a remarkable coincidence that a very rare form of carcinoma happened to have similar morphological features to what were in fact wholly innocent cells in 1995 and 1996 is in my judgment a very powerful factor. Just as this coincidence factor seems to me a legitimate factor to weigh in the balance when assessing the conflicting pathology expert opinions in relation to the 1995 and 1996 biopsies, so it seems to me a legitimate factor to weigh in the balance when considering the question whether the 2001 carcinoma was a recurrent or new primary one.

Mr Grace QC relied on references to the 2001 tumour being a recurrence in Dr Harrison’s amended definitive report dated 3^rd October 2001, Professor Fisher’s report dated 1^st October 2001, Mr Rhys-Evans’ letter of 12^th December 2002, Professor Langdon’s letter of 21^st February 2002 and Mr Bridger’s letter of 2^nd April 2001. I do not consider that Professor Fisher’s letter supports Mr Grace QC’s argument and note that Professor Sloan agrees with Professor Fisher’s explanation that he was using the word “recurrent” in his report in an observational sense. The contrast he was seeking to make in his conclusion that “this is more likely to represent recurrent spindle-cell (sarcomatoid) carcinoma than a post irradiation sarcoma” was not between recurrence and new radiogenic primary, but rather between carcinoma and sarcoma. Nor, in my view, does Dr Harrison’s amended report of 3 October 2001 take matters any further, both because he merely reproduces Professor Fisher’s conclusion verbatim and because in his own original report dated 14^th September 2001, written before he sent the biopsy to Professor Fisher for a second opinion, Dr Harrison had concluded that: “ The history indicates that there is a post-irradiation malignancy of soft tissue and severely dysplastic mucosa that have become apparent since the last of the previous biopsies in June 2001 (391/01).” I have already indicated that that revealed yet a further flawed interpretation of the earlier 2001 biopsies and in any event suggested a post-irradiation malignancy. As to Mr Rhys-Evans’ letter dated 12^th February 2002 there is nothing in that letter to suggest that he was applying his mind to the pathogenic origins of Mrs Manning’s carcinoma as at January 2002 as distinct from referring to the fact that it was not the first time she had had a carcinoma.

In his letter dated 2^nd April 2001 Mr Bridger wrote:

Although it is apparent from those extracts that Mr Bridger had not reached any conclusion or diagnosis, it is fair to say that it is implicit that the only possibility which he was contemplating was recurrence as distinct from a new radiogenic primary. It is a reasonable inference that if he had considered a new radiogenic to be a realistic possibility he would have referred to it. To that extent Mr Bridger’s letter supports the expert opinions of Dr Plowman and Mr Brown. Professor Langdon’s letter dated 21 February 2002 carries the matter no further since it does no more than refer to Professor Fisher’s conclusion to which I have already referred.

The flip side of Mr Grace QC’s submission that Mrs Manning’s 2001 carcinoma cannot have been, or at least was very unlikely to have been a new radiogenic primary, is that it was a recurrence, or as he preferred to label it in the interests of clarity a persistence of original 1993 SQC, albeit this time in the form of a mutated SPCC. It is thus necessary to test the strength of the argument that the 2001 carcinoma was not a new radiogenic primary by reference to an assessment of the strength of Ms Mishcon’s attack on Mr Grace QC’s case that it was probably a recurrence.

Mr Grace QC in his written closing submissions summarised that case as follows:

The tumour cells had been “stunned” by the RT to use Professor Sloan’s words or “knocked back” to use Dr Plowman’s words; and/or

Its growth was slowed by genetic factors; and/or

It was anyway not a fast-growing tumour;

The Claimant’s case as to aetiology is neatly summarised by the following extract from Professor Langdon’s book: “Recurrences after radiotherapy tend to be deeply infiltrating and the extent can be difficult to define; Indeed it is quite common for the superficial part of the tumour to disappear completely and mucosa heal over it, yet malignant cells survive in the deeper part of the tumour and continue to spread in muscle or bone. Furthermore the roots of tumour spread following radiotherapy are unpredictable and no longer follow the usual pattern.”

It produces no symptoms, because this is the nature of oral tumours until the tumour invades sensory nerve fibres (see again Professor Langdon’s book); but

By the autumn of 2000 it had got to a sufficient size to produce symptoms of pain;

Thereafter its growth accelerated as a result of

Spread into better oxygenated, less radiation damaged

Genetic factors; and/or

The hyperbaric oxygen treatment in 2001.

Mr Grace QC submitted that the whole of that sequence of events is and always has been supported by all the Claimant’s experts as the most probable explanation of events. The steps in the sequence were both individually, and collectively accumulatively logical and even the Defendants’ experts did not condemn them out of hand. Thus he submitted that Professor Speight agreed that it was possible that the spindle-cells of 1996 represented dormant malignant cells which may have emerged in 2001, even though he considered it highly unlikely. He also conceded the possibility that SPCC cells could lie dormant for 5 years or more, albeit he said this must be very rare. In addition Professor Speight said that he had experience of late recurrences at up to 15 years.

Ms Mishcon advanced two related submissions as to why a recurrence in 2001 was improbable. The first, under the heading Volume Doubling Times/Gompertzian Theory, was broadly to the effect that working backwards from April 2001, if one applies the 2 month volume doubling time to be inferred from the quadrupling of the size of the tumour between the MRI scans of 26^th April 2001 and 22^nd January 2002 estimated by Dr Lewis-Jones and then makes allowance for the Gompertzian theory that tumour cells grow more quickly when they are small it is unlikely that any cancer cells were present in 1996. If that is right if follows that the 2001 carcinoma must have been a new primary rather than a recurrence or persistence of a cancer already present in 1996. Ms Mishcon’s related submission was that it would have been very unusual for a carcinoma to recur twice in two years (September 1995 and December 1996) and then to lie dormant and not recur again for a further four years.

Ms Mishcon’s first submission was based on two assumptions: first that because the inference from Dr Lewis-Jones’ evidence was that the volume doubling time of the tumour was two months in the period between April 2001 and January 2002, the tumour would, subject to the second assumption have been growing at the same volume doubling rate from inception, and second that because of the Gompertzian theory the volume doubling rate would have been shorter and the tumour would have been growing more quickly in its early stages when it was microscopic. For both propositions she relied heavily on the evidence of Dr Barley. That evidence was hotly disputed by Dr Plowman. On the first point both oncologists agreed that an average figure for tumour volume doubling time for head and neck carcinoma is about 45 days. This was based on figures in Professor Steel’s textbook of 1997. According to Dr Barley those figures showed that 90% of head and neck squamous carcinomas are within the range of 33 to 150 days. This was a topic on which Dr Plowman was extensively cross-examined. Doctor Plowman’s fundamental and strongly held view to which I shall refer shortly was that the Gompertzian model of exponential growth with late retardant slowing in the rate of growth is not an iron law. It does not apply in every case and in particular did not apply in this case. However he had a fallback argument broadly to the effect that if one assumed that the volume doubling time of Mrs Manning’s tumour was roughly 150 days in the period between December 1996 and January 2001, i.e. at the outer end of Professor Steel’s range, it was possible for there to have been cancer cells present in 1996. He did however accept that on the balance of probabilities if one applied a two month doubling time there probably was not cancer present and that if the Gompertzian theory is right and when a tumour is very small it grows at its fastest rate, cancer was even less likely to have been present, albeit only slightly less likely because the retardation is often not great. Thus in order for cancer to be present on the balance of probabilities assuming that the Gompertzian model was applicable in this case it would be necessary for Mrs Manning’s doubling time between 1996 and 2001 to have been outside the 90% range of Professor Steel’s statistics.

However Dr Plowman was adamant that the Gompertzian theory is not an iron law of universal application. It is apparent from the closing written submissions that the lawyers on both sides had different recollections and/or manuscript notes of a particular passage at the conclusion of Dr Plowman’s cross-examination when he was asked whether he accepted that most oncologists go along with the Gompertzian theory. This is not surprising since the parties did not have available to them transcripts of the oral testimony. In fact the question was asked twice and his answers were as follows:

It is clear that Dr Plowman’s evidence was to the effect that most oncologists agree that not all tumours behave according to the exponential growth doubling times enunciated by Gompertz. The reference in the passages cited to Fujitsa and Henk are in the former to a paper recording that 16.7% of recurrences of SPCC occur after 5 years and the evidence of Dr Henk at this trial that about 10% of recurrences occur after 5 years.

The powerful starting point of Dr Plowman’s evidence on this point is based in simple logic.:

Some support for Dr Plowman’s evidence that the Gompertzian theory is not an iron law which makes it possible with accuracy to identify with precision in any given case the speed of growth of a tumour over a period of years and hence its size at particular times within that period is to be found in evidence from the expert pathologists. They were asked a series of written questions prior to their joint meeting about volume doubling time and what if any inferences could be drawn therefrom. In particular they were asked if they agreed that had the doubling time in this case been constant the tumour volume in December 1996 (calculated by extrapolation) would be about 0.05 cubic millimetres? With the caveat that they are not experts in this area their answer was : “ We know of no accurate data that would enable retrospective calculation of tumour size over a prolonged period.” It was also the evidence of Dr Woolgar and Professor Sloan that in their experience the rate of growth of tumour varies within the lifetime of the tumour, probably due to genetic factors. Further the proposition that tumour growth rate inevitably slows down is not supported by the observation by Ellis and Corio (specifically in the context of SPCC): “ Particularly noted in several cases, however, was a sudden rapid increase in the size of the tumour.”

The question begged by Dr Plowman’s logic-based attack on the universal applicability of Gompertzian theory is: If late recurrences and slow-growing tumours do not fit the picture of constant volume doubling subject to late retardation, what is the scientific explanation for them?

Doctor Plowman described Gompertzian kinetics as a growth model consisting of exponential logarithmic growth where a single cell becomes two, the two become four and so on. As they get larger and their blood supply is less able to keep up with the growth of the tumour, the growth rate falls away from doubling either due to the inadequate blood supply or cell loss. Doctor Plowman’s evidence was that this model of retarded exponential growth is not a universal or iron law because various genetic malformation mutations of genes that drive tumours forward will affect growth rates. For that reason what he described as “ the rather simple logarithmic growth, Gompertzian kinetics, does not apply to many tumours and particularly ones that recur late. When asked if this latter point was just another way of saying the same thing, Dr Plowman said that it was not. In other words it is not just late recurrent tumours that are affected by genetic malformation mutations of genes which affect growth rates. “It is a way of saying that there are some tumours that do not obey these relatively simple kinetic models. We are beginning to understand why: because genetic mutations within cancer cells which are, after all, an unstable population of cells, can influence different growth rates at different times of their natural history. Q – What can influence different growth rates? A – Mutations within what is called oncogenes, which are the genes within a cell which can drive a cancer cell into either longer survival to divide many times or accelerate growth rates. Q – So mutations in oncogenes drive growth rates? A – Absolutely. The relevance of that my lord is that it is not always possible to quote growth rate for, say, squamous cell carcinoma of the head and neck or spindle-cell carcinoma. The growth rate may well be more capricious and it could well differ at different times in the natural time.”

There was much discussion during the questioning of Dr Plowman of a particular oncogene known as P53. Ms Mishcon put to him a paper by Professor Sorensen which suggested that P53 gene mutations are less frequent in squamous carcinomas occurring in non-smoking young patients who do not drink alcohol than in young smokers or in the general population. In re-examination Mr Grace QC referred him to a paper by Popovtzer which referred to the Sorensen paper but reported that: “ In contrast, Regezi et al and Atula et al compared the P53 mutation, P21 rb, in young and older patients and found no significant difference and Lingen et al demonstrated high levels of P53 mutations among young, non-smoking patients and stated that the aetiology for the mutation in these patients is different and therefore may lead to a unique disease behaviour. Shantz et al suggested that SCC in young patients is the result of an imbalance between free radical induced chromosomal damage and the inability to repair the mutational event, which is more common in younger patients, but found no definite gene abnormality characteristic in young patients.” Doctor Plowman’s response to these various papers was that this is research in progress. “P53 is by no means the only oncogene, but it is called the gatekeeper of the human genome; it is a tumour suppressant gene that stops cells from growing uncontrolled; it is a very important gene. And it is important in head and neck cancer.” He later added: “It is a controversial subject and I think I said that when I wrote it, but there is no doubt that to account for different behaviours in growth rates of cancers, one nowadays no longer looks at the Gompertzian model but one looks at the oncogenes and their driving forces for the cancer. Q – To account for different growth rates in cancer these days? A – Yes…. I am not refuting the Gompertzian model, but one has to look at other events that occur during the natural history of a tumour which may drive it forward or alter it’s behaviour. … The simple idea of tumours going two, four, eight, sixteen, thirty two, sixty four etc is probably too facile a concept and one which certainly does not fit with, say, very late behaviour, a very late declaration of recurrences…or why some tumours metastasise and some tumours do not. So the behaviour of tumours which has just been put down to be capricious in the past is now starting to have a more understood basis. Q – As a result of the unravelling of the human gene? A – Yes.”

Doctor Plowman’s central point was that cancer cells can vary in their growth rate at various times. The Gompertzian idea is based on simple tumours in mouse models and in some human cancers the growth is more complex than that although the precise genetic mechanism or mechanisms by which those growth rates are affected is only beginning to be understood as a result of research into oncogenes and tumour suppressant genes. There is likely to be some genetic instability which leads to a change in growth rates of tumours at different times. In cross-examination Dr Plowman rejected a suggestion put to him (based on Dr Barley’s evidence) that P53 can only slow down cell growth for a very short time after radiation and certainly not for a few years. Asked what conclusion he drew from the reference in the Ellis and Corio paper to a sudden rapid increase in the size of the tumour noted in several cases of SPCC, Dr Plowman said that his tenet was that SPCCs have some genetic instability and can change their growth rate towards a more rapid pattern. In that respect they are no different from all cancer cells which have genetic instability. Mutations of oncogenes and suppressor genes are instrumental in initiating cancer by allowing cells to be released from normal body controls. After a tumour has been initiated tumour oncogenes and/or suppressor genes in combination by further mutation can alter subsequent growth patterns which may vary as time goes on.

Doctor Plowman accepted that these subsequent mutations are more recognised for accelerating than decelerating growth rate however he could see no reason why mutations in oncogenes and/or suppressant genes would not slow rates of tumour growth. It is harder to observe and identify the slowing down effect on growth of mutations in oncogenes and suppressant genes because where a tumour is treated the subsequent slowing in the growth rate tends to be attributed causally to the treatment. In principle there is no reason why mutations in oncogenes and/or suppressant genes should not slow down the growth rate of tumours because cancer cells are unstable and there are mutational events occurring in their natural history. It was put to Dr Plowman in cross-examination that breast cancer shows that recurrence tends to occur in lower grade hormone sensitive tumours. Doctor Plowman’s response was that there are some high grade tumours which are not hormone sensitive which also recur late where it is not possible to ascribe the late recurrence to oestrogen.

In addition to natural genetic instability and mutations in oncogenes and/or suppressant genes, Dr Plowman’s evidence was that the after effects of radiation treatment are also capable of inhibiting or slowing down the growth rate of cancer cells. In his report Professor Sloan, having referred to the Fujita paper which reported that local recurrence is not rare in the period of more than 5 years after treatment [of mobile tongue tumours by RT ] said : “ In lay terms, it appears that radiotherapy can sometimes merely “stun” cancer cells. Most cancer cells die after radiation treatment but some cells appear to survive and undergo genetic ‘evolution’. They are trapped in radiation scar tissue which has a reduced blood supply. Even years later the cancer can recur in the tissues. Sometimes the genetic change results in the cancer having a different appearance to that in the original biopsy…” Having said that he agreed with Professor Sloan, Dr Plowman was shown by Mr Grace QC an extract from Dr Barley’s report in which he wrote: “ It could be argued that, owing to the very poor blood supply near the site of the tumour following a high dose radiotherapy, residual cancer cells may grow relatively slowly for several years and be detectable under a microscope, long before becoming evident clinically.” Asked whether he agreed with that Dr Plowman answered: “Yes I think that is a slightly more eloquent way of putting it than stunned, but it is the same thing.”

Dr Plowman elaborated further in cross examination. He cited three reasons why he did not hold with the Gompertzian model as applicable to Mrs Manning between 1996 and 2001: first that the model does not account for late recurrences; second that the late acceleration in 2001 could have been caused by genetic mutations; and third that it ignores the effect of RT. On the latter point he said that one would not expect the tumour to grow between 1996 and 2001 with the same doubling times as in 1993-1994 or as in 2001-2002. The former preceded the RT treatment of the tumour and by the time of the latter the tumour may have grown outside the high dose region of bad soil created by the RT and would thus be free to take off at the same or a higher rate of growth due to mitosis.

Any application of Gompertzian theory to Mrs Manning between 1996 and 2001 would have to include what Dr Plowman described as retardation constants in the form of heavily irradiated tissue, lack of oxygen, lack of blood supply and fibrosis. A sub-lethal dose of RT to cells could cause delay in mitotic rate. Thus Mrs Manning may have had more retardation constants early on after RT and then the tumour may have found more fertile soil once it outgrew the irradiated area. It would not necessarily have the same growth rate before and after RT.

Moreover RT may have killed faster growing cells, leaving slower growing cells to survive. By causing fibrosis and scarring in the irradiated tissues it is likely that RT will inhibit the growth of many surviving tumour cells because such tissues will be less well oxygenated. In this context Mr Grace Q.C. relied on the following statement in : “Carcinoma of the Oral Cavity-Management of The Primary Tumour” by Professor Langdon and Dr Henk: “Recurrences after radiotherapy tend to be deeply infiltrating and the extent can be difficult to define; indeed it is quite common for the superficial part of the tumour to disappear completely and mucosa heal over it, yet malignant cells survive in the deeper part of the tumour and continue to spread in the muscle or bone. Furthermore the routes of tumour spread, following radiotherapy are unpredictable and no longer follow the usual patterns.”

Dr Plowman also referred to the pathology evidence as to the relative absence of mitosis as arguing strongly against Mrs Manning’s tumour being aggressive in the sense of having a short doubling time, even if it presented as a polypoid SPCC in September 1995 and/or December 1996. In this his evidence was consistent with that of Dr Barley who said that if there was a tumour in September 1995 and December 1996 it would not have been fast growing.

For all these reasons Dr Plowman was emphatic that that it is not possible to infer from a two month doubling time between April 2001 and January 2002 that there must have been at most a two month doubling time between 1993 and 2001.

Doctor Plowman agreed with Ms Mishcon that the literature shows that there is no difference in the average recurrence time after treatment by brachytherapy as distinct from any other kind of treatment such as surgery. But he pointed out that there is nonetheless a significant minority of late recurrences. Further Mr Grace QC in closing pointed out that this statistic does not undermine the force of Dr Plowman’s point in that surgical treatment of cancer could also affect growth rates by cutting off the blood supply and producing scar tissue as infertile ground for any surviving cancer cells to grow in. Doctor Plowman made the further point that since there will always be a spectrum of growth rates as reflected in the Steel spectrum of 45 to 155 days doubling time, it is always possible that cells surviving RT would have grown faster without it.

Doctor Plowman emphasised that the Gompertzian model is based on studies of unperturbed cancer, whereas if a tumour grows in soil so heavily irradiated as to cause a radiogenic ulcer (which is what he believes occurred to Mrs Manning in 1995/6) and then grows in the base of the necrotic ulcer the growth rate will be knocked back. He added that even if the alleged tumour presented in 1995/1996 as a polypoid SPCC(as suggested in parts of his evidence by Professor Sloan)the relative absence of mitosis observed in the September 1995 and December 1996 biopsies argued strongly against the tumour being aggressive in the sense of a short doubling time and fast growth rate).

Doctor Plowman said that he did not hold with the Gompertzian model as an explanation when considering the rate of growth of Mrs Manning’s tumour between 1996 (assuming it was there) and 2001. It does not account for late relapses in cancer generally, it ignores the radiation undergone by Mrs Manning, and Dr Plowman would not expect the tumour to have grown with the same doubling times during that period either as in the period 1993-1994 or as in the period in 2001 when the tumour had grown outside the high dose region of “bad soil” at which point it’s growth rate could take off.

In his written closing submissions Mr Grace QC relied on three further unknown variables which make it impossible to treat the Gompertzian model as a reliable guide as to the expected size of any cancer in 1996 working back from its size in 2001. The first is that it is impossible to determine when the decline in the tumour’s growth rate (due to the tumour outgrowing its oxygen supply) postulated by the Gompertzian theory occurred. The second is that it is not known how many cells survived the RT and BT in 1994.

The third is the intensive hyperbaric oxygen treatment (a total of 60 dives) undergone by Mrs Manning between 26^th April 2001 and 22^nd January 2002, the period in which Dr Lewis Jones estimated a quadrupling in size of the tumour. Mr Grace QC submitted that any Gompertzian conclusions that might otherwise be drawn from the growth rate of the tumour between those two dates are confounded by that intensive hyperbaric oxygen treatment on the basis that that treatment may itself to an indeterminate extent have contributed to that growth rate between those dates, such that it is impossible to identify reliably a doubling rate unaffected by the hyperbaric oxygen treatment to which Gompertzian principles could be applied for the purpose of the exercise of working backwards from April 2001(when by definition growth rates would not have been affected by hyperbaric oxygen treatment) in order to estimate the size of any cancer present in 1996.

On the hyperbaric oxygen point, all three pathology experts agreed in their joint report that such treatment is inappropriate in the presence of recurrent tumour and that it may promote tumour growth. Doctor Plowman in his report stated that although he did not think that such treatment would have affected the growth greatly, it is theoretically possible that it would give hypoxic tumour cells more viability. Doctor Barley in his report referred to the effect of hyperbaric oxygen treatment obliquely. Referring to the rapid progress in the growth of the tumour from March 2001 onwards he said: “This rate of growth is consistent with a poorly differentiated or sarcomatoid squamous carcinoma which may double in volume within a week or two without the use of hyperbaric oxygen.” (emphasis added). The natural inference from the emphasised words is that Dr Barley recognised that hyperbaric oxygen treatment is liable to accelerate the growth rate of a tumour. In cross-examination, when Mr Grace QC asked Dr Barley to confirm this inference, he did so, albeit not without a considerable degree of reluctance and prevarication, which it was hard to interpret as other than reflecting a reluctance to acknowledge points inconsistent with the defendants’ case which, in my judgment, permeated his evidence. Thus for example on two occasions he denied that hyperbaric oxygen treatment may cause tumours to grow more rapidly, but on two other occasions he accepted that it is possible and he also accepted that if he had had a patient who was receiving hyperbaric oxygen therapy with a view to promoting tissue healing and then discovered that the patient was suffering from cancer he would have stopped the treatment very quickly.

More generally on this aspect of the case I found Dr Barley’s evidence somewhat unsatisfactory and, in so far as it differed from that of Dr Plowman, far less persuasive. Ms Mishcon’s primary submission that if one applies Gompertzian theory to the inferred doubling time of the tumour between April 2001 and January 2002 it is unlikely that any cancer cells were present in 1996 was based in large part on Dr Barley’s evidence. That evidence was subjected to close cross-examination, by the end of which it emerged that a number of propositions which, at the outset, had been presented as clear cut and straightforward were in fact more complex, equivocal and/or contentious.

At the heart of Dr Barley’s evidence was his assertion that it is an inevitable fact of life, or iron rule as it came to be referred to, that where you know the doubling rate of a tumour at a particular point, the doubling time of the tumour must have been shorter earlier on and thus the tumour must have been growing more quickly earlier on. That is because by the time the tumour is large enough to be detected 90% of the cells being produced are dying immediately through lack of oxygen which inevitably slows down the growth of the tumour as it gets bigger. He also said that it is an iron law of biology that all late recurrences of SQC or SPCC of the head and neck must have a slow doubling rate at the point of detection and that the rate of growth of tumours is faster when they are small and slows down as they get bigger.

At one point Dr Barley said that this was an iron rule accepted among oncologists. At another point he said that the rule has no exceptions. However elsewhere Dr Barley volunteered that tumours do not “on the whole” change their nature and behaviour, the implication being that there are occasions on which they do just that. He also accepted that sometimes a tumour may be influenced by other factors to grow more quickly. He cited the example of breast cancer which may be influenced by changes in hormone levels and the example of melanomas which it has been suggested is controlled by the body’s immune response such that when the immunity wanes the melanoma has an opportunity to recur. Although he said that there is no evidence that hormones or immune response have a significant effect on the growth of head and neck cancers, the significant concession was that the so called iron rule is in fact subject to exceptions, the full ambit of which is not known.

Confusingly at one point Dr Barley accepted that it is possible for a tumour to start growing slowly and then speed up but not to start fast then slow down and then speed up. He accepted that the former proposition can occur because of what Dr Plowman, rightly as he thought, described as genetic abnormalities causing an increase in the rate of cell division. On its face this appears inconsistent with the so-called iron rule. Doctor Barley sought to reconcile the two propositions on the basis that any increase in cell division due to genetic abnormalities would be outbalanced by the normal Gompertzian rule. However this appeared to be based not on evidence or logic but assertion. Moreover Dr Barley then retreated and accepted that there could be a net increase in the tumour growth rate even after taking account of Gompertzian theory, albeit that the acceleration caused by genetic abnormality would have been even greater without Gompertzian theory. In other words put simply he accepted that genetic abnormalities can lead to a tumour growth rate accelerating. When it was put to him in cross-examination that within the life of a tumour there can be differing growth rates he explicitly agreed, albeit saying that they could not slow down. But then he accepted even the latter as a theoretical possibility because of impairment of the blood supply or impairment of oxygenation. Thus he accepted, albeit grudgingly, that RT can impair tumour growth to some extent. However he went on to say that when cancer cells are trapped in fibrous scar tissue as a result of RT it is not possible that they become less able to grow thus reducing the growth rate. When Mr Grace QC drew his attention to a paragraph in his report to suggest that its contents were inconsistent with that piece of evidence, Dr Barley reacted defensively indicating even before any question was put that he was alive to the inconsistency:

By this stage Mr Grace QC had not read out any part of the relevant paragraph. The paragraph read as follows:

It could be argued that, owing to the very poor blood supply near the site of the tumour following high dose radiotherapy, residual cancer cells may grow relatively slowly for several years, and be detectable under a microscope, long before becoming evident clinically. However, it has been my personal experience that local recurrence within the high dose volume is usually detected within a few months of completing treatment. Although cancer cells may be visible in the area where the tumour was a few months after completion of treatment, they may not be viable. However if there is evidence of residual squamous carcinoma more than 6 months (but less than 18 months) after treatment, especially if there is an associated tumour or ulcer, the majority of head and neck teams would treat this as recurrent cancer. Recurrence is very uncommon more than 2 years after radical treatment, and after 3 tears without evidence of recurrence a patient with head and neck cancer is usually considered to be cured.”

Mr Grace QC, rightly in my judgment, pointed out that the natural inference of the first sentence is that Dr Barley accepted that it was a perfectly respectable argument. Doctor Barley had to agree that he had indeed intended to say that it could be put forward as an argument, albeit not one with which he agreed. However the basis of his disagreement he said was the rate of growth of head and neck cancer in general and that of Mrs Manning in particular, the latter point being in my judgment entirely circular, the very question in issue being whether it is possible to infer by extrapolation what that rate of growth was. In my view Mr Grace QC was right to suggest that the first sentence of the paragraph is inconsistent with Dr Barley’s immediately preceding evidence which prompted him to show Dr Barley the paragraph.

There then followed an exchange about what causes late recurrent cancers after RT, which Dr Barley ascribed to the intrinsically slow rate of growth of the recurring tumour. When asked if that intrinsic rate of growth can never be altered Dr Barley’s answer was: “It does not usually, no.” This was a further answer which by necessary implication accepted that there can be exceptions to the so-called iron rule. Given the weight of evidence as to the existence of a considerable minority of late recurring head and neck SPCCs and SQCs and Dr Plowman’s point that there must be some explanation for them, Dr Barley’s concession, albeit not apparently made with any great enthusiasm, seemed to me telling. So was his response when asked how he would explain the reference in Ellis and Corio to it being particularly noted in several cases that there was a sudden rapid increase in the size of tumour. Doctor Barley’s response was to point to a graph that Dr Plowman added to the joint oncologist’s statement showing how volume doubling can give the impression of rapid growth occurring suddenly when the tumour becomes detectable. What Dr Barley did not explain is why that suggested explanation is any more plausible than, let alone necessarily correct to the exclusion of, the more obvious explanation, namely that in those cases for some reason or other the growth rate of the tumours accelerated.

Doctor Barley made a number of additional concessions in the course of his evidence. The first was that if, as he asserted, Mrs Manning’s tumour grew faster before presentation in December 1993 than between treatment in 1994 and the 1995 and 1996 biopsies then the slowing down of the growth rate (assuming that cancer was in fact present in September 1995 and December 1996) could be explained if after treatment in 1994 Mrs Manning was left with just one or two malignant cells. By parity of reasoning it would seem to follow that if the effect of those biopsies had been inadvertently to excise a part of a tumour present leaving only a few cells behind, particularly if they were deep to the mucosa, that could account for a prolonged period of relatively slow growth thereafter before the comparatively rapid growth rate in between April 2001 and January 2002.

The second concession was that it is impossible to know, even assuming the Gompertzian model applied in this case, when the moment of Gompertzian falling off of growth rate occurred.

The third was that the so-called iron rule in fact, according to Dr Barley, does not apply throughout the life span of the growth of a tumour, but only kicks in after the first 10 or 15 doublings. This rather important gloss on the Gompertzian iron law only emerged late on in the cross-examination. In the light of all these concessions it was perhaps not surprising that more fundamentally Dr Barley accepted that it is not possible accurately to extrapolate back on the rate of doubling in Mrs Manning’s case because the cell cycle time for her tumour is not known.

In my judgment the argument based on Gompertzian and retrospective extrapolation of volume doubling rates does not prove that there cannot have been cancer present in September 1995 or December 1996 or even that cancer was not present on the balance of probabilities. While it is one of the factors to weigh in the balance on the defendant’s side of the scales it is not one to which in my judgment very much weight should be attached.

Ms Mishcon’s second submission was that it would have been very unusual for a carcinoma to recur twice in two years (September 1995 and December 1996) and then to lie dormant and not recur again for a further four years.

The oral surgeons in their joint report agreed that it would be possible but highly unlikely for an SPCC to lie dormant for five years or more. In answer to the question: “How many cases have you seen or heard about where a moderately differentiated squamous carcinoma recurs as a spindle cell carcinoma then lies dormant for more than five years after completing treatment before becoming an extremely aggressive cancer? Is it possible for this to occur?”, they agreed that such a scenario had never been seen, discussed or published to their knowledge, but it could occur. The unlikelihood of this was emphasised by Mr Watt-Smith and Dr Barley.

In cross-examination Mr Brown confirmed that in his opinion it would be highly unlikely but possible for an SPCC to have recurred twice within two and a half years and then lain dormant for the next four years. In cross-examination Dr Plowman said that the biggest difficulty he had had in his cross-examination was accounting for the fact that Mrs Manning’s tumour did not become overt more quickly after 1996. In evidence in chief he acknowledged that the slowness with which the tumour developed if it was a recurrence in 2001 was a weakness in the claimant’s case.

All three pathology experts agreed in their joint report that it would be very rare but nonetheless possible for SPCCs to lie dormant for five years or more. Specifically in the context of the present case they all agreed that it is possible that the spindle cells in the December 1996 biopsy which they agreed were highly suspicious for SPCC represented dormant malignant cells which may have emerged in 2001.While Professor Speight considered that to be highly unlikely Professor Sloan and Dr. Woolgar were of the view, on the basis of having seen the later specimens and with knowledge of Mrs Manning’s clinical history that they are the same cells as the ones in the 2001 tumour and that they were dormant for some or all of the intervening period.

This is undoubtedly one of the stronger factors arguing against recurrence in January 2001. However, it remains the case that this was a factor which was taken into account by both Dr Plowman and Mr Brown and which did not prevent them from reaching the very clear conclusion that in fact the 2001 cancer was probably recurrence rather than a new primary. Equally it was taken into account by Professor Sloan and Dr Woolgar and it did not prevent them from reaching the no less clear conclusion that there was probably cancer present in Mrs Manning in September 1995 and December 1996. As many of the experts on both sides had occasion to comment, there are, in Dr Plowman’s words, things which do not square on either side of the arguments on this case. It was certainly not suggested by any of the experts that this was a knock out blow on the recurrence versus new primary issue.

Moreover the Defendants’ argument rested in part on a premise which was not accepted by Dr Plowman and whose evidential basis was questionable. The premise was that the tumour grew rapidly between its inception and detection in December 1993, again grew rapidly after the RT treatment in February 1994 leading up to the December 1995 and December 1996 biopsies and thereafter slowed down or lay dormant between December 1996 and the autumn of 2000. The first part of that premise, namely that the tumour grew rapidly between its inception and its detection in December 1993 rested on the assertion of Dr Barley to that effect. However it became clear in cross-examination that this assertion was based not on any concrete evidence but on speculation on Dr Barley’s part.

Thus at the end of his evidence in chief Dr Barley asserted that Mrs Manning’s tumour had grown rapidly during the six months between June and December 1993. In cross-examination it emerged that this assertion was based on an assumption by Dr Barley that the tumour had been one centimetre in diameter in June 1993, from which it grew to the 2.5 centimetres which was recorded in Mrs Manning’s notes in December 1993. This assumption turned out to be just that, an assumption. It was not based on any evidence. There was no evidence in the factual part of the case as to the size of the tumour in June 1993 or indeed at any date before December 1993.

Dr Barley it turned out was basing his assertion on three matters: first his recollection that it had been suggested that Mrs Manning had symptoms “for about six months before she was seen by Professor Langdon in December 1993”, second, the proposition that usually a tumour is a centimetre in diameter before it is clinically detectable and third, an assertion that on the balance of probabilities Mrs Manning’s tumour would have grown at a similar rate to that of a moderate to poorly differentiated head and neck cancer with a volume doubling time of about 45 days.

As to the first matter, Dr Barley’s recollection of the evidence was incorrect. What Professor Langdon had recorded in his letter dated 10 December 1993 to Dr Henk was that Mrs Manning “has been aware of an ulcer on the lateral border of her tongue for at least six months.” (Emphasis added). It is thus unknown when Mrs Manning first became aware of the tumour and Mr Grace QC was right to suggest to Dr Barley that any attempt to assess the growth rate of the tumour prior to December 1993 must be pure speculation since there is no second point of time prior to December 1993 at which it is possible to fix the dimension of the tumour. As to the second matter, Dr Barley’s proposition turned out in cross-examination to be no more than a suggestion made by him without any authority in the literature to support it. As to the third matter, when it was put to Dr Barley that his assertion was no more than a reference to the median of the Steel figures of a range of 33 to 150 days, Dr Barley accepted that that was correct, adding: “But we have only these statistics to go on I’m afraid”. In my judgment it is a non sequitur to say that because 45 days per doubling is the median figure in a range representing 90% of tumour growths, it therefore follows that in any particular case the volume doubling rate was on the balance of probabilities 45 days. If that were the case it would follow that in a population of 100 patients with SPCC on the balance of probabilities each and therefore all of the 100 on the balance of probabilities had a 45 day doubling rate. This seems to me to be a false equation between the concept of the median and the concept of evidence that in a particular case a particular growth rate can be said to be identifiable on the balance of probabilities. This part of Dr Barley’s evidence prompted the response from Mr Grace QC: “You grasp at figures do you not if it suits your case because essentially I suggest you are seeking to act as an advocate in this case and not an expert at all.” While in my view overstated as a criticism it was hard to escape the impression that there was perhaps more than a grain of truth in it.

As to the growth rate between the RT treatment in January and February 1994 and September 1995 and December 1996 Dr Plowman did not accept that the tumour must have grown more quickly in that period and then slowed down between December 1996 and the autumn of 2000. He pointed out that the claimant’s case is that the cancer present in September 1995 and December 1996 manifested itself microscopically on the biopsy but not clinically. Dr Plowman’s view was that the tumour, having been knocked back by RT and BT in early 1994 thereafter grew slowly or as he put it grumbled along from early 1994 to late 2000. He considered that the evidence in 1996 as to the absence of mitoses argues strongly in favour of a growth rate which was slower than a two months doubling time. Thus on analysis what was presented as a pattern of quick (pre-December 1993), quick (February 1994 to December 1996), slow (December 1996 to autumn 2000), quick (January 2001 to April 2002) may in fact have been a pattern of slow (inception of tumour to autumn 2000) quick (January 2001 to April 2002). That brings one back to Ms Mishcon’s first submission based on Gompertzian rates about which I have already expressed my views.

In relation to the speed of growth between early 1994 and September 1995 and then between September 1995 and December 1996, some support for Dr Plowman’s evidence that assuming that cancer was present on both occasions the rate of growth was not especially quick came from Dr Barley. In cross examination he accepted that if (which of course he did not believe) cancer was present in September 1995 and December 1996 the growth rate of the tumour first between treatment in February 1994 and the September 1995 biopsy and then between the latter biopsy and the December 1996 biopsy would have been relatively slow and certainly within the range of head and neck cancer growth rates: as he put it not rapid but not slow. This further undermines the clear cut suggestion of a quick slow quick pattern of growth of the putative tumour.

Ms Mishcon in her written closing submissions relied on an answer from Dr Plowman in cross-examination to the effect that if the 1995 biopsy had millions of cancer cells in it, it would be highly unusual for it then to have gone dormant for five years and that he would be surprised if it had not become clinically manifest sooner than 2001. That of course begs the question whether in fact there were millions of cancer cells in the September 1995 biopsy. However a few minutes later, it was pointed out to Dr Plowman that Professor Sloan had said that in the December 1996 biopsy there were no atypical mitotic figures and few mitotic figures in a field. This prompted Dr Plowman to say that it is a feature of aggressively growing tumours that under a high power microscope you will see five or more mitotic figures in a field. If there were not that many in the December 1996 biopsy that in Dr Plowman’s view supported the proposition that the tumour was not growing aggressively at that stage, since a highly aggressive tumour would have quite a few mitotic figures visible.

This coincided with his evidence that there is a spectrum for malignancies and that just because a malignancy changes its morphology from squamous to spindle cell that does not necessarily mean that it is going to grow faster. Thus he did not accept that the presence of spindle cells even if malignant in 1996 necessarily meant that they had a high mitotic rate and thus must have been aggressive and fast growing. This led Dr Plowman to qualify his earlier answer, which is relied on by Ms Mishcon. He said that even if there were millions of cancer cells present in 1996 he would not necessarily have expected the cancer to be clinically obvious before 2002 unless the doubling time was short. He would have expected to have seen a recurrence before 2001, but not necessarily. It would depend on the growth rate and the absence of mitosis argued against there being a fast doubling time.

Professor Sloan, Mr Brown and Dr Plowman were in broad agreement that the long dormancy period may be explicable in part by the location of a few carcinoma cells deep in the tongue. As referred to above this may have been compounded by the effects of RT and/or the small number of cells left behind after RT and BT in 1994 and/or the September 1995 and December 1996 biopsies. Ms Mishcon pointed out in her written closing submissions that Professor Sloan in evidence accepted that if the cancer cells which he believed had been left behind by the RT/BT in early 1994 had mutated to SPCC and produced a lesion and ulcerated by 1995, they were not inactive in that period. Thus there would still need to be an explanation for how they could have been active between 1994 and 1996 and then become inactive for the next four years. This of course begs the question whether the September 1995 lesion and ulceration was caused by the cancer if it was still there. Although it is right that in cross-examination Professor Sloan expressed for the first time the view that the September 1995 biopsy may have been a polyploid spindle cell carcinoma, Mr Grace QC pointed out during cross-examination of another witness that it is not a necessary part of the claimant’s case that the persistent cancer manifested itself clinically in September 1995 or December 1996 but merely that it was microscopically present. In fact it appeared to be Dr Plowman’s view that although the original cancer had not been completely killed off by the RT and BT and was present in September 1995 and December 1996, the ulceration in September 1995 may well have not been caused by the cancer cells. In his view it was perfectly possible, indeed probable that the original cancer, to the extent that it survived the RT/BT slowly grumbled away probably deep in the tongue and very possibly stunted in its growth by the effects of the RT/BT until it grew out of the sterile zone and became clinically manifest in January 2001.

Nonetheless there was undoubtedly a tension between that part of the evidence of Professor Sloan which suggested that the September 1995 and December 1996 lesions were polypoid SPCCs and Dr Plowman’s evidence that the ulceration in September 1995 may well have not been caused by the cancer cells which he, like Professor Sloan, nonetheless believed were present. Ms Mishcon relied on Professor Speight’s evidence that although it is theoretically possible to have a deep recurrence his guess was that only 20% of such recurrences may be deep and that he had never seen or read about an SPCC arising from the deep tissues, which he felt was very unlikely. Against that Mr Grace QC pointed out (i) that SQC can and indeed frequently does recur as SPCC, (ii) that the pathology experts all agreed that it is possible for a recurrence of a tongue tumour following RT to develop deep to the mucosal surface of the tongue and that they have all seen cases where this has occurred, although none of them had sufficient experience of post radiotherapy tongue recurrences to define whether that is “normal” (iii) that the oral surgeon experts also agreed that recurrences of tongue tumour following RT can develop deep to the mucosal surface, (iv) that the oncology experts also agreed that in their clinical experience recurrence of squamous carcinoma of the tongue following RT can be either superficial or deep in muscle or both and (v) that Dr Henk and Professor Langdon in their book state that recurrences after RT tend to be deep and indeed that the mucosa heals:

“Recurrences after radiotherapy tend to be deeply infiltrating and the extent can be difficult to define; indeed it is quite common for the superficial part of the tumour to disappear completely and mucosa heal over it, yet malignant cells survive in the deeper part of the tumour and continue to spread in muscle or bone. …”

Mr Grace QC also cited in support of the plausibility of a relatively long period of apparent dormancy of the tumour two bits of evidence from the literature. The first was an extract from Professor Langdon’s book reporting that between 27 and 50% of patients with oral cancer present for treatment with late lesions, one of the explanations for which is that oral cancer is not usually painful until such time as either the ulcer becomes secondarily infected or the tumour invades sensory nerve fibres. In other words the tumours tend not to be symptomatic and therefore not diagnosed until a late stage and not until tumour invades nerve fibres. The second bit of evidence was the Ellis and Corio paper which recorded that only a minority of patients with SPCC suffer pain and symptoms.

Ms Mishcon in her closing submissions submitted that it is generally accepted by the experts that SPCC is a more aggressive tumour than SQC and that the more poorly differentiated the tumour the more aggressive it usually is. The original SQC in 1993 she said was moderately to poorly differentiated and the SPCC which emerged in 2001 was poorly differentiated. She prayed in aid an article co-written by Professor Sloan in 1990 about SPCC which said: “The literature now contains reports of more aggressive behaviour and this has been our experience also. Few authors emphasise this aggressive clinical behaviour …”. She thus preyed in aid the assertion that SPCC is regarded as being an aggressive fast growing tumour as a strong indication that it was not present in 1995 or 1996 on the basis that it would be unlikely to have been inactive and slow growing over a period of over five years.

Against that Mr Grace QC cited a passage in Professor Sloan’s report which said that: “Even in 1971 it was stated in the WHO Blue Book that oral spindle carcinoma ‘may have a low mitotic rate and does not always show a high degree of malignancy’. In my opinion it is highly likely that the tumour grew slowly in the bulk of the tongue between 1996 and 2001. During this time the tumour could progress and infiltrate the tongue until, after a period of more rapid growth during 2001 it reached a large size.” This is consistent with the evidence of Mr Brown who said that: “If the tumour was more deeply placed clearly that would not become apparent for much longer” and “My own experience is that tumours grow at different rates and speeds”. Moreover both Dr Woolgar and Professor Sloan said that in their experience the rate of growth of a tumour varies within its lifetime probably due to genetic factors.

Mr Grace QC also prayed in aid papers by Sue et al and Popovtzer et al in support of the submission that SPCC is not invariably aggressive and fatal. It is true that Mr Brown said that it would be very unusual for someone to survive if SPCC had gone untreated for four to five years and that the fact that Mrs Manning had survived without treatment between December 1996 and the autumn of 2000 was an argument against SPCC being present in 1995 and 1996. However, against that I have already referred to Dr Plowman’s evidence that the low mitotic rate in 1995 and 1996 points against Mrs Manning’s tumour being fast growing and aggressive and Dr Barley’s evidence that if cancer was present in September 1995 and December 1996 the growth rate from February 1994 until those two dates would not have been particularly fast. In addition Dr Plowman in cross-examination stated that the fact that the morphology of Mrs Manning’s tumour mutated from SQC to SPCC does not imply that it was therefore aggressive. According to him one gene determines the morphology change from SQC to SPCC, another determines the rate of growth.

This issue is linked to the general statistics on late recurrence of SQC. It was generally agreed by the experts that most local recurrences of SQC occur within the first two to three years. This is consistent with the findings of the Fujitsa study that 66.7% of local recurrences studied occurred within two years after treatment. However, it was also agreed that there is a significant and established pattern of late recurrences. Dr Barley estimated recurrences after five years at 10%, Dr Plowman at slightly less than 10%. It is however of note that the Fujitsa paper reported that in their clinic 25.6% of local recurrences, higher than in previous reports, occurred after five years. In patients where the tumour was T1 as many as 8 of 14 recurrences occurred after five years and of 15 recurrences in patients treated solely by BT (Mrs Manning was of course treated by both RT and BT) 6 recurred after five years. Fujitsa added that: “Reports show that local recurrence is not rare in the period of more than five years after treatment (12.5%, 11.6%, 15.4%), we believe therefore that a periodical follow up should be continued for more than five years, even if the lesion might be T1, which is a good indication for [BT] alone treatment. Indeed this latter point was highlighted in the overall conclusion of the paper: “… we also recommend longer follow-up periods; more than five years might be necessary for late local recurrences and for secondary cancer”.

There is a striking similarity between the evidence that only 10% of second primaries occur as carcinomas as distinct from sarcomas and the evidence that recurrences of SQC after five years is in the region of 10% (although higher according to Fujitsa). This underlines the difficulty in this case, namely that whether, as Mr Manning submitted, the 2001 cancer was a late recurrence or, as the Defendants submitted, it was a new primary, it was a very unusual occurrence. The fact that it was unusual does not mean that it did not happen. Indeed the one thing we do know about this case for sure is that whatever was the nature of Mrs Manning’s cancer in 2001 it was very rare and very unusual.

Standing back and looking at this evidence in the round it seems to me to fall a long way short of showing that the 2001 primary cannot have been a recurrence. Once it is accepted that whichever version of events is correct it will of necessity involve a number of very unusual features, it does not seem to me that the evidence on growth rates, dormancy and deep location of the tumour is of such a character or weight as to displace the inference to be drawn from the powerful effect of the overwhelming evidence as to the unlikelihood if not impossibility of the January 2001 cancer being a new primary if not a recurrence.

Both the September 1995 and December 1996 biopsies healed over. Ms Mishcon submitted in her written closing submissions that this was a strong indication that malignancy was not present on either occasion. This was undoubtedly one of her strongest arguments. All the experts agreed that it would be very unusual for a biopsy wound to heal if malignancy were present. Ms Mishcon further submitted that the experts agreed that if the 1995 lesion, which measured 1.8 x 1.5 x 0.8 cm was an SPCC which had been cut through it was extremely surprising that it healed over with no clinical signs or symptoms for fifteen months. This point is linked with her submission that if the lesions and ulceration in September 1995 and December 1996 were caused by cancer cells, as she submitted was implicit in Professor Sloan’s late suggestion at trial that the clinical evidence pointed to the presence of polypoid SPCCs, there would still need to be an explanation for how they could have been active between 1994 and 1996 and then become inactive for the next four years.

Mr Grace QC in response pointed out that it is the claimant’s case that it was the biopsy, as distinct from the tumour, which was of those dimensions and submitted that the biopsy contained only a small minority of suspicious cells. More generally there was a consensus that it is to use Dr Plowman’s words “perfectly possible” for the epithelium to heal over even if there is SPCC. That was the evidence of Dr Henk, Mr Brown, Dr Plowman and Dr Woolgar. Indeed Professor Sloan said in evidence that he had actual experience of a case in which that happened, albeit the cancer was discovered relatively shortly after the mucosa healed over so that it is impossible to know how long it would have taken before the cancer would have manifested itself had it not been independently detected. Moreover Dr Plowman said that it would be perfectly possible for the tumour to remain grumbling for some time after the epithelium healed over. Ms Mishcon submitted that the experts were generally agreed that it would be virtually impossible for a biopsy wound to heal if there were malignant cells on or close to the surface. To that Mr Grace QC responded by referring to Dr Woolgar's evidence that after incomplete surgical removal of a tumour, that is to say without clear or any margins, the wound may heal despite the remaining presence of tumour. It was also the evidence of Dr Plowman, with which Mr Brown and Professor Sloan agreed, that it was perfectly possible, indeed likely that a few cells left behind grew down into the tongue and that in that event it would have been possible for the cancer to grow slowly over a period of years undetected until it invaded the sensory nerves leading to the pain in the autumn of 2000 which Dr Henk said was almost certainly caused by the carcinoma.

There was undoubtedly a tension between that part of Professor Sloan’s evidence which suggested that at the time of the September 1995 and December 1996 biopsies there were polypoid SPCCS and Dr Plowman’s evidence that the ulceration in September 1995,may well have not been caused by the cancer cells which he, no less than Professor Sloan, believed were present. Mr Grace QC was right that it is not a necessary part of the Claimant’s case that the persistent cancer for which he contends manifested itself clinically in September 1995 or December 1996. If Dr Plowman is right and the lesions and ulceration were not caused by cancer cells even though some were present Ms Mishcon’s point loses much of its force. It is also right that the notion of a polypoid SPCC was not a necessary part of Professor Sloan’s diagnosis of SPCC. It did not appear to have been based on his examination of the biopsies and had not formed part of his original report or been mentioned in the joint experts report. He raised it at trial saying that it had occurred to him for the first time listening in court to the evidence of Mrs Manning’s clinical history. Nonetheless it still strikes me as legitimate for Ms Mishcon to point out that if Professor Sloan was right there would need to be an explanation for how cancer cells could have been active between 1994 and 1996 and then become inactive for the next four years. That such an explanation is possible emerged from the evidence which I have summarised in this section and the section of the judgment dealing with dormancy and deep recurrence.

To my mind although, taken together with the long dormancy issue, this is probably the strongest argument pointing against the presence of cancer in September 1995 and December 1996, the two critical points are first that it was not established that this factor meant that it was impossible for there to have been cancer on those dates and second that both Mr Brown and Dr Plowman maintained their strong view that the 2001 cancer was a recurrence(and Professor Sloan maintained his strong view that cancer was present in September 1995 and December 1996) notwithstanding this factor which was drawn to their attention.

Thus for example it was put to Mr Brown that: “If the 1996 biopsy was positive it would be unusual not to heal? A. That is right. It is certainly an unusual point about the case. Q. Does it alter your view on the balance of probabilities looking at all the evidence as to what happened? A. No I think that I would still go with the progression from 1995 where there was suspicion of cells and in 1996 they were highly suspicious and then to a tumour which was evident. It is possible that that progress could have been a slow ongoing process and on the balance of probability to this particular case I would say that is the most likely explanation. But that largely is based on the site, the size of the cells when it was diagnosed and also the similarity of the cells as I explained.” In that respect this factor was the same as the fact that it would be unusual for Mrs Manning to have survived an untreated SPCC from 1996 to 2000 and unlikely for an SPCC to lie dormant for that time. Again both those points were put to Mr Brown and he maintained his position that not withstanding them he believed that on a balance of probabilities the 2001 tumour was a recurrence.

I have given this matter the most careful consideration. I have reviewed in great detail both the factual and expert evidence and I have reflected long and hard on the competing submissions. At the end of this process I have reached the clear conclusion that the weight of evidence points very strongly to the 2001 carcinoma having been a recurrent or persistent form of the original SQC which was treated in February 1994 and not a new second radiogenic primary.

My reasons are apparent in the preceding analysis. In short I am persuaded that it is highly unlikely if not impossible that the 2001 tumour was a new radiogenic cancer. Although, as I have pointed out, it could accurately have been said in for example 1996 that it would be unusual if Mrs Manning were to suffer a recurrence in 2001 with no intervening clinical manifestations and even more unusual with one or two intervening clinical manifestations, so too could it have accurately been said that it would be most unusual if she were to develop a second radiogenic carcinoma (as distinct from a sarcoma) as soon after the RT and BT treatment of February 1994 as 2001.

However it seems to me that the proposition that the 2001 carcinoma was a new radiogenic primary goes beyond merely the improbable. The combination of the facts that it presented on the same site as the original carcinoma and that, when it presented, the mucosa was intact, takes this beyond the merely improbable to the realm of the extremely unlikely if not virtually impossible. The defendants on analysis seem to me to have no convincing answers to these points. When added to the fact that by common consent 2001 was statistically too early for a new radiogenic primary, that the chances of Mrs Manning developing a new radiogenic primary were exceedingly small, that only one in ten second primaries present as carcinomas and that all three pathology experts agreed that there were morphological similarities between the cells in the September 1995 and December 1996 biopsies and the 2001 acknowledged cancer, these factors were very powerful indeed. They are supported by the element of coincidence. Ms Mishcon suggested that the claimant's case was based on little more than the coincidence argument. For the reasons I have given this does not seem to me correct. It is, however, a free standing and independently powerful point in favour of the claimant. Both SQC and SPCC are very rare forms of cancer. Mrs Manning had SQC in 1993 and SPCC in 2001. In September 1995, at a time when Professor Langdon was convinced that her cancer had returned, the biopsy revealed cells which were morphologically similar to the very rare SPCC found in 2001. The same is the case in respect of the December 1996 biopsy with the added factor that Professor Sloan and in particular Dr Woolgar were particularly struck by the progression as between the pre-September 1995 biopsies and the September 1995 biopsy the December 1996 biopsy and the 2001 biopsies. Indeed it is that progression which, while of course wholly inadmissible in considering whether there was a breach of duty of care, at which point hindsight is inadmissible, played an important part in the strongly held opinions of Professor Sloan and Dr Woolgar that cancer was present in September 1995 and December 1996.

For present purposes it seems to me legitimate, without pre-judging the dispute between Professor Sloan and Dr Woolgar on the one hand and Professor Speight on the other as to whether the biopsy slides in September 1995 and December 1996 contained cancerous cells, to give weight to the consideration that it would be an extraordinary coincidence if there was in fact no cancer present but nonetheless they both contained features which were strikingly similar to the very rare form of oral carcinoma which in fact presented itself in 2001. Finally I place very great weight on the opinions of Dr Plowman and Mr Brown in both of whom I had as I have indicated very great confidence. Although ultimately it is for the court to make findings of fact, it is inevitable in so technical an area as this that where there are conflicting opinions and a mass of evidence pointing in opposite directions, the court is bound to be guided by the views and analysis of those of the expert witnesses whom it finds the most persuasive and reliable.

I have of course given the most careful consideration to the various arguments relied on by Ms Mishcon as pointing to the improbability of there having been a recurrence in 2001. In relation to some of them, as I have endeavoured to explain, I was not persuaded, having heard all the evidence, that they were improbable or as improbable as submitted by the Defendants. In relation to others there is in my judgment undoubtedly force in Ms Mishcon’s arguments. However I was not persuaded that any of them was of such a character as to compel the conclusion that a recurrence in 2001 would be beyond the merely improbable and in the territory of the extremely unlikely if not virtually impossible. In that critical regard they differed in my judgment from at least two of the arguments against there having been a new radiogenic primary. In addition doing my best to weigh all the competing arguments and evidence as to the probabilities and improbabilities I am of the view that the balance of probabilities points clearly in favour of the contention advanced on behalf of Mr Manning.

In these circumstances I have reached the clear conclusion that on the balance of probabilities the 2001 primary was not a new radiogenic primary but a recurrence or persistence of the original SQC.

It is against that background that I turn to the vexed question of the disputed expert pathology evidence. I do so on the basis that although I retain an open mind on that dispute in my judgment it would require very strong evidence to justify a conclusion that there was not cancer present in September 1995 or December 1996. That is because such a conclusion would be inconsistent with the conclusion which I have reached that the evidence points strongly to the February 2001 carcinoma having been a recurrence. Were that inconsistency to be resolved in favour of a finding that there was no cancer present in September 1995 or December 1996 that would require a finding that the 2001 carcinoma was a new primary, something which, as I have indicated, was in my judgment highly unlikely if not impossible. Plainly if the pathology evidence justified such a finding it would be the duty of the court as best it could to resolve the conflict between two apparently inconsistent putative findings.

All three experts were agreed that the September 1995 biopsy contained features which were suspicious for SPCC and that the December 1996 biopsy contained features which were highly suspicious for SPCC. In fact in his evidence Professor Speight said that in his view there were features of the September 1995 biopsy which were also highly suspicious. Professor Sloan and Dr Woolgar accepted that without the benefit of hindsight and in particular their examination of the 2001 and 2002 biopsies it would not be possible to make a definitive diagnosis of SPCC. That was principally because of the absence of epithelial dysplasia and foci of SQC, the two smoking guns as they came to be known in the trial, for SPCC.

It follows, as Ms Mishcon pointed out, that the so called stigmata of malignancy which led Professor Sloan and Dr Woolgar to the conclusion that SPCC was in fact present on both occasions must be at least in theory consistent both with SPCC and with a non-malignant innocent explanation. Indeed it was common ground between in particular Professor Sloan and Professor Speight that the principal areas of difference of opinion between them reflected not any difference in observation but rather differences of interpretation. Professor Speight described the job of the pathologist as being “to distinguish between different types of cells based on their morphology and appearance. One must be able to tell the difference between types of normal spindle-shaped cells, based on their size, shape, intensity of staining and their context/location.” Professor Sloan described it as a skill learned from training and experience which is “about recognising the pattern, the architecture of the tissue and the cells in the tissue and being able to classify that as a particular diagnostic entity and recognise that in the current world literature.” Elsewhere he described histopathology as “more of a clinical art in its recognition of cells and tissues and patterns of immunostaining.” Although both sides sought to bolster their conclusions by a number of ancillary arguments based on inference, at the heart of the difference of opinion between the experts lay different interpretations of what they saw in the biopsy slides. Self evidently this presents the court with considerable difficulties, not least because the court was circumscribed by being limited to seeing a number of photographs taken respectively by Professor Speight and Professor Sloan of individual fields within the slides. Not only do these photographs represent only a small percentage of the totality of the cells and patterns which were observed by the experts. In addition Professor Sloan emphasised that a large part of the process of interpretation involves spending quite a long time roving over the biopsy under the microscope at different levels of intensity and that patterns, impressions and features which emerge during such a process cannot always be reproduced or demonstrated by a single photograph or series of photographs. Both for that reason and because by definition the court has no training, experience or skill in the clinical art of pathology, inevitably a not inconsiderable part of the process of seeking to resolve these differences of opinion must depend on the view taken by the court of the reliability and persuasiveness of the evidence given by the experts.

The task was made no easier by the fact that the opposing opinions were strongly held on both sides. Doctor Woolgar in her report said that with hindsight she was around 70-80% certain that there was a tumour present in the September 1995 biopsy which she described as less certain than she was that SPCC was present in the December 1996 biopsy. In examination in chief she clarified that she had not thereby intended to suggest that there was a possibility however small that the tumour began some time between the two biopsies. Rather it was intended to reflect her view that there was less histological evidence of tumour in 1995 than 1996. On reflection she said that what she meant and should have written was that there was the same probability of cancer being present in both biopsies which she put at 70-80%.

In the course of a very protracted and exhausting cross-examination Dr Woolgar accepted that she had been wrong in three respects: First in her interpretation of the epithelial cells in the September 1995 biopsy, second in her interpretation of the so called “archipelago” in the December 1996 and third in respect of the statement in her report that there had been atypical mitoses in the December 1996 biopsy. Nonetheless at the end of that gruelling process Dr Woolgar remained of the view that on the overall balance of probabilities SPCC was present in both September 1995 and December 1996, albeit not to the 70% degree of likelihood to which she had referred in her report and at the outset of her evidence.

Professor Sloan was no less convinced that Mrs Manning had SPCC in September 1995 and December 1996. He too was subjected, quite properly, to intensive and close cross-examination. Towards the end of his evidence at my suggestion he re-examined the December 1996 biopsy slides under a microscope in his old university laboratory and returned to court with some additional photographs which he had taken over the weekend. By this stage he too, like Dr Woolgar, had accepted that his initial view that there were atypical mitoses in the December 1996 biopsy was wrong. Nonetheless the experience of re-examining the slides confirmed him in the strength of his conviction that Mrs Manning already had SPCC by this time. When asked what was the degree of his conviction his answer was that it was in the region of 75% probability.

On the other side of the fence Professor Speight was no less trenchant in his views. On the September 1995 biopsy he had only a 10% doubt as to the presence of malignancy on the H and E slide which was largely removed by the immunostaining. As to the December 1996 biopsy, in the joint experts report although he agreed that it contained cells that were highly suspicious of SPCC and that it is possible that those spindle-cells represented dormant malignant cells which may have emerged in 2001 he thought that this was highly unlikely and highly improbable.

In his written closing submissions Mr Grace QC submitted that the outcome of the case depends very substantially upon the courts impression of the expert witnesses. He was referring not only to the pathologists but also the oncologists and surgeons. In her reply submissions Ms Mishcon agreed that the outcome of the case depends very much on the courts’ impression of the expert witnesses, but qualified that agreement by the further submission that since the whole case turns upon the evidence of the pathology experts, it is the impression that they gave which is important. As is already apparent I do not accept that latter submission. For the reasons which I have given thus far the factual and expert evidence on the many aspects of the disputed issue of whether the 2001 tumour was on the balance of probabilities a recurrent or radiogenic new primary SPCC was in my judgment of critical importance to the resolution of the ultimate question whether SPCC was present in September 1995 and/or December 1996. On those aspects of the case it was the evidence of the surgeons and oncologists which was of most importance and, as I have indicated, my views have been greatly influenced by my impression of those expert witnesses.

In the light of my analysis of the issues in the case set out in the previous section of this judgment, the evidence of the pathology experts while important was not in my view determinative of the ultimate outcome of the case. I have already given my reasons for rejecting the attacks on the bona fides of the three pathology experts made respectively by Mr Grace QC and Ms Mishcon. In addition both counsel prayed in aid departures in the oral testimony of the opposing expert(s) from what had appeared in their reports and/or the joint report on aspects of the breach of duty allegations in support of submissions that they were unreliable. I have referred to those departures in the breach of duty section of this judgment. There is in my view some fairly limited force in those submissions on both sides and I have carefully considered them and have taken them into account. More substantively Ms Mishcon submitted that as mentioned above Dr Woolgar accepted in cross-examination that she had been wrong in three technical aspects of her analysis of the biopsies. That is correct. In respect of one of them Professor Sloan, accepted that he too had been wrong. Both Dr Woolgar and Professor Sloan in their reports expressed the opinion that insufficient attention or weight had been given by Dr Harrison to the presence in the December 1996 biopsy of atypical mitotic figures.

Ms Mishcon also submitted that because Dr Woolgar agreed with Professor Speight that Professor Sloan was wrong to say that there were suspicious cells at the deeper aspect of the 1995 biopsy (after cross examination) that he was also wrong in his interpretation of the archipelago in the December 1996 biopsy, it follows that Professor Sloan was also wrong in those two major areas of interpretation. I do not accept that latter submission which seems to me a non sequitur. In my judgment it does not follow from the fact that on these two points of interpretation Dr Woolgar agreed on the balance of probabilities with Professor Speight that therefore their view on them is correct and Professor Sloan’s is incorrect.

Ms Mishcon went on to submit that both Dr Woolgar and Professor Sloan accept that there are two choices of interpretation in relation to the September 1995 and December 1996 biopsies, namely that SPCC was present or it was a reactive healing process in the presence of a chronic ulcer. Both agreed that the choice is largely a matter of interpretation. Given that both Professor Sloan and Dr Woolgar had made what she described as such serious errors of interpretation Ms Mishcon submitted that the evidence of Professor Speight who had not been shown to have made any such error should be preferred. Again I do not accept that submission. In relation to the issue of atypical mitotic figures, Professor Sloan in cross-examination explained that when he reviewed the slides before writing his original report he had interpreted some of the cells in the December 1996 biopsy (but not the September 1995 biopsy) as atypical mitotic figures. In particular he saw what he regarded as a striking and conspicuous mitotic figure in the photograph on page 56 of the green trial bundle. His interpretation of the slides on his own had been that there were some normal mitotic figures, some apoptotic cells and more than one atypical mitotic figure scattered throughout the spindle-cell proliferation. At the joint experts meeting Professor Sloan said that the experts looked at these suspicious cells and discussed them at length. He said that he came away unconvinced that he had in fact seen atypical mitotic figures and that Professor Speight had convinced him looking at the slide through a double-headed microscope that the cells which he had thought were atypical mitotic cells were not.

He said that it is difficult to distinguish between mitotic and atypical mitotic figures adding that he had seen one pathologist think that a particular figure was an atypical cell and another think that it was not. At trial Professor Sloan confirmed that the particular cell in the left hand photograph on page 56 which also appeared in Professor Speight’s photograph at page 320 of the green trial bundle, was one in respect of which he could not be certain whether it was atypical or not. He did however remain of the view that on the balance of probabilities it was a mitotic figure and not an apoptotic figure as Dr Harrison had believed it to be. He thought that most competent pathologists would recognise it as a mitotic figure. He was also certain that a number of cells in that region which Dr Harrison had identified as apoptotic were in fact mitotic. He felt very confident about recognising apoptotic cells because he had spent quite a lot of time with a PhD student looking at such cells on H and E sections so that he was familiar with their morphology. He had examined a PhD on the counting of mitotic and apoptotic figures in SPCC.

In my judgment Professor Sloan’s change of opinion in respect of atypical mitotic figures did not evidence a lack of skill in recognition on his part. On the contrary it demonstrated an open-minded approach and a willingness to reconsider initial opinions in the light of new material and alternative views. In fact it lent greater force to those of his key conclusions which remained unaffected both by his detailed discussions with Professor Speight, his consideration of the evidence at trial and his cross-examination. He modestly and generously expressed great respect for Professor Speight and said that he reviewed his own opinions in the light of the differences of view which emerged when he read Professor Speight’s report and met him at the joint experts meeting. What was very powerful was Professor Sloan’s account of how his review of the slides shortly before trial and again on the weekend during the trial when he re-examined the 1996 slides left him more convinced than ever that they evidenced SPCC.

There were a number of features both of his original report and the joint experts report which he accepted in cross-examination did not accurately reflect his views. In relation to the latter (and in particular the passage “our diagnosis: chronic ulcer with evidence of radiation damage” referring to the September 1995 biopsy), he candidly accepted that he had taken his eye off the ball in signing off on the joint report despite the fact that it contained propositions with which he did not agree. The context was that a draft was prepared based on notes typed at the joint experts meeting by Dr Woolgar many of which both she and Professor Sloan said recorded things said by Professor Speight rather than views with which they had all agreed. The intention was that they would serve as a basis for amendment in email discussion. There then followed a series of email exchanges which led to some changes but did not make all the corrections which Professor Sloan candidly admitted he should have insisted on. He ascribed this partly to the fact that he had never prepared a joint experts report before and partly to the fact that it occurred at a time when he was very busy changing jobs.

In relation to the allegedly suspicious cells at the deeper aspect of the September 1995 biopsy and Professor Sloan’s interpretation of the archipelago, I do not accept the validity of the arithmetical approach urged on me by Ms Mishcon. It does not follow from the fact that two experts hold one opinion and a third holds a different opinion that the former must be right or even that it is right on the balance of probabilities. That strikes me as too simplistic an approach. It depends on what view one forms of the experts and how the issues in question fit in with the wider picture.

In relation to Dr Woolgar there was in my view more force in Ms Mishcon’s submissions. Although it seemed to me necessary to make considerable allowance for the fact that Dr Woolgar was plainly exhausted by the lengthy cross-examination (following as it did a long period, and far longer than she had expected, sitting in court listening to other evidence) so that some of her concessions may have owed more to exhaustion than a genuine change of heart, nonetheless her changes of opinion led me to treat her views with some caution. However with Dr Woolgar, just as with Professor Sloan, I was very struck by two things. The first was the strength of her initial views that Mrs Manning had SPCC in 1995 and 1996. The second was that despite the concessions made in cross-examination and lengthy exposure to Professor Speight’s contrary views, she remained adamant at the end of her cross-examination that Mrs Manning had cancer in September 1995 and December 1996.

Both Professor Sloan and Dr Woolgar were of the clear opinion that further biopsies taken both in September 1995 and December 1996 would have revealed SPCC. Professor Sloan said in relation to the September 1995 biopsy that if a further biopsy had been taken it would probably have revealed spindle-cells invading the deeper tissue and/or a focus of conventional squamous carcinoma. That would have led to a firm diagnosis of SPCC and triggered Professor Langdon to do salvage surgery. Similarly, in relation to the December 1996 biopsy he believed that a deeper biopsy, had it been taken, would probably have shown spindle-cells in the muscle or foci of conventional spindle-cell carcinoma. He believed that the 2001 carcinoma arose from cells left behind in 1996 in the deeper tissue which grew slowly in the deeper tissues after the 1996 biopsy healed over. He believed that a small focus of just a few malignant cells were left behind which grew slowly in the tongue and eventually manifested in November 2000 when Mrs Manning developed pain and speech problems which he believed (as did Dr Henk) was almost certainly the carcinoma cells invading the nerves of the tongue.

Doctor Woolgar also said that if a deeper biopsy into the muscle had been performed in December 1996 on the balance of probabilities it would just as in the case of September 1995, have revealed a spindle-cell carcinoma. These answers supported from a pathological perspective the opinion given by Dr Plowman from an oncological perspective that cancer was present in 1996.

It is convenient in this context to record that both Dr Plowman and Professor Sloan expressed the clear opinion that if cancer was in fact present in December 1996 it is likely that such cancer would have been revealed on a further biopsy. In the joint oncologists report the question had been posed: “The biopsy taken by Professor Langdon on 2^nd December 1996 was 2 millimetres deep and did not include any muscle. If tumour was then present would a deeper biopsy probably have revealed the tumour?” Doctor Plowman’s answer was that “ a larger deeper biopsy would have been desirable and may have clarified the diagnosis of persisting carcinoma.” At trial he confirmed that on the balance of probabilities he thought that it would have done so because he believed that there were cancer cells deep to the superficial area which was clinically apparent. Cancer was probably going on in the base, the deeper structures and statistically a bigger bite from that area, a bigger divot would have been more likely to have given it. If there were in fact spindle-cell carcinoma cells deep in the biopsy that made it even more likely that they would have shown up in a further deeper biopsy. Professor Sloan said that if SPCC was in fact present in 1995 and/or 1996 it is highly likely that a further biopsy would have revealed the underlying tumour. A surgeon such as Professor Langdon if presented with the information that the original biopsy was highly suspicious for SPCC would not have taken that lightly and would have removed a substantial amount of tissue in order to prove a diagnosis one way the other. No surgeon would have taken that lightly. This latter point, which is of course an essential part of the chain of causation which needs to be proved for the claim to succeed, was not challenged by the Defendants.

The fact that as they both openly acknowledged their diagnosis was heavily influenced by the benefit of hindsight and in particular what they regarded as the striking similarity between features of the September 1995, December 1996 and 2001/2002 biopsies did not in my view in any way diminish the persuasiveness or validity of their opinions. In their view viewed as a continuum the slides demonstrated an evolution of the original cancer cells whose progression could clearly be seen. They were also struck by the marked difference between the 1994 and July 1995 biopsies on the one hand, and the September 1995 and December 1996 biopsies on the other, the latter showing a progressive busyness which Dr Woolgar said was the first thing that struck her when she viewed the slides. This busyness was the opposite of what would have been expected as the length of time from the BT/RT with its creation of radiation damaged fibroblasts increased. Nor could it plausibly be explained clinically or pathologically as a reaction to local trauma or ulceration. This was particularly so in the case of the December 1996 biopsy where there was no evidence of clinical ulceration as distinct from ulceration visible microscopically.

In relation to the so called archipelago there was a fundamental difference of opinion between Professor Speight and Professor Sloan on whether a number of cells which stained positive in immunostaining and of the 1996 slides carried out not by Dr Harrison but as a forensic exercise for the purpose of the trial, and which were found in the connective tissue were properly diagnosable as malignant epithelial cells which had invaded the connective tissue or were in fact innocent rete pegs which were in fact connected to the epithelium, the connection being invisible on the photograph of the immunostaining by virtue of what was described at the trial as the effect of sectioning.

This latter sectioning point was one which formed a recurring theme in Professor Speight’s evidence. It is a well-known and established fact among pathologists that it sometimes happens that because of the way in which sections of a biopsy are cut a misleading impression may be given. This can either take the form of making cells have an appearance which they do not in real life possess or it can make a cell appear to be isolated whereas in real life it is connected to the epithelium.

Overall I had great confidence in Professor Sloan. He was immensely experienced and distinguished in the field. He also struck me as a careful, diligent thoughtful and entirely open-minded expert who was genuinely committed, first to arriving at the right conclusion and then to doing his best to assist the court. His willingness to reconsider his opinions in the light of changing evidence or differing opinions gave added weight to the persuasiveness of his views.

The court’s task was not made easier by the fact that Professor Speight was also an impressive witness. Like Professor Sloan he was immensely distinguished and experienced. Like Professor Sloan he too changed some of his opinions as between his report and his testimony. Thus in the context of breach of duty he wrote in his report in relation to the December 1996 biopsy: “Normally, faced with suspicious features in a biopsy, a pathologist would prepare deeper levels so as to examine more tissue. There is evidence in the report that Dr Harrison was suspicious and may not have prepared levels.” This appeared to accept the allegation to which it responded that Dr Harrison was negligent in failing to take deeper levels in respect of the December 1996 biopsy. At trial Professor Speight argued that it was not necessary for Dr Harrison to have done so. Mr Grace QC submitted that Professor Speight could not properly reconcile his report with his testimony on this point and that the court could not reconcile it either. In my view there is some force in that submission.

In my view more striking was the apparent lack of consideration which Professor Speight had given prior to the trial to the effect of the acknowledged false negative rate on immunostaining on the unreliability of a 90% innocent view based on H and E slides alone. When the point was put to him and its implication explored with him he accepted the logic of the Claimant’s argument that the false negative rate rendered a 90% innocent view unreliable and would oblige a reporting pathologist to alert the surgeon to the existence of residual doubt. I found this somewhat surprising. In relation to Mr Grace QC’s submission that Professor Speight’s attempts to explain away all suspicious features by a “sectioning effect” were altogether too facile and unnecessarily favoured the Defendants’ position since there is no reason why the random effect of sectioning should always favour the innocent explanation rather than malignancy, I saw a certain amount of force in it. It was common ground between the parties that many of the features relied on by Professor Sloan and Dr Woolgar as pointing to malignancy were also consistent with an innocent explanation. The process of reaching a view as to which was the correct diagnosis thus necessarily involved either a judgment based on experience and recognition or inferences to be drawn from external evidence such as clinical context or comparison with the 2001 and 2002 biopsies or both. When Professor Speight argued that a particular feature was explicable by reference to a sectioning effect, it was not always clear which part if any of that process led him to that conclusion. This was of particular importance in the context of the debate about whether the positive stained cells in the archipelago in the December 1996 biopsy were innocent rete pegs or malignant cells.

I would not wish by these observations to give the impression that I found Professor Speight other than an authoritative expert who, as Ms Mishcon pointed out, on occasion volunteered a point favourable to the Claimant. However, while I did not for a moment consider that he did not genuinely believe in the correctness of the Defendants’ case, or that he was not doing his best to assist the court, I did sometimes feel that, perhaps because he was convinced in the correctness of their case, he was less open-minded than Professor Sloan. It is also fair to point out that there was a lack of clarity and arguably some inconsistency as between Professor Speight’s report and his oral testimony as to whether the plump and pleomorphic cells within the connective tissue which he described in the H and E sections of the September 1995 biopsy as forming small sheets of spindle-cells were, as he said in the written report, consistent with atypical fibroblasts as a consequence of radiation damage (“radiation fibroblasts”) or as he suggested in oral testimony, were proliferating fibroblasts associated with a healing ulcer. It thus seemed to me that it could fairly be said of Professor Speight as well as of Professor Sloan and Dr Woolgar that he was not entirely consistent in his opinions throughout.

It was common ground that for the purposes of this case the features of stigmata of malignancy for which a pathologist would be looking are (1) Pleomorphism (which Professor Speight in evidence in chief described as the most important feature a pathologist would look for, including variable shapes and sizes of nuclei and nucleoli.) (2) Hyperchromatism (3) Increased cellularity. Hyper cellularity. (4) The arrangement or pattern of the cells (5) Mitoses and (6) Invasion or infiltration. Mitoses can be either typical or atypical. If atypical that is a strong indicator of malignancy. It is also the case that the more mitotic figures there are the greater the suspicion of malignancy. However it is also the case that in a malignant tumour mitoses may be sparse (see Ellis and Corio). It was also common ground (a) that a diagnosis of malignancy does not require that all these features or stigmata are present and (b) that these stigmata both individually and cumulatively are consistent both with malignancy and with an innocent explanation. It is thus readily apparent to what extent diagnosis depends on interpretation on the one hand and inferences to be drawn from external evidence such as the clinical context (which Professor Speight described as 90% of the diagnostic process), comparison with other biopsies and other matters on the other hand. At one point in his evidence Professor Sloan said that interpreting biopsies and making a diagnosis is not just a question of drawing up a list of stigmata of malignancy.

It will also be readily apparent from the earlier parts of this judgment that it is not possible, in answering the question whether cancer was present in September 1995 and/or December 1996, to do so by reference to the biopsies and the expert evidence thereon in isolation from the evidence as to whether the 2001 carcinoma was more likely to have been a recurrent or a new radiogenic primary.

It was common ground between the three experts that both the September 1995 biopsy and the December 1996 biopsy contained stigmata of malignancy. That is why they all agreed that both biopsies were highly suspicious. Where they parted company was in their interpretation of the stigmata.

Professor Sloan was convinced with the benefit of hindsight that the December 1996 biopsy contained evidence of the presence of SPCC. He was particularly struck in reaching that conclusion by what he regarded as the striking similarity between some of the cells and arrangements in the December 1996 biopsy and those in the 2001 and 2002 biopsies. While he accepted that the malignant features were more developed and prominent in the latter than the former, he considered that to be entirely to be expected and consistent with a recurring tumour which grew over a period of years. Like Dr Woolgar he was also struck by the hypercellularity or busyness of the biopsy which he did not consider to be reasonably explicable either as the long-term effect of radiation damage or as healing process associated with a chronic ulcer. In this he was also supported by Dr Woolgar. His conclusion relied also on his interpretation of the islands of epithelial cells in the archipelago which stained positive in immunostaining and which he interpreted as evidence of the malignant invasion of the connective tissues. In this he was originally supported by Dr Woolgar but found himself ultimately in a minority, Dr Woolgar having accepted in cross-examination that because the archipelago was not materially further away from the epithelium than were two acknowledged rete pegs the archipelago was more likely to be rete pegs whose true nature was disguised by the sectioning effect.

Professor Sloan said that his conclusions were supported by some of the photographs in evidence but emphasised two points: first that photographs do not accurately reproduce what the pathologist sees down the microscope, which enables greater magnification and the study in detail of individual cells in a multitude of fields together with the gaining of an overall impression of the pathology; and second that the photographs which he adduced were intended only as examples of particular features, of which he had seen many more on the slides under the microscope. This latter point is important. I have already mentioned that it was suggested to Professor Sloan by Ms Mishcon that he was lying when he said that he had seen more examples of malignant bands on the deeper aspect of the biopsy when he reviewed it over the weekend during the trial than the single example contained in one of the photographs he adduced on the following Monday morning. I have already said that I entirely accept that Professor Sloan was telling the truth in this regard.

I have carefully reviewed and indeed re-read several times all the evidence on this aspect of the case. That includes the three original experts reports, Dr Harrison’s original report, the joint experts report, the relevant clinical records going back to 1994 and the transcripts ( and where appropriate my notes) of the oral testimony of the three experts and Dr Harrison. I have also reviewed and studied at great length all the photographs adduced by the experts together with their respective annotations thereon and the detailed oral and written submissions on this aspect of the case by Mr Grace QC and Ms Mishcon. I have given the matter a great deal of anxious consideration. I have been struck by the force of a number of Ms Mishcon’s submissions and troubled by the apparent inconsistency between Professor Sloan’s conclusion and certain features of the evidence to which both he and Professor Speight drew attention. I have of course taken into account the respects in which Dr Woolgar did not support Professor Sloan’s conclusion and those aspects of Professor Sloan’s evidence which represented a departure from things he had previously said. All these matters have given me long pause for thought. However I accept Professor Sloan’s conclusion. In my judgment there was SPCC present in December 1996.

It would further lengthen an already very long judgment to set out in minute detail the entirety of the process of reasoning by which I have reached this conclusion and all the matters which have contributed to it. I highlight below a number of the more important factors.

First I found Professor Sloan to be the most persuasive of the three experts. It was quite clear to me that he had an unshakeable conviction that SPCC was present and that each time he revisited the slides this conviction was strengthened. Second, I was struck by the fact that, even though Professor Speight was able to satisfy himself that the various features to which he drew attention in his report were consistent and indeed more probably explicable by innocent explanations, he too had been struck initially by the presence of what he described as highly suspicious features and by the similarity of some of those features with the 2001 and 2002 biopsies. Third I was unpersuaded by the Defendants’ submission that it was more probable that the hypercellularity had an innocent explanation (whether the long-term effect of RT or the short-term effect of a chronic ulcer) than a malignant or sinister one, (although of course the burden of proof on this as in all issues was for the Claimant). Indeed the contention that the explanation was a healing reaction to a chronic ulcer was in my view at odds with the clinical evidence as to the nature of Mrs Manning’s nodule.

It was accepted by Professor Speight that the December 1996 hypercellularity was more prominent and obvious than in the previous biopsies. Indeed there was a progression from the May 1994 biopsy through the July 1995, September 1995 and December 1996 biopsies which showed a pattern of increasing busyness. I was persuaded by the force of Dr Woolgar’s and Professor Sloan’s evidence that one would ordinarily expect hypercellularity to decrease rather than increase the more time elapsed since RT. Similarly I was persuaded by the force of Mr Grace QC’s submission that if one has regard to the evidence of the clinical context of the four biopsies, it would be surprising if the degree of hypercellularity in December 1996 was the result of a healing process caused by a chronic ulcer. In May 1994 Mrs Manning had an ulcer which had been present for three months. In December 1996 there was no clinical ulcer at all. Professor Langdon described a very small nodule, 5 millimetres maximum in diameter and his clinical notes explicitly record: “Not ulcerated.” Professor Langdon was asked about the difference between a nodule and an ulcer. His answer was: “It was an elevated little lump looking like a pimple in fact, but critically it was covered by normal and healthy healed mucosa epithelium. It was not ulcerated at all…. the surface of it was covered by healed mucosa and there was not any ulceration or any destruction of the epithelium.” Professor Speight pointed out that the December 1996 biopsy revealed non-clinically evident ulceration but he accepted that the fact there was no clinical evidence of ulceration implies that the ulceration visible on the slides was very small.

In addition because Dr Henk’s clinical notes record that as late as 14 October 1996 on examination there were no signs of recurrence of carcinoma and Mrs Manning’s neck was clear, there is no evidence that there was any non-clinically apparent ulceration present earlier than 19 November 1996 when Mrs Manning first presented at Professor Langdon’s clinic with the fibrous nodule, which was itself not described clinically as ulcerated. Against that background I found Professor Speight’s reluctance to accept that the contrast between the clinical context in May 1994 and December 1996 suggested that the much greater hypercellularity in December 1996 was unlikely to have been caused by a healing reaction to an ulcer unconvincing. His suggestion that it all depends on the nature of the two ulcers, even if theoretically correct, ignores the fact that the May 1994 ulcer was described by Professor Langdon as “indolent non-healing ulcer”. Professor Speight when this was put to him had misremembered that it was a fairly small healing ulcer. However even when it was pointed out to him that it was neither healing nor small (which he then had to accept, it being 10 by 5 millimetres) Professor Speight refused to accept the force of Mr Grace QC’s point. This is despite the fact that he accepted that the fact that the proliferating granulation tissue in May 1994 was not as proliferating as it was in 1995 and 1996 is what made the September 1995 and December 1996 biopsies suspicious and what made him look at them so carefully. I found Professor Speight’s evidence on this even less convincing when he seized on a mention by Mr Grace QC in cross-examination of a reference in Dr Harrison’s biopsy report to the presence of candidosis and suggested for the first time that the increased cellularity in December 1996 could at least in part be explained by the candidosis. When asked why he had not thought of that theory before Professor Speight’s answer was: “Because you have just reminded me of it Mr Grace but I had not regarded it as being particularly important because the cellularity could be explained by the presence of a chronic healing ulcer, but by reminding me of the infection that would give me a reason which I could put to you which may alter the cellularity in this particular biopsy, but I have to be honest and say I had not thought of it as being important until you reminded me.”

This passage in Professor Speight’s cross-examination served to underline the impression I had already formed that on analysis Professor Speight’s evidence while showing that the December 1996 hypercellularity could have been caused by a healing process reacting to a chronic ulcer, fell short of demonstrating that it probably was so caused. It also left me feeling that Professor Speight was more concerned to defend his original position than to respond to the evidence and arguments on their merits.

I am further fortified in my conclusion on this point by evidence from Professor Sloan that by December 1996 one would not expect hypercellularity due to RT because following RT tissues tend towards being hypocellular and also by his evidence that if, as was the case in December 1996, it is not possible for the clinician to detect an ulcer clinically the ulcer must have been minimal, and that the amount of healing reaction one is likely to find on histology depends upon the severity of the ulceration. If there is an extensive ulceration you would expect a more extensive healing reaction. Both these points, the latter of which strikes me as common sense, argue against either RT or healing response to an ulcer as being the probable explanation for the hypercellularity in the December 1996 biopsy.

I was very struck by the extent to which Dr Woolgar had been herself struck by the increased busyness and hypercellularity in the December 1996 biopsy and the fact that it was more hypercellular than the September 1995 one and that both were far more hypercellular than the May 1994 and July 1995 ones. She said it was the first thing she noticed and it was thoroughly unexpected. I found her evidence on this which she maintained throughout and despite close cross-examination very persuasive. It was of course the same as that of Professor Sloan.

Fourth I found Professor Sloan’s evidence on the archipelago more persuasive than that of Professor Speight. That remains the case notwithstanding the fact that Dr Woolgar changed camps on this issue in cross-examination. The difference of interpretation on this point was fully discussed at the joint experts meeting and Professor Sloan, who has great respect for Professor Speight, took on board his interpretation but remained unpersuaded by it. In his view the islands of suspicious cells in the archipelago shown on photograph 54 right and 55 left in the green trial bundle were individual cytokeratin spindle-cell evidencing the presence of SPCC. Although Dr Woolgar in cross-examination accepted that they were not materially further from the epithelium than the larger figures which all three experts accepted were probably innocent and the result of tangential sectioning, Professor Sloan was adamant that even if they are not too deep in the tissue to be the result of tangential sectioning. Professor Speight’s interpretation was wrong because the cells are morphologically similar to cells seen in the acknowledged SPCC in the 2001 and 2002 biopsies. In cross-examination Professor Sloan accepted that the archipelago was within the area of the acknowledged rete pegs and therefore not as deep in the connective tissue as he had originally interpreted it to be. However he remained firmly of the view that the islands were malignant rather than innocent migrating epithelial cells having regard to the pattern and distribution of the cells

Fifth, I found Professor Sloan’s evidence in relation to the supplemental photographs of the December 1996 biopsy produced by Professor Speight which he commented on when he was recalled for the second time both persuasive and convincing. Professor Speight produced 10 photos of contiguous or overlapping parts of the interface between the biopsy and the tissue remaining on Mrs Manning’s tongue. This was referred to as the west coast. There was also a photograph of the whole biopsy in which the location of the other 10 photographs was identified.

Professor Sloan identified and described features in photographs 3,4,5 and 6 which he regarded as evidence of SPCC. Professor Speight had interpreted the disputed cells as being innocent fibroblasts whereas Professor Sloan interpreted them as suspicious interlacing bands of spindle and kite shaped cells such as are found in SPCC. He supported his interpretation by saying that they were strikingly similar to those in the 2001 SPCC. In relation to the interlacing bands, while he acknowledged that they were less prominent than in the 2001 and 2002 biopsies, he said that this was only to be expected in the evolution of the SQC into the SPCC.

He said that although the bands were not in the classical basket weave form associated with SPCC, photos 5 and 6 showed interlacing bands which were visible and photos 3 and 4 showed bands from which it could be inferred that they were interlacing. Acknowledging as inevitably one must the court’s complete lack of experience and expertise in this area, I found Professor Sloan’s evidence persuasive and which is more important, I found it more persuasive than that of Professor Speight in relation to these photos. I also take into account the fact that Professor Sloan was again at pains to emphasise the basic limitation of photographs as a diagnostic tool as distinct from looking under the microscope. He said that when pathologists do their external quality assurance they always insist on having original slides circulated so that they can look in their own microscopes rather than just digital images because although they can be used to illustrate points it is difficult to get all the information in a static digital photograph. He said that if ever he is asked for a second opinion by email and is emailed an image he always asks for the original slide and said that he would not pass an opinion on a digital image by email for that reason.

For that reason among others in deciding as between the two competing expert views I have relied in part on my greater confidence in Professor Sloan as an expert witness as well as on my own observation of and reaction to the photos. I have also taken into account the fact that I was persuaded by Professor Sloan’s evidence on two associated matters.

The first is his evidence that if the abnormal appearances in photographs 4 to 6 were the result of radiation damage he would have expected them to have the same appearance as the photographs 1,2,3 and 7,8,9, and 10 which he said were the classical picture of post-radiation therapy. Instead of seeing a very cellular picture in photos 3,4,5 and 6 one would have expected to see the whole biopsy looking uniform.

The second was his evidence that the suspicious features in photos 3 to 6 could definitely not be explicable as a consequence of the ulcer because there would be no reason if that were the explanation why those features were not also present in the other photographs.

Sixth in his report Professor Sloan had written that “there are interlacing bands of spindle-cells and kite-shaped cells, most prominent towards the deep aspect of the biopsy. These cells do not have the features of radiation damaged fibroblasts and represent a spindle-cell proliferation.” In response to Ms Mishcon’s suggestion to him in cross-examination that the reason he had not produced photographic evidence of such interlacing bands was that he had not seen them on the slides and that they did not exist, Professor Sloan at my suggestion reviewed the biopsy slides and returned with four photos. Photograph 56D in the green bundle showed the locations (marked A and B) of two areas of which he had taken photographs on the weekend, respectively 56E (in relation to area A) and 56F and 56G (in relation to area B). Area A and area B overlapped to a small extent. Both A and B were roughly in the middle of the photograph of the biopsy viewed from north west to south east. Area B included the line of the surgical margin. On photo 56E which Professor Sloan agreed was in the more superficial part of the biopsy nearer the epithelium he said that the majority of the cells were suspicious spindle-cells. What made them suspicious was the large nuclei, the prominent nucleoli and the cell density that is to say the hypercellularity.

He accepted that it was not possible in photo 56E to appreciate the fascicles or banding arrangement. Photo 56F he described as the area referred to in his report where he had said that there were bands more prominent towards the deep margin. He annotated his copy of 56F to show scattered suspicious spindle-cells, including a pleomorphic cell and the best example of a suspicious spindle-cell, a small nucleus and a large nucleus (the variation between which he cited as an example of pleomorphism). He also identified bands or fascicles of cells in different orientations. The latter were very noticeable even to the untrained judicial eye. He identified a distinct band of parallel arranged cells with adjacent cells appearing to be cutting a cross-section which he said implied an interlacing arrangement. He also identified what he described as a less obvious additional parallel band of pleomorphic spindle-cells in the top left of 56F.

He pointed out nuclei with variable shape and intensity, some quite small, some with dark stains, others quite large and prominent. He said there were suspicious spindle-cells not only in the bands or fascicles but also scattered around the photo. He described the hypercellularity on the slide as worrying. When asked to compare the cells in 56F with those in photo 56A which was taken from the 26^th February 2001 biopsy, Professor Sloan commented that features were strikingly similar. He said that the fascicles in 56F were probably more prominent that those in 56A but that the cells and the arrangement were strikingly similar. The striking similarity in the cells consisted in the large nuclei prominent nucleoli and the spindle-shapes. The similarity in the arrangements was the parallel bands adjacent to cross-sections.

Photo 56G which he marked as “showing fascicle at deep margin” was taken of the same area as appeared in 56F but at high magnification. Professor Sloan annotated a fascicle of parallel cells, another fascicle of parallel cells at a divergent angle, a suspicious spindle-cell with hyperchromatic nucleus and smaller cells with hyperchromatic nuclei with the comment: “Note variation in size”.

The relevance of the contrast between the cell with the large hyperchromatic nucleus and other cells with more slender less intense nuclei was that it is a feature of pleomorphism that the cells are varied in shape and size which Professor Sloan says adds to the suspicion.

Asked if it is conceivable that 56F and 56G could be healing tissue given that they were at the deep margin he said he believed that it was SPCC. He was very impressed with the morphological similarity to the 2001 tumour. He contrasted other areas of the December 1996 biopsy which he believed showed healing tissue at the margin, for example at the bottom right of the surgical margin on 56D.

I have already referred to the suggestion by Ms Mishcon in cross-examination that Professor Sloan was lying when he said that he had seen other interlacing bands at the deep margin. Professor Sloan’s response was that the reason that he only photographed one interlacing band at the deep margin was to give an example. He could have taken more photographs but thought that it was sufficient just to give an example and show the most prominent. His analysis was that there was a focus of SPCC in the deeper tissue and that 56F shows the top part or edge of an SPCC.

Professor Sloan said that the features in box B, hypercellularity, pleomorphism and the patterns of the cells were suspicious for SPCC. They were all present in the agreed February 2001 carcinoma. Taken on their own he regarded that particular combination of features as highly suspicious. What made him conclude with hindsight that it was not just suspicious but actually SPCC was what he regarded as the striking similarity between what he saw in 1996 and what can be seen in 2001. It was at this point that he repeated that he thought there was in the region of a 75% probability that this was SPCC.

Professor Sloan was cross-examined closely on these photographs. He accepted that the band in the top left corner of 56F was not at the deep margin, but pointed out that the one in the bottom right hand corner was. It was put to him that one would expect to see mitoses in an SPCC, whereas there are none in 56F or 56G. Professor Sloan thought the explanation was that the degree of differentiation in the 1996 was higher than in the 2001 biopsy, although as he pointed out everybody was agreed that there were some mitotic figures in the December 1996 biopsy.

Professor Sloan accepted, as of course he had to, that in the December 1996 biopsy, as in the September 1995 biopsy, there was evidence of neither epithelial dysplasia nor a focus of SQC, the two smoking guns for a diagnosis of SPCC. His explanation was that there must have been SQC in the deeper tissue left behind in Mrs Manning’s tongue which would have been revealed had a further deeper biopsy been performed. However the absence of visible evidence of either of these phenomena did not undermine his conviction that SPCC was present in December 1996. It merely reduced the degree of probability from 100% to 75%.

Seventh, I accept Professor Sloan’s evidence as to the striking similarity between aspects of the December 1996 biopsy and the 2001 and 2002 biopsies. It was this factor, coupled with the evolving patterns in the biopsies from May 1994 to 2002 evidencing the progression of the tumour according to Professor Sloan and Dr Woolgar which first convinced Professor Sloan that there was SPCC present in September 1995 and December 1996. It was a recurring theme in his testimony to which he returned often when seeking to explain why he was so convinced that his interpretation was correct. All three experts agreed that there were similarities. Ms Mishcon however submitted that the similar features were also consistent with innocent fibroblasts and relied on Professor Speight’s interpretation that the latter was the better interpretation.

As with other aspects of the difference of views between the experts on the interpretation of the slides, I take into account Professor Sloan’s warning as to the limitations as to the degree to which it is possible to convey and adequately represent his conclusions on examining the slides by reference to photographs. I also take into account Professor Sloan’s acknowledgement that it is to be expected that the features in 2001 will not be exactly the same as those in 1996 both because the tumour would be expected to have evolved and less importantly because of the differences between the small sample in December 1996 and, the larger sample for example in February 2001. As with other aspects of the dispute on interpretation, I take into account my confidence in Professor Sloan as an expert witness as well as my own observations of the photographs. I also take into account, as with the other areas of interpretation, the inferences to be drawn from the wider aspects of the case, including the evidence as to whether the 2001 cancer is likely to have been a recurrence or a new radiogenic primary.

Taking all these matters into account as I have said I accept Professor Sloan’s evidence. One of the photographs relied on by Professor Sloan was photo 55 in the green trial bundle which showed the archipelago. He said that the cells in this photograph showed a striking similarity to the CK stained cells in the right hand photograph on the same page taken from the 2002 biopsy. Ms Mishcon’s submission on that was that given that on the balance of probabilities the archipelago is innocent and does not contain malignant spindle-cells there can be no such similarity. That submission of course depends upon her submission that the archipelago is on the balance of probabilities innocent, a proposition which relied on her submission that because Professor Sloan was in a minority on this issue it followed that he must be wrong on the balance of probabilities. I have already explained why I reject that submission. I note that no alternative submissions were made to show that the cells were not in fact strikingly similar on the assumption that I were to hold as I do that the archipelago is not innocent.

Ms Mishcon criticised Professor Sloan’s and Dr Woolgar’s inability to demonstrate a convincing cord on photograph 56B, which Professor Sloan compared with the right hand photograph on the same page taken from the 2002 biopsy. Professor Sloan’s answer which I found convincing was that the photograph had not been taken to show a cord but rather to demonstrate increased density. He said that all the suspicious cells in the bottom left hand of the photograph were in a broad cord which was why he and Dr Woolgar had struggled to draw bands of cord.

The two photographs on page 56 of the green trial bundle compared cells taken on high magnification in the December 1996 and 2002 biopsies. Professor Sloan included them to show the striking similarity between some of the cells in the tiny field in December 1996 and the accepted 2002 carcinoma cells. He identified in particular one cell in the left hand photograph which he described as a spindle-cell with a worryingly elongated nucleus and worrying hypochromatism. The fact that the cells in the two fields were strikingly similar rather than identical was the reason for his inclusion of the photographs in that it demonstrated the process of de-differentiation which he observed in the evolution of the cells and patterns as between the successive biopsies. Professor Speight accepted that the cells in these two photographs were similar in some respects while pointing out that there were also differences.

Ms Mishcon cited the photographs on 56A of the green trial bundle taken from the February 2001 biopsy as showing marked differences to the 1995 and 1996 biopsies. One she said showed interlacing bands typical of SPCC, the other showed four mitotic figures in a small field, for which there was no comparable photo of the 1995 or 1996 biopsies. In fact Professor Sloan was very impressed with the morphological similarity between his supplemental photo 56F taken from field B of the December 1996 biopsy and the 2001 biopsies. He regarded the features including the fascicles in 56F as strikingly similar to those in 56A. The strikingly similar features were large nuclei, prominent nucleoli, spindle-shaped cells and parallel bands adjacent to cross sections.

Having considered both Professor Speight’s evidence and Ms Mishcon’s submissions I could detect no obvious error in Professor Sloan’s interpretation or conclusion which of course coincides with the conclusions which I have drawn on the evidence that the 2001 carcinoma is more likely to have been a recurrence that a new radiogenic primary.

Ms Mishcon relied on a number of submissions as to the improbability of there having been SPCC present in December 1996. I have already referred to some of them. One was the absence of both the two SPCC smoking guns, namely epithelial dysplasia or a focus of squamous cell carcinoma. This is of course a powerful point which I have weighed in the balance. It is not however a knockout blow. All of the experts agreed that one would normally expect to find evidence of either epithelial dysplasia or conventional squamous cell carcinoma in a biopsy when SPCC was present. Ellis and Corio state: “As a requirement for inclusion in this study, all cases showed either foci of squamous cell carcinoma or evidence of dysplasia of the mucosal epithelium.” Batsakis and Suarez state: “ Is the fact that not all candidate lesions for a diagnosis of sarcomatoid carcinoma demonstrate a detectable epithelial differentiation in the sarcomatous component a contraindication to the diagnosis? Not if elements of a squamous cell carcinoma are found or the spindle-cell elements exhibit cytomorphological evidence of malignancy, regardless of absent epithelial markers.”

Professor Speight said that although it is impossible to have SPCC without epithelial dysplasia or squamous cell carcinoma, it is possible in cases of extensive ulceration that neither would be seen on a microscopic examination. However he said that this was not the case in September 1995 or December 1996 as there was clearly visible epithelium, despite the ulceration. However Lucas states: “Areas showing the usual appearances of SCC [as distinct from epithelial dysplasia] may be … quite difficult to find” and Barnes states: “ The former component (SQC) is often small and elusive, requiring numerous sections for demonstration.” These latter comments in the literature are consistent with Professor Sloan’s opinion that a further and deeper biopsy would have revealed a focus or foci of squamous cell carcinoma. The bimorphic nature of SPCC means that different areas may have different morphology.

In addition both Professor Sloan and Professor Speight agreed that in the case of a deep recurrence of SQC as SPCC it is possible to have an SPCC without epithelial dysplasia or SQC. It is of course the Claimant’s case supported by Mr Brown, Dr Plowman, Professor Sloan and Dr Woolgar that Mrs Manning’s SPCC was a deep recurrence. All three pathology experts agreed in the joint report that it is possible that the spindle-cells seen in the December 1996 biopsy represent dormant malignant cells which may have emerged in 2001 although Professor Speight considered that to be highly unlikely and highly improbable.

Professor Speight accepted that a deep recurrence was a possibility in December 1996. He did not accept that it was a possibility in the September 1995 biopsy on the basis that both he and Dr Woolgar agreed that the base of that biopsy was composed of radiation fibrosis and damaged muscle whereas in the December 1996 biopsy the suspicious cells that all three experts saw were on the base of the biopsy. He did not suggest that even if for that reason there was no SPCC in the September 1995 biopsy there cannot have been SPCC in the December 1996 biopsy because he accepted that the exception to the normal requirement for epithelial dysplasia or foci of squamous cell carcinoma would still apply in December 1996 on the basis that an SPCC could have arisen in 1996 from cells left in the tissue after the RT in 1994. Moreover Professor Speight also accepted even in respect of the September 1995 biopsy that even if the suspicious cells were, as he thought, relatively superficial it was possible that there may also have been other malignant cells at a deeper level left behind after the RT, albeit he thought that very unlikely. The absence of evidence of in the December 1996 biopsy of epithelial dysplasia and foci of SQC does not either on its own or in combination with Ms Mishcon’s other submissions alter my conclusion that on the balance of probabilities SPCC was present in 1996.

I have given very careful consideration to the evidence and submissions as to the significance and weight to be attached to the absence in the December 1996 biopsy of evidence of either epithelial dysplasia or foci of SQC. I have of course taken it into account but neither on its own nor in combination with Ms Mishcon’s other submissions does it alter my conclusion that Professor Sloan was right in his diagnosis that SPCC was present in December 1996.

Another important submission of Ms Mishcon was that the natural inference to be drawn from the absence of positive CK staining is that there was no SPCC present in the December 1996 biopsy. This was another powerful argument in the Defendants’ favour. I have referred in the context of the breach of duty allegations to the significant false negative rate when SPCC does not stain positively despite being present. It was 35% in the cases studied by Lewis and Olsen, an average of 42% in the other studies summarised in a table in that paper and, although he criticised the latter, Professor Speight accepted that the false negative rate might be as high as 25%.

Of course the false negative rate has a different significance in the context of whether on the balance of probabilities SPCC was present in 1996 than in the context of whether it was negligent of Dr Harrison to make a definitive diagnosis of innocence in the face of such a rate. Taken in isolation from all other evidence and all other considerations a 75% true negative rate would point to the absence of SPCC in December 1996 (and for that matter in September 1995 where the suspicious cells did not stain positive for CK). However this is not the only piece of evidence. It is merely one part of a much larger jigsaw. It is possible that Mrs Manning had SPCC in December 1996 and that it happened to be one of the 25% of SPCCs which do not stain CK positive, just as it is theoretically possible that she had a new radiogenic carcinoma in early 2001 and that it was one of the 10% of new radiogenic primaries which present as a carcinoma rather than a sarcoma.

Ms Mishcon submitted that none of the main reasons for false negatives applied to either the September 1995 or December 1996 biopsies. Those were lack of epithelium in the specimen, loss of keratin markers in the tumour through de-differentiation and sampling error. In fact the Lewis and Olsen paper added a fourth which was insufficient sensitivity of detection methods including fixation and processing variables.

As to the first, she submitted that there was ample evidence of epithelium which stained positively thereby giving an internal control showing that the immunostaining had worked. While that is true, it is not a complete answer because it is possible that malignant cells of epithelial origin may have been present elsewhere in the tongue and would have been detected in a further biopsy.

As to the second, Ms Mishcon submitted that it could not apply because tumours become less differentiated and lose their markers as they grow and in February 2001 between 33 and 40% of the SPCC cells stained positively for CK. Mr Grace QC’s response to that submission was to submit that tumours do not always become more de-differentiated as time goes on. In support of this submission he prayed in aid the evidence of Dr Plowman that tumour cell populations are unstable with variable biology which may change over time and that cells in the same tumour can differentiate or de-differentiate in different ways. This was accepted in principle by Professor Speight. Doctor Plowman also said that a change in morphology from SQC to SPCC does not necessarily imply a change in differentiation and that tumours do not always de-differentiate. He also said that if the morphology of the cells was, as suggested by Professor Sloan and Dr Woolgar, the same in 2001 as in 1995 and 1996 the cells would not have been less differentiated in 2001 than in 1995 and 1996. This latter point did not strike me as a very good one since Professor Sloan’s evidence was more qualified. All three experts agreed that the scattered atypical lozenge or kite-shaped tumour cells in the September 2001 biopsy showed similar morphological features to those in the September 1995 and December 1996 biopsies. Professor Sloan and Dr Woolgar were of the view that they were the same cells. But I do not think that they went so far as to describe them as identical in appearance. In relation to the arrangements and in particular the interlacing bands Professor Sloan, although on one occasion describing the pattern as more prominent in an earlier biopsy than a later biopsy, elsewhere said that they were more pronounced in 2001 and 2002 which was to be expected given a process of de-differentiation. On the other hand both Professor Sloan and Dr Woolgar were of the view that many of the morphological features in the September 1995 and December 1996 biopsies were strikingly similar to those in the 2001 and 2002 biopsies.

Mr Grace QC also relied on the fact that only a small proportion of cells in any one tumour may stain positive for CK. He cited in support Batsakis and Suarez: “The percentage of cells coloured by cytokeratin entigen-antibody reactions has varied from 10% or less to more than 90%.” He also cited Lewis et al: “Staining for keratin often was focal” and on the following comment in Batsakis and Suarez: “ The spindle-cells in some tumours will show a pure epithelial differentiation, while those in other tumours will exhibit only a mesenchymal differentiation.”

As to sampling error it was of course Professor Sloan’s contention that the squamous cell carcinoma element would have been revealed in the part of Mrs Manning’s tongue that was not biopsied and that would not be inconsistent with the Batsakis and Suarez finding that in some cases only 10% of cells are coloured by cytokeratin reactions.

Mr Grace QC also relied on Dr Woolgar’s evidence in her report that SPCC cells can express both epithelial and mesenchymal (connective tissue) markers. “Cytokeratin expression can be demonstrated in the spindle-cells in 40 to 85% of cases (World Health Organisation Classification of Tumours, Pathology and Genetics Head and Neck Tumours 2005). The staining is often confined to sporadic cells within the tumour and the most useful epithelial markers are AE/1 to AE/3, CK/1,CK/18 and EMA. The spindle-cells express vimentin (and often other mesenchymal filaments) – with the result that the tumour is often uniformly strongly positive with vimentin (often thought of as a connective tissue marker) yet negative or only focally and weakly positive with epithelial markers. This can mislead an unwary pathologist.” He also relied on table 2 in the Lewis et al paper which showed 100% of the spindle-cells staining positive for vimentin (as did the 1996 biopsy) and the evidence of all three pathology experts that vimentin is not a reliable means of distinguishing fibroblasts from carcinoma in what I regarded as an effective answer to Ms Mishcon’s reliance on the positive vimentin staining in the December 1996 as pointing against SPCC.

Mr Grace QC also pointed out that different stains were used for the 1996 biopsies (CK/1 and CK/19 by Dr Harrison and AE/1 to 3 and MNF/116 by Dr Woolgar) to those used for 2001 (CAM 5.2.) Finally he relied on the fact that the islands in the archipelago stained positive in the 1996 biopsy and it is of course Professor Sloan’s evidence that they were malignant cells.

Taken all in all in my view the CK staining point is one of the stronger arguments pointing against the presence of SPCC in December 1996 (and also in September 1995). Nobody however suggested that it was a knockout blow and in my view it is far from being that.

Ms Mishcon relied on the clinical context of the December 1996 biopsy in that, unlike September 1995 when Professor Langdon was sure that she had a recurrence of carcinoma, he did not believe that to be the case. Against that December 1996 fell well within the period in which a recurrence could normally be expected. In addition Professor Sloan and Dr Woolgar pointed to the very strong inference to be drawn from the developing patterns to be found in the successive biopsies.

One of the many complications in this case has been the multiplicity of overlapping issues. I have sought to divide my analysis into two broad areas: the evidence on whether the 2001 primary was probably a recurrence or a new radiogenic primary and the question whether the factual and expert pathology evidence pointed to the presence of SPCC in the December 1996 biopsy. Although it is convenient and indeed essential for the purpose of clarity to analyse these two areas separately it is at some point necessary to draw the strands together. If the clinical and expert pathology evidence showed that there was no SPCC present in December 1996, the 2001 primary cannot have been a recurrence. If the 2001 carcinoma cannot have been a new radiogenic primary, there must have been SPCC present in December 1996. Absent certainty on either of these points, the evidence on both areas needs to be weighed together. In my judgment the factual and expert pathology evidence is far from showing that there was definitely no SPCC present in December 1996. In my view it shows on a balance of probabilities that SPCC was probably present in December 1996. Taken together with my finding that it was very unlikely that the 2001 primary was a new radiogenic primary in my view the factual and expert pathology evidence points on a clear balance of probabilities to the presence of SPCC in December 1996.

In the light of the unchallenged evidence of Dr Plowman, Professor Sloan and Dr Woolgar that if SPCC was present in December 1996 it would have been picked up in a further and deeper biopsy and having regard to all the relevant evidence I further find that if Professor Langdon had performed a further and deeper biopsy in December 1996 as I have already found he would probably have done but for Dr Harrison’s breach of duty of care, such a biopsy and/or any associated MRI scan would on the balance of probabilities have disclosed the existence of SPCC.

In that eventuality it was common ground that Professor Langdon would have performed salvage surgery and he gave evidence to that effect. On the 2^nd of November 2007 Ms Mishcon formally conceded on behalf of the Defendants that if SPCC (or indeed SQC) was present in December 1996 and had been diagnosed and treated Mrs Manning would on the balance of probabilities have survived. It follows that in my judgment the Claimant is entitled to recover from the Defendants damages for bereavement and dependency under the Fatal Accidents Act 1976, damages for the estate under the Law Reform (Miscellaneous Provisions) Act 1934 including damages for the pain and suffering and loss of amenities suffered by Mrs Manning during her lifetime, and interest on such loss and damage pursuant to statute as a result of Dr Harrison’s negligence in December 1996.

If I am right in my findings in relation to December 1996,both as to the proof of breaches of duty of care and as to causation, nothing material turns on the question whether there was cancer present in September 1995. However against the possibility that I may be wrong in either or both of those findings it is necessary to record my finding on the question whether cancer was also present in September 1995 since, if it was and if I am right in my findings that there were breaches of duty of care in September 1995,the overall result is the same and the wider claim to damages (i.e beyond those flowing from the admitted breaches of duty of care in 2001) succeeds.

Yet again there was a division of opinion between the experts: Professor Sloan and Dr Woolgar believed that on the balance of probabilities cancer was present, Professor Speight believed that it was not. Yet again Professor Sloan and Dr Woolgar accepted that in the absence of epithelial dysplasia and foci of SQC it was only possible to make a diagnosis with the benefit of hindsight and a comparison of the December 1996 biopsy slides with those that came later as well as those that came before.

As Ms Mishcon rightly pointed out one of the three suspicious features in the September 1995 biopsy on which Dr Woolgar originally based her conclusion was agreed at trial by all three experts to be innocent. That was the marked proliferation of the surface epithelium at the edge of the ulcer with epithelial processes appearing to be detached from the surface and almost blending with the granulation tissue. Professor Speight interpreted these as innocent epithelial cells migrating as part of the healing process. At trial Professor Sloan agreed in evidence in chief and Dr Woolgar accepted this in cross examination.

The two remaining suspicious features relied on by Professor Sloan and Dr Woolgar were the presence and arrangement of the spindle cells and the hypercellularity of the biopsy. All three experts agreed that these were suspicious features of the biopsy. Professor Speight said they were highly suspicious and in one sense even more suspicious than the December 1996 biopsy.

Professor Speight in his report referred to prominent plump polygonal and spindle cells with large open nuclei with prominent nucleoli scattered throughout the ulcer, squamous epithelium showing some evidence of atypia with prominent enlarged nuclei and suspicious pleomorphic cells scattered within the tissue. He said there were features suspicious for recurrent squamous cell carcinoma, although he concluded that the immunostaining(which had in fact not been done by Dr Harrison but were done for the trial) showed that the spindle cells were not epithelial, indicating that there was no evidence of malignancy within the biopsies.

Professor Sloan in his report said that in his opinion : “the first appearance of the SPCC is seen in the September 1995 biopsy, where there are bands of lozenge-shaped spindle cells. The diagnosis would have been difficult. The malignant cells are few in number and are in cords on the deeper aspect of the biopsy. The presence of radiation induced scar tissue tends to distract and contrasts with the typical straightforward diagnosis of carcinoma where the malignant cells tend to form abnormal sheets. It should be recognised that it is easier with hindsight, knowing the morphological features of the spindle-cell carcinoma in later specimens. Nevertheless a competent oral pathologist should be concerned about even small islands or cords of cells in a post radiation ulcer. In this situation the possibility of a recurrent carcinoma should be raised in the pathology report and deeper biopsies requested.”

Professor Sloan confirmed in evidence that that remained his view, adding that in hindsight he believed the lesion was part of an SPCC and that if Professor Langdon had taken a deeper biopsy it would probably have revealed spindle cells invading the deeper tissue and/or a focus of conventional squamous carcinoma.

Dr Woolgar in her report wrote that “The granulation tissue includes interlacing bands of plump cells which largely account for the "busyness" of the tissue at low magnification. The epithelial proliferation and the cellularity of the granulation tissue are worrisome…The increase in cellularity due to reactive benign fibroblast proliferation usually occurs soon after radiotherapy and hence, I would be uneasy in explaining this late increased cellularity as an innocent reaction to radiotherapy. I would have issued a report that clearly indicated the presence of worrisome features and my uncertainty in distinguishing reactive post-radiation features from possible neoplastic features, and I would have recommended a repeat biopsy if there was ongoing clinical concern or continued suspicion of malignancy…. I am less certain about Specimen 4: Slides 457/95, parts 1 and 2 (King's College Hospital; received 15 September 1995; reported 19 September 1995). With hindsight, I strongly suspect tumour is present (I am around 70-80% certain).”

Ms Mishcon pointed out that whereas Professor Sloan said that with the benefit of hindsight the malignant cells were scattered throughout the biopsy but there were more in cords on the deeper aspect, the evidence of Dr Woolgar and Professor Speight was that the suspicious spindle cells were in the granulation tissue. If there were no malignant cells on the deep aspect of the biopsy Professor Speight said that it would not have been possible for the putative cancer to have been a deep recurrence in which case any SPCC could not have come either from below or(because of the absence of epithelial dysplasia)from above. There seemed to me to be force in that point, although of course it depended for its force on the assumption that Professor Speight was right and Professor Sloan was wrong on whether there were suspicious cells on the deeper aspect. Ms Mishcon further submitted that the hypercellularity could be explicable as a reaction associated with a healing process due to the July 1995 biopsy.

Mr Grace QC pointed to the contrast between Professor Speight’s evidence in his report suggesting that the sheets of spindle cells were “quite consistent” with radiation fibroblasts and his evidence at trial that the suspicious cells were proliferating fibroblast as a result of a healing ulcer. He submitted that Professor Speight’s attempt to explain away the appearance of the suspicious cells as the result of a plane of sectioning effect was facile and unconvincing on the basis that there was no reason why the random sectioning of cells should render them innocent as opposed to malignant. Ms Mishcon’s response in her reply submissions was that Professor Speight had advanced a very good reason why the random sectioning of cells could make them innocent, namely that it made them appear pleomorphic when in reality they were not. This did not seem to me to address the sting of Mr Grace QC’s point, which was not that the random sectioning could not be the explanation of the pleomorphism but rather that there was no convincing evidence that it was in fact the explanation rather than the malignant one contended for by Professor Sloan having regard to the bands and the similarity with the 2001 biopsy.

Ultimately there were a number of factors which contributed to my conclusion that there was SPCC present in 1995.I refer to some of them, although inevitably an overall balancing process involves consideration of all the competing arguments and evidence. I was again persuaded by Professor Sloan’s evidence both as to what appears on the photos of the slides and as to what he saw more generally under the microscope and his interpretation thereof. I was persuaded by the strength of both Professor Sloan’s and Dr Woolgar’s conviction that the hypercellularity was greater than would have been expected even allowing for the July 1995 ulcer. I was persuaded by the same factor which they emphasised in relation to December 1996,namely the increasing pattern of cellularity between the successive biopsies, the unexpected contrast between those of May 1994 and those of September 1995 and December 1996 and the similarity between the features in the September 1995 biopsy with some of those in the later biopsies. I took into account my finding that there was SPCC present in December 1996 which to my mind would have added very considerably to the co-incidence factor were it to be the case that all the suspicious features in September 1995 were in fact innocent despite their similarity to features in what on my finding would be SPCC present in 1996 as well as in 2001-2002. I also took into account the clinical context. Although one aspect of that assisted the Defendants, namely the July 1995 ulcer as a possible innocent explanation for the fibroblasts, the background of Professor Langdon’s certainty that there was a recurrent carcinoma in September 1995 plainly helps the Claimants. I also took into account my finding that the 2001 carcinoma was a recurrent or persistent one and not a new radiogenic primary.

As in the case of my finding that there was cancer present in December 1996, in the light of the unchallenged evidence of Dr Plowman, Professor Sloan and Dr Woolgar to which I have referred in the context of causation in December 1996 and having regard to all the relevant evidence, I further find that if Professor Langdon had performed a further and deeper biopsy in September 1995 as I have already found he would probably have done but for Dr Harrison’s breach of duty of care, such a biopsy and/or any associated MRI scan would on the balance of probabilities have disclosed the existence of SPCC.

In that eventuality it was common ground that, as in December 1996, Professor Langdon would have performed salvage surgery and he gave evidence to that effect. As also mentioned above on 2^nd November 2007 Ms Mishcon formally conceded on behalf of the Defendants that if SPCC (or indeed SQC) was present in September1995 and had been diagnosed and treated Mrs Manning would on the balance of probabilities have survived. It follows that in my judgment the Claimant is entitled to recover from the Defendants damages for bereavement and dependency under the Fatal Accidents Act 1976, damages for the estate under the Law Reform (Miscellaneous Provisions) Act 1934 including damages for the pain and suffering and loss of amenities suffered by Mrs Manning during her lifetime, and interest on such loss and damage pursuant to statute as a result of Dr Harrison’s negligence in September 1995.

I referred at an early part of this judgment to the admission of the Defendants that due to the breaches of duty of care on the part of Dr Harrison and Professor Johnson in respect of the February, June and August 2001 biopsies the diagnosis of Mrs Manning’s cancer, which should have been in February 2001, was avoidably delayed until September 2001. In those circumstances it is not necessary for me to make detailed findings in relation to the allegations of negligence against Professor Johnson and Dr Harrison in respect of 2001 since the effect of the admissions is that the Claimant is entitled to all such damages as flow from the fact of that delay. As mentioned earlier the main head of those damages is in respect of the appalling and avoidable pain and suffering that Mrs Manning suffered as a result of the delay in diagnosis. It does not include the damages flowing from the fact that she ultimately died of the cancer since it was accepted by the Claimant that even with a diagnosis in February 2001 there would have been a less than 50% chance of her having survived.