David John Saunders v Central Manchester University Hospitals NHS Foundation Trust

The Claimant seeks damages for personal injury and consequential losses arising out of alleged clinical negligence during surgery to reverse an ileostomy at Trafford General Hospital in March 2012.

Shortly after that surgery, the Claimant became seriously unwell and it was discovered that his entire colon was ischaemic. The colon had to be removed. As a result, the Claimant now has a permanent ileostomy. He has suffered other unpleasant consequences including protracted infection of the rectal stump and the need for further surgery. Unsurprisingly, this has impacted on many aspects of his life and has caused the Claimant much distress. It is the Claimant’s case that the surgery was negligently performed resulting in damage to the blood supply to the bowel.

The Defendant denies liability, contending that the damage was done by a naturally occurring blood clot.

The parties are agreed that these are the only realistic explanations for the damage to the Claimant’s bowel although each one represents a very rare occurrence. I must therefore decide which is the more likely, considering all the evidence I have heard.

The claim was originally listed before me for trial in relation to liability and quantum. However, recent developments in the Claimant’s condition caused the parties to agree that quantum could not sensibly be determined at this stage. I also note that a secondary allegation made by the Claimant in relation to the management of the rectal stump was abandoned after the surgeon, Mr Mazarelo, had given his evidence. I am therefore only considering the issue of liability in relation to the primary allegation of surgical negligence.

The Claimant was aged 60 at the time of his surgery in 2012. He first came under the care of Mr Felix Mazarelo, a consultant colorectal surgeon, in 2010 when he was diagnosed with a rectal tumour. Following radiotherapy, the tumour was excised and the end of the rectum was joined to the side of the sigmoid colon. That type of anastomosis (join) carries a significant leak rate. Therefore, a defunctioning loop ileostomy was performed to divert the faeces into a bag until the anastomosis had healed. The intention was to reverse the ileostomy once it was established that healing had occurred and that there was no evidence of leakage. Like most patients, that was what the Claimant wanted.

The Claimant’s medical history included a myocardial infarction in 2006 and ischaemic heart disease. He had smoked for many years. He had high cholesterol and suffered from hypertension.

Mr Mazarelo was an experienced surgeon. He qualified in 1973 and was appointed to his consultant post with the Defendant in 2001. He told me that he conducted all aspects of the surgery to reverse the ileostomy himself.

The surgery took place on 20^th March 2012. Mr Mazarelo said that it was entirely straightforward. This is reflected by the short operation note made by Mr Mazarelo. There is nothing within the Claimant’s notes to suggest that there had been any complications and he was returned to the ward, the operation having seemingly gone as expected.

Post-operatively, the Claimant appeared to be recovering well. The notes suggest that he was mobile, eating and drinking and passing urine. He had opened his bowels. All his observations were entirely normal. He was discharged from hospital on Friday 23^rd March.

The Claimant subsequently became very unwell. By the early hours of Sunday 25^th March, he was sufficiently ill that his wife called an ambulance. On arrival at hospital he was in a shocked state with evidence of severe sepsis. He was resuscitated with intra-venous fluids, antibiotics and oxygen. Mr Mazarelo then carried out an emergency laparotomy. He described the Claimant as being at death’s door.

Fortunately, the Claimant survived the emergency surgery. There is no dispute that the large bowel was entirely ischaemic and had to be removed. A further ileostomy was fashioned. The Claimant was initially cared for on ITU. Eventually, he could be discharged from hospital, but he suffered recurrent problems which I do not need to go into at this stage.

Naturally, the Claimant has no direct knowledge of what happened during the surgery on 20^th March 2012. His case is that iatrogenic damage (damage caused by the surgery) is the only realistic and plausible explanation for the findings from the emergency laparotomy on 25^th March. The allegation is that injury was caused to a branch of the superior mesenteric artery which was the main artery supplying the blood the bowel. It is contended that such was caused by the application of excessive traction or torsion during the ileostomy reversal. Such an injury would not have happened without a lack of proper care on the surgeon’s part. Therefore, it amounts to a breach of duty.

The Defendant denies that damage was done during the surgery. The Defendant’s case is that the necrosis of the bowel was caused by vascular occlusion as a result of an acute arterial thrombosis, probably related to pre-existing atherosclerotic disease. This was not related to the surgery but was a naturally occurring mesenteric infarction, similar to a myocardial infarction, although much rarer.

Mr Mazzag’s written closing submissions began by acknowledging that:

“The Claimant bears the burden of proof throughout. It is accepted that the Defendant does not have to prove anything.”

The Claimant must prove both that damage occurred during the surgery and that such damage resulted from a lack of proper care on the part of the surgeon.

In considering the factual issue as to whether damage was done during surgery or through natural causes, care must be taken not to resort too readily to the burden of proof. In Barnett v Medway NHS Foundation Trust [2017] EWCA Civ 235, the Court of Appeal reviewed the authorities in the context of factual causation in a clinical negligence action, citing Verlander v Devon Waste Management [2017] EWCA Civ 835. I have in mind that, as Auld LJ stated at paragraph 19 of that case:

“a judge should only resort to the burden of proof where he is unable to resolve an issue of fact or facts after he has unsuccessfully attempted to do so by examination and evaluation of the evidence.”

Further (paragraph 24 of Verlander):

“such resort is only necessary where on the available evidence, conflicting and/or uncertain and/or falling short of proof, there is nothing left but to conclude that the claimant has not proved his case. The burden of proof remains part of our law and practice – and a respectable and useful part at that – where a tribunal cannot on the state of the evidence before it rationally decide one way or the other.”

The Claimant has not asserted that the principle res ipsa loquitur applies in this case. A useful summary of the approach to cases such as this where a patient suffers injury under general anaesthetic and so cannot give evidence as to what actually happened and usually cannot call any factual witnesses to support his case is to be found in O’Connor v The Pennine Acute Hospitals NHS Trust [2015] EWCA Civ 1244. At paragraph 60, Jackson LJ said:

“More recent authority has tended to the view that res ipsa loquitur is not a principle of law at all. There is no reversal of the burden of proof. The so-called res ipsa loquitur cases are merely cases in which, on the totality of the evidence, the court was able to make a finding of negligence. It has always been the position that courts can make findings of fact by means of inference when there is no direct evidence of the events in issue.”

He then cited with approval the principles summarised by Brooke LJ in Ratcliffe v Torbay Health Authority [1998] PIQC P170. I will not set out that summary again here but have had regard to it.

I note too the reference to Thomas v Curley [2013] EWCA Civ 117. In that case, the claimant suffered an injury to her bile duct during an uncomplicated operation. The expert witnesses offered various possible mechanisms by which the injury may have been caused. None of these was consistent with the exercise of proper skill and care. In the absence of any satisfactory explanation from the defendant’s expert or from any other quarter, the judge was entitled to conclude from all the evidence that negligence had been proved.

Applying these authorities to the facts of this case, I must first seek to resolve the factual issue as to whether the damage was done during surgery or as a result of a naturally occurring blood clot. In doing so, I recognise that I am choosing between two rare events but that they are considered to be the only plausible explanations. I must therefore examine and evaluate all the available evidence to see which is the more likely.

If I conclude that injury occurred during the surgery, I may be able to draw an inference that it was the result of a lack of proper skill and care on the surgeon’s part. However, this is not a foregone conclusion. I will bear in mind that the experts agree that this was a straightforward procedure and that Mr Burgess has not put forward any mechanism by which surgical damage could have resulted despite the exercise of reasonable skill and care. The Claimant is not necessarily required to prove the exact mechanism of injury. It may be enough to show that there are a number of possible explanations but that none are consistent with the exercise of proper skill and care. However, I must stand back and look at all the evidence to assess whether the Claimant has proved, on the balance of probabilities, that his injury was caused by surgical negligence.

I also note that, on the facts of this case, consideration of the mechanism of injury is relevant when evaluating the likelihood of the competing explanations for the damage. Therefore, there is an overlap between the issue of factual causation and breach of duty and it is not possible to wholly divorce consideration of one from the other.

I heard evidence from the Claimant and his wife, Angela Saunders. As might be expected, much of the evidence in their statements went to quantum rather than liability. Given the way that the trial developed and the narrowing of issues, Mrs Saunders’ evidence can be put to one side.

The timing of the onset of symptoms is of significance. The Claimant’s statement contained the short assertion “Soon after discharge I began to feel more unwell.” Mr Mazzag asked for permission to introduce some further detail. I allowed that on the basis that the evidence was first put into writing. This produced a three-page handwritten statement. This important issue clearly should have been addressed in advance. However, Mr Eccles was able to cross-examine the Claimant by reference to the medical notes. The Claimant struck me as an entirely honest witness, doing his very best to give a truthful and accurate account. The combination of the notes and his evidence gave me a good evidential picture of the Claimant’s condition between the operation on 20^th March and his readmission on 25^th March and I am satisfied that the late admission of additional evidence from the Claimant did not prejudice either party.

The Defendant called Mr Mazarelo. He was able to give direct evidence as to the surgery on 20^th March and his findings on 25^th March. Mr Mazarelo had provided two statements dated 23^rd March 2017 and 22^nd December 2017. The second statement was prepared after receipt of the experts’ joint statement. It dealt with an important feature in the case, namely the findings on 25^th March. It is of relevance when considering the expert evidence to know whether the blood supply to the terminal ileum (part of the small bowel) was compromised. Therefore, whether there was necrosis in this area in addition to the colon is of significance.

In his first statement, Mr Mazarelo had said that when he carried out the laparotomy on 25^th March:

“The entire colon was found to be ischaemic. The colon and 19cm of small bowel was found to be dead.”

He attached to his statement various extracts from the medical notes, including a pathology report dated 31^st March 2012. The result was recorded as being signed off by him on 1^st April 2012. That report was seemingly consistent with what Mr Mazarelo said in his statement. However, the second statement claimed that it was an error to say that the 19cm of small bowel was found to be dead. He said that the last 19cm of small bowel was not ‘dead’. The entire colon was. He explained that the terminal part of the small bowel was removed as it incorporated the site of the ileostomy reversal and he did not want to leave that in situ.

Mr Mazarelo was cross-examined extensively on this issue. He told me that when he operated he did not think the small bowel looked dead. That was not the reason he removed it. However, he did accept the pathology report which he had signed and, on that basis, accepted the 19cm was not viable. He distinguished between something that is macroscopically necrotic – as the colon was here – and something which is not obviously abnormal to the naked eye but is abnormal under a microscope. Having accepted that the pathology report was accurate, he conceded that this meant that his first statement was accurate. He did though stand by the clarification in his second statement that the portion of small bowel was not removed because it looked ‘dead’ but because he wanted to remove the site of the ileostomy reversal, as leaving it would risk further complications.

I thought that Mr Mazarelo gave his evidence in an entirely straightforward way. He was not evasive at all. He gave considered answers to questions. In his closing submissions, Mr Mazzag described Mr Mazarelo as a “careless witness; adamant he was right when he was wrong; and a confusing and confused witness.” I do not agree at all. My impression was that he was generally careful and was willing to make concessions as appropriate. I clearly have to analyse his evidence very carefully and to take account of the apparent discrepancy in his statements. However, I certainly do not dismiss him as a generally unreliable witness. Like the Claimant, I regarded him as truthful witness, doing his best to assist the court.

I heard all the non-expert witnesses on the first day. The following morning, Mr Eccles told me that further enquiries had suggested that additional evidence may be available casting doubt on the contents of the pathology report. I allowed the parties some time to discuss the position. Mr Eccles then produced some written evidence which he sought permission to rely upon. He accepted that admitting it would inevitably lead to the trial being adjourned. The Defendant’s position was that this was important evidence as it would wholly undermine the Claimant’s case. He also sought permission to amend the Defence.

The attempt to introduce this further evidence came far too late. The experts had proceeded on the basis that the pathology report was correct and had each given their (differing) opinions on that basis. All the non-expert witnesses had given their evidence. Mr Mazarelo had accepted the contents of the pathology report on oath. I considered it much too late for the Defendant to seek to wholly change the nature of their case. In the circumstances, I refused the Defendant’s application and I did not read the evidence.

Some concern was ventilated in the course of the application about the fact that Mr Eccles had revealed the nature of the additional evidence he wished to admit and whether that would have a prejudicial effect on the trial. In the event, I do not believe it caused any particular difficulty when the experts were giving their evidence. It is certainly not something that has played any part in my consideration of the evidence. I must decide the case on the evidence that is before me. I have the pathology report and I have Mr Mazarelo’s confirmation that it was accurate. I proceed on the basis that the contents of the pathology report are correct.

Each party called an eminently qualified expert in colorectal surgery. Mr Savvas Papagrigoriadis was instructed on behalf of the Claimant and Mr Phillip Burgess for the Defendant. The experts agreed that an acute arterial occlusion had occurred. However, they differed as to the likely cause of the occlusion. Mr Papagrigoriadis favoured an iatrogenic cause whereas Mr Burgess thought the likely explanation was a naturally occurring thrombus.

Naturally, each party asked me to prefer the evidence of their expert. Both Counsel contrasted the experts, and each invited me to say that theirs was more impressive. The reality is that the two experts had very different styles. Mr Burgess was robust but at times appeared unwilling to reflect on alternative viewpoints. Mr Papagrigoriadis was more reflective but was sometimes a little vague. Neither approach was particularly unusual. Each had its advantages and disadvantages. Resolving the issues arising out of the expert evidence requires detailed analysis and cannot depend on a stylistic impression of who was the ‘better’ expert.

Both experts provided clear reports that were easy to read; thorough and attractively presented with useful diagrams attached. However, their joint statement was disappointing. It was 60 pages long and did not fulfil the purpose identified in CPR 35PD 9.2 “to agree and narrow issues”. It seemed to me that the difficulty may have arisen not through the fault of the experts but through the way in which the agendas were drafted. I say “agendas” because, for reasons not explained to me, there had apparently been two separate agendas that the experts were required to consider. Both involved repetitive questions for the experts and far from producing a focus on the real issues, the result was a document that served only to confuse rather than assist.

I can see no good reason why the parties were unable to agree a single agenda in this case. Perhaps greater input from Counsel may have assisted. The joint statement is an important document. It ought to be possible to read it and to understand the key issues and each expert’s position on those issues. Sometimes less is more as far as the agenda is concerned. Parties should adopt a common sense and collaborative approach rather than allowing this stage of the litigation to become a battleground. Frankly, the approach to the joint statement in this case achieved nothing of value.

The fundamental question in this case is whether the necrosis of the Claimant’s colon was caused by iatrogenic damage or by a naturally occurring thrombus. Consideration of the following points assists in determining the issue:

From a lay perspective, it is fair to say that there appears to be a temporal link between the surgery and the injury. Five days after the operation, the Claimant was critically unwell.

Mr Papagrigoriadis relies upon this close connection in time as an important feature in support of iatrogenic damage. He told me that if he were looking at this case in the context of a clinical governance review, he would start from the position that something must have happened in the surgery. He said that the picture is of a man going in for intermediate severity surgery, going out and 36 hours later he is very unwell. Superficially, at least, it is attractive to think that there must be a connection. However, Mr Burgess suggested that had the Claimant sustained damage to the blood supply of the bowel during the operation, the effects would have been apparent much sooner and certainly before his discharge from hospital on 23^rd March.

The medical and nursing notes reveal nothing untoward during the post-operative period and up to discharge. By the time he was discharged, he had been eating and drinking; he was passing urine normally; he had opened his bowels and was described as fully mobile. All his observations were entirely normal. Two sets of observations were recorded on 23^rd March. The first was timed at 7.00 a.m.; no time has been recorded for the second set, but they must have been taken some time later and before the Claimant was discharged.

The Claimant agreed that he had been progressing well up to the morning of 23^rd March. His recollection was that he did not feel as well by the afternoon when he was discharged. He said that he felt weak and left hospital in a wheelchair and that he felt worse than he had the day before. However, he was frank in accepting that his recollection was a little vague. He also agreed that, at the time, he felt as he expected to after surgery, although now with hindsight he regards that as the time when he began to become unwell.

The Claimant was clear that he was feeling rough when he went to bed on Saturday 24^th March. He was sufficiently unwell that his wife called an ambulance at around 3 to 4 a.m. The ambulance records note a 5-day history of feeling generally unwell, weak and dizzy. On admission at A & E a history was given of him being unwell for 5 days post-op. It was then said that he had been generally unwell the past few days, was dizzy and had “poor oral intake”. The Claimant agreed his wife must have given this history. I bear in mind that she did so while her husband was critically ill. There seems to be some confusion between when the Claimant had his surgery and when he became unwell.

My interpretation of all the records and the Claimant’s evidence is that he had displayed no abnormal symptoms up until his discharge. He felt somewhat worse when he was home but initially his symptoms were as he expected after surgery and following reduction in his pain medication. However, his condition deteriorated on Saturday 24^th March and he was noticeably unwell when he went to bed that night. He continued to deteriorate and was critically ill when admitted to hospital on the Sunday morning.

Mr Burgess’s evidence was that an occlusive event causing infarction of the bowel would usually result in the rapid onset of symptoms with the patient becoming critically unwell within 6 to 12 hours.

Mr Papagrigoriadis appeared to accept that an acute event causing complete obstruction would be likely to produce symptoms within hours. However, he considered that the onset of symptoms could be delayed if damage caused by twisting or partial tearing produced a “pseudoaneurysm” or if damage to a vein produced a haematoma inside the mesentery which expanded and caused compression of the artery later. In the joint statement, he suggested that

“this is not likely to have been a complete obstruction which occurred in one moment but a gradual process which evolved during the next 24 hours”.

He further suggested that the bowel would have been paralysed in the hours immediately after the operation and that it would not be surprising to see symptoms only developing as the patient began eating, drinking and passing bowel movements. In the joint statement, he suggested that the bowel would mobilise over 48 to 72 hours post-surgery.

Having considered the evidence of both experts, I find that although the onset of symptoms was superficially close in time to the surgery, the timing does not fit with an acute event during the surgery causing immediate arterial occlusion. There was no sign of an evolving problem up until the Claimant’s discharge. He had been eating and drinking and had opened his bowels by then. I cannot say that the delay in onset was so great as to exclude iatrogenic damage. However, I do consider that the symptoms came on later than would have been expected if the artery had been occluded at the time of the surgery. Four days had passed before the Claimant became significantly unwell. Even taking account of Mr Papagrigoriadis’s evidence as to bowel immobilisation, it seems that the onset of symptoms due to iatrogenic injury would usually have been expected to have occurred earlier.

An understanding of the anatomy of the region is necessary when looking at the nature of the damage suffered by the Claimant.

I was provided with some helpful anatomical diagrams of the colon and its blood supply. It is important to bear in mind that, like many things in life, anatomy is not a precise science. Every human being is different and will display natural variations. What the surgeon sees when operating on the abdomen is very different from the neat diagrams in the textbooks.

During the trial, it emerged that there was some dispute between the two experts as to the ‘normal’ anatomy of the blood supply to the bowel. At first blush, it was surprising that two experts from the same discipline had differing views on this. However, I have come to the conclusion that this simply reflects natural variability. Mr Burgess told me that the anatomy of this region can be “tremendously variable”. I note that the various diagrams produced all had subtle differences. In their joint statement, the experts agreed:

“The exact distribution of blood supply and contribution to each part of the bowel is variable and reliant on collaterals.”

In my judgment, care must be taken not to be too dogmatic about the circulation of the blood supplying the bowel.

The Claimant’s blood supply to the left of his colon had been affected by his cancer surgery in 2011. The inferior mesenteric artery was divided so that he had lost the supply from the branches on that side. The left colon was therefore dependent on the marginal artery of Drummond. The branches on the right side, including the middle colic, the right colic and the ileocolic remained. The body can adapt so that the Claimant could manage without his inferior mesenteric artery. Mr Burgess suggested that there would probably have been a physiological response with the middle colic artery becoming more substantial to compensate for the loss of the inferior mesenteric artery.

In the body, the blood vessels are not all distinctly visible but are embedded in a fatty envelope of tissue. In the Claimant’s case it is known that his mesentery was short. This was noted by Mr Mazarelo at the emergency surgery on 25^th March. When he tried to fashion the new ileostomy on the left side the bowel looked ischaemic, so he put it to the right instead. Mr Papagrigoriadis postulated that the Claimant’s anatomy was such that it was easy to do damage. He suggested that just a small amount of pulling would be detrimental in a patient with a short mesentery.

The Claimant had a parastomal hernia which was repaired at the time of the surgery on 20^th March. He is also likely to have had some adhesions as a result of his previous surgery.

Mr Burgess maintains that the site of the occlusion was anatomically remote from the operative field. In their joint statement, the experts agreed that the anatomical position of the colon is relatively fixed. In comparison the small bowel is usually very mobile, and several feet can easily be brought out through the small incision used during closure of a loop ileostomy. Mr Burgess says that it is important to appreciate that the middle colic artery and the marginal artery of Drummond are remote from the site of the surgery on the ileum.

Mr Papagrigoriadis agrees that the area of damage was outside the immediate area of the surgery but points to literature which indicates that injuries can occur at remote locations. He agreed that there are no reports in the literature of iatrogenic damage during ileostomy reversal causing total failure of the large bowel. However, he said that the marginal artery of Drummond is known to be particularly vulnerable to damage.

An important part of the reasoning underpinning Mr Papagrigoriadis’s opinion is the extent and distribution of the damage. According to the pathology report, there was ischaemic necrosis affecting the large bowel and the terminal ileum.

I accept that Mr Mazarelo’s recollection of his findings at the emergency surgery on 25^th March were truthful and accurate. He told me that the operation stuck in his mind as he thought he was going to lose his patient. I accept that. I thought he was entirely forthright in what he said about the operation and in his acceptance of the pathology report. I therefore proceed on the basis that the colon was visibly ‘dead’ but that the necrosis of the terminal ileum was not apparent until microscopically examined.

Mr Papagrigoriadis is firmly of the view that damage could only have occurred to the entire colon and the terminal ileum if the marginal artery of Drummond became occluded. Had there been a clot to the superior mesenteric artery, the whole of the small bowel would have been affected and the Claimant would not have survived. Had there been a clot to any one of the three vessels on the right – the middle colic, the right colic and the ileocolic – that would not have been sufficient to produce the extensive damage seen. Although he accepted that nothing is impossible in medicine, Mr Papagrigoriadis did not think a spontaneous thrombus could account for occlusion of the marginal artery of Drummond. He described the marginal artery of Drummond as the “safety valve to survive ischaemic events” and said that he had never seen a spontaneous clot there in clinical practice or in the reported literature.

It is known that the middle colic artery was pulseless at the surgery on 25^th March. Occlusion of this artery alone would not cause damage to the terminal ileum which is supplied by the ileocolic artery.

Mr Burgess was of the view that the middle colic artery was probably the main source of the blood supply to the Claimant’s colon and that interruption of that would result in colonic infarction on both right and left sides. He accepted that this would not explain all the damage but said that the clot may propagate as the bowel infarcts. Infarction causes associated inflammatory reaction and there will be an inexorable progression with damage becoming more widespread over a number of hours. He also suggested that the changes shown under the microscope may have resulted from loss of vascularity when the portion of ileum was resected. He did not accept that damage to the terminal ileum excluded a naturally occurring thrombus.

Mr Mazzag suggested that Mr Burgess only introduced the concept of the clot propagating at a late stage to explain the damage to the terminal ileum which otherwise would not fit with his theory. However, it appeared to me that this was just a one of a range of possible explanations. Mr Burgess had consistently expressed the opinion that the injury was caused by a natural thrombus although he had taken the damage to the distal part of the small bowel into account.

I consider that the pattern of damage lends some support to the Claimant’s case but that it is not decisive. The evidence of both experts leads me to the view that it is impossible to be precise about how damage will develop. Having accepted Mr Mazarelo’s evidence as to his findings on 25^th March, I believe that the necrosis was more established in the colon than the terminal ileum fitting with a progressive situation where damage became more widespread over a number of hours. I also note that Mr Papagrigoriadis told me that by the time of the emergency surgery on 25^th March the dead bowel would have altered the mesentery so much with generalised oedema that it may have been difficult to notice a haematoma or other signs of damage. That would also seem to fit with a pattern of extensive damage regardless of precisely where the occlusion started.

It is agreed that the Claimant was at an increased risk of thrombotic events. He had atherosclerotic disease and had suffered a myocardial infarction in 2006. He was a smoker and had hypertension and high cholesterol. However, there was no evidence of atherosclerotic disease in the aorta or superior mesenteric artery being identified on scans either before or since 2012. Mr Papagrigoriadis thought it unlikely that there would be an atherosclerotic occlusion of the middle colic artery without some evidence of changes in the aorta or superior mesenteric artery.

The risk of suffering a spontaneous mesenteric event is low, about 1 per 100,000 of the population. Only about 20 to 30% of these cases result from thrombotic occlusion at the site of a previous atherosclerotic stricture. More cases result from embolic occlusion. The Claimant did not, however, have any predisposing factors putting him at an increased risk of embolism. Although the Claimant’s risk of suffering a thrombotic mesenteric occlusion was increased, I bear in mind that it remained a tiny risk.

The experts agreed in their joint statement that any operative procedure carries some risk of arterial occlusion because of change in blood flow, atherosclerosis or embolism. Mr Burgess accepted that the operation on 20^th March would not have increased the risk significantly although it could go some way to explaining the coincidence of a clot occurring soon after the surgery.

I conclude that the Claimant was at a slightly increased risk of a natural thrombotic event compared to the general population but that his risk could still be considered to be very low indeed.

The Claimant can offer no clear explanation as to what happened in the course of the surgery to damage the bowel. The only direct evidence about the operation came from Mr Mazarelo. He described the procedure and said that it was not a difficult operation. He did all steps himself. He strongly refuted the suggestion that he had used excessive traction. There was no unusual twisting or anything that might have damaged a vein. In short, he could not see that he had done anything that might have caused an injury.

I have already said that I found Mr Mazarelo to be a generally careful witness. Although there was an apparent discrepancy in his evidence about whether it was an error to say that the 19 cm of terminal ileum was dead, I did not regard that as indicative of any general lack of care. I accept the explanation he gave in the witness box that his first statement had been drafted by reference to the pathology report but that it had not been apparent to him at the time that the portion of the ileum was dead and that is not why he removed it. Although quite a lot of his cross-examination centred on this, in the end I thought that it was a peripheral point and it did not undermine Mr Mazarelo’s credibility.

I accept that Mr Mazarelo did not notice anything unusual or have any reason to think any damage had been done at the time of the surgery on 20^th March. Mr Papagrigoriadis suggested that there had been an unrecognised injury and said that it was perfectly possible for damage to be done without the surgeon ever being aware of it.

It is also to be noted that there was no sign of mesenteric injury or haematoma at the time of the emergency surgery on 25^th March.

Mr Papagrigoriadis readily accepted that he had started from the position that something must have happened during the surgery and had then asked what was likely to have happened. His approach was based upon the injury being close in time and location to the operation site. He had not found any other explanation that could account for the damage and therefore concluded that it had to be iatrogenic. This was not a recognised complication of surgery. He had looked at the literature and it had never been reported previously. The fact that damage had happened therefore indicated that Mr Mazarelo had fallen below the standard of care to be expected.

Mr Papagrigoriadis found it much more difficult to explain what Mr Mazarelo was likely to have done wrong. He said it would be presumptuous to say what had happened. He suggested various possibilities, including accidental incision of a vessel but then indicated that was not proposed here. He appeared to settle on either excessive tension or twisting. He said twisting might occur in trying to divide adhesions and could happen without the surgeon even being aware of the adhesions. Alternatively, the Claimant’s short mesentery may have made it easier to damage through pulling.

Mr Papagrigoriadis’s attempts to explain how damage could be done without the surgeon being aware of it did raise questions as to whether iatrogenic damage would necessarily evidence a lack of proper care. He relied on the possibility that adhesions or the unusually short mesentery had played a part. However, when then pressed as to whether, if that was the case, the injury would provide evidence of Mr Mazarelo doing anything wrong he was vague and then reverted to saying that such damage was not a recognised complication.

Mr Papagrigoriadis said that he had never seen a spontaneous clot of the marginal artery of Drummond but that it was known to be vulnerable to damage. During re-examination he suggested that all surgeons had done damage in that area. He said: “usually you recognise and correct it”. I asked him whether he was saying that the negligence was in not detecting the damage rather than causing it, if that was something all surgeons had done. His response as not entirely clear. At one point, Mr Papagrigoriadis said that he was not saying Mr Mazarelo had done anything wrong, that was for the court to determine, but the fact of the injury caused him to maintain that something had gone wrong during the surgery.

Mr Burgess told me that he could not understand how traction or twisting during an ileostomy could result in catastrophic failure of the blood supply to the colon. He said that the procedure required mobilisation of only a small segment of the small bowel. The site being operated on was anatomically distant from the marginal artery of Drummond. He accepted that traction injuries could occur but could not comprehend that pulling on the small bowel could damage the blood supply to the colon to the extent that it was totally compromised without the surgeon noticing anything had happened.

This is a difficult case. The Claimant’s case is that the only plausible explanation for the damage to his colon and terminal ileum was surgical error. The Defendant contends that a natural thrombotic event shortly after the surgery is more likely. Both explanations represent extremely rare occurrences. It is agreed that neither has previously been described in medical literature. There have been no reported cases of mesenteric infarction occurring as a natural complication of an ileostomy closure. Equally, there have been no reported cases of iatrogenic injury to the marginal artery of Drummond during such surgery.

The Claimant has no way of knowing what actually happened during the surgery and his expert, Mr Papagrigoriadis, has not, in my judgment, offered a clear explanation of the likely mechanism of surgical injury, although he offers a number of possibilities. He relies upon the coincidence of the damage being sustained shortly after the ileostomy surgery and says, in essence, that something must have happened.

Analysis of the expert evidence as to aetiology by reference to the pattern of damage, the proximal relationship to the surgery and the Claimant’s anatomy and past medical history does not produce a clear answer. There are factors pointing both ways.

I consider that the pattern of damage provides some support for the Claimant’s case but that the temporal link is less clear. The delayed presentation suggests that the arterial supply was not directly occluded at the time of the operation. Mr Papagrigoriadis’s theory depends upon the subsequent expansion of a haematoma or other gradual process evolving in the hours and days after the surgery, when it is known that the Claimant was well with no abnormal observations up to his discharge on 23^rd March. The timing is such that, even based on Mr Papagrigoriadis’s opinion, it is at the very margin of what might be considered a temporal connection. I consider that a delay of four days before the onset of significant symptoms suggests that very real care must be taken not to assume that the injury is related to the surgery. I would regard the delayed onset as providing some support for the Defendant’s case.

I have summarised key aspects of the experts’ evidence but have, of course, taken the totality of their evidence into account. I have carefully reviewed all the expert reports, the joint statement and the medical literature provided, in addition to considering the experts’ oral evidence.

I am not able to conclusively exclude the possibility of either of these rare events by reference to the expert evidence alone.

I must then stand back and ask whether the Claimant has proved his case that the damage was caused by surgical negligence on a balance of probabilities.

The real difficulty for the Claimant is the absence of a clear explanation of the likely mechanism of injury during surgery which was anatomically remote from the site of injury. In my judgment, Mr Papagrigoriadis’s evidence on this was somewhat vague and shifting. He admitted that he was starting from the position that something must have happened. He offered various possible explanations, but it was clear he found the mechanism difficult to explain. He settled on the likely cause being excessive traction. Having heard Mr Mazarelo’s evidence, he suggested it may have been an assistant rather than Mr Mazarelo himself who was to blame. However, Mr Mazarelo said that he performed all the steps himself.

During cross-examination, Mr Papagrigoriadis postulated that the Claimant’s anatomy was such that it was easy to do damage. He suggested that the presence of adhesions and/or the short mesentery may have been a contributory factor. However, he still found it very difficult to say what Mr Mazarelo was likely to have done wrong.

I am conscious of the difficulty facing the Claimant in explaining a surgical injury while he was under anaesthetic. I recognise the need for care in evaluating the evidence of Mr Mazarelo. I accept that even the most experienced surgeon can make mistakes and that injury could occur without him recognising that he had done anything wrong.

However, I do have clear evidence from Mr Mazarelo, which I accept, that nothing unusual happened in the operation and that it was an entirely straightforward procedure. He could not see how he could have damaged the marginal artery of Drummond during a normal ileostomy reversal. Neither could the Defendant’s expert, Mr Burgess.

The effect of the expert evidence is that there are two competing explanations, namely surgical injury or natural causes. Neither has previously been reported in the medical literature as a complication causing catastrophic injury to the colon following an ileostomy reversal. However, it is agreed that no other plausible explanations exist.

I am not persuaded that the occurrence of a spontaneous thrombotic event can be excluded on the basis of the expert evidence. When I then put the evidence of Mr Mazarelo into the balance, it is difficult to see how surgical damage occurred. Mr Papagrigoriadis’s evidence did not persuade me that any of the postulated mechanisms of injury were in fact likely to have occurred during the surgery described to me by Mr Mazarelo.

In those circumstances, I am not satisfied that the Claimant has established, on a balance of probabilities, that his injury resulted from surgical damage.

Even if I had been persuaded it was more likely than not that damage occurred during surgery, Mr Papagrigoriadis suggested that the Claimant’s anatomy may have been such that it was particularly easy for damage to be done. He was not clear as to how, in those circumstances, it could be said that the damage resulted from Mr Mazarelo doing something wrong such that he could be said to have fallen below the standard to be expected of a reasonably competent surgeon.

On the basis of all the evidence before me, the Claimant has not established that his injury was caused by negligence on the part of Mr Mazarelo.

This claim therefore fails and must be dismissed.