Buxton v Abertawe Bro Morgannwg University Local Health Board

The claimant in this action, Mr. Matthew Buxton, was born on 17 October 1982, so he is now aged 27 years. He suffers from short-sight and started to wear spectacles in his childhood to correct that defect in his vision. From his teenage years he started to wear contact lenses in place of spectacles.

Mr. Buxton studied computer science at Swansea University. Since graduating he has been employed as a computer software developer.

In September 2005 Mr. Buxton was living in Cardiff. However, he had obtained a job in Swansea, which he was due to commence on 26 September.

On 19 September 2005 Mr. Buxton found that his right eye was red and painful and he found it difficult to open the eye. He consulted an optician, who referred him at once to Cardiff Eye Clinic (“the Clinic”) at the University Hospital of Wales. The notes of the diagnosis made and treatment advised on that occasion were put in evidence at this trial. As they were somewhat difficult both to read and to interpret, without assistance, it is convenient to quote the transcription, including the aids to interpretation, set out by Mr. Nicholas Phelps Brown, a consultant ophthalmologist instructed on behalf of Mr. Buxton, in his report dated 8 June 2008:

“19.9.05: “Referral from Optometrist – Asda Opticians – Red (R[ight]) eye – large patch keratitis – had it for last 2 x w[ee]ks

– No improvement – Diagnosis (Rt) healing dendritic ulcer (RT) HSV [herpes simplex virus keratitis) – Treatment Oc [ointment] Zovirax 5x/day – g [eyedrops] cyclopentolate [pupil relaxing eyedrops] 1% bd [twice daily] g Keterolac [nonsteroidal anti-inflammatory] – Follow up 1 week Eye Casualty”

19.9.05: “PC [present complaint] Red R[igh]t Eye – HPC [history of present complaint] onset 2/52 [2 weeks] ago – P[atien]t woke with red tender R[ight]E[ye] – C[ontact]L[ens] wearer – been on CPL [chloramphenicol = antibiotic eye drop]

– PMH [past medical history] Hx [history] of cold sores. -” The right visual acuity was 6/24 [25%] improving to 6/12 [50%] with a pinhole. The left visual acuity was 6/4 [100%+]. The diagram of the right eye shows a typical dendritic ulcer across the central area of the cornea. The anterior chamber showed cells +.”

Mr. Buxton was advised to return to the Clinic a week later. What was then found was recorded in a letter of referral from the Clinic to Singleton Hospital, Swansea (“the Hospital”) dated 26 September 2005, also transcribed, in part, with some interpretative comments, by Mr. Phelps Brown in his report:

What all of this means Mr. Phelps Brown explained in his report:-

“5.1

Herpes simplex virus (HSV) is the virus causing the common cold sore. When it affects the cornea [the transparent front element of the eye], it produces surface ulceration called dendritic ulceration. This is so called because it produces a branching pattern. The dendritic pattern is highly characteristic of Herpes simplex corneal ulceration and leads to confident diagnosis of this condition. However, the dendritic pattern is occasionally mimicked by some other causes of keratitis. The ulceration is initially confined to the surface where it represents a breakdown in the continuity of the surface epithelium [the transparent skin of the cornea].

5.2

The symptoms of herpetic corneal ulceration are pain, watering, blurred vision, photophobia [light sensitivity] and eye redness. The patient often has a history of a previous event.”

However, as Mr. Phelps Brown went on to explain in his report, dendritic ulceration was not the only possible consequence of herpes simplex virus (“the Virus”) affecting the eye:-

“5.3

Herpes virus keratitis [corneal inflammation] is potentially very damaging. The corneal ulceration is associated with a varying degree of inflammation of the anterior segment of the eye. There may be stromal keratitis [inflammation of the corneal substance] or uveitis [inflammation of the pigmented parts of the eye]. The virus invasion of the stroma is evidenced by the beginning of white cellular infiltration along the line of the dendritic ulcer and it may then spread more extensively in the corneal stroma. It may affect the central area of the cornea with an immune response producing a characteristic circular ring infiltrate called disciform keratitis. The corneal sensation becomes reduced. The uveitis is characterised by the deposition of inflammatory cells on the corneal endothelium [the back surface of the cornea], by inflammatory cells and by protein flare in the anterior chamber of the eye. There may be a sufficient accumulation of cells to cause a hypopyon [layer of pus]. The white of the globe of the eye is inflamed.”

Mr. Phelps Brown then considered in his report the appropriate treatment of herpes virus keratitis:-

“5.4

The treatment of Herpes virus keratitis [corneal ulceration and inflammation] is with antiviral agents, of which the most effective is Aciclovir (Zovirax). This is usually given in ointment form and may additionally be given orally when there is corneal stromal involvement. Ganciclovir may also be given systemically. It is also usual to give a pupil relaxing eye drop such as Cyclopentolate. An antibiotic eyedrop may be added if it is considered that there may be secondary bacterial infection. Zovirax ointment is somewhat toxic to the eye and may cause punctuate epithelial keratopathy. When this occurs, the clinician will wish to reduce the Zovirax treatment, provided that the corneal condition is being controlled.

5.5

Anti-inflammatory agents may also be needed when the corneal stroma is affected or if there is uveitis. The antiinflammatory agents that are most effective in suppressing the inflammation are corticosteroid eye drops, but the corticosteroid eye drops carry the risk of initiating or of aggravating herpetic corneal ulceration. Corticosteroid eye drops vary in their power to treat inflammatory conditions. The more powerful corticosteroid eye drops also have the greater tendency to aggravate the herpetic condition. They also have a tendency to increase intraocular pressure. Pred Forte [a strong prednisolone eye drop] is the most powerful corticosteroid eye drop. The use of corticosteroids in herpetic eye disease needs to be covered by the use of the antiviral agent Zovirax.

5.6

Topical corticosteroids should never be used in the treatment of dendritic ulcers (Oxford Textbook of Ophthalmology Vol. 1 eds Easty and Sparrow, Oxford University Press 1999 p426) and should not be given until the ulceration is healed. Corticosteroids may then be given in the treatment of stromal disease “Do not use potent steroids in the treatment of stromal disease if possible; instead try to use the minimal dosage of steroid that will achieve control of the inflammation. – Where full strength, or dilutions of topical corticosteroids are applied, an antiviral ‘umbrella’ should be used simultaneously (Oxford Textbook Vol. 1 p427).

5.7

The non-steroidal anti-inflammatory eye drops such as Keterolac do not carry the risk of aggravating the herpetic ulceration, nor the risk of raising the ocular pressure, but are less effective in suppressing corneal inflammation.”

In simple terms, therefore, the Virus attacking the eye may cause dendritic ulceration, or stromal keratitis (of which a particular type is disciform keratitis), or uveitis, also called iritis, or any combination of these. The most effective means of tackling stromal keratitis is by use of corticosteroid eye drops. The most powerful such eye drops is Prednisolone Forte. However, the use of corticosteroids can damage the eye if dendritic ulceration has not healed at the time of application. The reason was explained in Oxford Textbook of Ophthamology, Vol. 1, (“the Oxford Book”) at page 426:-

“Topical corticosteroid should never be used to treat dendritic ulcers because the virus can replicate freely in the presence of steroid-induced local immunosuppression, leading to enlargement of the ulcer.”

Consequently, if dentritic ulceration and stromal keratitis were both present in an eye a decision would have to be made as to how to treat each condition, given the risk of exacerbating the dentritic ulceration if the most effective means of combating the stromal keratitis were adopted to cope with that condition.

On the occasion of his attendance at the Clinic on 26 September 2005 Mr. Buxton was advised not to work for a week, but to make contact with the Hospital as soon as possible. He told me in cross-examination that he accepted the advice not to work for a week, and he made contact with the Hospital the next day, 27 September 2005.

The authority responsible for the Hospital was Swansea NHS Trust (“the Trust”). The defendant in this action, Abertawe Bro Morgannwg University Local Health Board, is the statutory successor to the Trust, via Abertawe Bro Morgannwg University NHS Trust.

Mr. Buxton attended at the Hospital at about 6.30 on the evening of 27 September 2005. There he saw a lady doctor, Dr. Tan. Dr. Tan did not give evidence in this action and all that is known of how she assessed the condition of Mr. Buxton’s right eye prior to prescribing is what she set out in the notes which she made, which again Mr. Phelps Brown transcribed in his report:-

“4.4

27.9.05: The right visual acuity was 6/12+2 [60%] improving to 6/9 [67%] with a pinhole. “ – Painful red RE approximately 3/52 [for 3 weeks] - Cardiff 19.9.05 Dendritic ulcer g oflox [ofloxacillin = antibiotic] added 26.9.05 for infiltrates – pt felt eye getting worse following 2 job interviews

– photophobia, pain ++, blurring, headache, - ”

4.5

The examination of the right eye showed “v photophobic to examine – florid injection [eye redness]. The diagram of the cornea shows a hatched in area below the centre which may represent epithelial ulceration or stromal infiltration. “faint outline of dendritic c [with] small dots of epith [epithelial] defect along dendritic of subepith infiltrates. The anterior chamber showed “cells +”. The right ocular pressure was 22 and the left 20 [normal range 10-21]. “Imp [impression] (R) Disciform keratitis c healing dendritic c iritis – Plan G Acyclovir [Acyclovir = Zovirax] 5x day – G cyclopentolate 1% bd – G predforte – see 1/52 [in a week].”

Dr. Tan therefore prescribed, and Mr. Buxton started to use, Prednisolone Forte.

How matters developed thereafter was revealed by the notes made in the Hospital, which Mr. Phelps Brown transcribed, but which Mr. Jeffrey Hillman, a consultant ophthalmic surgeon instructed on behalf of the defendant, summarised in his report dated 31 July 2009 prepared for the purposes of this action:

“3.6

He was reviewed on 2^nd October 2005 when he was complaining of increased pain and significantly reduced vision since the previous day. On examination visual acuities were recorded as Count Fingers right eye and 6/5 left eye. A clear diagram illustrates a very injected red eye with a hazy cornea and a round central corneal lesion measuring 4 mm in vertical diameter and 4.2 mm in horizontal diameter described as “dense central ulcer/infiltrate. no obvious perineuritis.

↓corneal sensation. ?early ring infiltrate. (not typically geographic)”. Intraocular pressure was recorded as 20 mm and there was no view of the fundus. The possible differential diagnosis was recorded as “1. ? worsening HSK due to topical steroids. *2. acanthamoeba keratitis * - chronic course, c/l wearer. ring infiltrates. 3 2◦ bacterial infection of HSK”.

3.7

The management plan was for corneal scrape for diagnostic material and a note was made that it was not possible to culture the contact lens as it had been discarded by the patient. After discussion with a Mr. Rathod treatment was started with hourly preservative-free Gentamicin and Cefuroxime (antibiotic) drops together with oral Acyclovir.

3.8

He was reviewed at 2.15 p.m. on 2^nd October 2005 and a note made that the right corneal sensation was slightly reduced compared with the left but was still present. The central corneal lesion was measured as 4 mm x 4 mm with a note “epith defect, … illegible … infiltrates …”. A diagnosis was made of right disciform keratitis with a sick endothelium and secondary bacterial infection. Treatment was continued with Cefuroxime and Gentamicin intensive antibiotic drops and Cyclopentolate (pupil-dilating) drops and oral Acyclovir. A note timed at 17:20 hrs reported that no organisms had been seen on initial examination of the corneal specimens.

3.9

When reviewed on 3^rd October 2005 right vision was recorded as Count Fingers with a note that he felt that vision had improved. The right eye was noted to be very injected with a round central epithelial defect with infiltration. He was reviewed later the same day by the specialist registrar who again recorded the round central area of epithelial defect and corneal infiltration with reduced sensation and a few inflammatory cells in the anterior chamber.

3.10

A third examination was recorded on 3rd October 2005 (untimed) with a diagram showing a wavy edge of epithelium hopefully advancing over and healing the epithelial defect. A small hypopyon (less than 1 mm) was noted. Treatment was continued as before.

3.11

When reviewed on 4^th October 2005 at 9.00 a.m. he was noted to be more comfortable with the epithelial defect shown on the diagram as much smaller and about 20% of the previous size. A note was made that the appearance appeared to be improving intensive Cefuroxime and Gentamicin hourly antibiotics were continued by day only and the other medication was continued.

3.12

When reviewed on 4^th October 2005 the corneal epithelial defect was noted to have healed further with an amoeboid shape and stromal haze over the previously inflamed round area. Treatment was continued.

3.13

On 5^th October 2005 visual acuities were recorded as 6/24 (improving to 6/12+1 on pinhole test) right eye and 6/4 left eye. He was noted to be feeling better and the eye looked less injected. The round inflamed area is shown on a diagram with one or two small epithelial defects and a note was made that there was no hypopyon. The intensive antibiotics were reduced to two hourly by day. When reviewed later that day by the specialist registrar a note was made that the central corneal infiltration was less and there were no epithelial defects and the anterior chamber was quiet with a few keratic precipitates. Plans were made for discharge on treatment.

3.14

He was reviewed on 7^th October 2005 when the central inflamed area was noted to present a hazy stroma which was clearing with clear surrounding cornea and quiet anterior chamber. He was discharged home on two hourly antibiotic drops by day and Acyclovir ointment five times daily with the Cyclopentolate 1% drops restarted.

3.15

He was reviewed on 10^th October 2005 when right vision was recorded as 6/12, improving to 6/9-2 on pinhole test. The eye was noted to be less injected with scattered punctuate epithelial erosions over the central corneal area. The drops were reduced to four times daily.

3.16

When reviewed on 14^th October 2005 right vision was recorded as 6/24, improving to 6/12-1 on pinhole test. The right eye was assessed as unchanged and treatment supplemented with Celluvisc lubricant drops.

3.17

On 17th October 2005 a note was made that he had no pain. A clear diagram illustrates the abnormal central corneal area which presented no epithelial defects but some white opacities. Treatment was changed to Ofloxacin (antibiotic) drops with Acyclovir (anti-viral) ointment.

3.18

When reviewed on 24th October 2005 he was noted to feel better but with vision worse without the dilating drops. Right vision was recorded as Count Fingers. The central corneal opacification was noted to be less intense and he was noted to have some blepharitis. The Ofloxacin was discontinued and treatment continued with an ointment which I cannot read and Acyclovir ointment five times daily.

3.19

At review on 31^st October 2005 the infiltrate was noted to be less and treatment was continued. On 1^st November 2005 right vision was recorded as 6/36+1 with glasses improving to 6/12 on pinhole test. Central corneal haze was noted with no ulceration. Treatment was continued with Ganciclovir five times daily.

3.20

When reviewed on 9^th December 2005 right vision was recorded as 6/12 improving to 6/9 on pinhole test. Central corneal scarring was noted and a three week reducing dosage of Ganciclovir was prescribed.

3.21

When reviewed on 10^th February 2006 right vision was recorded as 6/18+2 improving to 6/9+2 on pinhole test and he was noted to be symptom free. A diagram illustrates right central corneal scarring with no active ulceration. At that consultation he was discharged with the offer to return to the eye casualty in any emergency.”

While it perhaps does not emerge clearly from that summary, Mr. Buxton was detained in hospital between 2 and 10 October 2005. On 17 October 2005 he resumed the employment which he began on 26 September 2005, but in which he had thus far only worked half a day.

It was common ground that, following the prescription of Prednisolone Forte by Dr. Tan, and the use of that medicament by Mr. Buxton between 27 September 2005 and 2 October 2005, he was found, on 2 October 2005 to be suffering from an epithelial ulceration of his right eye. The cause of that ulceration was in dispute between the parties. The case for Mr. Buxton was that the cause was the use of Prednisolone Forte at a time when the dendritic ulcer already diagnosed had not healed. On behalf of the defendant, on the other hand, it was contended that the cause was stromal keratitis. I shall return to the evidence relevant to the cause of the ulceration found on 2 October 2005.

The consequences for Mr. Buxton, after treatment, of the ulceration found on 2 October 2005 was one of the matters addressed in a joint statement (“the Joint Statement”) produced by Mr. Phelps Brown and Mr. Hillman for the purposes of this action as to those matters in which they were in agreement and those matters about which they disagreed.

In the Joint Statement Mr. Phelps Brown and Mr. Hillman answered questions 8, 9 and 10 (the nature of the questions emerging from the answers given) as follows:-

“8.

When Mr. Hillman examined the Claimant on 16^th January 2008 he measured visual acuity with contact lenses as 6/24 right eye and 6/6 left eye. With a suitable over refraction spectacle lens right vision improved to 6/12 (equivalent to 80% of normal visual acuity). When Mr. Phelps Brown examined the Claimant on 4^th June 2008 he found visual acuities of Right eye 6/18 (equivalent to 67% of normal visual acuity) and Left eye 6/6 corrected by contact lens with no improvement on over refraction. We are agreed of the clinical findings of a feint round scar in the superficial central cornea.

We are agreed that the corneal scarring will cause a degree of glare to direct bright lights e.g. in night driving and we would agree that this will give a reduced contrast of images. In the absence of the aggravated ulcer we would expect a lesser degree of corneal scarring with a lesser degree of glare and improved contrast sensitivity.

We are agreed that in the absence of exacerbation of the ulcer, the probability is of a visual acuity outcome of the order of 6/9 (equivalent to 91% of normal visual acuity) with less corneal scarring.

9.

We are agreed that there is a risk of recurrence of herpes simplex corneal ulceration, which has not been altered by the management.

10.

We are agreed that the Claimant will require medical treatment if and when a corneal ulcer recurs. We are agreed that an annual review by an optometrist is indicated, but this is not changed by the medical treatment.”

Mr. Phelps Brown agreed in cross-examination that the difference between his measurement of the visual acuity of Mr. Buxton’s right eye and the measurement of Mr. Hillman was such as one might expect of testing on a separate occasion, as it amounted to the ability to read one line more or less of the standard optician’s eye chart.

Mr. Buxton explained in his witness statement prepared for the purposes of this action the consequences for him of his right eye being in the condition in which it is:

“24.

I am no longer attending medical appointments but I have been left with a permanent reduction in the sight of my right eye and glaring of lights at night. Having the sight in my right eye has affected me at home as well but I just get on with it. I have had accidents where I have dropped things on the floor because my sight is not good.

25.

I have learned to live with it and have adapted to using mainly my left eye. Whenever I watch the television I get a headache as my left eye compensates for my right. When I drive at night time I find that the lights glare quite badly and this is disorientating. Therefore, I try to avoid driving at night as the glare is quite distracting. Driving during the day is now fine.

26.

In general terms, the symptoms I have been suffering from since my discharge from hospital are a considerable lack of vision in my right eye. It is hazy and blurry vision and I cannot make out objects at a distance and cannot read or write very well with my right eye at any distance. I also suffer from glare from light sources. At no point was I advised not to use my contact lenses, but, in any event, I did not do so.

27.

These symptoms have had a combined affect [sic] on me. As well as the physical symptoms, I get very frustrated and annoyed and depressed due to the complications with my vision. I am not, however, on any specific medication. I do take painkillers to help me with the migraines associated with my lack of vision when they are severe.

....

29.

When I returned to work, I struggled to read the computer screens. My right eye would not open fully and my left eye became strained and tired as it was compensating for the right eye. The first month or so back at work was extremely difficult for me. As my right eye still had issues opening fully I felt immensely tired all through the day and having to concentrate for a long period of time was very difficult. I remember we had some (all day) training when I first joined and trying to look at a projector screen for a long period of time was really hard and very tiring, I was practically falling asleep in them as I could not concentrate (which obviously did not look good).

30.

My work revolves around computers and staring at monitors for lengthy periods of time. This gives me migraines due to the lack of vision in my right eye and with my left eye over compensating for this. This slows my work down as I cannot work continuously for extended periods of time. The headaches also cause me nausea from time to time.

....

32.

In terms of my hobbies, my snooker and pool playing is affected. Whilst I still can play these games recreationally, my relative lack of vision hinders my play. I am also no longer able to undertake gymnastics as I used to because I need good vision in both eyes for my balancing, spotting landing points and the other aspects which I am sure will be clear to anyone who has watched gymnastics on the television. I also find going to the cinema or watching TV for any period of time much more difficult than I used to as I swiftly get headaches after doing so.

33.

I used to go to the gym 3 or 4 times per week and go swimming. In the first few weeks after I was discharged from hospital I could not do this because my eye was still infectious. I remember that all my office equipment had to be cleaned as well to prevent infection. I am able to go to the gym and swim now as the virus has cleared up.

34.

I only take painkillers for my migraines and headaches if they are severe. This is because I do not want to rely on painkillers for the rest of my life. I suffer from both anxiety and depression. The depression is because of my lack of vision and the anxiety is because I was worried about my potential job loss. I have not had any professional counselling but I have relied on support from my family and friends for this.”

In his oral evidence Mr. Buxton explained that he gets slight double vision, with a sort of blurred copy of what he is seeing overlain on a clear view. He said that he got headaches every day, and that he sometimes bumped into a door frame. At work he had to take breaks from looking at a monitor screen to deal with headaches or nausea. However, relatively short breaks, of five minutes or so, seemed to be sufficient to deal with the onset of headaches or nausea.

Mr. Buxton claimed damages in this action against the defendant, as the statutory successor to the Trust, for the alleged negligence of Dr. Tan in prescribing Prednisolone Forte at a time when the dendritic ulceration in Mr. Buxton’s right eye had not healed. That, essentially, was the issue relevant to liability in this action.

The position adopted on behalf of the defendant was that, as at 27 September 2005, Mr. Buxton’s right eye was sufficiently healed for it to be a matter of clinical judgment whether to prescribe Prednisolone Forte, and it could not be said that, in the circumstances, the prescription of Prednisolone Forte was negligent, or, using the language which the defendant seemed to prefer, “substandard”.

In the result there were, it seemed, two matters upon which the question whether the defendant was liable in damages to Mr. Buxton depended. The first was what, as a matter of fact, was the condition of Mr. Buxton’s right eye on 27 September 2005 when Dr. Tan saw him and prescribed Prednisolone Forte. The second was whether, given that condition, no reasonably competent ophthalmologist would have prescribed Prednisolone Forte, or any other corticosteroid. It was no part of the case for Mr. Buxton at the trial that, if it was otherwise appropriate for a corticosteroid to be prescribed, Prednisolone Forte should not have been prescribed, because it was too strong. It is necessary to make that point because both Mr. Phelps Brown and Mr. Hillman agreed in the Joint Statement, in answer to question 6, that, if they had been considering prescribing a corticosteroid to treat stromal keratitis, they would have prescribed a “weaker” one in preference to a “stronger” one.

As I have explained, the evidence as to what was the condition of Mr. Buxton as at 27 September 2005 was really to be found only in the medical notes. Mr. Buxton himself gave evidence as to his perception of how he was, but, while I accept without reservation the evidence of Mr. Buxton, by whom I was very impressed, he does not profess any medical qualification, and his own account of how he was feeling is not of much assistance on the critical points of the condition of the dendritic ulcer from which he was at that time suffering in his right eye or the development of stromal keratitis in that eye.

The notes made at the Clinic on 19 September 2005 recorded that the dendritic ulcer in Mr. Buxton’s right eye was then “healing”. However, the eye was red, and the prescription of the non-steroidal anti-inflammatory Keterolac indicated, according to the evidence of Mr. Hillman in cross-examination, that there were signs of stromal keratitis, but the prescribing doctor considered that it was not then appropriate to prescribe a steroidal anti-inflammatory.

What was found at the Clinic on 26 September 2005 was noted in the letter dated that day, from which I have quoted. There was a degree of inconsistency in what was recorded. The text of the letter included, “on examination his dendritic ulcer had healed but there was [sic] 2 areas of round Epithelial defects with microinfiltrate”. A diagram included in the letter showed an eye with “healing/improving dendritic ulcer” and two “ED with microinfiltrate”. It is tempting to conclude that what the author of the letter meant to convey was that the dendritic ulcer had healed, apart from two epithelial defects with microinfiltrates. It seems unlikely that the author would have used the word “healed” in the main text unless he or she thought that the ulcer was close to achieving that condition, but the diagram was differently marked. The use of the words, “but there was 2 areas of round Epithelial defects with microinfiltrate” after the word “healed” in the main text suggests that that form of words was intended as a qualification to the statement that the ulcer had healed. There was no other indication in the letter of a respect in which the dendritic ulcer had not healed.

The interpretation which I have placed upon the letter dated 26 September 2005 appears to be consistent with the note made by Dr. Tan about 27 ½ hours later at the Hospital, “faint outline of dendritic c small dots of epith defect along dendritic of subepith infiltrates”. She recorded her impression of a right eye with “Disciform keratitis c healing dendritic c iritis”. She thus diagnosed Mr. Buxton’s eye as suffering from those three pathologies.

I was invited by both parties to treat the observations of Dr. Tan made on 27 September 2005 as accurate, so far as they went.

It is, I think, material to note what was observed when Mr. Buxton was next seen at the Hospital, on 2 October 2005. As transcribed and interpreted by Mr. Phelps Brown what was recorded on that occasion was:-

“ “– on g Cyclo [cyclopentolate] – Oc ACV [Aciclovir] – g Pred Forte – g Ciloxan [antibiotic] 2 – Now increased pain since yesterday – much reduced vision”. The right visual acuity was CFs [counts fingers]. The eye was “injected +++ - Hazy cornea throughout Dense central ulcer/infiltrate – No obvious perineuritis [inflammation characteristic of acanthamoeba keratitis] – reduced corneal sensation -?early ring infiltrate – (not typically geographic) – Imp – 1 ?Worsening HSK [herpes stromal keratitis] due to topical steroids. 2. Acanthamoeba keratitis – chronic course C/L wear ring infiltrate. 3 2 [secondary] Bacterial infection of HSK”. The diagram shows the central 4 mm of the cornea affected by ulceration. “Plan – Scrapes – Gram stain – Wet specimen – Conj swab - ”. He was admitted: “Imp (R) Disciform keratitis > sick endothelium + secondary bacterial infect – Plan g Cef [cefuroxime = antibiotic] g Gent [gentamicin = antibiotic] g Cyclo [cyclopentolate pupil relaxing] ACV [oral Acyclovir] 400 m 5x day – Gram stain – No organisms seen 0 pus.”

Those notes did not make any reference in terms to a dendritic ulcer.

In the result I find that, when Mr. Buxton saw Dr. Tan on 27 September 2005 at the Hospital he had a dendritic ulcer on his right eye which had healed save for small dots of epithelial defect along the dendritic ulcer of sub-epithelial infiltrates. The presence of those dots meant, as I think was common ground between Mr. Phelps Brown and Mr. Hillman, that strictly the dendritic ulcer had not healed. I was invited by Mr. Timothy Meakin, who appeared on behalf of Mr. Buxton, to make findings as to whether the ulcer was “active”, by which I think that he meant whether viral replication was taking place. The evidence put before me does not enable me to reach any conclusion on that issue. The fact that the ulcer had, on my findings, almost healed showed at least that Mr. Buxton’s body was winning the battle against the Virus at that point, but it is not possible to conclude simply from the progress of healing, that viral replication was not taking place. It was suggested at one point in cross-examination that the fact that the process of healing had not completed indicated that the Virus was still active. I am not sure that that follows, although it was, perhaps, possible that there was still some life in the Virus. However, for reasons to which I shall come, I do not think that actually it mattered, so far as liability was concerned, whether the Virus was active or not as at 27 September 2005.

The evidence of Mr. Phelps Brown was that no reasonably competent ophthalmologist could have prescribed a corticosteroid for stromal keratitis if the affected eye was also affected by a dendritic ulcer. Mr. Hillman took a different view. His position was that, in a patient suffering both from a dendritic ulcer and stromal keratitis, it was a matter of judgment whether to concentrate upon the ulcer or the stromal keratitis, and a matter of judgment by what means to treat whichever condition it was resolved to treat. The principal relevant factors in making the decision were, in no particular order, the fact that prescription of corticosteroid to combat the stromal keratitis exposed the dendritic ulcer to the risk of exacerbation as the virus would be free to replicate in a local environment of immuno-suppression; the fact that there were nonsteroid anti-inflammatories available with which to combat the stromal keratitis; the fact that the most effective means of combating stromal keratitis was by use of corticosteroids; and the fact the risk of serious damage to sight is greater with stromal keratitis than with a dendritic ulcer.

In the Joint Statement Mr. Phelps Brown and Mr. Hillman set out their views as to what a reasonably competent ophthalmologist should have done when confronted with the disease from which Mr. Buxton was suffering as at 27 September 2005 in this way:

“We are in agreement with regard to the treatment up to the 27^th September 2005. We agree that it is appropriate to prescribe steroids to treat underlying disciform keratitis at the point at which a herpes simplex dendritic corneal ulcer is healed. Our disagreement is with regard to the interpretation of the notes entry “feint outline of dendritic c small dots of epith defect along dendritic + subepith infiltrates”. Mr. Phelps Brown points out the recorded diagnosis of “R disciform keratitis c healing dendritic c iritis”. On the basis of this Mr. Phelps Brown interprets the notes as indicating that whilst the dendritic ulcer was “healing” it had not at that stage “healed”. Mr. Phelps Brown expresses the opinion that the ulcer should not be regarded as healed until there is complete epithelial healing of the ulcer itself. Mr. Hillman bases his opinion on the record of clinical findings as described above and interprets this as showing that there were dots of epithelium along the line of the previous ulcer which were staining with diagnostic Fluorescein stain and in those areas the epithelium had not healed. However, he interprets this as indicating that the ulcer (as opposed to the epithelium) had healed sufficiently to allow the use of steroid drops.”

As matters turned out, it was unfortunate that Mr. Hillman used the expression “healed sufficiently” in answering question 1 in the Joint Statement, mirroring the use of that expression, and similar expressions, in his report. The use of these expressions led to misunderstanding which occupied quite a lot of time at the trial. Mr. Hillman was asked in cross-examination to define the words “healed sufficiently”. He was also asked to contrast that formulation with other expressions used in his report, in particular “not completely healed”, “not fully healed” and “almost healed”. I am satisfied, having heard the evidence of Mr. Hillman, that the point which he was seeking to make was that, in his opinion, the degree to which the dendritic ulcer had healed when Dr. Tan saw it on 27 September 2005 was such that a reasonably competent ophthalmologist could have decided that the balance of the various risks which I have mentioned was tipped in favour of tackling the stromal keratitis by the most effective means of combating that condition. He was not seeking to say, for example, that when a dendritic ulcer was 80% healed, or 90% healed, a reasonably competent ophthalmologist could decide to prescribe corticosteroids for a stromal keratitis which was also present. He was simply pointing out that, as the healing of the dendritic ulcer proceeded, there would come a time when the balance of risk passed from being tipped in favour of avoiding the possibility of encouraging the Virus to continue its attack on the dendritic ulcer to being tipped in favour of grappling the stromal keratitis as effectively as possible. I do not think that actually Mr. Phelps Brown differed from the concept. His view was that that balance did not tip until the dendritic ulcer was completely healed, and that no reasonably competent ophthalmologist could have thought otherwise in September 2005.

Another diversion from a consideration of the real issues in this action which was encountered in the course of the trial was emphasis on the concept of “clinical judgment”. From time to time during the hearing that phrase seemed to have acquired the status of a panacea. It excused all. If a matter was one of “clinical judgment”, it was irreproachable. That prompted the attack on the concept that it was immaterial to the circumstances of the present action because, so it was contended, it was clear beyond peradventure that no reasonably competent ophthalmologist could possibly have considered that it was appropriate to prescribe corticosteroids at a time at which there was a dendritic ulcer which was not completely healed.

However, again on analysis the difference between the parties was nothing like as extreme as appeared. In the end I think that it was accepted on behalf of Mr. Buxton, as logically it had to be, that any decision of a doctor to prescribe treatment (or actually to take no action), following a diagnosis involved an exercise in clinical judgment. The criticism was not of the fact of the exercise of clinical judgment, but of the particular judgment made by Dr. Tan. That emerged most clearly in paragraph 18 of the written closing submissions of Mr. Meakin, where he set out, in effect, the case of Mr. Buxton as to what judgment Dr. Tan ought to have made.

In the end, therefore, the point upon which liability turned in this action was a very narrow one, whether, as Mr. Phelps Brown contended, no reasonably competent ophthalmologist could have decided on 27 September 2005, in the light of the agreed fact that the dendritic ulcer in Mr. Buxton’s right eye had not healed completely, that it was appropriate to prescribe corticosteroids for the stromal keratitis.

One might have thought that, if matters were as clear, from a medical perspective, as Mr. Phelps Brown contended, that had, perhaps, been noted in appropriate medical literature. However, that did not appear to be the case. Mr. Phelps Brown relied, in relation to medical literature, simply on the Oxford Book. The material passages were at page 426 and at page 427:-

“(page 426)

Treatment The objective of treatment is to inhibit viral replication and at the same time reduce the inflammatory and immune reaction in the stroma, which, if ignored can lead to lasting damage to stromal collagen fibrils. Topical corticosteroid should never be used to treat dendritic ulcers because the virus can replicate freely in the presence of steroid-induced local immunosuppression, leading to enlargement of the ulcer. Such ulcers are known as amoeboid or geographic because of diffuse viral spread both within the epithelium and to the stroma.

(page 427)

Indications for antiviral use Antivirals must be used in the treatment of primary herpes simplex keratitis, in association with systemic acyclovir where there is a significant mucocutaneous or facial eruption. As dendritic ulceration may act as a portal of entry for bacteria and not uncommonly cause a secondary bacterial abscess, an adjunctive topical antibiotic is advisable.

In recurrent disease, antivirals should be used prophylactically where the trigger factors are known. Patients with frequent recurrences should have a topical antiviral available to instil immediately they become symptomatic, and should be advised to seek medical advice as soon as possible.

Treatment of stromal disease requires careful management. The presence of active inflammation must be recognized and documented. Do not use potent steroids in the treatment of stromal disease if possible; instead try to use the minimal dosage of steroid that will achieve control of the inflammation. Always taper down a potent steroid through lesser dilutions to avoid rebound of inflammation. Where full-strength, or dilutions of, topical corticosteroid are applied, an antiviral ‘umbrella’ should be used simultaneously. Since this may be for long periods, antivirals with low toxicity should be employed.”

Those passages did not support the view of Mr. Phelps Brown. All one could really derive from the reference on page 426 was that topical corticosteroid should not be used to treat dendritic ulcers. That was not in dispute before me. Dr. Tan had not prescribed Prednisolone Forte to treat Mr. Buxton’s dendritic ulcer, but to treat his stromal keratitis. The principal message of the passage on page 427 relevant to the present case was that, when using steroids to combat stromal keratitis, one should use the lowest strength of steroid which was effective. Again that was not in dispute before me. The authors of the Oxford Book did not appear to address at all the treatment of a dendritic ulcer and stromal keratitis when both were present.

Attached to the report of Mr. Hillman were extracts from the third edition, 1995, of Clinical Ophthalmology written by Jack Kanski. He also did not in terms appear to deal clearly with the treatment of a dendritic ulcer and stromal keratitis when both were present. However, at page 110 he considered the treatment for stromal necrotic keratitis. He wrote:

“Treatment of stromal keratitis is controversial, difficult and frequently unsatisfactory. The first aim is to heal any active epithelial lesions with active antiviral agents. If after 14 days there is no evidence of active epithelial disease, but the epithelium is still not healed, treatment is similar to that for trophic keratitis (i.e. lubricant ointments, pressure patching or a bandage contact lens). Once the epithelium has been healed, the stromal reaction may diminish. However, in resistant cases with incapacitating symptoms and severe anterior uveitis, the cautious use of steroids, combined with topical antiviral and antibiotic cover, will be necessary to relieve symptoms and prevent severe corneal scarring.”

Mr. Meakin relied on that passage, and a similar passage on the next page concerned with the treatment of disciform keratitis, as supporting the opinion of Mr. Phelps Brown. The passage on page 111 read:-

“Treatment is much more satisfactory than that of stromal necrotic keratitis. The first aim is to heal any associated epithelial lesion. As disciform keratitis is usually unassociated with severe discomfort, small lesions away from the visual axis may be observed. However, if the visual axis is involved, topical steroids combined with antiviral cover are required. Initially the steroid drops and antivirals are given four times daily. As improvement occurs, the strength of steroid may be reduced and the antivirals administered three times daily. In general, less than 0.25% prednisolone twice daily does not require antiviral cover. The steroids should be tapered over a period of several weeks, although some patients will need one drop of a weak concentration once a day for a prolonged period of time to prevent rebound. Periodic attempts should be made to taper the dose further or to stop medication altogether.”

Mr. Buxton did not suffer from stromal necrotic keratitis, but from disciform keratitis. Mr. Kanski appeared to take the view that in the treatment of disciform keratitis, while the first aim was to heal any associated epithelial lesion, steroids might be applied, if the visual axis was involved, in combating the keratitis in advance of the healing of the epithelial lesion, but it cannot be said that his opinion on that question was entirely clear. What may be more significant was that he did not say in terms that steroids should not be used until the epithelial lesion was healed, and one might have expected him to say that in terms, if that was his view.

In the end I was not persuaded that the evidence of Mr. Phelps Brown that no reasonably competent ophthalmologist could have prescribed corticosteroid for stromal keratitis at a time when there was present in the relevant eye a dendritic ulcer which had not healed was correct. If his view were well-founded, the point was elementary and incontrovertible, yet that view was not in terms recorded as shared by any other ophthalmologist in any of the medical literature which was put before me. Moreover, the identification by Mr. Hillman of the factors relevant to be evaluated and balanced by an ophthalmologist confronted by both a dendritic ulcer and stromal keratitis was not challenged in cross-examination or other than implicitly (in that it was inconsistent with his expressed view) by Mr. Phelps Brown. Mr. Phelps Brown did not suggest that Mr. Hillman was in error in stating that a greater risk to sight was presented by stromal keratitis than by a dendritic ulcer. I was persuaded that logic and common sense supported the position of Mr. Hillman. Any doctor confronted by a patient suffering from two conditions has to determine in what order, and by what means, to address each condition. If and insofar as the possible means of treating one might have implications on the progress of the other, an assessment has to be made of the advantages and disadvantages of each possible course available. Depending upon the circumstances, it might be appropriate to treat one condition and ignore the other altogether, or to treat one first, and then the other, or to treat each at the same time. If each condition is to be treated at the same time, it is necessary to consider whether, and if so how, the possible means of treating one condition might affect adversely the progress of the other. If the treatment of one condition can only be undertaken at some risk to the progress of the other, it is essential to assess the extent of the risk, the seriousness of the outcome if the risk eventuates, and the seriousness of the outcome for the other condition if the course contemplated is not taken. That is, in its essence, what Mr. Hillman considered that a reasonably competent ophthalmologist confronted by Mr. Buxton on 27 September 2005 with his right eye demonstrating the signs which it then did had to do. On the evidence of her notes, that is what Dr. Tan seems to have done, for she identified, correctly, it appears, the relevant conditions, and decided how to treat each. I am not satisfied on the evidence that her decision could be characterised as such as no reasonably competent ophthalmologist could have made.

It was common ground that when examined next after 27 September 2005, that is to say, on 2 October 2005, it was found that Mr. Buxton’s right eye was suffering from epithelial ulceration. At question 6 of the Joint Statement Mr. Phelps Brown and Mr. Hillman were asked to say whether they were agreed as to the cause of that ulceration. What they wrote in answer was:

“The clinical note is unclear in that the lesion is described as a “dense central ulcer/infiltrate”. It is not entirely clear whether this refers to an ulcer or an infiltrate, or an ulcer with an infiltrate. We incline to interpret this with the latter view. We are agreed that as the ulcer is not described as “geographic” this does not indicate a classical steroid-aggravated herpes simplex ulcer, but it does not exclude this diagnosis. We interpret the reference to “infiltrate” as indicating that there was some degree of underlying disciform keratitis. In Mr. Phelps Brown’s opinion the balance of probabilities is that the ulceration was steroid aggravated. Mr. Hillman disagrees with this view on the basis that the ulcer was not of the geographic shape which is usual for steroid aggravated herpes simplex ulceration.”

The only evidence put before me relevant to the issue whether the ulceration found on 2 October 2005 had been caused by the aggravation of the dendritic ulcer by the Virus operating freely in the immuno-suppressive environment created by the use of corticosteroid or by the effects of stromal keratitis consisted of the notes of the attendance on 2 October 2005, as interpreted by Mr. Phelps Brown and Mr. Hillman. They agreed what was the relevant note, and how it should be interpreted. What they did not agree about was what conclusion should be drawn from that interpretation. While they did agree that the ulcer, as described, did not indicate a classical steroid-aggravated herpes simplex ulcer, Mr. Phelps Brown concluded, I think only from the temporal link between the consultation with Dr. Tan on 27 September 2005 and the date of the next consultation, that the cause of the ulcer seen on 2 October 2005 was the use of Prednisolone Forte. Mr. Phelps Brown thus attributed no significance to the fact that the ulcer described on 2 October 2005 did not look like a steroid-aggravated ulcer. Mr. Hillman was influenced by the look of the ulcer to conclude that the cause of the ulcer was not the use of Prednisolone Forte.

I think that it was common ground that the other possible causes considered by the maker of the notes of 2 October 2005, acanthamoebia keratitis and bacterial infection, were probably eliminated as live possibilities by the facts that tests taken on 2 October 2005 showed no bacterial growth and that, had there been acanthamoeba, the condition would not have resolved, as it did in fact resolve, without anti-amoebic treatment.

It was for Mr. Buxton to prove that the cause of the ulcer found on 2 October 2005 was the use of Prednisolone Forte. In my judgment he failed to do so. His case amounted to no more than post hoc, ergo propter hoc. The fact that the ulcer found on 2 October 2005 was not described in the way one would expect if it were the original dendritic ulcer aggravated by steroids was positive evidence against the contention advanced on behalf of Mr. Buxton. The fact that the appearance of the ulcer was not sufficient to exclude the possibility that it had been caused as was contended on behalf of Mr. Buxton was simply not enough, on a balance of probabilities, to prove that that was how the ulcer had in fact been caused.

I have already set out the evidence as to the effect upon Mr. Buxton of the condition in which he is left in the right eye, and the progress of his improvement from 2 October 2005 until his discharge from hospital. Had it been necessary to assess general damages for pain and suffering and loss of amenity, I think that it would have been important to recognise that, on any view, Mr. Buxton was destined to be left with a defective right eye. As I have indicated, I was much impressed by Mr. Buxton. Refreshingly, he has accepted the hand which Fate has dealt, and sought to make the best of his circumstances. I am entirely confident that his evidence as to the effects of the defects in his right eye which he gave was accurate, and in no way exaggerated. The headaches and nausea of which he spoke are important aspects of the case, as are the quality of the sight in the right eye and the element of double-vision. I should have assessed general damages for pain and suffering and loss of amenity in this case at £15,000.

It was contended on behalf of Mr. Buxton that an award should be made in his favour to compensate him for the disadvantage which he would be at on the open labour market, were he to lose his employment. I think that the nature of his employment, and the qualifications and experience which he has obtained in that area, mean that any disadvantage would be slight. Nonetheless, I am persuaded that there is an element of disadvantage, and, had it been appropriate, I should have awarded compensation in the sum of £5,000 in respect of that disadvantage.

There was no great challenge to the claims of Mr. Buxton for special damages which were pursued at trial. The sums were modest, and were for loss of earnings between 26 September 2005 and 17 October 2005, and for the cost of taxis to work for a period of 22 days, during which Mr. Buxton was unable to drive, and five taxi trips to hospital. The points made on behalf of the defendant in respect of these claims were, first, that, on his own evidence, Mr. Buxton was not intending to work for a week from 26 September 2005, having been advised at the Clinic not to do so, and, second, that, if he had not taken a taxi to work, he would have incurred expense in driving himself by car. I think that each of these points was well-taken. Had it been appropriate to assess special damages, I should have awarded Mr. Buxton loss of earnings from and including Tuesday, 4 October until, and including, Friday, 14 October 2005 (9 working days), and deducted from the claim in respect of taxi fares a sum of £80, that being the sum which Mr. Buxton told me he spent on petrol each month at the end of 2005. The claim in respect of taxi fares to work covered 22 working days, which is, for practical purposes, a month.

In the result the action fails and is dismissed.