Lai Ping Wah v. China Insurance Co. Ltd. and Anotehr
Read the full judgment text of HCPI 874/1997 on BabelCite. This High Court CFI judgment was delivered on 25 November 1999.
1. On September 18th 1994, Madam Ku Lai Kwan, then 38 years' of age, was travelling as a passenger in a coach which came into collision with two railway units at a level crossing. She was thrown out of the coach onto the road surface in what must have been an horrific experience for the coach passengers. She sustained serious injuries but they were not life-threatening.
Cited by 2 cases
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HCPI000874/1997 HCPI 874/97 IN THE HIGH COURT OF THE HONG KONG SPECIAL ADMINISTRATIVE REGION COURT OF FIRST INSTANCE PERSONAL INJURIES ACTION NO. 874 OF 1997 ________________
________________ Coram: The Hon. Mr. Justice Seagroatt in Court Dates of Hearing: 7 - 10, 13 - 15 and 28 September 1999 Date of Handing Down of Judgment: 25 November 1999 _______________ J U D G M E N T _______________ 1. On September 18th 1994, Madam Ku Lai Kwan, then 38 years' of age, was travelling as a passenger in a coach which came into collision with two railway units at a level crossing. She was thrown out of the coach onto the road surface in what must have been an horrific experience for the coach passengers. She sustained serious injuries but they were not life-threatening. 2. Her direct injuries seemed to be on the mend by the end of 1994 but from February 1995 - perhaps even from December 1994 - her general physical state declined progressively without remission. In February 1995 there was some complaint of frontal scalp pain; by July 1995 she was blind in her left eye, retrobulbar neuritis having been diagnosed in April, and there was deterioration in vision in her right eye. She became totally blind in or about March 1996 and there was progressive weakness in her legs requiring her to use a frame to walk. 3. Paraplegia had set in from about May 1996 onwards and further deterioration led to tetraplegia. She never improved and following admission to hospital on 7th March 1998 with indications of chest infection she died ten days later of pneumonia as a complication of what was then diagnosed as multiple sclerosis. 4. The crucial question is whether the neurological deterioration and developing disorder or disorders were attributable to her original injuries or were a coincidental development despite the fact that there was a steady course of ill-health from the time of her admission to hospital following the accident. Post-Accident Hospital History 5. A distilled examination of her injuries and progress and treatment in respect of them, is an essential preliminary. She was admitted to Tuen Mun Hospital at 1357 hrs. on the 10th September 1994. 6. The significant hospital records made their appearance relatively late in the course of this trial, during the evidence of Dr. Huang on behalf of the Plaintiff, although he and the consultant neurologist for the Defendants, Dr. Yu Yuk Ling, had considered the records and annexed some of the pages to their respective reports. However this is clearly a case in which a legible and chronologically ordered bundle of such reports was material to the basic considerations. Notwithstanding the absence of such it has been possible to piece together the deceased's course of treatment for her injuries and what developed, albeit painstakingly. 7. An undated history sheet (but probably made on the day of admission) records as her complaints:
The clinical findings were:
The note refers to X-rays of cervical spine, chest and left leg. No fractures were seen.
8. Sheet B of the Nursing Kardex which records the progress and intervention and evaluation, confirms that the facial laceration was sutured on the ward under local anaesthetic on 10th September. Abdominal and Chest X-rays were carried out. 9. The operation record of 11th September deals with the wound to the left calf region. Reverting to the Nursing record for the same day, there is a note of abdominal and wound pain. On the 12th September a neck collar was applied and there was a complaint of dizziness after the X-ray was taken, which persisted through the 13th & 14th September in a mild form. Also on the 14th September is recorded exploration of wounds under local anaesthetic without more detail. 10. Mild back pain was noted on 16th September with neck pain and tenderness intruding on the following day and ribs pain on the 18th September. There was a transient episode of dizziness on the 19th September. 11. Thereafter little of note is recorded save possibly the removal of pieces of broken glass from right hand and left leg on the 28th September and a piece of glass from the elbow, possibly, on the following day. 12. The discharge/transfer summary dated 26th October, some six weeks or so after the accident, refers to a fracture of the left inferior pubic ramus and also of the right little toe, as well as the left leg laceration. She was then walking with a stick. The final note says that "at least four sessions of removal of glass beads under LA (Local Anaesthetic) during WFV(?) have been carried out." 13. She was back in hospital on the 7th November 1994, less than two weeks later. She was still walking with a stick. Apart from hip pain and left shin pain there was complaint of increased right forehead pain. The notes are almost indecipherable after this point save for a reference "to neurosurgery for post-concussional syndrome". 14. This was also an attendance on the 8th November. The history repeats the essential injuries. There is a reference to transient loss of consciousness. The current complaints were right forehead numbness throughout the whole day and reduced sensation over right forehead. There seems to be no apparent distinction between the two areas but a drawing refers to loss of sensation over the right supraorbital nerve. 15. She returned on the 25th November complaining of hypersensitivity of the scalp above the scar, exaggerated by touching, and increased sleeplessness. The healing process of the nerve ending was explained to her and medication (including panadol) was prescribed. 16. There is an entry relating to a visit on the 12th December 1994 which as far as I can tell is restricted to the pelvic and little toe injuries. It notes a 'follow-up' in two months time. 17. On the 30th December 1994 she was still complaining of numbness on the right forehead, and pain that can be controlled by analgesic. There was no blurred vision and she was walking steadily. 18. She attended her planned follow-up on the 21st February 1995. She was still complaining of right frontal scalp pain with reduced sensation on the right side. There was no vomiting and no blurred vision and she could get to sleep. One month later (29th March 1995) it is recorded "still mild symptoms." It may be risky to put this in the context of the previous attendance but she was attending hospital again, earlier than anticipated - on 21st February; she had been told to come again in three months time. 19. The next entry is unclear but logically it must be after 29th March and probably after 25th April 1995. I think it is either the 3rd or 23rd May. It is confined to continuing complaint of back pain - the range of movement of her spine and her straight leg raising were noted to be full. The entry is by the same person who wrote the entry for 5th June 1995 and the topic is the same. 20. It is at this stage one needs to look back and take stock of her progress. The orthopaedic injuries were recovering reasonably well. However there may have been some persisting sensory deficit, which varied in intensity. 21. Over this period of time - about 7 months - her treatment had of course been geared to her physical injuries. She moved onto a régime of medication. However, of significance as it later appears, is the number of tetanus toxoid injections she received and their timing. The first was on the day of the accident. The second, a booster was on the 22nd October and the third, a further booster was on the 20th April 1995. 22. Medical records do not of course tell the whole story of a patient's injuries and condition particularly where admission is as an emergency following a motor accident. We have no contemporaneous statement by Madam Ku but a comprehensive statement in relation to her injuries, disabilities and continuing problems dated 16th July 1996, about 22 months after the precipitating event. 23. Immediately following the collision she recalls two periods of unconsciousness. Her head, face and left leg were covered by engine oil. She said the oil staining of her head was still present the following day when members of her family visited and had difficulty in recognising her. She may be mistaken about this. Bearing in mind her forehead laceration had been stitched on the day of admission and surgery on the severe laceration of the left leg was carried out in the early hours of the 11th September it is inconceivable that she would not have been properly washed and toiletted in the injured areas. On the other hand some engine oil may well have contaminated the open wounds. 24. She describes three facial wounds (corresponding to one of the diagrams in the medical records) all of which were sutured . An open injury over her right shoulder was left to heal of its own accord; her ribs were injured and painful for three months. The wound to her left lower leg was undoubtedly severe. She also had a wound to her right inner leg which required sutures. The medical records also confirm what she says about the glass splinters in her legs. At the time she was writing her health had already taken a serious downturn though she makes no mention of those developments. 25. Her medical records from late April 1995 record the beginning and the inexorable progress of that deterioration. 26. Five days after her third tetanus toxide injection those records state:
27. Many notes are unclear - at the end of that entry for 25th April is noted "admit for CT scan." 28. On the 2nd May is a note saying progressive reduction of left eye vision and then total blindness within 3 days. MR1 scan was booked with follow up in three weeks. The next entry, one month later, is short, refers only to pain in the right hip and makes no mention of the MR1. 29. An entry for 14th May, 1996 refers to the MR1 of May 1995 as confirming left optic neuritis. The bundle of records is so hopelessly disorganised that it is difficult to follow her progress but other records refer to admission in July 1995. Of significance is the reference by Madam Ku to experiencing blurring of vision following her third anti-tetanus vaccination. On 7th July, which is the start of the series of notes following her admission, she said she experienced the day before, sudden onset of reduced right eye vision after waking from sleep. There were no other complaints. 30. The diagnosis was recorded as Optical neuritis leading to idiopathy or secondary demyelinating disease (multiplesclerosis). An entry for the 18th July 1995 records as the diagnosis "bilateral Optic Neuritis." She was discharged home. 31. She must have been admitted again in September 1995 because there is an entry to that effect on 14th May 1996 noting bilateral lower limb twitching and weakness with a diagnosis of multiple sclerosis - transverse myelitis (inflammatory disease of the spinal cord). In May 1996 she complained of intermittent pain over the right parietal region with numbness and paraesthesiae over the right upper face and occasional tinnitus. An entry, possibly as a clinical finding, records 'paraesthesia over V1, V2 - reduced sensation.' 'No other cranial nerve (or neurological?) deficit.' There was reduced power in her lower limbs and she was chair bound. A full medical was booked for the following day with a follow-up in one month. 32. The next apparent entry (though I anticipate that there must be others in the intervening period somewhere in the volume of records) is dated 16th October 1996. It does not record anything new. 33. 12th March 1997 notes "multiple sclerosis - wheelchair bound" but that entry and the next two (19th March and 16th July 1997) contain nothing else of note. 34. The last two entries are for 7th October and 4th November 1997. The former does not indicate much other than her continued decline. Part of the diagnosis written on the second occasion is not legible; what is, legible reads "M.S. and transverse myelitis and blind both eyes". She was of course wheelchair bound. Within five months she had died. The Neurological Debate 35. Her diagnosis has been variously recorded as multiple sclerosis, Devic's Syndrome and other forms of demyelinating disease but the overall tendency has been to apply the label of multiple sclerosis. No post-mortem was carried out so that fact has imposed some limitation upon the clinical and other material available. The point at issue is what was probably the correct diagnosis of her unhappy condition and was it caused by the trauma or any of the necessary aspects of the treatment for the injuries suffered by her. 36. I have had the advantage of hearing at length from two distinguished neurologists, Dr. Huang Chen Ya and Dr. Yu Yuk Ling respectively on behalf of the Plaintiff and the Defendants. They have considered a number of studies recorded for their profession in authoritative publications which have helped to shed some light on the difficult aspects of this case. There are differences in their respective conclusions and how they approach this body of limited evidence which on any view is derived from an almost infinitesimal proportion of sufferers from this crippling demyelinating disease whatever form it takes. 37. Before I proceed to consider their evidence in detail I need to refer to a medical report from the consultant neurologist Dr. Edmond Woo who examined the deceased in late March 1997; by that time she was already totally blind and wheelchair bound. 38. This report formed no part of the Plaintiff's case but Mr. Sakhrani on behalf of the Defendants sought to adduce it without consent. I declined to allow him to do so. In any event the report should not be adduced on it own without oral evidence because there were a number of matters in it which were quite unclear as to source and foundation. I invited the parties to agree what contents were capable of agreement between them by a joint discussion with Dr. Woo and a consideration of his notes. No agreement was forthcoming - which did not surprise me - and so any reference to or reliance upon contents of that report was fraught with difficulty and I was not likely to accord it much significance. Apart from his examination of Madam Ku, Dr. Woo had only the reports from government hospitals to rely upon and an orthopedic report from the consultant Dr. Arthur Chiang. 39. The history related by him is taken in part from those written sources. Regrettably they were not wholly accurate. Some of it is likely to have come from the patient. It is not wholly reliable. He records that a diagnosis of multiple sclerosis was made. We know from a more detailed examination of records and reports that the diagnosis was not a wholly confident one. We do know that some form of unremitting progressive idiopathy had brought her to the condition Dr. Woo saw. 40. In his neurological examination Dr. Woo did not itemise what tests he conducted. In the context of this case his assessment in respect of her facial/cranial neurological deficits was of some potential consequence but that was not to be known by Dr. Woo at the time. His comment at the end (in effect his conclusion) is probably the most important part of his report:
He could not have anticipated the debate that was likely to follow and which has occupied this Court for a significantly longer period of time than was estimated. 41. Dr. Huang's report of 21st May 1999 draws attention to a repeated reference in the ward notes to Devic's Syndrome with the discharge summary diagnosing multiple sclerosis, and the inter-changeable use of the terms. 42. An examination of the various investigations which she underwent is highly relevant and Dr. Huang sets those out. They are crucial to his assessment.
Dr. Huang identifies the course of Madam Ku's disease as relapsing and progressive, with the clinical evidence showing optical nerve and spinal cord involvement with an absence of abnormality in the brain. 43. The sensory impairment on the right side of Madam Ku's face was noted by Dr. Fong To Sang in his report of 7th January, 1997 when referring to an examination of 14th May 1996 at Tuen Mun Hospital. A diagnosis of multiple sclerosis (with left optic atrophy) had been made on referral. The report says, "There was also subjective numbness of right upper face. Examination revealed, inter alia, paraesthesia of right V1 and V2 cranial nerves." She had of course sustained a laceration over the forehead, as illustrated by diagrams, which had required suturing. 44. Dr. Woo refers in his report to her beginning to experience tingling and paraesthesiae over the right side of her head and face intermingled with paroxysms of pain. Dr. Woo did not have the medical records available, only a few reports and Madam Ku's recollection 21/4 years after the event, and of course has not given evidence in this case, and his report has not been admitted into evidence. I am not prepared to rely upon any deduction in that report in the circumstances of this case and I say that with no disrespect to Dr. Woo. Although on a number of occasions Mr. Sakhrani has referred to a number of matters in that report I am not prepared to allow them in by a side wind for the reasons set out. 45. Dr. Huang refers to the well-illustrated facial and forehead injuries which required suturing and may well have accounted for the sensory impairment. 46. If Madam Ku's disease was multiple sclerosis simpliciter Dr. Huang is of the view that it is unlikely that her injuries sustained in the accident caused her subsequent neurological illness. But, he points out, recent years have produced studies which suggest that not all cases of Devic's Syndrome are due to multiple sclerosis. The controversy is as to whether Devic's Syndrome is just a variant of multiple sclerosis. 47. This case has followed this debate closely whilst noting that case studies, although inevitably confined to a very small number of individuals, nonetheless may provide a possible explanation or alternative approach to diagnostic signs which should properly be regarded as questioning conventional acceptance or wisdom. By that token are the boundaries of medical knowledge and advance pushed out further. 48. Taking the learned medical papers in chronological sequence Mandler et al, in a paper entitled "Devic's Neuromyelitis Optica - A Clinicopathological Study of 8 patients" published in the Annals of Neurology 1993 (under the auspices of the American Neurological Association) reported that the clinical, imaging, CSF and pathological features are sufficiently distinctive from those usually observed in multiple sclerosis. The major difference between these patients - five of whom died and thus afforded evidence from post - mortem - and multiple sclerosis patients was the absence of brainstem, cerebellum and cognitive findings in the former group even after several years of follow-up in some cases - "The important negative imaging finding was the absence of white matter abnormalities in head MR1s. On the contrary, multiple white matter abnormalities are usually seen in head MR1s of MS patients." 49. The paper concluded with the author's belief that Devic's Syndrome was, in the strict sense, a distinctive clinicopathological entity, different from multiple sclerosis. More studies were required to find the aetiology of the Syndrome. The reference to "The necrotising nature of the myelopathy with involvement of large areas of the spinal cord grey matter being a hallmark in Devic's Syndrome but not in multiple sclerosis" is of importance in the case of Madam Ku, as were the diagnostic criteria set out at the end of the paper. 50. The 1996 paper of O'Riordan et al in the Journal of Neurology, Neurosurgery and Psychiatry reported on twelve patients, eleven of whom were women, with an average age of 35.1 years but the range was 14 to 61 years, so the average is not in itself a significant factor. The study was undertaken to help clarify, whether or not Devic's Syndrome is a variant of multiple sclerosis. Eleven of the twelve underwent MR1 of the brain and spinal cord, as did Madam Ku. In five cases the brain MR1 was normal, and in five others there were multiple deep white matter lesions. The conclusion put forward was that Devic's Syndrome is a distinctive disorder with some clinical, CSF and MR1 features different from those found in classic multiple sclerosis. In most cases a specific aetiology was not identified but an immunological mechanism of tissue damage seemed likely. 51. Mandler's paper was referred to (and of course very much in mind) and the similarities were identified. Other studies were identified and no doubt played some part in the overall conclusion including a study by Fazekas et al in 1994. 52. From these recent studies, we move to the 1998 edition of McAlpine's "Multiple Sclerosis". A number of statements are worth citing in the context of Madam Ku's case:
53. Returning to O'Riordan's study and earlier reports, from which the preceding statement is drawn, it points out that the cases "have several clinical, prognostic, imaging and immunological features which distinguish them from the typical case of multiple sclerosis but several might reasonably have been classified as having primary neurological vasculitis or acute disseminated encephalomyelitis and, in our view, the majority of adult patients with persistent neurological deficits reported as having Devic's Syndrome have multiple sclerosis ......"
54. Paty and Ebers' "Multiple Sclerosis" (1998) says (at page 305)"-
55. As a result of his consideration of these authoritative publications and the case studies Dr. Huang set Madam Ku's features against the subjects of Mandler's and O'Riordan's case studies:
56. There were a number of features therefore which were unusual for multiple sclerosis - additionally the spinal cord lesion was limited to the thoracic region. In multiple sclerosis the majority of lesions were in the cervical cord. Dr. Huang concludes that the clinical diagnosis of Madam Ku's condition was that she was suffering from Devic's Syndrome, distinct from multiple sclerosis. 57. Dr. Yu Yuk Ling first provided a report for the Defendants in August 1998. He referred to the first symptom of neurological impairment appearing in December 1994. He had relied upon a somewhat equivocal passage in Dr. Woo's report for that and it is by no means clear that in relation to her complaints of paraesthesiae and numbness in 1994 this was anything more than sensory impairment as a consequence of the lacerations, the latter being well-documented. 58. He appears to accept that her condition was indeed Devic's Syndrome but then concludes that multiple sclerosis was the proper diagnosis as being the most common cause of Devic's Syndrome. He does not agree with Dr. Huang's opinion that her condition was that of Devic's Syndrome distinct from Multiple Sclerosis. However he accepts that the clinical picture of Madam Ku's disease was "unusual or atypical for multiple sclerosis in its classical presentation" though there have been such atypical cases of multiple sclerosis. 59. One of the studies (1989) led by Dr. Yu which had Dr. Huang (and Dr. Woo) in the team, included a patient whose clinical features were similar to those of Madam Ku save that that patient had "a small MS lesion" in the brain whereas Madam Ku had none. Autopsy of the patient confirmed multiple sclerosis with definitive evidence in the brain. The absence of CSF oligoclonal bands is a common feature in Chinese patients with multiple sclerosis. Dr. Yu concludes with the statement that on available evidence the most common cause of Devic's Syndrome is multiple sclerosis. I do not understand Dr. Huang to disagree with that as a premise. However from that premise Dr. Yu states that the underlying cause of Madam Ku's illness was probably multiple sclerosis. By that he must mean that statistically she is more likely to have Devic's Syndrome caused by multiple sclerosis that from any other cause. She remains however unusual, or atypical, in her clinical presentation. 60. There is no doubt that Dr. Yu places great significance on what he regards as the onset of neurological symptoms in December 1994. He links Dr. Fong's 1996 report (and hospital record of 14th May 1996) with Dr. Edmund Woo's reference mentioned earlier. He thinks that this may well have been detected in November 1994 relying on the Tuen Mun hospital record of 8th November 1994 noting "non-specific scalp tenderness and neuralgia". With this Dr. Huang takes issue reminding us in fact of the numerous facial lacerations three of which required suturing. These were soft tissue injuries. The findings were essentially subjective. Dr. Fong included in his report (24th August 1995) when referring to that November 1994 attendance that she was "overall quite unremarkable." Dr. Yu himself did not regard Dr. Fong's report reliable (of 24th August 1995 I assume, though probably that of 7th January 1997, as well) preferring to rely on Dr. Woo's report of April 1997. I have already dealt with the difficulties inherent in Dr. Woo's report and the need to exclude it from consideration in this case. 61. Dr. Yu also links his conclusions from the November and December 1994 entries in the records with the mention by Dr. Arthur Chiang (who saw Madam Ku in January 1997) and Dr. Woo (March 1997) of "gradual clumsiness of the right leg... She developed a right foot-drop" [Dr. Woo] in February 1995 - "In about February to March 1995 she noted that there was weakness in the right leg." [Dr. Chiang]. The two doctors are reporting complaints by Madam Ku. 62. In her Statement Madam Ku refers to the wound in her right inner shank which had also been debrided and sutured; we know that there had been pain over her right inguinal area from the physiotherapists notes on 18th September 1994, and it was her right inferior pubic ramus which had been fractured. 63. There is no entry in the medical records relating to the right leg in February 1995. The record for 25th April 1995 which is largely concerned with her loss of vision in her left eye also records "No limb numbness/weakness ... No neurological deficit ...gait steady" and a word which I cannot read followed by "equal" which in the above context must relate to the lower limbs. There is no note to accord with what either Dr. Chiang or Dr. Woo were told. Dr. Huang pointed out that the entry for 7th July 1995 in the neurological testing includes normal power in all four limbs. The entries and history on a contemporaneous basis do not support the contention of neurological deficit of this nature made by Dr. Yu at that stage. 64. One of the arguments advanced by Dr. Yu against the notion of tetanus toxoid vaccination having precipitated her neurological decline is his assertion that the November or December 1994 neurological symptoms (in the head) predated her second dose of tetanus toxoid. In fact this is not so. She had received her second tetanus toxoid vaccination on 22nd October 1994. Her third vaccination was on 20th April 1995 only 3 days before the drastic symptoms in her vision appeared. It is to this topic of tetanus toxoid vaccinations that I now turn. Tetanus toxoid 65. It is true that there is no documented case study showing tetanus toxoid as having caused the development of Devic's Syndrome. But Dr. Huang points out the clear temporal link between the third tetanus vaccination and the optic neuropathy. The hospital record for the 23rd April 1995 (2 days before the entry for the 25th April) records the increasing reduction in the vision of the left eye over three days. She had been registered at Tuen Mun at 9:09 p.m. that day. There is an entry stating "insidious onset ... no trauma recently". The date of this record has perhaps been overlooked, though not by Dr. Huang, in the effort to piece together and establish some sequence in all these records - hither to we have been concentrating on the entry for the 25th April. Given the nature of her admission - "urgent" is recorded - and with a complaint of loss of vision, great care would be taken to ascertain from the patient when she first noticed the problem or onset. The answer, as recorded was three days earlier "(3/7)". 66. Dr. Huang draws attention to a letter from a group of Turkish doctors (Topaloglu and others) to "The Lancet" published in January 1992. It was in response to an earlier report by a group of doctors identifying cases of central nervous system demyelination following immunisation with recombinant hepatitis B vaccine, raising a possible immunological mechanism. 67. A healthy 11 year old girl suffered rapid onset of visual deterioration and weakness following a booster dose of tetanus toxoid. She was diagnosed with optic neuritis. Both eyes were affected. She also had bilateral papillitis and spastic paraparesis. Her condition deteriorated until about two weeks following the vaccination. Regrettably the copy of the document is not legible enough to see how many months elapsed before full recovery. It appears that there had been (by that time) several reported cases of neurological reactions to tetanus toxoid including polyradiculoneuritis and relapsing neuropathy. "Most cases have shown a benign course and recovery." Obviously some have not. Optic neuritis and myelitis have been reported after rubella immunisation. Relapse has been reported with further injections of tetanus toxoid. 68. Dr. Topaloglu's letter led to another in the May issue of "The Lancet" from a group of three doctors in the Department of Neurology at the Royal Brisbane Hospital in Australia. They had managed a patient with acute transverse myelitis - that also followed a tetanus toxoid booster. Twelve days after his initial presentation he was admitted with flaccid areflexic paralysis of the legs associated with sensory loss to T6. (In Topaloglu's patient there had been sensory loss also - to T4). An MR1 brain scan was normal. Oligoclonal bands were not detected. They concluded that although it is possible that the myelopathy in their patient "occurred independently of vaccination the timing and absence of an alternative explanation may implicate tetanus toxoid." 69. In the Italian Journal of Neurological Science for May 1994 is a short report from the Ospedale Civile Maggiore of Verona entitled "Acute radiculomyelitis after antitetanus vaccination," which Dr. Huang obtained from Medline which I think is a website. The authors were reporting a case of transverse myelitis with a radicular component, which arose acutely following the administration of tetanus toxoid and had a partially favourable course [My underlining.] The conclusion drawn was immunisation with vaccines or sera can cause lesions of immunomediated pathogenesis involving the central nervous system (which includes the optic nerve) and the peripheral nervous system. Although the neurological complications described as following upon antitetanus vaccinations are rare in themselves they are rarer still when affecting the central nervous system. 70. These three reports highlight the rarity of the situation but indicate by reason of their existence, the possibility of neurological complications, including those in the central nervous system, following upon tetanus toxoid administration, with both benign and adverse results following treatment. 71. At this stage it is pertinent to consider a report in the Journal of Neurological Sciences of 1978 (37) (Pollard and Selby) of what was then described as a unique case history of a 42 year old patient who suffered three episodes of a demyelinating neuropathy, each following an injection of tetanus toxoid. In the discussion section is stated -
72. As long ago as 1948, half a century ago now, reference had been made in Barnworth to repeated neurologic involvement following a second or third innoculation, although to the authors (in 1978) there was no known case containing such detail. Further in the report appears the following:
73. The clinical features on each occasion of the demyelinating neuropathy consequent upon the tetanus toxoid injection were characteristic of acute idiopathic polyneuropathy. In the majority of cases this (AIP) is a uniphasic disease but in some patients it follows a chronic relapsing or progressive course - such was the course in Madam Ku's case. Recurrence of disease has been reported following further exposure to some known antecedents such as surgery or vaccination. 74. The final paper on this topic is a report from three doctors in Baltimore, Maryland, U.S.A. presented originally at the 42th Annual Assembly of the American Academy of Physical Medicine and Rehabilitation in Washington D.C. in October 1980 (almost two decades ago) and published in July 1982. 75. There are some remarkable similarities between the position of the case study, a 33 year old man who "inadvertently received three tetanus toxoid injections for minor trauma over a five-month period and subsequently developed profound mixed sensorimotor polyneuropathy", and that of Madam Ku. Over a period of two years diagnostic studies suggested segmental demyelination and axonal neuropathy. This was the 14th reported case of peripheral neuropathy following tetanus toxoid vaccination, to the authors' knowledge. 76. Dr. Yu's view of the evidence afforded by this series of case studies across the years is an understandably cautious one: there is no proof that tetanus toxoid vaccination causes Devic's Syndrome. In his earlier report Dr. Yu had not considered the tetanus toxoid vaccinations of any significance despite their obvious consideration, in the reports to which Dr. Huang referred, over twenty years. I assume that the reason is that Dr. Yu is dismissive of them for the explanation he has given. He was largely concerned with the question of whether the trauma (i.e. the range of injuries themselves) were collectively or individually in any respect responsible for her neurological disease. He concentrated principally on the head injury. 77. The reasons essentially for Dr. Yu's rejection of the tetanus toxoid injections (second or third) as the cause of Devic's Syndrome, is, apart from the absence of a reported case of Devic's Syndrome following such immunisation, the contrast between Madam Ku's relapsing and progressive disease and the benign course and recovery "of most cases". Therein perhaps lies a weak link in Dr. Yu's argument. There are cases of continuing and permanent neurological deficit. The deficit is wide-ranging in nature. He also considered that the onset of Devic's Syndrome predated the tetanus toxoid booster injection. That as we now know is incorrect. The tetanus toxoid booster (of 20th October) pre-dated any arguably neurological symptom (whether in November or December 1994) and the third injection predated the manifestation of optic neuritis. The other factors 78. Madam Ku had suffered a period, probably two periods, of loss of consciousness, at the scene. It is not possible to determine the overall length of these with precision, but it was probably no more than an hour in duration. There were of course several wounds to her forehead. 79. The mechanism of such an injury and its immediate effect can produce a breakdown in the blood brain barrier in the brain, exposing the central nervous system to the cellular and molecular constituents of the blood and activating or predisposing an immunological attack on the central nervous system. The risk of immunological attack could be increased if combined with tetanus toxoid. 80. Finally there is the other risk factor associated with the engine oil which she described as covering her facial and body wounds for some time. No doubt this had been cleaned away before she received any treatment to her wounds but the debridément of her left leg wound - a substantial and extensive injury - took place many hours later. It required further debridément and drainage by reason of infection on the 7th October, almost one month later. Dr. Huang states the possibility of engine oil acting as an immunological adjuvant providing an additional risk. There is some evidence from experiments in relation to inducing experimental allergic encephalomyelitis (EAE) in animals which suggests that paraffin oil and mineral oil with other adjuvants can enhance the development of EAE - this can be further enhanced by the injection of tetanus toxoid reactive lymphocytes. Dr. Yu questions the validity of such tests and conclusions being applied to a consideration of human reactions. He discounts the period of unconsciousness as a factor in the development of Madam Ku's neurological disorder. In his view Madam Ku suffered a mild head injury with a maximum duration of unconsciousness of 1 1/2 hours. 81. In commenting on Dr. Arthur Chiang's view that the temporal association between the accident and the onset of the disease in a person of pre-accident good health, would cause the possibility of the accident "triggering off or causing an early appearance of symptoms of this disease" to be strongly considered (Dr. Chiang was of course speaking as an orthopedic consultant not as a neurologist) Dr. Yu was constrained to concede in evidence that "we have a temporal association between trauma and the development of disease "...." "A very striking proximity." 82. In relation to the engine oil factor Dr. Yu's view was that there were many unknowns. There was a slim theoretical possibility unsupported by evidence and that any link was highly unlikely; - but he "cannot entirely exclude that such a mechanism exists but it is highly unlikely that this is what happened." 83. Dr. Yu's approach, which is inevitably a proper and careful one as one would expect of a distinguished consultant Neurologist, has been premised, in part, upon his contention that if the theories of head trauma and/or tetanus toxoid as causative factors were true, there would have been some report that Devic's Syndrome was caused by head injury with or without tetanus toxoid. Had there been such a report my task would have been that much easier and this litigation would have proceeded on a much simpler basis. 84. Dr. Yu added in the course of his evidence that it cannot be proved that there is no link (between such factors and the disease) but there is very strong evidence of no link as far as is known. One should be aware of the possibility that in other cases there may be a link but it is necessary to provide evidence of such a link. If no evidence is provided it remains a remote possibility. 85. Dr. Yu, taking the strict clinical approach to the evidence contained in the reported studies, concluded that the evidence demonstrates that head injuries, do not cause Multiple Sclerosis or Devic's Syndrome. This is not the approach I have to adopt. The evidence does not prove the positive but it cannot be said that it proves the negative. The reason for this is clear enough. The case studies represent a minuscule number of patients and it is not possible to extrapolate from their limited variety such a conclusion. But the tetanus toxoid reports have a significance of their own. 86. In fact the legal approach is a good deal simpler than that. Whereas the medical profession seeks the aetiology of a disorder or clinical state of affairs with a logically progressive sequence of events and cause and effect, the courts do not look for a Plaintiff to establish a chain of causation-the "irrefragable chain of causation" in Lord Kilbrandon's words in McGhee v. National Coal Board 1973. 1. W.L.R. at p.10 - only a probability, a state of circumstances which drives one, on a common sense practical approach, to a certain conclusion. Lord Reid encapsulated this in his speech in McGhee:
and Lord Simon similarly in Alphacell Ltd. v. Woodward 1972 A.C. at p.847:
87. I do not find it difficult to apply this concept to the facts of this case. The temporal link between the accident and direct injuries and the development of the disease, in whatever form it took, is of overwhelming significance, and I have been aided in that conclusion by the evidence of both Dr. Huang and Dr. Yu. - Dr. Yu's "striking proximity" is the phrase which cannot be bettered and in its application displaces the strict critical and clinical analysis which he applied in his cautious approach. 88. Dr. Huang has built into the clinical approach the experience manifested by the case studies - in particular the known potential of tetanus toxoid to cause neurological disorder in the broad sense. 89. I accept his evidence. It provides the medical link to the practical temporal link. Either the injuries themselves or the contamination, or the necessary tetanus toxoid injections, collectively or individually, led to the development of Devic's Syndrome - and I accept Dr. Huang's view that this was probably a case of Devic's, independent of Multiple Sclerosis. The proximity of the third tetanus injection to the rapid, irreversible optic neuritis - a gap of three days - was both striking and devastating. To ignore that proximity would be to fly in the face of human understanding and no one has sought to do that. 90. If the complaints of Madam Ku in early November 1994 - and I prefer Dr. Huang's view that this was more likely a sensory rather than a neurological problem - were nonetheless a manifestation (the first) of a neurological disorder, one cannot overlook that only a little over two weeks had elapsed since she had received her second tetanus toxoid injection. I bear in mind that it was not until May 1996 that there was any reference in the hospital records to this being regarded as of neurological significance and Dr. Huang astutely makes the point that this reference may have been coloured by the then recent diagnosis of multiple sclerosis [The trigeminal nerve involvement]. 91. The deceased's injuries led directly to the development of Devic's Syndrome by the chain of events reviewed. The Defendants are liable for the deteriorating and ultimately fatal consequences of these injuries and illness. The third tetanus injection caused a neurological reaction within an extremely short period - less than 3 days - and the optic neuritis. Devic's Syndrome followed from this and not from multiple sclerosis. The second tetanus toxoid injection may earlier have precipitated a neurological reaction. Although I prefer the evidence suggesting the November/December 1994 complaints were sensory in nature resulting from the healing of the facial/head wounds, I do not rule out entirely the possibility of some earlier tetanus toxoid induced neuropathy presenting a problem at or about this time. To the same extent there may well have been other deleterious factors directly caused by the accident which contributed to her decline. Quantum Pain, Suffering and loss of amenity. 92. It is not necessary for me to rehearse the catalogue of injuries suffered by this lady as a direct result of the accident, and the progressive decline in her physical faculties and senses following the onset of what I have found to be the consequential disease. 93. Three and a half years elapsed between the accident and her death. The direct physical injuries themselves would have left a degree of permanent impairment. The facial lacerations, with permanent cosmetic disfigurement, would have been of significance to her; although we have no photographs to illustrate the lacerations to both legs, we have from measurements alone, some idea of the injury to her left leg, which required further surgical treatment when infection set in. The fracture would probably, in a woman, have left some permanent discomfort. It never did return to a normal state though it is impossible to know when it reached a final state in view of the neurological decline. 94. The loss of sight in her left eye in April 1995, six or seven months after the accident, must have been frightening to say the least. By July/August 1995, less than a year after the accident, her vision in her right eye was reducing quickly. There was some short-term control, but by March of the year following she was totally blind. She survived for two more years as she declined from a state of hemi-paresis to one of paraplegia, being wheelchair bound, and finally to quadriplegia. 95. It is impossible to appreciate the state of hopelessness and despair which must have set in. Persistent decline, dependency on others, little if any realistic hope of relief, must have made her life one of absolute misery, however resilient her nature. She must have known too that there was never any realistic chance of reversing her state, and responsible medical opinion could never have held that out to her as possibility. 96. Over that period she endured continuous discomfort, medical tests, treatment and investigations, none of which was going to avail her anything other than a prognosis of gloom following a diagnosis of some uncertainty. 97. In my view damages should be no less than $1,000,000.00. The Defendants in their Answer to the Plaintiff's Statement of Damages did not even try to deal with the question of a figure under this head of damages, to embrace the situation where all injury and disease and finally her death, were attributable to the Defendant's admitted negligence. Accordingly there was no argument to set against that on behalf of the Plaintiff.
98. The Plaintiff's Statement of Damages calculates these in the sum of $335,575.80. I award this sum.
99. At the time of the accident she had in her savings account a little over $89,000.00. 100. Between then and the date of trial, virtually five years, it is claimed that she would have saved 25% of her earnings and the calculated figure is therefore a little over $124,000.00. 101. At her death she was 38 years of age. Assuming she would have worked until she was 60 years of age the multiplier appropriate for a further 22 working years is 12. Five years have elapsed. At the date of trial her earnings would have been approximately $11,000.00 per month - $132,000.00 per annum. A multiplier of 7 (the balance of the 12 years) produces $924,000.00, 25% of which is $231,000.00. That together with $124,000.00, totalling $355,000.00 will be the award under this head.
102. This is fixed by statute. The figure is $150,000.00.
103. She commenced employment with Triumph in 1992. She paid 5% of her salary into their fund. Her employers paid a like sum. Accepting the calculations in the Plaintiff's Statement of Damages, the benefit she would have received on retirement, allowing for accelerated receipt, would have been $34,650.00. Other items of Special Damages
104. The total is $100,000.00. I accept these as reasonable.
105. These too are reasonable at $7,000.00 over 3 1/2 years.
106. This inevitably is a contentious item. There is likely to be an overlap with normal expenditure on food. 107. $12,500.00 is a reasonable allowance.
108. $10,000.00 is claimed. I have no doubt that a claim for services to his wife over and above this loss would have been justified $10,000.00 is therefore the reasonable minimum figure.
109. These total $30,500.00. It is a reasonable figure. Given the head of damages for services which was not pursued I award this sum much of which reflects the work of the Plaintiff (the deceased's husband) carried out by him for his late wife's benefit.
110. This was an item needed for almost the last two years of her life. The total is $11,500.00.
111. The account totalled $34,800.00. 112. The total cost of these miscellaneous items is $206,300.00. If the Defendants feel that any of the items were nonetheless excessive and ought to have been subjected to greater scrutiny and challenge than I have been able to do, they have only themselves to blame. The whole purpose of a detailed Statement of Damages is to afford the Defendants the opportunity of setting out a detailed case in relation to such items which they cannot agree. They do this by serving a comprehensive Answer, advancing a clear argument as to why an item should not be allowed or why it should be allowed only in part or only on a certain basis. A simple statement that an item is not agreed will not suffice. If Defendants are incapable of putting forward such an Answer it is not for the trial judge to do their work for them. The best he can do is to assess the reasonableness of such items. In this case the original Answer by the Defendants was hopelessly inadequate and deficient, and the Amended Answer submitted during the course of this trial was no better. I declined to give leave to the Defendants to rely on it. Summary
113. There will therefore be judgment for the Plaintiff for $2,081,525.80 with costs to be taxed if not agreed, together with interest as provided for above.
Representation: Miss Jacqueline Pinto instructed by the Director of Legal Aid for the Plaintiff. Mr. Ashok Sakhrani instructed by Messrs. Deacons, Graham & James for the Defendants. |
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