Damages
124The finding I have made about Mr Hennessy's unreliability as a medical historian means that the facts relevant to determination of the quantum issues in this case need to be based upon other objectively determined and satisfactory evidence.
125Because most of the doctors who saw Mr Hennessy for the purpose of this case were not given the full picture by way of history, their evidence, which is mostly very supportive of him, needs to be put to one side. It is axiomatic that the opinions expressed are only as good as the assumptions made.
126To find reliable objectively determined evidence one must look to the medical evidence. In this regard, there are four doctors who seem to have more or less the full picture. They are the general practitioner, Dr Owen Brookes, Dr Deveridge, Dr Peter Giblin and Dr Edward Schutz. The three specialists were medico-legal referees qualified for the purpose of the case. Each of them was provided with the complete clinical picture by way of contemporaneous reports for the purpose of the preparation of his last report. Dr Giblin and Dr Schutz gave oral evidence.
127In cases like this, where the determination of the right history is critical to the determination of the quantum of damages by application of the compensatory principle, the views of a treating general practitioner who has been the plaintiff's physician both before and after the relevant accident will often be of great value, especially where his or her views are expressed in a non-contentious or non-forensic context. I have the benefit of having received in evidence (Exhibit FF) the referral letter of Dr Brookes to Dr Mark Davies, the operating surgeon, dated 27th August 2005. I think it important to set out Dr Brookes's description of the development of Mr Hennessy's condition in full. It is in the following terms:
Thank you for seeing Shane Hennessy, age 23 yrs, for review. I understand you have spoken to George Pitsis and we have been managing Shane in tandem, so I thought it important to put in my 2 cents worth.
He has a history of lumbar back pain. Initially a short self limited episode in 1997. In 2002 he had a work related injury which resulted in a protracted course but he did slowly return to work over 4-5/12. CT scans at the time showed disc prolapse. He did have some sciatica. I think the pain never completely settled but he was able to satisfactorily return to work. He was assessed by the spine service at St George Hospital but as there was no operable lesions, I suspect that they weren't particularly interested and Shane was unimpressed by the orthopaedic surgeon. An MRI was performed.
In November, last year, his back flared up following a big weekend gardening/landscaping.
In March, 2005, he slipped and fell again at work, slipping on a wet step and landing forwards on the ground. He was unable to get up without asssistance. He has had symptoms which might be consistent with radicular pain on the left side. Since then his course has been very slow with minimal reduction in pain. A repeat MRI scan has been performed but this does not
appear to be much changed from previous, according to the report.
Shane is bored at home and was keen to return to some form of work but the extended time to travel to the city by public transport was a disaster.
He has had an injection into the nerve root sheaf with some temporary improvement. He has been referred to Henry Lam for pain management. Otherwise he remains unfit for any but the
mildest of activity.
I have been loathe to suggest surgical management. His pain largely settled with conservative management last time and in the past he has had other injuries which were slow to settle and yet with time did so completely.
I find Dr Brookes description of the development and progress of the plaintiff's condition to be illuminating and consistent with what I regard as other objective evidence.
128Much was properly made in argument by the defendants of the past medical history. The relevant factors are: back injury in 1997; the work related injury in 2002, which appeared to involve some degree of disc lesion with ongoing symptomatology; the incident involving heavy gardening in November 2004; and the referral to a spinal surgeon, Dr. Diwan. Of course, the complaints advanced to Dr Diwan were significant.
129Much of this is put in context by Dr Brookes's report and given that he was a treating doctor over many years, his impression of some sciatica at the time of the 2002 injury settling, a significant flare-up in 2004 and Dr Diwan not being interested as he considered there was no operable lesion, is a very valuable impression formed by an experienced medical practitioner engaged in the ongoing management of Mr Hennessy's condition. Moreover, his impressions are borne out by other evidence. In his letter to Dr Brookes (there are two versions of it, one dated 20 January 2005 and the other 20 February 2005), as I have recorded above, Dr Diwan did not find any objective signs of radiculopathy: he said "lower limb neurology is normal". He did not diagnose operable disc lesion on the basis of his clinical examination, which to my mind is significant. His diagnosis was of a pars defect without spondylolisthesis. Both Dr Giblin and Dr Schutz regarded a unilateral pars defect as of no real clinical significance. Moreover, Dr Diwan did not suggest surgery. Rather, he "foreshadowed ... the possibility of an injection program". All of this confirms Dr Brookes opinion at the time.
130It is true that there is no report from Dr Diwan commenting upon the MRI scan of 4th February 2005 requested by him which, as I have said, demonstrated a left sided disc protrusion at L4/5 affecting the exiting sciatic nerve root.
131Dr Brookes recorded that that MRI was similar to the post-accident MRI carried out on 23rd May 2005 by the same radiologist, at least in Dr Brookes's words "according to the report". Dr Schutz is of the view that the pathology shown on each MRI scan was identical and that Mr Hennessy's condition was the same both before and after 21st March 2005. The operation that was necessary after March 2005 was equally necessary before.
132 I also bear in mind as an objective fact, the plaintiff was able to carry on full time work as a security guard until 21st March 2005 with a loss of only one day with severe back pain, namely 13st January 2005. Moreover, that he suffered a significant, and perhaps ongoing, flare-up of symptoms following the heavy gardening/landscaping work at home in November 2004 demonstrates that, at that time, he regarded himself as up for that type of activity. The security guard work at the container terminal involved some moderately heavy activities. Crates of bats, which were as I understand it, some form of identification issued to visitors entering the terminal had to be collected and moved. According to Mr Taylor's evidence they weighed between 10 and 15 kilograms. Ms Picone confirmed that his activity was required of guards, according to my impression, not infrequently.
133I accept, however, that the pathology shown in the pre-accident MRI and CT scan had an effect upon his ability to perform heavy work such as heavy gardening, and that this degree of incapacity was a consequence of the work injury he suffered in 2002.
134Although one must avoid the post hoc ergo propter hoc fallacy, it is significant that there seems to have been a great change in his symptomatic presentation after the injury of 21st March 2005. Dr Brookes thought he then developed "radicular pain on the left side". It is to be borne in mind that Dr Pitsis, whom Mr Hennessy saw on referral from Dr Brookes in around June 2005, received the "correct history". He was told that Mr Hennessy "has never been 100 per cent following" the 2002 injury "but well enough to continue working".
135Dr Pitsis also received a history of very severe lower back pain and associated radicular pain bilaterally worse on the left. He recorded finding an "associated positive slump test worse, on the left, with a normal neurological examination otherwise noted". I infer that this is a finding of a neurological sign. Dr Pitsis thought it evident that Mr Hennessy had a left 4/5 disc protrusion with associated left L4 nerve root impingement as indicated by the May MRI report "and supported by clinical findings". In January 2005, Dr Diwan did not diagnose L4/5 disc protrusion because he did not make clinical findings which supported that diagnosis.
136The question of whether the MRI scans of February 2005 and May 2005 show the same pathology was addressed by Drs Giblin and Schutz in their reports and in their oral evidence.
137In his report of 26th June 2013 Dr Giblin recorded that he noticed fluid in the facet joints on his examination of the May 2005 MRI scan. In evidence he described this as evidence of a significant post traumatic clinical event lasting from within 72 hours to six between six weeks and three months of the trauma (304.50-305.5T). Although, Dr Giblin regarded that sign as evidence of significant trauma, from his consideration of the MRI scan, he would not have recommended surgery basically because of the presence of epidural fat around the nerve. The epidural fat is a protective covering and "is one of the very first anatomical structures to disappear in an x-ray when that nerve is under compression" (305.10T), I took this to mean there is no point decompressing a nerve root by removing the disc protrusion or bulge because it was not compressed.
138As I have said, Mr Hennessy has undergone three operations. He first saw the operating neurosurgeon, Dr Mark Davies on 27th September 2005. Dr Davies did not get an accurate history of the previous injury. However, he did record what he regarded as signs of radiculopathy being asymmetrical limitation of straight leg raising, worse on the left and a reduced left knee and ankle jerk. His diagnosis was left L4 radiculopathy secondary to foramenal L4/5 disc lesion. At the surgery on 15th November 2005 he found the following:
Shallow left posterolateral/foramenal L4/5 disc lesion. Focal tear in foramen. Small amount subligamenatous sequestrated material adjacent to L4 nerve root.
Dr Giblin was of the view that those operative findings of a displaced piece of disc material "would be consistent with the mechanism and history of injury". I asked him the following question:
Q. And does that have any connection with what you said about the fluid in the facet joints?
A. Yes, exactly, direct causal connection (305.40T).
It should be recorded that Dr Giblin would not have operated under those conditions. He regarded the pathology disclosed on the MRI scan as not severe enough to warrant it. However that may be, his evidence supports the view that there was an increment in the pathology because of the injury of 21st March 2005 being the sequestrated disc material and the recency of the trauma causing that increment is supported by the finding of fluid in the facet joints not commented upon by the radiologist when he prepared his report of 24th May 2005.
139Dr Schutz agreed that fluid in facet joints is an indication of inflammation which could be due to "an acute significant trauma" or trauma in the form of an ongoing or intermittent aggravation of pre-existing aggravation. He could not distinguish between them. He would accept that the fluid could be present for six to twelve weeks. But if due to "inflammation without ... specific cause" then it would dissipate when the inflammation settled (318.10 - .35T).
140I formed the impression that Dr Schutz was very disenchanted with Mr Hennessy for giving him the wrong history in the first place. I must say this is understandable. But it did seem to colour his views and affect his evidence: see 325.15T; 328.35 - .45T.
141On reviewing the contemporaneous medical material, he formed a strong view that the pathology remained the same throughout subject to periodic flare-ups following specific trauma, but basically unchanged. If there was a need for surgery, which he seemed to accept there was, it was due to the underlying condition, not any aggravation which may have occurred on 21st March 2005 which he regarded as temporary and self-limiting, lasting a period of weeks only.
142He accepted, however, that the underlying condition is susceptible to the effects of trauma of different kinds (335.5T). And that the incident of 21st March 2005, if it occurred, is capable of being a significant incident of trauma (335.10T). In his view if one accepted from March 2002 an ongoing cyclical situation of flair-ups and remissions followed by an incremental worsening of an ongoing type after March of 2005 then the incident in March of 2005 is "the primary cause" (335.20 - .40T). However it was clear that Dr Schutz thought that the nature of the complaints made to Dr Diwan in January 2005 weighed heavily against the idea that there was any "supposed changed" in March 2005.
143The second surgery occurred on 28th February 2006. The background, according to Dr Davies, is that Mr Hennessy developed a recurrence of his left leg pain, following what the surgeon had regarded as successful surgery. It was decided to undergo a re-exploration of his spine. As Dr Davies explained in his report of 7th March 2006, his intention had been to remove "the existing dynamic stabilisation device, perform a redo discectomy and insert a new prosthesis". During surgery he became aware of the pars interarticularis/inferior articular defect at L4 which he regarded as "not visible on imaging". During surgery he decided that this was evidence that the L4/5 segment was unstable. He also found a disc bulge with a small recurrent sequestrated foramenal component. He said "both pathologies were causing marked L4 nerve root compression". He carried out a complete foraminotomy and rhizolysis of the left L4 nerve root together with a single level spinal fusion at L4/5. This produced "immediate relief of [Mr Hennessy's radicular leg pain".
144It is fair to say that both Dr Giblin and Dr Schutz were somewhat puzzled by Dr Davies deciding to perform a fusion during surgery because he'd found a pars defect. Dr Schutz doubted that a unilateral defect would cause instability and Dr Giblin regarded treating a defect with a fusion as superseded by modern practice (308.45T). Dr Giblin thought the presence of the defect in conjunction with a recurrent sequestrated disc was significant. But he would not have carried out a fusion (308.15 - .35T).
145Initially signs following the surgery were good, as I have said, and by August 2006 Dr Davies thought the x-rays were indicating that the fusion was going to be solid. As at September 2006, Mr Hennessy seems to have got back to some form of light part-time work in a static position for a couple of hours a day. Dr Davies doubted he would be able to sustain that type of work for 12 hours on end. He needed to be more mobile. However, he did not last long in this position because he redeveloped back pain which was slowly worsening within about a month.
146By April 2007, his condition had deteriorated significantly. He was complaining of constant back and severe bilateral leg pain, namely in the left leg. He was on very strong narcotic pain killing medication. On examination, there was marked restriction of all spinal movements and there were some inconsistent neurological signs on the left. Sophisticated radiological techniques showed that the fusion was not solid. There was a "halo" around the L5 screws by which the fusion was fixed at that level. Dr Davies considered that the halo was a pseudoarthrosis at L4/5 permitting "micro movement" which would be a significant contributor to ongoing pain. Dr Giblin said that this indicated that the fusion surgery had failed. In these circumstances, Dr Giblin was of the view that further surgical attempt was "a reasonable option". The third operation was carried out in August 2007 by way of a revision of the spinal fusion.
147The situation since then unfortunately has not been one of improvement. Rather Mr Hennessy has been treated with a large variety of different modalities to manage his pain from psychological and psychiatric consultation to specialist pain-management physicians. He has received nerve stimulator treatment and a series of analgesics, antidepressants and pain modifying drugs, according to Dr Brookes's report of 12th September 2012.
148He has applied for employment unsuccessfully and he failed to finish a private investigation course which was recommended by a vocational agency because he was physically unable to complete the course due to his disabilities. All this has been compounded by his psychological state. However, the psychiatrists are of the view that his mental problems are caused by the severity of his physical disability. Dr Brookes provided the following opinion:
It is my opinion that Mr Hennessy is now unemployable due to his chronic pain and psychological scarring. The severity of his symptoms preclude meaningful employment. He is psychologically unsuited to sedentary employment and his physical disabilities make sitting and driving for periods impossible.
His prognosis is poor. He may improve with time, but his disabilities are unlikely to allow employment.
149It is notable that Dr Giblin is of the view that Mr Hennessy has a guarded prognosis in terms of any return to work. In his last report of 27th June 2013 Dr Deveridge, armed with all relevant material, adhered to his view that there had been a material aggravation of a pre-existing spinal condition, particularly at the L4/5 disc protrusion which led to the need for medical and surgical treatment. Dr Deveridge did not expect Mr Hennessy to return to gainful employment. There is an ongoing need for high dose narcotic medication. The medication itself would prevent him from performing even sedentary duties of a responsible nature. He requires domestic home care assistance. Dr Deveridge does not expect there to be any further surgery.
150In his report of 5th October 2009, Dr Schutz found extensive post-operative fibrous tissue-scarring on looking at the post-operative MRI scans. He said of that phenomenon, in evidence, the following (332.10T):
Well, we are seeing Mr Hennessy who has unresolved symptoms despite surgery. And one of the causes of persisting symptoms in the radicular nerve root distribution is pathology involving the nerve root. The surgeon has taken away the prolapsed disc ... but perineural fibrosis, that is scar tissue around the nerve, is invariable after any sought of operation, but sometimes it becomes a significant problem, hence I have referred to extensively to post-operative fibrosis. In other words, I think that that is probably greater - at the high end of expectations and possibly the cause of ongoing radicular symptoms.
Dr Schutz said that the phenomenon was induced by the first operation. This probably accounts for the high level of ongoing pain. Dr Schutz was of the view that with some allowance for freedom of movement Mr Hennessy could work "in a light and variable clerical activity".