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You are here: BAILII >> Databases >> Scottish Court of Session Decisions >> Lawson (AP) v Lothian Health Board [1999] ScotCS 105 (5 May 1999) URL: http://www.bailii.org/scot/cases/ScotCS/1999/105.html Cite as: [1999] ScotCS 105

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The pursuer in this action of reparation in respect of medical negligence broke his lower left leg while playing football in Edinburgh on Sunday, 12 January 1992. He sustained fractures of the left tibia and fibula. He was taken to the Orthopaedic Trauma Unit in the Royal Infirmary in Edinburgh where he underwent an operation involving the internal fixation or nailing of the broken bones. That operation was carried out successfully. In the course of his subsequent recovery from that operation the pursuer developed a condition known as compartment syndrome in the lower left leg. In order to deal with that condition surgical intervention in the form of a fasciotomy was required. On the evening of 15 January 1992 the pursuer was accordingly taken to the operating theatre in the Royal Infirmary where a fasciotomy was carried out by Mr John F Keating, at that time a senior registrar and now a senior lecturer in orthopaedic surgery in the University of Edinburgh and an honorary consultant in orthopaedic surgery in the Royal Infirmary and Princess Margaret Rose Hospitals in Edinburgh. On behalf of the pursuer it is claimed that in the course of carrying out that fasciotomy operation Mr Keating negligently damaged the posterior tibial nerve in the pursuer's left lower leg. In particular it is averred that the nerve was "partially severed, or damaged when stretched or pulled".

In the event that it is established that Mr Keating negligently inflicted such damage on the posterior tibial nerve, parties are agreed by Joint Minute on the amount of damages which should be awarded.

The anatomy of the lower leg was the subject of discussion and description in the evidence and for an understanding of the issues raised in the case it is appropriate to give a simplified description of the relevant aspects. The muscles of the lower leg, below the knee, may be grouped together in what are conveniently described as four compartments, each of the compartments being bounded by a thicker membrane known as the fascia. The arrangement of the compartments may be seen schematically in horizontal cross-section in the diagram No 25D of process. To the rear of the lower leg is the superficial posterior compartment. On the outer aspect of the lower leg lies the lateral compartment. On the forward aspect of the limb is the anterior compartment. And lying between the anterior and superficial posterior compartments is to be found the fourth compartment, namely the deep posterior compartment which extends medially towards the inside surface of the leg.

Within the superficial posterior compartment are to be found the soleus muscle and the gastrocnemius (lateral head and medial head) muscles. These muscles have the function of enabling the foot and toes to be lowered as a whole. Within the deep posterior compartment are grouped (i) the tibialis posterior muscle, whose purpose is to enable the ankle to be pointed downwards and to support the arch of the foot; (ii) the flexor digitorum longus muscle, which allows the four small toes to be pointed downwards and (iii) the flexor hallucis longus muscle which provides a similar function respecting the hallux, or big toe. The anterior compartment contains by contrast muscles which enable the foot and toes to be pulled up, namely the tibialis anterior, the extensor digitorum longus and the extensor hallucis longus. The lateral compartment includes within it the peroneus longus and peroneus brevis muscles, which enable the foot and ankle to be pointed outwards.

Turning to the nerves which supply and activate those various muscle groups the principal nerve stemming from the spinal cord and supplying all of them is the sciatic nerve which, having passed down the thigh bifurcates at or a little above the knee to become (a) the tibial nerve and (b) the common peroneal nerve. The latter nerve - the common peroneal - provides, after division into the deep and superficial peroneal nerve, the nerve input necessary to operate the muscles in the anterior and lateral compartments, that is to say, those extensor muscles which enable the foot and toes to be pulled up and those muscles affecting eversion of the foot. The tibial nerve, following the bifurcation with the peroneal nerve runs down the back of the knee in the area known as the popliteal fossa. It then enters the superficial posterior compartment and at about that point of entry one finds branches leading from it which supply the necessary nervous input to the soleus muscle and the two gastrocnemius muscles. As it descends further down the leg the tibial nerve passes beneath the soleus muscle. As it does so, it moves from the superficial posterior compartment into the deep posterior compartment and is described thereafter as the posterior tibial nerve. At about the same point branches from the posterior tibial nerve feed into the muscles of the deep posterior compartment, ie, tibialis posterior, flexor digitorum longus and flexor hallucis longus whose functions have already been briefly described. The posterior tibial nerve continues down the leg in what might be crudely described as the middle of the leg, and in due course forks, at about the level of the ankle, into the medial and lateral plantar nerves.

Compartment syndrome involves an increase in the hydrostatic pressure within one or more of the compartments. In its typical form, in the case of the lower leg, the patient suffers an injury such as a fracture of the tibia or fibula which may produce bleeding within the compartment. The fascia being tough and fibrous the compartment cannot expand sufficiently to accommodate the pressure arising from that escape of blood. The increasing pressure causes impairment of the blood supply to the muscle tissue. With inadequate diffusion of blood to that tissue the muscles may become ischaemic and in doing so produce waste fluids which in turn further increase pressure within the compartment which in turn further inhibits the blood supply. In effect there develops a vicious cycle. Nerve tissue is likewise dependant on a supply of blood. The increasing hydrostatic pressure and its inhibition of the blood supply therefore also endanger the viability of the nerve tissue. The development of compartment syndrome following tibial fractures is variable in a sense that many patients do not have this complication whereas unfortunately some others do.

A patient suffering from compartment syndrome experiences severe pain and sometimes, in addition, pins and needles. Where the pain from the original fracture or other trauma appears not to settle but rather to worsen and become out of proportion to the pain usually to be expected from the original injury, compartment syndrome may be suspected. It is also possible to measure the pressure at a point within a compartment by inserting an instrument known as a pressure monitor. The anterior compartment is the one which most readily allows the insertion of a pressure monitor.

In its normal, typical form compartment syndrome presents as an acute condition within a few hours of the injury to the limb. Much more unusually however, some accident victims develop a late compartment syndrome some days after the original injury. The reasons for this are not clearly understood or well established. It may be that the original traumatic injury inflicted damage on certain muscles which causes them to lose their blood supply and die. The ensuing physiological mechanisms produce increased fluids within the compartment as necrosis develops. There may also be a late resumption of bleeding from the original injury which either by itself, or in combination with the production of fluids from the necrosis of muscle tissue, may result in increased pressure within the muscle compartments of the lower leg.

The recognised treatment for compression syndrome, whether classical or late, is fasciotomy, that is to say the making of an opening in the fascia in order to decompress the compartment. Although it is not necessarily the case that more than one compartment will be affected, all the medical witnesses were agreed that standard practice when undertaking a fasciotomy of the lower limb was to open all four compartments. That standard procedure involves making two longitudinal incisions in the skin, one on the medial side of the lower leg in order to decompress the superficial and deep posterior compartments and another skin incision on the lateral side in order to decompress the anterior and lateral compartments. The location and length - typically six inches or a little more - of the skin incisions is illustrated on Production No 25E. Having incised the skin and underlying fatty tissues on the medial side to expose the bluey grey structure of the fascia the surgeon is then able, by pulling the skin and fatty tissue back a little, to make an incision in the superficial posterior compartment and thereafter, by pulling the skin and fatty tissue forward a little, to make an incision in the deep posterior compartment. Similarly in the case of the lateral skin incision, the surgeon is able by pulling the skin respectively a little back or forward to make from the single skin incision two incisions in the fascia of the lateral and anterior compartment respectively. On making the fascia incisions, particularly if the compartment is under pressure, the muscle tissue may pout or protrude from the fascia incision.

If the incision in the fascia reveals muscle tissue which is plainly dead, that tissue should be removed and the surgeon would then proceed to a further stage of removing that necrotic tissue. The incisions in the fascia are left open subsequent to the fasciotomy, in order that the viability of the underlying muscle and nerve tissues may be assessed following the resumption of the blood supply.

As already indicated above, the pursuer was admitted to the Orthopaedic Trauma Unit of the Royal Infirmary of Edinburgh on Sunday 12 January 1992 following his football injury. He was noted inter alia as having sustained a closed shaft fracture of the middle third of the tibia. It was also noted that there was no neurovascular compromise and no sign of a compartment syndrome. (No 9 of process, page 10). On the following day, 13 January 1992, Mr Court Brown, consultant orthopaedic surgeon, carried out a routine operation to fix and nail the fractured tibia. At the beginning of that operation a pressure monitor was inserted in the anterior compartment to measure compartment pressure. It disclosed pressures ranging between 30 - 35mm of mercury, regarded by the medical witnesses as normal. The pressure monitor was left in place after the operation so that monitoring of compartment pressure might continue. On the morning of 14 January 1992 the pressure monitor was removed, the in situ readings being between 24 and 29mm.

No criticism is made of the decision to remove the pressure monitor at that point. Indeed Professor Rowley, professor of orthopaedic and trauma surgery in Dundee, who was tendered as a witness for the pursuer described the decision as being very reasonable. It is convenient at this point to record that Professor Rowley also acknowledged that in 1992 the trauma unit in the Royal Infirmary in Edinburgh monitored post-operative compartment pressure as a matter of routine and in doing so went beyond what was normal custom and practice in the average hospital. It may also be recorded at this point that there was largely undisputed evidence that the Edinburgh Unit had considerable reputation for its expertise in treating trauma victims and in its study and treatment of compartment syndrome.

Reverting to the history of events, at about 1800 hours on Wednesday 15 January 1992 the nursing notes recorded the pursuer as having a temperature of 38.4ºC and the medical staff were informed. Thereafter follows a nursing note that the pursuer was complaining of "severe pain in his left leg and toes numb". There was also a note that "patient also states he cannot feel his 4 left toe (great)". The patient's temperature was then recorded at 38.6ºC. At 2210 hours the pursuer was given an injection of morphine sulphate, a potent analgesic, and at 2350 hours was taken to the operating theatre where an emergency fasciotomy operation was carried out by Mr Keating. The note of the operation dictated by Mr Keating very shortly after its conclusion is transcribed in these terms:

The hospital notes further record that on 17 January 1992 the pursuer was seen by Mr Court Brown whose dictated note is transcribed thus:-

On the following day, 18 January, Mr Court Brown carried out a re-exploration of the left leg wound but found nothing significant. There was a little dead muscle which he resected. His dictated note of the operation then contains in its transcription the following:-

On 29 January 1992 the pursuer was transferred from Edinburgh to Dundee Royal Infirmary to be near to his home and family during his further recuperation and the nerve conduction studies desiderated by Mr Court Brown were in due course carried out in Dundee. Evidence was given in relation to those studies by a Dr Foster, a consultant in clinical neurophysiology.

The evidence given by Dr Foster was in some respects highly technical and was not always easy to follow. For the moment it is perhaps sufficient to record that a principal finding pertinent to the posterior tibial nerve was produced by an "inching" study - which involved the placing of electrodes on the surface of the skin at roughly one inch intervals along the course of the nerve. That study gave an indication of injury to the posterior tibial nerve having been sustained somewhere between one and two inches below the operation scar on the inner aspect of the pursuer's leg. In a passage in his report of 22 July 1994 (24/1 of process) Dr Foster expressed himself thus -

In his oral evidence, Dr Forster made clear that this site of clear change in amplitude, indicative of some injury to the posterior tibial nerve, was not between the two tips of the operation scar but was somewhere between one and two inches distal to the distal tip - "the tip nearest the ground" - of the operation scar (201F, cf. 206B, 235D). Dr Forster also made clear that the injury to the posterior tibial nerve in that area could not have involved the complete severing of the nerve. (238).

It was also apparent from the nerve conduction studies that the pursuer was unable to activate a large number of muscles served by the deep peroneal nerve and the superficial peroneal nerve and by the tibial nerve (before it becomes the posterior tibial nerve). In particular, the pursuer was unable to activate the gastrocnemius muscles which are enervated by branches from the tibial nerve in the superficial posterior compartment.

So far as the pursuer's further treatment and recuperation is concerned, putting matters shortly, the pursuer never recovered any effective voluntary movement of his left ankle or foot. In October 1994 he underwent a fusion operation of the left ankle and subsequently an attempt was made at tendon transfer which failed.

It is averred on behalf of the pursuer that in the course of the fasciotomy operation "the posterior tibial nerve of the pursuer's left leg was damaged at or about the point where it passed the pursuer's left knee". It is then further averred that - "the said nerve was partially severed, or damaged when stretched or pulled". In Article 3 of Condescendence it is averred that any surgeon of ordinary skill exercising reasonable care would have avoided causing damage to the pursuer's posterior tibial nerve.

Although it will be necessary to revert to the matter later, it is convenient to observe at this point that it was generally accepted by all the medical witnesses that traumatic injury to the posterior tibial nerve was not a recognised possible risk of a lower limb fasciotomy against which particular care had to be taken. The posterior tibial nerve lies well within the deep posterior compartment. There was some disagreement as to the precise depth at which it lay from the medial surface of the leg but it appeared that in an adult male it might be one to two inches. In opening the fascia a surgeon would not require to approach or expose the posterior tibial nerve.

The defenders for their part aver inter alia that any damage sustained to the posterior tibial nerve occurred in consequence of compression ischaemia. That contention was disputed by the pursuer's witnesses, principally Professor Rowley, who, having formed the view that the damage was not ischaemic concluded that the only other option was a trauma inflicted by the surgeon in the course of the fasciotomy.

I find it convenient to consider first the issue of ischaemic damage.

The witnesses tendered on behalf of the defenders - Mr Keating, Mr Court Brown and a further consultant orthopaedic surgeon, Mr James Graham - all expressed the view that any deficits in the pursuer's posterior tibial nerve were attributable to ischaemic damage arising from interference with the supply of blood to the nerve during the development and persistence of the compartment syndrome.

As I understood it, one of the main reasons for which Mr Court Brown reached that view was the wide extent of the pursuer's disabilities. The pursuer's inability to move his ankle and foot was quite generalised. One was not talking of dysfunction only in the muscles enervated by the posterior tibial nerve. To explain the wider dysfunction there would have to be a problem which interfered with all the major nerves of the lower limb and that could really only be an ischaemic problem. Moreover, looking more closely at the posterior tibial nerve, the enervation to the flexor hallucis longus, the flexor digitorum longus and the tibialis posterior muscles came off the posterior tibial nerve about half way up the tibia, that is to say, well above the area of change of amplitude in the course of the posterior tibial nerve identified in the nerve conduction "inching" studies. There must therefore be some damage to the posterior tibial nerve above that area and the most likely cause of that damage was ischaemia induced by increased pressure in the deep posterior compartment during the development and persistence of the compartment syndrome. The deep posterior compartment and the anterior compartment were the compartments most commonly involved, at least in the classic, acute compartment syndrome. It was however more difficult to generalise in the case of late compartment syndrome because it was a condition much less frequently encountered. Mr Court Brown explained that although in January 1992 he had found it difficult to believe that the pursuer had anoxic (ie. ischaemic) damage to such a complete degree as to prevent him having any voluntary movement of his foot or ankle, knowledge and experience of late compartment syndrome had increased since 1992. Late compartment syndrome manifested itself in a different and more insidious way. It often had a different mechanism. While it would be unusual to get extensive ischaemic damage in acute compartment syndrome which is decompressed quickly, it was now becoming more recognised that in late compartment syndrome, such as that suffered by the pursuer, the damage was already there and even the prompt decompression by fasciotomy would not produce the same successful results as could be obtained in classic acute compartment syndrome.

Mr James Graham was from December 1976 until his retiral from active NHS practice in 1996 a consultant orthopaedic surgeon at the Western Infirmary and Gartnavel General Hospitals in Glasgow. His opinion was similar to that held by Mr Court Brown. Starting from the clinical findings that the pursuer was unable to move his left foot or ankle and the indications from the nerve conduction studies of nerve damage which affected a large number of muscles in the left lower limb, Mr Graham stated that in his view the only possible causes were a severing of the sciatic or tibial nerve or catastrophic damage to the artery or increased pressure in all four compartments of the lower leg producing ischaemia of the nerves and thus leading to loss of function in those nerves. Severing of the sciatic or tibial nerve could of course not have occurred in any fasciotomy of the lower limb and the vascular changes in the leg which would have accompanied the second possibility were wholly absent. Similarly, Mr Graham pointed to the fact that the pursuer appeared to have lost the ability to use the gastrocneumius muscles which in any view were enervated by the tibial nerve in the superficial posterior compartment before it had become the posterior tibial nerve. The pursuer's extensive disability could thus only be ascribed to ischaemic damage.

Mr Keating also considered that any damage in the function of the posterior tibial nerve was the consequence of the compartment syndrome. The deep posterior compartment is, after the anterior compartment the compartment, most commonly involved in compartment syndrome and the other compartments were also affected to a greater or lesser degree in most compartment syndrome cases. In the present case the deep posterior compartment was very close to the fracture site. Cases of compartment syndrome undoubtedly could produce permanent ischaemic damage to the nerve tissues, particularly if not decompressed sufficiently quickly. It was Mr Keating's opinion that any nerve damage was most likely to have been due to ischaemia as a consequence of the compartment syndrome possibly combined with or exacerbated by direct injury or trauma to a nerve at the time of the fracture and the displacement of the bone ends.

When invited to respond to the proposition that the injury to the pursuer's posterior tibial nerve arose from compression ischaemia Professor Rowley appeared to give two principal reasons for rejecting that suggestion. First, on his understanding of matters the pursuer went into the fasciotomy operation with complete ability to move his foot and ankle and since on emerging from the operation the pursuer was unable to move his foot and ankle and also had numbness on the sole it had to be concluded that an event had occurred during the conduct of the operation which had caused damage to the nerve. That view appeared to be supported by Professor Rowley's understanding that the "inching" study indicated that something was happening locally within the compass of the medial operation scar. The other principal strand of Professor Rowley's reasoning was his understanding that at the fasciotomy operation the deep posterior compartment was found not to be under pressure and accordingly ischaemic damage could not have arisen. Professor Rowley had not seen any such ischaemic damage to the posterior tibial nerve in those cases of compartment syndrome which he had seen, particularly in blast injuries in war zones in Kenya and Afghanistan. In elaboration of this strand the professor pointed to the operation note dictated by Mr Keating, which he construed as plainly indicating that the muscles within the deep posterior compartment were healthy. The phrase which Mr Keating had employed was "the muscle adjacent to the fracture site was quite contused but otherwise the muscles appeared to be viable". Muscle tissue was less resilient to ischaemic damage than nerve tissue. Accordingly had there been sufficient pressure within the deep compartment to inflict ischaemic damage on the posterior tibial nerve the muscles of the deep posterior compartment would clearly have shown ischaemia. Although there was very elevated pressure recorded on the monitor in the anterior compartment (sufficiently high to suggest a doubt as to the accuracy of the reading) Professor Rowley did not consider that it followed that other compartments might also be under pressure. In particular the interosseous membrane between the anterior and deep posterior would provide a "bastion of resistance" to pressure. Professor Rowley did however agree that standard procedure in any fasciotomy would involve making an incision in each of the four compartments in order to relieve the pressure.

Dr Forster was also sceptical about the view that the damage to the posterior tibial nerve was ischaemic. He considered that nerves were resilient to compressive injury and that it took pressure of a significant amount and duration before permanent ischaemic damage might be suffered by a nerve. Dr Forster pointed out that tourniquets were used to create a bloodless field in surgery and pressures of up to 300mm for periods of up to three hours were commonly used without leading to permanent adverse effect on the nerve tissue. Dr Forster's understanding was that only three hours had elapsed from the symptoms being noted until decompression. The timescale was such that ischaemia would not be an issue unless there were some major local compression at the site of damage or within the compartment.

As Mrs Smith, who appeared for the pursuer, pointed out in her submissions, certain of the matters relied upon by Professor Rowley and Dr Forster were accepted by some of the defenders' witnesses. Thus Mr Keating, Mr Court Brown and Mr Graham all agreed as a generality that nerve tissue was more resilient than muscle tissue to loss of blood supply, at least in the sense that nerve tissue had greater ability to make a long term recovery. Mr Keating and Mr Graham had agreed that identification of a specific site of nerve injury would be more indicative of a traumatic insult than compressive ischaemic injury. Her submission in regard to the nature of the injury was that on the evidence ischaemia was not the likely cause. In particular she submitted there was evidence that the deep posterior compartment was not under elevated pressure. No monitor readings were of course available since a monitor had not been inserted in the deep posterior compartment. The operation note did not record anything to the effect that there was pressure. Had there been signs of elevated pressure a surgeon would have recorded that in his operation note. All that Mr Keating had recorded was that the muscle was quite contused. However, said Mrs Smith, that was simply bruising from the footballing injury and apart from Mr Keating no other witness had suggested that the bruised muscle tissue might be the sequel to or indicative of pressure within the deep posterior compartment.

Mr Campbell, who appeared for the defenders, put forward in relation to this issue the submission that in important respects the evidence of Professor Rowley was based on mistaken or unjustified assumptions. Professor Rowley had assumed that the pursuer could fully move his foot and ankle when he went into the fasciotomy operation but there was evidence that such was not the case. The pursuer himself deponed (13B-D) that after the nailing operation and before the fasciotomy he could not in fact move his toes or ankle. Mr Graham in his evidence had highlighted the nursing note entries - already set out above - which indicated in his view clear abnormal neurological signs. In cross-examination Professor Rowley had indeed accepted (135) that there were indications of abnormal neurological signs prior to the fasciotomy operation. This did not give any proper basis for the professor's assumption that all was completely well prior to the fasciotomy and that therefore an untoward event must have occurred during the conduct of the operation. Further it was neither true nor correct to say that on carrying out the fasciotomy Mr Keating had found that the tissues within the deep posterior compartment were not under pressure. The operation note dictated by Mr Keating immediately after the operation did not say so. What Professor Rowley sought to read into a single sentence was contradicted by Mr Keating's evidence in which Mr Keating explained that in the absence of a monitor a surgeon would not record pressure as such but would briefly record what he observed. Mr Keating had recorded the sequelae of pressure, namely contusion in the muscle tissues. Mr Court Brown (419-420) did not regard the findings noted as indicating that the deep posterior compartment was not under pressure. Further, Professor Rowley's evidence proceeded on the mistaken assumption that the area of damage identified in Dr Forster's "inching" studies was within the area of the medial operation scar whereas, as Dr Forster had clarified in his oral evidence, it was some one to two inches below the lower or distal end of the operation scar.

Counsel for the defenders further submitted that Dr Forster's dismissal of ischaemic damage, and his whole reference to the supposed tourniquet analogy, proceeded on the wrong assumption of the whole compartment syndrome suddenly developing and enduring for a mere three hours. Plainly there was a background of pain from the original fracture, and as explained by Mr Keating (288-291), the syndrome may be developing and may exist for some time the patient being in any event in receipt of pain killing drugs. In his own evidence the pursuer had explained how he was in pain and receiving morphine but the then point arrived when the morphine was no longer controlling the pain. That was not at all inconsistent with the gradual onset of pressure in the compartments until eventually the inability of the analgesic drugs to mask the increasing pain led to the noting by the nursing staff of the abnormal neurological signs. The supposed tourniquet analogy was not a true analogy and was inappropriate to the development, over time, of compartment syndrome pressures, particularly in the unusual case of the development of a late compartment syndrome.

Leaving aside for the present the probabilities or improbabilities inherent in the alleged act of negligence as such, and adjudicating simply on the medical arguments for or against ischaemic damage I have come to the conclusion that the evidence led on behalf of the defenders is to be preferred.

I am in agreement with Mr Campbell that the evidence given by Professor Rowley proceeded on assumptions which Mr Campbell properly characterised as being in the event unsound for the reasons he gave and which I have already summarised and need not repeat. My distinct impression was that Professor Rowley attached notable weight to the fact that, on his reading of Dr Forster's report of 22 July 1994 (No 24/1 of process) the area of damage to the posterial tibial nerve identified in the "inching" studies was within the immediate area subjacent to the fasciotomy incision. Dr Forster's report is ambiguous as to the location of that point and I well understand that Professor Rowley read it in the way in which he evidently did - that is to say a point of injury two inches or so below the end of the operation scar nearest to the knee, and thus subjacently within the area of the incision. In giving evidence Professor Rowley preceded Dr Forster who made clear that, as already explained, the relevant site of that apparent nerve injury was some two inches below the lower end of the scar, that is to say the end nearest to the ankle. Not only is that location outwith the area of surgical intervention but, as was explained Mr Court Brown and Mr Graham, it was located too distally to account for the pursuer's inability to operate the muscles of the deep posterior compartment which draw their enervation higher up the posterior tibial nerve. On that matter Dr Forster (239) was in agreement with Mr Court Brown and Mr Graham.

It also appeared to me that neither Professor Rowley nor Dr Forster had any persuasive explanation for the generalised nerve damage from which the pursuer unfortunately suffers. Professor Rowley accepted that he had difficulty in explaining the common peroneal picture (130ff) and when cross-examined (113ff) in relation to the gastrocnemius and soleus muscles he appeared unwilling or unable to give any clear answers. Dr Forster also had difficulty in explaining the generalised picture of dysfunction. He did suggest (251) that scarring or adhesions might be an explanation for the pursuer's inability to operate these various muscles but on that particular point deferred to the views of the orthopaedic surgeons. That suggestion was effectively and emphatically discounted by Mr Court Brown (452).

It also has to be borne in mind that the pursuer's case was not a classic acute compartment syndrome but took the much less common form of a late compartment syndrome. As Mr Court Brown explained, in the latter form a different precipitating mechanism may be involved such as a developing necrosis of muscle fibre and the whole process may be much more insidious. Recently gained experience of late compartment syndrome indicated that decompression, even brought about promptly, did not achieve the same results as in the classic form. Mr Keating (277ff) also pointed out that the late compartment syndrome was an uncommon event and was rather non-typical in presentation.

It was not really disputed that the orthopaedic trauma unit of the Royal Infirmary in Edinburgh has a particular reputation for clinical research in this field. Mr Court Brown, a distinguished member of that unit, has had a particular interest in tibial fractures which led in turn to a special interest in compartment syndrome. With appropriate modesty of demeanour he accepted that he was an expert in the subject (402-4). Mr Keating did his senior registrar training in the Edinburgh Royal Infirmary Trauma Unit in 1991 and 1992 and having done so had a particular awareness of compartment syndrome. He had a particular interest in tibia fractures. (It may be noted that having been informed of the pursuer's condition on the evening of 15 January 1992, he was in no doubt as to what had to be done and carried out the fasciotomy as a matter of considerable urgency). It was of course not disputed that Professor Rowley had experience in treating compartment syndrome. Particularly, as he said, he had experience of dealing with the victims of war in Kenya and Afghanistan. However, he did not claim any particular expertise or specialised knowledge in the particular matter of late compartment syndrome. Counsel for the defenders remarked that a surgeon not having particular specialised knowledge of compartment syndrome - and especially the very uncommon late compartment syndrome - may not fully appreciate the potential for late compartment syndrome to cause lasting ischaemic damage, even if treated promptly after the eventual observation of the development of the symptoms. I consider that to be an apposite observation.

The other facet to which attention must be given is the nature of the alleged negligence and its probability. As has been already indicated, fasciotomy of the lower limb is not seen as being an operation carrying any risk of surgical injury to the posterior tibial nerve if carried out in the standard fashion. Professor Rowley agreed that injury to the posterior tibial nerve was an unlikely event, the surgical work being relatively superficial. There was, he said, no risk of actually cutting the posterior tibial nerve because "although it is adjacent it is far enough away not to require exposure as routine and a surgeon using normal surgical techniques and skill should not encounter it or put it at risk in any way" (58). Having then been asked by counsel for the pursuer how, assuming lack of care, a surgeon might cut the nerve, Professor Rowley responded thus -

Under encouragement from counsel the Professor moved from speculation to envisaging as a "strong possibility", that in the act of opening up the incision in the fascia a surgeon, if he caught the nerve, might tear it in part and pull it in part.

On the other hand, for his part, Dr Forster adverted (162) to the nerve being "fairly stretchy, .... a very resilient piece of tissue". By explanation of what he meant by resilience he went on to say this -

Mr Court Brown (423) considered it extremely unlikely that surgical damage could be sustained by the posterior tibial nerve in the course of the fasciotomy; It was a straightforward operation and there was no requirement to go into the deep posterior compartment itself "beyond a very very few millimetres"; and it was next to impossible if the lesion to the nerve were one to two inches or so below the point at which the lower end of the operation scar finished.

Mr Graham was also of the opinion that it would have been very difficult to damage the posterior tibial nerve when carrying out the operation in the correct manner. He likened it to taking a knife to the skin of a heated haggis and whenever the skin is burst the haggis burst open. Muscles did the same on the incision of the fascia. There was no need for any surgeon to go any deeper. It would be even more difficult to damage the nerve at the location indicated in the inching studies -

Perhaps more importantly, Mr Graham pointed out that there was no need to go down to that level because the great bulk of the muscles of the posterior compartment were not there but lay at a higher level.

On the evidence I conclude that the infliction of surgical damage to the posterior tibial nerve during a simple fasciotomy is at best improbable and it is yet more highly improbable that injury might be inflicted to the posterior tibial nerve at the location indicated in the "inching" study. That high improbability is in my view reinforcement of the view which I take of the other evidence to the effect that the damage to the pursuer's posterior tibial nerve was caused by ischaemia during the development and persistence of the late compartment syndrome.

In his evidence to the Court Mr Keating denied having done anything which might have injured the posterior tibial nerve. He explained (279ff) that he carried out the fasciotomy on the deep and superficial posterior compartments in a wholly normal fashion. Since the muscle tissue had an appearance of viability, no excision of the muscle was carried out. He considered that the contusion to the muscle tissue indicated that there was a degree of pressure. Mr Keating further stated that since the nerve was fairly deep in the centre of the leg it required a fairly extensive exposure to get to it and so "one would have to have made a deliberate attempt to be exposing this nerve to be first of all anywhere near it. I didn't do this in this case. I did not damage this nerve surgically." Mr Keating also denied ever having placed his finger in the wound and having moved it up or down in the manner envisaged by Professor Rowley. Mr Keating further denied having attempted to reach at any stage the inside of the pursuer's leg below the level of the incision or having had any cause to do so. In that regard he said -

Mr Keating stressed that a normal fasciotomy carried no possibility of direct injury or traction on the posterior tibial nerve because it did not require the surgeon to make any manoeuvre whatsoever to expose the nerve or place traction on it. He put matters thus (at 362) -

Counsel for the pursuer submitted that Mr Keating's denial of having inflicted surgical damage on the posterior tibial nerve was not credible. She said that Mr Keating "protesteth too much" and had a defensive attitude stemming from a pride which was his downfall. Other points affecting his credibility were made in relation to the general discussion of the probability of improbability of ischaemic damage which I have already addressed. Relating particularly to the demeanour of Mr Keating I reject Mrs Smith's submission that Mr Keating was not a credible witness. His denial of the allegation of negligence was repeated, and at times forceful, but in my view that was in fair measure a reflection of the frequency and strength with which the allegation was put to him by the cross-examiner. In the light of his own evidence and the evidence of the other eminent surgeons giving evidence in this case I think that Mr Keating is wholly correct in saying that to have inflicted the injury on the posterior tibial nerve in a fasciotomy as claimed by the pursuer, the surgeon would have to go far outwith the appropriate field of surgery. That is not something which could have been done in any way unwittingly or by mere oversight. I believe and accept Mr Keating's evidence that he did not do anything of that kind.

I have of course every sympathy for the pursuer who has had the extreme misfortune to develop the unusual condition of a late compartment syndrome and who has, in consequence, been left with very significant difficulties.

However, notwithstanding my sympathy for the pursuer I am unable to hold that any fault or negligence on the part of Mr Keating has been established. I shall therefore uphold the second and third pleas-in-law for the defenders and assoilzie them.