Article of the Month: July/August 2013
The Woolley and Roe Case - How the reputation of spinal anaesthesia was damaged in the UK
Dr Patrick Magee
Consultant Anaesthetist, Royal United Hospital Bath
Presented at the Royal College of Anaesthetists, Churchill House, London, 31st Otober 2008
Proceedings of the History of Anaesthesia Society 2008; 40: 14-17
The case of Woolley and Roe, which was heard at the High Courts of Justice in October 1953, had a significantly damaging effect on the practice of spinal anaesthesia in the UK for several decades thereafter. As such it is worthy of periodic review to remind ourselves that spinal anaesthesia was not always as low risk as nowadays.
The spinal anaesthetics and aftermath
On Monday October 13th 1947, at Chesterfield Hospital, Dr JM Graham was the visiting anaesthetist for an operating list which included Cecil Roe and Albert Woolley. Roe was the first patient of the morning and was to have a semilunar cartilage removed. Woolley was the third patient and was to have a hydrocele repaired. A second unnamed patient, who died of his surgical illness postoperatively, was to have a laparotomy for gastrointestinal obstruction. All three patients were given spinal anaesthesia as 10 ml of 1/1500 cinchocaine into the subarachnoid space. Roe experienced headache and back pain as soon as the spinal needle was inserted, as well as a burning sensation at the operative site which suggested inadequate analgesia. Woolley suffered no immediate discomfort. By the next day, however, both patients had developed an acute myelopathy that involved the nerve roots of the cauda equina and the lower spinal cord. Clinically the condition presented as a flaccid paralysis and loss of sensation over the legs, the lower abdominal wall and the peri-anal area, as well as loss of bowel and bladder control. These symptoms were common to both patients; there were no signs of meningism and lumbar puncture the week after showed normal CSF. The second patient had died five days postoperatively from his surgical illness, but had shown some signs of neurological damage. Woolley and Roe were moved in November to the Wharncliffe Hospital in Sheffield under the care of Dr James Carson for their continued neurological care. After some initial improvement in the first month or so, their symptoms worsened to a painful spastic paraparesis which persisted for the remainder of their lives. In May 1948, a second lumbar puncture in both patients revealed a dry tap, which was an ominous result, indicating a blockage to CSF flow in the thoracic region. In December 1948 both patients were discharged home, but continued to deteriorate such that Roe was readmitted in May 1949. In May 1950 Roe had a laminectomy performed in Birmingham by Professor Brodie Hughes. At operation his findings included arachnoid cysts in the thoracic cord under pressure which were drained, and a mass of arachnoidal adhesions around the cauda equina. During this period Roe’s symptoms became very much worse, as did Woolley’s.
The court case
Woolley and Roe sued the Ministry of Health as trustees of the hospital, Dr Graham himself and Ciba, the manufacturer of the cinchocaine. In particular, Dr Graham was accused of having failed to prevent the introduction of infective material into the spinal, of having failed to prevent the introduction of carbolic acid, and of having failed to have supervised the sterilization process. When the case came to court in October 1953 [1], the plaintiffs’ expert witness was Professor Robert MacIntosh. As an expert who had published a book in 1951, considered as a definitive contemporary text on spinal anaesthesia, he was closely questioned by counsel. In particular he was questioned on the method of sterilization of both needles and ampoules, and the value or otherwise of the dyed phenol solution used to sterilize ampoules. Although his recommendation in 1953 for sterilization was autoclaving, he recognized that not everybody would have used this method in 1947. The method of sterilizing needles and syringes in Chesterfield was by boiling for twenty minutes and rinsing in sterile water, and the method of sterilizing ampoules was by soaking in a phenol solution. The possibility of invisible cracks in the ampoule, through which phenol could leak inwards was unknown before MacIntosh’s publication. The plaintiffs’ case rested on the allegation of leakage of phenol from the sterilizing bath of dyed phenol, in which the ampoules were immersed, through invisible cracks in the ampoules to contaminate the cinchocaine. Other anaesthetic expert witnesses were called, as were a surgeon and two neurologists. The non- anaesthetic witnesses believed that the phenol was not at issue, rather the act of spinal anaesthesia itself or nupercaine itself were the cause of the problem. Despite evidence being presented in court, which raised the possibility of other causes, phenol contamination was accepted by the judge as the cause of the injuries. However, Dr Graham was not judged to have been negligent because although by 1953 the possibility of phenol leakage into ampoules was known about through MacIntosh’s book, in 1947 it was not. At an early stage of the trial, counsel for Ciba demonstrated to everyone’s satisfaction that the manufacturing and storage process of the ampoules was satisfactory and safe and Ciba were exonerated. The plaintiffs received no compensation, a decision which was upheld at the Appeal in April 1954.
Review of the case
In a review of the case by Hutter [2] in 1990, it was pointed out that phenol had been used to treat chronic pain from 1954, and that it had produced very different symptoms and neurological signs from those of Woolley and Roe; indeed phenol was used to treat spastic paraparesis rather than being a cause of it. Hutter also pointed out that invisible cracks were another unlikely cause, since there had been no previous injuries either at Chesterfield Hospital or anywhere else which could be attributed to this cause. It was also unlikely that, the cinchocaine labels having come off in the phenol soaking process, the ampoules were misidentified, since no other similar sized ampoules of different medicines were found, and all three patients received analgesia from the contents of the ampoules. Hutter concludes that the most likely cause is the water in the steriliser. The steriliser had been filled with descaling fluid, consisting of phosphoric and hydrochloric acid, in the days preceding the relevant Monday morning. The descaling process was not directly supervised by Dr Graham, the senior theatre nurse had gone off on holiday on the preceding Saturday, and her assistant had gone off sick at lunchtime on the Monday. Hutter discusses the possible mechanism of damage of the descaling fluid as a contaminant. There is no direct information about the damage that can be caused by phosphoric acid, but we know from the neurotoxicity caused by Chloroprocaine (pH 3.3) what can happen, and from the pulmonary damage caused by aspiration of gastric contents. Nupercaine binds avidly to tissue proteins and associated acidic contaminants will cause coagulation, vascular thrombosis and consequent ischaemia, protein destruction and intracellular enzyme destruction. Phosphoric acid is toxic at a pH of 5.5, and if we hypothesize that a 1 molar solution of the acid is diluted by a factor of 100 000, the resulting solution has a pH of 5. Clearly the tissue damage caused by the acid is attenuated by dilution, but factors aggravating local damage include the fact that cerebrospinal fluid is a poor buffer, there is no local metabolism in the CSF, and diffusion of the substance out of the CSF for metabolism elsewhere is hindered in the presence of local vascular thrombosis. Factors in favour of an acidic contaminant in the case of Roe were the presence of a large skin ulcer at the needle entry point and the headache and backache which he suffered at the time. Furthermore, as local anaesthetic agents are weak bases, they are more highly ionized in an acidic environment, which limits their ability to cross neural membranes and exert their action; Roe’s poor quality analgesia backs up this state of affairs. Although it does so slowly, neural tissue is capable of repair and regeneration, and this explains the partial recovery in neurological function by Woolley and Roe. However, this was followed by the development of fibrous tissue and a chronic adhesive arachnoiditis with arachnoid cyst formation and spinal cord compression. These were the pathological findings at Roe’s laminectomy in 1950 and at autopsy following his death.
There was a good deal of unease among medical opinion of the time at the decision of the judge based on the phenol explanation, and Dr Graham himself, when interviewed by Maltby [3] some thirty years later, indicated that he had never believed that invisible cracks in the ampoule with phenol seepage were a likely cause of the disaster. It is probable that this case led directly to the demise of spinal anaesthesia in the UK for at least 25 years. It is worth pondering, that if a similar case were heard today, whether an anaesthetist would not be found negligent under similar circumstances. Indeed the summary by Lord Denning at the Appeal of the case in 1954, while expressing sympathy for the plight of the patients’ suffering, speaks volumes about the desire of the law of the time to protect the medical profession against spurious claims of negligence, where misadventure is the real explanation [3].
References
1. Cope RW. The Woolley and Roe Case; Woolley and Roe versus Ministry of Health and Others. Anaesthesia 1954; 9: 249-270
2. Hutter CDD. The Woolley and Roe case; a reassessment. Anaesthesia 1990; 45: 859-864
3. Maltby JR, Hutter CD, Clayton KC. The Woolley and Roe case. British Journal of Anaesthesia 2000; 84: 121-126
The spinal anaesthetics and aftermath
On Monday October 13th 1947, at Chesterfield Hospital, Dr JM Graham was the visiting anaesthetist for an operating list which included Cecil Roe and Albert Woolley. Roe was the first patient of the morning and was to have a semilunar cartilage removed. Woolley was the third patient and was to have a hydrocele repaired. A second unnamed patient, who died of his surgical illness postoperatively, was to have a laparotomy for gastrointestinal obstruction. All three patients were given spinal anaesthesia as 10 ml of 1/1500 cinchocaine into the subarachnoid space. Roe experienced headache and back pain as soon as the spinal needle was inserted, as well as a burning sensation at the operative site which suggested inadequate analgesia. Woolley suffered no immediate discomfort. By the next day, however, both patients had developed an acute myelopathy that involved the nerve roots of the cauda equina and the lower spinal cord. Clinically the condition presented as a flaccid paralysis and loss of sensation over the legs, the lower abdominal wall and the peri-anal area, as well as loss of bowel and bladder control. These symptoms were common to both patients; there were no signs of meningism and lumbar puncture the week after showed normal CSF. The second patient had died five days postoperatively from his surgical illness, but had shown some signs of neurological damage. Woolley and Roe were moved in November to the Wharncliffe Hospital in Sheffield under the care of Dr James Carson for their continued neurological care. After some initial improvement in the first month or so, their symptoms worsened to a painful spastic paraparesis which persisted for the remainder of their lives. In May 1948, a second lumbar puncture in both patients revealed a dry tap, which was an ominous result, indicating a blockage to CSF flow in the thoracic region. In December 1948 both patients were discharged home, but continued to deteriorate such that Roe was readmitted in May 1949. In May 1950 Roe had a laminectomy performed in Birmingham by Professor Brodie Hughes. At operation his findings included arachnoid cysts in the thoracic cord under pressure which were drained, and a mass of arachnoidal adhesions around the cauda equina. During this period Roe’s symptoms became very much worse, as did Woolley’s.
The court case
Woolley and Roe sued the Ministry of Health as trustees of the hospital, Dr Graham himself and Ciba, the manufacturer of the cinchocaine. In particular, Dr Graham was accused of having failed to prevent the introduction of infective material into the spinal, of having failed to prevent the introduction of carbolic acid, and of having failed to have supervised the sterilization process. When the case came to court in October 1953 [1], the plaintiffs’ expert witness was Professor Robert MacIntosh. As an expert who had published a book in 1951, considered as a definitive contemporary text on spinal anaesthesia, he was closely questioned by counsel. In particular he was questioned on the method of sterilization of both needles and ampoules, and the value or otherwise of the dyed phenol solution used to sterilize ampoules. Although his recommendation in 1953 for sterilization was autoclaving, he recognized that not everybody would have used this method in 1947. The method of sterilizing needles and syringes in Chesterfield was by boiling for twenty minutes and rinsing in sterile water, and the method of sterilizing ampoules was by soaking in a phenol solution. The possibility of invisible cracks in the ampoule, through which phenol could leak inwards was unknown before MacIntosh’s publication. The plaintiffs’ case rested on the allegation of leakage of phenol from the sterilizing bath of dyed phenol, in which the ampoules were immersed, through invisible cracks in the ampoules to contaminate the cinchocaine. Other anaesthetic expert witnesses were called, as were a surgeon and two neurologists. The non- anaesthetic witnesses believed that the phenol was not at issue, rather the act of spinal anaesthesia itself or nupercaine itself were the cause of the problem. Despite evidence being presented in court, which raised the possibility of other causes, phenol contamination was accepted by the judge as the cause of the injuries. However, Dr Graham was not judged to have been negligent because although by 1953 the possibility of phenol leakage into ampoules was known about through MacIntosh’s book, in 1947 it was not. At an early stage of the trial, counsel for Ciba demonstrated to everyone’s satisfaction that the manufacturing and storage process of the ampoules was satisfactory and safe and Ciba were exonerated. The plaintiffs received no compensation, a decision which was upheld at the Appeal in April 1954.
Review of the case
In a review of the case by Hutter [2] in 1990, it was pointed out that phenol had been used to treat chronic pain from 1954, and that it had produced very different symptoms and neurological signs from those of Woolley and Roe; indeed phenol was used to treat spastic paraparesis rather than being a cause of it. Hutter also pointed out that invisible cracks were another unlikely cause, since there had been no previous injuries either at Chesterfield Hospital or anywhere else which could be attributed to this cause. It was also unlikely that, the cinchocaine labels having come off in the phenol soaking process, the ampoules were misidentified, since no other similar sized ampoules of different medicines were found, and all three patients received analgesia from the contents of the ampoules. Hutter concludes that the most likely cause is the water in the steriliser. The steriliser had been filled with descaling fluid, consisting of phosphoric and hydrochloric acid, in the days preceding the relevant Monday morning. The descaling process was not directly supervised by Dr Graham, the senior theatre nurse had gone off on holiday on the preceding Saturday, and her assistant had gone off sick at lunchtime on the Monday. Hutter discusses the possible mechanism of damage of the descaling fluid as a contaminant. There is no direct information about the damage that can be caused by phosphoric acid, but we know from the neurotoxicity caused by Chloroprocaine (pH 3.3) what can happen, and from the pulmonary damage caused by aspiration of gastric contents. Nupercaine binds avidly to tissue proteins and associated acidic contaminants will cause coagulation, vascular thrombosis and consequent ischaemia, protein destruction and intracellular enzyme destruction. Phosphoric acid is toxic at a pH of 5.5, and if we hypothesize that a 1 molar solution of the acid is diluted by a factor of 100 000, the resulting solution has a pH of 5. Clearly the tissue damage caused by the acid is attenuated by dilution, but factors aggravating local damage include the fact that cerebrospinal fluid is a poor buffer, there is no local metabolism in the CSF, and diffusion of the substance out of the CSF for metabolism elsewhere is hindered in the presence of local vascular thrombosis. Factors in favour of an acidic contaminant in the case of Roe were the presence of a large skin ulcer at the needle entry point and the headache and backache which he suffered at the time. Furthermore, as local anaesthetic agents are weak bases, they are more highly ionized in an acidic environment, which limits their ability to cross neural membranes and exert their action; Roe’s poor quality analgesia backs up this state of affairs. Although it does so slowly, neural tissue is capable of repair and regeneration, and this explains the partial recovery in neurological function by Woolley and Roe. However, this was followed by the development of fibrous tissue and a chronic adhesive arachnoiditis with arachnoid cyst formation and spinal cord compression. These were the pathological findings at Roe’s laminectomy in 1950 and at autopsy following his death.
There was a good deal of unease among medical opinion of the time at the decision of the judge based on the phenol explanation, and Dr Graham himself, when interviewed by Maltby [3] some thirty years later, indicated that he had never believed that invisible cracks in the ampoule with phenol seepage were a likely cause of the disaster. It is probable that this case led directly to the demise of spinal anaesthesia in the UK for at least 25 years. It is worth pondering, that if a similar case were heard today, whether an anaesthetist would not be found negligent under similar circumstances. Indeed the summary by Lord Denning at the Appeal of the case in 1954, while expressing sympathy for the plight of the patients’ suffering, speaks volumes about the desire of the law of the time to protect the medical profession against spurious claims of negligence, where misadventure is the real explanation [3].
References
1. Cope RW. The Woolley and Roe Case; Woolley and Roe versus Ministry of Health and Others. Anaesthesia 1954; 9: 249-270
2. Hutter CDD. The Woolley and Roe case; a reassessment. Anaesthesia 1990; 45: 859-864
3. Maltby JR, Hutter CD, Clayton KC. The Woolley and Roe case. British Journal of Anaesthesia 2000; 84: 121-126
