Anaesthesia, 1975, Volume 30, pages 778-782 C A S E REPORT
Paraplegia following epidural analgesia
P H I L I P P A D. H A R R I S O N
The technique of epidural analgesia has become popular in recent years and the method has proved to be safe in experienced hands. Complications are rare but, in a review of the world literature, Dawkins found eighteen cases of permanent neurological damage.' A further case is presented in this communication and the mechanism discussed. Case report
A 47-year-old housewife was admitted for abdominal hysterectomy for fibroids in September 1968. A small simple vulval tumour was also noted. Physical examination revealed no other abnormality except that blood pressure was 160/100 mmHg. The haemoglobin was 13.3 g% Anaesthesia nnd surgery
Papaveretum 20 mg and hyoscine 0.4 mg were administered intramuscularly as premedication. Lumbar epidural block was performed without technical difficulty in the L4-5 interspace and 30 ml 1.5% lignocaine in isotonic solution containing adrenaline 1 in 200,000 was injected. Light general anaesthesia was maintained during operation using thiopentone, nitrous oxygen and oxygen and the Magill circuit. Abdominal total hysterectomy and right salpingo-oophorectomy were carried out via a midline incision with the patient in 5" head down tilt. The blood pressure was recorded at frequent intervals and, because systolic pressure fell to 55 mmHg, .lo00 ml 4.2% dextrose in 0.18% saline solution were infused and atropine 0.2 mg was administered intravenously to counteract a bradycardia. Pressor drugs were not used in the belief that the consequent vasoconstriction militates against increased tissue perfusion. The abdominal operation was completed; the patient was then placed in lithotomy position for removal of the vulval tumour, which was excised quickly and without difficulty. Systolic blood pressure was now 65 mmHg. Philippa D. Harrison, MRCPE, Neurologist, Conyers House, Skerne, Driffield, N. Humberside.
778
Paraplegia following epidural analgesia
779
Postoperative course Immediate. The systolic pressure fell to 50 mmHg for a short time after transfer to the postoperative room and a further 500 ml of 4.2% dextrose in 0.18% saline was infused. Ninety minutes after cessation of surgery systolic pressure was 70 mmHg. The patient was fully conscious, but complained of inability to move her legs and she had paraesthesiae in the feet. First postoperative day. The patient suffered continuing inability to move her legs and paraesthesiae in the feet. Clinical examination confirmed a partial paralysis of the lower limbs. Neurological examination. The patient was examined by a neurologist on the seventh postoperative day. She was complaining of moderately severe pain in the mid-lumbar region. Examination revealed a severe motor weakness involving flexion adduction of the hip; this was more pronounced in the left leg and there was moderate weakness of extension and abduction. Extension of the knees was severely affected and flexion was weak. All movements at the ankle were weak with the exception of eversion. Knee and ankle jerks were absent but the plantar responses were flexor. There was sensory loss to pin-prick involving the L4-5 segments with relative sparing below SI. It was concluded that the patient was suffering from a bilateral root or plexus lesion. A histamine flare reaction was compatible with an intraspinal lesion. X-ray of the lumbar spine revealed a disc degeneration at the L3-4 interspace. The first postoperative month. The motor power gradually improved and, after 4 weeks, the patient was allowed home using a walking frame. The sensory deficit was unchanged. 24 years later (June 1970). The main disability was inability to raise the left foot clear of the ground. Examination revealed wasting of the quadriceps, the anterior tibia1 compartments and the right calf. The left foot was cold and cyanosed. Motor weakness involved flexion and extension of the left knee and dorsiflexion of the left foot and toes. The knee jerks were present but the ankle jerks were not. The right plantar reflex was absent but the left was flexor. Sensory loss had not changed since the original examination. Vibration sense was impaired at the ankle joints but position sense was normal. 3 years later (December 1970). The patient was admitted to hospital following diarrhoea and vomiting. There was hepatomegaly and a clinical diagnosis of carcinomatosis was made. The patient died shortly afterwards. Postmortem examination. The diagnosis of carcinomatosis was confirmed but the primary site could not be determined; unfortunately the spinal cord was not examined. Discussion The spinal cord receives its blood supply from the anterior spinal artery which supplies the anterior two-thirds of the cord and from paired posterior spinal arteries. The anterior spinal artery arises from the union of a branch from each vertebral artery and passes caudally on the anterior surface of the cord. It receives paired tributaries accompanying each nerve root but only a few are large enough to contribute to flow in the main vessel. These larger tributaries are usually unpaired and their number and segmental level are variable. The largest and most caudal ventral radicular artery is the
780
Philippa D.Harrison
artery of Adamkiewicz, found most frequently on the left side. It may accompany any root from T8 to L4 but is commonest at the level of T9' and is found in the lumbar region in only 20% of subjects. The vascular supply of the roots themselves is strictly segmental. Infarction of the spinal cord is more common than was once thought3 and may result from local causes or as a result of generalised hypoxia or fall in perfusion pressure. The classical clinical picture is one of flaccid paraplegia with loss of tendon reflexes and loss of sensation to pin-prick below the affected level. Considerable recovery is likely if there is ischaemia without infarction. Davies, Solomon & Levene4 and Urquhart Hay5 have reported spinal cord infarction following lumbar epidural analgesia and this has been attributed to diminished perfusion pressure coupled with vasoconstriction due to adrenaline. A review of the literature has suggested an incidence of permanent neurological damage in 0.02% of patients in a total of 32,718 epidural blocks.6 A degree of hypotension is accepted as a normal concomitant of epidural blockade levels of 80 mmHg6 and 60 mmHg' systolic arterial pressure have been regarded as acceptable. The proponents of total spinal analgesia believe that, given adequate ventilation and oxygenation, a systolic pressure as low as 35 mmHg is adequate as it is greater than the sum of venous pressure and the osmotic pressure of the plasma, always provided that peripheral resistance is abolished by vasodilatation consequent on sympathetic blockade.* In the case here reported systolic pressure varied between 50 and 70 mmHg. There is no evidence that any renal, cerebral or cardiac abnormality occurred. The neurological complication arising in the immediate postoperative period and followed.by a progressive recovery of motor power appears compatible with a vascular lesion or an epidural haematoma. The distribution of motor weakness and sensory loss is not compatible with infarction of the cord. The sensory loss, maximal at L4-Sl bears a direct relation to the level of injection and clearly denotes involvement of sensory nerve roots. Adrenaline, because of its known vasoconstrictor action, is a hazard when used in tissues with a restricted blood supply. Briddle & Androsg have demonstrated the role of adrenaline as a primary spinal analgesic when used in a hyperbaric solution in a saddle block technique. No adverse effects were reported. Catterburg & Insausti'' published eleven cases of paraplegia in association with epidural block; adrenaline used in concentrations between 1 in 160,000 and 1 in 80,000 was considered causal. A concentration of 1 in 200,000 is now accepted as optimal with the aim of reducing toxic reactions and potentiating quality and duration of blockade. Ellis, Hillman & Simpson," however, believe that duration of local analgesic drugs is prolonged only when adrenaline is combined with hypotension. Epidural veins are thin-walled and contain little or no muscle'2 which suggests that increase in duration of analgesia is attributable to reduced arterial and arteriolar flow. Another possible source of damage to nerve roots lies in the addition of preservatives to local analgesic solution^.'^ The lignocaine used in the case reported here was prepared in the hospital pharmacy in sealed containers, the solution made isotonic with saline, contained no additive, and the ampoule was sterilised by autoclaving. Allergy to lignocaine has been reported14 but is rare. There was no evidence regarding previous exposure to lignocaine in this patient. The drugs used for local analgesia can cause tissue necrosis in certain circum-
Paraplegia following epidural analgesia
78 1
stances, the action being determined by concentration, dose and duration of exposure to the drug.” Metabolic or respiratory acidosis are associated with an increased uptake of some drugs by the brain and spinal cord.16 The latency and quality of epidural blockade are improved when carbonated salts of lignocaine and prilocaine are used and a similar effect might be expected in the presence of metabolic a~id0sis.l~ The most likely cause of the neurological deficit in this patient appears to be nerve root ischaemia as a result of lowered perfusion pressure and vasoconstriction. Associated involvement of the lumbar cord cannot be excluded definitely. Electromyelography was not carried out. The presence of an epidural haematoma cannot be ruled out. The case has been reported to the sub-committee formed by the Association of Anaesthetists of Great Britain and Ireland to collect information on neurological complications which occur following epidural or spinal analgesia. Summary
A case of neurological damage associated with lumbar epidural block is presented. Muscle paralysis and sensory loss were found in the immediate postoperative period and there was partial recovery of muscle power. The possible mechanisms of nerve damage are discussed. Acknowledgments
The author wishes to thank R. Pilkington Esq. MD, MRIOG, Consultant Gynaecologist, H. Moon, Esq. FFARCS, formerly Senior House Officer, and R. S . Atkinson, MB, FFARIS Consultant Anaesthetist, Southend-on-Sea General Hospital, Essex for details of this case. References 1. DAWKINS, C.J.M. (1972) Complications of epidural analgesia. In: Proceedings of the Symposium on Epidural Analgesia in Obstetrics, p. 67 (Ed. by A. Doughty). H. K. Lewis, London. 2. MANNEN, T. (1966) Vascular lesions in the spinal cord of the aged: a clinico-pathological study. Geriatrics, 21, 151. 3 . Editorial (1974) Lancet, ii, 1299. 4. DAVIES, A., SOLOMON, B. & LEVENE, A. (1958) Paraplegia following epidural anaesthesia. British Medical Journal, ii, 654. 5 . URQUHART-HAY, D. (1969) Paraplegia following epidural analgesia: case report. Anaesthesia, 24, 461. 6. DAWKINS,C.J.M. (1969) An analysis of the complications of extradural and caudal block. Anaesthesia, 24, 554. R.S. (1973) Synopsis of Anaesthesia, 7th edn. J. Wright & Sons, Bristol. 7. LEE,J.A. & ATKINSON, 8. GRIFFITHS, H.W.C. & GILLIES, J. (1948) Thoraco-lumbar splanchnicectomy and sympathectomy : anaesthetic procedure. Anaesthesia, 3, 134. 9. BRIDDLE,H.D.& ANDROS, G.J. (1950) Primary spinal anesthetics effect of epinephrine. Anesthesia and Analgesia: Current Researches, 29, 156. 10. CATTERBURG, J. & INSAUSTI, T. (1964) Paraplejias consecutivas a anestesia peridural (estudio clinico y experimental). Reuista de la Asociacion Medica Argentina, 78, 1. 11. ELLIS,R.H., HILLMAN, G. & SIMPSON, B.R.J. (1970) The duration of action of local analgesic drugs in thoracic extradural analgesia. In : Progress in Anaesthesiology: Proceedings of rhe Fourth World Congress of Anaesthesiologists. London 1968, p. 1241 (Ed. by T. B. Boulton et al.).Excerpta Medica International Congress Series, No. 200.
782
Philippa D. Harrison
12. PEARCE,D.J. (1957) The role of posture in laminectorny. Proceedingx of the Royal Society of Medicine, 50, 109. 13. NATHAN,P.W. & SEARS,T.A. (1961) Action of methyl hydroxybenzoate on nervous conduction. Nature, 192, 668. 14. NOBLE, D.S. & PIERCE,G.F.M. (1961) Allergy to lignocaine: a case history. Lancet, ii, 1436. 15. NATHAN,P.W., SEARS,T.A. & SMITH,M.C. (1965) Effects of phenol solutions on the nerve roots of the cat: an electrophysiological and histological study. Journal of the Neurological Sciences, 2, 7. 16. ROTH,L.J. & BARLOW,C.F. (1961) Drugs in the brain: autoradiography and radioassay techniques permit analysis of penetration by labeled drugs. Science, 134, 22. P.R., JOYAL,A.C. & BINNEY,J.C. (1963) Local anesthetic drugs: penetration from the 17. BROMAGE, spinal extradural space into the neuraxis. Science, 140,392.
Paraplegia following epidural analgesia
P H I L I P P A D. H A R R I S O N
The technique of epidural analgesia has become popular in recent years and the method has proved to be safe in experienced hands. Complications are rare but, in a review of the world literature, Dawkins found eighteen cases of permanent neurological damage.' A further case is presented in this communication and the mechanism discussed. Case report
A 47-year-old housewife was admitted for abdominal hysterectomy for fibroids in September 1968. A small simple vulval tumour was also noted. Physical examination revealed no other abnormality except that blood pressure was 160/100 mmHg. The haemoglobin was 13.3 g% Anaesthesia nnd surgery
Papaveretum 20 mg and hyoscine 0.4 mg were administered intramuscularly as premedication. Lumbar epidural block was performed without technical difficulty in the L4-5 interspace and 30 ml 1.5% lignocaine in isotonic solution containing adrenaline 1 in 200,000 was injected. Light general anaesthesia was maintained during operation using thiopentone, nitrous oxygen and oxygen and the Magill circuit. Abdominal total hysterectomy and right salpingo-oophorectomy were carried out via a midline incision with the patient in 5" head down tilt. The blood pressure was recorded at frequent intervals and, because systolic pressure fell to 55 mmHg, .lo00 ml 4.2% dextrose in 0.18% saline solution were infused and atropine 0.2 mg was administered intravenously to counteract a bradycardia. Pressor drugs were not used in the belief that the consequent vasoconstriction militates against increased tissue perfusion. The abdominal operation was completed; the patient was then placed in lithotomy position for removal of the vulval tumour, which was excised quickly and without difficulty. Systolic blood pressure was now 65 mmHg. Philippa D. Harrison, MRCPE, Neurologist, Conyers House, Skerne, Driffield, N. Humberside.
778
Paraplegia following epidural analgesia
779
Postoperative course Immediate. The systolic pressure fell to 50 mmHg for a short time after transfer to the postoperative room and a further 500 ml of 4.2% dextrose in 0.18% saline was infused. Ninety minutes after cessation of surgery systolic pressure was 70 mmHg. The patient was fully conscious, but complained of inability to move her legs and she had paraesthesiae in the feet. First postoperative day. The patient suffered continuing inability to move her legs and paraesthesiae in the feet. Clinical examination confirmed a partial paralysis of the lower limbs. Neurological examination. The patient was examined by a neurologist on the seventh postoperative day. She was complaining of moderately severe pain in the mid-lumbar region. Examination revealed a severe motor weakness involving flexion adduction of the hip; this was more pronounced in the left leg and there was moderate weakness of extension and abduction. Extension of the knees was severely affected and flexion was weak. All movements at the ankle were weak with the exception of eversion. Knee and ankle jerks were absent but the plantar responses were flexor. There was sensory loss to pin-prick involving the L4-5 segments with relative sparing below SI. It was concluded that the patient was suffering from a bilateral root or plexus lesion. A histamine flare reaction was compatible with an intraspinal lesion. X-ray of the lumbar spine revealed a disc degeneration at the L3-4 interspace. The first postoperative month. The motor power gradually improved and, after 4 weeks, the patient was allowed home using a walking frame. The sensory deficit was unchanged. 24 years later (June 1970). The main disability was inability to raise the left foot clear of the ground. Examination revealed wasting of the quadriceps, the anterior tibia1 compartments and the right calf. The left foot was cold and cyanosed. Motor weakness involved flexion and extension of the left knee and dorsiflexion of the left foot and toes. The knee jerks were present but the ankle jerks were not. The right plantar reflex was absent but the left was flexor. Sensory loss had not changed since the original examination. Vibration sense was impaired at the ankle joints but position sense was normal. 3 years later (December 1970). The patient was admitted to hospital following diarrhoea and vomiting. There was hepatomegaly and a clinical diagnosis of carcinomatosis was made. The patient died shortly afterwards. Postmortem examination. The diagnosis of carcinomatosis was confirmed but the primary site could not be determined; unfortunately the spinal cord was not examined. Discussion The spinal cord receives its blood supply from the anterior spinal artery which supplies the anterior two-thirds of the cord and from paired posterior spinal arteries. The anterior spinal artery arises from the union of a branch from each vertebral artery and passes caudally on the anterior surface of the cord. It receives paired tributaries accompanying each nerve root but only a few are large enough to contribute to flow in the main vessel. These larger tributaries are usually unpaired and their number and segmental level are variable. The largest and most caudal ventral radicular artery is the
780
Philippa D.Harrison
artery of Adamkiewicz, found most frequently on the left side. It may accompany any root from T8 to L4 but is commonest at the level of T9' and is found in the lumbar region in only 20% of subjects. The vascular supply of the roots themselves is strictly segmental. Infarction of the spinal cord is more common than was once thought3 and may result from local causes or as a result of generalised hypoxia or fall in perfusion pressure. The classical clinical picture is one of flaccid paraplegia with loss of tendon reflexes and loss of sensation to pin-prick below the affected level. Considerable recovery is likely if there is ischaemia without infarction. Davies, Solomon & Levene4 and Urquhart Hay5 have reported spinal cord infarction following lumbar epidural analgesia and this has been attributed to diminished perfusion pressure coupled with vasoconstriction due to adrenaline. A review of the literature has suggested an incidence of permanent neurological damage in 0.02% of patients in a total of 32,718 epidural blocks.6 A degree of hypotension is accepted as a normal concomitant of epidural blockade levels of 80 mmHg6 and 60 mmHg' systolic arterial pressure have been regarded as acceptable. The proponents of total spinal analgesia believe that, given adequate ventilation and oxygenation, a systolic pressure as low as 35 mmHg is adequate as it is greater than the sum of venous pressure and the osmotic pressure of the plasma, always provided that peripheral resistance is abolished by vasodilatation consequent on sympathetic blockade.* In the case here reported systolic pressure varied between 50 and 70 mmHg. There is no evidence that any renal, cerebral or cardiac abnormality occurred. The neurological complication arising in the immediate postoperative period and followed.by a progressive recovery of motor power appears compatible with a vascular lesion or an epidural haematoma. The distribution of motor weakness and sensory loss is not compatible with infarction of the cord. The sensory loss, maximal at L4-Sl bears a direct relation to the level of injection and clearly denotes involvement of sensory nerve roots. Adrenaline, because of its known vasoconstrictor action, is a hazard when used in tissues with a restricted blood supply. Briddle & Androsg have demonstrated the role of adrenaline as a primary spinal analgesic when used in a hyperbaric solution in a saddle block technique. No adverse effects were reported. Catterburg & Insausti'' published eleven cases of paraplegia in association with epidural block; adrenaline used in concentrations between 1 in 160,000 and 1 in 80,000 was considered causal. A concentration of 1 in 200,000 is now accepted as optimal with the aim of reducing toxic reactions and potentiating quality and duration of blockade. Ellis, Hillman & Simpson," however, believe that duration of local analgesic drugs is prolonged only when adrenaline is combined with hypotension. Epidural veins are thin-walled and contain little or no muscle'2 which suggests that increase in duration of analgesia is attributable to reduced arterial and arteriolar flow. Another possible source of damage to nerve roots lies in the addition of preservatives to local analgesic solution^.'^ The lignocaine used in the case reported here was prepared in the hospital pharmacy in sealed containers, the solution made isotonic with saline, contained no additive, and the ampoule was sterilised by autoclaving. Allergy to lignocaine has been reported14 but is rare. There was no evidence regarding previous exposure to lignocaine in this patient. The drugs used for local analgesia can cause tissue necrosis in certain circum-
Paraplegia following epidural analgesia
78 1
stances, the action being determined by concentration, dose and duration of exposure to the drug.” Metabolic or respiratory acidosis are associated with an increased uptake of some drugs by the brain and spinal cord.16 The latency and quality of epidural blockade are improved when carbonated salts of lignocaine and prilocaine are used and a similar effect might be expected in the presence of metabolic a~id0sis.l~ The most likely cause of the neurological deficit in this patient appears to be nerve root ischaemia as a result of lowered perfusion pressure and vasoconstriction. Associated involvement of the lumbar cord cannot be excluded definitely. Electromyelography was not carried out. The presence of an epidural haematoma cannot be ruled out. The case has been reported to the sub-committee formed by the Association of Anaesthetists of Great Britain and Ireland to collect information on neurological complications which occur following epidural or spinal analgesia. Summary
A case of neurological damage associated with lumbar epidural block is presented. Muscle paralysis and sensory loss were found in the immediate postoperative period and there was partial recovery of muscle power. The possible mechanisms of nerve damage are discussed. Acknowledgments
The author wishes to thank R. Pilkington Esq. MD, MRIOG, Consultant Gynaecologist, H. Moon, Esq. FFARCS, formerly Senior House Officer, and R. S . Atkinson, MB, FFARIS Consultant Anaesthetist, Southend-on-Sea General Hospital, Essex for details of this case. References 1. DAWKINS, C.J.M. (1972) Complications of epidural analgesia. In: Proceedings of the Symposium on Epidural Analgesia in Obstetrics, p. 67 (Ed. by A. Doughty). H. K. Lewis, London. 2. MANNEN, T. (1966) Vascular lesions in the spinal cord of the aged: a clinico-pathological study. Geriatrics, 21, 151. 3 . Editorial (1974) Lancet, ii, 1299. 4. DAVIES, A., SOLOMON, B. & LEVENE, A. (1958) Paraplegia following epidural anaesthesia. British Medical Journal, ii, 654. 5 . URQUHART-HAY, D. (1969) Paraplegia following epidural analgesia: case report. Anaesthesia, 24, 461. 6. DAWKINS,C.J.M. (1969) An analysis of the complications of extradural and caudal block. Anaesthesia, 24, 554. R.S. (1973) Synopsis of Anaesthesia, 7th edn. J. Wright & Sons, Bristol. 7. LEE,J.A. & ATKINSON, 8. GRIFFITHS, H.W.C. & GILLIES, J. (1948) Thoraco-lumbar splanchnicectomy and sympathectomy : anaesthetic procedure. Anaesthesia, 3, 134. 9. BRIDDLE,H.D.& ANDROS, G.J. (1950) Primary spinal anesthetics effect of epinephrine. Anesthesia and Analgesia: Current Researches, 29, 156. 10. CATTERBURG, J. & INSAUSTI, T. (1964) Paraplejias consecutivas a anestesia peridural (estudio clinico y experimental). Reuista de la Asociacion Medica Argentina, 78, 1. 11. ELLIS,R.H., HILLMAN, G. & SIMPSON, B.R.J. (1970) The duration of action of local analgesic drugs in thoracic extradural analgesia. In : Progress in Anaesthesiology: Proceedings of rhe Fourth World Congress of Anaesthesiologists. London 1968, p. 1241 (Ed. by T. B. Boulton et al.).Excerpta Medica International Congress Series, No. 200.
782
Philippa D. Harrison
12. PEARCE,D.J. (1957) The role of posture in laminectorny. Proceedingx of the Royal Society of Medicine, 50, 109. 13. NATHAN,P.W. & SEARS,T.A. (1961) Action of methyl hydroxybenzoate on nervous conduction. Nature, 192, 668. 14. NOBLE, D.S. & PIERCE,G.F.M. (1961) Allergy to lignocaine: a case history. Lancet, ii, 1436. 15. NATHAN,P.W., SEARS,T.A. & SMITH,M.C. (1965) Effects of phenol solutions on the nerve roots of the cat: an electrophysiological and histological study. Journal of the Neurological Sciences, 2, 7. 16. ROTH,L.J. & BARLOW,C.F. (1961) Drugs in the brain: autoradiography and radioassay techniques permit analysis of penetration by labeled drugs. Science, 134, 22. P.R., JOYAL,A.C. & BINNEY,J.C. (1963) Local anesthetic drugs: penetration from the 17. BROMAGE, spinal extradural space into the neuraxis. Science, 140,392.
