Painful sciatic neuropathy following cardiac surgery P. Kempster”
E. Byrne
Neurology Registrar, Department of Neurology, St Vincent’s Hospital, Melbourne, Vic.
Neurologist, Departments of Medicine and Neurology, St Vincent’s Hospital, Melbourne, Vic.
P. Gates
A. Wilson
Neurologist, Department of Neurology, St Vincent’s Hospital, Melbourne, Vic.
Cardiothoracic Surgeon, Open-Heart Surgery Unit, St Vincent’s Hospital, Melbourne, Vic.
Abstract: Ten patients developed bilateral asymmetrical lower limb sensori-motor or motor deficits associated with prominent causalgic pain after cardiac surgery. The clinical and electrophysiological abnormalities indicated bilateral proximal sciatic nerve lesions, although in several cases the distinction from a diffise ischaemic axonopathy was diEcult to make. This pattern of postcardiac surgery peripheral neurological dysfunction has not been previously described but is likely to relate either to the intra-operative posturing technique for access to the saphenous veins and/or the upright posture used to nurse patients in the immediate post-operative period and is in keeping with the previously demonstrated susceptibility of peripheral nerves to pressure palsy during cardiac surgical procedures. (Aust NZ J Med 1991; 21: 732-735.) Key words: Cardiac surgery, sciatic nerve, peripheral neuropathy, causalgia.
INTRODUCTION Focal central nervous system deficits and neuropsychological dysfunction are relatively common Injury to the complications of cardiac peripheral nervous system appears to be less frequent although two large prospective s t ~ d i e sdocument ~.~ post-cardiacsurgical peripheral nervous system complications in approximately 12% of patients. Upper limb radiculoplexopathy related to nerve stretching by sternal retraction is seen most frequently., In most cases, this involves the distribution of the C8-Tl nerve roots or lower trunumedial cord of the brachial p l e ~ u s . Mononeuropathy ~.~ affecting cranial, upper and lower limb nerves constitutes the remainder of peripheral nervous system lesions. Spontaneous resolution of nerve dyshnction is usually seen over several months and pain is usually not a prominent symptom. These features are in keeping with previous information concerning the spectrum of peripheral neurological complications of general surgical proceduress.6although the peripheral nervous system complication rate would appear to be considerably
higher following cardiac surgery. We describe ten patients who developed bilateral but asymmetrical lower limb peripheral neurological dyshnction associated with prominent causalgic pain following cardiac’ operations. This pattern of nerve damage has not previously been identified.
PATIENTS AND METHODS Ten patients with bilateral painful lower limb neuropathy were identified between 1980 and 1986. All underwent cardiac surgery at the St Vincent’s Hospital Cardiothoracic Unit. During this period 3599 coronary artery bypass graft (CABG)operations, 1021 cardiac valve replacements and 219 combined procedures were performed. All patients were male; mean age was 61 years (43-69). Co-existing medical conditions in the patients with lower limb neuropathy were: peripheral vascular disease (three cases), hypertension (three cases), diabetes mellitus, chronic obstructive airways disease, and previous cerebral infarction (each in one case). Standard anaesthetic, perfusion and surgical techniques were used and intraoperative
Reprint requests to: Dr Peter Gates, Department of Neurology, St Vincent’s Hospital, Victoria Parade, Fitzroy 3065, Melbourne, Australia. The material described in this manuscript was presented at the Australian Association of Neurologists’ Annual Scientific Meeting in May 1987. *Present appointment: Neurologist, Monash Medical Centre, Melbourne, Victoria.
732
Aust NZ J Med 1991; 21
KEMPSTER ET AL.
TABLE 1 Summary of Clinical and Neurophysiological Findings
Clinical Features \ge
Motor
Senwry
Nerve Conduction Studies
______
Common peronpal nerve Amplitude (uV)
Velocity
(msec
F wave
I)
Posterior ribial nerve Amplitude (uV)
Velocity (m W C ')
F wave
Surd Nerve Sensori Potentlal
Electromvography L'eneri.drion -~
65
++
67
++
54 63 64 68
43 65 55 69
+
++ 0
++ 0
+ + 0
++
++
I1
++
++ ++
I +
++
+ I + I
60 200 N A N N N -
30
43 N A N 33 N -
-
-
A A
~
A
N
-
A 1000 N N
A -
A A 39
-
A
-
N N N ~
-
~
-
-
A ~
A A A A N
GMPS BFGMPS QUAST BFGM
N
~
A
N
-
-
~
~~
-
EDB TA ST RF lAGN EDBAHBTA t D B AH5 TA EDB AHB ~
~
~
ratJons Clinical involvement - I I =severe + = mild 0 = nil :onduction studies - N = normal A =absent - = not performed nyographic muscle sampling - EDB - extensor digitorum brevis AHB = abductor hallucis brevis TA= (ibidliS antefior GN -gastrocnemius :eps femoris ST = semitendinosis, QUA = quadriceps fernoris GM - gluteus maximus PS = L5 paraspinal muscles
nic heparinisation and hypothermia (26 "-28 "C) employed routinely. Disposable membrane nators in use were: Cobe bubble oxygenator, membrane lung, Bentleigh bubble oxygenator, q bubbler and Gambro membrane. Mean cardinonary bypass time was 84 minutes (42-125). patients undergoing CABG surgery had coronary donated from the saphenous venous system and gs were postured by large rounded pads placed .d the thighs or buttocks to facilitate surgical 3. The tenth patient had a mitral valve replaceand it is possible that the legs were also postured imilar manner but this could not be determined. itients were nursed in an upright sitting position returning to the open heart surgery intensive care iperatively. All patients were examined by a dogist after the appearance of neurological toms. Time from surgery until neurological ination ranged from one day to several months.
ULTS :ase report is presented to illustrate typical clineatures and electrophysiological findings. The s of the other nine patients are outlined in Table 1 -year-old man with a past history of chronic uctive airways disease required CABG surgery .ay 1986 because of unstable angina pectoris. e saphenous vein grafts (from the right leg) and nternal mammary artery graft were performed; Jpulmonary bypass time was 85 minutes. On lpting to mobilise on the day following surgery sticed weakness in his legs. Within a few days he oped burning discomfort over the soles of both nd also had some shooting pain from the knees C L S C I A T I C NEUROPATHY
down to the feet which tended to be worse at night. Pressure ulceration of both heels had also developed post-operatively. On examination several weeks after surgery there was wasting with fasciculation of anterior tibial and calf muscle groups bilaterally. Knee flexion and all movements of the ankles and toes were weak bilaterally although this was more marked on the left. The knee and adductor jerks were normal but biceps femoris and ankle jerks were absent bilaterally. Light touch and pinprick sensation were impaired over the plantar and dorsal surfaces of the feet and on lateral and posterior aspects of calves with some sparing medially. Foot pulses were palpable. Neurophysiological tests were performed three months post-operatively at which time his symptoms were unchanged. Left common peroneal nerve conduction velocity was 30.2 mlsec with compound motor potential amplitude in the extensor digitorum brevis muscle reduced to 60 microvolts. There was no response to stimulation of the left posterior tibial or left sural nerves. Electromyography of the left semitendinosus, biceps fernoris, tibialis anterior and extensor digitorum brevis muscles showed fibrillation potentials and reduction in recruitment patterns with maximum voluntary contraction consistent with denervation. Electromyography of the left quadriceps, gluteus maximus and L5 paraspinal muscles was normal. All ten patients had painful lower limb sensory symptoms which were largely confined to the skin below the knees (six symmetrical, four asymmetrical). Six described prominent cutaneous burning sensations and five had dysaesthetic response to light tactile stimulation of the skin. Symptoms were worse at night in five patients and were associated with subiective motor restlessness. All had detectable distal lower limk sensory impairment on examination, chiefly affecting light touch, pinprick and thermal sensation. Seven 733 Aust NZ J Mcd 1991; 21
patients had additional motor involvement (severe in five). This was always asymmetrical and involved muscles below the knee although three patients also had weakness of the knee flexor muscles. When a motor deficit was marked, symptoms were usually present when normal consciousness returned after surgery although unpleasant sensory phenomena often took several days to appear. Patients with milder and predominantly sensory disturbances usually experienced a delay of several days until the development of first post-operative symptoms. Two patients developed post-operative heel skin pressure necrosis. Gradual recovery of sensory symptoms occurred in four patients without significant motor involvement after a mean period of 14 months (two-32). The remainder continue to experience painful dysaesthesia. Motor deficits showed little spontaneous improvement, and were largely unchanged after periods of observation o f u p to four years. Electrophysiology studies were performed in seven cases (Table 1). In cases with sensori-motor involvement, loss of amplitude of compound motor and sensory potentials and mild to moderate slowing of conduction velocities was found. Electromyographic evidence of denervation was detected in five patients; this was confined to muscles innervated by the sciatic nerves. Electromyography and nerve conduction studies performed in one case of isolated sensory disturbance were within normal limits apart from absence of F wave potentials. Upper limb nerve conduction studies were performed in one case and these were normal. Sural nerve biopsy was not performed on any patient.
DISCUSSION We have encountered a distinct syndrome of distal, asymmetrical and painhl sensori-motor or sensory lower limb neurological disturbance with causalgic features following cardiac surgery. The neurophysiological findings were consistent with a proximal focal site of axonal damage or an axonal peripheral neuropathy. There appeared to be no common predisposing circumstances other than the fact that all patients underwent surgery in the same hospital and received generally similar peri-operative management. No common factor in relation to surgeon, anaesthetist, cardiac bypass equipment, cardiac bypass time or predisposing illness was present. We believe that these lesions were produced by bilateral sciatic nerve compression although the distinction from a diffuse axonal peripheral neuropathy was difficult to make clinically in several mildly affected cases. The marked asymmetry of motor deficits and focal involvement of the hamstring musculature in several cases are best explained by asymmetrical proximal sciatic nerve pathology, and this hypothesis would be consistent 734
with previous experience concerning peripheral neurological complications of cardiac surgery. Mononeuropathy occurs relatively frequently after CABG surgery, suggesting a vulnerability of individual peripheral nerve^.^,^ This may relate to prolonged nerve pressure during a surgical procedure performed under the lowered arterial perfusion pressure provided by cardiopulmonary bypass. Intraoperative hypothermia has been shown to correlate with increased risk for mon~neuropathy~ in CABG surgery and was routinely used in all of the present cases. Cold may predispose to injury secondary to pressure or stretching.’ Lower limb causalgia occurs with proximal sciatic lesions8 and characteristically produces unpleasant sensory symptoms largely confined to the feet. Post-operative sciatic neuropathy not caused by direct nerve trauma is recognised as a complication of general surgical procedures.6,9Surgery performed in the lithotomy position appears to predispose to postoperative sciatic neuropathy, suggesting that nerve stretching and compression are aetiological factomh The fact that this pattern of post-cardiac surgery neuropathy had not been identified in previous large prospective surveys led to a search for causative factors related to local surgical and peri-operative management. In CABG surgery at St Vincent’s Hospital it was usual to posture the legs with pads or rolls placed under the upper thighs or buttocks to facilitate surgical access for dissection of saphenous vein grafts by slightly flexing, abducting and externally rotating the legs. This technique may render the sciatic nerves at increased risk for pressure palsy especially where the nerve runs subcutaneously after emerging from beneath the gluteus maximus muscle in the upper thigh. However, despite modification of this posturing method, further cases were encountered, several of whom had evidence of buttock and heel pressure necrosis. Further enquiries revealed that patients were being routinely nursed in the immediate post-operative period in a sitting position with the axis of the trunk vertical and at a 90 degree angle to the outstretched lower limbs. During this time, patients were usually intubated, drowsy and unable to move. On the basis that this form of posturing was likely to contribute to sciatic nerve pressure, post-operative nursing care was also altered and patients were postured with their upper body tilted no more than 30 degrees above the horizontal. Following institution of this measure, one further case of painful lower limb neuropathy was encountered over the next 36 months. Our experience suggests that the sciatic nerves, in common with other peripheral nerves, are susceptible to pressure-related damage in the course of cardiac surgery. Centres performing open heart surgical procedures should examine their methods for posturing patients during the intra-operative and post-operative
Aust NZ J Med 1991; 21
KEMPSTER ET AL.
periods to minimise the risk of this unpleasant and intractable post-operative complication. Postscript One of the authors (PG) has subsequently had communication from several other neurologists regarding identical cases operated on at other institutions and has personally seen such a case where cardiac surgery was performed in New Zealand. These observations indicate that this complication is not unique to St Vincent’s Hospital, Melbourne. Date of submission: 8 March 1991
References I. Javid H, Tnfo HM, Najifi H, Dye WS, Hunter JA. Neurological abnormalities following open-heart surgery. J Thorac Cardiovasc Surg 1969; 58: 502-9. 2. Sotaniemi KA, Juolasmaa A, Hokksnen E T . Neuropsychological outcome after open-heart surgery. Arch Neurol 1981; 38: 2-8.
3. Yhaw PJ, Bates D, Cartlidge NEF, Heaviside D: Julian UG, Shaw DA. Early neurological complications of coronary artery bypass surgery. Br Med J 1985; 291: 1384-7. 4. Lederrnan RJ, Breuer AC, Henson M R et al. Petipheral nervous system complications of coronarv artery bypass graft surgerv. Ann Neurol 1982; 12: 297-301. 5. Dhuner KG. Nerve injuries following operations: a survey of cases occurring during a six year period. Anesthesiology 1950; 11: 289-97. 6. Parks HJ. Postoperative peripheral neuropathies. Surgery 1973; 74: 348-57. 7. Thomas PK, Holdorff B. Neuropathy due to physical agcnrs. In: Dyck PJ, Thomas PR, Lamberr E H (eds). Peripheral neuropathp, 2nd editiou (volume 2). l‘hiladelph~a: Saunders, 1984; 1479- 1 5 1 1. 8. Sunderland S. I’ain mechanisms in causalgia. J Neurol Neurosurg Psychiatry 1976; 39: 471-80. 9. Stewart JD, Angus E, Gendron 11. Sciatic neuropathies. Br Med J 1983; 287: 1!08-9.
Case Reports s stated in the June issue, Case Reports to the Journal will be published as Letters to the Editor and the Letters section increased accordingly. T h e restrictions of length (500 words) and number of references (six) which presently apply to Letters will apply also to Case Reports published in this section. Only 1 table or 1 figure is permitted. (Case reports submitted prior to the June publication will, if accepted, be published in their current form.)
A
PAINFUL SCIATIC NEUROPATHY
Aust NZ J Med 1991; 21
735
E. Byrne
Neurology Registrar, Department of Neurology, St Vincent’s Hospital, Melbourne, Vic.
Neurologist, Departments of Medicine and Neurology, St Vincent’s Hospital, Melbourne, Vic.
P. Gates
A. Wilson
Neurologist, Department of Neurology, St Vincent’s Hospital, Melbourne, Vic.
Cardiothoracic Surgeon, Open-Heart Surgery Unit, St Vincent’s Hospital, Melbourne, Vic.
Abstract: Ten patients developed bilateral asymmetrical lower limb sensori-motor or motor deficits associated with prominent causalgic pain after cardiac surgery. The clinical and electrophysiological abnormalities indicated bilateral proximal sciatic nerve lesions, although in several cases the distinction from a diffise ischaemic axonopathy was diEcult to make. This pattern of postcardiac surgery peripheral neurological dysfunction has not been previously described but is likely to relate either to the intra-operative posturing technique for access to the saphenous veins and/or the upright posture used to nurse patients in the immediate post-operative period and is in keeping with the previously demonstrated susceptibility of peripheral nerves to pressure palsy during cardiac surgical procedures. (Aust NZ J Med 1991; 21: 732-735.) Key words: Cardiac surgery, sciatic nerve, peripheral neuropathy, causalgia.
INTRODUCTION Focal central nervous system deficits and neuropsychological dysfunction are relatively common Injury to the complications of cardiac peripheral nervous system appears to be less frequent although two large prospective s t ~ d i e sdocument ~.~ post-cardiacsurgical peripheral nervous system complications in approximately 12% of patients. Upper limb radiculoplexopathy related to nerve stretching by sternal retraction is seen most frequently., In most cases, this involves the distribution of the C8-Tl nerve roots or lower trunumedial cord of the brachial p l e ~ u s . Mononeuropathy ~.~ affecting cranial, upper and lower limb nerves constitutes the remainder of peripheral nervous system lesions. Spontaneous resolution of nerve dyshnction is usually seen over several months and pain is usually not a prominent symptom. These features are in keeping with previous information concerning the spectrum of peripheral neurological complications of general surgical proceduress.6although the peripheral nervous system complication rate would appear to be considerably
higher following cardiac surgery. We describe ten patients who developed bilateral but asymmetrical lower limb peripheral neurological dyshnction associated with prominent causalgic pain following cardiac’ operations. This pattern of nerve damage has not previously been identified.
PATIENTS AND METHODS Ten patients with bilateral painful lower limb neuropathy were identified between 1980 and 1986. All underwent cardiac surgery at the St Vincent’s Hospital Cardiothoracic Unit. During this period 3599 coronary artery bypass graft (CABG)operations, 1021 cardiac valve replacements and 219 combined procedures were performed. All patients were male; mean age was 61 years (43-69). Co-existing medical conditions in the patients with lower limb neuropathy were: peripheral vascular disease (three cases), hypertension (three cases), diabetes mellitus, chronic obstructive airways disease, and previous cerebral infarction (each in one case). Standard anaesthetic, perfusion and surgical techniques were used and intraoperative
Reprint requests to: Dr Peter Gates, Department of Neurology, St Vincent’s Hospital, Victoria Parade, Fitzroy 3065, Melbourne, Australia. The material described in this manuscript was presented at the Australian Association of Neurologists’ Annual Scientific Meeting in May 1987. *Present appointment: Neurologist, Monash Medical Centre, Melbourne, Victoria.
732
Aust NZ J Med 1991; 21
KEMPSTER ET AL.
TABLE 1 Summary of Clinical and Neurophysiological Findings
Clinical Features \ge
Motor
Senwry
Nerve Conduction Studies
______
Common peronpal nerve Amplitude (uV)
Velocity
(msec
F wave
I)
Posterior ribial nerve Amplitude (uV)
Velocity (m W C ')
F wave
Surd Nerve Sensori Potentlal
Electromvography L'eneri.drion -~
65
++
67
++
54 63 64 68
43 65 55 69
+
++ 0
++ 0
+ + 0
++
++
I1
++
++ ++
I +
++
+ I + I
60 200 N A N N N -
30
43 N A N 33 N -
-
-
A A
~
A
N
-
A 1000 N N
A -
A A 39
-
A
-
N N N ~
-
~
-
-
A ~
A A A A N
GMPS BFGMPS QUAST BFGM
N
~
A
N
-
-
~
~~
-
EDB TA ST RF lAGN EDBAHBTA t D B AH5 TA EDB AHB ~
~
~
ratJons Clinical involvement - I I =severe + = mild 0 = nil :onduction studies - N = normal A =absent - = not performed nyographic muscle sampling - EDB - extensor digitorum brevis AHB = abductor hallucis brevis TA= (ibidliS antefior GN -gastrocnemius :eps femoris ST = semitendinosis, QUA = quadriceps fernoris GM - gluteus maximus PS = L5 paraspinal muscles
nic heparinisation and hypothermia (26 "-28 "C) employed routinely. Disposable membrane nators in use were: Cobe bubble oxygenator, membrane lung, Bentleigh bubble oxygenator, q bubbler and Gambro membrane. Mean cardinonary bypass time was 84 minutes (42-125). patients undergoing CABG surgery had coronary donated from the saphenous venous system and gs were postured by large rounded pads placed .d the thighs or buttocks to facilitate surgical 3. The tenth patient had a mitral valve replaceand it is possible that the legs were also postured imilar manner but this could not be determined. itients were nursed in an upright sitting position returning to the open heart surgery intensive care iperatively. All patients were examined by a dogist after the appearance of neurological toms. Time from surgery until neurological ination ranged from one day to several months.
ULTS :ase report is presented to illustrate typical clineatures and electrophysiological findings. The s of the other nine patients are outlined in Table 1 -year-old man with a past history of chronic uctive airways disease required CABG surgery .ay 1986 because of unstable angina pectoris. e saphenous vein grafts (from the right leg) and nternal mammary artery graft were performed; Jpulmonary bypass time was 85 minutes. On lpting to mobilise on the day following surgery sticed weakness in his legs. Within a few days he oped burning discomfort over the soles of both nd also had some shooting pain from the knees C L S C I A T I C NEUROPATHY
down to the feet which tended to be worse at night. Pressure ulceration of both heels had also developed post-operatively. On examination several weeks after surgery there was wasting with fasciculation of anterior tibial and calf muscle groups bilaterally. Knee flexion and all movements of the ankles and toes were weak bilaterally although this was more marked on the left. The knee and adductor jerks were normal but biceps femoris and ankle jerks were absent bilaterally. Light touch and pinprick sensation were impaired over the plantar and dorsal surfaces of the feet and on lateral and posterior aspects of calves with some sparing medially. Foot pulses were palpable. Neurophysiological tests were performed three months post-operatively at which time his symptoms were unchanged. Left common peroneal nerve conduction velocity was 30.2 mlsec with compound motor potential amplitude in the extensor digitorum brevis muscle reduced to 60 microvolts. There was no response to stimulation of the left posterior tibial or left sural nerves. Electromyography of the left semitendinosus, biceps fernoris, tibialis anterior and extensor digitorum brevis muscles showed fibrillation potentials and reduction in recruitment patterns with maximum voluntary contraction consistent with denervation. Electromyography of the left quadriceps, gluteus maximus and L5 paraspinal muscles was normal. All ten patients had painful lower limb sensory symptoms which were largely confined to the skin below the knees (six symmetrical, four asymmetrical). Six described prominent cutaneous burning sensations and five had dysaesthetic response to light tactile stimulation of the skin. Symptoms were worse at night in five patients and were associated with subiective motor restlessness. All had detectable distal lower limk sensory impairment on examination, chiefly affecting light touch, pinprick and thermal sensation. Seven 733 Aust NZ J Mcd 1991; 21
patients had additional motor involvement (severe in five). This was always asymmetrical and involved muscles below the knee although three patients also had weakness of the knee flexor muscles. When a motor deficit was marked, symptoms were usually present when normal consciousness returned after surgery although unpleasant sensory phenomena often took several days to appear. Patients with milder and predominantly sensory disturbances usually experienced a delay of several days until the development of first post-operative symptoms. Two patients developed post-operative heel skin pressure necrosis. Gradual recovery of sensory symptoms occurred in four patients without significant motor involvement after a mean period of 14 months (two-32). The remainder continue to experience painful dysaesthesia. Motor deficits showed little spontaneous improvement, and were largely unchanged after periods of observation o f u p to four years. Electrophysiology studies were performed in seven cases (Table 1). In cases with sensori-motor involvement, loss of amplitude of compound motor and sensory potentials and mild to moderate slowing of conduction velocities was found. Electromyographic evidence of denervation was detected in five patients; this was confined to muscles innervated by the sciatic nerves. Electromyography and nerve conduction studies performed in one case of isolated sensory disturbance were within normal limits apart from absence of F wave potentials. Upper limb nerve conduction studies were performed in one case and these were normal. Sural nerve biopsy was not performed on any patient.
DISCUSSION We have encountered a distinct syndrome of distal, asymmetrical and painhl sensori-motor or sensory lower limb neurological disturbance with causalgic features following cardiac surgery. The neurophysiological findings were consistent with a proximal focal site of axonal damage or an axonal peripheral neuropathy. There appeared to be no common predisposing circumstances other than the fact that all patients underwent surgery in the same hospital and received generally similar peri-operative management. No common factor in relation to surgeon, anaesthetist, cardiac bypass equipment, cardiac bypass time or predisposing illness was present. We believe that these lesions were produced by bilateral sciatic nerve compression although the distinction from a diffuse axonal peripheral neuropathy was difficult to make clinically in several mildly affected cases. The marked asymmetry of motor deficits and focal involvement of the hamstring musculature in several cases are best explained by asymmetrical proximal sciatic nerve pathology, and this hypothesis would be consistent 734
with previous experience concerning peripheral neurological complications of cardiac surgery. Mononeuropathy occurs relatively frequently after CABG surgery, suggesting a vulnerability of individual peripheral nerve^.^,^ This may relate to prolonged nerve pressure during a surgical procedure performed under the lowered arterial perfusion pressure provided by cardiopulmonary bypass. Intraoperative hypothermia has been shown to correlate with increased risk for mon~neuropathy~ in CABG surgery and was routinely used in all of the present cases. Cold may predispose to injury secondary to pressure or stretching.’ Lower limb causalgia occurs with proximal sciatic lesions8 and characteristically produces unpleasant sensory symptoms largely confined to the feet. Post-operative sciatic neuropathy not caused by direct nerve trauma is recognised as a complication of general surgical procedures.6,9Surgery performed in the lithotomy position appears to predispose to postoperative sciatic neuropathy, suggesting that nerve stretching and compression are aetiological factomh The fact that this pattern of post-cardiac surgery neuropathy had not been identified in previous large prospective surveys led to a search for causative factors related to local surgical and peri-operative management. In CABG surgery at St Vincent’s Hospital it was usual to posture the legs with pads or rolls placed under the upper thighs or buttocks to facilitate surgical access for dissection of saphenous vein grafts by slightly flexing, abducting and externally rotating the legs. This technique may render the sciatic nerves at increased risk for pressure palsy especially where the nerve runs subcutaneously after emerging from beneath the gluteus maximus muscle in the upper thigh. However, despite modification of this posturing method, further cases were encountered, several of whom had evidence of buttock and heel pressure necrosis. Further enquiries revealed that patients were being routinely nursed in the immediate post-operative period in a sitting position with the axis of the trunk vertical and at a 90 degree angle to the outstretched lower limbs. During this time, patients were usually intubated, drowsy and unable to move. On the basis that this form of posturing was likely to contribute to sciatic nerve pressure, post-operative nursing care was also altered and patients were postured with their upper body tilted no more than 30 degrees above the horizontal. Following institution of this measure, one further case of painful lower limb neuropathy was encountered over the next 36 months. Our experience suggests that the sciatic nerves, in common with other peripheral nerves, are susceptible to pressure-related damage in the course of cardiac surgery. Centres performing open heart surgical procedures should examine their methods for posturing patients during the intra-operative and post-operative
Aust NZ J Med 1991; 21
KEMPSTER ET AL.
periods to minimise the risk of this unpleasant and intractable post-operative complication. Postscript One of the authors (PG) has subsequently had communication from several other neurologists regarding identical cases operated on at other institutions and has personally seen such a case where cardiac surgery was performed in New Zealand. These observations indicate that this complication is not unique to St Vincent’s Hospital, Melbourne. Date of submission: 8 March 1991
References I. Javid H, Tnfo HM, Najifi H, Dye WS, Hunter JA. Neurological abnormalities following open-heart surgery. J Thorac Cardiovasc Surg 1969; 58: 502-9. 2. Sotaniemi KA, Juolasmaa A, Hokksnen E T . Neuropsychological outcome after open-heart surgery. Arch Neurol 1981; 38: 2-8.
3. Yhaw PJ, Bates D, Cartlidge NEF, Heaviside D: Julian UG, Shaw DA. Early neurological complications of coronary artery bypass surgery. Br Med J 1985; 291: 1384-7. 4. Lederrnan RJ, Breuer AC, Henson M R et al. Petipheral nervous system complications of coronarv artery bypass graft surgerv. Ann Neurol 1982; 12: 297-301. 5. Dhuner KG. Nerve injuries following operations: a survey of cases occurring during a six year period. Anesthesiology 1950; 11: 289-97. 6. Parks HJ. Postoperative peripheral neuropathies. Surgery 1973; 74: 348-57. 7. Thomas PK, Holdorff B. Neuropathy due to physical agcnrs. In: Dyck PJ, Thomas PR, Lamberr E H (eds). Peripheral neuropathp, 2nd editiou (volume 2). l‘hiladelph~a: Saunders, 1984; 1479- 1 5 1 1. 8. Sunderland S. I’ain mechanisms in causalgia. J Neurol Neurosurg Psychiatry 1976; 39: 471-80. 9. Stewart JD, Angus E, Gendron 11. Sciatic neuropathies. Br Med J 1983; 287: 1!08-9.
Case Reports s stated in the June issue, Case Reports to the Journal will be published as Letters to the Editor and the Letters section increased accordingly. T h e restrictions of length (500 words) and number of references (six) which presently apply to Letters will apply also to Case Reports published in this section. Only 1 table or 1 figure is permitted. (Case reports submitted prior to the June publication will, if accepted, be published in their current form.)
A
PAINFUL SCIATIC NEUROPATHY
Aust NZ J Med 1991; 21
735
