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NEUROLOGICAL SEQUELAE OF SPINAL ANAESTHESIA
" / would have everie man write what he knowes and no
BRITISH
JOURNAL
OF
more."—MONTAIGNE
ANAESTHESIA NOVEMBER 1989
VOLUME 63, No. 5
EDITORIAL NEUROLOGICAL SEQUELAE OF SPINAL ANAESTHESIA
Downloaded from http://bja.oxfordjournals.org/ at Monash University on June 18, 2015
taining the local anaesthetic—they were sterilized by immersion in this fluid. As the possibility of such occurrences had not appeared in the literature until 3 years after the anaesthetics [4], no negligence was held to have occurred. In spite of this, the effect of the case, coming so soon after the Foster Kennedy review and attracting considerable publicity, was to cause the virtual demise of spinal anaesthesia in the U.K. Only a very few determined enthusiasts continued to use the technique. The response to these events elsewhere was more scientific. In direct response to Foster Kennedy, Dripps and Vandam [5] reviewed meticulously the outcome of more than 10000 spinal anaesthetics. There were no major sequelae and any minor ones were mostly transient. Since then, many other papers have been written on this subject (see [6] for a review), and they lead to the same conclusion. Correctly conducted spinal anaesthesia should be very safe, Gynecology and Obstetrics and so was read widely but if it is performed badly then problems may by surgeons. It had a major impact, even though occur. Consider what a little phenol is believed to it was deficient in details of the anaesthetic have done to Woolley and Roe to see how procedures. In particular, there was no mention of susceptible the spinal cord is to damage! the conditions under which the blocks were given What else may lead to such tragedies? A or of the competence and standing of the decreasing minority still believe that local administrators. In spite of this, the article anaesthetics can be irritant. This may be true of concluded that "paralysis below the waist is too very acid solutions, but far more dangerous are large a price to pay in order that the surgeon should those containing preservative. For instance, in the have a fine relaxed field, and that the method should U.S.A. in recent years, paraplegia after the be rigidly reserved for those patients unable to accept accidental intrathecal injection of chloroprocaine a local or general anaesthetic." has been attributed to the bisulphite added to the In the U.K. particularly, this warning was solution as a preservative [7]. Other acknowledged reinforced by the " Woolley and Roe" case [3]. In causes in addition to chemical contamination of 1953, two patients sued the Ministry of Health the injected solution include infection caused by and others for damages for permanent paraplegia poor sterilization of drugs and equipment or an that followed spinal anaesthetics given by one inadequate aseptic technique, direct needle anaesthetist during the same operating list in trauma, pressure from a blood clot caused by 1947. Eventually the courts accepted the evidence needle trauma, cord ischaemia from poorly of Professor (later Sir) Robert Macintosh that the managed hypotension and vasoconstrictors added damage was caused by leakage of phenol through to the local anaesthetic to prolong its duration of undetected cracks in the glass ampoules con- action. The practitioner of spinal anaesthesia must It is usual to think of the neurological sequelae that may follow spinal anaesthesia as affecting only those parts of the nervous system that lie near the point of injection. Such sequelae may range from transient, localized disorders of nerve function, through loss of control of the urinary and rectal sphincters, to permanently incapacitating paraplegia. The first recorded case was published [1] just 8 years after the first spinal anaesthetics were given, but the great concern on this problem dates from the period after World War II. In 1950, a paper written by Foster Kennedy, an eminent New York (but Queen Square trained) neurologist, appeared with the title "The grave spinal cord paralyses caused by spinal anesthesia" [2]. It was a comprehensive review of a collection of neurological catastrophes following spinal anaesthesia and still provokes serious reflection on being read today. It was published in Surgery,
506
patients who required cardiorespiratory resuscitation during spinal anaesthesia and who developed neurological sequelae that do not fit the above categories. Caplan and colleagues described 14 cases of "sudden" cardiac arrest during spinal anaesthesia in relatively young and healthy patients [10]. All were resuscitated, but suffered ischaemic brain damage which was severe in six and led to death. Of the other eight, only one recovered to achieve a reasonable degree of independence. The authors acknowledged that retrospective analysis is fraught with difficulty, but identified two contributory patterns of management. The first was the use of sufficient • supplementary medication to produce a sleep-like state. The doses of sedation used were not excessive, but it should be noted that extensive blocks were present—the mean documented level before the cardiac arrest was T4. Such a block produces considerable deafferentation and the effects of small doses of sedative drugs may be exaggerated, resulting in increased risk of ventilatory inadequacy or airway obstruction. As cyanosis was noted close to the time of the arrest in 50 % of the patients, inadequate alveolar ventilation seems a likely aetiological factor. This implies earlier failure either to observe or to recognize the simple clinical features of airway obstruction or inadequate chest excursion. As a number of patients received supplementary oxygen, airway obstruction may have been the more important problem. Although the authors suggested that respiratory insufficiency may have played an important role, they commented on the "overall adequacy of basic anesthesia care". It is hard to reconcile the two statements if personal observation of the patient by the anaesthetist is considered an integral part of basic care. Such an analysis refutes the final conclusion of the paper—that spinal anaesthesia "carries a poorly understood potential for sudden cardiac arrest and severe brain injury in healthy patients".
A point correctly emphasized in the report by Caplan and his colleagues was that, in the presence of sympathetic block, hypoxia and hypercapnia may produce central and peripheral cardiovascular depression instead of the more usual stimulation. This would provide a mechanism for the cardiac arrest and also relate to the second contributary pattern recognized by the authors. This was a failure to appreciate the interaction between sympathetic block and the mechanisms of cardiorespiratory resuscitation. In essence,
Downloaded from http://bja.oxfordjournals.org/ at Monash University on June 18, 2015
recognize all these possibilities and control his technique to ensure that they are eliminated. Neurological complications respond poorly, if at all, to treatment, so they must be prevented. Gentleness, precision and careful manual control (Bromage's "gossamer touch") are essential for technical success and the avoidance of trauma and its consequences. The aseptic technique should be meticulous, as must be the procedures for preparing and sterilizing equipment, therefore high quality disposable syringes and needles are a great advantage. Some individuals may not be able to attain such high standards and should be encouraged to confine themselves to less demanding methods. For instance, recent reports of 32 cases of major neurological sequelae in Nicaragua were investigated by a panel of international experts who found that they were in essence war casualties [A. Fortuna, personal communication]. Economic breakdown led to falling standards in almost all aspects of practice, but most significantly, it appeared that drugs containing preservatives and equipment contaminated with detergents were used. This should be a warning to all of what can happen when standards decline. A second group of neurological sequelae of spinal anaesthesia, which are not quite as well recognized as the spinal cord and nerve root lesions considered above, include single transient palsies of the third, fourth, sixth, seventh or eighth cranial nerves. Overt lesions occur usually in association with post lumbar puncture headache, but may occur without, and are thought also to result from leakage of CSF. The reported incidence varies, but this is perhaps a reflection of how assiduously they are sought, as detailed evaluation has revealed a high incidence of minor degrees of hearing loss [8]. This same study found no hearing loss in similar patients given an extradural block, helping to confirm that the cause was leakage of CSF. Any patient who becomes aware of such a cranial nerve palsy should be reassured that it is likely to be transient, but obviously must be observed carefully until resolution occurs. It is important to remember that continued leakage of CSF after lumbar puncture may lead to the formation of intracranial haematoma [9]. Cranial nerve palsy should be treated in the same way as spinal headache. The use of fine-gauge needles and atraumatic lumbar puncture are obvious preventive measures. Recently there has been a report of a group of
BRITISH JOURNAL OF ANAESTHESIA
NEUROLOGICAL SEQUELAE OF SPINAL ANAESTHESIA
methoxamine 1-2 mg should be given. At intermediate heart rates, a combined alpha and beta agonist such as ephedrine 3-6 mg may be more suitable. If repeated doses are needed, it may be simpler to give a larger dose by the i.m. route. A poor response to i.v. drugs should always lead to reassessment of the extent of blood loss. In summary, spinal anaesthesia may affect the nervous system adversely in different ways. Because nervous tissue has such a poor potential for recovery, it is essential that such mishaps are prevented. An understanding of the potential hazards, coupled with a careful technique should make spinal anaesthesia a routine, safe technique that realizes its great potential as a method of providing pain relief and good operating conditions. J.A.W. Wildsmith and The late J. Alfred Lee REFERENCES 1. Urban K. Uber lumbalanaesthesie. Wiener Medizin Wochschrift 1907; 57: 31-32. 2. Kennedy, F, Effron AS, Perry G. The grave spinal cord paralyses caused by spinal anesthesia. Surgery, Gynecology and Obstetrics 1950; 91: 385-388. 3. Cope RW. The Woolley and Roe case. Anaesthesia 1954; 9: 249-270. 4. Sternberg, BL. Ampule contamination in spinal anesthesia. Anesthesiology 1950; 11: 257-258. 5. Dripps RD, Vandam LD. Longterm follow-up of patients who received 10098 spinal anesthetics. I: Failure to discover major neurological sequelae. Journal of the American Medical Association 1954; 156: 1486-1491. 6. Lee JA, Atkinson RS, Watt MJ. Sir Robert Macintosh's Lumbar Puncture and Spinal Analgesia Intradural and Extradural, 5th Edn. Edinburgh: Churchill Livingstone, 1985. 7. Covino BG. Current controversies in regional anaesthesia. In: Scott DB, McClure JH, Wildsmith JAW, eds. Regional Anaesthesia 1884-1984. Sodertalje: I.C.M. AB, 1984; 74-81. 8. Wang LP, Fog J, Bove M. Transient hearing loss following spinal anaesthesia. Anaesthesia 1987; 42: 1258-1263. 9. Newrick P, Read D. Subdural haematoma as a complication of spinal anaesthesia. British Medical Journal 1982; 28S: 341-342. 10. Caplan RA, Ward RJ, Posner K, Cheney FW. Unexpected cardiac arrest during spinal anesthesia: a closed claims analysis of predisposing factors. Anesthesiology 1988; 68: 5-11. 11. Keats AS. Anesthesia mortality—a new mechanism. Anesthesiology 1988; 68: 2-4. 12. Charlton JE. The management of regional anaesthesia. In: Wildsmith JAW, Armitage EN, eds. Principles and Practice of Regional Anaesthesia. Edinburgh: Churchill Livingstone, 1987; 37-61.
Downloaded from http://bja.oxfordjournals.org/ at Monash University on June 18, 2015
cardiac massage requires the presence of vasomotor tone to "generate" perfusion pressure when the heart is compressed. In the absence of sympathetic tone, cardiac massage may produce little or no cerebral blood flow. The implication is that a vasopressor (probably adrenaline) should be given at a very early stage in the treatment of cardiac arrest in a patient with extensive sympathetic block. The argument in favour of vasopressors was extended further in the editorial [11] accompanying the report. The point was made that, at one time, vasopressors were used to treat hypotension from any cause. It was soon recognized that such therapy was counterproductive in the hypovolaemic patient, but this led to an aversion to the use of these drugs in any situation and produced the illogical vogue for volume loading both to prevent and to treat hypotension during regional anaesthesia. This vogue continues even though evidence [12] suggests that it may be both harmful and ineffective, or at best only slowly effective. If the patient is hypovolaemic, fluid must be given urgently, as the patient's compensatory reflexes are impaired by the block. However, if the hypotension results mainly from sympathetic block, it is more logical to utilize drug therapy. Management of sympathetic block to avoid catastrophic consequences for the patient has a number of aspects. First, the anaesthetist should attempt to limit the extent of the block so that the amount of sympathetic paralysis is minimal. Second, the patient should be maintained in a slight head-down tilt to maintain venous return. Third, oxygen should be administered when arterial pressure is reduced or following the administration of sedative drugs. If the latter are used, airway patency and ventilatory excursion should be the subjects of constant observation by the anaesthetist. The usual equipment should be immediately available for dealing with problems. Finally, if the arterial pressure does decrease to a value that is considered unacceptable for the individual patient, it should be treated promptly by i.v. administration of an appropriate drug. Patients respond in different ways to various treatment options, but the following is a useful scheme for initial treatment (subsequent measures will depend on the response). If the heart rate is slow, increments of atropine 0.2 mg may be sufficient therapy. At heart rates in excess of 80-90 beat min"1, a pure alpha agonist such as
507
BRITISH
JOURNAL
OF
more."—MONTAIGNE
ANAESTHESIA NOVEMBER 1989
VOLUME 63, No. 5
EDITORIAL NEUROLOGICAL SEQUELAE OF SPINAL ANAESTHESIA
Downloaded from http://bja.oxfordjournals.org/ at Monash University on June 18, 2015
taining the local anaesthetic—they were sterilized by immersion in this fluid. As the possibility of such occurrences had not appeared in the literature until 3 years after the anaesthetics [4], no negligence was held to have occurred. In spite of this, the effect of the case, coming so soon after the Foster Kennedy review and attracting considerable publicity, was to cause the virtual demise of spinal anaesthesia in the U.K. Only a very few determined enthusiasts continued to use the technique. The response to these events elsewhere was more scientific. In direct response to Foster Kennedy, Dripps and Vandam [5] reviewed meticulously the outcome of more than 10000 spinal anaesthetics. There were no major sequelae and any minor ones were mostly transient. Since then, many other papers have been written on this subject (see [6] for a review), and they lead to the same conclusion. Correctly conducted spinal anaesthesia should be very safe, Gynecology and Obstetrics and so was read widely but if it is performed badly then problems may by surgeons. It had a major impact, even though occur. Consider what a little phenol is believed to it was deficient in details of the anaesthetic have done to Woolley and Roe to see how procedures. In particular, there was no mention of susceptible the spinal cord is to damage! the conditions under which the blocks were given What else may lead to such tragedies? A or of the competence and standing of the decreasing minority still believe that local administrators. In spite of this, the article anaesthetics can be irritant. This may be true of concluded that "paralysis below the waist is too very acid solutions, but far more dangerous are large a price to pay in order that the surgeon should those containing preservative. For instance, in the have a fine relaxed field, and that the method should U.S.A. in recent years, paraplegia after the be rigidly reserved for those patients unable to accept accidental intrathecal injection of chloroprocaine a local or general anaesthetic." has been attributed to the bisulphite added to the In the U.K. particularly, this warning was solution as a preservative [7]. Other acknowledged reinforced by the " Woolley and Roe" case [3]. In causes in addition to chemical contamination of 1953, two patients sued the Ministry of Health the injected solution include infection caused by and others for damages for permanent paraplegia poor sterilization of drugs and equipment or an that followed spinal anaesthetics given by one inadequate aseptic technique, direct needle anaesthetist during the same operating list in trauma, pressure from a blood clot caused by 1947. Eventually the courts accepted the evidence needle trauma, cord ischaemia from poorly of Professor (later Sir) Robert Macintosh that the managed hypotension and vasoconstrictors added damage was caused by leakage of phenol through to the local anaesthetic to prolong its duration of undetected cracks in the glass ampoules con- action. The practitioner of spinal anaesthesia must It is usual to think of the neurological sequelae that may follow spinal anaesthesia as affecting only those parts of the nervous system that lie near the point of injection. Such sequelae may range from transient, localized disorders of nerve function, through loss of control of the urinary and rectal sphincters, to permanently incapacitating paraplegia. The first recorded case was published [1] just 8 years after the first spinal anaesthetics were given, but the great concern on this problem dates from the period after World War II. In 1950, a paper written by Foster Kennedy, an eminent New York (but Queen Square trained) neurologist, appeared with the title "The grave spinal cord paralyses caused by spinal anesthesia" [2]. It was a comprehensive review of a collection of neurological catastrophes following spinal anaesthesia and still provokes serious reflection on being read today. It was published in Surgery,
506
patients who required cardiorespiratory resuscitation during spinal anaesthesia and who developed neurological sequelae that do not fit the above categories. Caplan and colleagues described 14 cases of "sudden" cardiac arrest during spinal anaesthesia in relatively young and healthy patients [10]. All were resuscitated, but suffered ischaemic brain damage which was severe in six and led to death. Of the other eight, only one recovered to achieve a reasonable degree of independence. The authors acknowledged that retrospective analysis is fraught with difficulty, but identified two contributory patterns of management. The first was the use of sufficient • supplementary medication to produce a sleep-like state. The doses of sedation used were not excessive, but it should be noted that extensive blocks were present—the mean documented level before the cardiac arrest was T4. Such a block produces considerable deafferentation and the effects of small doses of sedative drugs may be exaggerated, resulting in increased risk of ventilatory inadequacy or airway obstruction. As cyanosis was noted close to the time of the arrest in 50 % of the patients, inadequate alveolar ventilation seems a likely aetiological factor. This implies earlier failure either to observe or to recognize the simple clinical features of airway obstruction or inadequate chest excursion. As a number of patients received supplementary oxygen, airway obstruction may have been the more important problem. Although the authors suggested that respiratory insufficiency may have played an important role, they commented on the "overall adequacy of basic anesthesia care". It is hard to reconcile the two statements if personal observation of the patient by the anaesthetist is considered an integral part of basic care. Such an analysis refutes the final conclusion of the paper—that spinal anaesthesia "carries a poorly understood potential for sudden cardiac arrest and severe brain injury in healthy patients".
A point correctly emphasized in the report by Caplan and his colleagues was that, in the presence of sympathetic block, hypoxia and hypercapnia may produce central and peripheral cardiovascular depression instead of the more usual stimulation. This would provide a mechanism for the cardiac arrest and also relate to the second contributary pattern recognized by the authors. This was a failure to appreciate the interaction between sympathetic block and the mechanisms of cardiorespiratory resuscitation. In essence,
Downloaded from http://bja.oxfordjournals.org/ at Monash University on June 18, 2015
recognize all these possibilities and control his technique to ensure that they are eliminated. Neurological complications respond poorly, if at all, to treatment, so they must be prevented. Gentleness, precision and careful manual control (Bromage's "gossamer touch") are essential for technical success and the avoidance of trauma and its consequences. The aseptic technique should be meticulous, as must be the procedures for preparing and sterilizing equipment, therefore high quality disposable syringes and needles are a great advantage. Some individuals may not be able to attain such high standards and should be encouraged to confine themselves to less demanding methods. For instance, recent reports of 32 cases of major neurological sequelae in Nicaragua were investigated by a panel of international experts who found that they were in essence war casualties [A. Fortuna, personal communication]. Economic breakdown led to falling standards in almost all aspects of practice, but most significantly, it appeared that drugs containing preservatives and equipment contaminated with detergents were used. This should be a warning to all of what can happen when standards decline. A second group of neurological sequelae of spinal anaesthesia, which are not quite as well recognized as the spinal cord and nerve root lesions considered above, include single transient palsies of the third, fourth, sixth, seventh or eighth cranial nerves. Overt lesions occur usually in association with post lumbar puncture headache, but may occur without, and are thought also to result from leakage of CSF. The reported incidence varies, but this is perhaps a reflection of how assiduously they are sought, as detailed evaluation has revealed a high incidence of minor degrees of hearing loss [8]. This same study found no hearing loss in similar patients given an extradural block, helping to confirm that the cause was leakage of CSF. Any patient who becomes aware of such a cranial nerve palsy should be reassured that it is likely to be transient, but obviously must be observed carefully until resolution occurs. It is important to remember that continued leakage of CSF after lumbar puncture may lead to the formation of intracranial haematoma [9]. Cranial nerve palsy should be treated in the same way as spinal headache. The use of fine-gauge needles and atraumatic lumbar puncture are obvious preventive measures. Recently there has been a report of a group of
BRITISH JOURNAL OF ANAESTHESIA
NEUROLOGICAL SEQUELAE OF SPINAL ANAESTHESIA
methoxamine 1-2 mg should be given. At intermediate heart rates, a combined alpha and beta agonist such as ephedrine 3-6 mg may be more suitable. If repeated doses are needed, it may be simpler to give a larger dose by the i.m. route. A poor response to i.v. drugs should always lead to reassessment of the extent of blood loss. In summary, spinal anaesthesia may affect the nervous system adversely in different ways. Because nervous tissue has such a poor potential for recovery, it is essential that such mishaps are prevented. An understanding of the potential hazards, coupled with a careful technique should make spinal anaesthesia a routine, safe technique that realizes its great potential as a method of providing pain relief and good operating conditions. J.A.W. Wildsmith and The late J. Alfred Lee REFERENCES 1. Urban K. Uber lumbalanaesthesie. Wiener Medizin Wochschrift 1907; 57: 31-32. 2. Kennedy, F, Effron AS, Perry G. The grave spinal cord paralyses caused by spinal anesthesia. Surgery, Gynecology and Obstetrics 1950; 91: 385-388. 3. Cope RW. The Woolley and Roe case. Anaesthesia 1954; 9: 249-270. 4. Sternberg, BL. Ampule contamination in spinal anesthesia. Anesthesiology 1950; 11: 257-258. 5. Dripps RD, Vandam LD. Longterm follow-up of patients who received 10098 spinal anesthetics. I: Failure to discover major neurological sequelae. Journal of the American Medical Association 1954; 156: 1486-1491. 6. Lee JA, Atkinson RS, Watt MJ. Sir Robert Macintosh's Lumbar Puncture and Spinal Analgesia Intradural and Extradural, 5th Edn. Edinburgh: Churchill Livingstone, 1985. 7. Covino BG. Current controversies in regional anaesthesia. In: Scott DB, McClure JH, Wildsmith JAW, eds. Regional Anaesthesia 1884-1984. Sodertalje: I.C.M. AB, 1984; 74-81. 8. Wang LP, Fog J, Bove M. Transient hearing loss following spinal anaesthesia. Anaesthesia 1987; 42: 1258-1263. 9. Newrick P, Read D. Subdural haematoma as a complication of spinal anaesthesia. British Medical Journal 1982; 28S: 341-342. 10. Caplan RA, Ward RJ, Posner K, Cheney FW. Unexpected cardiac arrest during spinal anesthesia: a closed claims analysis of predisposing factors. Anesthesiology 1988; 68: 5-11. 11. Keats AS. Anesthesia mortality—a new mechanism. Anesthesiology 1988; 68: 2-4. 12. Charlton JE. The management of regional anaesthesia. In: Wildsmith JAW, Armitage EN, eds. Principles and Practice of Regional Anaesthesia. Edinburgh: Churchill Livingstone, 1987; 37-61.
Downloaded from http://bja.oxfordjournals.org/ at Monash University on June 18, 2015
cardiac massage requires the presence of vasomotor tone to "generate" perfusion pressure when the heart is compressed. In the absence of sympathetic tone, cardiac massage may produce little or no cerebral blood flow. The implication is that a vasopressor (probably adrenaline) should be given at a very early stage in the treatment of cardiac arrest in a patient with extensive sympathetic block. The argument in favour of vasopressors was extended further in the editorial [11] accompanying the report. The point was made that, at one time, vasopressors were used to treat hypotension from any cause. It was soon recognized that such therapy was counterproductive in the hypovolaemic patient, but this led to an aversion to the use of these drugs in any situation and produced the illogical vogue for volume loading both to prevent and to treat hypotension during regional anaesthesia. This vogue continues even though evidence [12] suggests that it may be both harmful and ineffective, or at best only slowly effective. If the patient is hypovolaemic, fluid must be given urgently, as the patient's compensatory reflexes are impaired by the block. However, if the hypotension results mainly from sympathetic block, it is more logical to utilize drug therapy. Management of sympathetic block to avoid catastrophic consequences for the patient has a number of aspects. First, the anaesthetist should attempt to limit the extent of the block so that the amount of sympathetic paralysis is minimal. Second, the patient should be maintained in a slight head-down tilt to maintain venous return. Third, oxygen should be administered when arterial pressure is reduced or following the administration of sedative drugs. If the latter are used, airway patency and ventilatory excursion should be the subjects of constant observation by the anaesthetist. The usual equipment should be immediately available for dealing with problems. Finally, if the arterial pressure does decrease to a value that is considered unacceptable for the individual patient, it should be treated promptly by i.v. administration of an appropriate drug. Patients respond in different ways to various treatment options, but the following is a useful scheme for initial treatment (subsequent measures will depend on the response). If the heart rate is slow, increments of atropine 0.2 mg may be sufficient therapy. At heart rates in excess of 80-90 beat min"1, a pure alpha agonist such as
507