514
P. C. GORDON ET AL. the use of topical ice slush. Ann Thorac Surg 1989; 48:764-768.
11. Abd AG, Braun NMT, Baskin MI, O'Sullivan MM et al. Diaphragrnatic dysfunction after open heart
surgery: treatment with a rocking bed. Ann Intern Med 1989; 111:881-886. 12. Brown KA, Hoffstein V, Byrick RJ. Bedside diagnosis of bilateral diaphragmatic paralysis in a ventilator-dependent patient after open-heart surgery. Anesth Analg 1985; 64: 1208-121 O. 13. Laub GW, Muralidharan S, Chen C, Perritt A et al. Phrenic nerve injury. A prospective study. Chest 1991; 100:376-379. 14. Hamilton JR, Tocewicz K, Elliott MJ, de Leval M et al. Paralysed diaphragm after cardiac surgery in
IS. Braun SR, Sufit RL, Giovannoni R, O'Connor M et al. Intermittent negative pressure ventilation in the treatment of respiratory failure in progressive neuromuscular disease. Neurology 1987; 37:1874-1875. 16. Eposito RA, Spencer FC. The effect of pericardial
insulation on hypothermic phrenic nerve injury during open-heart surgery. Ann Thorac Surg 1987; 43:303-308. 17. Wheeler WE, Rubis U, Jones CW, Harrah JD.
Etiology and prevention of topical cardiac hypothermia-induced phrenic nerve injury and left lower lobe atelectasis during cardiac surgery. Chest 1985; 88:680-683.
children: Value for plication. Eur J Cardiothorac Surgery 1990; 4:487-490.
Extensive Central Neural Blockade Following Interscalene Brachial Plexus Blockade D. P. McGLADE* Department of Anaesthesia, Preston and Northcote Community Hospital, Melbourne, Victoria Key Words: ANAESTHESIA TECHNIQUES, REGIONAL: brachial plexus, interscalene block; COMPLICATIONS: central neural blockade
Although the interscalene approach to the brachial plexus has been recognised for over 60 years, 1 it has only more recently gained popularity in the field of regional anaesthesia due to the work of Winnie. 2 Several complications of this technique have been described. However, these are felt to be infrequent enough to justify its continued place in anaesthetic practice. The following describes an uncommon but wellrecognised complication of the technique, involving high central neural blockade, unconsciousness and apnoea. This may have resulted from an inadvertent subarachnoid injection oflocal anaesthetic solution, but there are certain unusual aspects of the case which cast doubt on this diagnosis. CASE REPORT A healthy 17-year-old male was admitted to hospital with severe lacerations of the left forearm. *F.F.A.RACS .. StafT Specialist. Address forCorrespondence/Reprints: Dr. D. P. McGlade, Staff Specialist, Department of Anaesthesia, Royal Women's Hospital, 132 Grattan Street, Carlton, Victoria 3053, Australia. Accepted for publication May 1, 1992
The next day the patient presented to the operating theatre for suturing of the lacerations, Premedication had been omitted and in the anaesthetic room intravenous access was secured via an indwelling cannula through which midazolam 2.5 mg was administered. Vital signs included a blood pressure of 125/75 mmHg and pulse rate of 80/minute, Using a 23 gauge standard-bevel needle, a left interscalene block was then attempted. The needle was initially inserted in the direction recommended by Winnie, 2 medially, dorsally and slightly caudally, to a depth of between 20 and 25 mm, and the transverse process of C6 was encountered. The needle was then repositioned anteriorly and paraesthesia was obtained in the upper forearm. Following negative aspiration and an uneventful 2 ml test dose given to exclude intravascular administration, a total of 28 ml of lignocaine 1.5% with adrenaline 1:200,000 was slowly injected. Approximately two minutes after the completion of the injection, the patient described paraesthesia and weakness, first in the left arm and then rapidly progressing to involve the right arm. This was then followed by weakening of the voice and the Anaesthesia and Intenslre Care, Vol. 20. No. 4, Norember, 1992
515
CASE REPORT
complaint of nausea, at which stage 100% oxygen was delivered by face mask. The patient objected to this by thrashing movements of the head and lower half of the body, with the arms remaining motionless. Over the next few minutes apnoea ensued and gentle positive pressure ventilation was applied. Gradually body movements ceased and examination revealed dilated non-reacting pupils, absent corneal reflexes and flaccid limbs. Haemodynamically the patient remained stable with a systolic BP of 110 with no requirement for intravenous volume loading or the use of vasopressor agents. Positive pressure ventilation was maintained via the facemask for the duration of the apnoeic episode which lasted 15 minutes. Spontaneous ventilatory efforts then resumed and within two minutes were judged to be clinically adequate by rate and depth of anaesthetic bag movement. Otherwise the patient remained motionless and unconscious. At this stage, considering the stable condition of the patient and the relatively benign nature of the proposed operation, it was decided to proceed with surgery. Following a period with the patient spontaneously breathing 100% oxygen, and without the use of any sedative or muscle relaxant agents, laryngoscopy was performed and the patient intubated, with no laryngeal, cardiovascular or other response being noted. Surgery was then carried out with the patient breathing spontaneously 70% nitrous oxide in oxygen with isoflurane 0.25% to avoid any potential for awareness. Vital signs at this stage included a systolic blood pressure of 95 mmHg, heart rate of 90/min, peripheral arterial oxyhaemoglobin saturation of 97% and an endtidal C02 level of 45 mmHg. These remained stable throughout the procedure. With the institution of inhalational anaesthesia, the pupils which had previously appeared dilated and non-reacting became constricted. At the completion of surgery, approximately 90 minutes after the performance of the block, inhalational agents were ceased and the patient promptly awoke with apparent full neurological recovery except for analgesia and some persistent weakness in the left arm. This subsided over the next hour. Monitoring was continued in the highdependency area for the next three hours, with no untoward events occurring. Later, on questioning, the patient revealed that he could recall the onset of difficulty with breathing and the application of the facemask, but nothing further until awakening at the end of the operation. He was discharged from hospital the following day. Anaesthesia and Intensi,'e Care, Vo!. la, No. 4, NOI'ember, 1991
DISCUSSION
Since the interscalene brachial plexus block is a paravertebral technique, there is always the potential for producing extensive central neural blockade, either subarachnoid,3 subdural or epidural. 4 ,5 Dural penetration by the local anaesthetic needle may result from inappropriately deep positioning of the needle-tip through an intervertebral foramen, or from a needle inserted to an appropriate depth inadvertently entering a dural cuff extending out from the intervertebral foramen along a nerve root. The technique also involves needle insertion into an area where intravascular injection into either the vertebral artery or vein is possible, with either complication causing potentially serious central nervous system disturbances. However, there have been several reports of extensive bilateral blockade following this technique which defy obvious anatomical explanation and the authors postulate other possible methods of spread of solution, such as via prevertebral fascial planes. 6,7 In this case subarachnoid injection is supported by several features. First, there was a rapid onset of an ascending block initially involving cervical nerve roots bilaterally, then progressing to involve the brainstem with the development of dysphonia through to apnoea and unconsciousness with dilated, non-reacting pupils witin a few minutes. Spread caudally was difficult to assess as the onset of lower-limb flaccidity coincided with that of brainstem anaesthesia. The duration of the unconsciouness and extensive neurological blockade would appear to be similar to that of previously documented cases of subarachnoid injections of relatively massive volumes of local anaesthetic from either a cervical3or lumbar8 level. A similar neurological picture may also result from inadvertent subdural deposition of local anaesthetic at a cervical level due to the continuity of the subdural space from vertebral to intracranial levels through the foramen magnum. 9 The epidural space, however, does not extend intracranially and massive epidural injection of local anaesthetic is therefore very unlikely in this case. There are two aspects ofthis case that are worthy of note. The first is the haemodynamic stability displayed by the patient. Whereas profound hypotension has previously been observed in the context of a total spinal anaesthetic occurring as a consequence of an attempted interscalene brachial plexus block, 3 this was obviously not the case here. Some authors would claim that this supports the explanation of inadvertent subdural administration, in so far as certain previous case reports have demonstrated extensive levels of sensory blockade with remarkable maintenance of
516
D. P. McGLADE
cardiovascular stability.9,lo,11 The explanation for this is unknown, but as the preferred distribution of solutions injected into the subdural space has been described as mainly along its dorsal aspect and in a cephalad direction, 8 injection from a mid-cervical level could conceivably result in a spread which spared the preganglionic sympathetic outflow arising from the ventral aspect of the thoracolumbar spinal cord. Of greater interest is the relatively short-lived period of apnoea observed, in so far as ventilation resumed in the presence of what appeared to be ongoing brainstem anaesthesia. This is not inconsistent with case reports documented by Bromage,8 where following inadvertent subarachnoid injection of large doses of local anaesthetic solution in attempted epidural blockade, the duration of unconsciousness not uncommonly exceeded that of apnoea. In a previous study on total spinal anaesthesia by Evans l2 using large volumes of local anaesthetic solution administered from a lumbar level, it was demonstrated that apnoea, while being usual, was not universal. However, what was noted in that study was prolonged and profound motor blockade of the lumbar plexus, i.e. those nerve roots in the immediate vicinity of the site of administration. Motor control of respiration is principally via the phrenic nerve to the diaphragm, with lesser input from the intercostal and accessory nerves to their respective muscle groups. Given the proximity of the phrenic nerve roots (C3, 4, 5) to the site of interscalene injection (C6), if this were a case of inadvertent total spinal anaesthesia due to subarachnoid administration of massive amounts of local anaesthetic, then it would be difficult to explain the prompt return of ventilation which occurred. On the other hand, with inadvertent subdural administration it may be theoretically possible to have relative sparing of motor fibres as well as the preganglionic sympathetic fibres due to the predominantly dorsal distribution of local anaesthetic solution previously proposd. This situation of profound sensory blockade with relatively minor motor disturbance occurring in the context of subdural blockade has been described.lO Apnoea of a similar duration has also been described following probable injection of local anaesthetic into the vertebral artery during an attempted interscalene brachial plexus block. 13 However, in contrast, that case was associated with
maintenance of consciousness in the presence of tetraplegia and aphonia, i.e. the 'locked-in syndrome', and the patient's condition subsequently progressed to involve haemodynamic instability and convulsions. Finally, this case and others l4 continue to emphasise the importance of patient monitoring and the necessity for the ready availability of resuscitation equipment when performing major regional techniques. REFERENCES
1. Labat G, Brachial plexus block; Details of technique with lantern slide demonstration. Br J Anaesth 192627; 4: 174-176. 2. Winnie AP. Interscalene brachial plexus block. Anesth Analg 1970; 49:455-466. 3. Ross S, Scarborough CD. Total spinal anaesthesia following brachial plexus block. Anesthesiology 1973; 39:458. 4. Scammell SJ. Inadvertent epidural anaesthesia as a complication of interscalene brachial plexus block. Anaesth Intens Care 1979; 7:56-57. 5. Kumar A, Battit GE, Froese AB, Long MC. Bilateral cervical and thoracic epidural blockade complicating interscalene brachial plexus block. Anesthesiology 1971; 35:650-652. 6. Cobcroft MD. Bilateral spread of analgesia with interscalene brachial plexus block. Anaesth Intens Care 1976; 4:73. 7. Lombard TP, Couper JL. Bilateral spread of analgesia following interscalene brachial plexus block. Anesthesiology 1983; 58:472-473. 8. Bromage PR. Complications and Contraindications. In: Epidural Analgesia. W. B. Saunders Co., Philadelphia 1978; 655-665. 9. Bruyns T, Devulder J, Verrneulen H, De Colvenaer L, Rolly G. Possible inadvertent subdural block following attempted stellate ganglion blockade. Anaesthesia 1991; 46:747-749. 10. Pearson RMG. A rare complication of extradural analgesia. Anaesthesia 1984; 39:460-463. 11. Manchanda VN, Murad SHN, Shilyansky G, Mehringer M. Unusual clinical course of accidental subdural local anesthetic injection. Anesth Analg 1983; 62:1124-1126. 12. Evans TI. Total spinal anaesthesia. Anaesth Intens Care 1974; 2:158-163. 13. Durrani Z, Winnie AP. Brainstem toxicity with reversible locked-in syndrome after intescalene brachial plexus block. Anesth Analg 1991; 72:249-252. 14. Edde RR, Deutsch S. Cardiac arrest after interscalene brachial plexus block. Anesth Analg 1977; 56:446-447.
Anaesthesia and Inlensi)'e Care, Va!. 20, No. 4, No)'ember, 1992
P. C. GORDON ET AL. the use of topical ice slush. Ann Thorac Surg 1989; 48:764-768.
11. Abd AG, Braun NMT, Baskin MI, O'Sullivan MM et al. Diaphragrnatic dysfunction after open heart
surgery: treatment with a rocking bed. Ann Intern Med 1989; 111:881-886. 12. Brown KA, Hoffstein V, Byrick RJ. Bedside diagnosis of bilateral diaphragmatic paralysis in a ventilator-dependent patient after open-heart surgery. Anesth Analg 1985; 64: 1208-121 O. 13. Laub GW, Muralidharan S, Chen C, Perritt A et al. Phrenic nerve injury. A prospective study. Chest 1991; 100:376-379. 14. Hamilton JR, Tocewicz K, Elliott MJ, de Leval M et al. Paralysed diaphragm after cardiac surgery in
IS. Braun SR, Sufit RL, Giovannoni R, O'Connor M et al. Intermittent negative pressure ventilation in the treatment of respiratory failure in progressive neuromuscular disease. Neurology 1987; 37:1874-1875. 16. Eposito RA, Spencer FC. The effect of pericardial
insulation on hypothermic phrenic nerve injury during open-heart surgery. Ann Thorac Surg 1987; 43:303-308. 17. Wheeler WE, Rubis U, Jones CW, Harrah JD.
Etiology and prevention of topical cardiac hypothermia-induced phrenic nerve injury and left lower lobe atelectasis during cardiac surgery. Chest 1985; 88:680-683.
children: Value for plication. Eur J Cardiothorac Surgery 1990; 4:487-490.
Extensive Central Neural Blockade Following Interscalene Brachial Plexus Blockade D. P. McGLADE* Department of Anaesthesia, Preston and Northcote Community Hospital, Melbourne, Victoria Key Words: ANAESTHESIA TECHNIQUES, REGIONAL: brachial plexus, interscalene block; COMPLICATIONS: central neural blockade
Although the interscalene approach to the brachial plexus has been recognised for over 60 years, 1 it has only more recently gained popularity in the field of regional anaesthesia due to the work of Winnie. 2 Several complications of this technique have been described. However, these are felt to be infrequent enough to justify its continued place in anaesthetic practice. The following describes an uncommon but wellrecognised complication of the technique, involving high central neural blockade, unconsciousness and apnoea. This may have resulted from an inadvertent subarachnoid injection oflocal anaesthetic solution, but there are certain unusual aspects of the case which cast doubt on this diagnosis. CASE REPORT A healthy 17-year-old male was admitted to hospital with severe lacerations of the left forearm. *F.F.A.RACS .. StafT Specialist. Address forCorrespondence/Reprints: Dr. D. P. McGlade, Staff Specialist, Department of Anaesthesia, Royal Women's Hospital, 132 Grattan Street, Carlton, Victoria 3053, Australia. Accepted for publication May 1, 1992
The next day the patient presented to the operating theatre for suturing of the lacerations, Premedication had been omitted and in the anaesthetic room intravenous access was secured via an indwelling cannula through which midazolam 2.5 mg was administered. Vital signs included a blood pressure of 125/75 mmHg and pulse rate of 80/minute, Using a 23 gauge standard-bevel needle, a left interscalene block was then attempted. The needle was initially inserted in the direction recommended by Winnie, 2 medially, dorsally and slightly caudally, to a depth of between 20 and 25 mm, and the transverse process of C6 was encountered. The needle was then repositioned anteriorly and paraesthesia was obtained in the upper forearm. Following negative aspiration and an uneventful 2 ml test dose given to exclude intravascular administration, a total of 28 ml of lignocaine 1.5% with adrenaline 1:200,000 was slowly injected. Approximately two minutes after the completion of the injection, the patient described paraesthesia and weakness, first in the left arm and then rapidly progressing to involve the right arm. This was then followed by weakening of the voice and the Anaesthesia and Intenslre Care, Vol. 20. No. 4, Norember, 1992
515
CASE REPORT
complaint of nausea, at which stage 100% oxygen was delivered by face mask. The patient objected to this by thrashing movements of the head and lower half of the body, with the arms remaining motionless. Over the next few minutes apnoea ensued and gentle positive pressure ventilation was applied. Gradually body movements ceased and examination revealed dilated non-reacting pupils, absent corneal reflexes and flaccid limbs. Haemodynamically the patient remained stable with a systolic BP of 110 with no requirement for intravenous volume loading or the use of vasopressor agents. Positive pressure ventilation was maintained via the facemask for the duration of the apnoeic episode which lasted 15 minutes. Spontaneous ventilatory efforts then resumed and within two minutes were judged to be clinically adequate by rate and depth of anaesthetic bag movement. Otherwise the patient remained motionless and unconscious. At this stage, considering the stable condition of the patient and the relatively benign nature of the proposed operation, it was decided to proceed with surgery. Following a period with the patient spontaneously breathing 100% oxygen, and without the use of any sedative or muscle relaxant agents, laryngoscopy was performed and the patient intubated, with no laryngeal, cardiovascular or other response being noted. Surgery was then carried out with the patient breathing spontaneously 70% nitrous oxide in oxygen with isoflurane 0.25% to avoid any potential for awareness. Vital signs at this stage included a systolic blood pressure of 95 mmHg, heart rate of 90/min, peripheral arterial oxyhaemoglobin saturation of 97% and an endtidal C02 level of 45 mmHg. These remained stable throughout the procedure. With the institution of inhalational anaesthesia, the pupils which had previously appeared dilated and non-reacting became constricted. At the completion of surgery, approximately 90 minutes after the performance of the block, inhalational agents were ceased and the patient promptly awoke with apparent full neurological recovery except for analgesia and some persistent weakness in the left arm. This subsided over the next hour. Monitoring was continued in the highdependency area for the next three hours, with no untoward events occurring. Later, on questioning, the patient revealed that he could recall the onset of difficulty with breathing and the application of the facemask, but nothing further until awakening at the end of the operation. He was discharged from hospital the following day. Anaesthesia and Intensi,'e Care, Vo!. la, No. 4, NOI'ember, 1991
DISCUSSION
Since the interscalene brachial plexus block is a paravertebral technique, there is always the potential for producing extensive central neural blockade, either subarachnoid,3 subdural or epidural. 4 ,5 Dural penetration by the local anaesthetic needle may result from inappropriately deep positioning of the needle-tip through an intervertebral foramen, or from a needle inserted to an appropriate depth inadvertently entering a dural cuff extending out from the intervertebral foramen along a nerve root. The technique also involves needle insertion into an area where intravascular injection into either the vertebral artery or vein is possible, with either complication causing potentially serious central nervous system disturbances. However, there have been several reports of extensive bilateral blockade following this technique which defy obvious anatomical explanation and the authors postulate other possible methods of spread of solution, such as via prevertebral fascial planes. 6,7 In this case subarachnoid injection is supported by several features. First, there was a rapid onset of an ascending block initially involving cervical nerve roots bilaterally, then progressing to involve the brainstem with the development of dysphonia through to apnoea and unconsciousness with dilated, non-reacting pupils witin a few minutes. Spread caudally was difficult to assess as the onset of lower-limb flaccidity coincided with that of brainstem anaesthesia. The duration of the unconsciouness and extensive neurological blockade would appear to be similar to that of previously documented cases of subarachnoid injections of relatively massive volumes of local anaesthetic from either a cervical3or lumbar8 level. A similar neurological picture may also result from inadvertent subdural deposition of local anaesthetic at a cervical level due to the continuity of the subdural space from vertebral to intracranial levels through the foramen magnum. 9 The epidural space, however, does not extend intracranially and massive epidural injection of local anaesthetic is therefore very unlikely in this case. There are two aspects ofthis case that are worthy of note. The first is the haemodynamic stability displayed by the patient. Whereas profound hypotension has previously been observed in the context of a total spinal anaesthetic occurring as a consequence of an attempted interscalene brachial plexus block, 3 this was obviously not the case here. Some authors would claim that this supports the explanation of inadvertent subdural administration, in so far as certain previous case reports have demonstrated extensive levels of sensory blockade with remarkable maintenance of
516
D. P. McGLADE
cardiovascular stability.9,lo,11 The explanation for this is unknown, but as the preferred distribution of solutions injected into the subdural space has been described as mainly along its dorsal aspect and in a cephalad direction, 8 injection from a mid-cervical level could conceivably result in a spread which spared the preganglionic sympathetic outflow arising from the ventral aspect of the thoracolumbar spinal cord. Of greater interest is the relatively short-lived period of apnoea observed, in so far as ventilation resumed in the presence of what appeared to be ongoing brainstem anaesthesia. This is not inconsistent with case reports documented by Bromage,8 where following inadvertent subarachnoid injection of large doses of local anaesthetic solution in attempted epidural blockade, the duration of unconsciousness not uncommonly exceeded that of apnoea. In a previous study on total spinal anaesthesia by Evans l2 using large volumes of local anaesthetic solution administered from a lumbar level, it was demonstrated that apnoea, while being usual, was not universal. However, what was noted in that study was prolonged and profound motor blockade of the lumbar plexus, i.e. those nerve roots in the immediate vicinity of the site of administration. Motor control of respiration is principally via the phrenic nerve to the diaphragm, with lesser input from the intercostal and accessory nerves to their respective muscle groups. Given the proximity of the phrenic nerve roots (C3, 4, 5) to the site of interscalene injection (C6), if this were a case of inadvertent total spinal anaesthesia due to subarachnoid administration of massive amounts of local anaesthetic, then it would be difficult to explain the prompt return of ventilation which occurred. On the other hand, with inadvertent subdural administration it may be theoretically possible to have relative sparing of motor fibres as well as the preganglionic sympathetic fibres due to the predominantly dorsal distribution of local anaesthetic solution previously proposd. This situation of profound sensory blockade with relatively minor motor disturbance occurring in the context of subdural blockade has been described.lO Apnoea of a similar duration has also been described following probable injection of local anaesthetic into the vertebral artery during an attempted interscalene brachial plexus block. 13 However, in contrast, that case was associated with
maintenance of consciousness in the presence of tetraplegia and aphonia, i.e. the 'locked-in syndrome', and the patient's condition subsequently progressed to involve haemodynamic instability and convulsions. Finally, this case and others l4 continue to emphasise the importance of patient monitoring and the necessity for the ready availability of resuscitation equipment when performing major regional techniques. REFERENCES
1. Labat G, Brachial plexus block; Details of technique with lantern slide demonstration. Br J Anaesth 192627; 4: 174-176. 2. Winnie AP. Interscalene brachial plexus block. Anesth Analg 1970; 49:455-466. 3. Ross S, Scarborough CD. Total spinal anaesthesia following brachial plexus block. Anesthesiology 1973; 39:458. 4. Scammell SJ. Inadvertent epidural anaesthesia as a complication of interscalene brachial plexus block. Anaesth Intens Care 1979; 7:56-57. 5. Kumar A, Battit GE, Froese AB, Long MC. Bilateral cervical and thoracic epidural blockade complicating interscalene brachial plexus block. Anesthesiology 1971; 35:650-652. 6. Cobcroft MD. Bilateral spread of analgesia with interscalene brachial plexus block. Anaesth Intens Care 1976; 4:73. 7. Lombard TP, Couper JL. Bilateral spread of analgesia following interscalene brachial plexus block. Anesthesiology 1983; 58:472-473. 8. Bromage PR. Complications and Contraindications. In: Epidural Analgesia. W. B. Saunders Co., Philadelphia 1978; 655-665. 9. Bruyns T, Devulder J, Verrneulen H, De Colvenaer L, Rolly G. Possible inadvertent subdural block following attempted stellate ganglion blockade. Anaesthesia 1991; 46:747-749. 10. Pearson RMG. A rare complication of extradural analgesia. Anaesthesia 1984; 39:460-463. 11. Manchanda VN, Murad SHN, Shilyansky G, Mehringer M. Unusual clinical course of accidental subdural local anesthetic injection. Anesth Analg 1983; 62:1124-1126. 12. Evans TI. Total spinal anaesthesia. Anaesth Intens Care 1974; 2:158-163. 13. Durrani Z, Winnie AP. Brainstem toxicity with reversible locked-in syndrome after intescalene brachial plexus block. Anesth Analg 1991; 72:249-252. 14. Edde RR, Deutsch S. Cardiac arrest after interscalene brachial plexus block. Anesth Analg 1977; 56:446-447.
Anaesthesia and Inlensi)'e Care, Va!. 20, No. 4, No)'ember, 1992
