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Anesthesia for craniotomy in a patient with previous paralytic polio
Journal of Clinical Anesthesia (2008) 20, 210–213
Case report
Anesthesia for craniotomy in a patient with previous paralytic polio Puthuvassery Raman Suneel MD (Associate Professor)a , Prabhat Kumar Sinha MD (Associate Professor)a,⁎, Koniparambil Pappu Unnikrishnan MD (Assistant Professor)a , Mathew Abraham MS, MCh (Assistant Professor)b a
Department of Anesthesiology, Sree Chitra Tirunal Institute of Medical Sciences and Technology, Thiruvananthapuram, Kerala, India PIN 695011 b Department of Neurosurgery, Sree Chitra Tirunal Institute of Medical Sciences and Technology, Thiruvananthapuram, Kerala, India PIN 695011 Received 18 September 2006; revised 22 July 2007; accepted 10 August 2007
Keywords: Anesthesia, nondepolarizing neuromuscular relaxants; Poliomyelitis
Abstract Poliomyelitis remains endemic in many developing nations. Patients may develop residual muscle weakness in one or more limbs after an attack of poliomyelitis in childhood. We report an adult patient who presented for right temporal cortical grid placement. He had childhood poliomyelitis and, while showing no evidence of postpolio syndrome, demonstrated excessive sensitivity to nondepolarizing muscle relaxants and developed prolonged muscle weakness during the postoperative period. © 2008 Elsevier Inc. All rights reserved.
1. Introduction Poliomyelitis is still endemic in many developing nations. Many patients may develop residual muscle weakness in one or more limbs after a poliomyelitis attack in childhood. Such polio survivors can develop new onset of progressive muscle weakness and fatigue in skeletal or bulbar muscles more than 15 years later. This situation has been described as the postpolio syndrome [1,2]. Patients having this disorder have excessive susceptibility to neuromuscular blockers [2,3]. We report the case of a patient who had no evidence of postpolio ⁎ Corresponding author. Department of Anesthesiology and Perioperative Medicine, University Hospital, University of Western Ontario, 339 Windermere Road, London, Canada N6A 5A5. E-mail address: [email protected] (P.K. Sinha). 0952-8180/$ – see front matter © 2008 Elsevier Inc. All rights reserved. doi:10.1016/j.jclinane.2007.08.005
syndrome, but nevertheless showed excessive sensitivity to nondepolarizing muscle relaxants, and developed weakness while in the intensive care unit (ICU).
2. Case report A 38-year-old man weighing 65 kg (body mass index = 25), with medically refractory complex partial seizures, presented for right temporal cortical grid placement. The patient had paralytic poliomyelitis at the age of three and had developed weakness of the left upper limb and right lower limb that resolved. At the time of presentation, the patient was receiving carbamazepine, 200 mg, twice daily for seizure control. Serum levels of carbamazepine were not
Anesthesia for craniotomy in post poliomyelitis measured before surgery. The patient had no history of drug allergies. On examination, the affected limbs had grade 4/5 power with minimal muscle wasting (muscle power was graded as per medical research council scale, in which grade 0 = complete paralysis, grade 1 = flicker of contraction, grade 2 = power detectable only when gravity is ruled out, grade 3 = limb can be held against force of gravity but not against examiner's resistance, grade 4 = some degree of weakness, usually described as poor, fair, or moderate strength, and grade 5 = normal power). The patient was premedicated with oral diazepam, 5 mg, and intramuscular (IM) glycopyrrolate, 0.2 mg, one hour before his scheduled surgery. Anesthesia was induced with propofol, 2 mg/kg, and fentanyl, 4 μg/kg, and pancuronium, 6 mg, was used to facilitate tracheal intubation and for muscle relaxation. Apart from routine monitoring, neuromuscular monitoring was also done using a peripheral nerve stimulator (Innervator 272, Fisher and Paykel Healthcare, Auckland, NZ). We chose the left posterior tibial nerve for peripheral nerve stimulation. Intubation was accomplished when there was absence of any response to train-of-four (TOF) stimuli. Anesthesia was maintained with oxygen, nitrous oxide, and isoflurane, along with fentanyl infusion (1 μg/kg per hr). During the maintenance phase, pancuronium was titrated to maintain the presence of at least one twitch on TOF. During the 6-hour procedure, the patient received an additional 2 mg of pancuronium. At the end of surgery, two hours later, the patient had three twitches on a TOF count with fade. Residual muscle relaxation was reversed with intravenous (IV) neostigmine, 3 mg, and glycopyrrolate, 0.6 mg. He was assessed with double-burst stimulation, which showed two twitches of equal strength (no fade). Once the patient was fully awake and moving all four limbs on command with satisfactory respiratory parameters, his trachea was extubated. Postextubation, the patient was capable of sustained head lift for more than 5 seconds, he was able to speak, and he had stable vital function. One hour after he was taken to the ICU, he was given 500 mg of amikacin. Within 15 minutes of the amikacin injection, the patient complained of weakness in all limbs but denied any respiratory difficulty. On examination, the left upper and right lower limb showed grade 1/5 power, whereas the right upper and left lower limbs had 3/5 power. The patient was awake, able to speak, had adequate respiratory movements, and normal arterial blood gases and electrolytes. Measured peripheral temperature at this time was normal. Train-of-four and double-burst stimulation on the right and left posterior tibial nerves showed no fade on visual estimation. In spite of this finding, he was administered neostigmine, 2 mg, and glycopyrrolate, 0.4 mg, IV on the assumption of persistent neuromuscular block. Immediately thereafter, his muscle power improved to grade 3/5 in the left upper and right lower limbs, whereas power of the right upper and left lower limbs improved to 4/5, but still he could not manage a sustained handgrip or head lift. Because the patient did not have any respiratory difficulty, no further neostigmine was adminis-
211 tered. His muscle power continued to improve and attained preoperative levels in all limbs 6 hours after surgery.
3. Discussion Atypical muscle weakness in our patient could have been the result of (a) inadequate reversal of pancuronium, (b) amikacin-induced muscle weakness, (c) postpolio syndrome, or (d) neurologic deficit after intracranial surgery. The dose of neostigmine required to reverse a neuromuscular blocker is 0.05 to 0.07 mg/kg [4]. We used 3 mg of neostigmine in our patient, which is an adequate dose for his ideal body weight. Furthermore, the dose required to reverse the action of the neuromuscular blocker is not only a function of its dose but also the degree of neuromuscular block present at the time of reversal [5]. Our patient had three twitches on a TOF count before the administration of neostigmine, and hence, complete recovery from neuromuscular block was expected after neostigmine. Atypical muscle weakness also could be a result of redistribution of neostigmine, as the duration of action of pancuronium is longer than that of neostigmine [4]. However, we would expect generalized muscle weakness, with possible respiratory compromise, which was not present in our patient. It is known that patients with remote history of poliomyelitis may show excessive susceptibility to neuromuscular blocking agents [6]. Our patient required less neuromuscular blocker during the entire period of surgery in spite of having only mild residual paralysis from a poliomyelitis attack in childhood. One hour after reversal of muscle relaxation, the patient developed new muscle weakness in his limbs but no weakness of the respiratory muscles. However, his neuromuscular response to TOF and double-burst stimulation (ie, absence of fade) did not correlate with his clinical state. This muscle weakness might have been aggravated by amikacin, which is an aminoglycoside antibiotic [7,8]. Aminoglycoside antibiotics can cause weakness, even in the absence of neuromuscular blocking agents [4]. The mechanism of action of aminoglycoside-induced block has been studied in detail. Neomycin, another aminoglycoside antibiotic, reduces the amount of transmitter released from the presynaptic membrane in response to an action potential. Neomycin also alters the calcium influx into the presynaptic nerve terminal, thereby reducing the amount of acetylcholine release [9,10]. The potentiation of neuromuscular block produced by an aminoglycoside antibiotic is known to be resistant to the effects of neostigmine [10]. Calcium is more reliable and predictable than neostigmine for the reversal of neuromuscular block produced by neomycin [10,11]. Calcium interacts with, or competes with, neomycin during some part of the prejunctional process before the release of acetylcholine. However, calcium should not be used for two reasons: first, the antagonism is not sustained, and second, it
212 may prevent the antibacterial action of the antibiotic [4]. In our patient, administration of neostigmine partially reversed the neuromuscular block. This fact suggests that the muscle weakness in our patient may not have been entirely attributable to amikacin and that the exaggerated response might have been because of the presence of residual postpolio muscle weakness. Lambert et al [2] recently reviewed the anesthetic implications in patients having postpolio syndrome. Postpolio syndrome refers to a constellation of signs and symptoms; the chief symptom is new onset muscle weakness, which develops after 15 years or more after recovery from the initial attack of poliomyelitis [1]. The etiology of this weakness is probably because of time-related loss of enlarged motor units after paralytic poliomyelitis [2]. However, our patient did not have postpolio syndrome; he only had remote history of poliomyelitis. To our knowledge, there is only one study in the literature that suggests that patients with a remote history of polio have increased sensitivity to neuromuscular blocking agents [6]. Our case is unique in that our patient had prolonged muscle weakness after aminoglycoside administration, after apparently recovering complete muscle power after reversal of the neuromuscular blocker. Our patient's neuromuscular response to TOF and doubleburst stimulation (ie, absence of fade) did not correlate with his clinical state. From earlier reports it can be expected that a paretic limb will be more resistant to the effects of neuromuscular blocking agents [12,13]. During recovery, the paretic limbs show adequate recovery of TOF whereas the patient may still have TOF fade on the nonparetic limbs and may well be susceptible to respiratory depression. After denervation, there may be an increase of cholinergic receptors. These extrajunctional areas may be more chemosensitive, resulting in a decreased threshold to acetylcholineinduced muscular response [12,13]. In the presence of neomycin, the characteristic TOF suppression may be present after administration of a neuromuscular blocking agent, but a tetanic stimulus does not result in fade. Neomycin also produces posttetanic exhaustion [14]. Because of these phenomena, the monitoring of the TOF and tetanic response may be inadequate to monitor the degree of neuromuscular block in the presence of aminoglycosides. The effect of double-burst stimulation in this scenario has not been described. It is likely that our patient suffered more on account of his postpolio state rather than the amikacin administration. However, because of the temporal sequence observed in our patient, it is possible that amikacin may have aggravated the recurarizing effect of the residual muscle relaxant. As we have mentioned, our patient showed no signs of respiratory muscle weakness despite developing postoperative muscle weakness most likely because there was no effect on the respiratory muscles during his acute poliomyelitis. Hypothermia prolongs the duration of action of neuromuscular blocking agents [15]; however, the efficacy
P.R. Suneel et al. of neostigmine is not altered by mild hypothermia [16]. Because the patient's measured peripheral temperature was normal, his muscle weakness could not have been because of hypothermia. Patients receiving chronic anticonvulsant therapy show resistance to neuromuscular blockers except for mivacurium [17]. Furthermore, patients receiving chronic carbamazepine therapy have increased clearance of neuromuscular blocking agents [18]. Because our patient was receiving carbamazepine therapy, it was expected that he would require more neuromuscular blockers and to reverse quickly. Therefore, carbamazepine administration cannot be the reason for the prolonged postoperative muscle weakness. Occurrence of muscle weakness in postpolio patients after neurosurgery or spine surgery easily can be confused with postoperative neurologic deficits, though this was ruled out in our patient from the atypical limb weakness and clear sensorium. Repeating the dose of neostigmine not only helped in differentiating this condition from other neurosurgical causes but also averted the need for further investigation. Postpolio patients have a low threshold for neuromuscular blocking agents and are prone to redevelop muscle weakness when exposed to drugs such as aminoglycosides. Thus, not only postpolio syndrome, but also a history of poliomyelitis itself, can be considered a risk factor for increased muscle weakness in the postoperative period.
References [1] Gawne AC, Halstead LS. Post-polio syndrome: pathophysiology and clinical management. Crit Rev Phys Rehabil Med 1995;7:147-88. [2] Lambert DA, Giannouli E, Schmidt BJ. Postpolio syndrome and anesthesia. Anesthesiology 2005;103:638-44. [3] Liu S, Modell JH. Anesthetic management for patients with postpolio syndrome receiving electroconvulsive therapy. Anesthesiology 2001; 95:799-801. [4] Naguib M, Lien CA. Pharmacology of muscle relaxants and their antagonists. In: Miller RD, editor. Miller's anesthesia. 6th ed. New York: Elsevier Churchill Livingstone; 2005. p. 481-572. [5] Dorsch JA, Dorsch SE. Understanding anesthesia equipment. 4th ed. Philadelphia: Lippincott Williams and Wilkins; 1996. p. 849-77. [6] Gyermek L. Increased potency of nondepolarizing relaxants after poliomyelitis. J Clin Pharmacol 1990;30:170-3. [7] Jedeikin R, Dolgunski E, Kaplan R, Hoffman S. Prolongation of neuromuscular blocking effect of vecuronium by antibiotics. Anaesthesia 1987;42:858-60. [8] Gilliard V, Delvaux B, Russell K, Dubois PE. Long-lasting potentiation of a single-dose of rocuronium by amikacin: case report. Acta Anaesthesiol Belg 2006;57:157-9. [9] Elmqvist D, Josefsson JO. The nature of neuromuscular block produced by neomycine. Acta Physiol Scand 1962;54:105-10. [10] Hasfurther DL, Bailey PL. Failure of neuromuscular blockade reversal after rocuronium in a patient who received oral neomycin. Can J Anaesth 1996;43:617-20. [11] Singh YN, Harvey AL, Marshall IG. Antibiotic-induced paralysis of mouse phrenic nerve-hemi diaphragm preparation, and reversibility by calcium and neostigmine. Anesthesiology 1978;48:418-24. [12] Graham DH. Monitoring neuromuscular block may be unreliable in patients with upper-motor-neuron lesions. Anesthesiology 1980;52: 74-5.
Anesthesia for craniotomy in post poliomyelitis [13] Moorthy SS, Hilgenberg JC. Resistance to non-depolarizing muscle relaxants in paretic upper extremities of patients with residual hemiplegia. Anesth Analg 1980;59:624-7. [14] Lee C, Chen D, Barnes A, Katz RL. Neuromuscular block by neomycin in the cat. Can Anaesth Soc J 1973;23:527-33. [15] Caldwell JE, Heier T, Wright PM, et al. Temperature-dependent pharmacokinetics and pharmacodynamics of vecuronium. Anesthesiology 2000;92:84-93.
213 [16] Miller RD, Roderick LL. Pancuronium-induced neuromuscular blockade, and its antagonism by neostigmine at 29, 37, and 41 c. Anesthesiology 1977;46:333-5. [17] Spacek A, Neiger FX, Spiss CK, Kress HG. Chronic carbamazepine therapy does not influence mivacurium-induced neuromuscular block. Br J Anaesth 1996;77:500-2. [18] Roth S, Ebrahim ZY. Resistance to pancuronium in patients receiving carbamazepine. Anesthesiology 1987;66:691-3.
Case report
Anesthesia for craniotomy in a patient with previous paralytic polio Puthuvassery Raman Suneel MD (Associate Professor)a , Prabhat Kumar Sinha MD (Associate Professor)a,⁎, Koniparambil Pappu Unnikrishnan MD (Assistant Professor)a , Mathew Abraham MS, MCh (Assistant Professor)b a
Department of Anesthesiology, Sree Chitra Tirunal Institute of Medical Sciences and Technology, Thiruvananthapuram, Kerala, India PIN 695011 b Department of Neurosurgery, Sree Chitra Tirunal Institute of Medical Sciences and Technology, Thiruvananthapuram, Kerala, India PIN 695011 Received 18 September 2006; revised 22 July 2007; accepted 10 August 2007
Keywords: Anesthesia, nondepolarizing neuromuscular relaxants; Poliomyelitis
Abstract Poliomyelitis remains endemic in many developing nations. Patients may develop residual muscle weakness in one or more limbs after an attack of poliomyelitis in childhood. We report an adult patient who presented for right temporal cortical grid placement. He had childhood poliomyelitis and, while showing no evidence of postpolio syndrome, demonstrated excessive sensitivity to nondepolarizing muscle relaxants and developed prolonged muscle weakness during the postoperative period. © 2008 Elsevier Inc. All rights reserved.
1. Introduction Poliomyelitis is still endemic in many developing nations. Many patients may develop residual muscle weakness in one or more limbs after a poliomyelitis attack in childhood. Such polio survivors can develop new onset of progressive muscle weakness and fatigue in skeletal or bulbar muscles more than 15 years later. This situation has been described as the postpolio syndrome [1,2]. Patients having this disorder have excessive susceptibility to neuromuscular blockers [2,3]. We report the case of a patient who had no evidence of postpolio ⁎ Corresponding author. Department of Anesthesiology and Perioperative Medicine, University Hospital, University of Western Ontario, 339 Windermere Road, London, Canada N6A 5A5. E-mail address: [email protected] (P.K. Sinha). 0952-8180/$ – see front matter © 2008 Elsevier Inc. All rights reserved. doi:10.1016/j.jclinane.2007.08.005
syndrome, but nevertheless showed excessive sensitivity to nondepolarizing muscle relaxants, and developed weakness while in the intensive care unit (ICU).
2. Case report A 38-year-old man weighing 65 kg (body mass index = 25), with medically refractory complex partial seizures, presented for right temporal cortical grid placement. The patient had paralytic poliomyelitis at the age of three and had developed weakness of the left upper limb and right lower limb that resolved. At the time of presentation, the patient was receiving carbamazepine, 200 mg, twice daily for seizure control. Serum levels of carbamazepine were not
Anesthesia for craniotomy in post poliomyelitis measured before surgery. The patient had no history of drug allergies. On examination, the affected limbs had grade 4/5 power with minimal muscle wasting (muscle power was graded as per medical research council scale, in which grade 0 = complete paralysis, grade 1 = flicker of contraction, grade 2 = power detectable only when gravity is ruled out, grade 3 = limb can be held against force of gravity but not against examiner's resistance, grade 4 = some degree of weakness, usually described as poor, fair, or moderate strength, and grade 5 = normal power). The patient was premedicated with oral diazepam, 5 mg, and intramuscular (IM) glycopyrrolate, 0.2 mg, one hour before his scheduled surgery. Anesthesia was induced with propofol, 2 mg/kg, and fentanyl, 4 μg/kg, and pancuronium, 6 mg, was used to facilitate tracheal intubation and for muscle relaxation. Apart from routine monitoring, neuromuscular monitoring was also done using a peripheral nerve stimulator (Innervator 272, Fisher and Paykel Healthcare, Auckland, NZ). We chose the left posterior tibial nerve for peripheral nerve stimulation. Intubation was accomplished when there was absence of any response to train-of-four (TOF) stimuli. Anesthesia was maintained with oxygen, nitrous oxide, and isoflurane, along with fentanyl infusion (1 μg/kg per hr). During the maintenance phase, pancuronium was titrated to maintain the presence of at least one twitch on TOF. During the 6-hour procedure, the patient received an additional 2 mg of pancuronium. At the end of surgery, two hours later, the patient had three twitches on a TOF count with fade. Residual muscle relaxation was reversed with intravenous (IV) neostigmine, 3 mg, and glycopyrrolate, 0.6 mg. He was assessed with double-burst stimulation, which showed two twitches of equal strength (no fade). Once the patient was fully awake and moving all four limbs on command with satisfactory respiratory parameters, his trachea was extubated. Postextubation, the patient was capable of sustained head lift for more than 5 seconds, he was able to speak, and he had stable vital function. One hour after he was taken to the ICU, he was given 500 mg of amikacin. Within 15 minutes of the amikacin injection, the patient complained of weakness in all limbs but denied any respiratory difficulty. On examination, the left upper and right lower limb showed grade 1/5 power, whereas the right upper and left lower limbs had 3/5 power. The patient was awake, able to speak, had adequate respiratory movements, and normal arterial blood gases and electrolytes. Measured peripheral temperature at this time was normal. Train-of-four and double-burst stimulation on the right and left posterior tibial nerves showed no fade on visual estimation. In spite of this finding, he was administered neostigmine, 2 mg, and glycopyrrolate, 0.4 mg, IV on the assumption of persistent neuromuscular block. Immediately thereafter, his muscle power improved to grade 3/5 in the left upper and right lower limbs, whereas power of the right upper and left lower limbs improved to 4/5, but still he could not manage a sustained handgrip or head lift. Because the patient did not have any respiratory difficulty, no further neostigmine was adminis-
211 tered. His muscle power continued to improve and attained preoperative levels in all limbs 6 hours after surgery.
3. Discussion Atypical muscle weakness in our patient could have been the result of (a) inadequate reversal of pancuronium, (b) amikacin-induced muscle weakness, (c) postpolio syndrome, or (d) neurologic deficit after intracranial surgery. The dose of neostigmine required to reverse a neuromuscular blocker is 0.05 to 0.07 mg/kg [4]. We used 3 mg of neostigmine in our patient, which is an adequate dose for his ideal body weight. Furthermore, the dose required to reverse the action of the neuromuscular blocker is not only a function of its dose but also the degree of neuromuscular block present at the time of reversal [5]. Our patient had three twitches on a TOF count before the administration of neostigmine, and hence, complete recovery from neuromuscular block was expected after neostigmine. Atypical muscle weakness also could be a result of redistribution of neostigmine, as the duration of action of pancuronium is longer than that of neostigmine [4]. However, we would expect generalized muscle weakness, with possible respiratory compromise, which was not present in our patient. It is known that patients with remote history of poliomyelitis may show excessive susceptibility to neuromuscular blocking agents [6]. Our patient required less neuromuscular blocker during the entire period of surgery in spite of having only mild residual paralysis from a poliomyelitis attack in childhood. One hour after reversal of muscle relaxation, the patient developed new muscle weakness in his limbs but no weakness of the respiratory muscles. However, his neuromuscular response to TOF and double-burst stimulation (ie, absence of fade) did not correlate with his clinical state. This muscle weakness might have been aggravated by amikacin, which is an aminoglycoside antibiotic [7,8]. Aminoglycoside antibiotics can cause weakness, even in the absence of neuromuscular blocking agents [4]. The mechanism of action of aminoglycoside-induced block has been studied in detail. Neomycin, another aminoglycoside antibiotic, reduces the amount of transmitter released from the presynaptic membrane in response to an action potential. Neomycin also alters the calcium influx into the presynaptic nerve terminal, thereby reducing the amount of acetylcholine release [9,10]. The potentiation of neuromuscular block produced by an aminoglycoside antibiotic is known to be resistant to the effects of neostigmine [10]. Calcium is more reliable and predictable than neostigmine for the reversal of neuromuscular block produced by neomycin [10,11]. Calcium interacts with, or competes with, neomycin during some part of the prejunctional process before the release of acetylcholine. However, calcium should not be used for two reasons: first, the antagonism is not sustained, and second, it
212 may prevent the antibacterial action of the antibiotic [4]. In our patient, administration of neostigmine partially reversed the neuromuscular block. This fact suggests that the muscle weakness in our patient may not have been entirely attributable to amikacin and that the exaggerated response might have been because of the presence of residual postpolio muscle weakness. Lambert et al [2] recently reviewed the anesthetic implications in patients having postpolio syndrome. Postpolio syndrome refers to a constellation of signs and symptoms; the chief symptom is new onset muscle weakness, which develops after 15 years or more after recovery from the initial attack of poliomyelitis [1]. The etiology of this weakness is probably because of time-related loss of enlarged motor units after paralytic poliomyelitis [2]. However, our patient did not have postpolio syndrome; he only had remote history of poliomyelitis. To our knowledge, there is only one study in the literature that suggests that patients with a remote history of polio have increased sensitivity to neuromuscular blocking agents [6]. Our case is unique in that our patient had prolonged muscle weakness after aminoglycoside administration, after apparently recovering complete muscle power after reversal of the neuromuscular blocker. Our patient's neuromuscular response to TOF and doubleburst stimulation (ie, absence of fade) did not correlate with his clinical state. From earlier reports it can be expected that a paretic limb will be more resistant to the effects of neuromuscular blocking agents [12,13]. During recovery, the paretic limbs show adequate recovery of TOF whereas the patient may still have TOF fade on the nonparetic limbs and may well be susceptible to respiratory depression. After denervation, there may be an increase of cholinergic receptors. These extrajunctional areas may be more chemosensitive, resulting in a decreased threshold to acetylcholineinduced muscular response [12,13]. In the presence of neomycin, the characteristic TOF suppression may be present after administration of a neuromuscular blocking agent, but a tetanic stimulus does not result in fade. Neomycin also produces posttetanic exhaustion [14]. Because of these phenomena, the monitoring of the TOF and tetanic response may be inadequate to monitor the degree of neuromuscular block in the presence of aminoglycosides. The effect of double-burst stimulation in this scenario has not been described. It is likely that our patient suffered more on account of his postpolio state rather than the amikacin administration. However, because of the temporal sequence observed in our patient, it is possible that amikacin may have aggravated the recurarizing effect of the residual muscle relaxant. As we have mentioned, our patient showed no signs of respiratory muscle weakness despite developing postoperative muscle weakness most likely because there was no effect on the respiratory muscles during his acute poliomyelitis. Hypothermia prolongs the duration of action of neuromuscular blocking agents [15]; however, the efficacy
P.R. Suneel et al. of neostigmine is not altered by mild hypothermia [16]. Because the patient's measured peripheral temperature was normal, his muscle weakness could not have been because of hypothermia. Patients receiving chronic anticonvulsant therapy show resistance to neuromuscular blockers except for mivacurium [17]. Furthermore, patients receiving chronic carbamazepine therapy have increased clearance of neuromuscular blocking agents [18]. Because our patient was receiving carbamazepine therapy, it was expected that he would require more neuromuscular blockers and to reverse quickly. Therefore, carbamazepine administration cannot be the reason for the prolonged postoperative muscle weakness. Occurrence of muscle weakness in postpolio patients after neurosurgery or spine surgery easily can be confused with postoperative neurologic deficits, though this was ruled out in our patient from the atypical limb weakness and clear sensorium. Repeating the dose of neostigmine not only helped in differentiating this condition from other neurosurgical causes but also averted the need for further investigation. Postpolio patients have a low threshold for neuromuscular blocking agents and are prone to redevelop muscle weakness when exposed to drugs such as aminoglycosides. Thus, not only postpolio syndrome, but also a history of poliomyelitis itself, can be considered a risk factor for increased muscle weakness in the postoperative period.
References [1] Gawne AC, Halstead LS. Post-polio syndrome: pathophysiology and clinical management. Crit Rev Phys Rehabil Med 1995;7:147-88. [2] Lambert DA, Giannouli E, Schmidt BJ. Postpolio syndrome and anesthesia. Anesthesiology 2005;103:638-44. [3] Liu S, Modell JH. Anesthetic management for patients with postpolio syndrome receiving electroconvulsive therapy. Anesthesiology 2001; 95:799-801. [4] Naguib M, Lien CA. Pharmacology of muscle relaxants and their antagonists. In: Miller RD, editor. Miller's anesthesia. 6th ed. New York: Elsevier Churchill Livingstone; 2005. p. 481-572. [5] Dorsch JA, Dorsch SE. Understanding anesthesia equipment. 4th ed. Philadelphia: Lippincott Williams and Wilkins; 1996. p. 849-77. [6] Gyermek L. Increased potency of nondepolarizing relaxants after poliomyelitis. J Clin Pharmacol 1990;30:170-3. [7] Jedeikin R, Dolgunski E, Kaplan R, Hoffman S. Prolongation of neuromuscular blocking effect of vecuronium by antibiotics. Anaesthesia 1987;42:858-60. [8] Gilliard V, Delvaux B, Russell K, Dubois PE. Long-lasting potentiation of a single-dose of rocuronium by amikacin: case report. Acta Anaesthesiol Belg 2006;57:157-9. [9] Elmqvist D, Josefsson JO. The nature of neuromuscular block produced by neomycine. Acta Physiol Scand 1962;54:105-10. [10] Hasfurther DL, Bailey PL. Failure of neuromuscular blockade reversal after rocuronium in a patient who received oral neomycin. Can J Anaesth 1996;43:617-20. [11] Singh YN, Harvey AL, Marshall IG. Antibiotic-induced paralysis of mouse phrenic nerve-hemi diaphragm preparation, and reversibility by calcium and neostigmine. Anesthesiology 1978;48:418-24. [12] Graham DH. Monitoring neuromuscular block may be unreliable in patients with upper-motor-neuron lesions. Anesthesiology 1980;52: 74-5.
Anesthesia for craniotomy in post poliomyelitis [13] Moorthy SS, Hilgenberg JC. Resistance to non-depolarizing muscle relaxants in paretic upper extremities of patients with residual hemiplegia. Anesth Analg 1980;59:624-7. [14] Lee C, Chen D, Barnes A, Katz RL. Neuromuscular block by neomycin in the cat. Can Anaesth Soc J 1973;23:527-33. [15] Caldwell JE, Heier T, Wright PM, et al. Temperature-dependent pharmacokinetics and pharmacodynamics of vecuronium. Anesthesiology 2000;92:84-93.
213 [16] Miller RD, Roderick LL. Pancuronium-induced neuromuscular blockade, and its antagonism by neostigmine at 29, 37, and 41 c. Anesthesiology 1977;46:333-5. [17] Spacek A, Neiger FX, Spiss CK, Kress HG. Chronic carbamazepine therapy does not influence mivacurium-induced neuromuscular block. Br J Anaesth 1996;77:500-2. [18] Roth S, Ebrahim ZY. Resistance to pancuronium in patients receiving carbamazepine. Anesthesiology 1987;66:691-3.