Br. J. Anaesth. (1975), 47, 523
ANAPHYLAXIS TO SUXAMETHONIUM Two Case Reports J. M. MANDAPPA, P. M. CHANDRASEKHARA AND R. G. NELVIGI SUMMARY
Several drugs used in anaesthesia, including tubocurarine, have been shown to liberate histamine leading to major reactions (Paton, 1959). The first case of hypersensitivity to suxamethonium was reported by Smith (1957) and this was followed by other reports (Kepes and Haimovici, 1959; Fellini, Bernstein and Zaunder, 1963; Jerums, Whittingham and Wilson, 1967; Eustace, 1967; Bele-Binda and Valeri, 1971; Katz and Mulligan, 1972). We wish to report two further cases of anaphylactic reaction to suxamethonium. CASE REPORTS
Case No. 1. A male patient aged 35 years was anaesthetized for excision of the head of radius on May 8, 1969. He had been a healthy man and had no history of previous anaesthesia. Routine laboratory investigations and clinical examination revealed no abnormality. The patient denied any history of asthma or allergic reactions to drugs. Premedication was with pethidine 50 mg and atropine 0.5 mg i.m. 45 min before anaesthesia. Thiopentone 200 mg followed by suxamethonium (Midarine) 75 mg were administered i.v. After inflation of the lungs with 100% oxygen, the trachea was intubated with a 10-mm cuffed Magill tube. Within 1 min there was marked tachycardia and in the next minute the radial pulse became impalpable, and only the carotid pulse remained palpable. An erythematous rash of the face, chest, abdomen and forearms appeared. There was mild bronchospasm with copious secretions in the pharynx. The patient was ventilated with pure J.
M.
MANDAPPA;
P.
M.
CHANDRASEKHARA;
NELVIGI; Department of Anaesthesiology, Medical College, Hubli, Karnataka, India.
R.
G.
Karnatak
oxygen and methoxamine was administered i.v. Promethazine 10 mg was given as an nntihistaminic. The arterial pressure was found to be 50/70 mm Hg systolic. The patient regained consciousness and normal respiration. The endotracheal tube was removed and oxygen therapy continued from a face mask. Since the arterial pressure remained low and unstable, dexamethasone 8 mg was given i.v. This was ineffective and another 8 mg was given. The arterial pressure increased to 115/72 tnm Hg and remained steady. The operation was postponed and the patient was treated with a steroid regimen. The bacteriological reports on the infusion fluid and the administration set were negative. Sensitivity tests for pethidine, atropine and thiopentone were negative. A skin test for suxamethonium on the 4th day after the episode while the patient was still receiving steroids, showed a circular weal formation of 1 inch in diameter. This persisted for nearly 2 hr, whereas no reaction was observed with saline on the other forearm. The operation was planned for May 17, 1969, and the patient was given twice the maintenance dose of steroid from 2 days before anaesthesia and on the day of operation. Premedication was with atropine 0.5 mg, given i.m. 45 min before anaesthesia. Anaesthesia was induced with thiopentone 8 ml (2.5%) i.v., and, after 2 min during which there was no untoward response, a further 3 ml was given. After making sure that there was no reaction to thiopentone, diluted suxamethonium in incremental doses of 25 mg was given slowly into the drip. The total dose required to produce ideal conditions for endotracheal intubation with this method of administration was 75 mg. Within 2 min signs of anaphylaxis were evident. In view of our experience with the previous reaction and the treatment neces-
Downloaded from http://bja.oxfordjournals.org/ at University of California, Davis on January 28, 2015
Anaphylaxis to suxamethonium in patients who gave no history of allergy is presented in this report. The diagnosis of anaphylaxis was based on a rapid onset of tachycardia, arterial hypotension, erythematous patches and oedema, and a positive reaction to a sensitivity test.
524 sary for it, a total dose of 24 mg of dexamethasone was administered through the drip intermittently together with an appropriate dose of promethazine and methoxamine. Arterial pressure and pulse rate were unstable for 2 hr. The operation was postponed again. For personal reasons the patient had to leave the hospital without operation. A subsequent sensitivity test for suxamethonium showed a marked weal and flare response that persisted for more than 2 hr.
Skin sensitivity tests on the forearm with saline as control, were negative for atropine, but for suxamethonium there was an indication of a weak positive response: only a weal appeared without a flare. This test was repeated 12 days after stopping of the steroids. Then there was a marked weal and flare response with serous oozing from the test site without any systemic effects. This positive response lasted for more than 2 hr. The second test was also
read against saline as control on the opposite forearm. DISCUSSION
The clinical features of a rapid onset of tachycardia, arterial hypotension, flushing and oedema after suxamedionium in both patients is suggestive of anaphylaxis. This view is supported by the absence of a history of allergic manifestations or drug sensitivity, and a positive intradermal test to suxamethonium after stopping the administration of steroids in both patients. A doubtful positive skin test with only a weal response in the first instance in both patients could be attributed to the continued treatment with steroids. In the first patient, in whom suxamethonium was used for the second time, steroid therapy could not prevent the adverse reaction. On this occasion the reaction may have been the result of drug idiosyncrasy or sensitivity reaction in addition to anaphylaxis (Jerums, Whittingham and Wilson, 1967). REFERENCES
Bele-Binda, N., and Valeri, F. (1971). A case of bronchospasm induced by succinylcholine. Can. Anaesth. Soc J., 18, 116. Bourns, J. G., Collier, H. O. J., and Somers, G. F. (1952). Succinylcholine muscle relaxant of short duration. Lancet, 1, 1225. Eustace, B. R. (1967). Case report: suxamethonium induced bronchospasm. Anaesthesia, 22, 638. Fellini, A. A., Bernstein, R. L., and Zaunder, H. L. (1963). Bronchospasm due to suxamethonium: report of a case. Br. J. Anaesth., 35, 657. Jerums, G., Whittingham, S., and Wilson, P. (1967). Anaphylaxis to suxamethonium: a case report. Br. J. Anaesth., 39, 73. Katz, A. M., and Mulligan, P. G. (1972). Case report: Bronchospasm induced by suxamethonium. Br. J. Anaesth., 44, 1097. Kepes, E. R., and Haimovici, H. (1959). Allergic reaction to succinylcholine. J^AM.A., 171, 548. Lehmann, H., and liddel, J. (1964). Suxamethonium sensitivity. Br. Med. J., 1, 501. Paton, W. D. M. (1959). The effects of muscle relaxants other than muscular relaxation. Anesthesiology, 20, 453. Smith, N. L. (1957). Histamine release by suxamethonium. Anaesthesia, 12, 293. L'ANAPHYLAXIE AU SUXAMETHONIUM RESUME
Ce rapport prfeente l'anaphylaxie au suxamethonium chez les patients qui n'ont pas indiqui d'antcoidents en matiere a'allergie. Le diagnostic d'anaphylazie etait bas£ sur un declenchement rapide de la tachycardie, de rhypotension arterielle, de plaques erythemateuses et de l'oedeme et sur une reaction positive a un test de sensibility.
Downloaded from http://bja.oxfordjournals.org/ at University of California, Davis on January 28, 2015
Case No. 2. A healthy female patient aged 16 years with no history of asthma or allergy was scheduled for tonsillectomy on March 6, 1974. Findings on clinical and laboratory examinations were normal. Premedication was with atropine 0.5 mg injected i.m. 45 min before anaesthesia. Anaesthesia was induced with nitrous oxide, oxygen, trichloroethylene and ether. A nasotracheal tube was passed with the aid of 50 mg of suxamethonium (Scoline). Within 5 min there was tachycardia (140 beats/min) and arterial hypotension (80/40 mm Hg). The anaesthetic administration was stopped and the patient was ventilated with pure oxygen. There were manifestations of skin reaction with flushing and erythematous patches over the chest and upper limbs, with marked oedema of the face and eyelids. Immediately, dexamethasone 8 mg was given i.v. The arterial pressure increased to 100/60 mm Hg and the pulse rate was 90 beats/min. Return of spontaneous ventilation and consciousness were observed at this time. Meanwhile, chlorpheniratnine maleate 10 mg and calcium gluconate 10 ml (10%) were given through the intravenous infusion. When all was well, the patient was again anaesthetized with nitrous oxide, oxygen and trichloroethylene and the operation was completed. A steroid regimen was continued for 5 days after the operation.
BRITISH JOURNAL OF ANAESTHESIA
ANAPHYLAXIS TO SUXAMETHONIUM ANAPHYLAXIE AUF SUXAMETHONIUM
525 ANAFILAXIS PARA SUXAMETONIUM
ZUSAMMENFASSUNG
SUMARIO
Anaphylaxie auf Suxamethonium bei Patienten, die keine frflhere Allergieanfalligkeit gezeigt haben, wird in diesem Bericht vorgelegt. Die Anaphylaxie-Diagnose beruhte auf einem rapiden Eintreten von Tachykardie, arterielkr Hypotension, erythemat6sen Flecken und Odem, sowie einer positiven Reaktion auf einen Sensitivita'Otest.
Se presenta en este infonne la anafilaxis para suxanaetonium en pacientes que no presentaron historial de alergia. El diagnostico de anafilaxis se baso en una rapida inidaci6n de taquicardia, hipotension arterial, mancbas eritematosas y edema, y una reacckSn positiva a una prueba de sensibilidad.
Downloaded from http://bja.oxfordjournals.org/ at University of California, Davis on January 28, 2015
ANAPHYLAXIS TO SUXAMETHONIUM Two Case Reports J. M. MANDAPPA, P. M. CHANDRASEKHARA AND R. G. NELVIGI SUMMARY
Several drugs used in anaesthesia, including tubocurarine, have been shown to liberate histamine leading to major reactions (Paton, 1959). The first case of hypersensitivity to suxamethonium was reported by Smith (1957) and this was followed by other reports (Kepes and Haimovici, 1959; Fellini, Bernstein and Zaunder, 1963; Jerums, Whittingham and Wilson, 1967; Eustace, 1967; Bele-Binda and Valeri, 1971; Katz and Mulligan, 1972). We wish to report two further cases of anaphylactic reaction to suxamethonium. CASE REPORTS
Case No. 1. A male patient aged 35 years was anaesthetized for excision of the head of radius on May 8, 1969. He had been a healthy man and had no history of previous anaesthesia. Routine laboratory investigations and clinical examination revealed no abnormality. The patient denied any history of asthma or allergic reactions to drugs. Premedication was with pethidine 50 mg and atropine 0.5 mg i.m. 45 min before anaesthesia. Thiopentone 200 mg followed by suxamethonium (Midarine) 75 mg were administered i.v. After inflation of the lungs with 100% oxygen, the trachea was intubated with a 10-mm cuffed Magill tube. Within 1 min there was marked tachycardia and in the next minute the radial pulse became impalpable, and only the carotid pulse remained palpable. An erythematous rash of the face, chest, abdomen and forearms appeared. There was mild bronchospasm with copious secretions in the pharynx. The patient was ventilated with pure J.
M.
MANDAPPA;
P.
M.
CHANDRASEKHARA;
NELVIGI; Department of Anaesthesiology, Medical College, Hubli, Karnataka, India.
R.
G.
Karnatak
oxygen and methoxamine was administered i.v. Promethazine 10 mg was given as an nntihistaminic. The arterial pressure was found to be 50/70 mm Hg systolic. The patient regained consciousness and normal respiration. The endotracheal tube was removed and oxygen therapy continued from a face mask. Since the arterial pressure remained low and unstable, dexamethasone 8 mg was given i.v. This was ineffective and another 8 mg was given. The arterial pressure increased to 115/72 tnm Hg and remained steady. The operation was postponed and the patient was treated with a steroid regimen. The bacteriological reports on the infusion fluid and the administration set were negative. Sensitivity tests for pethidine, atropine and thiopentone were negative. A skin test for suxamethonium on the 4th day after the episode while the patient was still receiving steroids, showed a circular weal formation of 1 inch in diameter. This persisted for nearly 2 hr, whereas no reaction was observed with saline on the other forearm. The operation was planned for May 17, 1969, and the patient was given twice the maintenance dose of steroid from 2 days before anaesthesia and on the day of operation. Premedication was with atropine 0.5 mg, given i.m. 45 min before anaesthesia. Anaesthesia was induced with thiopentone 8 ml (2.5%) i.v., and, after 2 min during which there was no untoward response, a further 3 ml was given. After making sure that there was no reaction to thiopentone, diluted suxamethonium in incremental doses of 25 mg was given slowly into the drip. The total dose required to produce ideal conditions for endotracheal intubation with this method of administration was 75 mg. Within 2 min signs of anaphylaxis were evident. In view of our experience with the previous reaction and the treatment neces-
Downloaded from http://bja.oxfordjournals.org/ at University of California, Davis on January 28, 2015
Anaphylaxis to suxamethonium in patients who gave no history of allergy is presented in this report. The diagnosis of anaphylaxis was based on a rapid onset of tachycardia, arterial hypotension, erythematous patches and oedema, and a positive reaction to a sensitivity test.
524 sary for it, a total dose of 24 mg of dexamethasone was administered through the drip intermittently together with an appropriate dose of promethazine and methoxamine. Arterial pressure and pulse rate were unstable for 2 hr. The operation was postponed again. For personal reasons the patient had to leave the hospital without operation. A subsequent sensitivity test for suxamethonium showed a marked weal and flare response that persisted for more than 2 hr.
Skin sensitivity tests on the forearm with saline as control, were negative for atropine, but for suxamethonium there was an indication of a weak positive response: only a weal appeared without a flare. This test was repeated 12 days after stopping of the steroids. Then there was a marked weal and flare response with serous oozing from the test site without any systemic effects. This positive response lasted for more than 2 hr. The second test was also
read against saline as control on the opposite forearm. DISCUSSION
The clinical features of a rapid onset of tachycardia, arterial hypotension, flushing and oedema after suxamedionium in both patients is suggestive of anaphylaxis. This view is supported by the absence of a history of allergic manifestations or drug sensitivity, and a positive intradermal test to suxamethonium after stopping the administration of steroids in both patients. A doubtful positive skin test with only a weal response in the first instance in both patients could be attributed to the continued treatment with steroids. In the first patient, in whom suxamethonium was used for the second time, steroid therapy could not prevent the adverse reaction. On this occasion the reaction may have been the result of drug idiosyncrasy or sensitivity reaction in addition to anaphylaxis (Jerums, Whittingham and Wilson, 1967). REFERENCES
Bele-Binda, N., and Valeri, F. (1971). A case of bronchospasm induced by succinylcholine. Can. Anaesth. Soc J., 18, 116. Bourns, J. G., Collier, H. O. J., and Somers, G. F. (1952). Succinylcholine muscle relaxant of short duration. Lancet, 1, 1225. Eustace, B. R. (1967). Case report: suxamethonium induced bronchospasm. Anaesthesia, 22, 638. Fellini, A. A., Bernstein, R. L., and Zaunder, H. L. (1963). Bronchospasm due to suxamethonium: report of a case. Br. J. Anaesth., 35, 657. Jerums, G., Whittingham, S., and Wilson, P. (1967). Anaphylaxis to suxamethonium: a case report. Br. J. Anaesth., 39, 73. Katz, A. M., and Mulligan, P. G. (1972). Case report: Bronchospasm induced by suxamethonium. Br. J. Anaesth., 44, 1097. Kepes, E. R., and Haimovici, H. (1959). Allergic reaction to succinylcholine. J^AM.A., 171, 548. Lehmann, H., and liddel, J. (1964). Suxamethonium sensitivity. Br. Med. J., 1, 501. Paton, W. D. M. (1959). The effects of muscle relaxants other than muscular relaxation. Anesthesiology, 20, 453. Smith, N. L. (1957). Histamine release by suxamethonium. Anaesthesia, 12, 293. L'ANAPHYLAXIE AU SUXAMETHONIUM RESUME
Ce rapport prfeente l'anaphylaxie au suxamethonium chez les patients qui n'ont pas indiqui d'antcoidents en matiere a'allergie. Le diagnostic d'anaphylazie etait bas£ sur un declenchement rapide de la tachycardie, de rhypotension arterielle, de plaques erythemateuses et de l'oedeme et sur une reaction positive a un test de sensibility.
Downloaded from http://bja.oxfordjournals.org/ at University of California, Davis on January 28, 2015
Case No. 2. A healthy female patient aged 16 years with no history of asthma or allergy was scheduled for tonsillectomy on March 6, 1974. Findings on clinical and laboratory examinations were normal. Premedication was with atropine 0.5 mg injected i.m. 45 min before anaesthesia. Anaesthesia was induced with nitrous oxide, oxygen, trichloroethylene and ether. A nasotracheal tube was passed with the aid of 50 mg of suxamethonium (Scoline). Within 5 min there was tachycardia (140 beats/min) and arterial hypotension (80/40 mm Hg). The anaesthetic administration was stopped and the patient was ventilated with pure oxygen. There were manifestations of skin reaction with flushing and erythematous patches over the chest and upper limbs, with marked oedema of the face and eyelids. Immediately, dexamethasone 8 mg was given i.v. The arterial pressure increased to 100/60 mm Hg and the pulse rate was 90 beats/min. Return of spontaneous ventilation and consciousness were observed at this time. Meanwhile, chlorpheniratnine maleate 10 mg and calcium gluconate 10 ml (10%) were given through the intravenous infusion. When all was well, the patient was again anaesthetized with nitrous oxide, oxygen and trichloroethylene and the operation was completed. A steroid regimen was continued for 5 days after the operation.
BRITISH JOURNAL OF ANAESTHESIA
ANAPHYLAXIS TO SUXAMETHONIUM ANAPHYLAXIE AUF SUXAMETHONIUM
525 ANAFILAXIS PARA SUXAMETONIUM
ZUSAMMENFASSUNG
SUMARIO
Anaphylaxie auf Suxamethonium bei Patienten, die keine frflhere Allergieanfalligkeit gezeigt haben, wird in diesem Bericht vorgelegt. Die Anaphylaxie-Diagnose beruhte auf einem rapiden Eintreten von Tachykardie, arterielkr Hypotension, erythemat6sen Flecken und Odem, sowie einer positiven Reaktion auf einen Sensitivita'Otest.
Se presenta en este infonne la anafilaxis para suxanaetonium en pacientes que no presentaron historial de alergia. El diagnostico de anafilaxis se baso en una rapida inidaci6n de taquicardia, hipotension arterial, mancbas eritematosas y edema, y una reacckSn positiva a una prueba de sensibilidad.
Downloaded from http://bja.oxfordjournals.org/ at University of California, Davis on January 28, 2015
