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| CASE REPORT |
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| Year : 2014 | Volume
: 28
| Issue : 1 | Page : 43-44 |
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Anaphylaxis with pancuronium bromide
Langpoklakpam Chaoba Singh1, Sanjeev Singh2, Arti Singh3, Kulsum4
1 Department of Anaesthesia, RIMS, Imphal; Department of Critical Care Medicine, NHIMS, Bengaluru, Karnataka, India
2 Department of Cardiac Anaesthesia, NHIMS, Bengaluru, Karnataka, India; Department of Anaesthesia and Intensive Care, School of Medical Sciences, College of Health Sciences, Kwame Nkrumah University of Science and Technology, Kumasi, Ghana, West Africa
3 University Health Services, Kwame Nkrumah University of Science and Technology, Kumasi, Ghana, West Africa
4 Department of Anaesthesia, Zainoel Abidin Hospital, Banda Aceh, Indonesia
| Date of Web Publication | 24-Jun-2014 |
Correspondence Address:
Dr. Sanjeev Singh
Department of Anaesthesia and Intensive Care, School of Medical Sciences, College of Health Sciences, Kwame Nkrumah University of Science and Technology, Kumasi, Ghana, West Africa
 Source of Support: None, Conflict of Interest: None  | Check |
DOI: 10.4103/0972-4958.135232
Anaphylactic reactions occurring during anaesthesia remain a major cause of concern for anaesthesiologists. Serious and occasionally fatal anaphylactic reaction may occur when a patient is exposed to a drug for the first time. On time prompt recognition and treatment of the acute event by the attending anaesthesiologist and subsequent determination of the responsible agents with strict avoidance of subsequent administration of all incriminated cross reacting compounds is very important. However, correct identification of the causative compound immediately is not always straightforward. In this case report, we summarized the alarming rare causes of anaphylaxis during anaesthesia and the diagnostic approach of this rare but potentially life-threatening complication and management. Keywords: Anaphylaxis, Anaesthesia, Neuromuscular blocking agent, Pancuronium
How to cite this article:
Singh LC, Singh S, Singh A, Kulsum. Anaphylaxis with pancuronium bromide. J Med Soc 2014;28:43-4 |
| Introduction | |  |
The incidence of anaphylaxis during anaesthesia has been reported to range from 1 in 4000 to 1 in 25,000. [1] Neuromuscular blocking agents induce about 50-60% of anaphylactic reactions during anaesthesia. [2] The incidence is estimated to be of the order of 1:980-1:20,000 by the Boston Collaborative Drug Surveillance Survey. [3] Three out of four cases of anaphylaxis to muscle relaxants occur in females, suggesting cross-reactivity with ammonium compounds in personal care products. [1] As the incidence of anaphylactic reactions during anaesthesia is low, determining the risk of anaphylaxis to individual neuromuscular blocking drugs (NMBDs) would require a study of over 30 million patients. [4]
Here, we are reporting anaphylaxis to pancuronium, which is a very rare event but can be life-threatening. Intradermal test studies suggest low-risk agents (e.g., pancuronium, vecuronium), intermediate (rocuronium) and higher-risk agents (e.g., alcuronium, succinylcholine) in their propensity to cause allergy. [5]
| Case Report | | |
A 59-year-old hypertensive and diabetic obese male with American Society of Anaesthesiologists (ASA)-III, Mallampati class-III (predicted difficult intubation), morbidly obese (class II-WHO 2004) having body mass index of 36.5 was posted for elective coronary artery bypass grafting (CABG). Premedicated in the morning with oral diazepam 5 mg, pantoprazole 40 mg and metoprolol 25 mg with sips of water. Monitoring was done in the operation theater as per ASA standards and difficult intubation trolley was kept ready. A peripheral cannula 16G was inserted in right hand and intravenous normal saline started. After local infiltration with 2% lidocaine 1 ml radial arterial cannula 20G was inserted in right hand. Preoperative vitals were stable with blood pressure of 130/70 mm Hg and heart rate of 70/min. Induction was done with propofol 1 mg/kg, fentanyl 150 μg and the patient was intubated after giving succinylcholine 1 mg/kg. After intubation, the blood pressure was 136/85 mm Hg, heart rate was 74/min and saturation was 100%. The patient was put on anaesthesia ventilator and was given 6 mg of pancuronium intravenously. Within few seconds of giving pancuronium vitals started deteriorating, the blood pressure dropped to 58/32 mm Hg, with heart rate of 45/min and saturation of 80%. Rashes appeared on the chest. Immediately, injection adrenaline 0.5 mg and atropine 0.6 mg was given intravenously. The patient was ventilated with 100% oxygen and fast infusion of normal saline was given 600-700 ml. Injection chlorphenaramine 10 mg, hydrocortisone 200 mg was given intravenously and adrenalin infusion 2000 μg in 50 cc was started in titrating doses. During the course, electrocardiography was normal, respiratory system examination revealed air entry bilaterally equal and scattered wheezing. The random blood sugar was 134 mg/dl, arterial blood gas showed metabolic acidosis with pH - 7.28, HCO 3 − 21.3 (STD), and base deficit - 4.0. After few minutes, the patient was stabilized with blood pressure of 124/78 mm Hg and heart rate of 87/min. Elective CABG was postponed. After 45 min, patient started breathing spontaneously and lifting neck on command then patient was extubated. Later patient was nebulized (with NS + adrenalin+ salbutamol + budecort solutions) and shifted to the intensive care unit (ICU) with adrenalin infusion at titrating dose. ICU stay was uneventful. The patient did not have a prior history of any allergy. We revised the drugs used in the OT and, as the event occurred after the administration of pancuronium, we suspected it to be anaphylaxis to pancuronium. After 3 h of the event, we collected the blood sample for mast cell tryptase (MCT) testing, which showed the beta subunit of 4.6 ng/l and ratio of total to beta subunit seven, confirming the event of anaphylaxis. After 6 weeks, we performed intradermal testing, which identified pancuronium to be the offending agent.
| Discussion | | |
Mast cell tryptase is the single most useful test to confirm an anaphylactic event. [6] MCT is an enzyme that is released from activated mast cells. MCT levels begin to rise within 30 min of an anaphylactic reaction and remain high for approximately 6 h. The level of the beta subunit of MCT more than 3 μg/l and ratio of total MCT to beta subunit <10 is a very sensitive indicator of an anaphylactic event during anaesthesia. [7] However, the most valuable method of assessing the relative likelihood of a NMBD to cause anaphylaxis is to determine intradermal sensitivity in a population of patients known to be relaxant reactors. [4] Radioimmunoassay testing helps to identify a responsible agent, especially when cutaneous tests are negative. [6]
Greater severity of anaphylaxis observed in patients receiving β-blockers might relate, in part, to a blunted response to epinephrine administered to treat anaphylaxis. [8] Epinephrine administered to a patient taking a β-blocker can produce unopposed alpha-adrenergic and reflex vagotonic effects, possibly leading to hypertension and the risk of cerebral hemorrhage. [9] In patients receiving β-blockers, increased propensity not only for bronchospasm, but also decreased cardiac contractility with perpetuation of hypotension and bradyarrhythemia might exist. [10]
Anaphylaxis can occur with any drug we use in our day to day anaesthesia practice. Therefore, proper documentation in anaesthesia notes and preserving records for further reference is necessary. Patients detected with these allergies should be advised to keep proper records of this information to be able to inform any other medical practitioner who sees them at a later date. Educating the patients about allergy or anaphylaxis to a drug is very important with providing medic alert identification bands for the prevention of any untoward event in the future.
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