EDITOR: A 20-yr-old mother, 50 kg in weight, with a history of vaginal bleeding for 1 week was diagnosed to have miscarried. Her uterus of 15 weeks' size was evacuated twice under general anaesthesia within a week and histology of the curettings suggested a hydatidiform mole. She was given oral amoxycillin and metronidazole as there were signs of pelvic sepsis and was sent home with a follow-up appointment for 2 weeks, which she failed to keep. One month later, she was transported urgently to hospital from a rural healthcare centre with a 12-h history of malathion poisoning following oral intake with suicidal intent. She had received a stomach washout, a bath, pralidoxime 1 g and atropine 1.2 mg intravenously (i.v.) and atropine 7.2 mg in a saline i.v. infusion, plus furosemide. She had been conscious at presentation in the rural healthcare centre but collapsed soon after with a pulse rate of 58 beats min−1, pinpoint pupils, muscle twitching and vomiting. On arrival at the hospital, she was conscious with a pulse rate of 64 beats min−1, blood pressure of 100/70 mmHg and she was not cyanosed. She was given more atropine 3.0 mg (it was our routine practice to use atropine to maintain a heart rate >100 beats min−1 in acute organophosphate poisoning) and pralidoxime 0.5 g every 8 h (total dose 4 g) with additional i.v. saline and dextrose over the next 24 h. Thirty-six hours after admission, she developed abdominal distension, lower abdominal tenderness, pallor and evidence of free fluid in abdomen. Her blood pressure was steadily decreasing (90/50 mmHg): intraperitoneal bleeding was suspected and an urgent laparotomy was advised. Clinically, there was no respiratory weakness, no use of accessory muscles of respiration and no movements of the alae nasi. Further resuscitation consisted of 1.5L 0.9% NaCl i.v. and 1 unit of blood. No premedication was given. She was calm, conscious but pyrexial with a blood pressure of 90/50 mmHg and pulse of 110 beats min−1 just before surgery. The patient was anaesthetized with meperidine 50 mg 1 mg kg−1 i.v., while breathing halothane (0.5% increasing to 2%) in N2O/O2 and a cricoid pressure was applied. After atracurium 10 mg i.v., the trachea was intubated with a 7.5-mm cuffed tube and her lungs were ventilated (14 breaths min−1, I:E ratio 1:2, tidal volume 400 mL) using a Bain-type breathing system and a volume preset mechanical ventilator. Anaesthesia was maintained by halothane 0.25% in a mixture of 60% N2O in O2. Further atracurium 10 mg was given 40 min after the first dose. No other medication was used during surgery. At laparotomy, she had a profusely bleeding perforation at the posterior wall of the uterus owing to an invading choriocarcinoma and a hysterectomy was performed. Perioperative blood loss including peritoneal cavity contents was approximately 3 L. Four units of blood were transfused in addition to i.v. crystalloids used to maintain her blood pressure at >100 mmHg systolic perioperatively. Pulse oximetry showed a SPO2 >97% and electrocardiogram (ECG) showed a sinus rhythm during surgery. Respiration was assisted for 45 min after the last dose of atracurium until adequate spontaneous respiration was established postoperatively. No neostigmine was given and the trachea was extubated. The patient was conscious, able to raise her head off the pillow momentarily and there was no respiratory distress (SPO2 = 96%). During the first 12 h postoperation, the urine output was 800 mL. The patient required no further atropine (there was neither bradycardia nor an increase in respiratory tract secretions) and pralidoxime was discontinued. Pain relief was maintained by diclofenac 50 mg i.m. twice a day and oral acetaminophen 1 g as required. Convalescence was prolonged owing to profuse diarrhoea that resolved gradually over 6-7 days. She received i.v. fluids for 5 days and metronidazole, ampicillin and gentamicin for 7 days before referral to an oncology centre. She had no clinical evidence of proximal or distal muscle weakness or features of any cranial nerve palsies. Malathion is an organophosphorus pesticide that inactivates human carboxylic esterase enzymes including acetyl cholinesterase if absorbed. This leads to an accumulation of endogenous acetylcholine at sites of cholinergic transmission that results in excess salivation, respiratory distress, a decreased level of consciousness, abdominal pain, vomiting, diarrhoea and pupillary constriction [1]. This initial acute cholinergic phase usually lasts 48-72 h and may be followed by an 'intermediate syndrome' [2] in which there is transient (5-10 days) muscle weakness often requiring respiratory assistance by artificial means. Some may develop a late-onset polyneuropathy [2]. During these clinical phases, the neuromuscular transmission is deranged owing to a variety of evolving reasons including excess acetylcholine and pre-and postsynaptic nicotinic receptors, myopathic changes, demyelination of peripheral nerves and spinal cord lesions [3]. Even after 'apparent' recovery, patients may suffer major catastrophes following administration of neuromuscular-blocking agents suggesting the restoration process of the damage done is very slow or else is indeed permanent. Baker and Sedgwick [4] demonstrated jitter (a sensitive indicator of impending failure of transmission at the neuromuscular junction) on single-fibre electromyography (EMG) even up to 2 yr after organophosphate poisoning when there were no detectable clinical signs or symptoms of weakness. Anaesthesia in acute organophosphate poisoning incorporates a multitude of problems. The initial severe acetylcholine receptor stimulation involving both central and peripheral nervous systems is associated with skeletal muscle stimulation, autonomic disturbances leading to bradycardia, bronchospasm, pulmonary oedema, high or low blood pressure and direct myocardial depression. The use of drugs metabolized by cholinesterase, e.g. succinylcholine and mivacurium, could exert very prolonged activity and should be avoided [5]. The cardiovascular instability (hypotension, hypertension, dysrrhythmias [6]) and respiratory dysfunction (due to bronchospasm, excessive secretions and muscle weakness) may also impose major anaesthetic risks. This patient was in acute cholinergic phase (it was <48 h since the ingestion of malathion) when an anaesthetic was required. There are no published guidelines concerning anaesthesia during acute organophosphate poisoning, although theoretical speculations about what interactions may be expected were available [7]. Thus, a technique of anaesthesia that would cause minimal disability during and after surgery was adopted. Both organophosphate compounds and atropine high doses are known to produce neuropsychiatric effects, i.e. behavioural disturbances. Therefore, the implication of premedication was unpredictable and hence none was used. Nevertheless, the patient was calm. The compromized cardiovascular function and hypotension in the patient did not appear to be related purely to blood loss, as there was no quick recovery following volume repletion. She was also not induced with an i.v. agent as available drugs (thiopental, propofol) were known myocardial depressants and there was no means of assessing the degree of myocardial dysfunction (e.g. echocardiography) preoperatively. Therefore, halothane inhalation with continuous ECG and SPO2 monitoring and cricoid pressure was chosen as it could be discontinued in the event of a complication. Although halothane cannot be considered the ideal agent under these circumstances - owing to its dysrythmogenicity and prominent myocardial depression effects - it was the only inhalation anaesthetic agent available in our hospital. Nevertheless, it did not produce a dysrhythmia. This could perhaps be attributed to the very brief use of a higher concentration (2%) of halothane for induction followed by the use of a low concentration (0.25%) for maintenance. Meperidine was selected as the analgesic agent as morphine could have aggravated bronchospasm and the vagotonic effects of organophosphate. Altered and unpredictable neuromuscular effects of organophosphate poisoning almost preclude the use of any muscle relaxant. However, muscle relaxation was essential for intubation and surgery in the patient. Atracurium was used for muscle relaxation as its degradation was not primarily dependent on any enzyme or biological function. Although, theoretically, an increase in the atracurium requirement was expected due to cholinesterase inhibition (as acetylcholine concentrations at the neuromuscular junction receptor are likely to be increased as a result of organophosphate overdose and cholinesterase inhibition), the converse was observed in the present patient. This is difficult to explain. However, during the intermediate syndrome and late-onset polyneuropathy, there is a definite increase in sensitivity to muscle relaxants. It is also noteworthy that the patient subsequently did not develop a clinically obvious intermediate syndrome. This could be coincidental, but non-requirement for any atropine postoperation suggests that some of the absorbed poison may have been removed with the haemorrhage. The blood transfusions may also have replenished some of the decreased stores of acetyl cholinesterase. Postoperatively, parenteral diclofenac was used for pain relief and no obvious side-effects were observed. Narcotics were not used due to the fear of summation with the anticipated respiratory difficulties. The patient's blood pressure was stable during and after the operation. The diarrhoea that developed postoperation is a recognized late clinical feature of oral malathion poisoning. This case history thus illustrates that a safe anaesthetic is possible with the use of inhalation anaesthesia, atracurium and meperidine in the presence of acute organophosphate poisoning. Regrettably, no clinical trial will be ethical in this context. Therefore, collation of rare clinical experiences as in the present case will be necessary to develop a consensus. C. D. A. Goonasekera C. J. B. Pethiyagoda C. L. K. Attapattu M. D. Nagarathne Department of Anaesthesia; Base Hospital, Matale, Sri Lanka