Atropine toxicity in a neonate.

The patient was a 2.2 kg, 30-day-old male with a partial airway obstruction secondary to cystic hygromata enlarging in the floor of the mouth and subcutaneously throughout the anterior neck. He was brought to the operating room for emergency resection of these rapidly enlarging masses. After he was given atropine sulphate 0.1 mg, anaesthesia was induced with halothane and then maintained with 50% nitrous oxide in oxygen by controlled ventilation facilitated by tubocurarine 1.7 mg. After 5 hours of surgery ths curare was reversed with neostigmine 0.25 mg mixed with atropine sulphate 0.1 mg, and the nitrous oxide was discontinued. The only other medications that the patient had received that day were ampicillin 100 mg and dexamethasone 1 mg. The child was returned to the recovery room with a nasal endotracheal tube in place. Upon arrival in the recovery room, the patient's respiration was spontaneous and regular. He had a normal sinus arrhythmia with a rate of 140/min, and his rectal temperature was 36.1°C. He was lethargic but initially responsive to simple stimuli with eye opening and sucking. He developed some intermittent shaking movements which increased in duration and frequency over the first 2-3 postoperative hours to a severe opisthotonictype seizure activity. By 3£ hours he was in a state of near status-opisthotonos. During this time his temperature had increased to 37.1°C. His pulse had slowed from 140 to 120 beats/min, and his breathing had become irregular with periods of apnoea lasting up to 15 sec in duration. His pupils, noted to be widely dilated since surgery, were unresponsive to light. Despite adequate fluid replacement and a palpably distended bladder, he had not passed urine spontaneously since before surgery. His mucous membranes and skin were dry and unflushed. Laboratory data in the recovery room, including arterial gases, e.c.g., haemoglobin concentration, white blood count, and serum electrolyte, glucose and calcium concentrations, were all within normal limits. Despite the fact that routinely used doses of atropine had not been exceeded, the child's symptoms suggested the possibility of the central anticholinergic syndrome associated with belladonna alkaloid poisoning. To test this possibility, 0.07 mg of the anticholinesterase physostigmine salicylate was given to the child i.v. Within 2 minutes he had stopped his siezure activity, opened