Asystole in the prolonged QT syndrome 573 experimental evidence of its relationship with the sympathetic nervous system and the long OT syndrome. Am Heart J 1975;89:45-80. 4 Shwartz PJ. The long OT syndrome. Am Heart J 1975;89:378. 5 Milne JR, Ward OE. The long OT syndrome: effects of drugs and left Stellate ganglion block. Am Heart J 1982;104:194. 6 James NJ, James TN, Frogatt P. Observations on the pathophysiology of the long OT syndrome with special reference to the neuropathology of the heart. Circulation 1978;57:221.Correspondence to Dr J M Rennie, Special Care Baby Unit, Liverpool Maternity Hospital, Oxford Street, Liverpool 7. Received 13 January 1984Complete recovery after profound acidosis (pH 6.49) M I KHAN, M T MILLER, AND Nf BARTLETT Department of Paediatrics, Baragwanath Hospital, Johannesburg, South Africa SUMMARY We describe an infant with profound acidosis caused by chronic therapeutic salicylate poisoning. The confirmed arterial blood pH of 6-49 must be close to the limit of tolerable acidity and is the lowest such value in our experience. Full recovery was made.Case report A 21/2 month old infant weighing 3-6 kg presented to the paediatric emergency ward with a three day history of a dry non-productive cough, diarrhoea, and vomiting. During the preceding three days she had reportedly received approximately 125 mg aspirin three times daily (administered by the mother) in an attempt to alleviate symptoms. The mother also reported that the infant had had generalised convulsions lasting 10 minutes on the day of admission.Clinical examination showed an infant who was somnolent, dehydrated, hypothermic (temperature 35°C), hyperpnoeic (respiratory rate 72/minute), shocked (systolic blood pressure 50 mmHg), and anuric. There was clinical evidence of extensive, right sided, middle and lower lobe pneumonia. The infant's weight, head circumference, and length were well below normal. Arterial blood gas analysis and serum urea, creatinine, and electrolyte determinations confirmed a profound metabolic acidosis with respiratory compensation and hypertonic dehydration.Initial baseline laboratory values were as follows: pH 6-82; Paco2, 13-1 mmHg; Pao2, 40-8 mmHg; bicarbonate 3-4 mmol/l; base deficit 32-0 mmol/l; oxygen saturation 36-7%; serum sodium 163 mmoll 1; serum potassium 7-3 mmol/l; serum urea 38-7 mmolIl; serum creatinine 230 umol/l; serum osmolality 397; and whole blood glucose 18-2 mmol/l. A serum salicylate concentration of 1-36 mmol/l (reference value less than 0-36 mmol/l) and a high anion gap acidosis confirmed chronic, salicylate overdosage. A blood specimen for prothrombin index failed to clot and a bleeding time (Ivy method) of 20 minutes confirmed a bleeding diathesis. A lumbar puncture on admission was normal.Sodium bicarbonate 8-5% (2 mmolUkg) was given intermittently in addition to a continuous infusion at a rate of 0-03 mmol/kg/minute. While measures were taken to correct the severe metabolic acidosis and dehydration the patient developed generalised convulsions which were controlled ...

No abstract