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Maternal ketoacidosis complicating acute starvation in pregnancy

Case report A 22-year-old primigravida presented with a 5-day history of severe vomiting at 35 weeks’ gestation. She had had no diarrhoea and she denied all drug abuse. She was apryexial and tachypnoeic. There was persistent tachycardia and she was hypertensive (140/95 mmHg). Urinalysis revealed heavy ketonuria and proteinuria (4+). Breath sounds were normal and there was no abdominal tenderness. The fundal height was compatible with dates. Cardiotocography showed an unreactive tachycardia with shallow unprovoked decelerations. Pulmonary embolism was excluded by a normal V/Q isotope scan. Arterial blood gases revealed a normal PO2 (15 ́9 kPa) but with profound metabolic acidosis (pH 7 ́23, a low PCO2, and a base excess of ± 19 mmol/l). The serum lactate was normal and anion-gap was calculated to be 25 mmol/l (8± 16 mmol/l). Her blood glucose was normal (4 1́ mmol/l) and salicylate was undetectable. Her electrolytes and liver function tests were normal. The maternal ECG was normal. The acidosis was corrected with of an infusion of bicarbonate (50 ml of 8 ́4% sodium bicarbonate over 60 minutes) together with a modi® ed Alberti regimen (sliding scale human insulin together with an infusion of 10% dextrose containing 20 mmol of potassium chloride at 60 ml per hour). A male weighing 2 ́7 kg was delivered by emergency caesarean section. There was no abruption and he had an Apgar score of 9 at 5 minutes. The cord blood pH was 7 ́04 with a base excess of ± 16 mmol/l. The infant developed respiratory distress and required ventilation for 3 days. He made good progress thereafter. Repeat maternal acid-base status shortly after delivery revealed a rising pH (7 3́1) and a closing of the base de® cit (± 10 mmol/l). The mother’s blood pressure measurements were within acceptable limits and anti-hypertensive treatment was not needed. Similarly, anticonvulsant therapy was not required. The maternal acid-base status returned to within normal limits 24 hours of delivery. Serial blood glucose measurements were all normal. At follow-up the mother was well. Discussion The commonest cause of non-hypoxic metabolic acidosis is uncontrolled type I diabetes. Euglycaemic diabetic ketoacidosis can occur rarely but this woman was clearly not diabetic after delivery. Other causes of metabolic acidosis include renal tubular acidosis, salicylate poisoning, alcohol abuse and severe diarrhoea, but these were all excluded. We believe that our patient had ketoacidosis secondary to accelerated starvation, possibly as a result of pre-eclampsia-induced vomiting. Metabolic acidosis has been reported in severe pre-eclampsia but with the biochemical features of anaerobic acidosis (Wheeler et al., 1996); here the acidosis appeared to have resulted from accumulation of ketones and not lactate. Ketosis from starvation develops more quickly in pregnancy (Metzger et al., 1982). Although gestational ketosis is usually a benign condition, the accumulation of ketones in this woman appears to have resulted in a profound acidosis. The clinical message is that protracted vomiting in late pregnancy requires prompt treatment with rehydration and anti-emetic drugs if maternal and fetal complications are to be prevented (Land et al., 1992).