Four case studies of severe metabolic acidosis in pregnancy

Arterial blood gas analysis in cases of metabolic acidosis reveals primary decrease in pH and bicarbonate, and secondary (compensatory) reduction in pCO₂. The most common cause of metabolic acidosis is increased production of endogenous metabolic acids, either lactic acid, in which case the condition is called lactic acidosis, or keto-acids, in which case the condition is called ketoacidosis. 

Ketoacidosis most commonly occurs as an acute and life-threatening complication of type I diabetes, due to severe insulin deficiency and resulting reduced glucose availability for energy production within cells (insulin is required for glucose to enter cells). Keto-acids accumulate in blood as a result of metabolism of fats mobilized to fill the energy gap created by reduced availability of glucose within cells. 

Starvation is also associated with reduced availability of (dietary) glucose and potential for ketoacidosis, although compared with diabetic ketoacidosis, starvation ketoacidosis is rare, usually mild and not life-threatening. Except, that is, when it occurs during pregnancy. 

In a recently published paper the authors outline four cases of severe starvation ketoacidosis, all occurring in the third trimester of pregnancy, following prolonged vomiting over a period of days. All four women presented for emergency admission in a very poorly state and still vomiting with severe partially compensated metabolic acidosis (bicarbonate in the range of 8-13 mmol/L and base deficit in the range of 14-22 mmol/L). 

All four required transfer to intensive care and premature delivery of their babies by emergency Cesarean section. Fortunately vomiting ceased immediately, and resolution of the severe life-threatening metabolic disturbance followed within 4-12 hours of delivery. 

Biochemical confirmation of starvation ketoacidosis as the cause of the severe metabolic acidosis was made by the finding of low-normal or reduced blood glucose (excluding diabetic ketoacidosis); normal lactate (excluding lactic acidosis); and 4+ ketones in the urine of all four women. 

In an extended discussion of the case histories the authors provide a comprehensive review of the pathogenesis of starvation ketoacidosis in pregnancy, as well as its diagnosis and management.