Fulminant diabetes mellitus has recently been recognised as a distinct clinical entity. In this condition -cell destruction rapidly leads to hyperglycaemia and ketoacidosis. Previous cases have only been reported in Asian women, often associated with a poor neonatal outcome.
A Caucasian woman presented at 29+6 weeks gestation with two weeks of malaise, followed by four days of fever, dyspneoa, vomiting, polyuria and polydipsia. She was dehydrated and feverish with 1+ proteinuria, 4+ ketonuria and white cell count 15.7. Symphysis-fundal height was 38cm. Treatment for a suspected UTI was initiated as glucose tests were normal (random glucose 5.5mmol, fasting glucose 7.0mmol). Deterioration occurred over 24 h with increasing dyspnoea and tachycardia. A repeat random blood glucose was 13 and blood gas analysis demonstrated a severe metabolic acidosis (pH 7.08, bicarbonate 7).
New onset diabetes presenting as diabetic ketoacidosis (DKA) was considered unlikely (due to the short duration of symptoms, previously normal glucose level and only mildly elevated glucose level (range 10–15)). ITU management was therefore initially supportive. Persistently elevated glucose levels were stabilised with an insulin infusion and DKA resolved. Subsequent basal bolus regime required rapid increments to achieve normo-glycaemia. Ultrasound confirmed a macrosomic fetus with polyhydramnios. Pregnancy was closely monitored until 33+3 weeks when further deterioration prompted caesarean delivery of a healthy son weighing 3330g. Diabetes requiring insulin has persisted post partum.
Notably, on admission to ITU, amylase was mildly elevated (405). Elevated serum amylase has previously been reported where fulminant diabetes develops during pregnancy prior to DKA being observed.
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