21kPa. Diabetic ketoacidosis was diagnosed and treated

according to hospital guidelines. Over the next six hours, the patient’s symptoms rapidly improved. At the time of diagnosis of DKA, cardiotocograph (CTG) monitoring was pathological with reduced baseline variability which returned to normal within 24 hours of initiation of DKA treatment. Following treatment of DKA, bicarbonate level rose to 17mmol/L and remained at this LGK-974 order level until delivery, two weeks later. The patient went into spontaneous labour; however, in view of the suspected macrosomia, she underwent an uncomplicated lower segment caesarean section resulting in the delivery of a live female weighing 4.34kg with APGAR scores of 8, 9 and 10 at 1, 5 and 10 minutes, although the cord pH was 6.9. The baby had severe neonatal hypoglycaemia, with blood glucose 1.5mmol/L, necessitating admission to the neonatal intensive care unit and treatment with intravenous dextrose for 48 hours. The patient had a six-week postpartum OGTT which showed impaired glucose tolerance with a fasting glucose of 3.9mmol/L and a two-hour glucose of 9.3mmol/L. Both mother and child were well at last contact. This case highlights the fact that Y-27632 datasheet women with GDM are at risk of developing DKA in later pregnancy. Recognised risk factors for DKA in pregnant patients with T1DM include infection, vomiting, treatment non-compliance, new onset diabetes, insulin pump failure,

corticosteroids and beta-adrenergic drugs.1,3 The likely precipitant in this case of GDM was administration of corticosteroids. The use of steroids in patients Farnesyltransferase with DM is associated with a significant worsening of glycaemic

control for up to 48 hours after steroid administration.6 In pregnant women with DM who receive antenatal steroids, blood glucose control can be achieved with additional insulin, either calculated according to prior insulin requirements or via an insulin sliding scale.6,7 Venous glucose at diagnosis of DKA may be considerably lower in pregnant than in non-pregnant women. In one case-control study the blood glucose levels were compared in 90 pregnant and 286 non-pregnant females at diagnosis of DKA, and were found to be significantly lower in pregnant women with DKA: 16.3±4.6 and 27.5±4.8mmol/L (mean±SD), respectively.8 The reduced glucose level at presentation of DKA in pregnant women with DM, as in this case, may present diagnostic difficulties. All patients with DM, including those with GDM, who are unwell or present with any combination of nausea, vomiting or reduced calorific intake, should be assessed for the possibility of DKA9 with serum urea and electrolytes, venous blood gases and testing of blood or urine for ketones regardless of blood glucose readings. Acid-base balance in pregnancy is characterised by a physiological hyperventilatory response leading to a primary respiratory alkalosis.