LAUSR

A 40-year-old, G10P4 13/40 woman presented with drowsiness and incoherence. Limited history revealed vomiting, altered sensorium and no alcohol intake. Blood pressure was 60/40 mmHg with sinus tachycardia of 140 b.p.m. Neurological examination demonstrated diplopia, gaze-evoked nystagmus, bilateral dysmetria and dysdiadochokinesia, proximal bilateral lower limb weakness 2/5, with clonus. She received fluid resuscitation, electrolyte replacement, antiemetics, thiamine 300 mg three times a day for hyperemesis gravidarum (HG) and empirical antibiotics for possible sepsis. Infective screen was subsequently negative. Consistent with HG, she had anaemia, abnormal electrolytes and elevated liver enzymes (Table 1). Brain magnetic resonance imaging (MRIB) supported the diagnosis of Wernicke encephalopathy (WE) (Fig. 1). Intravenous thiamine was increased to 500 mg three times a day and continued for her 19-day hospitalisation. Within 24 h, her cognition improved. She required blood transfusions, electrolytes and refeeding monitoring and was diagnosed with gestational transient thyrotoxicosis (GTT) (Table 1). High vagal tone from HG and WE caused prolonged cardiac pauses, treated with escitalopram. Collateral history revealed 6 weeks of HG, 10 kg weight loss and 3 weeks of ataxia. At discharge, she could walk 40 m with a four-wheel walker (4WW) and had persistent cognitive deficits. After pregnancy counselling, oral thiamine 100 mg daily was continued until delivery. MRIB 4 months after diagnosis showed near-complete resolution of lesions. Complex maternal indications resulted in caesarean section at 36/40 delivering a 2464-g newborn, Appearance, Pulse, Grimace, Activity, Respiration (APGAR) scores of 6, 7 and 9, requiring ventilatory support for 30 min of life in special care nursery, but the baby was otherwise healthy. Postpartum, she could walk 100 m with a 4WW. Cognitive changes remained consistent with Wernicke–Korsakoff syndrome. Baby remained healthy at 4 months old. WE is a severe manifestation of thiamine deficiency. Pregnancy results in increased thiamine demand; HG and GTT, as in this patient, can rapidly deplete stores with a risk of WE. GTT was diagnosed by the absence of goitre, negative thyroid antibodies and subsequent normalisation of thyroid function. Her anaemia was caused by malnutritionrelated marrow failure as a result of HG. Deranged liver enzymes in HG, as in this patient, carry an increased risk of