Endocrine Abstracts

A previously healthy 12 year old girl presented to the emergency department with loss of consciousness and increased work of breathing. She was unwell for 3 days prior to presentation with vomiting and lethargy. There was a 3 week history of polydipsia and weight loss. On assessment, Glasgow Coma Scale (GCS) was 7/15, pupils size 3, equal but poorly responsive. She was hypertensive BP 140/70 mmHg, HR 113 bpm, and capillary refill time 5 seconds. There was left arm decorticate posturing on exam, with no other focal neurology noted. Initial investigations revealed blood glucose 22 mmol/L, ketones 4.8 mmol/L, pH unrecordable, Na 132 mmol/L, K 4.5 mmol/L and CRP<5 mg/L. Urine toxicology was negative. The working diagnosis was severe diabetic ketoacidosis (DKA) with clinical evidence of cerebral oedema. She was intubated and ventilated and resuscitated with 3% hypertonic saline. DKA protocol was commenced and she received IV Ceftriaxone to treat possible sepsis. CT brain reported no acute abnormality or cerebral oedema. She extubated later that day but was not moving her limbs or talking and she did not appear to recognise her parents. Following consultation with Neurology, a repeat CT brain with contrast was performed, which ruled out sagittal vein thrombosis. EEG reported generalised slowing with superimposed rhythmic fast activity with anterior predominance; findings consistent with moderate encephalopathy and the possibility of a locked-in or brain-stem syndrome. She improved clinically within 24 hours; GCS 15/15, she was alert, orientated, moving all 4 limbs, and communicating appropriately. A diagnosis of metabolic encephalopathy secondary to severe DKA was reached. She was switched to subcutaneous insulin after 48 hours on the DKA protocol. On follow up, she has no apparent cognitive or motor impairments. Metabolic encephalopathy is an extremely rare but potentially devastating complication of DKA. This is the first reported case of metabolic encephalopathy complicating DKA in the paediatric population. While our patient was critically ill, her encephalopathy was transient and reversible. The aetiology is still poorly understood. A high clinical suspicion, along with strict monitoring of fluids and electrolyte balance is necessary to ensure early detection, appropriate management and improved long-term outcome in this group.