Endocrine Abstracts

Case presentation: A 35-year-old man presented to the emergency department (ED) in a confused and agitated state. His past medical history was significant for poorly controlled type 1 diabetes, complicated by background diabetic retinopathy. He was taking basal/bolus insulin and had a history of diabetic ketoacidosis (DKA) eleven years prior. He also had multiple sclerosis however disengaged with neurology services and was non-compliant with interferon therapy. Prior to admission he worked as a caretaker in a school, smoked ten cigarettes per day, took excess alcohol and smoked cannabis twice per week. Following initial investigations, he was found to be in DKA. Unfortunately, despite timely and appropriate management his neurological symptoms and behavioural disturbance persisted. Biochemistry revealed DKA (pH 7.17, blood ketones 8 mmol/l and blood glucose 26 mmol/l). Alcohol levels were undetectable, urine and serum toxicology screens were negative. Excluding ketosis, acidosis and hyperglycaemia there were no significant abnormalities in other biochemical or haematological investigations. HbA1c was 70 mmol/mol (8.5%). Analysis of cerebrospinal fluid (CSF) on the second day of admission revealed an elevated protein at 61 mg/dl with normal glucose 6.3 mol/l, erythrocytes 86 u/l and leucocytes 1/uL. Serum and CSF extended viral PCR was negative. Neuroimaging revealed temporal lobe abnormalities consistent with an encephalopathic process. The patient underwent extensive investigation looking for evidence of autoimmune, infective, metabolic, toxic and paraneoplastic encephalopathy, with no obvious cause demonstrated. Temporal lobe biopsy showed marked astrocytic gliosis without evidence of vasculitis, inflammation, infarction or neoplasia. Electroencephalogram was consistent with an encephalopathic process. A diagnosis of metabolic encephalopathy secondary to DKA was reached.

Results and treatment: In addition to his initial treatment for DKA followed by basal/bolus insulin, the patient was also given high dose intravenous thiamine and a reducing regimen of chlordiazepoxide. He received empiric antiviral treatment and folic acid supplementation. Subsequent treatment was largely supportive, involving a multidisciplinary team of occupational therapy, physiotherapy, social care and neuropsychology. Despite neuro-rehabilitation, the patient’s cognitive function remained impaired up to 18 months post presentation and he ultimately required residential care.

Conclusion and points for discussion: DKA poses a serious and significant neurological risk to patients with diabetes mellitus. To our knowledge this is the second case report of metabolic encephalopathy as an acute complication of DKA. The aims of this report are to highlight metabolic encephalopathy as a complication of DKA and to explore the current research in diabetic related brain injury.