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A 35-year-old unmarried man living alone was brought to the emergency department with acute abdominal pain mainly in the epigastric region. He could not provide any detailed history regarding his presenting complaint but had no fever or other constitutional symptoms. He was known to have diabetes mellitus, but we had no information on any other medical history. Following admission to hospital, his Glasgow Coma Scale score deteriorated rapidly over 24–48 hours from 14/15 to 4/15, and he was intubated and ventilated. His pupils were symmetrical at 4 mm in diameter and were slowly reactive. Deep tendon reflexes were globally diminished with reduced muscle tone, and plantar responses were down going. The remaining neurological examination including cranial nerve function and optic fundi was normal, and there was no neck stiffness. His blood pressure on admission was 190/100 mmHg with a pulse rate of 90 beats per minute. The random plasma glucose level was 19.8 mmol/L and his arterial blood gases showed a high anion gap metabolic acidosis (pH 6.7). Serum electrolytes showed a normal level of serum sodium of 135 mmol/L, but a raised serum potassium level of 5.7 mmol/L. Serum calcium and magnesium levels were normal. Ketone bodies were present in the urine but not in the serum. His renal function was gradually deteriorating with a raised serum creatinine level of 308 μmol/L. CT scan of the head on admission was normal. Cerebrospinal fluid contained 1.48 g/L of protein, 3.7 mmol/L of glucose (paired plasma glucose of 7.9 mmol/L), 0 polymorphs, 4 lymphocytes and red blood cells (1750×106 cells/L). Electroencephalogram showed generalised slow delta activity throughout the record suggesting encephalopathy or encephalitis. Urine toxicology screen was negative for cocaine, methamphetamine, morphine, tetrahydrocannabinoids, amphetamine, barbiturates, benzodiazepine, methadone and tricyclic antidepressants.
Question 1: What clinical syndrome best describes this presentation?
He was previously well and presented acutely with epigastric pain but soon became unconscious with very …
Acknowledgements We acknowledge the contributorship of the patient, patient’s family and colleagues of the Institute of Neurology, National Hospital of Sri Lanka.
Funding The authors have not declared a specific grant for this research from any funding agency in the public, commercial or not-for-profit sectors.
Competing interests None declared.
Patient consent for publication Consent obtained directly from the patient(s).
Provenance and peer review Not commissioned; externally peer reviewed by Jeremy Chataway, London, UK.