Endocrine Abstracts

History: A 31-year-old gentleman with morbid obesity, hypertension and congenital blindness presented with 2 days of vomiting and drowsiness.

Examination: On presentation, he was in diabetic ketoacidosis (DKA).

• GCS: 11 • Widespread non-blanching rash • Abdomen: diffusely tender, soft

Investigation results: • CRP > 320 • Creatinine 360 • Neutrophils 17 • Amylase 32 • CXR clear • Antibodies for T1DM and lipid profile sent

Diagnostic challenges, Management and course: Without a history of Type 1 diabetes, the cause of DKA was unclear. Suspected precipitants included meningitis or intra-abdominal infection. He was started on IV ceftriaxone and aciclovir, with CT imaging arranged. CTAP showed pancreatic tail oedema, suggestive of acute pancreatitis. Despite 8 hours of DKA therapy, acidosis persisted (pH 6.9, HCO₃ 4), requiring ICU admission and 72 hours of haemofiltration, after which renal function improved. Further results: triglycerides 35 mmol/l, HbA1c 150, T1DM antibodies negative. Repeat CTAP confirmed necrotising pancreatitis (distal body/tail) with splenic vein thrombosis.

Learning points: 1. Rising metabolic syndrome can lead to uncommon DKA triggers. • Here, undiagnosed type 2 diabetes (HbA1c 150) progressed to type 3c (pancreatogenic) following pancreatitis due to severe hypertriglyceridemia. 2. Hypertriglyceridemia should be considered as a cause of pancreatitis. 3. Splenic vein thrombosis may complicate pancreatitis and the pro-thrombotic state of DKA, emphasising the role of thromboprophylaxis. 4. Fluid resuscitation in morbid obesity:are we underfilling?