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Endocrine Abstracts (2018) 55 P04 | DOI: 10.1530/endoabs.55.P04

West Middlesex University Hospital, London, UK.

During starvation, ketone bodies acetoacetate and 3-D-hydroxybutyrate are freely soluble energy substrates made by the liver. Their major role is to supply an alternative glucose substrate for the brain under conditions of medium- and long-term energy restriction. The most common cause of pathological ketoacidosis is poorly controlled type 1 diabetic mellitus triggering uncontrolled hyperglycaemia. Other common causes are alcoholic ketoacidosis and fasting ketosis. In non-diabetic patients developing significant metabolic acidosis, important differentials include salicylate poisoning, methanol or ethylene glycol poisoning, elevated serum lactate levels, uremic acidosis or malnutrition with extremely poor oral intake. Clinically, fasting is rarely a suspected cause of significant metabolic acidosis. A 46-year-old patient with a 20-year history of multiple sclerosis presented to the emergency department for the second time in a 72-hour period with intractable vomiting. Regular medications were sertraline and topiramate. She had a Glasgow coma score 14, respiratory rate 28 breaths per minute, heart rate 90 beats per minute, blood pressure 110/65 mmHg. The patient was clinically dehydrated and exhibited Kussmaul breathing. Initial venous blood gas (VBG) showed a metabolic acidosis pH 7.005, pCO2 3.55 kpa, lactate 0.96, HCO3 7.5 mmol/l (22 – 26), base excess −23.6 m Default (−2 to +2), blood glucose 5 mmol/l, blood ketones 4.8 mmol/l (<0.6 mmol/l). Admission bloods ruled out paracetamol and salicylate poisoning, uraemia (urea 3.4 mmol/l), acute renal failure (normal urea: creatinine ratio and eGFR >90 ml/min per 1.73 m2) and tumour lysis syndrome – serum uric acid 205 micromol/l (155–357). The patient had a high anion gap metabolic acidosis 17.6 mEq/l. She was started on a fixed rate insulin infusion (FRII) as per diabetic ketoacidosis (DKA) protocol and intravenous sodium bicarbonate 1.26%. Repeat VBG showed a worsening metabolic acidosis pH 6.97, base excess −26.6 mEq/l, bicarbonate 4.3 mmol/l. She was admitted to the high dependency unit. Her ketosis resolved after 24 hours on FRII and IV sodium bicarbonate. Starvation ketoacidosis is a rare but important differential diagnosis for metabolic acidosis.This case is unique on account of severity of ketoacidosis in a young, relative healthy patient. An exaggerated response to fasting has been described in pregnant patients, the elderly and young infants. There are currently no set guidelines for treatment of this patient subgroup but use of FRII in conjunction with IV sodium bicarbonate has proven to be successful in reversing the metabolic acidosis.

Volume 55

Society for Endocrinology Endocrine Update 2018

Society for Endocrinology 

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