Endocrine Abstracts

Stress hyperglycaemia is a widely recognised feature of critical illness. Spontaneous hypoglycaemia, by contrast, is an underappreciated but serious complication. Here I present three cases encountered over 12 months in a single teaching hospital.

Case 1: 59 year old female. Admitted with fever and leg pain. Cellulitis diagnosed and antibiotics commenced. Hours later, she became unresponsive and shocked, with evident necrotising fasciitis. She had metabolic acidosis, lactate 10.0 mmol/L. Capillary blood glucose was 0.8 mmol/L and serum cortisol was only 169 nmol/. Unfortunately, she deteriorated further and died shortly afterward. A post-mortem revealed bilateral adrenal haemorrhage.

Case 2: 43 year old male. Presented with respiratory distress following a viral prodrome. Blood gas analysis showed metabolic acidosis, lactate 7.0 mmol/L. Laboratory tests showed leukopaenia, coagulopathy, acute kidney injury and hepatic failure. He became diaphoretic and aggressive, followed by PEA arrest. Capillary blood glucose was 0.8 mmol/L. Unfortunately, he died on ITU 8 days later from multiorgan failure.

Case 3: 49 year old female. Admitted with abdominal pain, fever, diarrhoea and vomiting. She developed disorientation and confusion with capillary blood glucose 1.8 mmol/L. Tests revealed coagulopathy, acute kidney injury and hepatic failure. Cortisol was appropriate at 1261 nmol/L. After antibiotics and glucocorticoids in intensive care, she made a full recovery and remains under investigation for an as yet undiagnosed systemic inflammatory condition.

Spontaneous hypoglycaemia in critical illness is associated with high mortality – in one study of 7820 patients with acute MI, 136 (1.7%) experienced spontaneous hypoglycaemia (mean glucose 2.5 mmol/L), which was associated with a doubling of mortality. Increased metabolic demand requires effective mobilisation of energy stores to maintain blood glucose concentrations. Hypoglycaemia is most often found in the context of hepatic failure (disruption of glycogenolysis and gluconeogenesis), or bilateral adrenal haemorrhage (glucocorticoid insufficiency). It remains unknown whether treatment or avoidance of hypoglycaemia improves outcomes in critical illness.