Differentials
Hyperosmolar hyperglycaemic state (HHS)
SIGNS / SYMPTOMS
Patients are typically older than patients with diabetic ketoacidosis and usually have type 2 diabetes. Older nursing home residents with poor fluid intake are at particularly high risk.
Symptoms evolve insidiously over days to weeks.[1]
Mental obtundation and coma are more frequent.[1] Focal neurological signs (hemianopia and hemiparesis) and seizures are also seen.[126] Seizures may be the dominant clinical feature.[127]
INVESTIGATIONS
Serum glucose is >33.3 mmol/L.[1] Total serum osmolality is usually >320 mmol/kg. Effective serum osmolality is >300 mmol/kg.[1]
Urine ketones are normal or only mildly positive (less than 2+). Serum ketones are <3 mmol/L.[1]
Anion gap is variable but typically <12 mmol/L.
Total chloride deficit is 5-15 mmol/kg.
ABG: arterial pH is typically ≥7.30, whereas in DKA it ranges from 7.00 to 7.30. Arterial bicarbonate is ≥15 mmol/L.[1]
Lactic acidosis
SIGNS / SYMPTOMS
The presentation is identical to that of diabetic ketoacidosis. In pure lactic acidosis, the serum glucose and ketones should be normal and the serum lactate concentration should be raised.
Starvation ketosis
SIGNS / SYMPTOMS
Starvation ketosis results from inadequate carbohydrate availability resulting in physiologically appropriate lipolysis and ketone production to provide fuel substrates for muscle. The condition develops over many days and is suggested by a prolonged history of dietary intake <2090 kJ/day (500 kcal/day).[1]
INVESTIGATIONS
Blood glucose is usually normal.[18] Although the urine can have large amounts of ketones, the blood rarely does. Arterial pH is normal and the anion gap is at most mildly elevated.[18] Serum bicarbonate concentration usually >18 mmol/L due to renal compensation.[11] If electrolyte intake is also limited, then electrolyte disturbances will eventually occur.[11]
Alcoholic ketoacidosis
SIGNS / SYMPTOMS
Classically, these are people with long-standing alcohol use disorder for whom ethanol has been the main caloric source for days to weeks. The ketoacidosis occurs when for some reason alcohol and caloric intake decreases (such as a recent binge culminating in vomiting and acute starvation).[1]
INVESTIGATIONS
The presence of ketoacidosis without hyperglycaemia in a patient with long-standing alcohol use is virtually diagnostic of alcoholic ketoacidosis.[11] Total ketone bodies are much greater than in diabetic ketoacidosis, with a higher beta-hydroxybutyrate to acetoacetate ratio of 7:1 versus 3:1 in DKA.[18]
Salicylate poisoning
SIGNS / SYMPTOMS
Can be differentiated by history and laboratory investigation. Salicylate intoxication produces an anion gap metabolic acidosis usually with a respiratory alkalosis.
INVESTIGATIONS
The plasma glucose is normal or low, ketones are negative, osmolality is normal, and salicylates are positive in blood and/or urine.[18]
Ethylene glycol/methanol intoxication
SIGNS / SYMPTOMS
Methanol and ethylene glycol also produce an anion gap metabolic acidosis without hyperglycaemia or ketones.
Uraemic acidosis
SIGNS / SYMPTOMS
Uraemia can develop with chronic kidney disease, especially the later stages, or with acute kidney injury if loss of kidney function is rapid. Uraemic symptoms include fatigue, anorexia, nausea, vomiting, pruritus, metallic taste, restless legs, and altered mental status. Physical examination findings such as asterixis and pericardial rub (due to uraemic pericarditis), among others, may be noted.[129]
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