Lab Case 16 – Interpretation

55 year old female with alcohol intoxication

Issues –

altered mental state – alcohol, other



risk of seizures

chronic alcohol abuse – liver disease, GI bleed, cerebellar disease, haematologic abnormlities

Severe metabolic alkalosis – pH 7.65, HCO3 54, BE 30

Compensation: expected CO2 = 0.7XHCO3 + 20 = 57.8

actual CO2 = 49 – reasonable early compensation, will be limited by central response

LFT – high bilirubin, GGT, ALT – chronic alcoholic liver disease, consider acute hepatitis

significant hypoNa, hypoK, hypoCL – classically occurs in loss of stomach fluids – eg. vomiting

high Urea, normal Creatinine – pre renal from vomiting and dehydration, consider GI bleed

FBC – essentially normal but consistent with chronic alcohol abuse

Lactate high – volume depletion

Anion gap = 4 – low normal

Osmolality 247 – very low


55 year old female with sever hypoCl, hypoK, metabolic alkalosis. This occurs with gastric outlet obstruction, however severe vomiting may account for this. Requires K replacement.

Severe hypo osmolar hypoNa with elevated urea – large volume loss and fluid shifts will account for this, secondary to vomiting. Must exclude GI bleed ie. secondary to peptic ulcer disease. Close monitoring for seizures. Cosiderations in volume replacement – CPM.

Consider chronic peptic ulcer disease and gastric outlet obstruction in this patient.

Other causes of metabolic alkalosis:

Endocrine – Conn’s, Cushing’s

Renal tubular acidosis

Excess HCO3 ingestion – antacid use/ abuse

Diuretic abuse/ use