36 year old lady with a triple acid – base disorder:

Severe high anion gap metabolic acidosis

Normal anion gap metabolic acidosis

Respiratory acidosis

pH very low => acidaemia

Low HCO3, -ve BE => metabolic acidosis

Anion gap = 20.5 — high

Causes: DKA (normal glucose) and sepsis (CRP <1) and renal failure (low Urea and Creat) unlikely. Volume depletion contributory (lactate mildly elevated), however must check ketones – alcoholic/ starvation ketoacidosis likely to be the main contributor. Consider drug co-ingestants.

Compensation: expected CO2 = 18, actual 28 => additional respiratory acidosis, incomplete compensation. Aspiration pneumonia, drug related

Delta gap = 0.5 => mixed high and normal anion gap acidosis. Saline rehydration, RTA (normal K, consider NSAID abuse in view of history)

LFT show elevated GGT => chronic alcohol abuse, no evidence of hepatitis or obstruction.

Low Urea and creatinine – possible reduced muscle mass due to chronic alcohol abuse/ starvation.

Very low PO4 levels occur in chronic alcoholics and require replacement to prevent myocardial dysfunction and life threatening arrhythmias.

Triple acid base disorder likely due to alcoholic/ starvation ketoacidosis with contributory factors being possible respiartory complication ( pneumonia, drug related) and saline rehydration. drug co-ingetion must be considered in this patient. Abdominal pain may be caused by gastritis (no biochemical evidence of hepatitis or billiary disease). Bowel obsruction/ perforated PUD must be excluded.

Excessive vomiting may also cause a metabolic alkalosis due to loss of HCL – but not a major factor here.

Treatment of alcoholic ketoacidosis is aimed at corrected volume depletion and replacing glycogen stores. Use a combination of dextrose and saline as required. If not initially shocked, use 10% dextrose infusion at 100ml/hr. monitor BSL.

Carbohydrate and fluid replacement reverse the pathophysiologic derangements that lead to AKA by increasing serum insulin levels and suppressing the release of glucagon and other counterregulatory hormones. Dextrose stimulates the oxidation of NADH and aids in normalizing the NADH/NAD⁺ ratio. Fluids alone do not correct AKA as quickly as do fluids and carbohydrates together.

Remember to replace thiamine in chronic alcoholics prior to dextrose administration to prevent Wernicke’s encephalopathy. Alcohol withdrawal chart is mandatory for those patients admitted to hos[ital