Write a short note on hypokalaemia.

Definition

Hypokalaemia is a serum potassium below 3.5 mEq/L, classified as mild (3.0–3.5), moderate (2.5–3.0) and severe (< 2.5 mEq/L, or symptomatic at any level). It is the commonest electrolyte abnormality in hospital practice.

Causes

Renal loss (urinary potassium > 20 mEq/day):

• Diuretics — loop and thiazide — the commonest cause.
• Hyperaldosteronism — primary (Conn's syndrome) and secondary; Cushing's syndrome; liquorice ingestion.
• Renal tubular acidosis types 1 and 2.
• Hypomagnesaemia — a critically important and frequently missed cause.
• Bartter and Gitelman syndromes; amphotericin B, aminoglycosides, cisplatin.
• Post-obstructive diuresis, recovery phase of acute tubular necrosis.

Gastrointestinal loss (urinary potassium < 20 mEq/day):

• Vomiting and nasogastric aspiration (loss is largely renal, driven by the accompanying alkalosis and volume depletion), severe diarrhoea, laxative abuse, villous adenoma, fistulae, ileostomy.

Transcellular shift into cells:

• Insulin therapy (especially during treatment of diabetic ketoacidosis), beta-2 agonists (salbutamol), metabolic alkalosis, refeeding syndrome, hypokalaemic periodic paralysis, thyrotoxicosis, and treatment of megaloblastic anaemia with vitamin B12.

Inadequate intake: alcoholism, anorexia nervosa, prolonged fasting — rarely the sole cause.

Clinical Features

• Neuromuscular: weakness (proximal, ascending), fatigue, cramps, hyporeflexia; severe depletion causes flaccid paralysis and rhabdomyolysis; ileus from smooth muscle involvement — abdominal distension and constipation.
• Cardiac: palpitations, ventricular ectopics and arrhythmias, and markedly increased risk of digoxin toxicity — hypokalaemia potentiates digoxin binding.
• Renal: nephrogenic diabetes insipidus with polyuria and polydipsia; metabolic alkalosis; long-standing depletion causes interstitial nephropathy.
• Metabolic: impaired insulin release with glucose intolerance; worsening of hepatic encephalopathy through increased renal ammoniagenesis.

ECG Changes

• Flattening and inversion of the T wave
• Prominent U waves — the classic sign, best seen in the precordial leads
• ST segment depression
• Prolonged PR interval, and apparent QT prolongation (in reality QU prolongation)
• Ventricular ectopics, and in severe cases ventricular tachycardia, torsades de pointes and fibrillation

Investigations

Serum potassium, magnesium, sodium, chloride, bicarbonate, calcium and creatinine; arterial or venous blood gas to identify accompanying acid-base disorder; spot urinary potassium and the transtubular potassium gradient to separate renal from extrarenal loss; ECG; and, where indicated, aldosterone and renin (for Conn's syndrome), thyroid function, and a drug review.

The acid-base pattern is diagnostically useful: hypokalaemia with metabolic alkalosis suggests vomiting, diuretics or hyperaldosteronism; hypokalaemia with metabolic acidosis suggests diarrhoea or renal tubular acidosis.

Management

• Correct magnesium first or simultaneously. Potassium cannot be replaced successfully in the presence of hypomagnesaemia, because magnesium deficiency increases renal potassium wasting through ROMK channels. This is the single most common reason for refractory hypokalaemia.
• Oral replacement is preferred where the patient can take it and depletion is mild to moderate — potassium chloride is the salt of choice, and is also appropriate where there is coexisting alkalosis.
• Intravenous replacement for severe hypokalaemia, arrhythmia, or when the oral route is unavailable. Potassium must be diluted and infused slowly, preferably via a large vein or central line for higher concentrations, with continuous cardiac monitoring for rapid infusion. Never give undiluted potassium as a bolus.
• Treat the underlying cause — withdraw or modify diuretics, add a potassium-sparing agent, control vomiting or diarrhoea, treat hyperaldosteronism.
• Monitor serum potassium frequently during replacement, and recheck after correction, since rebound hyperkalaemia can occur once shifts reverse.