Hypokalaemia in children

Hypokalaemia is generally caused by increased losses or trans-cellular shift and rarely due to decreased intake. 

Serum K level does not reflect total body K stores, as intra-cellular K is approximately 30-times higher.

Factors affecting renal regulation of Potassium include renal function, serum K level, Aldosterone & Acid-Base status.

Hypokalaemia is defined as a plasma potassium level less than 3.5mmol/L.

 

Serum Potassium level <3mmol/L is moderate; < 2.5 mmol/L is severe & <2mmol/L is critical

Causes of hypokalaemia

Intracellular shift

– Alkalosis

– Insulin e.g. during IV infusion in DKA

– Re-feeding syndrome

– Medications (Salbutamol, theophylline, etc)

– Hypokalaemic periodic paralysis

Increased renal losses

– Renal tubular acidosis (proximal or distal)

– Congenital adrenal hyperplasia

– Renin secreting tumors

– Gitelman syndrome & Bartter syndrome

– Drugs (loop and thiazide diuretics, aminoglycosides, corticosteroids)

– Ureterosigmoidostomy

– Mineralocorticoid excess (Cushing syndrome, hyperaldosteronism)

– Hypomagnesemia

Increased Extra-renal losses

– Diarrhea, Laxative overuse

– Vomiting, nasogastric suction

– Potassium binding resins (sodium polystyrene sulfonate)

Decreased intake or low stores

– Malnutrition, Anorexia nervosa

– Parenteral nutrition with less Potassium

Clinical Presentation

Symptoms are nonspecific but can be related to muscular weakness or cramps or cardiac dysfunction.

Severe hypokalaemia (K <2.5 mmol/L) may cause muscle weakness (neck flop, abdominal distension, constipation, ileus) and produce cardiac arrhythmias.

– Presence of hypertension suggests hyperaldosterone state, renal artery stenosis or glucocorticoid excess.

– Relative hypotension and alkalosis suggests diuretic use, or a tubular disorder like Gitelman syndrome.

– If Hypokalaemia & Metabolic Acidosis, consider Diarrhoeal losses / Renal Tubular Acidosis / DKA

– If Hypokalaemia & Metabolic Alkalosis, consider persistent vomiting (e.g. Pyloric Stenosis) or NG free drainage losses; or diuretic use; or Bartter and Gitelman syndromes.

-Life threatening complications of severe hypokalaemia: arrhythmias, rhabdomyolysis, diaphragmatic weakness, and paralysis

Investigations

– Repeat U&E with a ‘good sample’ to ensure hypokalaemia is true

– Also check renal function, acid-base status & Magnesium level

– ECG changes include flattened T wave, depressed ST segment, and the appearance of a U wave (after T wave), Heart block, SVT or Ventricular fibrillation.

Treatment

– Reduce ongoing loss

– Consider reversible causes e.g. Salbutamol

– If diuretic required, change to a potassium sparing diuretic

– ACE-inhibitor useful in Gitelman and Bartter syndromes

Oral Potassium replacement for mild to moderate hypokalaemia with 2-4 mmol/kg/ day in 3 or 4 divided doses (maximum 20mmol per dose)

Intravenous KCl administration if unable to take orally or severe hypokalaemia (<2.5 mmol/L) with associated ECG changes.

Peripherally, IV infusion can contain up to 40 mmol/L of KCl concentration (give maximum 10mmol per hour).

Through a Central line, higher concentrations of KCl above 40mmol/L can be given in HDU or PICU setting

Give 0.5 mmol/kg (maximum 20mmol per hour), given over 1 hour under continuous cardiac monitoring and repeat serum K level after 1–2hr