POTASSIUM DISORDERS

Potassium is the principle intracellular cation, essential to maintain resting membrane potential of cells (along with major extracellular cation - sodium) and consequently, adequate excitability of neurons and contractility of muscles.

Normal serum potassium levels are 3-5 mEq/L. More than 90% of potassium is present in body fluids, rest being in bones, cartilages and connective tissue.

Physiology: Dietary intake of potassium is usually adequate and rarely affects serum potassium levels. Maintenance of normokalemia mainly depends on:

• Renal excretion, regulated by serum K⁺ levels, blood pH and hormones, e.g. aldosterone.

• Transcellular movements during blood pH changes- Potassium moves out of the cell during acidosis (leading to ECF hyperkalemia) and into the cell during alkalosis (leading to ECF hypokalemia).

Hypokalemia is the commonest electrolyte abnormality in sick children, defined as S. potassium levels lt;3 mEq/L. Causes: Severe diarrhea or vomiting is the commonest cause of acute hypokalemia, while persistent hypokalemia usually indicates underlying renal disease (Table 7.7). Pathophysiology: Low extracellular potassium levels slow down the post-depolarization return of potassium into the cells, delaying process of repolarization and leading to impaired neuromuscular excitability.

Clinically, hypokalemia presents with signs of impaired neuromuscular excitability, as follows:

• Skeletal muscle involvement, e.g. limb weakness, hypotonia, hyporeflexia, abdominal distension and respiratory muscle paralysis. Rhabdomyolysis is a rare but important complication.

• Smooth muscle involvement, e.g. paralytic ileus, orthostatic hypotension, bradyarrhythmia.

• Characteristic ECG changes, which may precede clinical features in hypokalemia and include: (a) low voltage, (b) ST depression with flat/inverted T waves, (c) prolonged QTc interval, and (d) prominent U waves.

capability, manifesting as polyuria, polydipsia, meta­bolic alkalosis with secondary failure to thrive and nephrosclerosis.

Treatment: Symptomatic or severe hypokalemia (lt;2.5 mEq/L) must be treated with slow potassium chloride infusion (2 mEq/ml) in IV fluids as 0.5-1 mEq/kg over

TABLE 7.7: Causes of hypokalemia

a. Extrinsic losses:

- GIT: Diarrhea, vomiting, nasogastric drainage

- Urinary*:

Renal: Renal tubular acidosis, Bartter syndrome Endocrinal: Cushing syndrome, hyperaldosteronism Iatrogenic: Diuretics, e.g. furosemide

Metabolic: Diabetic ketoacidosis

- Skin: Profuse sweating

- t#8729; muscle mass: Severe malnutrition

b. Transcellular redistribution**

- Alkalosis/rapid correction of metabolic acidosis

c. Others: Familial hypokalemic periodic paralysis

*Urinary K⁺ lt;15 mEq/L indicate extra-renal loss of potassium.

**In acidosis, K⁺ moves out of the cell. Rapid correction leads to return of K⁺ intracellularly, causing hypokalemia.

1-2 hours, with monitoring every 2-4 hours. Potassium concentration in the infusate should never exceed 60 mEq/L.

Prolonged hypokalemia due to renal diseases or diuretics may be prevented or treated with oral potas­sium chloride (20 mEq/15 ml) given as 2-4 mEq/kg/ day, along with treatment of primary cause.

Hyperkalemia is defined as S. potassium levels gt;5.5 mEq/L. Serum potassium levels of gt;8.5 mEq/L are often fatal.

Causes: Acute renal failure is the commonest cause of hyperkalemia in children, apart from other causes given in Table 7.8.

Pathophysiology: High ECF potassium in hyperkalemia resists further efflux of potassium from the cells during depolarization, leading to slow membrane depolarization.

Clinically, these cases present with signs of neuro­muscular irritability, as follows:

• Neurological signs, e.g. muscular weakness, paresthesia, tetany, etc.

• Cardiac signs, e.g.

• Characteristic ECG changes in hyperkalemia may precede clinical features and often correlate with serum potassium levels, including: (a) peaked 'tented' T waves, (b) prolonged PR interval, (c) wide QRS complexes, and (d) flat or absent p waves in severe cases.

Treatment of hyperkalemia is an emergency in cases with serum levels gt;6.5 mEq/L or presence of ECG changes and must be treated with:

• Discontinuation of all potassium containing fluids and medications;

• IV calcium gluconate 10% (0.5-1 ml/kg) with cardiac monitoring to stabilize myocardial cell membrane and counteract cardiac toxicity of potassium.

• IV insulin infusion (0.3 U/kg) in 1 ml/kg of DW50% over 1 hour to enhance cellular uptake of potassium, co-transported with glucose.

• IV sodium bicarbonate (1-2 mEq/L over 30 min), to create an alkalotic state that facilitates re-entry of potassium into the cells.

• Dialysis in cases of refractory or life-threatening hyperkalemia, e.g. in acute renal failure or tumor-lysis syndrome.

• Prolonged mild/moderate hyperkalemia, e.g. in chronic renal disease/failure, may be treated with ion exchange resins, e.g. kayexalate or sodium polystyrene sulfonate given orally or rectally as 1 gm/kg/dose (Max 15 gm).

7.4