Definition (Pediatr Rev 1996;17:395)
• Serum K <3 mEq/L; common finding in hospitalized children and not usually further evaluated, just repleted; if assoc with sx or if persists, warrants further eval
Pathophysiology (Pediatr Clin North Am 1990;37:419)
• Majority of body K intracellular; 1° ion responsible for cell’s net negative charge
• Acute changes in K do not reflect body stores; but chronic changes do
• As such, hypokalemia presents with nerve and muscle dysfunction.
• [K+] can be lost from the body through renal or GI secretion or can be shuttled in and out of cells mediated by certain hormones or in exchange for H+
Etiologies (Pediatr Clin North Am 1990;37:419; Rose & Post. Clinical Physiology of Acid-Base & Electrolyte Disorders 2001:836; Pediatr Rev 2008;29:e50)
• ↑ renal excretion 2/2 primary tubulopathies (Bartter, Gitelman, Liddle, Fanconi, distal Type 1 RTA, proximal type 2 RTA), drugs (diuretics, cisplatin, amphotericin B), mineralocorticoid excess (Hyperaldosteronism, Cushing’s, exogenous mineralocorticoid, high renin state (RAS), CAH due to 17α-hydroxylase or 11β-hydroxylase deficiency)
• Diuretic use or w/ excretion of non-resorbable anions, which pull K w/ them in distal tube (i.e., bicarb, seen in alkalosis) & w/ hypomagnesaemia
• Bartter: Rare p/w hypoK and met alkalosis early (<6 yo); assoc w/ multiple genes; often w/ stunted growth and MR
• Gitelman: Rare p/w hypoK, generally normal Ca, hypoMg, met alkalosis; defect in Na–Cl channel in DT, more benign and incidentally dx’d in early adulthood, often p/w tetany (Q J Med 2010;103:741)
• Liddle: (Rare AD) similar to presentation of 1° hyperaldosteronism; gain of fxn mutation in Na channel at CT, so eval w/ low renin and aldo levels, HTN
• Nonrenal losses: GI losses: Vomiting, diarrhea (consider laxative abuse), NGT suction, fistulas, or ostomies. Rarely 2/2 clay ingestion or profuse sweating
• Shift of extracellular to intracellular fluid can be mediated by hormones (insulin or β2-catecholamines), by alkalosis (0.4 mEq/L per ↑ 0.1 pH), or w/ use of GM-CSF or treatment of megaloblastic anemias w/ B12 (settings of high-cell turn over). Transient hypoK also seen in trauma, concussions (J Trauma 2003;54:197)
• Pseudohypokalemia w/ metabolically active cells (i.e., inc WBC in AML) can consume K following blood draw resulting in spuriously low value)
Clinical Manifestations (Pediatr Rev 1996;17:395)
• Significant symptoms are unlikely unless [K+] <2.5 mEq/L but significant variability
• Neuromuscular: P/w weakness, ↓ reflexes, paralysis, ↓ GI motility, even ileus
• Can be severe enough to result in rhabdomyolysis
• Cardiac: Multi arrhythmias 2/2 ↑ automaticity and prolonged repolarization
• Premature ventricular beats, sinus bradycardia, AV blocks, paroxysmal atrial and junctional tachycardias (prolonged depol sets up for SVT), even VT or VF
• Classic EKG: PR and QRS shortening, T wave flattening, development of U wave
• Renal: W/ loss of renal concentrating ability and decreased responsiveness to ADH p/w polyuria and polydipsia; requires 2–3 wk of K depletion
Diagnostic Studies (Rose & Post.Clinical Physiology of Acid-Base & Electrolyte Disorders 2001:746; Pediatr Rev 2011;32:65)
• Chem 10 (w/ Ca, Mg, Phos), U/A, urine lytes (K, Na, Cl, Osm, Cr), pH, and BP, SOsm
• Spot urine [K+] <15 mEq/L suggests extrarenal losses but less sensitive w/ hypovolemia or w/ polyuria; 24 hr urine [K+] <25 mEq more definitive
• Transtubular potassium gradient (TTKG; can use if UNa > 25 & UOsm > POsm) = (UK)(POsm)/(PK)(UOsm) is typically 8–9 given normal dietary K intake & normal renal fx. TTKG < 3 c/w GI losses or inadequate K intake. HypoK & TTKG > 3 c/w renal loss
• In more complicated cases or w/ significant symptoms can check CK, cortisol, plasma renin activity, aldosterone level, 17-OH ketosteroids, EKG
• Urine [Cl−] useful: UCl <25 mEq/L strongly suggests of vomiting or diuretic effect (even after drug effect passed), if >40 mEq/L should assay urine for diuretic and if neg & pt normotensive, consider Bartter’s or Gitelman’s syndrome
Management (Pediatr Rev 1996;17:395)
• W/ severe sx or EKG Δ’s, IV repletion advised and accomplished with KCl
(0.5–1 mEq/kg IV × 1, repeat as needed). Need CV monitoring and central access if repleted at >0.5 mEq/kg/hr or >10 mEq/hr or with concentration >10 mEq/100mL
• In the asymp pt, oral repletion preferred and choice of K salt depends on etiology
• In metabolic acidosis (i.e., RTA) use K citrate
• In metabolic alkalosis use KCl
• If hypophosphatemic, use K phos
• If chronic K wasting, can require daily repletion for weeks w/ 3–5 mEq/kg qd
• Check and replete Mg, as K repletion is ineffective in the presence of hypoMg