Definition (Pediatr Rev 2004;25:350; Pediatr Rev 2011;32:240)
• Processes resulting in net loss of H+ or gain of HCO3−; alkalemia is a serum pH >7.44
Pathophysiology (Pediatr Rev 2004;25:350; Pediatr Rev 2011;32:240)
• Gain of HCO3− can be 2/2 ↑ intake, ↓ renal excretion, or volume contraction around stable amount of bicarbonate
• Healthy kidneys can excrete a large load of bicarbonate rapidly, so to maintain a metabolic alkalosis renal bicarbonate excretion must be impaired
• Renal bicarbonate excretion is impaired when prox tubule bicarb reabsorp is inc 2/2, dec effective circ volume and chloride depletion (results in 2° hyperaldo, dec tubular Cl− inhibiting Cl−/HCO3− exchanger), [K+] depletion (creates intracellular acidosis, stimulates H+/Na+ exchanger), or posthypercapnia adaptation
Clinical Manifestations (Pediatr Rev 1996;17:395; Pediatr Rev 2011;32:240)
• Can present w/ lethargy, confusion, and eventually seizures
• Can see tissue hypoxia, CNS effects, and muscular irritability
• Body compensates w/ respiratory acidosis and some w/ dec respiratory excursion
Etiologies (Pediatr Rev 2004;25:350; Pediatr Rev 2011;32:240)
• Can be divided into chloride responsive and chloride-unresponsive etiologies
• Chloride responsive (urinary Cl− <10 mEq/L)
• GI (emesis [pyloric stenosis], diarrhea, laxative abuse, villous adenoma, NGT suction)
• Diuretics (loop and thiazide), PCN, CF, posthypercapnic
• Chloride unresponsive (urinary Cl− >10 mEq/L)
• Adrenal dysfunction (hyperaldosteronism or Cushing syndrome)
• Exogenous steroids (glucocorticoids, mineralocorticoids, and licorice)
• Inherited channelopathies (Bartter syndrome and Gitelman syndrome)
• Alkali ingestion, large volume blood transfusions (due to citrate in blood)
• Edematous states Rx’d w/ diuretics (e.g., CHF, cirrhosis, nephrotic syndrome)
• Refeeding alkalosis
• Hypokalemia
Management (Rose & Post. Clinical Physiology of Acid-Base & Electrolyte Disorders 2001:551; Pediatr Rev 2011;32:240)
• Rx underlying condition and correct met alkalosis by renal secretion of HCO3−
• For saline responsive etiologies, provide IV saline (monitor efficacy via urine pH [which is <5 before therapy and rises to >7 w/ repletion] and UCl [which rises above 10mEq/L with tx]) and replete K as needed
• For saline unresponsive etiologies
• If edematous state (CHF, cirrhosis, nephrotic syndrome): Withhold diuretic if possible, acetazolamide, HCl, Arginine Chloride or dialysis
• Hypokalemia: Replete K
• Hyperaldosteronism: K-sparing diuretics/aldo antagonists or removal of parathyroid adenoma
Complications (Pediatr Rev 2004;25:350; Pediatr Rev 2011;32:240)
• Cardiac: Arteriolar constriction, refractory SVT, and ventricular arrhythmias
• Cerebral: Reduction of cerebral blood flow, tetany, seizures, lethargy, stupor
• Respiratory: Hypoventilation w/ hypercapnia and hypoxia
• Metabolic: HypoK, hypoMg and hypoPhos, stimulation of glycolysis, oxyhemoglobin dissociation curve shifts left