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Emergency And Acute Medicine: Hypokalemia
Basics
Description
Hypokalemia is defined as a serum potassium <3.5 meq />. Mild 3–3.5 mEq/L, moderate 2.5–3 mEq/L, severe <2.5 meq />. Occurs in up to 20% of inpatients and 14% of outpatients, commonly from diuretics or GI losses. Potassium is the major intracellular cation (98% intracellular) maintained by Na–K ATPase, insulin, β-agonists, and mineralocorticoids. Hypokalemia increases the intracellular–extracellular potassium gradient, alters depolarization thresholds, prolongs action potentials, and disrupts cellular function.
Etiology
Renal losses Diuretics, renal tubular disorders (RTA I and II), interstitial nephritis, drug toxicity (amphotericin, cisplatin), myeloma kidney, hyperaldosteronism (primary, secondary, exogenous), hypomagnesemia, osmotic diuresis, Bartter and Gitelman syndromes, Liddle syndrome, delivery of nonreabsorbable anions (bicarbonate, ketones, hippurate, penicillins).
GI losses Diarrhea, villous adenomas, laxative abuse, vomiting or NG suction, ureterosigmoidostomy, intestinal fistulae, ileostomy, cystic fibrosis.
Intracellular shift Alkalosis, insulin administration or refeeding, adrenergic excess (stress, β-agonists, theophylline), stimulants, hypokalemic periodic paralysis (familial or thyrotoxic), hypothermia.
Poor intake Rare alone; seen with malnutrition, eating disorders, dementia, or esophageal disease.
Diagnosis
Signs And Symptoms Neuromuscular weakness beginning in lower extremities and progressing proximally, paralysis with rapid severe hypokalemia, muscle cramps, tetany, rhabdomyolysis, paresthesias, fatigue. GI ileus and constipation. Cardiac dysrhythmias including PACs, PVCs, AV block, atrial or junctional tachycardias, VT/VF, and potentiation of digoxin toxicity. Renal concentrating defect causing polyuria and polydipsia.
Physical Exam Hypertension suggests mineralocorticoid excess or renal artery stenosis. Hypotension suggests GI loss or diuretics. Decreased reflexes and muscle tenderness may be present.
Diagnosis Tests And Interpretation
Lab Electrolytes, BUN, creatinine, glucose. Elevated bicarbonate suggests diuretics, vomiting, or mineralocorticoid excess; low bicarbonate suggests RTA or diarrhea. Urine potassium <20 meq /> suggests nonrenal loss or intracellular shift; >20 mEq/L suggests renal loss. Urine potassium–creatinine ratio <13 meq /> favors nonrenal loss; >13 mEq/g favors renal loss. Urine sodium <20 meq /> with high urine potassium suggests secondary hyperaldosteronism. Plasma renin differentiates primary vs secondary hyperaldosteronism. Check TSH and free T4 if indicated.
ECG Flattened T waves, ST depression, prominent U waves mimicking QT prolongation, small P waves, atrial and ventricular dysrhythmias.
Differential Diagnosis Primary cardiac disease, neuromuscular junction disorders, spinal cord disease, polyneuropathies, acute myopathies, cataplexy.
Treatment
Initial Stabilization/Therapy ABCs, IV access, cardiac monitoring.
Emergency Department Treatment/Procedures Replace potassium based on severity, symptoms, and comorbidities. Oral replacement preferred when possible. Identify and stop ongoing losses, treat vomiting or diarrhea, avoid glucose-containing fluids, and correct volume depletion and hypochloremia.
Medications
Oral potassium chloride Preferred. Mild to moderate: 10–20 mEq q6–12h. Moderate to severe: 40–60 mEq q8–12h.
Oral potassium citrate or gluconate Use in acidosis; less effective in alkalosis.
IV potassium chloride Indicated for severe hypokalemia, dysrhythmias, paralysis, or ongoing losses. Typical rate 10 mEq/h via peripheral line; higher rates require central access and close monitoring. Avoid dextrose solutions.
Adjuncts Magnesium sulfate 2 g IV if hypomagnesemia present. Correct volume and chloride deficits with normal saline.
Follow-Up And Disposition
Admission Criteria Need for IV potassium, dysrhythmias, profound weakness, ongoing losses, K <2.5 meq />, significant hypotension or hypertension, major comorbidities.
Discharge Criteria Asymptomatic, able to take oral potassium, reliable follow-up. Recheck electrolytes in 2–3 days.
Follow-Up Recommendations Continue replacement until potassium remains ≥3–3.5 mEq/L. Refer to nephrology if renal wasting suspected.
Pearls And Pitfalls
Correct hypokalemia before treating acidosis to prevent dangerous intracellular shifts. Avoid glucose during replacement. Check and correct magnesium if hypokalemia is refractory. Small potassium doses are sufficient in periodic paralysis or adrenergic states; excessive replacement risks rebound hyperkalemia.
Basics
Description
Hypokalemia is defined as a serum potassium <3.5 meq />. Mild 3–3.5 mEq/L, moderate 2.5–3 mEq/L, severe <2.5 meq />. Occurs in up to 20% of inpatients and 14% of outpatients, commonly from diuretics or GI losses. Potassium is the major intracellular cation (98% intracellular) maintained by Na–K ATPase, insulin, β-agonists, and mineralocorticoids. Hypokalemia increases the intracellular–extracellular potassium gradient, alters depolarization thresholds, prolongs action potentials, and disrupts cellular function.
Etiology
Renal losses Diuretics, renal tubular disorders (RTA I and II), interstitial nephritis, drug toxicity (amphotericin, cisplatin), myeloma kidney, hyperaldosteronism (primary, secondary, exogenous), hypomagnesemia, osmotic diuresis, Bartter and Gitelman syndromes, Liddle syndrome, delivery of nonreabsorbable anions (bicarbonate, ketones, hippurate, penicillins).
GI losses Diarrhea, villous adenomas, laxative abuse, vomiting or NG suction, ureterosigmoidostomy, intestinal fistulae, ileostomy, cystic fibrosis.
Intracellular shift Alkalosis, insulin administration or refeeding, adrenergic excess (stress, β-agonists, theophylline), stimulants, hypokalemic periodic paralysis (familial or thyrotoxic), hypothermia.
Poor intake Rare alone; seen with malnutrition, eating disorders, dementia, or esophageal disease.
Diagnosis
Signs And Symptoms Neuromuscular weakness beginning in lower extremities and progressing proximally, paralysis with rapid severe hypokalemia, muscle cramps, tetany, rhabdomyolysis, paresthesias, fatigue. GI ileus and constipation. Cardiac dysrhythmias including PACs, PVCs, AV block, atrial or junctional tachycardias, VT/VF, and potentiation of digoxin toxicity. Renal concentrating defect causing polyuria and polydipsia.
Physical Exam Hypertension suggests mineralocorticoid excess or renal artery stenosis. Hypotension suggests GI loss or diuretics. Decreased reflexes and muscle tenderness may be present.
Diagnosis Tests And Interpretation
Lab Electrolytes, BUN, creatinine, glucose. Elevated bicarbonate suggests diuretics, vomiting, or mineralocorticoid excess; low bicarbonate suggests RTA or diarrhea. Urine potassium <20 meq /> suggests nonrenal loss or intracellular shift; >20 mEq/L suggests renal loss. Urine potassium–creatinine ratio <13 meq /> favors nonrenal loss; >13 mEq/g favors renal loss. Urine sodium <20 meq /> with high urine potassium suggests secondary hyperaldosteronism. Plasma renin differentiates primary vs secondary hyperaldosteronism. Check TSH and free T4 if indicated.
ECG Flattened T waves, ST depression, prominent U waves mimicking QT prolongation, small P waves, atrial and ventricular dysrhythmias.
Differential Diagnosis Primary cardiac disease, neuromuscular junction disorders, spinal cord disease, polyneuropathies, acute myopathies, cataplexy.
Treatment
Initial Stabilization/Therapy ABCs, IV access, cardiac monitoring.
Emergency Department Treatment/Procedures Replace potassium based on severity, symptoms, and comorbidities. Oral replacement preferred when possible. Identify and stop ongoing losses, treat vomiting or diarrhea, avoid glucose-containing fluids, and correct volume depletion and hypochloremia.
Medications
Oral potassium chloride Preferred. Mild to moderate: 10–20 mEq q6–12h. Moderate to severe: 40–60 mEq q8–12h.
Oral potassium citrate or gluconate Use in acidosis; less effective in alkalosis.
IV potassium chloride Indicated for severe hypokalemia, dysrhythmias, paralysis, or ongoing losses. Typical rate 10 mEq/h via peripheral line; higher rates require central access and close monitoring. Avoid dextrose solutions.
Adjuncts Magnesium sulfate 2 g IV if hypomagnesemia present. Correct volume and chloride deficits with normal saline.
Follow-Up And Disposition
Admission Criteria Need for IV potassium, dysrhythmias, profound weakness, ongoing losses, K <2.5 meq />, significant hypotension or hypertension, major comorbidities.
Discharge Criteria Asymptomatic, able to take oral potassium, reliable follow-up. Recheck electrolytes in 2–3 days.
Follow-Up Recommendations Continue replacement until potassium remains ≥3–3.5 mEq/L. Refer to nephrology if renal wasting suspected.
Pearls And Pitfalls
Correct hypokalemia before treating acidosis to prevent dangerous intracellular shifts. Avoid glucose during replacement. Check and correct magnesium if hypokalemia is refractory. Small potassium doses are sufficient in periodic paralysis or adrenergic states; excessive replacement risks rebound hyperkalemia.
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