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BASICS

  • Serum potassium <3.5 mEq/L (normal 3.5–5 mEq/L)
  • Severity:
  • Mild: 3.0–3.5 mEq/L
  • Moderate: 2.5–3.0 mEq/L
  • Severe: <2.5 mEq/L

EPIDEMIOLOGY

  • Male = female prevalence
  • Common in >20% hospitalized patients (<3.6 mEq/L)
  • Higher prevalence in alcoholism, diuretic use, CKD, eating disorders, AIDS
  • Risk increased post bariatric surgery

ETIOLOGY AND PATHOPHYSIOLOGY

  • Decreased intake: poor diet (alcoholics, elderly), anorexia nervosa
  • GI losses: vomiting, diarrhea, laxative abuse, fistulas, bowel diversion, malabsorption
  • Intracellular shift: metabolic alkalosis, insulin excess, Ξ²2-agonists, hypokalemic periodic paralysis, toxins, refeeding syndrome, exercise
  • Renal potassium loss:
  • Drugs: loop and thiazide diuretics, amphotericin B, aminoglycosides, penicillins, clay
  • Mineralocorticoid excess (primary hyperaldosteronism, secondary causes, exogenous mineralocorticoids)
  • Osmotic diuresis (e.g., uncontrolled diabetes)
  • Renal tubular acidosis types I & II
  • Magnesium depletion
  • Glucocorticoid excess (Cushing syndrome, exogenous steroids, ectopic ACTH)
  • DKA treatment with inadequate potassium replacement
  • Genetic syndromes:
  • 11-Ξ²-hydroxysteroid dehydrogenase deficiency
  • Apparent mineralocorticoid excess
  • Congenital adrenal syndromes
  • Familial hypokalemic periodic paralysis
  • Bartter, Gitelman, Liddle syndromes

RISK FACTORS

  • Higher systolic BP
  • Diuretic use (thiazide, loop), ACE inhibitors
  • Low cholesterol, low BMI
  • Higher albumin-to-creatinine ratio

PREVENTION

  • Monitor potassium levels when starting diuretics
  • Address underlying causes and medication review

COMMON ASSOCIATED CONDITIONS

  • Acute GI illnesses with vomiting/diarrhea
  • Cardiac arrhythmias
  • Predictor of severe alcohol withdrawal syndrome

DIAGNOSIS

History

  • Diuretic use, malnutrition, GI losses
  • Symptoms: fatigue, cramps, muscle weakness
  • Polyuria, polydipsia, nocturia, heart failure symptoms

Physical Exam

  • Skeletal muscle weakness (proximal > distal)
  • GI hypomotility
  • Respiratory muscle weakness (risk respiratory failure)
  • Cardiovascular signs: hypotension, arrhythmias
  • Renal manifestations

Differential Diagnosis

  • Mainly lab diagnosis, exclude lab errors (e.g., leukocytosis)

Diagnostic Tests

  • Serum potassium <3.5 mEq/L
  • ECG: T wave flattening, U waves, arrhythmias
  • Urine potassium and chloride to differentiate renal vs nonrenal loss
  • Basic metabolic panel with Mg, Ca, phosphate
  • ABG for acid-base status
  • Serum digoxin level if relevant
  • Creatine kinase for rhabdomyolysis
  • Drug screens if suspicion

Interpretation

  • Urine potassium >15 mEq/day or spot urine K/Cr ratio >13 mEq/g suggests renal loss
  • TTKG >4 suggests renal potassium wasting
  • Metabolic acidosis with low urine K β†’ GI loss
  • Metabolic alkalosis with urine K wasting β†’ primary aldosteronism, diuretics, genetic syndromes

TREATMENT

General Measures

  • Correct underlying cause
  • Stop laxatives, use K-neutral or K-sparing diuretics
  • Treat diarrhea, vomiting
  • H2 blockers for nasogastric suction patients
  • Control hyperglycemia if present

Medication

  • Oral potassium preferred for stable patients (40–120 mEq/day in divided doses)
  • Hydration with water to reduce GI irritation
  • IV potassium for inability to tolerate oral or severe cases; max 10 mEq/hr peripheral, central line preferred >10 mEq/hr
  • Potassium chloride is preferred salt form
  • Magnesium replacement if hypomagnesemia present

Precautions

  • Monitor serum K closely to avoid hyperkalemia
  • More frequent checks in elderly, diabetics, renal failure patients
  • Insulin therapy in DKA requires aggressive potassium replacement

GERIATRIC CONSIDERATIONS

  • Elderly develop hypokalemia rapidly
  • Risk of paralysis, myonecrosis, falls

ISSUES FOR REFERRAL

  • Unexplained hypokalemia
  • Suspected aldosteronism or periodic paralysis
  • Refractory hypokalemia

ADMISSION CONSIDERATIONS

  • Cardiac manifestations or respiratory failure require inpatient care with cardiac monitoring
  • ICU care for life-threatening complications

ONGOING CARE

  • Monitor potassium and magnesium frequently during replacement
  • Adjust therapy based on clinical status and compliance

DIET

  • Increase potassium-rich foods: bananas, oranges, cantaloupe, prunes, dried fruits, beans, squash
  • Reduce sodium intake to minimize urinary potassium loss

PATIENT EDUCATION

  • Importance of adherence to supplements and diet
  • Awareness of symptoms and when to seek care

PROGNOSIS

  • Usually corrects in 24–72 hours after replacement
  • Resolves with treatment of primary cause
  • Associated with increased morbidity/mortality if cardiac arrhythmias occur

COMPLICATIONS

  • Hyperkalemia from overcorrection
  • Digoxin toxicity potentiation
  • Arrhythmias due to altered cardiac cell excitability

REFERENCES

  1. Palmer BF. A physiologic-based approach to the evaluation of a patient with hypokalemia. Am J Kidney Dis. 2010;56(6):1184-1190.
  2. Kardalas E, Paschou SA, Anagnostis P, et al. Hypokalemia: a clinical update. Endocr Connect. 2018;7(4):R135-R146.
  3. Asmar A, Mohandas R, Wingo CS. A physiologic-based approach to the treatment of a patient with hypokalemia. Am J Kidney Dis. 2012;60(3):492-497.
  4. Kovesdy CP, Matsushita K, Sang Y, et al. Serum potassium and adverse outcomes across the range of kidney function: a CKD Prognosis Consortium meta-analysis. Eur Heart J. 2018;39(17):1535-1542.
  5. Unwin RJ, Luft FC, Shirley DG. Pathophysiology and management of hypokalemia: a clinical perspective. Nat Rev Nephrol. 2011;7(2):75-84.

Clinical Pearls

  • Even mild to moderate hypokalemia in cardiac patients increases arrhythmia risk; repletion and monitoring critical.
  • Correct hypomagnesemia to effectively treat hypokalemia.
  • Young women with unexplained hypokalemia should be evaluated for bulimia nervosa.
  • Supplement potassium when prescribing diuretics; minimize dose of non-potassium-sparing diuretics.