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Emergency And Acute Medicine-Hyperkalemia
Basics
Description Potassium is primarily intracellular, with approximately 98% inside cells and 2% in the extracellular space. Normal serum potassium ranges from 3.5 to 5.0 mmol/L. Potassium excretion occurs mainly through the kidneys (≈90%) and to a lesser extent through the gastrointestinal tract (≈10%). Renal and extrarenal mechanisms regulate serum potassium via dietary intake, distal tubular function, acid–base balance, mineralocorticoids, insulin, catecholamines, osmolarity, and medications.
Etiology Decreased potassium excretion is the most common cause and is typically due to acute or chronic renal failure. Other causes include distal tubular disorders (acute interstitial nephritis, renal transplant rejection, sickle cell nephropathy, type IV renal tubular acidosis), mineralocorticoid deficiency (Addison disease, hypoaldosteronism), and medications such as ACE inhibitors, ARBs, beta-blockers, potassium-sparing diuretics, NSAIDs, cyclosporine, trimethoprim, and lithium. Intracellular to extracellular shifts occur with metabolic acidosis, hyperosmolar states, insulin deficiency, cell necrosis, rhabdomyolysis, hemolysis, chemotherapy, digitalis toxicity, succinylcholine, beta-blockers, alpha-agonists, and hyperkalemic periodic paralysis. Excess potassium load may result from trauma, tumor lysis, salt substitutes, oral potassium, potassium-containing antibiotics, or rapid transfusion of stored blood. Pseudohyperkalemia results from hemolysis during blood draw, thrombocytosis, extreme leukocytosis, or prolonged tourniquet use.
Diagnosis
Signs and symptoms Hyperkalemia is frequently asymptomatic, even at high levels. Neuromuscular manifestations include weakness that may progress to paralysis and dyspnea due to respiratory muscle involvement. Cardiac dysrhythmias may be the first presentation, with symptoms such as chest pain, palpitations, or syncope.
Physical exam Findings may include muscle weakness, paralysis in severe cases, and evidence of cardiac dysrhythmias.
Essential workup Serum potassium >5.0 mmol/L confirms hyperkalemia. Use a heparinized tube if pseudohyperkalemia is suspected.
Diagnosis tests and interpretation
Laboratory Obtain electrolytes, BUN, creatinine, and glucose. Renal failure typically shows elevated BUN and creatinine. Mineralocorticoid deficiency may present with hyponatremia. Type IV renal tubular acidosis causes mild metabolic acidosis. Arterial blood gases assess acid–base status. Creatine kinase should be checked if rhabdomyolysis is suspected. In patients with hyperkalemia and normal renal function, calculate the transtubular potassium gradient (TTKG); values >8 suggest extrarenal causes, while <6 indicate impaired renal excretion.
ECG Findings correlate imperfectly with potassium levels. Early changes include peaked T waves and shortened QT interval (5–6.5 mmol/L). Moderate elevations (6.5–8 mmol/L) may cause PR prolongation, loss of P waves, and QRS widening. Severe hyperkalemia (>8 mmol/L) can result in intraventricular blocks, bundle branch blocks, sine-wave patterns, and ventricular arrest. ECG may be normal despite life-threatening hyperkalemia.
Differential diagnosis Pseudohyperkalemia.
Treatment
Prehospital Treat suspected hyperkalemia-related dysrhythmias differently from standard ACLS. Administer inhaled beta-agonists, consider sodium bicarbonate in metabolic acidosis, and give calcium when hyperkalemia is suspected in unstable patients.
Initial stabilization/therapy Ensure airway, breathing, and circulation. Establish IV access and initiate continuous cardiac monitoring.
Emergency department management With ECG changes or instability, immediately antagonize cardiac membrane effects using calcium gluconate (awake patient) or calcium chloride (cardiac arrest). To shift potassium intracellularly, administer insulin with glucose, inhaled albuterol, and sodium bicarbonate (especially if acidotic). To remove potassium, restrict exogenous potassium, discontinue contributing medications, use loop diuretics if renal function permits, administer cation exchange resins for non-emergent cases, and initiate hemodialysis in renal failure. Special situations include urgent dialysis in renal failure, cautious calcium use in digoxin toxicity, and hydrocortisone for mineralocorticoid deficiency.
Medication Calcium gluconate 10% 10 mL IV over 2–5 min or calcium chloride 10% 10 mL IV; regular insulin 10 U IV with 50 mL D50W; albuterol 10–20 mg nebulized; sodium bicarbonate 44–132 mEq IV; furosemide 40–80 mg IV; sodium or calcium polystyrene sulfonate PO or PR; hydrocortisone 100 mg IV when indicated.
Follow-up and disposition
Admission criteria Most patients require admission due to delayed potassium redistribution and ongoing risk of rebound hyperkalemia.
Discharge criteria Mild hyperkalemia (<5.5 mmol/L) with clear reversible cause, demonstrated response to therapy, no anticipated rebound, and reliable early follow-up.
Issues for referral Address the underlying cause, commonly chronic kidney disease requiring nephrology follow-up and possible dialysis.
Follow-up recommendations Close monitoring and access to dialysis are essential for discharged patients.
Key points Clinical and ECG effects are more important than the absolute potassium value. Do not delay treatment when ECG changes indicate a hyperkalemic emergency. Hyperkalemia is often silent until severe—obtain an ECG early in at-risk patients. Use sodium bicarbonate cautiously to avoid volume overload.
Basics
Description Potassium is primarily intracellular, with approximately 98% inside cells and 2% in the extracellular space. Normal serum potassium ranges from 3.5 to 5.0 mmol/L. Potassium excretion occurs mainly through the kidneys (≈90%) and to a lesser extent through the gastrointestinal tract (≈10%). Renal and extrarenal mechanisms regulate serum potassium via dietary intake, distal tubular function, acid–base balance, mineralocorticoids, insulin, catecholamines, osmolarity, and medications.
Etiology Decreased potassium excretion is the most common cause and is typically due to acute or chronic renal failure. Other causes include distal tubular disorders (acute interstitial nephritis, renal transplant rejection, sickle cell nephropathy, type IV renal tubular acidosis), mineralocorticoid deficiency (Addison disease, hypoaldosteronism), and medications such as ACE inhibitors, ARBs, beta-blockers, potassium-sparing diuretics, NSAIDs, cyclosporine, trimethoprim, and lithium. Intracellular to extracellular shifts occur with metabolic acidosis, hyperosmolar states, insulin deficiency, cell necrosis, rhabdomyolysis, hemolysis, chemotherapy, digitalis toxicity, succinylcholine, beta-blockers, alpha-agonists, and hyperkalemic periodic paralysis. Excess potassium load may result from trauma, tumor lysis, salt substitutes, oral potassium, potassium-containing antibiotics, or rapid transfusion of stored blood. Pseudohyperkalemia results from hemolysis during blood draw, thrombocytosis, extreme leukocytosis, or prolonged tourniquet use.
Diagnosis
Signs and symptoms Hyperkalemia is frequently asymptomatic, even at high levels. Neuromuscular manifestations include weakness that may progress to paralysis and dyspnea due to respiratory muscle involvement. Cardiac dysrhythmias may be the first presentation, with symptoms such as chest pain, palpitations, or syncope.
Physical exam Findings may include muscle weakness, paralysis in severe cases, and evidence of cardiac dysrhythmias.
Essential workup Serum potassium >5.0 mmol/L confirms hyperkalemia. Use a heparinized tube if pseudohyperkalemia is suspected.
Diagnosis tests and interpretation
Laboratory Obtain electrolytes, BUN, creatinine, and glucose. Renal failure typically shows elevated BUN and creatinine. Mineralocorticoid deficiency may present with hyponatremia. Type IV renal tubular acidosis causes mild metabolic acidosis. Arterial blood gases assess acid–base status. Creatine kinase should be checked if rhabdomyolysis is suspected. In patients with hyperkalemia and normal renal function, calculate the transtubular potassium gradient (TTKG); values >8 suggest extrarenal causes, while <6 indicate impaired renal excretion.
ECG Findings correlate imperfectly with potassium levels. Early changes include peaked T waves and shortened QT interval (5–6.5 mmol/L). Moderate elevations (6.5–8 mmol/L) may cause PR prolongation, loss of P waves, and QRS widening. Severe hyperkalemia (>8 mmol/L) can result in intraventricular blocks, bundle branch blocks, sine-wave patterns, and ventricular arrest. ECG may be normal despite life-threatening hyperkalemia.
Differential diagnosis Pseudohyperkalemia.
Treatment
Prehospital Treat suspected hyperkalemia-related dysrhythmias differently from standard ACLS. Administer inhaled beta-agonists, consider sodium bicarbonate in metabolic acidosis, and give calcium when hyperkalemia is suspected in unstable patients.
Initial stabilization/therapy Ensure airway, breathing, and circulation. Establish IV access and initiate continuous cardiac monitoring.
Emergency department management With ECG changes or instability, immediately antagonize cardiac membrane effects using calcium gluconate (awake patient) or calcium chloride (cardiac arrest). To shift potassium intracellularly, administer insulin with glucose, inhaled albuterol, and sodium bicarbonate (especially if acidotic). To remove potassium, restrict exogenous potassium, discontinue contributing medications, use loop diuretics if renal function permits, administer cation exchange resins for non-emergent cases, and initiate hemodialysis in renal failure. Special situations include urgent dialysis in renal failure, cautious calcium use in digoxin toxicity, and hydrocortisone for mineralocorticoid deficiency.
Medication Calcium gluconate 10% 10 mL IV over 2–5 min or calcium chloride 10% 10 mL IV; regular insulin 10 U IV with 50 mL D50W; albuterol 10–20 mg nebulized; sodium bicarbonate 44–132 mEq IV; furosemide 40–80 mg IV; sodium or calcium polystyrene sulfonate PO or PR; hydrocortisone 100 mg IV when indicated.
Follow-up and disposition
Admission criteria Most patients require admission due to delayed potassium redistribution and ongoing risk of rebound hyperkalemia.
Discharge criteria Mild hyperkalemia (<5.5 mmol/L) with clear reversible cause, demonstrated response to therapy, no anticipated rebound, and reliable early follow-up.
Issues for referral Address the underlying cause, commonly chronic kidney disease requiring nephrology follow-up and possible dialysis.
Follow-up recommendations Close monitoring and access to dialysis are essential for discharged patients.
Key points Clinical and ECG effects are more important than the absolute potassium value. Do not delay treatment when ECG changes indicate a hyperkalemic emergency. Hyperkalemia is often silent until severe—obtain an ECG early in at-risk patients. Use sodium bicarbonate cautiously to avoid volume overload.
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