Ver el código de «Hyperkalemia»

==Background==
*Serum potassium >5.0 mEq/L (some define >5.5 mEq/L)
*'''Life-threatening when >6.5 mEq/L''' or with ECG changes
*Most common electrolyte disorder causing [[cardiac arrest]]
*Potassium homeostasis:
**98% intracellular (maintained by Na/K-ATPase)
**Renal excretion is primary mechanism of potassium regulation

===Causes===
*Decreased excretion (most common mechanism):
**[[Acute kidney injury]] / [[chronic kidney disease]]
**Medications: ACE inhibitors, ARBs, K-sparing diuretics (spironolactone, amiloride), NSAIDs, trimethoprim, heparin
**[[Adrenal insufficiency]] (hypoaldosteronism)
**Type 4 renal tubular acidosis
*Transcellular shift (K moves out of cells):
**Acidosis (metabolic acidosis shifts K extracellularly)
**Insulin deficiency / [[DKA]]
**Tissue destruction: [[rhabdomyolysis]], tumor lysis, hemolysis, burns
**Succinylcholine, beta-blockers, digitalis toxicity
**Hyperkalemic periodic paralysis
*Increased intake: excessive supplementation, salt substitutes (KCl)
*Pseudohyperkalemia: hemolyzed sample, prolonged tourniquet, thrombocytosis, leukocytosis
**Always repeat level if unexpected

==Clinical Features==
*Often asymptomatic until severe
*Muscle weakness, fatigue, paresthesias
*Ascending paralysis (may mimic [[Guillain-Barre]])
*'''Cardiac dysrhythmias''' (most dangerous manifestation)
*Nausea, vomiting, diarrhea

===ECG Changes (Progressive)===
*Peaked T waves (earliest change, typically >5.5 mEq/L)<ref>Montague BT, et al. Retrospective review of the frequency of ECG changes in hyperkalemia. Clin J Am Soc Nephrol. 2008;3(2):324-330. PMID 18235147</ref>
*Prolonged PR interval
*Widened QRS
*Loss of P waves
*Sine wave pattern (pre-arrest)
*Ventricular fibrillation / asystole
*'''ECG changes do NOT reliably correlate with K level''' — some patients arrest without warning

==Differential Diagnosis==
*Pseudohyperkalemia (hemolyzed specimen)
*[[Acute kidney injury]] / [[chronic kidney disease]]
*[[DKA]]
*[[Rhabdomyolysis]]
*Tumor lysis syndrome
*[[Adrenal insufficiency]]
*Medication effect

==Evaluation==
*'''Stat ECG''' (most urgent — look for peaked T's, widened QRS)
*BMP: potassium level, creatinine (renal function), glucose, bicarbonate
*Repeat K level if unexpected (rule out pseudohyperkalemia)
*VBG/ABG (acidosis evaluation)
*Digoxin level if on digoxin (hyperkalemia potentiates digitalis toxicity)
*Urinalysis (myoglobinuria if rhabdomyolysis)
*Consider: CK, uric acid, phosphorus (tumor lysis), cortisol (adrenal insufficiency)

==Management==
===Step 1: Cardiac Membrane Stabilization===
*Calcium (does NOT lower K; protects myocardium from arrhythmia):
**Calcium gluconate 10%: 10-20 mL IV over 2-3 minutes (preferred; less tissue necrosis if extravasates)
**Calcium chloride 10%: 5-10 mL IV (via central line preferred; 3x more elemental calcium)
**Onset: 1-3 minutes; duration 30-60 minutes; may repeat in 5-10 min if ECG unchanged
**'''Give immediately if ECG changes present or K >6.5'''
*Caution in [[digoxin toxicity]]: calcium may worsen toxicity → use cautiously or consider digibind first

===Step 2: Shift Potassium Intracellularly===
*Insulin + Glucose (most reliable):<ref>Mahoney BA, et al. Emergency interventions for hyperkalaemia. Cochrane Database Syst Rev. 2005;(2):CD003235. PMID 15846652</ref>
**Regular insulin 10 units IV + D50W 25g (50 mL) IV
**Onset: 15-30 min; duration 4-6 hours; lowers K by 0.5-1.2 mEq/L
**Monitor glucose q30min x 4h (hypoglycemia occurs in up to 20%)
**Give D50 before or simultaneously with insulin
*Albuterol (nebulized):
**10-20 mg nebulized (4-8x standard asthma dose)
**Onset: 15-30 min; lowers K by 0.5-1.5 mEq/L
**Additive with insulin; 40% of patients are non-responders
*Sodium bicarbonate:
**50-100 mEq IV over 5-10 minutes
**Minimal effect as monotherapy; useful in setting of severe metabolic acidosis
**'''Do NOT rely on bicarb alone''' to lower potassium

===Step 3: Remove Potassium from Body===
*Loop diuretics (furosemide 40-80 mg IV): if adequate renal function
*Sodium polystyrene sulfonate (Kayexalate) 15-30g PO:
**Delayed onset (hours); controversial efficacy; risk of bowel necrosis
**Not recommended as acute treatment
*Patiromer (Veltassa) or sodium zirconium cyclosilicate (Lokelma):
**Newer potassium binders; better tolerated than Kayexalate
**Lokelma 10g PO may lower K within 1 hour
*Hemodialysis (most effective method of K removal):
**Indicated for: refractory hyperkalemia, severe renal failure, K >7 despite medical therapy

===Cardiac Arrest from Hyperkalemia===
*Standard ACLS + calcium 10-20 mL IV push
*Insulin + glucose + bicarb + albuterol simultaneously
*Avoid succinylcholine for intubation
*Consider emergent dialysis

==Disposition==
*Admit if K >6.0, ECG changes, renal failure, or ongoing cause
*ICU if severe (>7.0), ECG changes, or refractory to treatment
*Continuous telemetry for all admitted patients
*Consider discharge if mild hyperkalemia (5.0-5.5), known chronic cause, normal ECG, correctable precipitant

==See Also==
*[[Hypokalemia]]
*[[Acute kidney injury]]
*[[Diabetic ketoacidosis]]
*[[Rhabdomyolysis]]
*[[Cardiac arrest]]
*[[Digoxin toxicity]]

==References==
*Palmer BF. Managing hyperkalemia caused by inhibitors of the renin-angiotensin-aldosterone system. ''N Engl J Med''. 2004;351(6):585-592. PMID 15295051
*Weisberg LS. Management of severe hyperkalemia. ''Crit Care Med''. 2008;36(12):3246-3251. PMID 18936701
*Montford JR, Linas S. How dangerous is hyperkalemia? ''J Am Soc Nephrol''. 2017;28(11):3155-3165. PMID 28778861
*Long B, et al. An emergency medicine approach to hyperkalemia. ''Am J Emerg Med''. 2018;36(5):918-921. PMID 29548654

[[Category:Renal]]
[[Category:Critical Care]]