Hyperkalemia
Adult-Gerontology Acute Care Practice Guidelines
Definition
A.Serum potassium concentration of greater than 5.5 mEq/L (see Box 5.3).
Incidence
A.Most common in patients with renal disease (impaired potassium elimination).
Pathogenesis
A.Causes.
1.Redistribution (a net shift of potassium from intracellular to extracellular space).
2.Total body excess (due to increased potassium ingestion or impaired potassium elimination).
BOX 5.3
Potassium in Humans
•Normal serum potassium concentration is 3.5 to 5.5 mEq/L.
○Serum potassium levels represent extracellular potassium.
○The vast majority (~98%) of total body potassium is intracellular.
•Kidneys excrete 90% to 95% of dietary potassium, with the remaining excreted by the gut.
•Physiologic functions.
○Cellular metabolism.
○Glycogen and protein synthesis.
○Regulation of the electrical action potential across cell membranes.
Predisposing Factors
A.High potassium, low sodium diets.
B.Potassium supplements.
C.Renal insufficiency.
Subjective Data
A.Common complaints/symptoms.
1.General malaise.
2.Weakness.
3.Gastrointestinal complaints.
a.Nausea and vomiting.
b.Diarrhea.
4.Neuromuscular.
a.Muscle twitching.
b.Cramping.
c.Weakness.
d.Ascending paralysis.
e.Paresthesia.
f.Hyperreflexia.
Physical Examination
A.Inspect and assess for volume/hydration status: Skin, mucous membranes, and jugular venous distension.
B.Assess for cardiac and renal comorbidities.
1.Auscultate and evaluate heart and lung.
2.Perform neurological examination.
Diagnostic Tests
A.Initial laboratory tests.
1.Serum potassium (preferably plasma).
2.Venous or arterial CO2 or HCO3 and/or pH.
B.Other laboratory tests.
1.Complete chemistry panel.
2.Complete blood count.
3.Drug levels (i.e., digoxin).
4.Trans-tubular potassium gradient (TTKG).
a.[Urine potassium/plasma potassium]/[urine osmolarity/plasma osmolarity].
b.Assessment of the kidney’s capability to appropriately conserve potassium.
c.Valid only if the patient is not taking any diuretics or drugs to block the renin–angiotensin–aldosterone system (RAAS), the urine osmolarity is greater than 300 mOsm/kg, and the urine sodium is greater than 25 mEq/L.
d.Should be greater than 10 during hyperkalemia, indicating that the kidneys are trying to remove potassium.
C.Cardiac function tests.
1.EKG changes including:
a.Peaked T-waves, prolonged PR-interval, widened QRS complex, and shortened QT-interval.
b.Progressive worsening as potassium rises.
c.Brady arrhythmias.
d.Ventricular fibrillation.
e.Asystole.
Differential Diagnosis
A.Pseudohyperkalemia.
1.Hemolysis during blood draw.
2.Preexisting hemolysis (e.g., sickle cell disease, transfusion reaction, drug induced).
3.Sampling error (i.e., collected above the level of an infusion).
4.Polycythemia.
5.Thrombocytosis (>500,000 to 1 million/mm³): Potassium release when clots are formed.
6.Leukocytosis (>100–200,000/mm³): Elevated potassium in serum but not in plasma.
7.Familial pseudohyperkalemia.
B.Redistribution of intracellular potassium (shifts from intracellular to extracellular fluid).
1.Metabolic acidosis or diabetic ketoacidosis: Insulin deficiency.
2.Muscular injury (e.g., trauma and rhabdomyolysis).
3.Succinylcholine.
4.Digoxin overdose.
5.Reduced effective plasma volume/hypertonic state.
a.Severe dehydration.
b.Heart failure.
c.Liver failure.
6.Hyperkalemic periodic paralysis.
7.Medications (toxicity): Beta-blockers, succinylcholine;,and digitalis.
C.Impaired elimination.
1.Kidney failure: Acute versus chronic.
2.Medication-induced.
a.Potassium-sparing diuretics.
b.Angiotensin-converting enzyme (ACE) inhibitors.
c.Angiotensin receptor blockers (ARBs).
d.Aldosterone antagonists.
e.Nonsteroidal anti-inflammatory drugs (NSAIDs).
f.Trimethoprim.
g.Heparin.
3.Decreased action of aldosterone/aldosterone deficiency.
a.Medications: ACE inhibitors; ARBs; NSAIDs; potassium-sparing diuretics; antibiotics (trimethoprim, penicillin G potassium); clonidine; cyclosporine; heparin; and others.
b.Type IV renal tubular acidosis.
c.Hyporeninemic hypoaldosteronism.
d.Addison’s disease (primary adrenal insufficiency).
e.Gordon’s syndrome (Type II pseudohypoaldosteronism).
4.Hypocalcemia.
D.Increased ingestion (requires impaired elimination).
Evaluation and Management Plan
A.Step 1—Cardiac stabilization (stabilize the action potential in the myocardium).
1.Intravenous calcium administered as calcium gluconate or calcium chloride transiently stabilizes cardiac muscle but does not decrease serum potassium.
a.Calcium gluconate contains 4.65 mEq Ca++/g and calcium chloride contains 13.6 mEq Ca++/g. Adjust doses accordingly.
2.Transient but immediate effect.
3.1 to 2 g given immediately and prior to other therapies (i.e., intravenous bicarbonate), and may be repeated as needed.
4.Central line preferred (especially for calcium or high doses of calcium gluconate).
B.Step 2—Shift potassium to intracellular space.
1.10 units intravenous insulin with 50 mL dextrose 50% to prevent hypoglycemia. Repeat as needed. Monitor glucose and potassium.
2.High dose β-agonists such as nebulized albuterol.
3.Sodium bicarbonate in acidotic patients.
a.Note: Correcting acidosis can also lower calcium levels. Give intravenous calcium before intravenous bicarbonate.
C.Step 3—Remove excess potassium.
1.Potassium-wasting diuretics; adequate dosing for renal function.
2.Potassium binders.
a.Sodium polystyrene sulfonate (Kayexalate) given as 15 to 30 g PO every 4 to 6 hours or 30 to 60 g per retention enema.
b.Patiromer (Veltassa) as 8.4 g PO once daily.
D.Step 4—Dialysis. Consult a nephrology expert.
1.Assess all electrolytes and acid–base balance and treat as indicated with nephrology.
Follow-Up
A.Continue to monitor potassium levels for 24 to 48 hours after the last dose of medication to account for the half-life of all medications.
B.Consider chronic treatment, which also includes potassium restriction and increased potassium elimination.
1.Dietary potassium restriction.
2.Discontinuation of medications associated with hyperkalemia.
3.Potassium-wasting medications (diuretics or potassium binders).
C.Follow-up with nephrology and cardiology as needed until potassium is normalized.
Consultation/Referral
A.Consult nephrology for any refractory electrolyte disorder with or without acute kidney injury (AKI) or chronic kidney disease (CKD).
B.Consult endocrinology for any uncontrolled diabetes.
Special/Geriatric Considerations
A.Sodium polystyrene sulfonate (Kayexalate) is associated with bowel obstruction. Use with caution in all populations but especially patients at risk for slow gastrointestinal motility.
B.The high doses of β-agonists required to shift potassium intracellularly can cause tachycardia. Use with caution in patients with preexisting arrhythmias, and other at-risk populations.
C.Patients with CKD and end-stage renal disease (ESRD) as well as high risk of history of cardiac arrhythmias have a higher risk of mortality with hypokalemia than hyperkalemia. Monitor carefully.
D.Patients with chronic hyperkalemia may not require acute lowering of potassium levels for baseline potassium in the absence of EKG changes or other signs/symptoms.
Bibliography
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