Complicates 1.1% – 10% of hospital admissions.

Defined as greater than 5-5.5 mEq per liter.

Hyperkalemia-chronic elevation of potassium can occur with no increase of total body potassium.

Acute elevations of potassium usually produced by shifts of potassium from the intracellular fluid to the extracellular fluid.

Causes include: decreased GFR, acute renal failure, chronic renal failure, Addison’s disease, hyporeninemic hypoaldosteronism, use of potassium sparing diuretics, voltage-dependent renal tubular acidosis, use of trimethoprim-sulfamethoxazole, use of angiotensin-converting enzyme inhibitors, acidosis, Beta-adrenergic blockade, cell destruction by trauma, burns, tumor lysis, rhabdomyolysis, hemolysis, diabetic hyperglycemia, hyperkalemic periodic paralysis and succinylcholine use.

Particularly common in chronic kidney disease and heart failure, both conditions in which protective medications include renin-angiotensin-aldosterone system medications and may lead to increased plasma potassium.

Affects an estimated 14-20% of patients with chronic kidney disease.

Reasons for elevated potassium levels in patients with chronic kidney disease include: increased potassium intake, altered potassium management by the kidneys, aldosterone resistance, acidosis, and lack of insulin.

There is an increased risk of hyperkalemia in type 4 renal tubular acidosis, which occurs in patients with diabetes and overt nephropathy and may lead to impaired urinary excretion of potassium.
Abnormalities in potassium distribution caused by tissue injury, normal anion gap metabolic acidosis, and increased tonicity may also be present with hyperkalemia.

Can cause potentially life-threatening cardiac arrhythmias and is associated with a poor prognosis in certain patient populations.

Linked to increased adverse cardiovascular complications.

Incidence increasing as the prevalence of chronic kidney disease and diabetes are increased.

Associated with acute myocardial infarction as there is increased use of beta blockers, mineralcorticoid receptor antagonists, and renin-angiotensin aldosterone system antagonists causing hyperkalemia.

Hyperkalemia is common in patients hospitalized for acute myocardial infarction and is associated with marked increases in mortality even with mild elevations in potassium levels (Grodzinsky A et al).

Associated with medications: spirinolactone, renin-angiotensin-aldosterone system inhibitorrs, eplerenone, and potassium supplements.

Increased use of renin-angiotensin-aldosterone system (RAAS) inhibitors, and increase in chronic kidney disease, heart failure and diabetes have led to a higher prevalence of hyperkalemia, and hyperkalemic related hospitalizations and deaths.

Chronic renal disease predisposes to hyperkalemia by impaired glomerular filtration rate, a frequently high dietary potassium intake relative to residual renal function, extracellular shift of potassium caused by the metabolic acidosis of renal insufficiency, and treatment with renin-angiotensin-aldosterone system blockers that inhibit renal potassium excretion.

Risk factors for a Hyperkalemia in patients with CKD include: advancing renal impairment, comorbidities such as diabetes, hypertension, and heart failure, and a potassium enriched diet.

Key risk predictors for hyperkalemia development in CKD are an estimated GFR of less than 45 mL/minutes per 1.73 m2, a baseline serum K level greater than 4.5 millequivalents per liter prior to starting renin-angiotensin-aldosterone system inhibitor therapy.

Pseudohyperkalemia occurs with thrombocytosis or leucocytosis and is most common with myeloproliferative disorders.

Most important clinical manifestation is cardiac excitability.

Mild symptoms of high blood potassium concentrations include unusual skin sensations, muscle weakness, or fatigue, but more severe symptoms such as flaccid paralysis of the limbs, slow heart rate, and even shock can occur.

Hyperkalemia may decrease the velocity of impulse conduction in the nerves and muscles, including cardiac tissues, leading to cardiac dysfunction and neuromuscular consequences, such as muscle weakness, paresthesia, nausea, diarrhea, and others. 

Initial manifestation of ECG changes is peaked T waves which occurs when potassium is 6.5 meq/L or higher.

Peaked T waves are caused by hyperkalemic induced accelerated repolarization of the cardiac action potential.

When potassium levels reach 7-8 meq/L cardiac excitability is decreased and the PR interval is prolonged which is followed by loss of P waves and widening of the QRS complex.

Can induce inactivation of sodium permeability and lead to impairment of cardiac muscle excitability.

When serum potassium exceeds 8-10 meq/L sine wave patterns may appear on the ECG and cardiac standstill can occur.

Progression from peaked T waves to a sine wave may occur rapidly and correlation between potassium level and ECG abnormalities is not clear-cut.

The presence of peaked T waves and hyperkalemia indicates the need for hospitalization, while more advanced changes are treated as medical emergencies.

Hospitalization generally not needed if ECG is normal, renal status is stable, no other major metabolic or electrolyte abnormalities exist and the potassium is less than 6.5 meq/L.

All patients with potassium levels of 8 meq/L should be admitted to the hospital.

Among patients with hyperkalemia and diabetic kidney disease patiromer at doses of 4.2-16.8 g b.i.d. results in significant decreases in serum potassium levels after four weeks of treatment, lasting through 52 weeks Bakris GL et al).

In patients receiving hemodialysis, who are at risk for hyperkalemia after a long interdialytic, interval hyperkalemia is associated with an increased risk of major cardiovascular events and mortality.

Treatments include: 1)glucose plus insulin, sodium bicarbonate or beta-agonists which shift potassium from the extracellular to the intracellular fluid, 2)efforts to increase potassium elimination from the body such as dialysis, diuretics and exchange resins, and 3)use of calcium to decrease cardiac excitability.

Emergency treatment includes: calcium gluconate 10%, 5-30 mL IV or calcium chloride 5%, 5-30 mL IV (antagonizes cardiac onduction abnormalities), NaHCO3 44-88 meq (1-2 ampules) IV, regular insulin 5-10 units IV, plus glucose 50% 25 gm IV.

Available therapies for treatment which include insulin, Beta2 stimulants, and sodium bicarbonate promote translocation of potassium from the extracellular space to the intracellular space, providing just temporary benefit for approximately 1-4 hours.

The initial management of hyperkalemia may include: The use of loop diuretics, either alone or in combination with size or diuretics, which enhance urinary excretion of potassium by increasing flow and sodium delivery to the distal nephron.
Diuretic therapy is less effective in patients with advanced CKD or end stage renal disease.

Hyperkalemia in chronic kidney disease can be managed by down titrating or discontinuing RAAS  inhibitor therapy or limiting dietary potassium.

To remove potassium from the body requires the use of exchange raisins, diuretics, or dialysis.

The use of nonspecific polymeric exchange resins is presently the mainstay of the acute removal of potassium but has an uncertain efficacy, poor side effect profile and is associated was serious gastrointestinal adverse events particularly when administered with sorbitol.

Inhaled albuterol helpful in mild hyperkalemia.

Low salt intake promotes hyperkalemia. Thanks again

Limiting dietary potassium is associated with only slight reductions in serum potassium.

Sodium polystyrene sulfonate-oral 15-30 gm in 20% sorbitol, rectal 50 gm in 20% sorbitol.

The long-term pharmacological management of hyperkalemia has utilized sodium poly styrene sulfonate, a resin that exchanges potassium for sodium in the colon. 
Sodium polystyrene sulfonate is poorly tolerated and can cause gastrointestinal adverse effects, often leading to poor adherence.

Sodium zirconium cyclosilicate, also known as ZS-9, is a highly selective in organic cation exchanger designed to entrap potassium in the intestine.

Sodium zirconium cyclosilicate given to outpatients with hyperkalemia reduced serum potassium to normal levels within 48 hours compared with placebo.

Sodium zirconium cyclosilicate treatment for hyperkalemia is a non-polymer compound that exchanges potassium for sodium and hydrogen ions in the gastrointestinal tract, 
Patiromer, a polymer, that exchanges potassium for calcium ions in the gastrointestinal tract.
Sodium zirconium cyclosilicate and patiromer remove bound potassium ion via the feces. 
Sodium zirconium cyclosilicate and patiromer ate viable alternatives to sodium polystyrene sulfate in the management of hyperkalemia in patients with chronic kidney disease.
Sodium zirconium cyclosilicate and patironer Improve taste, texture, and appearance compared to polystyrene sulfate.
Sodium zirconium cyclosilicate has a rapid onset of action of one hour and is able to restore normal kalemia in our patients with severe hyperkalemia.

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