Scherr L et al. Management of hyperkalemia with a cation-exchange resin. Findings: Scherr and colleagues found a decrease in serum potassium by 1. Gruy-Kapral C et al. Effect of single dose resin-cathartic therapy on serum potassium concentration in patients with end-stage renal disease.
J Am Nephrol ; 9 10 : Findings: The authors found no difference in serum potassium levels at 12 hours. However, the results of their studies do not defend this conclusion. In the Flinn study, they were looking primarily at outcomes hours after administration. In the Scherr study, there was no control group and the decrease was seen at 24 hours, again, not what we would care about in the ED.
These two studies from the NEJM are the basis upon which kayexlate has been prescribed for 5 decades but they prove nothing except that patients given minimal dietary potassium their serum level will fall over 24 hours. Finally, we have a Cochrane Review Mahoney that states that potassium-absorbing resins have never been found to be effective in the first hours of treatment.
Alright, so a review of the literature shows that there is virtually no benefit in the emergent setting to the use of kayexalate. But is there a downside? As with all medications, there is. In this case, there is a rare but highly lethal complication of the drug: Colonic Necrosis.
A number of case reports and case series Lillemoe , Gerstman , Rogers , Bomback detail patients with kayexalate-associated colonic necrosis.
In fact, the FDA added a warning back in cautioning against the use of the drug for this reason. Given th e absence of any significant benefit, particularly in the emergent setting, and the potential for serious harm, this recommendation from the nephrology literature seems very reasonable:. So there you have it. More dogma-lysis on a medical myth that has been passed down from generation and purported for 50 years. All other therapies temporarily push K into cells. In: Brenner BM, ed.
Hyperkalemia revisited. Tex Heart Inst J. Retrospective review of the frequency of ECG changes in hyperkalemia. Clin J Am Soc Nephrol. Management of patients with acute hyperkalemia. Cardiac arrest in special circumstances: electrolyte abnormalities, poisoning, drowning, accidental hypothermia, hyperthermia, asthma, anaphylaxis, cardiac surgery, trauma, pregnancy, electrocution.
Emergency management of severe hyperkalemia guidelines for best practice and opportunities for the future. Pharmacol Res. Weisberg LS. Management of severe hyperkalemia. Crit Care Med. Albuterol for the treatment of hyperkalemia. Ann Pharmacother. Treatment of hyperkalemia: something old, something new. Kidney Int.
New questions on old drug for hyperkalemia. Kidney News. Evaluation of sodium polystyrene sulfonate dosing strategies in the inpatient management of hyperkalemia. Kayexalate sodium polystyrene sulfonate powder.
January Accessed January 20, FDA approves new drug to treat hyperkalemia. FDA news release. October 21, Accessed October 9, Veltassa patiromer for oral suspension prescribing information. Patiromer in patients with kidney disease and hyperkalemia receiving RAAS inhibitors. N Engl J Med. Relypsa Inc. FDA approves supplemental new drug application for Veltassa removing boxed warning regarding drug-drug interactions.
Press release. November 27, Accessed January 21, October 18, Accessed November 10, Sodium zirconium cyclosilicate ZS-9 : a novel agent for the treatment of hyperkalemia. Sodium zirconium cyclosilicate in hyperkalemia. May 27, Accessed November 20, This cannot be done in a patient with volume overload. The ideal candidate for bicarbonate therapy would be a patient with volume depletion, hyperkalemia, and metabolic acidosis, because isotonic bicarbonate may improve all three of these problems simultaneously.
What about volume resuscitation of a patient with hyperkalemia who doesn't have metabolic acidosis? Although normal saline is traditionally used in this situation, it has been proven in three randomized controlled trials to induce a hyperchloremic metabolic acidosis and worsen hyperkalemia not including Gutierrez discussed above; evidence explored here.
In contrast, Lactated Ringers is safe to use in hyperkalemic renal failure and is proven to cause less hyperkalemia than normal saline. Of everything discussed in this post, the danger of normal saline is supported by the strongest evidence three independent prospective double-blind RCTs.
Previously it was believed that there were three routes to emergently remove potassium from the body: stool using Kayexalate , urine kaliuresis , and dialysis. Removal of Kayexalate from the treatment algorithm simplifies matters and allows us to focus on kaliuresis, which can be extremely effective and is often under-utilized. For example, a recent review article on hyperkalemia failed to mention diuresis at all Elliott For a patient with life-threatening hyperkalemia, it is often reasonable to make a single attempt at kaliuresis prior to proceeding to dialysis or simultaneously to pursuing dialysis e.
Of course in some situations such as chronic anuric renal failure, kaliuresis is unlikely to succeed, so it may be more sensible to proceed immediately to dialysis. A loop diuretic e. For patients with life-threatening hyperkalemia and renal insufficiency, it may be reasonable to use multiple diuretics, as these will operate in a synergistic fashion by blocking potassium reabsorption at different sites in the nephron figure above.
The combination of a loop diuretic and thiazide is commonly used in diuretic-resistant patients, with increased efficacy and potassium loss Jentzer There is no evidence regarding the number or dose of diuretic which should be used.
For life-threatening hyperkalemia there is generally time for a single attempt at kaliuresis. Therefore, typically this attempt is fairly aggressive. For a patient with renal dysfunction who is expected to respond poorly, high doses of multiple agents may be considered e.
The risk of over-diuresis and electrolyte depletion may be minimized with close monitoring of electrolytes and repletion as needed. Urine output and volume status must be carefully monitored, with ongoing volume administration to return urinary losses and maintain a euvolemic state. In the absence of evidence, selection of the number and dosage of diuretics must be based on clinical judgement. For example, at Genius General we once admitted a pleasant elderly man with chronic renal failure complicated by hyperkalemia causing bradycardia and shock.
He wished never to undergo dialysis and was not amenable to this therapy even temporarily. Given probable death if he failed to respond promptly to diuretics, he was treated with maximal kaliuresis mg i.
He responded well, and ultimately required potassium and fluid repletion. In retrospect, he likely would have responded to a less aggressive diuretic regimen. However, in the face of life-threatening hyperkalemia, it may be safer to err on the side of over-treatment followed by meticulous replacement of electrolytes and fluid as needed.
Given that every liter of isotonic bicarbonate contains mEq of bicarbonate, this deficit correlates to roughly 1. Protects myocardium from toxic effects of calcium; no effect on serum potassium level. Shifts potassium out of the vascular space and into the cells; no effect on total body potassium. Consider 5 percent dextrose solution infusion at mL per hour to prevent hypoglycemia with repeated doses. Glucose unnecessary if blood sugar elevated above mg per dL Shifts potassium into the cells, additive to the effect of insulin; no effect on total body potassium.
Oral: 50 g in 30 mL of sorbitol solution Rectal: 50 g in a retention enema. Caution should be used in patients who take digoxin because calcium has been reported to worsen the myocardial effects of digoxin toxicity. Shifting potassium intracellularly is done using insulin or a beta 2 agonist Table 5 2 , 3. Insulin typically is given as 10 units intravenously with 50 mL of 50 percent glucose to counteract hypoglycemia.
Repeated doses can be given if the potassium level remains elevated. Inhaled beta2 agonists have a rapid onset of action. The effect of beta2 agonists is additive to that of insulin administration, and they can be taken together.
Intravenous beta2 agonists have been used in Europe, but they are not approved by the U. Food and Drug Administration. Sodium bicarbonate is no longer recommended to lower potassium, although it may be appropriate in patients with severe metabolic acidosis. Treatments that shift potassium into the cells have no effect on total body potassium. Potassium can be eliminated by renal excretion, gastrointestinal elimination, or dialysis.
The agents taken to lower total body potassium can interfere with tests to determine the cause of hyperkalemia. Thus, spot urine potassium, creatinine, and osmolality levels should be obtained before the agents are initiated; however, treatment should not be delayed while awaiting results.
Gastrointestinal excretion is accomplished using sodium polystyrene sulfonate Kayexalate , which binds potassium in the colon in exchange for sodium; it can be given orally or as a retention enema. The enema form is faster; the oral route can take four to six hours because it requires the resin to get to the colon before it takes effect.
Sodium polystyrene sulfonate often is given with sorbitol to decrease constipation. However, sorbitol can have intestinal complications, with reports of bowel necrosis and perforation in immunocompromised patients. Excretion of renal potassium can be increased with the use of diuretics, particularly loop diuretics e.
Patients with decreased kidney function may be relatively resistant to the effects of diuretics. If the patient is volume depleted, saline can be given with the diuretic. Hemodialysis or continuous renal replacement therapy are the treatments of last resort, with the exception of patients already receiving these therapies. Long-term treatment should be tailored to correcting the underlying cause of hyperkalemia.
Low-potassium diets should be discussed with patients, and medications that precipitated hyperkalemia should be discontinued if possible.
The use of loop diuretics or fludrocortisone will be needed for patients with hyporeninemic hypoaldosteronism whose hyperkalemia recurs or is chronic. The usual dosage of f ludrocortisone is 0. In some patients, hyporeninemic hypoaldosteronism is transitory and resolves after acute management; in others, long-term management with f ludrocortisone is required. Many patients tolerate long-term use of f ludrocortisone with no problems. The principal side effects are hypertension and f luid retention, which may respond to an added diuretic.
Although the question of appropriate treatment duration with f ludrocortisone has never been studied, one approach to management would be to slowly taper f ludrocortisone on an outpatient basis, and reinstate f ludrocortisone if potassium rises.
Hyperkalemia caused by the use of ACE inhibitors or angiotensin receptor blockers in patients with chronic renal failure and metabolic acidosis may respond to sodium bicarbonate supplementation.
Concomitant diuretic use limits the risk of volume overload. Already a member or subscriber? Log in. Interested in AAFP membership? Learn more. Address correspondence to James F. Calvert, Jr. Reprints are not available from the authors. Hyperkalemia in hospitalized patients: causes, adequacy of treatment, and results of an attempt to improve physician compliance with published therapy guidelines.
Arch Intern Med. Gennari FJ. Disorders of potassium homeostasis. Hypokalemia and hyperkalemia. Crit Care Clin. Therapeutic approach to hyperkalemia. Perazella MA. Drug-induced hyperkalemia: old culprits and new offenders. Am J Med. Drug-induced hyperkalemia [Letter Reply]. Pantanowitz L. Drug-induced hyperkalemia [Letter]. Cardiac arrest from succinylcholine-induced hyperkalemia. Am J Health Syst Pharm. Rates of hyperkalemia after publication of the Randomized Aldactone Evaluation Study.
N Engl J Med. Nephrotoxicity in the elderly due to co-prescription of angiotensin converting enzyme inhibitors and nonsteroidal anti-inflammatory drugs. J R Soc Med. DeFronzo RA. Hyperkalemia and hyporeninemic hypoaldosteronism.
Kidney Int. Hyporeninemic hypoaldosteronism in diabetic patients with chronic renal failure. Am J Nephrol.
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