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First confirm that the elevated level of serum K+ is genuine Potassium concentration can be measured in plasma rather than in serum to avoid leakage of potassium out of cells into the serum of the blood sample in the course of clotting, which may be observed in thrombocytosis Renal dysfunction should be ruled out at the initial assessment Treatment consists of withholding potassium and giving cation exchange resins by mouth or enema Sodium polystyrene sulfonate, 40 80 g/d in divided doses, is usually effective Emergent treatment of hyperkalemia is indicated if cardiac toxicity or muscular paralysis is present or if the hyperkalemia is severe (serum potassium > 65 7 mEq/L) even in the absence of ECG changes Insulin plus 10 50% glucose (5 10 g of glucose per unit of insulin) may be given to deposit K+ with glycogen in the liver (Table 21 7) Calcium may be given intravenously as an antagonist ion but not when digoxin toxicity is suspected, since calcium may augment the deleterious effects of digoxin on the heart Transcellular shifts of potassium can also be mediated by 2adrenergic stimulation Thus, one or two standard doses of nebulized albuterol can reduce serum K+ 05 1 mEq/L within 30 minutes after administration in dialysis patients, and this effect is sustained for at least 2 hours Sodium bicarbonate can be given intravenously as an emergency measure in severe hyperkalemia; the increase in blood pH
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Thiazide or loop diuretics and sodium bicarbonate may be effective in minimizing hyperkalemia Mild hyperkalemia that recurs often in patients in the absence of ACE inhibitor drug therapy is usually due to type IV renal tubular acidosis (RTA) Heparin inhibits aldosterone production by inhibiting the final enzymatic step in its manufacture in the adrenal glands, and thus can be a cause of hyperkalemia Trimethoprim is structurally related to amiloride and triamterene, and all three drugs inhibit renal potassium excretion through suppression of sodium channels in the distal nephron Serum potassium levels rise progressively over 4 5 days in patients treated with standard or high-dose trimethoprim (combined with sulfamethoxazole or dapsone), especially if there is concurrent CKD Over 50% of inpatients taking this drug have potassium levels over 5 mEq/L, and 20% have marked hyperkalemia (> 55 mEq/L) The potassium concentration returns to baseline after drug discontinuation Immunosuppressive drugs such as cyclosporine and tacrolimus can induce hyperkalemia in organ transplant recipients and especially in kidney transplant patients This is partly due to the suppression of basolateral Na+ K+-ATPase in principal cells Severe hyperkalemia and cardiovascular disturbances can be caused by the use of drugs with KATP channel-
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Table 21 7 Treatment of hyperkalemia
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EMERGENCY Modality Calcium Mechanism of Action Antagonizes cardiac conduction abnormalities Distributes K+ into cells Distributes K+ into cells Distributes K+ into cells Onset 0 5 minutes 15 30 minutes 15 60 minutes 15 30 minutes Duration 1 hour Prescription Calcium gluconate 10%, 5 30 mL intravenously; or calcium chloride 5%, 5 30 mL intravenously NaHCO3, 44 88 mEq (1 2 ampules) intravenously Regular insulin, 5 10 units intravenously, plus glucose 50%, 25 g (1 ampule) intravenously Nebulized albuterol, 10 20 mg in 4 mL normal saline, inhaled over 10 minutes K+ Removed from Body 0
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Bicarbonate Insulin Albuterol NONEMERGENCY Modality Loop diuretic
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1 2 hours 4 6 hours 2 4 hours
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Mechanism of Action Renal K+ excretion
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Duration of Treatment 05 2 hours
Prescription Furosemide, 40 160 mg intravenously or orally with or without NaHCO3, 05 3 mEq/ kg daily Oral: 15 30 g in 20% sorbitol (50 100 mL) Rectal: 50 g in 20% sorbitol
K+ Removed from Body Variable
Sodium polystyrene sulfonate (Kayexalate) Hemodialysis Peritoneal dialysis
Ion-exchange resin binds K+ Extracorporeal K+ removal Peritoneal K+ removal
1 3 hours
05 1 mEq/g
48 hours 48 hours
Blood flow 200 300 mL/min Dialysate [K+] ~ 0 Fast exchange, 3 4 L/h
200 300 mEq 200 300 mEq
Modified and reproduced, with permission, from Cogan MG Fluid and Electrolytes: Physiology and Pathophysiology McGraw-Hill, 1991
results in a shift of K+ into cells Hemodialysis or peritoneal dialysis may be required to remove K+ in the presence of protracted kidney injury Therapy of the precipitating event proceeds concurrently The severe hyperkalemia caused by the use of drugs with KATP channel-opening properties such as cyclosporine, isoflurane, or nicorandil (not yet available in the United States) can be successfully reversed by the administration of glibenclamide
de Denus S et al Quantification of the risk and predictors of hyperkalemia in patients with left ventricular dysfunction: a retrospective analysis of the Studies of Left Ventricular Dysfunction (SOLVD) trials Am Heart J 2006 Oct;152(4):705 12 [PMID: 16996842] Hebert LA Optimizing ACE-inhibitor therapy for chronic kidney disease N Engl J Med 2006 Jan 12;354(2):189 91 [PMID: 16407515] Hollander-Rodriguez JC et al Hyperkalemia Am Fam Physician 2006 Jan 15;73(2):283 90 [PMID: 16445274] Kettler RE Crush-related injury after disasters N Engl J Med 2006 Jun 8;354(23):2511 2 [PMID: 16760458] Palmer BF Managing hyperkalemia caused by inhibitors of the renin-angiotensin-aldosterone system N Engl J Med 2004 Aug 5;351(6):585 92 [PMID: 15295051] Singer M et al Reversal of life-threatening, drug-related potassium-channel syndrome by glibenclamide Lancet 2005 May 28 Jun 3;365(9474):1873 5 [PMID: 15924984]
Tran HA After the bender Am J Med 2006 Jun;119(6):487 90 [PMID: 16750961]
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