Hyperkalemia management

Patients with acute hyperkalemia usually require other therapies to manage hyperkalemia until dialysis can be initiated. Patients who present with cardiac abnormalities caused by hyperkalemia should receive calcium gluconate or chloride (1 g intravenously) to reverse the cardiac effects. Temporary measures can be employed to shift extracellular potassium into the intracellular compartment to stabilize cellular membrane effects of excessive serum potassium levels. Such measures include the use of regular insulin (5 to 10 units intravenously) and dextrose (5% to 50% intravenously), or nebulized albuterol (10 to 20 mg). Sodium bicarbonate should not be used to shift extracellular potassium intracellularly in patients with CKD unless severe metabolic acidosis (pH less than 7.2) is present. These measures will decrease serum potassium levels within 30 to 60 minutes after treatment, but potassium must still be removed from the body. Shifting potassium to the intracellular compartment, however, decreases potassium removal by dialysis. Often, multiple dialysis sessions are required to remove potassium that is redistributed from the intracellular space back into the serum. 

Electrolyte disturbances that develop in patients with tumor lysis syndrome should be managed aggressively to avoid renal failure from hyperphosphatemia and hypocalcemia and cardiac signs from hyperkalemia. One exception pertains to the use of intravenous calcium for hypocalcemia. Adding calcium may cause further calcium phosphate precipitation in the presence of hyperphosphatemia and should be used cautiously. 

Ora/ Adverse reactions may include nausea, vomiting, diarrhea, flatulence, and abdominal discomfort due to Gl irritation. They are best managed by diluting the preparation further, by taking with meals, or by dose reduction. Severe reactions may include hyperkalemia Gl obstruction, bleeding, ulceration, or perforation. 

In mild hyperkalemia—or after acute management of severe hyperkalemia by other measures—loop diuretics can significantly enhance urinary excretion of K+. This response is enhanced by simultaneous NaCI and water administration. 

Perazella MA. Trimethoprim-induced hyperkalemia Clinical data, mechanism, prevention and management. Drug Saf. 2000 22 227-236. 

Hypokalemia eventually develops in many patients who are placed on loop diuretics or thiazides. This can often be managed with dietary NaCl restriction. When hypokalemia cannot be managed in this way, or with dietary KC1 supplements, the addition of a potassium-sparing diuretic can significantly lower potassium excretion. While this approach is generally safe, it should be avoided in patients with renal insufficiency in whom life-threatening hyperkalemia can develop in response to potassium-sparing diuretics. 

Insulin is an endogenous hormone produced by fi-cells of islets of Langerhans of the pancreas, which consist of two chains of amino acids. It is required to be administered by a parenteral routes as it is destroyed when given orally. Insulin is used for the control of IDDM and in the emergency management of diabetic ketoacidosis.30 Insulin promotes the intracellular uptake of potassium and is used in hyperkalemia. Baker et al.31 have used insulin and glucagon in the treatment of liver disorders. Recent evidence indicates that the effects of insulin with glucose and potassium in ischemic heart disease have proved beneficial.32 It also is used in acute myocardial infarction.32... 

Life-threatening hyperkalemia after therapeutic barbiturate coma with thiopental has been described in three patients it was fatal in one (6). All the episodes occurred after the withdrawal of thiopental. Hypokalemia that is resistant to potassium replacement is common during thiopental coma and clinicians may choose to manage asjmptomatic barbiturate-induced hypokalemia expectantly in an attempt to avoid rebound hyperkalemia. 

Usually neither hyperkalemia nor hypokalemia pose a problem for the management of lithium treated patients. However, in lithium-treated subjects given thiazide diuretic, hypokalemia often develops [97]. This is due to the diuretic-induced increase in sodium delivery to the collecting tubule combined with the lithium-induced increase in urine flow. 

ACE inhibitors and ARBs slow the progression of diabetic kidney disease. A trial that was reported in 2000 confirmed that even nonmicroalbuminuric type 2 diabetic patients should be managed with ACE inhibitors or ARBs to prevent cardiovascular events.In addition to lowering systemic blood pressure, such patients also have lowered glomerular capillary blood pressure and protein filtration,ACE inhibitors and ARBs also reduce All-medi-ated effects on glomerular permeability and cell proliferation and fibrosis and should be incorporated into the treatment schedules of all patients with type 2 diabetes and those with type 1 diabetes and microalbuminuria, ACE inhibitors may exacerbate hyperkalemia in patients with advanced CKD and/or hyporeninemic hypoaldosteronism. In older patients with renal artery stenosis, they may cause a rapid decline in kidney function. Pooled data from large clinical trials indicated above show that only 1.5% of patients treated with ACE inhibitors or ARBs were withdrawn from trials because of hyperkalemia, and no deaths were reported as a consequence of hyperkalemia. ... 

Another related supportive care issue is electrolyte management. Hyperkalemia, hypermagnesemia, and hyperphosphatemia are common electrolyte disorders in patients with ARF who are unable to use their kidneys to maintain electrolyte balance. This is generally not a serious concern in patients who are achieving electrolyte control via RRT, but electrolytes should be monitored closely in all patients with ARF. 

In addition to CKD as a risk factor, other contributing factors should also be considered. This includes exposure to potassium-sparing diuretics -blockers, which work predominantly via 82-antagonistic effects to interfere with the extrarenal translocation of potassium into cells and ACEls, which may cause hyperkalemia by reducing aldosterone production. Polycitra, used for the treatment of metabolic acidosis, contains potassium citrate and should not be prescribed for patients with severe CKD. If hyperkalemia develops, management options are based on the degree to which potassium is elevated (see Chap. 50). 

Hyperkalemia is more common in patients with Stage 5 CKD therefore the discussion of treatment options focuses on interventions in this population. The majority of patients can be managed with a dietary potassium restriction of 50 to 80 mEq/day and alterations in dialysate potassium concentrations for patients receiving hemodialysis or peritoneal dialysis. Hyperkalemia is less common, however, in the peritoneal dialysis population due to differences in potassium transport. Constipation in patients with CKD can interfere with colonic potassium excretion therefore a good bowel regimen is important. For severe hyperkalemia hemodialysis is often required using a low-potassium dialysate bath (see Chap. 50). 

Acute decreases in renal function and hyperkalemia usually resolve over several days after ACEl or ARB therapy is discontinued. Occasional patients will require management of severe hyperkalemia, usually with sodium polystyrene sulfate (see Chap. 50). ACEl or ARB therapy may frequently be reinitiated, particularly for patients with congestive heart failure, after intravascular volume depletion has been corrected or the diuretic doses reduced. The development of mild renal insufficiency (serum creatinine concentration of 2 to 3 mg/dL) may be an acceptable trade-off for hemodynamic improvement in certain patients with severe congestive heart failure or renovascular disease not amenable to invasive management. Congestive heart failure patients with greater renal insufficiency may be best treated by substitution of hydralazine and nitrates for afterload reduction. 

Palmer BF. Managing hyperkalemia caused by inhibitors of the renin-ai iotensin-aldoster-one system. NEnglJ Med (2004) 351,585-92. 

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