Potassium therapy

Fath-Ordoubadi p Beatt KJ. Glucose-insulin-potassium therapy for treatment of acute myocardial infarction an overview of randomized placebo-controlled trials. Circulation 1997 96 1 152-1 156. 

Pemberton, J. Esophageal obstruction and ulceration caused by oral potassium therapy. Br. Heart J. 1970, 32, 267-268. 

Kassirer JP, Harrington JT. Diuretics and potassium metabolism a reassessment of the need, effectiveness and safety of potassium therapy. Kidney Int 1977 11 505-515. 

To date, there have been no pharmacoeconomic evaluations of the different pharmacotherapeutic alternatives to manage hypokalemia. The most economical source of potassium is from the diet. Thus patients receiving diuretic therapy should be instructed to increase their dietary intake of potassium-rich foods. By doing so, they may avert the need for exogenous potassium therapy. Additionally, oral potassium supplementation is much less expensive than intravenous supplementation by virtue of its ease of administration and lack of need... 

Renal tubular acidosis can occur during amphotericin B therapy [439,440]. Renal tubular acidosis and hykalemia can be easily corrected with oral potassium therapy [436,439,441]. Hydrocortisone and heparin are sometimes used in conjunction with polyene therapy to reduce toxic side effects [442]. The immediate reactions to intravenous amphotericin B therapy (nausea, vomiting and fever) can be controlled to some extent by usually antihistamines and hydrocortisone [443,444] but reports that some of the symptoms of nephrotoxicity may be overcome by mannitol supplementation [445] have been disputed [446]. 

Fmit and vegetable juices high in potassium have been recommended to correct hypokalemic alkalosis in patients on diuretic therapy. Apparendy the efficacy of this treatment is questionable. A possible reason for ineffectiveness is the low Ck content of most of these juices. Because Ck is high only in juices in which Na" is high, these have to be excluded (64). 

Ascites. Patients with cirrhosis, especially fiver cirrhosis, very often develop ascites, ie, accumulation of fluid in the peritoneal cavity. This is the final event resulting from the hemodynamic disturbances in the systemic and splanchnic circulations that lead to sodium and water retention. When therapy with a low sodium diet fails, the dmg of choice for the treatment of ascites is furosemide, a high ceiling (loop) diuretic, or spironolactone, an aldosterone receptor antagonist/potassium-sparing diuretic. 

Electrolyte imbalances that may be seen during therapy with a diuretic include hyponatremia (low blood sodium) and hypokalemia (low blood potassium), although other imbalances may also be seen. See Chapter 58 and Display 58-2 for the signs and symptoms of electrolyte imbalances. The primary care provider is notified if any signs or symptoms of an electrolyte imbalance occur. 

Hyperkalemia (increase in potassium in the blood), a serious event, may be seen with the administration of potassium-sparing diuretics. Hyperkalemia is most likely to occur in patients with an inadequate fluid intake and urine output, those with diabetes or renal disease tiie elderly, and those who are severely ill. In patients taking spironolactone, gynecomastia (breast enlargement in tiie male) may occur. This reaction appears to be related to both dosage and duration of therapy. The gynecomastia is usually reversible when therapy is discontinued, but in rare instances, some breast enlargement may remain. 

The nurse must closely observe patients receiving a potassium-sparing diuretic for signs of hyperkalemia (see Display 46-1), a serious and potentially fatal electrolyte imbalance The patient is closely monitored for hypokalemia during loop or thiazide diuretic therapy. A supplemental potassium supplement may be prescribed to prevent hypokalemia. The primary health care provider may also encourage the patient to include... 

Fbtassium-sparing diuretics Avoid eating foods high in potassium and avoid the use of salt substitutes containing potassium. Read food labels carefully. Do not use a salt substitute unless a particular brand has been approved by the primary health care provider. Avoid the use of potassium supplements. Male patients taking spironolactone may experience gynecomastia. This is usually reversible when therapy is discontinued. 

There is an additive bone marrow depression when methimazole or propylthiouracil is administered with otiier bone marrow depressants, such as the antineo-plastic drugs, or witii radiation therapy. When methimazole is administered with digitalis, there is an increased effectiveness of the digitalis and increased risk of toxicity. There is an additive effect of propylthiouracil when the drug is administered with lithium, potassium iodide, or sodium iodide When iodine products are administered with litiiium products, synergistic hypotiiyroid activity is likely to occur. 

Monitor and correct potassium, phosphorus, and magnesium ° Potassium levels may decrease with therapy... 

The major risk related to aldosterone antagonists is hyperkalemia. Therefore, the decision for use of these agents should balance the benefit of decreasing death and hospitalization from HF and the potential risks of life-threatening hyperkalemia. Before and within one week of initiating therapy, two parameters must be assessed serum potassium and creatinine clearance (or serum creatinine). Aldosterone antagonists should not be initiated in patients with potassium concentrations greater than... 

In patients without contraindications, spironolactone is initiated at a dose of 12.5 to 25 mg daily, or occasionally on alternate days for patients with baseline renal insufficiency. Eplerenone is used at a dose of 25 mg daily, with the option to titrate up to 50 mg daily. Doses should be halved or switched to alternate-day dosing if creatinine clearance falls below 50 mL/minute. Potassium supplementation is often decreased or stopped after aldosterone antagonists are initiated, and patients should be counseled to avoid high-potassium foods. At anytime after initiation of therapy, if potassium concentrations exceed... 

There is a paucity of clinical trial evidence comparing the benefit of diuretics to other therapies for symptom relief or long-term outcomes. Additionally, excessive preload reduction can lead to a decrease in CO resulting in reflex increase in sympathetic activation, renin release, and the expected consequences of vasoconstriction, tachycardia, and increased myocardial oxygen demand. Careful use of diuretics is recommended to avoid overdiuresis. Monitor serum electrolytes such as potassium, sodium, and magnesium frequently to identify and correct imbalances. Monitor serum creatinine and blood urea nitrogen daily at a minimum to assess volume depletion and renal function. 

All patients with ascites require counseling on dietary sodium restriction. Salt intake should be limited to less than 800 mg sodium (2 g sodium chloride) per day. More stringent restriction may cause faster mobilization of ascitic fluid, but adherence to such strict limits is very difficult. Patients usually respond well to sodium restriction accompanied by diuretic therapy.14,22,31,32 The goal of therapy is to achieve urinary sodium excretion of at least 78 mEq (78 mmol) per day.22 While a 24-hour urine collection provides this information, a spot urine sodium/ potassium ratio greater than 1.0 provides the same information and is much less cumbersome to perform. 

Diuretics are often required in addition to the sodium restriction described previously. Spironolactone and jurosemide form the basis of pharmacologic therapy for ascites. Spironolactone is an aldosterone antagonist and counteracts the effects of activation of the renin-angiotensin-aldosterone system. In hepatic disease not only is aldosterone production increased, but its half-life is prolonged because it is hepatically metabolized. Spironolactone acts to conserve the potassium that would be otherwise excreted because of elevated aldosterone levels. 

Develop a plan to provide symptomatic care of complications associated with ARF, such as diuretic therapy to treat volume overload. Monitor the patient s weight, urine output, electrolytes (such as potassium), and blood pressure to assess efficacy of the diuretic regimen. 

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. 

Monitor electrocardiogram continuously in patients with cardiac abnormalities until serum potassium levels drop below 5 mEq/L (5 mmol/L) or cardiac abnormalities resolve. Evaluate serum potassium and glucose levels within 1 hour in patients who receive insulin and dextrose therapy. Evaluate serum potassium levels within 2 to 4 hours after treatment with SPS or diuretics. Repeat doses of diuretics or SPS if necessary until serum potassium levels fall below 5 mEq/L (5 mmol/L). Monitor blood pressure and serum potassium levels in 1 week in patients who receive fludrocortisone. 

Moderate hypokalemia is defined as a serum potassium of 2.5 to 3.5 mEq/L (2.5 to 3.5 mmol/L) without ECG changes. In this setting, potassium replacement can usually be given orally at a dose of 40 to 120 mEq/day (40 to 120 mmol/day). Anecdotally, oral potassium supplementation (see Table 24-7) is often more effective in repleting moderate hypokalemia. For patients with an ongoing source of potassium loss, chronic replacement therapy should be considered. The potassium... 

Dextrose and insulin (with or without sodium bicarbonate) are typically given at the time of calcium therapy in order to redistribute potassium into the intracellular space. Dextrose 50% (25 g in 50 mL) can be given by slow IV push over 5 minutes or dextrose 10% with 20 units of regular insulin can be given by continuous TV infusion over 1 to 2 hours. The onset of action for this combination is 30 minutes and the duration of clinical effects... 

It is critically important to recognize that the treatments of hyperkalemia discussed thus far are transient, temporizing measures. They are intended to provide time to institute definitive therapy aimed at removing excess potassium from the body. Agents that increase potassium excretion from the body include sodium polystyrene sulfonate, loop diuretics, and hemodialysis or hemofiltration (used only in patients with renal failure). Sodium polystyrene sulfonate (Kayexalate , various manufacturers) can be given orally, via NG tube, or as a rectal retention enema and is dosed at 15 to 60 grams in four divided doses per day. 

Large doses of iodide inhibit the synthesis and release of thyroid hormones. Serum T4 levels may be reduced within 24 hours, and the effects may last for 2 to 3 weeks. Iodides are used most commonly in Graves disease patients prior to surgery and to quickly reduce hormone release in patients with thyroid storm. Potassium iodide is administered either as a saturated solution (SSKI) that contains 38 mg iodide per drop or as Lugol s solution, which contains 6.3 mg iodide per drop. The typical starting dose is 120 to 400 mg/day. Iodide therapy should start 7 to 14 days prior to surgery. Iodide should not be... 

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