Hypokalemia diuretics:chronic

Uses Chronic asthma Actions Topical steroid Dose Two inhalations tid-qid or 4 inhal bid Caution [C, ] Contra Component aU gy Disp Met-dose inhaler SE Cough, oral candidiasis Interactions T Risk of GI bleed W/ ASA, NSAIDs T effects W/ sakneterol, troleandomycin -1- effects W/barbiturates, hydantoins, pheny-toin, rifampin T effects OF diuretics, insulin, oral hypoglycemics, K supl, salicylates, somatrem, live virus vaccines EMS May affect glucose(hyperglycemia) monitor ECG for hypokalemia (flattened T waves) concurrent ASA/NSAID use may t risk of GI bleeding OD Acute OD unlikely to cause life-threatening Sxs, chronic OD may lead to S/Sxs of muscle weakness, and osteoporosis symptomatic and supportive... 

The chronic use of some diuretics may require the oral administration of potassium supplements or potassiumsparing diuretics that reduce urinary K+ excretion. This is true especially for patients with congestive heart failure and cirrhosis, who are particularly sensitive to K+ loss. The presence or absence of clinical symptoms of hypokalemia is quite closely related to serum K+ concentrations, and even small changes in extracellular K+ can have marked effects. Most patients begin to show symptoms when serum K+ levels fall below 2.5 mEq/L (from a normal value of approximately 5 mEq/L). 

Furosemide Loop diuretic Decreases NaCI and KCI reabsorption in thick ascending limb of the loop of Henle in the nephron (see Chapter 15) Increased excretion of salt and water reduces cardiac preload and afterload reduces pulmonary and peripheral edema Acute and chronic heart failure severe hypertension edematous conditions Oral and IV duration 2-4 h Toxicity Hypovolemia, hypokalemia, orthostatic hypotension, ototoxicity, sulfonamide allergy... 

Adverse effects Thiazide diuretics induce hypokalemia and hyperuricemia in 70% of patients, and hyperglycemia in 10% of patients. Serum potassium levels should be monitored closely in patients who are predisposed to cardiac arrhythmias (particularly individuals with left ventricular hypertrophy, ischemic heart disease, or chronic congestive heart failure) and who are concurrently being treated with both thiazide diuretics and digitalis glycosides (see p. 160). Diuretics should be avoided in the treatment of hypertensive diabetics or patients with hyperlipidemia. 

Early evidence linking thiazide-induced hypokalemia with dysrhythmias and sudden death was indirect and tenuous at best (50,51). One study suggested that diuretics are not responsible for the relation between hjrpokalemia and ventricular fibrillation in acute myocardial infarction (50). Chronic preoperative hypokalemia due to diuretics was not a risk factor for intraoperative dysrhjdhmias (52). Two large studies using 24-hour electrocardiographic monitoring failed to show a relation between diuretic-induced hypokalemia and ventricular dysrhythmias (53,54). 

When there is severe hypokalemia, it should not be attributed immediately to diuretic treatment. It may well be due to primary hyperaldosteronism, occult chronic liver disease, or abuse of licorice or laxatives. 

Figure 3. Sequential renal biopsies, separated by 10 years, in a patient with hypokalemia related to chronic diuretic abuse. Initial biopsy (on the left) shows proximal tubular cell vacuolization and mild interstitial inflammation. The subsequen t examination (on the right) demonstrates marked interstitial fibrosis, tubular atrophy and dropout.

The diuretics can result in an acute interstitial nephritis, which may have an immunologic basis and can persist, if undetected, as a chronic lesion leading to renal insufficiency. The acute form may or may not be associated with other hallmarks of an allergic phenomenon such as fever and rash, but eosinophilia and eosi-nophiluria are often present, if looked for. Thus far, this lesion has been associated with the administration of the thiazides and furosemide, but ethacrynic acid may also be involved. Persistent hypokalemia may also... 

Amiloride is used with thiazide or loop diuretics in hypertension, in congestive heart failure, in digitalis-induced hypokalemia, and in arrhythmias resulting from hypokalemia. Inappropriate use of amiloride may cause hyperkalemia (potassium >5.5 mEq/L), which may be fatal if not corrected, and may be more deleterious in elderly individuals and in patients with diabetes mellitus and renal impairment. The symptoms of hyperkalemia include fatigue, flaccid paralysis of the extremities, paresthesias, bradycardia, ECG abnormalities, and shock. Amiloride is not metabolized but is contraindicated in anuria, acute or chronic renal insufficiency, or in diabetic nephropathy. It should not be used with potassium preparations, and should be used cautiously with ACE inhibitors because these agents cause hyperkalemia. 

USE OF DIURETICS IN CLINICAL PRACTICE The majority of patients with heart failure will require chronic administration of a loop diuretic to maintain euvolemia. In patients with clinically evident fluid retention, furosemide typically is started at a dose of 40 mg once or twice/day and increased until an adequate diuresis is achieved. A larger initial dose may be required in patients with more advanced heart failure or with concurrent azotemia. Serum electrolytes and renal function should be monitored frequently in patients with preexisting renal insufficiency or those in whom a rapid diuresis is desirable. Once fluid retention has resolved, the diuretic dose should be reduced to the minimal level necessary to maintain euvolemia. Electrolyte abnormalities and/or worsening azotemia may supervene before euvolemia is achieved. Hypokalemia may be corrected by potassium supplementation or addition of a K-sparing diuretic. 

B. With chronic intoxication, visual disturbances, weakness, sinus bradycardia, atrial fibrillation with slowed ventricular response rate or junctional escape rhythm, and ventricular arrhythmias (ventricular bigeminy or trigeminy, ventricular tachycardia, bidirectional tachycardia, and ventricular fibrillation) are common. Accelerated junctional tachycardia and paroxysmal atrial tachycardia with block are frequently seen. Hypokalemia and hypomagnesemia from chronic diuretic use may be evident and appear to worsen the tachyarrhythmias. 

Most HE episodes in patients with chronic liver disease are precipitated by events such as oral protein load, gastrointestinal bleeding, obstipation, infection, especially peritonitis, hypokalemia and alkalosis complicating the use of diuretic drugs, administration of sedative drugs, for example for diagnostic procedures or induction of portal-systemic shunt via shunt operation or the TIPSS implantation. 

Tolerance to the diuretic action of caffeine was demonstrated more than 50 years ago and was shown to develop on chronic caffeine intake so that the clinical significance of hypokalemia and calciuria is difficult to evaluate. Although controversial, some epidemiological studies have implicated caffeine in the increased risk for poor calcium retention. For calcium intakes lower than 750 mg per day, increased rate of bone loss and lower bone density were reported. However, it has been suggested that the effect on bone of high caffeine intake requires a genetic predisposition toward osteoporosis. In individuals who ingest calcium recommended daily allowances, there is no evidence of any effect of caffeine on bone status and calcium economy. 

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