Diuretic metabolic alkalosis with

Hypokalemia is common in the patient with liver failure who has normal renal function. Poor nutritional intake and vomiting may initiate this disorder. Severe vomiting may lead to volume contraction metabolic alkalosis, with increased renal excretion of potassium. Secondary hyperaldosteronism, seen in the liver failure patient with intravascular depletion, also increases renal excretion of potassium. Loop diuretic therapy causes increased renal excretion of potassium, whereas diarrhea from lactulose therapy increases fecal excretion of potassium. All these conditions can lead to profound hypokalemia. Therefore, potassium requirements in the liver failure patient receiving specialized nutritional support often are increased substantially. 

The use of CA inhibitors as diuretics is limited by their propensity to cause metabolic acidosis and hypokalemia. Their use can be indicated in patients with metabolic alkalosis and secondary hyperaldosteronism resulting for example from aggressive use of loop diuretics. Furthermore, CA inhibitors are effective dtugs to produce a relatively alkaline urine for the treatment of cysteine and uric acid stones as well as for the accelerated excretion of salicylates. Perhaps the most common use of CA inhibitors is in the treatment of glaucoma. 

No unique signs or symptoms are associated with mild to moderate metabolic alkalosis. Some patients complain of symptoms related to the underlying disorder (e.g., muscle weakness with hypokalemia or postural dizziness with volume depletion) or have a history of vomiting, gastric drainage, or diuretic use. 

Metabolic alkalosis and respiratory acidosis can occur in patients with chronic obstructive pulmonary disease and respiratory acidosis who are treated with salt restriction, diuretics, and possibly glucocorticoids. 

In metabolic alkalosis and respiratory acidosis, pH does not usually deviate significantly from normal, but treatment can be required to maintain Pao2 and PaC02 at acceptable levels. Treatment should be aimed at decreasing plasma bicarbonate with sodium and potassium chloride therapy, allowing renal excretion of retained bicarbonate from diuretic-induced metabolic alkalosis. 

Oral Treatment of hypokalemia in the following conditions With or without metabolic alkalosis digitalis intoxication familial periodic paralysis diabetic acidosis diarrhea and vomiting surgical conditions accompanied by nitrogen loss, vomiting, suction drainage, diarrhea, and increased urinary excretion of potassium certain cases of uremia hyperadrenalism starvation and debilitation corticosteroid or diuretic therapy. 

Electrolyte imbalance and BUN increases Hyponatremia and hypochloremia may occur when amiloride is used with other diuretics. Increases in BUN levels usually accompany vigorous fluid elimination, especially when diuretic therapy is used in seriously ill patients, such as those who have hepatic cirrhosis with ascites and metabolic alkalosis, or those with resistant edema. 

Volume depletion of some degree occurs with all diuretics following prolonged use. This can cause problems, such as postural hypotension, in those with poor cardiac function. Volume depletion also causes a fall in glomerular filtration that can trigger homeostatic reflexes such as increased aldosterone and antidiuretic hormone secretion. This contributes to electrolyte disturbances, such as hypokalaemia and metabolic alkalosis. 

Acidosis and alkalosis are infrequent. Metabolic acidosis is a side effect of acetazolamide therapy and is due to bicarbonate loss in the PCT. All the K+-sparing diuretics can cause metabolic acidosis by H+ retention in the cells of the collecting duct. Metabolic alkalosis is associated with the loop and thiazide drugs. Reflex responses to volume depletion cause reabsorption of HCO-3 in the PCT and H+ secretion in the collecting tubule. 

Metabolic alkalosis is generally treated by correction of abnormalities in total body K+, intravascular volume, or mineralocorticoid levels. However, when the alkalosis is due to excessive use of diuretics in patients with severe heart failure, replacement of intravascular volume may be contraindicated. In these cases, acetazolamide can be useful in correcting the alkalosis as well as producing a small additional diuresis for correction of volume overload. Acetazolamide can also be used to rapidly correct the metabolic alkalosis that may develop in the setting of respiratory acidosis. 

Diuretic-induced metabolic alkalosis is another adverse effect that may further compromise cardiac function. This complication can be treated with replacement of K+ and restoration of intravascular volume with saline however, severe heart failure may preclude the use of saline even in patients who have received excessive diuretic therapy. In these cases, adjunctive use of acetazolamide helps to... 

Children with heart disease often require high-dose diuretic therapy, which can lead to hypochloremic metabolic alkalosis. There are limited data on the safety of acetazolamide in the treatment of hypochloremic metabolic alkalosis in children. In 28 patients, median age 2 (range 0.3-20) months who took acetazolamide 5 mg/kg for 3 days, there were no adverse events (36). There was no significant difference in any electrolyte concentration, except for serum HC03, which fell from 36 to 31 mmol/1, and serum chloride, which rose from 91 to 95 mmol/1. There was no change in urine output. Acetazolamide appears to be safe in very young patients when given for 3 consecutive days. 

Patients with congenital nephrogenic diabetes insipidus are often treated with a combination of a thiazide and a potassium-sparing diuretic, without consensus on the preferred potassium-sparing diuretic. A Japanese adult was systematically studied to determine the renal effects of hydrochlorothiazide plus amiloride and hydrochlorothiazide plus triamterene (1). The combination with amiloride was superior to that with triamterene in preventing excessive urinary potassium loss, hjrpokalemia, and metabolic alkalosis. These results suggest that amiloride is the preferred add-on therapy to hydrochlorothiazide in nephrogenic diabetes insipidus. 

Around 60-70% of the filtered sodium is usually reabsorbed in the proximal tubule therefore, acetazolamide could be expected to have a rather potent diuretic effect. However, it produces rather modest diuresis because most of the excess sodium leaving the proximal tubule can be reabsorbed in the more distal segments of the nephron. Furthermore, its diuretic action is progressively diminished by the development of hyperchloremic metabolic acidosis caused by the loss of bicarbonate ions into the urine (Martinez-Maldonado Cordova 1990, Rose 1989, 1991, Wilcox 1991). In humans, the primary indication for acetazolamide (as a diuretic agent) is the treatment of edema with metabolic alkalosis. 

The combination of respiratory and metabolic alkalosis is the most common mixed acid-base disorder. This mixed disorder occurs frequently in critically ill surgical patients with respiratory alkalosis caused by mechanical ventilation, hypoxia, sepsis, hypotension, neurologic damage, pain, or drugs, and with metabolic alkalosis caused by vomiting or nasogastric suctioning and massive blood transfusions. It may also occur in patients with hepatic cirrhosis who hyperventilate, receive diuretics, or vomit, as well as in patients with chronic respiratory acidosis and an elevated plasma bicarbonate concentration... 

This mixed disorder often occurs in patients with chronic obstructive pulmonary disease and chronic respiratory acidosis who are treated with salt restriction, dinretics, and possibly glncocorticoids. When diuretics are initiated, the plasma bicarbonate may increase because of increased renal bicarbonate generation and reabsorption, providing mechanisms for both generating and maintaining metabolic alkalosis. The elevated pH diminishes respiratory drive and may therefore worsen the respiratory acidosis. 

This patient s hypokalaemia and metabolic alkalosis can be explained by profound potassium depletion due to the use of diuretics with an inadequate intake of potassium.The principles of therapy are potassium supplementation and alteration of her drug regimen to one that will ameliorate potassium loss, e.g. use of an ACE inhibitor. 

Furosemide metabolic alkalosis hyperuricemia blood dyscrasias rashes lipid changes as with thiazide-type diuretics... 

The side effects of diuretics are discussed in Chapter 28. With regard to diuretic use in heart failure, the most important adverse sequelae of diuretics are electrolyte abnormalities, including hyponatremia, hypokalemia, and hypochloremic metabolic alkalosis. Both hypokalemia and renal wasting can be limited by administration of oral KCl supplements or a K -sparing diuretic. 

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