Metabolic acidosis hyperchloremic

Monitor for evidence of cerebral edema, noncardiogenic (permeability) pulmonary edema, acute respiratory distress syndrome, hyperchloremic metabolic acidosis, and vascular thrombosis... 

Crystalloids consist of electrolytes (e.g., Na+, Cl-, K1) in water solutions, with or without dextrose. Lactated Ringer s solution may be preferred because it is unlikely to cause the hyperchloremic metabolic acidosis seen with infusion of large amounts of normal saline. 

Szerlip H, Singer I Hyperchloremic metabolic acidosis after chlorine inhalation. Am J Met/ 77 581-582, 1984... 

Gynecomastia Gynecomastia may develop and appears to be related to dosage and duration of therapy. It is normally reversible when therapy is discontinued. Reversible hyperchloremic metabolic acidosis Reversible hyperchloremic metabolic acidosis, usually in association with hyperkalemia, occurs in some patients with decompensated hepatic cirrhosis, even in the presence of normal renal function. 

Hyperkalemia Significant hyperkalemia (sometimes associated with hyperchloremic metabolic acidosis) and hyperuricemia have been seen occasionally in individual patients. 

Carbonic anhydrase inhibitors were the forerunners of modern diuretics. They were discovered when it was found that bacteriostatic sulfonamides caused an alkaline diuresis and hyperchloremic metabolic acidosis. With the development of newer agents, carbonic anhydrase inhibitors are now rarely used as diuretics, but they still have several specific applications that are discussed below. The prototypical carbonic anhydrase inhibitor is acetazolamide. 

Acetazolamide, others Inhibition of the enzyme prevents dehydration of H2CO3 and hydration of CO2 Reduces reabsorption of HC03 in the kidney, causing self-limited diuresis hyperchloremic metabolic acidosis reduces body pH, reduces intraocular pressure Glaucoma, mountain sickness, edema with alkalosis Oral and topical preparations available duration of action 8-12 h Toxicity Metabolic acidosis, renal stones, hyperammonemia in cirrhotics... 

Colestyramine has been reported to have caused a hyperchloremic metabolic acidosis. 

Eaves ER, Korman MG. Cholestyramine induced hyperchloremic metabolic acidosis. Aust NZ J Med 1984 14(5) 670-2. 

Several sulfonamides, including co-trimoxazole in high doses, can produce hyperchloremic metabolic acidosis. This has even been seen in patients with extensive burns receiving topical mafenide (1077). Mafenide (Sulfamylon) and its metabolite para-sulfamoylbenzoic acid inhibit carbonic acid anhydrase, resulting in reduced reabsorption of bicarbonate and thus bicarbonate wasting. 

Inhibition of carbonic anhydrase activity profoundly depresses bicarbonate reabsorption in the proximal tubule. At its maximal safely administered dosage, 85% of the bicarbonate reabsorptive capacity of the superficial proximal tubule is inhibited. Some bicarbonate can still be absorbed at other nephron sites by carbonic anhydrase-independent mechanisms, and the overall effect of maximal acetazolamide dosage is about 45% inhibition of whole kidney bicarbonate reabsorption. Nevertheless, carbonic anhydrase inhibition causes significant bicarbonate losses and hyperchloremic metabolic acidosis. Because of this and the fact that HCO3" depletion leads to enhanced NaCl reabsorption by the remainder of the nephron, the diuretic efficacy of acetazolamide decreases significantly with use over several days. 

Pulse oximetry may indicate low oxygen saturation (Traub et al, 2002). While arterial blood gases usually indicate hypoxemia, carbon dioxide levels have been shown to be decreased, increased, or normal (Giiloglu et al, 2002 Traub et al, 2002). A hyperchloremic metabolic acidosis may show up on blood chemistries due to systemic absorption of hydrochloric acid. 

Mafenide is a topical sulfonamide that has been used for the treatment of burns but is now obsolete. Its adverse effects include hyperchloremic metabolic acidosis and (possibly) methemoglobinemia (1). Pulmonary insufficiency has been ascribed to mafenide acetate cream (SEDA-8,160). 

A 20-year-old man taking topiramate, valproate, and phenytoin had acute mental changes with hyperchloremic metabolic acidosis (46). He had been receiving a modest dose of topiramate for 9 months. His mental status returned to normal within 48 hours of withdrawal. 

An 11-year-old boy with refractory partial epilepsy who had been taking topiramate 300 mg/day for 13 months developed hyperventilation. He had a hyperchloremic metabolic acidosis with partial respiratory compensation. The hyperventilation and acidosis resolved after the administration of sodium bicarbonate and reduction of the dose of topiramate. 

Amiloride 5 mg/day 10 mg/day 50% 100% 100% Avoid Flyperkalemia with GFR < 30 ml/min, especially in diabetics may cause hyperchloremic metabolic acidosis No data No data No data... 

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. 

PTH increases the renal clearance of bicarbonate and phosphate. In hyperparathyroidism, a mild hyperchloremic metabolic acidosis may be observed whereas in nonparathyroid hypercalcemia, a mild hypochloremic metabolic alkalosis may be observed. Although hypophosphatemia is often seen in hyperparathyroidism, the measurement of serum phosphate is of limited value because hypophosphatemia is also found in hypercalcemic cancer patients. 

In the kidneys, PTH (1) induces 25-hydroxyvitamin D-la-hydroxylase, increasing the production of l,25(OH)2D, which stimulates intestinal absorption of both calcium and phosphate, (2) increases calcium reabsorption in the distal convoluted tubule of the nephron, (3) decreases reabsorption of phosphate by the proximal tubule, and (4) inhibits Na -H antiporter activity, which favors a mild hyperchloremic metabolic acidosis in hyperparathyroid states. 

The common N-terminal explains the ability of PTHrP to interact with the PTH/PTHrP receptor, mimicking the biological actions of PTH in classic target tissues, including bone and kidney. Like PTH, PTHrP causes hypercalcemia and hypophosphatemia t and increases urinary cyclic AMP. However, when compared with patients with primary hyperparathyroidism, patients with PTHrP-induced hypercalcemia have lower concentrations of l,25(OH)2D and more typically have metabolic alkalosis (instead of hyperchloremic metabolic acidosis), reduced distal tubular calcium reabsorption, and reduced and uncoupled bone formation. 

Potential adverse effects associated with hypertonic fluid administration for circulatory insufficiency include cellular crenation and damage caused by the dramatic fluid shifts, as well as peripheral vein destruction from their high osmolality. Also, in the case of hypertonic sodium chloride solutions, there are the possibilities of neurologic damage from hypernatremia and hyperchloremic metabolic acidosis from hyperchloremia. In the limited number of studies conducted in humans to date, such adverse effects have been uncommon and apparently of little clinical importance. ... 

Renal tubular acidosis refers to a group of disorders characterized by impaired tubular renal acid handling despite normal or near-normal glomerular filtration rates. These patients often present with hyperchloremic metabolic acidosis. 

In hyperchloremic metabolic acidosis, bicarbonate losses from the ECF are replaced by chloride and the SAG remains normal. This decrease in bicarbonate results from losses from the gastrointestinal tract, dilution of bicarbonate in the ECF space by the addition of sodium chloride solutions, or the addition of chloride-containing acids to the ECF. Common causes of metabolic acidosis with an increased or a normal SAG are listed in Table 51-5. 

Laboratory analysis reveals low serum sodium and high serum potassium concentrations. Patients often will present with hyperchloremic metabolic acidosis. Because the deficiency is in the min-eralocorticoid, replacement with fludrocortisone in a dose of 0.1 to 0.3 mg is usually effective. Patients should be followed for blood pressure response as well as electrolyte status. 

Proteinuria is characteristic of diabetic nephropathy (20). Patients with diabetes mellitus may have massive proteinuria and the nephrotic syndrome. Some of these patients never develop glomerulosclerosis. Hypertension develops but is rarely malignant. Plasma renin activity is normal or decreased. More commonly, hypo-reninemic hypoaldosteronism with hyperkalemia and mild hyperchloremic metabolic acidosis is found. 

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