Acidosis hyperchloremic

Metabolic acidosis Hyperchloremic, nonanion gap, metabolic acidosis is associated with topiramate treatment. This metabolic acidosis is caused by renal bicarbonate loss because of the inhibitory effect of topiramate on carbonic anhydrase. Generally, topiramate-induced metabolic acidosis occurs early in treatment, although cases can occur at any time during treatment. Bicarbonate decrements usually are mild to moderate rarely, patients can experience severe decrements to values below 10 mEq/L. Conditions or therapies that predispose to acidosis may be additive to the bicarbonate lowering effects of topiramate. If metabolic acidosis develops and persists, consider reducing the dose or discontinuing topiramate. 

A non-anion gap acidosis (hyperchloremic acidosis anion gap <16 mEq/L) is characterized by an acidosis where the anion gap is unchanged from the patient s baseline. This occurs as the decrease in serum bicarbonate is equaled by the rise in serum chloride [3]. Bicarbonate is typically lost from the gastrointestinal tract (i.e., diarrhea) or through the kidneys (i.e., renal tubular acidosis) [4]. Although a few metabolic disorders result in a non-anion gap acidosis (i.e., Fanconi-Bickel syndrome, OMIM 227810), a non-anion gap acidosis is typically not the result of an inborn error of metabolism. 

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

Hyperchloremic (nonanion gap) metabolic acidosis ° Consumption/loss of bicarbonate... 

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. 

Alkali therapy can be used to treat patients with acute severe metabolic acidosis due to hyperchloremic acidosis, but its role is controversial in patients with lactic acidosis. Therapeutic options include sodium bicarbonate and tromethamine. 

Hyperchloremic acidosis has been noted in some cases (B7, K13) this is presumably due to defective tubular reabsorption of bicarbonate. Phosphate-losing rickets or marked hypokalemia have not as yet been reported in galactosemia, but some cases show roentgenological evidence of osteoporosis (M2), and Holzel et al. (H8) record low levels of serum potassium. 

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. 

Hypersensitivity to these agents depressed sodium or potassium serum levels marked kidney and liver disease or dysfunction suprarenal gland failure hyperchloremic acidosis adrenocortical insufficiency severe pulmonary obstruction with inability to increase alveolar ventilation since acidosis may be increased (dichlorphenamide) cirrhosis (acetazolamide, methazolamide) long-term use in chronic noncongestive angle-closure glaucoma. 

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

Bile acid-sequestering resins Yes Reduces LDL n. Severe 11, with statin or niacin GI distress, hyperchloremic acidosis... 

GI tract obstruction, hyperchloremic acidosis, and osteoporosis secondary to calcium excretion may occur. 

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. 

The renal lesions which have been described in idiopathic hypercalcemia are not specific. Similar changes have been observed in hyperchloremic renal acidosis of infancy (B7, D7), in various other diseases of infancy and in hypervitaminosis D. It is interesting to note that a recent re-examination of the histological sections of Thatcher s cases of a quarter of a century ago showed that the changes there were essentially the same as those occurring in idiopathic hypercalcemia of infancy (Rl). 

The twins were referred subsequently to a metabolic specialist because of the suspicion of an inborn error of metabolism. Biochemical testing revealed each had a hyperchloremic (increased blood chloride concentration) metabolic acidosis that was more profound in Elizabeth. Serum levels of glucose and liver transaminases were normal. Urinary organic acids revealed modestly increased concentrations of lactate and ketone bodies. Blood samples and fibroblasts from skin biopsies from both girls were sent to an established diagnostic laboratory for genetic mitochondrial diseases. Tests of respiratory chain complex enzymatic activities were normal. 

Baseline and periodic serum bicarbonate levels to monitor for hyperchloremic, nonanion gap metabolic acidosis (i.e., decreased serum bicarbonate below the normal reference range in the absence of chronic respiratory alkalosis)... 

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. 

Carbonic anhydrase inhibitors should be used with caution in patients with respiratory acidosis or those with severe loss of respiratory capacity, and in patients with diabetes mellitus. They are contraindicated in patients with hepatic disease or insufficiency, reduced serum concentrations of sodium or potassium, adrenocortical insufficiency, hyperchloremic acidosis, or severe renal disease or dysfunction. They should also be avoided in patients taking salicylates. 

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). 

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