Ammonium chloride metabolic acidosis with

Hematological Effects. No information was located regarding the hematological effects of ammonia or ammonium compounds in humans following oral exposure. Repeated exposure to ammonium chloride in animals resulted in metabolic acidosis with related changes in bone metabolism and serum calcium. 

Megarbane B, Bruneel F, Bedos JP, et al. 2000. Ammonium chloride poisoning a misunderstood cause of metabolic acidosis with normal anion gap. Intensive Care Med 26(12) 1869. 

Dermatologic reactions Dermatologic reactions may occur exercise care when given to any patient receiving a drug with significant tendency to produce dermatitis. Toxic symptoms If serious toxic symptoms occur, administer ammonium chloride (8 g daily in divided doses for adults) 3 or 4 days a week for several months after therapy has been stopped acidification of the urine increases renal excretion by 20% to 90%. Exercise caution in renal function impairment and/or metabolic acidosis. 

The pH-buffering of extracellular fluid depends in part on the carbon dioxide/ bicarbonate equilibrium so that the intake of sodium bicarbonate is followed by a brief alkalosis and an increased excretion of sodium carbonate in the urine. Depending on its carbonate concentration, the pH of the urine may rise to 8.07. Large doses (80—100 g/day) of sodium bicarbonate were needed if the pH of stomach contents was to be maintained at 4 or over in patients with duodenal ulcers8. Oxidation of organic anions in the body to carbon dioxide and water permits the use of sodium citrate, lactate or tartrate instead of sodium bicarbonate. In an analogous manner the ingestion of ammonium chloride induces a brief acidosis as a result of the metabolic conversion of ammonia to urea and lowers the pH of the urine. 

Increased urinary calcium following exercise may be caused by the onset of metabolic acidosis associated with prolonged exercise. Elevation of urinary calcium has been noted in studies where metabolic acidosis was induced by feeding an acid ash diet (75), hydrochloric acid (76), or ammonium chloride (77). Renal tubular acidosis can also induce elevated urinary calcium (78). Walser (79) re-... 

Ammonium chloride, bicarbonate, and furosemide loading tests in an epileptic man with metabolic acidosis and episodic hypokalemia taking zonisamide showed evidence of distal renal tubular acidosis (9). On reexamination 7 weeks after zonisamide had been replaced with phenytoin, the renal tubular acidosis had resolved. 

The acid load test is occasionally used for the diagnosis of renal tubular acidosis, conditions in which metabolic acidosis arises from diminished tubular secretion of hydrogen ions. Ammonium chloride is administered orally in gelatin capsules. Urine samples are collected for the following 8 hours. With normal renal function, the pH of at least one sample should be less than 5.3. If necessary in a difficult diagnosis, the excretion rates of titratable acid and ammonium ion. and serum bicarbonate concentration, are all measured. This test should not be perl ormed on patients who are already acidotic or who have liver disease. 

Diuretic therapy is a common iatrogenic origin of metabolic disturbances of acid-base physiology. Diuretics are administered for their naturetic properties particularly in patients with cardiac, hepatic, pulmonary and renal disease, to rid the body of excess extracellular fluid. When the loss of sodium is matched by losses of other extracellular electrolytes in proportion to their extracellular concentrations, no disturbance of acid-base balance occurs. In cases where there is a disproportionate loss of bicarbonate, the result is metabolic acidosis. Conversely when there is an exaggeration of loss of ammonium or chloride ions by comparison with sodium, this leads to metabolic alkalosis. 

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