Ammonium chloride dosing

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. 

Emetics, when administered in small doses, act as expectorants and are used in inflammatory conditions of the respiratory tract to increase the bronchial secretion and render it less tenacious. The most commonly used expectorants are ipecac, ammonium chloride, and apomorphine. The last named is administered in doses of 1 mg in the form of an elixir or syrup. Apomorphine injected in subemetic doses of 1 to 2 mg is also used as a sedative in the delirium following anesthesia, in acute alcoholic psychosis, and in patients manifesting severe agitation prior to anesthesia. 

Sometimes, we may want to use a f-test in a way that differs from our previous approach. Say, for example, we are considering the use of urinary acidification to hasten the clearance of amphetamine from patients who have overdosed. An initial trial in rabbits is used to test the general principal. One group of rabbits receives ammonium chloride to induce a lower urinary pH and another group acts as controls. All rabbits receive a test dose of radio-labelled drug, the clearance of which is studied over a few hours. In this case, the question posed should be is there an increase in clearance rather than the standard is there a difference in clearance The former constitutes a one-sided question. 

Saul and Archer (1984) demonstrated that ammonia is oxidized to nitrate in the rat. Three male Sprague-Dawley rats were administered 15N-labeled ammonium chloride by gavage at a dose of 1,000 /rmol for 5 d. A significant amount (0.28 0.03 jUmol, mean SE) of excess 15N-labeled nitrate was found in the urine. 

The second exception was specific for HZSM-5 that had been acidified with ammonium chloride and which had large particle sizes. The differential heat curve at 416-423 K for these samples passed through a maximum at relatively low coverages. This behavior could be explained by the combination of three independent phenomena immobile adsorption, mass-transfer limitations, and preferential location of the most energetic acid sites in the internal pores of the zeolite structure. Apparently, the strongest sites were not accessible to ammonia when the first doses were introduced but became progressively covered when further ammonia was added. Electron paramagnetic resonance studies (93) provided data to support this hypothesis. 

Ammonium chloride, which is used as an expectorant in productive cough, can cause gastric irritation, acidosis, and hypokalemia in large doses (1). 

The dose of ammonium chloride can be calculated on the basis of the chloride deficit using the same method as for HCl, using the conversion of 20 g ammonium chloride providing 374 mEq of H . However, only half of the calculated dose of ammonium chloride should be administered so as to avoid ammonia toxicity. Ammonium chloride is available as a 26.75% solution containing 100 mEq in 20 mL, which should be further diluted prior to administration. A dilute solution may be prepared by adding 100 mEq of ammonium chloride to 500 mL of normal saline and infusing the solution at a rate of no more than 1 mEq/min. Improvement in metabolic stams is usually seen within 24 hours. CNS toxicity, marked by confusion, irritability, seizures, and coma, has been associated with more rapid rates of administration. Ammonium chloride must be administered cautiously to patients with renal or hepatic impairment. In patients with hepatic dysfunction, impaired conversion of ammonia to urea may result in increased ammonia levels and worsened encephalopathy. In patients with renal failure, the increased urea synthesis may exacerbate uremic symptoms. ... 

Ammonium chloride and other urine acidifiers, as well as probenecid and sulfinpyrazone, increase salsalate blood levels. Antacids in high doses and other urine alkalizers decrease salsalate blood levels. Corticosteroids enhance salsalate elimination. Food and antacids delay and decrease absorption of salsalate. 

Strontium-90 Alginate or aluminum hydroxide-containing antacids may reduce intestinal absorption of strontium. Dose 10 g, then 1 g 4 times daily. Barium sulfate may also reduce Sr absorption. Dose 100 g in 250 mL water PO. Calcium gluconate may dilute the effect of strontium. Dose 2 g in 500 mL PO or IV. Ammonium chloride is a demineralizing agent. Dose 3 g PO 3 times daily. 

A study in 6 healthy subjects found that the cumulative 72-hour urinary excretion of unchanged dextropropoxyphene was increased sixfold by acidification of the urine with oral ammonium chloride and reduced by 95% by alkalinisation with sodium bicarbonate the half-life of dextropropoxyphene was also shortened by ammonium chloride. The excretion of the active metabolite norpropoxyphene was much less dependent on urinary pH. However, the cumulative excretion of dextropropoxyphene and norpropoxyphene, even into acidic urine, accounted for less than 25% of the dose during 72 hours. ... 

A pharmacokinetic study in 5 healthy subjects given a 10-mg intramuscular dose of methadone found that the plasma half-life was 19.5 hours when the urine was made acidic (pH 5.2) with ammonium chloride, compared with 42.1 hours when the urine was made alkaline (pH 7.8) with sodium bicarbonate. The clearance of the methadone fell from 134 to 91.9 mL/minute when the urine was changed from acidic to alkaline. ... 

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