Urinary alkalinisers

Urinary alkalinisation increases the urine elimination of certain poisons by shifting the urine pH above 7.5 [1,21,79]. It is achieved by intravenous injection of a sodium bicarbonate solution. Raised pH of urine facilitates elimination of acidic drugs such as salicylates and barbiturates as they become ionised. The rate of reabsorption of an ionised drug into the blood is significantly lower than that of a non-ionised drug [1, 79]. In all cases however AC administration is more efficient than urinary alkalinisation [1,80]. It should be also kept in mind that WBI and urinary alkalinisation are relatively slow procedures which may cause delay with AC administration. 

The effect of urinary pH on the clearance of methadone is an established interaction, but of uncertain importance. Be alert for any evidence of reduced methadone effects in patients whose urine becomes acidic because they are taking large doses of ammonium chloride. Lowering the urinary pH to 5 with ammonium chloride to increase the clearance can also be used to treat toxicity. Theoretically, urinary alkalinisers such as sodium bicarbonate and acetazolamide may increase the effect of methadone. 

The urinary excretion of amfetamines is increased by urinary acidifiers (ammonium chloride) and reduced by urinary alkalinisers (sodium bicarbonate). 

A well established and well understood interaction but reports of problems in practice seem rare. The interaction has been exploited to increase the clearance of amfetamines in cases of overdose by acidifying the urine with ammonium chloride. Conversely it can represent an undesirable interaction if therapeutic doses of amfetamines are excreted too rapidly. Care is needed to ensure that amfetamine toxicity does not develop if the urine is made alkaline with sodium bicarbonate or another urinary alkaliniser, acetazolamide. 

Urinary alkalinisers can reduce the loss of diethylcarbamazine in the urine, whereas urinary acidifiers can increase the loss. The clinical importance of this is unknown. 

Urinary alkalinisers can increase the retention of quinine in man, and antacids can reduce the absorption of quinine in animals. None of these interactions appears to be of general clinical importance. 

Urinary alkalinisers (e.g. potassium or sodium citrate) and those antacids that can raise the urinary pH above 5.5 should not be used during treatment with methenamine because they inhibit its activation. 

Vitamin C 1 g three times daily was found to have no effect on the urinary excretion of methotrexate 45 mg given intravenously to a woman with breast cancer, despite the urine becoming more acidic at pH 5.9 (compare Methotrexate + Urinary alkalinisers , p.654). She was also receiving oral cyclophosphamide, propranolol, amitriptyline, perphenazine and prochlorperazine. No special precautions appear to be necessary. 

The interaction between ephedrine or pseudoephedrine and urinary alkalinisers are established but reports of adverse reactions in patients appear to be rare. Be aware that any increase in the adverse effects of these drugs (tremor, anxiety, insomnia, tachycardia, etc.) could be due to drug retention brought about by this interaction. Acetazolamide makes the urine alkaline and would be expected to interact with ephedrine and pseudoephedrine in the same way as sodium bicarbonate. 

Prescott LF, Balali-Mood M, Critchley JA, Johnstone AF, Proudfoot AT. Diuresis or urinary alkalinisation for salicylate poisoning Br Med (Clin Res Ed). 1982 285 1383-1386. 

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