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Compounds containing bromide ions—including potassium-, sodium-, and ammonium bromide—were once used as sedatives and anticonvulsants, and were a major ingredient in over-the-counter products (eg, Bromo-Seltzer, Dr. Miles' Nervine) until 1975. Bromides are still used to treat epilepsy in dogs. Bromism (chronic bromide intoxication) was once common; 10% of patients admitted to psychiatric hospitals once had measurable bromide levels. Bromism is now rare, but cases continue to be reported worldwide owing to bromide-based medications. Recent examples include: Cordial de Monell, a teething/colic medication recalled because of infant bromism (United States); pipobroman/Vercyte/Amedel, an alkylating agent used for polycythemia vera (UK); and bromovalerylurea/bromisoval, used as an analgesic (Taiwan); several of the aforementioned preparations are still available for purchase online or in certain countries. In 2007, table salt contamination led to the greatest recorded outbreak of bromide poisoning, with 467 officially recognized cases (Angola). Bromide is still found in photographic chemicals, in some well water, in bromide-containing hydrocarbons (eg, methyl bromide, ethylene dibromide, halothane), and in some soft drinks containing brominated vegetable oil. Foods fumigated with methyl bromide may contain some residual bromide, but the amounts are too small to cause bromide toxicity.


  1. Bromide ions substitute for chloride in various membrane transport systems, particularly within the nervous system. Bromide ions diffuse more readily through GABAA receptor–mediated chloride channels, enhancing inhibitory neuronal effects. Bromide is preferentially reabsorbed over chloride by the kidney, and chloride excretion further increases when bromide ion intake exceeds elimination. Up to 45% of chloride may be replaced in the body. With high bromide levels, the membrane-depressant effect progressively impairs neuronal transmission.

  2. Pharmacokinetics. The volume of distribution of bromide is 0.35–0.48 L/kg; bioavailability of bromide salts is nearly 100%. The half-life is 9–12 days, and bioaccumulation occurs with chronic exposure. Clearance is about 26 mL/kg/d; elimination is renal. Bromide is excreted in breast milk. It crosses the placenta, and neonatal bromism has been described.


The adult therapeutic dose of bromide is 3–5 g. One death has been reported after ingestion of 100 g of sodium bromide. Chronic consumption of 0.5–1 g per day may cause bromism.


Death is rare. Acute oral overdose usually causes nausea and vomiting from gastric irritation. Chronic intoxication can result in a variety of neurologic, psychiatric, GI, and dermatologic effects.

  1. Neurologic and psychiatric manifestations are protean and include restlessness, irritability, ataxia, confusion, memory impairment, hallucinations, schizophreniform psychosis, weakness, stupor, and coma.

  2. Gastrointestinal effects include nausea and vomiting (acute ingestion) and anorexia and constipation (chronic use).

  3. Dermatologic effects include acneiform, pustular, granulomatous, bullous, and erythematous rashes. Up to 25–30% of patients are affected.


Consider bromism in any confused or psychotic patient with a high serum chloride level and a low or negative anion gap. The serum ...

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