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Bromide was once used as a sedative and an effective anticonvulsant, and until 1975 it was a major ingredient in over-the-counter products such as Bromo-Seltzer and Dr. Miles' Nervine. Bromides are still used to treat epilepsy in dogs. Bromism (chronic bromide intoxication) was once common, accounting for as many as 5–10% of admissions to psychiatric hospitals. Bromism is now rare, but cases continue to be reported worldwide owing to bromide-based medications. Recent examples include the following: 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 bromovaleryurea/bromisoval, used as an analgesic (Taiwan). 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. Mechanism of toxicity

    1. Bromide ions substitute for chloride in various membrane transport systems, particularly within the nervous system. Bromide is preferentially reabsorbed over chloride by the kidney. Up to 30% 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. The half-life is 9–12 days, and bioaccumulation occurs with chronic exposure. Clearance is about 26 mL/kg/d, and elimination is renal. Bromide is excreted in breast milk. It crosses the placenta, and neonatal bromism has been described.

  2. Toxic dose. 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.

  3. Clinical presentation. 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, hallucinations, psychosis, weakness, stupor, and coma. At one time, bromism was responsible for 5–10% of admissions to psychiatric facilities.

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

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

  4. Diagnosis. Consider bromism in any confused or psychotic patient with a high serum chloride level and a low or negative anion gap. The serum chloride level is often falsely elevated owing to interference by bromide in the analytic test; the degree of elevation varies with the instrument.

    1. Specific levels. Assays are not readily available from most clinical laboratories. Endogenous serum bromide does not usually exceed 5 mg/L (0.06 mEq/L). The threshold for detection by usual methods is 50 mg/L. Therapeutic levels are 50–100 mg/L (0.6–1.2 mEq/L); levels above 3000 mg/L (40 mEq/L) may be fatal.

    2. Other useful laboratory studies include electrolytes, glucose, BUN, creatinine, and abdominal radiography (bromide is radiopaque).

  5. Treatment

    1. Emergency and supportive measures

      1. Protect the airway and assist ventilation ...

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