Bromides are well absorbed from the gastrointestinal (GI) tract. Their oral bioavailability is about 96%, and peak serum concentrations are reached within 2 hours. Bromide has a low volume of distribution (0.35–0.48 L/kg) and tends to concentrate in erythrocytes and neurons.[12,][13]
Serum bromide concentrations are expressed in several units, including mEq/L, mg/L, mg/dL, and mmol/L. The interpretation of recorded values is therefore subject to considerable confusion. Because of bromide's close relationship with chloride, its serum concentrations are best expressed in the equivalent mEq/L or mmol/L. Unit relationships are as follows:
Bromide is readily filtered by the glomeruli. Once in the tubular lumen, bromide competes with chloride for reabsorption with tubules having a higher affinity for bromide ion; therefore, chloride is preferentially excreted under typical circumstances. As a result, prolonged administration of bromide results in significant total-body loss of chloride. An intimate relationship exists between in situ chloride and bromide concentrations; the body maintains the molar sum of chloride and bromide ion at about 110 mmol/L.[12] The elimination half-life of bromide is 7 to 12 days; this half-life is increased with a salt-deficient diet.[1,][11,][12] Average renal bromide clearance is about 26 mL/kg per day. Bromide readily diffuses across the placenta and accumulates in fetal tissues. It is also secreted into breast milk.
Although animal studies have reported LD50 in the range of 2 to 5 g/kg, the reported human lethal dose is as low as 14 mg/kg. Nonetheless, experimental administration of up to 9 mg/kg/day of bromide for 12 weeks was reported to cause difficulty with concentration and sleepiness only. Bromide intoxication usually results from long-term overmedication, resulting in bromism.
Bromism is a clinical syndrome that consists of GI, dermatologic, and CNS manifestations (Box 96-1). GI manifestations include nausea, vomiting, a fetid odor on the breath, anorexia, and weight loss.[2] Dermatologic manifestations are found in as many as 30% of those with bromism[2]; bromoderma is the name given to the associated skin lesions. The most common lesion is an acneiform eruption on the face. Another frequent finding is an eruption resembling ecthyma, appearing on the lower extremities (nodose bromoderma). Other skin lesions include pemphigus-like, bromide-filled vesicles on the lower extremity, erythema multiforme, pyoderma gangrenosum, and bromoderma tuberosum (tumor-like lesions).
The neurobehavioral signs and symptoms of bromism are prominent. Behavioral disturbances include the appearance of a bromide dementia characterized by delirium, agitation, auditory and visual hallucinations, depression, and schizophrenic and manic-depressive psychosis. Hallucinosis may occur with an otherwise clear consciousness. Neurologic manifestations of bromism include dysarthria, hyporeflexia, and coma. An increased cerebrospinal fluid protein level occurs in 2% to 40% of patients.[14] Low-grade fever may be found in as many as 25% of cases.[2] Neurologic signs of bromism are slow to resolve and lag behind the decrease in serum bromide concentration because of the slow diffusion of bromide out of the CNS.[13] Among those who present with obtundation or coma, retrograde amnesia may develop. Ocular findings may also be striking in bromide intoxication and may consist of mydriasis, color disturbances, blurred vision, and micropsia or macropsia. These latter two syndromes are perceptual distortions in which objects appear smaller or larger, respectively, than they actually are. Ocular bobbing (opsoclonus) has been described in a patient with bromide encephalopathy.[15] Papilledema is occasionally found on funduscopic evaluation.
![:\](https://bluelight.org/xf/BL_Images/Orig_Emoji/wrygrin.gif "wry grin :\")
