Bromism

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Bromism
SpecialtyEmergency medicine, Psychiatry, Neurology Edit this on Wikidata

Bromism is the syndrome which results from the long-term consumption of bromine, usually through bromide-based sedatives such as potassium bromide and lithium bromide. Bromism was once a very common disorder, being responsible for 5 to 10% of psychiatric hospital admissions, but is now uncommon since bromide was withdrawn from clinical use in many countries and was severely restricted in others.

Presentation[edit]

Bromide rash
Neurological and psychiatric

Neurological and psychiatric symptoms are widely varied and may include the symptoms of restlessness, irritability, ataxia, confusion, hallucinations, psychosis, weakness, stupor and, in severe cases, coma.[1]

Gastrointestinal

Gastrointestinal effects include nausea and vomiting as acute adverse effects and anorexia and constipation with chronic use.[1]

Dermatological

Dermatological effects include cherry angiomas, acneiform, pustular and erythematous rashes.[1]

Causation[edit]

High levels of bromide chronically impair the membrane of neurons, which progressively impairs neuronal transmission, leading to toxicity, known as bromism. Bromide has an elimination half-life of 9 to 12 days, which can lead to excessive accumulation. Doses of 0.5 to 1 gram per day of bromide can lead to bromism. Historically, the therapeutic dose of bromide is about 3 to 5 grams of bromide, thus explaining why chronic toxicity (bromism) was once so common. While significant and sometimes serious disturbances occur to neurologic, psychiatric, dermatological, and gastrointestinal functions, death is rare from bromism.[1]

Bromism is caused by a neurotoxic effect on the brain which results in somnolence, psychosis, seizures and delirium.[2] Bromism has also been caused by excessive soda consumption, due to the presence of brominated vegetable oil, leading to headache, fatigue, ataxia, memory loss, and eventually inability to walk in one case.[3]

Diagnosis[edit]

Bromism is diagnosed by checking the serum chloride level, electrolytes, glucose, BUN and creatinine, as well as symptoms such as psychosis. Bromide is also radiopaque, so an abdominal X-ray may also help in the diagnosis.[1]

Treatment[edit]

There are no specific antidotes or protocols for bromide poisoning of the body. Although administering chloride (or dietary salt loading protocol) coupled with fluids can help the body to excrete bromide more quickly. Furosemide may help aid urinary excretion in individuals with renal impairment or where bromide toxicity is severe.[1] In one case, hemodialysis was used to reduce bromide's half-life to 1.38h, dramatically improving the patient's condition.[3]

Iodine deficiency is also linked to weaker (less detectable) forms of bromism.[citation needed] Iodine and bromine are closely related to each other in behavior and location on the periodic table. Bromine will tend to displace iodine in tissues and blood when there is an opportunity to do so. Supplementary intake of iodine should be preceded by a salt loading protocol, or consumption of dietary sulfur beforehand.[citation needed] Sulfur is required for sulfur metabolism chemistry in the body.

References[edit]

  1. ^ a b c d e f Olson, Kent R. (1 November 2003). Poisoning & drug overdose (4th ed.). Appleton & Lange. pp. 140–141. ISBN 978-0-8385-8172-8.
  2. ^ Galanter, Marc; Kleber, Herbert D. (1 July 2008). The American Psychiatric Publishing Textbook of Substance Abuse Treatment (4th ed.). United States of America: American Psychiatric Publishing Inc. p. 217. ISBN 978-1-58562-276-4.
  3. ^ a b "Bromism from Excessive Cola Consumption". Clinical Toxicology. 35: 315–320. 1997. doi:10.3109/15563659709001219. Retrieved 2016-01-18.

External links[edit]

Classification