| 词条 | Bromism |
| 释义 |
| name = Bromism | synonyms = | image = | alt = | caption = | pronounce = | field = | symptoms = | complications = | onset = | duration = | types = | causes = | risks = | diagnosis = | differential = | prevention = | treatment = | medication = | prognosis = | frequency = | deaths = }} 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disorder, being responsible for 5 to 10% of psychiatric hospital admissions, but is now uncommon since bromide was withdrawn from clinical use in many countries and was severely restricted in others.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
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 effects include nausea and vomiting as acute adverse effects and anorexia and constipation with chronic use.[1]
Dermatological effects include cherry angiomas, acneiform, pustular and erythematous rashes.[1] CauseHigh 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] DiagnosisBromism 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{{Cleanup|section|reason=no references or explanation of iodine and sulphur's connection to bromism|date=February 2019}}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.{{fact|date=February 2018}} 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.{{fact|date=February 2018}} References1. ^1 2 3 4 5 {{cite book |last1=Olson |first1=Kent R. |title=Poisoning & drug overdose |url=https://books.google.com/books?id=vuec3nTovyUC |edition=4th |date=1 November 2003 |publisher=Appleton & Lange |isbn=978-0-8385-8172-8 |pages=140–141 |chapter= |chapterurl= }} 2. ^{{cite book |last1=Galanter |first1=Marc |last2=Kleber |first2=Herbert D. |title=The American Psychiatric Publishing Textbook of Substance Abuse Treatment |url=https://books.google.com/books?id=6wdJgejlQzYC |edition=4th |date=1 July 2008 |publisher=American Psychiatric Publishing Inc |location=United States of America |isbn=978-1-58562-276-4 |page=217 |chapter= |chapterurl= }} 3. ^1 {{cite journal|title=Bromism from Excessive Cola Consumption |date=1997 |doi=10.3109/15563659709001219 |volume=35 |issue=3 |journal=Clinical Toxicology |pages=315–320|last1 = Horowitz|first1 = B. Zane}} External links{{Medical resources| DiseasesDB = | ICD10 = F13.2, G92, T42.6, T59.8 | ICD9 = {{ICD9|967.3}}, {{ICD9|E852.2}} | ICDO = | OMIM = | MedlinePlus = | eMedicineSubj = | eMedicineTopic = | MeshID = }}{{Poisoning and toxicity}} 6 : Neurological disorders|Substance-related disorders|Toxic effects of dietary elements|Syndromes affecting the nervous system|Syndromes affecting the gastrointestinal tract|Syndromes affecting the skin |
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