Hydrogen Bromide

CAS RN:10035-10-6

Treatment Overview

0.4.2 ORAL EXPOSURE
  • A) MANAGEMENT OF MILD TO MODERATE TOXICITY
    • 1) Care is symptomatic and supportive. Administer IV 0.9% sodium chloride to increase bromide elimination.
  • B) MANAGEMENT OF SEVERE TOXICITY
    • 1) Care is symptomatic and supportive. Orotracheal intubation may be necessary if CNS depression develops. Aggressively hydrate patient with 0.9% sodium chloride to enhance bromide excretion. Diuretics such as furosemide may further enhance bromide excretion. Consider hemodialysis in patients with severe toxicity, and those with impaired renal function or in whom diuresis is not effective or is contraindicated.
  • C) DECONTAMINATION
    • 1) Toxicity generally occurs with chronic ingestion. Consider activated charcoal only after large, recent ingestions in patients who are alert and can protect the airway. Gastric lavage is not indicated as acute ingestion is not life-threatening.
  • D) AIRWAY MANAGEMENT
    • 1) Endotracheal intubation should be performed in patients with excessive drowsiness and the inability to protect their own airway.
  • E) ANTIDOTE
    • 1) None
  • F) INTRAVENOUS FLUIDS
    • 1) Infusion of 0.9% sodium chloride enhances urinary bromide excretion. Give initial bolus of 10 to 20 mg/kg as clinically indicated, followed by an infusion 2 to 3 times the maintenance fluid rate. Discontinue infusion when symptoms have improved and the serum bromide level is less than 100 to 150 mg/dL.
  • G) DIURESIS
    • 1) Diuretics such as furosemide, ethacrynic acid, thiazides, or mannitol may be administered, in addition to intravenous sodium chloride, to obtain a urine flow of 3 to 6 mL/kg/hour. Administration may increase bromide clearance. Monitor fluid and electrolytes closely as hypernatremia may occur.
  • H) ENHANCED ELIMINATION
    • 1) The addition of diuretics, such as furosemide, ethacrynic acid, thiazides, and mannitol, to intravenous chloride therapy has been shown to increase urinary bromide excretion. Hemodialysis greatly increases bromide clearance, and is indicated in patients with severe toxicity, underlying renal insufficiency, or when attempts at intravenous chloride administration have been unsuccessful or are contraindicated.
  • I) PATIENT DISPOSITION
    • 1) HOME CRITERIA: Patients with inadvertent ingestions who are asymptomatic can be managed at home.
    • 2) OBSERVATION CRITERIA: Patients with deliberate overdose and symptomatic patients should be observed in a medical facility until free of symptoms.
    • 3) ADMISSION CRITERIA: All patients who are persistently symptomatic should be admitted.
    • 4) CONSULT CRITERIA: Consult a medical toxicologist or poison center for patients with significant toxicity or in whom the diagnosis is unclear.
  • J) PITFALLS
    • 1) Failure to discern the difference between bromide intoxication and bromine gas intoxication, which primarily causes pulmonary and dermatologic manifestations. Failure to consider the possibility of bromide intoxication with drugs containing bromides as the salt form.
  • K) PHARMACOKINETICS
    • 1) Bromide is well absorbed (95%). Volume of distribution is 0.35 to 0.48 L/kg and it is not protein bound. Eliminated renally, with a half-life of 12 days.
  • L) TOXICOKINETICS
    • 1) Half-life is shortened by various treatment modalities: Intravenous sodium chloride: 65 hours; osmotic diuresis: 37 hours; ethacrynic acid plus mannitol: 1.65 hours; oral furosemide plus lactated ringers: 26 hours; hemodialysis: 0.8 to 2.1 hours.
  • M) DIFFERENTIAL DIAGNOSIS
    • 1) Toxicologic and non-toxicologic causes of confusion and CNS depression (eg, barbiturates, benzodiazepines, lithium, phenytoin, carbamazepine, dementia, meningitis, CVA, CNS bleeding, tumor).
0.4.2 ORAL EXPOSURE
  • A) MANAGEMENT OF MILD TO MODERATE ORAL TOXICITY
    • 1) Within the first 12 hours of exposure, if burns are absent or grade I severity, patient may be discharged when able to tolerate liquids and soft foods by mouth. If mild grade II burns, admit for intravenous fluids, slowly advance diet as tolerated. Perform barium swallow or repeat endoscopy several weeks after ingestion (sooner if difficulty swallowing) to evaluate for stricture formation.
  • B) MANAGEMENT OF SEVERE ORAL TOXICITY
    • 1) Resuscitate with 0.9% saline; blood products may be necessary. Early airway management in patients with upper airway edema or respiratory distress. Early (within 12 hours) gastrointestinal endoscopy to evaluate for burns. Early bronchoscopy in patients with respiratory distress or upper airway edema. Early surgical consultation for patients with severe grade II or grade III burns, large deliberate ingestions, or signs, symptoms or laboratory findings concerning for tissue necrosis or perforation.
  • C) DECONTAMINATION
    • 1) INGESTION: In patients without vomiting or respiratory distress who are able to swallow, dilute with 4-8 ounces milk/water if possible shortly after ingestion; then NPO until after endoscopy. Neutralization, gastric lavage, and activated charcoal are all contraindicated. OCULAR: Copious irrigation until pH neutral. DERMAL: Remove contaminated clothes, brush off particulate corrosives, follow with copious irrigation. INHALATION: Humidified oxygen.
  • D) AIRWAY MANAGEMENT
    • 1) Aggressive airway management in patients with deliberate ingestions or any indication of upper airway injury. Severe edema may make intubation difficult; be prepared for surgical airway management (cricothyroidotomy) in patients with severe upper airway edema.
  • E) ENDOSCOPY
    • 1) Should be performed as soon as possible (preferably within 12 hours, not more than 24 hours) in any patient with acid ingestion. The grade of mucosal injury at endoscopy is the strongest predictive factor for the occurrence of systemic and GI complications and mortality. The absence of visible oral burns does NOT reliably exclude the presence of esophageal or gastric burns.
  • F) BRONCHOSPASM
    • 1) Treat with oxygen, inhaled beta agonists and consider systemic corticosteroids.
  • G) CORTICOSTEROIDS
    • 1) The use of corticosteroids to prevent stricture formation is controversial. Corticosteroids should not be used in patients with grade I or grade III injury, as there is no evidence that it is effective. Evidence for grade II burns is conflicting, and the risk of perforation and infection is increased with steroid use, so routine use is not recommended.
  • H) STRICTURE
    • 1) A barium swallow or repeat endoscopy should be performed several weeks after ingestion in any patient with grade II or III burns or with difficulty swallowing to evaluate for stricture formation. Recurrent dilation may be required. Some authors advocate early stent placement in these patients to prevent stricture formation.
  • I) SURGICAL MANAGEMENT
    • 1) Immediate surgical consultation should be obtained on any patient with grade III or severe grade II burns on endoscopy, significant abdominal pain, metabolic acidosis, hypotension, coagulopathy, or a history of large ingestion. Early laparotomy can identify tissue necrosis and impending or unrecognized perforation, early resection and repair in these patients is associated with improved outcome.
  • J) EYE INJURY
    • 1) Copious irrigation until pH neutral; perform slit lamp exam. Ophthalmology consult. Antibiotics and mydriatics may be indicated.
  • K) PATIENT DISPOSITION
    • 1) OBSERVATION CRITERIA: Patients with an acid ingestion should be sent to a health care facility for evaluation. Patients with an endoscopic evaluation that demonstrates no burns or only minor grade I burns and who can tolerate oral intake can be discharged to home.
    • 2) ADMISSION CRITERIA: Symptomatic patients, and those with endoscopically demonstrated grade II or higher burns should be admitted. Patients with respiratory distress, grade III burns, or extensive grade II burns, acidosis, hemodynamic instability, gastrointestinal bleeding, or large ingestions should be admitted to an intensive care setting.
  • L) PITFALLS
    • 1) The absence of oral burns does NOT reliably exclude the possibility of significant esophageal burns.
    • 2) Patients may have severe tissue necrosis and impending perforation requiring early surgical intervention without having severe hypotension, rigid abdomen, or radiographic evidence of intraperitoneal air.
    • 3) Patients with any evidence of upper airway involvement require early airway management before airway edema progresses.
    • 4) The extent of eye injury (degree of corneal opacification and perilimbal whitening) may not be apparent for 48 to 72 hours after the burn. All patients with acidic eye injury should be evaluated by an ophthalmologist.
  • M) DIFFERENTIAL DIAGNOSIS
    • 1) Alkaline corrosive ingestion, gastrointestinal hemorrhage, or perforated viscus.
0.4.3 INHALATION EXPOSURE
  • A) INHALATION: Move patient to fresh air. Monitor for respiratory distress. If cough or difficulty breathing develops, evaluate for respiratory tract irritation, bronchitis, or pneumonitis. Administer oxygen and assist ventilation as required. Treat bronchospasm with an inhaled beta2-adrenergic agonist. Consider systemic corticosteroids in patients with significant bronchospasm.
  • B) INHALATION: Administer oxygen. If respiratory symptoms develop obtain chest x-ray, monitor pulse oximetry and/or blood gases. Treat bronchospasm with inhaled beta2-adrenergic agonists. If acute lung injury develops, consider PEEP. Evaluate for esophageal, dermal and eye burns as indicated.
0.4.4 EYE EXPOSURE
  • A) DECONTAMINATION: Remove contact lenses and irrigate exposed eyes with copious amounts of room temperature 0.9% saline or water for at least 15 minutes. If irritation, pain, swelling, lacrimation, or photophobia persist after 15 minutes of irrigation, the patient should be seen in a healthcare facility.
  • B) CAUSTIC EYE DECONTAMINATION: Immediately irrigate each affected eye with copious amounts of water or sterile 0.9% saline for about 30 minutes. Irrigating volumes up to 20 L or more have been used to neutralize the pH. After this initial period of irrigation, the corneal pH may be checked with litmus paper and a brief external eye exam performed. Continue direct copious irrigation with sterile 0.9% saline until the conjunctival fornices are free of particulate matter and returned to pH neutrality (pH 7.4). Once irrigation is complete, a full eye exam should be performed with careful attention to the possibility of perforation.
  • C) EYE ASSESSMENT: The extent of eye injury (degree of corneal opacification and perilimbal whitening) may not be apparent for 48 to 72 hours after the burn.
0.4.5 DERMAL EXPOSURE
  • A) OVERVIEW
    • 1) DECONTAMINATION: Remove contaminated clothing and jewelry and irrigate exposed areas with copious amounts of water. A physician may need to examine the area if irritation or pain persists.
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