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Ammonia Toxicity Treatment & Management

  • Author: Steven Issley, MD, FRCPC; Chief Editor: Asim Tarabar, MD  more...
 
Updated: Dec 29, 2015
 

Approach Considerations

Management of toxic exposure to ammonia is largely supportive. Decontaminate the patient (if that was not done at the site of exposure) and support airway, breathing, and circulation (ABCs) as necessary. Provide warmed humidified oxygen.

Patients with facial or oral lesions from ammonia, like all patients with burns in these areas, are at high risk for developing laryngeal edema. Airway intervention should be aggressive.

Indications for tracheal intubation include the following:

Severe respiratory distress (hypoxemia, hypercapnia)

  • Stridor
  • Hoarseness
  • Deep facial burns
  • Burns identified by bronchoscopy or endoscopy
  • Depressed mental status

If intubation is necessary, use a large-size tube to prevent plugging by sloughed mucosa. Some experts consider procedural sedation preferable to rapid sequence intubation (RSI) because paralysis is risky in patients with a difficult and edematous airway. Furthermore, ventilation cannot be predicted to be successful if intubation fails in this context. Positive end respiratory pressure (PEEP) generally is useful (5 cm water minimum).

Beware of fluid over-resuscitation. Patients may have or may be developing acute lung injury (ALI).

Follow standard initial burn management; see Thermal Burns. Once the patient is adequately stable, irrigate the involved skin with tepid water for at least 15 minutes. Continue frequent regular irrigation for the first 24 hours, in addition to conventional burn management. Debride wounds and dress with 1% silver sulfadiazine (avoid using on face). Administer tetanus prophylaxis.

Irrigate eye injuries with copious amounts of tepid water for at least 30 minutes or until the conjunctival pH is 6.8-7.4; use pH indicator paper to monitor. Consult ophthalmology promptly because of risk of perforation and/or permanent eye damage.

Treat ingestions using the following steps:

  • Rinse mouth and dilute ingestion with approximately 250 mL of water or milk
  • Do not induce emesis, so as not to worsen injury with a second pass of toxin
  • Promptly arrange a gastroenterology consultation for subsequent endoscopic evaluation (not often performed before 12 hours post ingestion)

Corticosteroids are controversial therapies for ammonia inhalation injury. Many experts believe that corticosteroids may actually increase morbidity in these cases. However, corticosteroids are recommended to treat acute bronchospasm in patients with underlying reactive airways disease, and to treat chronic respiratory complications from acute inhalation injury.

Use of steroids for the treatment of caustic injuries after caustic ingestion is also controversial. However, patients exhibiting signs of airway edema after caustic exposure may benefit from intravenous (IV) dexamethasone (adults, 10 mg; children, 0.6 mg/kg up to a maximum of 10 mg).

In addition, use of IV corticosteroids can be considered in symptomatic patients with grade IIb (near-circumferential) caustic injuries, to reduce the formation of esophageal strictures. Antibiotics may also be given in these cases to counter the increased risk of mediastinitis.

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Prehospital Care

Prehospital care for patients exposed to ammonia includes the following:

  • Immediately remove the patient from the contaminated environment
  • Remove all the patient's clothing
  • Support ABCs as per advanced cardiac life support (ACLS) and advanced trauma life support (ATLS) guidelines (ACLS and ATLS guidelines may vary by region, according to training and legal responsibilities of prehospital care providers)

If the patient is sufficiently stable, begin copious skin and eye irrigation immediately. Continue irrigation for at least 20 minutes. Patients then can be covered with a dry, clean dressing and sheet. Provide a container for patients with ingestion exposure.

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Hospital Admission

The majority of patients with unintentional household ammonia exposure will have very mild symptoms and can be discharged safely if asymptomatic and able to tolerate oral intake. Admit patients to observation for at least 24 hours if they show significant and persistent signs, symptoms, or abnormalities in laboratory findings attributable to ammonia exposure. Admit unstable or potentially unstable patients to the intensive care unit.

Patients with ammonia ingestion may be discharged if endoscopy results are normal and oral intake is tolerated. Intentional ingestions require psychiatric evaluation.

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Antibiotics and Corticosteroids

The rationale for corticosteroid use after ammonia ingestion is that these agents may decrease the incidence and severity of esophageal strictures that occur during healing from significant alkaline injuries. Antibiotics are given because of the increased risk of mediastinitis associated with steroid use in patients with full-thickness esophageal alkaline corrosive burns.

Although controlled animal studies do support the use of these therapies, no well-controlled human trials have been performed. Consequently, corticosteroids and antibiotics should be administered only after consultation with a gastrointestinal specialist and surgeon.

If steroids are given, the recommended dose is 1-2 mg/kg/d of methylprednisolone for 3 weeks followed by gradual tapering. If antibiotics are given, a broad-spectrum antibiotic (eg, a second-generation cephalosporin) is appropriate.

Although patients with severe transmural burns are at risk for stricture formation, steroid therapy will not alter their risk. Thus, antibiotic therapy alone is recommended for this group to diminish their risk of mediastinitis.

Patients with extensive superficial ulceration or deep discrete or circumferential ulcerations are at risk for stricture formation and may benefit from steroid administration. Consider administering corticosteroids and antibiotics to this group of patients.

The decision to continue or stop corticosteroid and antibiotic therapy is based on endoscopic findings. Discontinue steroid and antibiotic therapies for patients with no injury or mild mucosal inflammation or ulceration, as they are not at risk for stricture formation.

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Contributor Information and Disclosures
Author

Steven Issley, MD, FRCPC Attending Physician, Department of Emergency Medicine, University Health Center, Toronto, ON

Disclosure: Nothing to disclose.

Coauthor(s)

Eddy S Lang, MDCM, CCFP(EM), CSPQ Associate Professor, Senior Researcher, Division of Emergency Medicine, Department of Family Medicine, University of Calgary Faculty of Medicine; Assistant Professor, Department of Family Medicine, McGill University Faculty of Medicine, Canada

Eddy S Lang, MDCM, CCFP(EM), CSPQ is a member of the following medical societies: American College of Emergency Physicians, Society for Academic Emergency Medicine, Canadian Association of Emergency Physicians

Disclosure: Nothing to disclose.

Joel Lockwood, MD Resident Physician, Department of Emergency Medicine, University of Toronto Faculty of Medicine, Canada

Joel Lockwood, MD is a member of the following medical societies: American College of Emergency Physicians, Emergency Medicine Residents' Association, Canadian Association of Emergency Physicians

Disclosure: Nothing to disclose.

Chief Editor

Asim Tarabar, MD Assistant Professor, Director, Medical Toxicology, Department of Emergency Medicine, Yale University School of Medicine; Consulting Staff, Department of Emergency Medicine, Yale-New Haven Hospital

Disclosure: Nothing to disclose.

Acknowledgements

Michael J Burns, MD Instructor, Department of Emergency Medicine, Harvard University Medical School, Beth Israel Deaconess Medical Center

Michael J Burns, MD is a member of the following medical societies: American Academy of Clinical Toxicology, American College of Emergency Physicians, American College of Medical Toxicology, and Society for Academic Emergency Medicine

Disclosure: Nothing to disclose.

Edmond A Hooker II, MD, DrPH, FAAEM Associate Professor, Department of Health Services Administration, Xavier University, Cincinnati, Ohio; Assistant Professor, Department of Emergency Medicine, University of Cincinnati College of Medicine

Edmond A Hooker II, MD, DrPH, FAAEM is a member of the following medical societies: American Academy of Emergency Medicine, American Public Health Association, Society for Academic Emergency Medicine, and Southern Medical Association

Disclosure: Nothing to disclose.

John T VanDeVoort, PharmD Regional Director of Pharmacy, Sacred Heart and St Joseph's Hospitals

John T VanDeVoort, PharmD is a member of the following medical societies: American Society of Health-System Pharmacists

Disclosure: Nothing to disclose.

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