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Ammonia Toxicity Clinical Presentation

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

History

The literature on ammonia toxicity in humans largely consists of case reports.[7] Despite lack of data, most of the literature is consistent regarding clinical presentation of ammonia toxicity. The effects of gaseous ammonia effects at various concentrations are as follows:

  • 25 ppm or less – Adverse effects highly unlikely
  • 25-50 ppm - Detectable odor; adverse effects unlikely
  • 50-100 ppm - Mild eye, nose, and throat irritation; tolerance may develop in 1-2 weeks with no adverse effects thereafter
  • 140 ppm - Moderate eye irritation; no long-term sequelae with exposures of less than 2 hours
  • 400 ppm - Moderate throat irritation
  • 500 ppm - Immediately dangerous to life or health (IDLH)
  • 700 ppm - Immediate eye injury
  • 1000 ppm - Directly caustic to airway
  • 1700 ppm - Laryngospasm
  • 2500 ppm - Fatality (after half-hour exposure)
  • 2500-6500 ppm - Sloughing and necrosis of airway mucosa, chest pain, acute lung injury (ALI), and bronchospasm
  • 5000 ppm - Rapidly fatal exposure

Inhalation injury

Symptoms of inhalational ammonia toxicity include rhinorrhea, scratchy throat, chest tightness, cough, and dyspnea; eye irritation from the ammonia gas may also be present. Symptoms usually subside within 24-48 hours. Absence of symptoms following inhalational exposure to ammonia essentially rules out significant injury. Individuals with reactive airway disease, such as asthmatics, are particularly sensitive to ammonia inhalation.

The first classification of injury from unintentional ammonia exposure, published in 1941 by Caplin, categorized cases as mild, moderate, or severe. Patients in the mild group presented with conjunctival and upper respiratory inflammation and pain but showed no signs of respiratory distress.[8] The moderate group presented similarly but with more exaggerated symptoms. The severe group presented in frank respiratory distress with productive cough, acute lung injury (ALI), and dysphagia.

With brief ammonia exposure, damage generally is limited to the upper airway mucosa. Brief exposures at very high concentrations, however, can be overwhelming and affect the entire respiratory system. People who are capable of escaping their environment usually are not subject to severe exposures, because they flee upon detection of ammonia's pungent odor.

Burns and cold injury

Gaseous ammonia combines with water of the skin, eyes, and airways to form ammonium hydroxide. This exothermic reaction results in both heat and chemical burns. Liquid ammonia freezes tissue on contact and may cause full-thickness tissue damage that penetrates deeper than the more conspicuous superficial chemical burns.

Concentrations greater than 10,000 ppm are required to cause skin damage. The eyes begin to feel irritated at concentrations of 50-100 ppm; at 700 ppm, immediate eye damage occurs.

Ingestion injury

Typical household ammonia products (3-10% ammonium hydroxide) have a pH of less than 12.5, although the pH of industrial solutions (up to 30% ammonium hydroxide) is often greater than 13. Because caustic alkali burns generally are thought to occur at a pH greater than 12.5, ammonia ingestions in the home usually do not lead to significant damage. However, Klein et al reported 3 cases of oropharyngeal and esophageal injury following intentional ingestion of household solutions with a pH less than 12.[9]

Patients present with oropharyngeal, epigastric, and retrosternal pain. Abdominal pain and other gastroenterologic symptoms may occur if ingestion causes perforation of a viscus (perforation may occur up to 24-72 hours post ingestion). Respiratory symptoms may be present if aspiration pneumonia or pneumonitis complicates ingestion.

Chloramine gas exposure

At low concentration, symptoms of chloramine gas toxicity include tearing, rhinorrhea, oropharyngeal burning, and cough. Although chloramine gases produce rapid onset of symptoms, these symptoms are mild enough that patients often do not remove themselves promptly from the toxic environment; thus, patients often present after a prolonged exposure time.

The physical examination following mild exposure reveals only mild wheezing and decreased air entry or may be entirely unremarkable. Patients with more significant exposure may present with dyspnea, pulmonary edema with secondary hypoxia, nausea, tracheobronchitis, toxic pneumonitis, intrapulmonary shunt, and/or pneumomediastinum. Note that pulmonary edema may ensue within minutes or be delayed for up to 24 hours following exposure.

Pulmonary function tests may reveal obstructive, restrictive, or combined patterns. The pulmonary artery occlusive pressure may be less than 17 mm Hg.

For more information, see Chlorine Toxicity.

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Physical Examination

Inhalation injury from ammonia is marked by the following findings:

  • Head, ears, eyes, nose, throat (HEENT) - Facial and oral burns and ulcerations
  • Respiration - Tachypnea, oxygen desaturation, stridor, drooling, cough, wheezing, rhonchi, and decreased air entry
  • Central nervous system (CNS) - Loss of consciousness (if exposure is massive)

Skin or eye contact with ammonia can result in burns or cold injury. Alkali burns to the skin are yellow, soapy, and soft in texture; with severe burns, skin turns black and leathery.

Burns to the eye penetrate particularly deeply and rapidly, leading to destruction of the inner structures within 2-3 minutes; this may progress to globe perforation. Ammonia typically causes more corneal epithelium and lens damage than other alkalis. Intraocular pressure and pH of the anterior chamber rise, resulting in a syndrome similar to acute narrow-angle glaucoma.

Other ophthalmic symptoms include the following:

  • Iritis
  • Corneal edema
  • Semi-dilated fixed pupil
  • Eventual cataract formation

With intentional ingestion of ammonia, hypovolemic shock may occur because of vomiting and third-spacing of intravascular fluid. HEENT findings may include edema of the lips, oropharynx, and upper airway.

On abdominal examination, patients may exhibit epigastric tenderness; mediastinitis and peritoneal signs may be present with viscus perforation, which can occur as late as 24-72 hours post ingestion. Respiratory manifestations include aspiration pneumonia and pulmonary edema.

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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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