Ammonia Toxicity Clinical Presentation
- Author: Steven Issley, MD, FRCPC; Chief Editor: Asim Tarabar, MD more...
The literature on ammonia toxicity in humans largely consists of case reports. 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
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. 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.
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.
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.
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:
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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