AUTHOR AND EDITOR INFORMATION

Section 1 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

INTRODUCTION

Section 2 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

Background

At room temperature, ammonia (NH₃) is a highly water-soluble, colorless, irritant gas with a unique pungent odor. Ammonia has a boiling point of -33°C and an ignition temperature of 650°C.

In 1993, anhydrous ammonia was the third most produced chemical by volume in the US. The farming industry uses approximately one third of the ammonia produced in the US as a component of fertilizer and animal feed. Industrial injury most often results from ammonia leaks in fertilizer tanks and hoses and toxic ammonia levels in animal buildings. Swine confinement buildings are particularly notorious for containing toxic levels of ammonia that often exceed threshold limit values. Because ammonia is liberated during combustion of nylon, silk, wood, and melamine, firefighters also are at risk for exposure to this irritant gas.

Before the 1970s, liquid ammonia stored under high pressure was widely used for refrigeration. Although Freon largely has replaced ammonia as a refrigerant, ammonia refrigeration is still used and numerous case reports exist of severe toxicity following accidental exposure.

Ammonia also is used in the production of explosives, pharmaceuticals, pesticides, textiles, leather, flame-retardants, plastics, pulp and paper, rubber, petroleum products, and cyanide. Furthermore, ammonia is a major component of many common household cleaning and bleaching products (eg, glass cleaners, toilet bowel cleaners, metal polishes, floor strippers, wax removers, smelling salts).

Permissible levels of exposure to toxic gases are defined by time-weighted average (TWA), short-term exposure limit (STEL), and concentration at which toxic gasses are immediately dangerous to life or health (IDLH). The TWA is defined as the concentration for an 8-hour workday of a 40-hour workweek that nearly all workers can be exposed to without adverse effects. Similarly, the STEL is the concentration to which an exposure of longer than 15 minutes is potentially dangerous and may produce immediate or chronic compromise to health. Anhydrous ammonia has a TWA of 25 ppm, an STEL of 35 ppm, and an IDLH of 500 ppm.

Although injury from ammonia most commonly is caused by inhalation, it also may follow ingestion or direct contact with eyes or skin. The clinical presentations of these injuries and their investigation and treatment are discussed in this article; chloramine gas inhalation injury also is discussed.

Pathophysiology

The most common mechanism by which ammonia gas causes damage occurs when anhydrous ammonia (liquid or gas) reacts with tissue water to form the strongly alkaline solution, ammonium hydroxide.

NH₃ + H₂O ®NH₄OH

This reaction is exothermic and capable of causing significant thermal injury.

Ammonium hydroxide also causes severe alkaline chemical burns to skin, eyes, and especially the respiratory system. Mild exposures primarily affect the upper respiratory tract, while more severe exposures tend to affect the entire respiratory system (see Clinical). The gastrointestinal tract also may be affected if ammonia is ingested.

Tissue damage from alkali is caused by liquefaction necrosis and typically penetrates far deeper than that caused by an equipotent acid. In the case of ammonium hydroxide, the tissue breakdown liberates water, thus perpetuating the conversion of ammonia to ammonium hydroxide. In the respiratory tract, this results in the destruction of cilia and the mucosal barrier to infection. Furthermore, secretions, sloughed epithelium, cellular debris, edema, and reactive smooth muscle contraction cause significant airway obstruction.

Airway epithelium can regain barrier integrity within 6 hours following exposure if the basal cell layer remains intact. However, damaged epithelium often is replaced by granular tissue, which may be one of the etiologies leading to chronic lung disease following ammonia inhalation injury.

Liquid anhydrous ammonia (-33°C) freezes tissue on contact. To put this in perspective, critical skin damage begins at -4°C and becomes irreversible at -20°C. The degree of tissue injury, however, is proportional to the duration and concentration of exposure.

Similarly, damage to the respiratory system is proportional to depth of inhalation, duration of exposure, concentration, and pH of the gas or liquid.

Ammonia is a product of protein catabolism and is metabolized by the liver. Normal blood ammonia levels range from 80-110 mcg/dL. This increases 10% with exposure to 25 ppm but is not considered harmful. Theoretically, patients with liver dysfunction are at increased risk for ammonia toxicity; however, currently no sufficient clinical evidence can confirm this.

Frequency

United States

Similar to previous years, in 2002, US poison control centers reported nearly 6000 cases of toxic ammonia exposure. Of exposures, 93% were unintentional, and 11% resulted in moderate to severe outcomes. Of note, in cases of household exposure, only 5% were moderate to severe.

Age

Of the 6000 toxic ammonia exposures reported in the American Association of Poison Control Centers' 2002 Annual Report, 70% occurred in adults and 20% occurred in children younger than 6 years.

• Ingestion of household solutions usually is accidental and occurs in young children; adult ingestions, however, most often are suicide attempts.
• Inhalation injury is almost always accidental. Because inhalation exposure generally occurs in an industrial setting, it usually is associated with working adults.

CLINICAL

Section 3 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

History

The literature on ammonia toxicity in humans largely consists of case reports. In a 1996 literature review, de la Hoz et al found only 94 previously reported cases; of these cases, 20 resulted in fatality and only 35 had clinical follow-up of one year or more. Despite lack of data, most literature is consistent regarding clinical presentation and treatment of ammonia toxicity.

• Gaseous ammonia effects at various concentrations are as follows:
  • 25 ppm or less - TWA

  • 25-50 ppm - Detectable odor; unlikely to experience adverse effects

  • 50-100 ppm - Mild eye, nose, and throat irritation; may develop tolerance in 1-2 weeks with no adverse effects thereafter

  • 140 ppm - Moderate eye irritation; no long-term sequelae in exposures of less than 2 hours

  • 400 ppm - Moderate throat irritation

  • 500 ppm - 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, pulmonary edema, and bronchospasm

  • 5000 ppm - Rapidly fatal exposure
• Inhalation injury
• • Because of its high water solubility, ammonia has a tendency to be absorbed by the water-rich mucosa of the upper respiratory tract. However, unlike most highly water-soluble irritant gases that tend to affect exclusively the upper respiratory tract, ammonia can damage proximally and distally.

  • In 1941, Caplin was the first to classify victims of accidental ammonia exposure; he described them as mild, moderate, and 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, pulmonary edema, and dysphagia.

  • Following a 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 can flee upon detection of ammonia's pungent odor; furthermore, absence of symptoms following inhalational exposure to ammonia essentially rules out significant injury.

  • Pain (oropharyngeal, retrosternal)

  • Dyspnea, hemoptysis - As expected, individuals with reactive airway disease, such as asthmatics, are particularly sensitive to ammonia inhalation.

  • Hoarseness

  • Dysphagia

  • Loss of consciousness

• Farming industry
  • In enclosed animal confinement buildings, ammonia is adsorbed by dust particles that transport it more directly to small airways. Because of this synergistic effect, symptoms have reportedly developed within minutes of entering animal confinement buildings.

  • Symptoms include rhinorrhea, scratchy throat, chest tightness, cough, dyspnea, and eye irritation and usually subside within 24-48 hours.
• Contact - 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
• • Typical household ammonia products (3-10% ammonium hydroxide) have a pH 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 when pH is 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 viscus perforation (perforation may occur up to 24-72 hours postingestion).

  • Respiratory symptoms may be present if aspiration pneumonia or pneumonitis complicates ingestion.

  • Smelling salts are a less common source of household ammonia ingestion. Often in capsule form, smelling salts, which contain approximately 20% ammonia, release a pungent odor when broken. Smelling salts are found in many first-aid kits as a treatment for syncope; unfortunately, children sometimes bite into them, resulting in minor esophageal burns and mild respiratory symptoms.

Physical

• Inhalation injury
• • Head, ears, eyes, nose, throat (HEENT) - Facial and oral burns and ulceration

  • Respiration - Tachypnea, oxygen desaturation, stridor, drooling, cough, wheezing, rhonchi, and decreased air entry

  • Central nervous system (CNS) - Loss of consciousness (if exposure is massive)

• Contact - Burns and cold injury
• • Skin - Alkali burns to the skin are yellow, soapy, and soft in texture. When burns are severe, skin turns black and leathery.

  • HEENT - 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 symptoms include iritis, corneal edema, semi-dilated fixed pupil, and eventual cataract formation.

• Ingestion
• • Cardiovascular - With intentional ingestion, hypovolemic shock may occur because of vomiting and third-spacing of intravascular fluid.

  • HEENT - Symptoms include edema of the lips, oropharynx, and upper airway.

  • GI - Patient may experience epigastric tenderness; mediastinitis and peritoneal signs may be present with viscus perforation, which can occur as late as 24-72 hours postingestion.

  • Respiratory - Aspiration pneumonia and pulmonary edema may occur.

DIFFERENTIALS

Section 4 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

Other Problems to be Considered

Other toxic inhalations or ingestions
Concomitant trauma
Reactive airway dysfunction syndrome (RADS)

WORKUP

Section 5 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

Lab Studies

• Complete blood count (CBC)
• Electrolytes, blood urea nitrogen (BUN), and creatinine
• Serial arterial blood gases (ABGs) in cases of significant respiratory distress
• • Metabolic acidosis

  • Respiratory alkalosis

  • Increased alveolar-arterial gradient

• Note that serum ammonia levels are of little value because they do not correlate with clinical condition. However, patients with compromised hepatic function may show increased serum ammonia levels because of less efficient metabolism.

Imaging Studies

• Chest x-ray (CXR)
• • Chest x-ray findings vary from normal to diffuse micronodular interstitial infiltrates. However, abnormal x-ray findings may take up to 48 hours to develop, even following severe exposure.

  • Other findings to consider are noncardiogenic pulmonary edema, acute respiratory distress syndrome (ARDS), secondary bacterial bronchopneumonia, and pneumomediastinum.

• Abdominal series (to rule out perforation following ingestion)

Other Tests

• Cardiac monitor
• Oxygen saturation monitor
• Pulmonary capillary wedge pressure (PCWP) monitoring (in cases of severe pulmonary edema or ARDS)
• Pulmonary function tests (PFTs) - Once acute emergency is controlled; useful to gauge severity and monitor progress and recovery
• • Obstructive lung disease (acute and chronic)

  • Restrictive lung disease (chronic)

• Ventilation/perfusion (V/Q) scan - May be useful to gauge severity or progress of disease; unlikely to change acute management
• • Ventilation deficits generally are more pronounced in the larger airways.

  • The ventilation scan also may show abnormal air trapping in the setting of lower airway obstruction.

• Slit-lamp examination with fluorescein staining, tonometry and conjunctival pH (see Physical: HEENT)

Procedures

• Perform bronchoscopy to assess respiratory tract damage following acute inhalation injury (in severe cases).
• • Airway edema, obstruction, and necrosis

  • Epithelial sloughing

  • Laryngitis and tracheitis

  • Diffuse alveolar damage

• Perform endoscopy for ingestion exposures. Indications are controversial; obtain a GI consultation. Perform endoscopy on symptomatic patients and patients with intentional ingestions within 48 hours following ingestion. The risk of perforation increases if endoscopy is performed more than 72 hours postingestion.
• • Laryngeal and epiglottic edema

  • Friable erythematous esophagus

  • Corrosive injury

TREATMENT

Section 6 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

Prehospital Care

• Immediately remove patient from the contaminated environment.
• Remove all clothing.
• Support airway, breathing, and circulation (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 following exposure. 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.

Emergency Department Care

• Decontaminate the patient (if not previously performed) and support ABCs as necessary. Provide warmed humidified oxygen.
• As with all burns, patients with facial or oral lesions are at high risk for developing laryngeal edema. Airway intervention should be aggressive.
• Indications for intubation include severe respiratory distress (hypoxemia, hypercapnia), stridor, hoarseness, deep facial burns, burns identified by bronchoscopy or endoscopy, and depressed mental status.
• • If intubation is necessary, use large size tube to prevent plugging by sloughed mucosa.

  • Some consider procedural sedation preferable to rapid sequence intubation (RSI) because paralysis is risky with a difficult and edematous airway. Furthermore, ventilation cannot be predicted as 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 noncardiogenic pulmonary edema.
• Follow standard initial burn management. (Discussion is beyond the scope of this article.)
  • Once patient is adequately stable, irrigate 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 conjunctival pH is 6.8-7.4; use pH indicator paper to monitor. Examine eye with slit-lamp and fluorescein staining.
  • Perform tonometry to determine if intraocular pressure is elevated.

  • 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 cc of water or milk.

  • Do not induce emesis, so as not to reproduce injury with a second pass of toxin.

  • Consult gastroenterology promptly for subsequent endoscopic evaluation (not often performed before 12 hours postingestion).

Consultations

When appropriate, immediately consult an intensivist, medical toxicologist, ophthalmologist (all eye injuries), gastroenterologist, and general and plastic surgeons.

MEDICATION

Section 7 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

Management of toxic exposure to ammonia is largely supportive, and medical therapy is directed at hypoxia, bronchospasm, pulmonary edema, hypovolemia, and burns of the skin and eyes.

Antibiotics and corticosteroids are controversial therapies following ammonia inhalation and ingestion exposures.

Although antibiotics and corticosteroids are often used in the acute treatment of patients with inhalation injury, neither has shown to improve outcome and many feel that corticosteroids may actually increase morbidity. Corticosteroids are recommended to treat bronchospasm in patients with underlying reactive airways disease and acute inhalation injury or for chronic respiratory complications that follow an acute inhalation injury.

Most authorities, however, do recommend both IV corticosteroid and antibiotic administration to symptomatic patients following ammonia ingestion. Corticosteroids are administered to decrease the incidence and severity of esophageal strictures that occur during healing from significant alkaline injuries. Antibiotics are given because of increased risk of mediastinitis associated 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; thus, corticosteroids and antibiotics should be administered in consultation with a gastroenterologist.

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

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. Furthermore, patients with severe transmural burns are at risk for stricture formation, but 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. Administer corticosteroid and antibiotics to this group of patients.

Drug Category: Bronchodilators

Bronchodilators selectively stimulate beta 2-adrenergic receptors of the bronchial tree and lungs. Bronchodilation results from relaxation of bronchial smooth muscle, which relieves bronchospasm and reduces airway resistance.

Drug Category: Diuretics

Are used to alleviate pulmonary edema. However, some believe that PEEP may be more useful than diuretics for optimizing oxygenation because pulmonary edema is secondary to alveolar capillary injury, not excess fluid. Nonetheless, a trial of diuretics poses little risk and may be used concomitantly with PEEP.

Drug Category: Antibiotics

Although expensive, topical Silvadene has antipseudomonal properties in addition to coverage for most gram-positive organisms.

For eye exposures, antibiotic eye preparations will reduce risk of infection secondary to tissue injury.

Drug Name	Ciprofloxacin (Ciloxan)
Description	Fluoroquinolone with activity against pseudomonads, streptococci, MRSA, S epidermidis, and most gram-negative organisms, but no activity against anaerobes. Inhibits bacterial DNA synthesis and growth. Neomycin 5% is described in much of the literature on ammonia-related eye injury; however, newer broad-spectrum antibiotics have fewer adverse effects
Adult Dose	1 gtt qid (prophylaxis)
Pediatric Dose	<12 years: Not recommended >12 years: Administer as in adults
Contraindications	Documented hypersensitivity
Interactions	Antacids, iron salts, and zinc salts may reduce serum levels; administer antacids 2-4 h before or after taking fluoroquinolones; cimetidine may interfere with metabolism of fluoroquinolones; ciprofloxacin reduces therapeutic effects of phenytoin; probenecid may increase ciprofloxacin serum concentrations; may increase toxicity of theophylline, caffeine, cyclosporine, and digoxin (monitor digoxin levels); may increase effects of anticoagulants (monitor PT)
Pregnancy	C - Safety for use during pregnancy has not been established.
Precautions	Prolonged use may result in overgrowth of nonsusceptible organisms, including fungi

Drug Name	Erythromycin (E-Mycin)
Description	Indicated for infections caused by susceptible strains of microorganisms and for prevention of corneal and conjunctival infections
Adult Dose	Apply 1-cm ribbon 4-8 times/d depending on severity of infection
Pediatric Dose	Apply as in adults
Contraindications	Documented hypersensitivity; viral, mycobacterial, or fungal infections of eye; patients using steroid combinations after uncomplicated removal of a foreign body from cornea also should avoid using this product
Interactions	None reported
Pregnancy	B - Usually safe but benefits must outweigh the risks.
Precautions	Do not use topical antibiotics to treat ocular infections that may become systemic; prolonged or repeated antibiotic therapy may result in bacterial or fungal overgrowth of nonsusceptible organisms and may lead to a secondary infection (take appropriate measures if superinfection occurs)

Drug Category: Anticholinergic agents

Induces cycloplegia by blocking the body's parasympathetic (cholinergic) effects in the eye. This is beneficial to prevent ciliary spasm.

Drug Name	Homatropine (Isopto Homatropine)
Description	Blocks responses of sphincter muscle of iris and muscle of ciliary body to cholinergic stimulation, producing pupillary dilation (mydriasis) and paralysis of accommodation (cycloplegia). Induces mydriasis in 10-30 min and cycloplegia in 30-90 min; these effects last up to 48 h.
Adult Dose	1 gtt into affected eye(s) once; may repeat in 24-48 h prn
Pediatric Dose	1 gtt into affected eye(s) once; may repeat in 24-48 h prn
Contraindications	Documented hypersensitivity; narrow-angle glaucoma
Interactions	None reported
Pregnancy	C - Safety for use during pregnancy has not been established.
Precautions	Caution in patients (eg, elderly patients) in whom increased intraocular pressure may be present; toxic anticholinergic systemic adverse effects can occur, but incidence is rare when used sparingly; adverse effects are more common in children, especially infants; compressing lacrimal sac by digital pressure for 1-3 min following instillation minimizes systemic absorption

Drug Name	Tropicamide (Mydriacyl)
Description	Blocks sphincter muscle of iris and muscle of ciliary body from responding to cholinergic stimulation
Adult Dose	1 gtt into affected eye(s) once
Pediatric Dose	Administer as in adults
Contraindications	Documented hypersensitivity
Interactions	None reported
Pregnancy	C - Safety for use during pregnancy has not been established.
Precautions	Caution in patients (eg, elderly patients) in whom increased intraocular pressure may be present; toxic anticholinergic systemic adverse effects can occur, but incidence is rare when used sparingly; adverse effects are more common in children, especially infants; compressing lacrimal sac by digital pressure for 1-3 min following instillation minimizes systemic absorption

Drug Category: Corticosteroids

Decrease the formation of fibroblasts on the cornea and may limit intraocular inflammation. However, may potentiate infection.

Drug Name	Fluorometholone (FML)
Description	Suppresses migration of polymorphonuclear leukocytes and reverses capillary permeability
Adult Dose	1 gtt q1-6h based on severity of inflammation for 7-10 d
Pediatric Dose	<2 years: Not established > 2 years: Administer as in adults
Contraindications	Documented hypersensitivity; herpes simplex; keratitis; viral and fungal diseases of the ocular structure
Interactions	None reported
Pregnancy	C - Safety for use during pregnancy has not been established.
Precautions	Prolonged use my result in elevated intraocular pressure or glaucoma

Drug Name	Rimexolone (Vexol)
Description	Decreases inflammation by suppressing migration of polymorphonuclear leukocytes and reversing increased capillary permeability.
Adult Dose	1 gtt q1-6h based on severity of inflammation for 7-10 d
Pediatric Dose	Not established
Contraindications	Documented hypersensitivity; viral, fungal, bacterial ocular infections
Interactions	None reported
Pregnancy	C - Safety for use during pregnancy has not been established.
Precautions	Caution in corneal or scleral perforation and posterior subcapsular cataracts

Drug Category: Local anesthetics

Used primarily for pain relief. Duration of action is relatively short-lived, limiting usefulness of local anesthetics outside of the hospital or clinic setting.

FOLLOW-UP

Section 8 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

Further Inpatient Care

• Admit patients to observation for at least 24 hours if they show significant and persistent signs, symptoms, or abnormalities in lab findings attributable to ammonia exposure.
• Admit unstable or potentially unstable patients to intensive care.
• Following ingestion, patients may be discharged if endoscopy results are normal and oral intake is tolerated.
• Intentional ingestions require psychiatric evaluation.

Complications

• Patients often develop chronic respiratory sequelae, particularly with severe ammonia exposures. In a case series by Close et al, exposed patients experienced gradual deterioration of pulmonary function during the first 2-6 months following exposure. A period of slight improvement was then observed, followed by stabilization of symptoms.
• Long-term effects of ammonia inhalation injury include the following:
• • Cough

  • Hoarseness

  • Obstructive and/or restrictive lung disease

  • Hyper-reactive airway disease and reactive airway dysfunction syndrome (RADS)

  • Impaired gas exchange

  • Residual parenchymal damage

  • Bronchiectasis and bronchiolitis obliterans (following massive exposure)

• It is postulated that chronic obstructive disease is secondary to airway lesions more than hyper-reactivity and, therefore, often minimally improved by bronchodilators.

Prognosis

• Most individuals with ammonia inhalation who survive the first 24 hours will recover.
• Patients begin showing improvement within 48-72 hours and may recover fully during this time if exposure was mild.
• For patients with more significant respiratory symptoms, recovery can be expected within several weeks to months.
• Interestingly, Arwood et al found that initial chest x-ray and PaO₂ poorly correlate with outcome and that physical examination on arrival is a more sensitive prognosticating factor.
• Montague and MacNeil, however, note that patients who do not develop chest x-ray findings are less likely to have chronic respiratory sequelae.

Patient Education

• For excellent patient education resources, visit eMedicine's Burns Center. Also, see eMedicine's patient education article Thermal (Heat or Fire) Burns.

MISCELLANEOUS

Section 9 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

Special Concerns

• Chloramine gas
• • Chloramines (NH₂Cl, NHCl₂) are highly water-soluble irritant gases formed when household bleach (5.25% sodium hypochlorite) is mixed with 5-10% ammonia solutions (usually cleaning products). Fumes contact moist mucous membranes, reacting with water to produce free ammonia gas (see Inhalation injury), hypochloric acid, and hypochlorous acid. The latter then reacts with water to form hydrochloric acid and nascent oxygen, a strong oxidizing agent with corrosive effects.

  • At low concentration, symptoms 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, and pulmonary artery occlusive pressure may be less than 17 mm Hg.

• Treat chloramine gas exposure as described under Emergency Department Care.
• • Sodium bicarbonate has been suggested to be an adjunct to supportive treatment, but little clinical experience with this treatment exists.

  • In Thomas and Storrow's case series of 22 patients with chloramine toxicity, treatment with sodium bicarbonate resulted in no clinical or statistical improvement.

REFERENCES

Section 10 of 10

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

• Am J Respir Crit Care Med. Respiratory health hazards in agriculture. Am J Respir Crit Care Med. Nov 1998;158(5 Pt 2):S1-S76. [Medline].
• Arwood R, Hammond J, Ward GG. Ammonia inhalation. J Trauma. May 1985;25(5):444-7. [Medline].
• Birken GA, Fabri PJ, Carey LC. Acute ammonia intoxication complicating multiple trauma. J Trauma. Sep 1981;21(9):820-2. [Medline].
• Burgess JL, Pappas GP, Robertson WO. Hazardous materials incidents: the Washington Poison Center experience and approach to exposure assessment. J Occup Environ Med. Aug 1997;39(8):760-6. [Medline].
• Caplin M. Ammonia-gas poisoning: 47 cases in a London shelter. Lancet. 1941;2:958-61.
• Close LG, Catlin FI, Cohn AM. Acute and chronic effects of ammonia burns on the respiratory tract. Arch Otolaryngol. Mar 1980;106(3):151-8. [Medline].
• Respiratory tract irritants. In: Ellenhorn MJ, Schonwald S, Ordog G, eds. Ellenhorn's Medical Toxicology: Diagnosis and Treatment of Human Poisoning. 2^nd ed. Baltimore: Lippincott, Williams & Wilkins; 1996:1519-25.
• Flury KE, Dines DE, Rodarte JR, Rodgers R. Airway obstruction due to inhalation of ammonia. Mayo Clin Proc. Jun 1983;58(6):389-93. [Medline].
• Goldfrank LR. Toxicological imaging, ophthalmologic principle, occupational and environmental toxics. In: Goldfrank's Toxicologic Emergencies. 5^th ed. Norwalk, Conn: Appleton & Lange; 1994:127, 368-9, 1183-1280.
• Haddad LM, Winchester JF, eds. Clinical Management of Poisoning and Drug Overdose. 2^nd ed. Philadelphia: WB Saunders Co; 1990.
• Klein J, Olson KR, McKinney HE. Caustic injury from household ammonia. Am J Emerg Med. Jul 1985;3(4):320. [Medline].
• Klein JD, Olson KR. Caustic injury from household ammonia, too. J Pediatr. Feb 1986;108(2):328. [Medline].
• Leung CM, Foo CL. Mass ammonia inhalational burns--experience in the management of 12 patients. Ann Acad Med Singapore. Sep 1992;21(5):624-9. [Medline].
• O'Kane GJ. Inhalation of ammonia vapour. A report on the management of eight patients during the acute stages. Anaesthesia. 38(12):1208-13. [Medline].
• Pascuzzi TA, Storrow AB. Mass casualties from acute inhalation of chloramine gas. Military Medicine. Feb 1998;163(2):102-4. [Medline].
• Perry GF Jr. Occupational medicine forum. J Occup Med. Oct 1994;36(10):1061-3. [Medline].
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Article Last Updated: Mar 14, 2007