DESCRIPTION

Anhydrous ammonia is a colorless alkaline gas, lighter than air, with a pungent choking odor.

FORMS AND USES

• Anhydrous ammonia (NH₃) is used in the production of fertilizers, dyes, plastics, synthetic fibers, and other chemicals and pharmaceuticals; commercial refrigerant gas; nitrogen fertilizer; and explosives.
• Aqueous ammonia is an ingredient in many household (usually at a concentration of 5% to 10%) and commercial (usually at concentrations above 25%) cleaning agents.

TOXIC DOSE

• Just a few drops of liquified anhydrous ammonia can cause severe airway burns and swelling.
• Large amounts of household ammonia (5% to 10%) must be ingested to produce injury.

PATHOPHYSIOLOGY

• Anhydrous ammonia is highly water soluble, forming highly caustic ammonium hydroxide when combined with water.
• Commercial aqueous solutions may cause severe alkali burns and liquefaction necrosis.
• Household products cause few effects unless very large amounts are involved.
• The combination of aqueous ammonia with hypochlorite bleaches may release chloramine and chlorine gases, which can cause irritant airway injury.

EPIDEMIOLOGY

• Ingestion of household products is common and typically accidental.
• Exposure to anhydrous or commercial strength aqueous ammonia is usually occupational.

CAUSES

Child neglect or abuse should be considered if the patient is less than 1 year of age, suicide attempt if the patient is over 6 years of age.

DRUG AND DISEASE INTERACTIONS

Ammonia may exacerbate reactive airway disease.

WORKPLACE STANDARDS

• ACGIH
  • TLV TWA is 25 ppm.
  • STEL is 35 ppm.
• OSHA
  • PEL TWA is 50 ppm, 35 mg/m³.
• NIOSH
  • PEL TWA is 25 ppm, 18 mg/m³.
  • IDLH is 300 ppm.

Section Outline:

• DESCRIPTION
• FORMS AND USES
• TOXIC DOSE
• PATHOPHYSIOLOGY
• EPIDEMIOLOGY
• CAUSES
• DRUG AND DISEASE INTERACTIONS
• WORKPLACE STANDARDS

SIGNS AND SYMPTOMS

• The severity of injury varies with the route, concentration, and duration of exposure.
• Inhalation of the anhydrous form causes rapid onset of respiratory symptoms, whereas inhalation of the household concentration typically produces no effect.

Vital Signs

• Tachycardia, tachypnea, and decreased pulse oximetry are common following inhalation.
• Hypertension has been reported.

HEENT

• Mucous membrane irritation is common (lacrimation, rhinorrhea, conjunctivitis, blepharospasm, drooling) from splash or inhalation exposure.
• Corneal burns, laryngeal edema, and laryngospasm may follow severe exposures.
• Oropharyngeal burns with epithelial desquamation may produce airway obstruction.

Dermatologic

• Erythema and dermatitis are common from contact exposure.
• Second- and third-degree burns are usually caused by contact with higher concentration commercial products.

Pulmonary

• Cough, chest pain, stridor, wheezing, bronchospasm, rhonchi and rales, chemical pneumonitis, and noncardiogenic pulmonary edema may occur following inhalation or aspiration.
• Pulmonary edema may be delayed following severe exposures.
• Upper airway edema may develop.

Gastrointestinal

• Nausea and vomiting are common following either inhalation or ingestion.
• Burns to the esophagus and stomach may follow ingestion of higher concentration commercial products or intentional large ingestion of lower concentration household products.

PROCEDURES AND LABORATORY TESTS

Essential Tests

No tests may be needed in asymptomatic patients following exposure to low-concentration products.

Recommended Tests

• Chest radiographs, arterial blood gases, and pulmonary function tests may help to evaluate injury.
• A chest radiograph is usually normal following mild to moderate exposures; infiltrates and pulmonary edema may not be evident for several hours.
• Bronchoscopy should be considered after a severe exposure because of the possibility of upper airway edema.
• Endoscopy should be performed to evaluate for burns within 24 hours following ingestion of high-concentration products or large amounts of lower concentration household products and in patients with oral burns, drooling, dysphagia, or abdominal pain.

Section Outline:

• SIGNS AND SYMPTOMS
  • Vital Signs
  • HEENT
  • Dermatologic
  • Pulmonary
  • Gastrointestinal
• PROCEDURES AND LABORATORY TESTS
  • Essential Tests
  • Recommended Tests

• After exposure to high-concentration products, the focus should be placed on aggressive airway management and early endotracheal intubation of patients with airway injuries.
• Dose and time of exposure should be determined for all substances involved.

DIRECTING PATIENT COURSE

The health-care professional should call the poison control center when:

• Respiratory or gastrointestinal symptoms are present.
• Signs and symptoms are not consistent with ammonia exposure.
• Coingestant, drug interaction, or underlying disease presents an unusual problem.

The patient should be referred to a health-care facility when:

• Attempted suicide or homicide is possible.
• Patient or caregiver seem unreliable.
• Symptoms are present.
• Coingestant, drug interaction, or underlying disease presents an unusual problem.

Admission Considerations

Inpatient management is warranted if:

• Patient is symptomatic.
• Patient was exposed to anhydrous ammonia or other high-concentration commercial product.

DECONTAMINATION

• Inhalation. Remove from exposure and provide 100% oxygen.
• Ingestion
  • Emesis should not be induced.
  • Dilution with oral administration of 4 to 6 ounces of milk or water may be useful.
• Dermal exposure
  • Skin should be irrigated with copious amounts of water, followed by thorough washing with soap and water.
  • Burned area should be covered with a sterile dressing after irrigation.
• Eye exposure
  • Exposed eyes should be irrigated with copious amounts of water; pH of cul-de-sac should be tested after irrigation to ensure neutral pH.
  • Slit-lamp examination should be performed, and patients with an ocular burn should be referred to an ophthalmologist immediately.

ANTIDOTES

There is no antidote for ammonia poisoning.

ADJUNCTIVE TREATMENT

• Bronchospasm should be treated with nebulized beta-₂-receptor agonist (albuterol).
• Ingestion of high concentration products (anhydrous or industrial products) is managed as an alkaline corrosive.
• Corticosteroids may reduce the degree of pulmonary injury, but their efficacy has not been proven in clinical trials.
• Skin burns are treated in the same manner as thermal burns.

Section Outline:

• DIRECTING PATIENT COURSE
  • Admission Considerations
• DECONTAMINATION
• ANTIDOTES
• ADJUNCTIVE TREATMENT

PATIENT MONITORING

Respiratory and cardiac function should be monitored continuously in symptomatic patients.

EXPECTED COURSE AND PROGNOSIS

• Toxicity usually develops within minutes (inhalation or aspiration) to hours (ingestion or skin exposures).
• Course depends on concentration of product and duration of exposure.
• Inhalation of high-concentration products may result in permanent pulmonary dysfunction.
• Ingestion of high-concentration products may cause esophageal strictures.

DISCHARGE CRITERIA/INSTRUCTIONS

• From the emergency department. Patients who are asymptomatic after toxic ingestion and patients with documented absence of gastrointestinal burns or first-degree burns and tolerating oral intake may be discharged after 6 hours observation and psychiatric evaluation, if needed.
• From the hospital. Patients with second- or third-degree burns may be discharged when they are tolerating oral feeding, with follow-up evaluation scheduled to detect stricture formation.

Section Outline:

• PATIENT MONITORING
• EXPECTED COURSE AND PROGNOSIS
• DISCHARGE CRITERIA/INSTRUCTIONS

Chest radiograph abnormalities may take hours to develop.

Toxic effect of corrosive aromatics, acids, and caustic alkalis.

See Also: SECTION IV, Caustics—Basic chapter.

RECOMMENDED READING

Close LG, Catlin FI, Cohn AM. Acute and chronic effects of ammonia burns of the respiratory tract. Arch Otolaryngol 1980;106:151-158.

Author: Edwin K. Kuffner

Reviewer: Richard C. Dart