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Ammonia - Emergency Department/Hospital Management

Acute Management Overview

Agent Identification

  • At room temperature, anhydrous ammonia is a colorless, highly irritating gas with a pungent, suffocating odor. It is lighter than air and flammable, with difficulty, at high concentrations and temperatures. It is easily compressed and forms a clear, colorless liquid under pressure. Ammonia dissolves readily in water to form ammonium hydroxide - an alkaline solution. The concentration of aqueous ammonia solutions for household use is typically 5% to 10% (weight:volume), but solutions for commercial use may be 25% (weight:volume) or more, and are corrosive. Anhydrous ammonia is stored and shipped in pressurized containers, fitted with pressure-relief safety devices, and bears the label "Nonflammable Compressed Gas". Despite not meeting the Department of Transport definition of flammable, it should be treated as such.
  • Anhydrous ammonia reacts with moisture in the mucous membranes to produce an alkaline solution (ammonium hydroxide). Exposure to ammonia gas or ammonium hydroxide can result in corrosive injury to the mucous membranes of the eyes, lungs, and gastrointestinal tract and to the skin due to the alkaline pH and the hygroscopic nature of ammonia.
  • Responders should obtain assistance in identifying the chemical(s) from container shapes, placards, labels, shipping papers, and analytical tests. General information on these identification technicques is located in the Emergency Response Guidebook.
  • Identification Tools - CHEMM-IST, WISER, Ammonia Chemical Properties
  • Devices (examples) - HazCat Industrial Chemical and Methamphetamine Identification Kit (Model KT1220 ) (solid and liquid), ChomAir Badges (vapor or gas), Safe Air Monitoring System (vapor or gas), Kitagawa Gas Detector Tubes (vapor), Sensidyne Gas Detection Tubes (vapor).
  • A comprehensive source for the selection of chemical identification equipment is the Guide for the Selection of Chemical Detection Equipment for Emergency First Responders, Guide 100-06, January 2007, 3rd Edition published by the Department of Homeland Security.

Rescuer Protection

  • Persons exposed only to ammonia gas generally do not pose substantial risks of secondary contamination.
  • However, clothing or skin soaked with industrial-strength ammonia or similar solutions may be corrosive to rescuers and may release harmful ammonia gas.
  • PPE required: Level B-C is generally adequate depending on the ambient temperature and distance from hot/warm zones (bring in HAZMAT for Level As PRN). Use butyl rubber or other glove materials with adequate breakthrough characteristics. Be aware that use of protective equipment by the provider may cause fear in children, resulting in decreased compliance with further management efforts.
  • Link to PPE, rescuer safety hospital management section
  • Link to reference section for acute event PPE related safety information

Ammonia Specific Triage

The following exposed persons should be evaluated at a medical facility:

  • Symptomatic patients complaining of persistent shortness of breath, severe cough, or chest tightness should be admitted to the hospital and observed until symptom-free. Pulmonary injury may progress for several hours.
  • Those who have eye or skin burns that cover a large surface area.
  • Those who have ingested ammonia.

Patient Release

  • In a mass casualty situation, asymptomatic patients who are reliable historians and those who experienced only minor sensations of burning of the nose, throat, eyes, and respiratory tract (with perhaps a slight cough) may be released. In most instances, these patients will be free of symptoms in an hour or less. They should be advised to seek medical care promptly if symptoms develop or recur.
  • If the treater feels that the patient has been exposed to a significant amount of ammonia, despite a relatively benign clinical appearance, if the incident involved a small number of patients, or the victims included young kids (especially infants or patients with special needs), they should be monitored in an ED "extended care" area for 6-12 hrs).

Decontamination

  • Victims exposed only to ammonia gas do not pose substantial risks of secondary contamination to personnel outside the Hot/Warm Zones.
  • Victims whose clothing or skin is contaminated with liquid ammonium hydroxide can secondarily contaminate response personnel by direct contact or through off-gassing ammonia vapor.
  • Link to hospital management section

Route of Exposure

  • Inhalation of ammonia may cause nasopharyngeal and tracheal burns, bronchiolar and alveolar edema, and airway destruction resulting in respiratory distress or failure. Ammonia's odor threshold is sufficiently low to acutely provide adequate warning of its presence (odor threshold = 5 ppm; OSHA PEL = 50 ppm). However, ammonia causes olfactory fatigue or adaptation, making its presence difficult to detect when exposure is prolonged. Anhydrous ammonia is lighter than air and will therefore rise (will not settle in low-lying areas); however, vapors from liquefied gas are initially heavier than air and may spread along the ground.
  • Skin/Eye Contact - the extent of injury produced by exposure to ammonia depends on the duration of the exposure and the concentration of the gas or liquid. Even low airborne concentrations (100 ppm) of ammonia may produce rapid eye and nose irritation. Higher concentrations may cause severe eye injury. Contact with concentrated ammonia solutions, such as some industrial cleaners (25%), may cause serious corrosive injury, including skin burns, permanent eye damage, or blindness. The full extent of damage to the eyes may not be clear until up to 1 week after the injury is sustained. Contact with liquefied ammonia can cause frostbite injury.
  • Ingestion - ingestion of ammonium hydroxide, while uncommon, results in corrosive damage to the mouth, throat, and stomach. Ingestion of ammonia does not normally result in systemic poisoning.

Clinical Signs and Symptoms

  • Respiratory - the extent of injury produced by exposure to ammonia depends on the duration of the exposure, the concentration of the gas, and the depth of inhalation. Even fairly low airborne concentrations (50 ppm) of ammonia produce rapid onset of eye, nose, and throat irritation; coughing; and narrowing of the bronchi. More severe clinical signs include immediate narrowing of the throat and swelling, causing upper airway obstruction and accumulation of fluid in the lungs. This may result in low blood oxygen levels and an altered mental status. Mucosal burns to the tracheobronchial tree can also occur. Immediate onset of laryngospasm with respiratory arrest can occur.
  • Dermal - dilute aqueous solutions (less than 5%) rarely cause serious burns but can be moderately irritating. Exposure to concentrated vapor or solution can cause pain, inflammation, blisters, necrosis and deep penetrating burns, especially on moist skin areas. Skin contact with compressed, liquid ammonia (which is stored at -28 °F) causes frostbite injury, and may also result in severe burns with deep ulcerations.
  • Ocular - ammonia has a greater tendency to penetrate and damage the eyes than does any other alkali. Even low concentrations of ammonia vapor (100 ppm) produce rapid onset of eye irritation. Contact with high concentrations of the gas or with concentrated ammonium hydroxide may cause swelling and sloughing of the surface cells of the eye, which may result in temporary or permanent blindness.
  • Gastrointestinal - nausea, vomiting, and abdominal pain are common symptoms following ingestion of ammonia. Ingestion of household ammonia (5-10%) has resulted in severe esophageal burns. Esophageal pain with swallowing, drooling and refusal of food suggest a more significant injury. Substernal chest pain, abdominal pain and rigidity suggest profound injury and potential perforation of the esophagus and/ or stomach.
  • Link to Toxic Syndromes
  • Link to Primary and Secondary Survey

Differential Diagnosis

  • Phosgene is distinguished by its smell in high concentrations and delayed onset of pulmonary edema.
  • Riot agents cause an acute onset of burning sensation in the eyes and upper airway without progression of symptoms. Riot agents do not cause laryngospasm except in hugh doses, and patients never develop symptoms of peripheral pulmonary edema.
  • Nerve agents induce watery secretions as well as respiratory distress, but have a host of other symptoms, such as miosis, seizures, rapidity of onset, that can distinguish them from pulmonary agents.
  • The respiratory toxicity of vesicants (i.e. mustard) is usually delayed but affects the central rather than the peripheral airway. Vesicant toxicity severe enough to cause dyspnea typically causes airway necrosis often with upper airway obstruction.
  • Link to Chemical Hazards Emergency Medical Management Intelligent Syndromes Tool (CHEMM-IST)

Treatment

Acute Patient Care Guidelines References