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Chapter: Modern Medical Toxicology: Asphyxiant Poisons: Toxic Gases

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Ammonia - Respiratory Irritants Asphyxiant Poison

Extremely irritant gas with a penetrating odour.

RESPIRATORY IRRITANTS

Ammonia

Physical Appearance

·              Extremely irritant gas with a penetrating odour.

·              It is highly water soluble (forming ammonium hydroxide which is an alkaline corrosive).

·              Aqueous ammonia is a colourless liquid with a strong alka- line reaction (pH 11.6) and a penetrating pungent odour. When heated to decomposition, it emits toxic fumes of ammonia and oxides of nitrogen.

Uses

·              Agriculture (fertiliser)

·              Mining

·              Manufacture of plastics and explosives

·              Refrigerant

·              Cleaning and bleaching agent

·              Treatment of syncope in the form of smelling salts.

·              Household ammonia is 5 to 10%. Strong ammonia solution is 28% (sold in pharmacies).

Clinical Features

·      Inhalation produces such severe upper airway irritation that the victim seldom remains exposed for more than an instant, unless he is trapped. Symptoms include lacrimation, cough, dyspnoea, convulsions, coma, and death. There is glottic and laryngeal oedema, sloughing of bronchial mucosa, and chemical pneumonitis with pulmonary oedema.

·              If recovery from the acute event is incomplete, a chronic condition may set in called reactive airways dysfunc-tion syndrome or RADS. This is a persistent, asthma-likesyndrome and is also referred to as irritant induced asthma. It is different from occupational asthma since there is no evidence of atopy in individuals suffering from RADS, and the agents involved are generally not considered to be immunologically sensitising. However it is true that RADS can occur as a chronic occupational condition in people who work with chemicals. The inflammatory response of the airways in RADS most probably has a neurogenic aetiology involving the release of substance P from unmyelinated sensory neurons or C fibres. Substance P is a well-known culprit in neurogenic inflammation. Management is best effected by immediate (and permanent) exclusion from the source of exposure and symptomatic measures, though the response to beta2 adrenergic agonist therapy is not as good as in occupational asthma.

·      Ingestion of ammonia solution produces corrosion of the alimentary tract and aspiration pneumonia. Nausea and vomiting occur frequently following ingestion. Swelling of the lips, mouth, and larynx, and oral or oesophageal burns may occur if concentrated ammonia solutions are ingested.

·      Dermal contact can result in deep, penetrating burns. Exposure to anhydrous ammonia stored at minus 280 F may produce frostbite injury with thrombosis of surface vessels and subsequent ischaemia and necrosis.

·      Ocular exposure can result in immediate and serious chemical burn with rapid penetration into the interior of the eye. Conjunctivitis, lacrimation, corneal irritation, and temporary or permanent blindness can result. Total corneal epithelial loss may occur. Ammonia has greater tendency than other alkalies to penetrate and damage the iris, and to cause burns and cataracts in cases of severe exposure. Iritis may be accompanied by hypopyon or haemorrhages, extensive loss of pigment, and severe glaucoma.

·      Chronic exposure in workers may lead to initial complaints of chronic cough, dyspnoea on effort, bilateral infiltrates on chest X-ray, and lung function indices reflecting ventilatory and diffusion abnormalities Asthma and laryngitis have been reported in workers chronically exposed to ammonia.

Usual Fatal Dose

·              About 5 to 10 ml of liquid ammonia.

·              Inhalation of the gas at concentrations above 5000 ppm can be rapidly fatal. Fatalities may also occur from exposure to ammonia concentrations of 2500 to 4500 ppm if inhaled for 30 minutes.

·              Mixing of ammonia with hypochlorite bleach results in the formation of chloramine, which causes a toxic pneumo- nitis (pulmonary oedema) following inhalation, and may produce residual pulmonary function abnormalities.

Diagnosis

·      Chest X-ray in dyspnoeic patients.

·      Early endoscopy to determine the extent of injury.

·      Barium swallow after 1 to 2 weeks to rule out oesophageal strictures.

·              Presence of ammonia in an unknown solution, stomach contents, or vomitus can be confirmed by placing an open bottle of concentrate HCl in the vicinity. This will produce copious white fumes of ammonium chloride. The determi-nation of ammonia in air may be done using an ammonia-specific electrode, second derivatives spectroscopy, ion chromatography, or colourimetrically.

Treatment

Ammonia blood levels are generally not useful indicators of exogenous ammonia exposure or toxicity. It is normally found in human blood at a concentration of 80 to 110 mcg/100 ml. There can be a four-fold or greater rise in blood ammonia in some toxic liver diseases because the urease needed to convert ammonia to urea is found only in the liver. A serum concentration of 1,000 to 10,000 mcg/100 ml is considered toxic.

·      Ocular exposure should be treated with prolonged irriga-tion with water (30 minutes or more) until the eye reaches neutral pH as tested with a litmus paper in the conjunctival sac.

·      Dermal exposure requires washing with soap and water, followed by copious irrigation with water alone. Frostbite should be treated in the standard manner.

·      Inhalation should be treated with oxygen, PEEP (positive end expiratory pressure), intubation, and bronchodilators. Intubation or tracheostomy may be life-saving following severe exposure if stridor, indicating laryngeal oedema, is present. Partial liquid ventilation has shown promise in preliminary studies.

·      If bronchospasm and wheezing occur, consider treatment with inhaled sympathomimetic agents.

·      In the case of ingestion, a small quantity of water or milk can be administered as a first-aid measure to dilute the chemical. Neutralisation with vinegar or weak acids is not recommended. Demulcents can be given. Do NOT attempt dilution in patients with respiratory distress, altered mental status, severe abdominal pain, nausea or vomiting, or patients who are unable to swallow or protect their airway. Diluents should not be force fed to any patient who refuses to swallow. Activated charcoal is of no benefit, and may induce vomiting and obscure endoscopy findings.

·              Stomach wash and emetics are contraindicated. Obtainconsultation concerning endoscopy as soon as possible, and perform endoscopy within the first 24 hours when indicated.

·      Antibiotics are indicated only when there is evidence of infection.

·      The use of corticosteroids for the treatment of caustic inges-tion is controversial.

Forensic Issues

·      While poisoning with ammonia is not very common, most of the cases reported are suicidal in nature. Since the solu-tion or gas even when weak has a distinct irritant smell, accidental poisoning is unlikely. Obviously, its properties preclude its choice for murder.

·              However, of late ammonia is being used as a spray to incapacitate victims of robbery. Serious eye injuries can result.

 

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