Alkalis - Corrosive(Caustic) Poisons

Alkalis and Other Caustics

ALKALIS

Alkalis commonly encountered in poisoning include ammonia (usually in the form of ammonium hydroxide), carbonates of sodium and potassium, and hydroxides of sodium, potassium, and calcium. Sodium hypochlorite is also increasingly being implicated.

Physical Appearance

Most of these occur as white powders or colourless solutions. Ammonia gas is colourless with a pungent, choking odour.

Uses

·              Ammonia gas—Smelling salts.*

·              Ammonium hydroxide (32.5% ammonia)—Paint, oil, and dirt remover, refrigerant.

·              Sodium hydroxide (caustic soda)—Drain cleaner, oven cleaner. Potassium hydroxide (caustic potash)—Drain cleaner, hearing aid batteries.

·              Sodium carbonate (washing soda)—Household cleaning agent, detergent.

·              Potassium carbonate—Household cleaning agent.

·              Sodium hypochlorite—Household bleach.

Usual Fatal Dose

·              About 10 to 15 gm for most alkalis.

·              About 15 to 20 ml for ammonia.

Mode of Action

Locally, alkalis produce liquefaction necrosis which results in extensive penetrating damage because of saponification of fats and solubilisation of proteins. Production of ulcers is common which may persist for several weeks. Oesophagus is more severely affected than the stomach in contrast to acids.

Clinical Features

Corrosion of GI mucosa with greyish pseudomembrane formation. Oesophagus is often severely affected resulting in dysphagia, vomiting, drooling, and haematemesis. Stridor is an important indicator of severe oesophageal injury.

There are four categories of alkali induced oesophagitis:

a. Non-ulcerative oesophagitis—from ingestion of mildirritants, resulting in 1st degree burns.

b.Mild ulcerative oesophagitis—from ingestion of weakbases. 2nd degree burns are produced. Strictures may develop.

c.Severe ulcerative oesophagitis—from ingestion ofstrong bases. There is severe dysphagia with vomiting which may subside after 2 to 3 days only to reappear as slowly progressive dysphagia after 4 to 6 weeks due to stricture formation. This may lead to total obstruction.

d.Oesophagitis with complications—apart fromoesophagitis, there are complications such as medi-astinitis, perforation, pericarditis, pulmonary oedema, laryngeal obstruction, etc.

It is important to perform oesophagoscopy and make accurate assessment as to the extent of local injury (Table 7.1). Contraindications to oesophagoscopy include upper airway obstruction and GI perforation.

Abdominal pain, diarrhoea, tenesmus. Skin involvement results in greyish, soapy, necrotic areas without charring.

Eye involvement can produce serious complications, and constitutes an ophthalmologic emergency.

Ammonia ingestion causes manifestations which are essen-tially similar to those seen with other alkalis, but respiratory symptoms are commonly super-added due to inhalation of fumes while swallowing.

Diagnosis

1.In stomach contents:

a. White, solid, slimy lumps, flakes, or granules.

b.Turns litmus paper blue.

c.Becomes warm on addition of water.

d.If exposed to air, becomes moist and gets dissolved.

e.Soapy or slimy feeling when touched with fingers.

f.Sharp penetrating odour in the case of ammonia.

2.Platinum wire flame test: Touch platinum wire to theunknown substance and then place it in a flame. Sodium gives an intense persistent yellow flame. Potassium gives a deep purple flame.

3.Fume test for ammonia: Place an open bottle of concen-trate Hcl near a sample of stomach contents, aspirate, or vomitus. Copious white fumes of ammonium chloride will emanate if ammonia is present. The test can also be done to detect the presence of ammonia in the atmosphere.

Treatment

·            Respiratory distress (especially in the case of ammonia) may require endotracheal intubation, cricothyroidotomy, or tracheostomy, depending on severity. Oxygen must be administered as necessary.

·            Diluents such as milk or water may be given as a first aid measure for alkali ingestion (no more than one or two glasses for an adult). If more than one hour has elapsed, this is usually not efficacious.

·            The following are absolutely contraindicated : emesis,gastric lavage, catharsis, and activated charcoal. Withhold all oral feeds initially.

·            Assess fluid and electrolyte balance.

·            Watch for development of complications and attend to them accordingly.

·            Some investigators recommend early surgical intervention and use of an intraluminal stent in patients with 2nd or 3rd degree oesophageal burns because perforation which requires surgical repair may otherwise be missed. Others have suggested that if the serum pH is less than 7.20 (because of lactic acidosis resulting from severe tissue necrosis), surgery should be immediately undertaken.

·            If circumferential 2nd degree or 3rd degree burns of the oesophagus are seen, exploratory laparotomy should be undertaken followed by gastric resection and oesopha-gectomy, in case gastric necrosis is evident at laparos-copy.

·              In the past, administration of corticosteroids was recom-mended to prevent stricture formation which was based on animal studies. But today most investigators appear to be of the opinion that high dose corticosteroid therapy in caustic ingestion predisposes the patient to infection and perforation as well as masks symptoms of devel-oping peritonitis or mediastinitis, and hence should be avoided. However, steroids may be effective in patients with dyspnoea, stridor, hoarseness, and other evidence of respiratory compromise, and may decrease laryngotra-cheal oedema thereby lessening respiratory dysfunction.

·            Use of prophylactic antibiotics is not recommended today. Most investigators feel that antibiotics should be administered only if there are signs of perforation or secondary infection.

·            An oesophagogram should be done at 3 weeks to evaluate the formation of strictures. Patients should be instructed to seek medical attention immediately when-ever they develop dysphagia.

·            Alkali injuries to the eye and skin should be irrigated copiously with water or saline for at least 20 to 30 minutes. Ophthalmologic consultation is mandatory. Topical antibiotics and steroids may help.

·            Patients who have suffered from stricture formation require long-term endoscopic follow-up for the presence of neoplastic changes of the oesophagus which may occur with a delay of several years or decades.

Autopsy Features

·      Characteristic odour (in the case of ammonia).

·      Brownish or greyish staining of skin.

·      Inflammatory oedema with corrosion and sliminess of the tissues of the oesophagus and stomach. The mucosa may be brownish owing to formation of alkaline haematin.

·              Congestion of respiratory tract and pulmonary oedema (especially in the case of ammonia).

Forensic Issues

·              Accidental poisoning occurs usually by mistaking an alkali solution for water, lemonade, beer, etc., because of careless storage of these chemicals in inadequately labeled, ordinary looking bottles or jars.

·              Industrial accidents involving these substances are reported from time to time.

·              Suicidal cases are occasionally encountered. Homicides from time to time.

·              Suicidal cases are occasionally encountered. Homicides are quite rare.

·              Ammonia may sometimes be sprayed or thrown on a victim to facilitate robbery.