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    ACID INGESTION

    DEFINITION

    Intake through the mouth or nose and subsequent swallowing of a
    chemical which, in solution, has a pH < 7.0 and is of sufficient
    strength or quantity to result in injury to tissues.

    TOXIC CAUSES 

    Any solution with an acidic pH has the potential to cause tissue
    injury when ingested.  The extent of injury depends not only on pH but
    on the volume ingested, the contact time, and concentration. The acids
    most frequently associated with significant pathology are sulphuric
    acid and hydrochloric acid.

    Hydrofluoric acid ingestion is associated with specific systemic
    toxicity and requires a different management approach to that of other
    acid ingestions.

    CLINICAL FEATURES

    Significant acid ingestion produces immediate pain in the mouth,
    pharynx and abdomen.  Other early symptoms associated with the
    gastrointestinal injury may include intense thirst, pain on
    swallowing, drooling of saliva, vomiting, haematemesis and malaena. 
    Non-gastrointestinal symptoms may include stridor and hoarse voice. 
    Inspection of the oropharynx may reveal areas of superficial burn
    which appear white or yellow and/or areas of deeper burn which appear
    grey or black and bleed easily.

    The absence of burns to the lips, mouth or throat does not imply an
    absence of significant burns to the oesophagus or stomach.

    Severe burns from acid ingestion may be associated with the
    life-threatening acute complications of oesophageal, gastric or
    intestinal perforation.  Oesophageal perforation is associated with
    chest pain, dyspnoea, fever, subcutaneous emphysema of the chest or
    neck, and a pleural rub.  A chest x-ray may show widening of the
    mediastinum, pleural effusions, pneumomediastinum, and pneumothorax. 
    Perforation of the stomach or small intestine is associated with
    clinical features of chemical peritonitis: fever, abdominal
    tenderness, guarding and rebound, and ileus.  Septic shock,
    multi-organ failure and death may complicate perforation. 

    Systemic toxicity due to other chemical properties of acids can occur
    following ingestion of acetic acid, arsenic and other heavy metal
    salts, cyanide, formic acid, hydrofluoric acid, hydrochloric acid,
    nitrates, sulfuric acid and phosphoric acid.

    An asymptomatic patient is unlikely to have severe injury although
    asymptomatic children may occasionally have a significant injury.

    DIFFERENTIAL DIAGNOSIS

    Alkali ingestion
    Allergic reaction with upper airways involvement
    Caustic or oxidant ingestion
    Foreign body ingestion
    Thermal burn
    Upper airways infection

    RELEVANT INVESTIGATIONS

    Symptomatic patients should undergo the following investigations:

         Arterial blood gas analysis
         Coagulation profile
         Complete blood count
         ECG
         Electrolytes
         Glucose
         Liver and renal function
         Radiological studies: Chest x-ray, upright abdominal film
         Type and cross-match
         Upper gastrointestinal endoscopy, ideally at 6 to 24 hours
         following exposure

    Upper gastrointestinal endoscopy should also be strongly considered
    for asymptomatic patients who have intentionally ingested a strong
    acid and children, where the history may be unreliable.

    Contrast oesophagography or thoracic CT is useful in the detection of
    perforation.

    TREATMENT

     Immediate (first) aid
    Do not induce vomiting.
    Do not attempt neutralisation.
    Do not give oral fluids
    Do rinse the mouth with water or saline.

     Hospital treatment
    Initial management is primarily supportive.  Particular attention
    should be directed to securing the airway, fluid resuscitation and
    provision of opioid analgesia.  Do not give activated charcoal as it
    will interfere with endoscopic evaluation. 

    Ongoing supportive care includes maintenance of adequate analgesia,
    fluid, electrolyte and pH balance, nutritional support, and monitoring
    for the development of complications.  Parenteral nutrition is
    necessary in more severe cases.

    Subsequent management and prognosis is largely dictated by findings at
    upper gastrointestinal tract endoscopy.  These are most frequently
    classified as:

          Grade 0     Normal examination
          Grade 1     Oedema or hyperaemia of mucosa
          Grade 2a    Superficial localised ulcerations, friability,
                      blisters
          Grade 2b    Grade 2a plus circumferential ulceration
          Grade 3     Multiple deep ulcerations, area of necrosis 

    Patients with deep discrete or circumferential ulceration or multiple
    ulcerations and/or areas of necrosis require more intensive supportive
    care and total parenteral nutrition or a feeding jejunostomy until
    healing is documented.  Patients with endoscopic findings of oedema,
    erythema, superficial ulceration, blistering or erosions, may be fed
    orally.

    Urgent laparotomy (without associated thoracotomy) with surgical
    resection of necrotic tissue and surgical repair is indicated in the
    presence of symptoms or signs of gastrointestinal perforation or where
    full thickness necrosis is found at endoscopy. 

    Corticosteroids are not indicated.

    Broad spectrum prophylactic antibiotics are not indicated unless there
    is evidence of gastrointestinal tract perforation or full thickness
    necrosis.

    CLINICAL COURSE AND MONITORING

    Monitoring of respiratory, cardiovascular, and renal systems and
    fluid, electrolyte and acid-base balance, in addition to regular
    clinical observation. Close observation is required until an
    evaluation of the gastro-intestinal tract can be made (preferably by
    endoscopy) or the patient is symptom free.  Severely poisoned patients
    should be considered for admission to an Intensive Care Unit.

    Patients should be followed for up to one year following recovery from
    a moderate or severe acid ingestion.  Assessment should be directed to
    nutritional status and any difficulties with eating, particular
    swallowing.

    LONG TERM COMPLICATIONS

    Tracheoesophageal fistulae may result from perforation of the anterior
    oesophageal wall.  The fistula may extend to involve the aorta; both
    types are fatal complications.

    Acid ingestions, that cause deep ulceration will result in oesophageal
    strictures in 70% of patients.  If full thickness necrosis occurs,
    strictures are highly likely.  Strictures do not develop following
    superficial mucosal ulceration (the muscularis mucosa is intact).

    Eighty percent of strictures will become symptomatic within two
    months.  Strictures may also involve the stomach but only 40% become
    symptomatic.  Strictures may rarely develop in the mouth and pharynx.

    AUTHOR(S)/PEER REVIEW

    Author:        Robert Dowsett
                   Consultant Toxicologist
                   Departments of Clinical Pharmacology and Emergency
                   Medicine
                   Westmead Hospital
                   Westmead, NSW 2145
                   Australia

    Peer review:   London, March 98: T. Della Puppa, L. Murray, A. Nantel,
                   M. Nicholls.