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.