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.