Diagnosis and assessment

Burning and blistering of the mouth suggests that there may be serious injury to the esophagus and stomach. In most cases there is severe pain in the mouth, anterior chest, or abdomen. The patient may have dysphagia with drooling of saliva. There may be vomiting with or without hematemesis. Excruciating retrosternal pain usually follows esophageal perforation, which is usually accompanied by subcutaneous emphysema of the neck and muscle rigidity of the left chest wall. On auscultation a pleuropericardial friction rub may be heard (Hamman's sign) and there may be signs of a left-sided hydropneumothorax. Peritonitis indicates gastric perforation.

Any respiratory distress is ominous and should alert one to possible upper airway compromise. Stridor is indicative of supraglottic edema, but hoarseness and even muteness are suggestive of laryngeal injury. Respiratory embarrassment may also be due to chemical pneumonitis or even pulmonary edema. As respiratory tract edema typically evolves over hours, patients must be observed carefully. Fever and tachycardia frequently accompany even moderate poisonings. Although certain signs such as stridor may be predictive of severe esophageal injury, these should not be relied upon to gauge severity as the absence of oropharyngeal burns does not exclude severe esophageal damage. Early endoscopy is mandatory in all cases where significant ingestion may have occurred.

An erect chest radiograph may show mediastinal air in esophageal perforation; there may be an associated hydropneumothorax or pleural effusions which are often small and usually left-sided. Rarely, contrast studies using water-soluble dyes may be needed to demonstrate esophageal perforation. Pneumonitis, which may be due to aspiration or inhalation of volatile vapors, may be evident. Free air under the diaphragm confirms gastric perforation. An abdominal film is less helpful but may show ileus.

Arterial blood gas measurement and continuous pulse oximetry are essential for any case where respiratory signs are evident or significant corrosive ingestion may have occurred. There may be metabolic acidosis which may reflect acid absorption or result from extensive tissue damage. Although most corrosive acids or alkalis are neutralized on contact with tissue, significant quantities may be absorbed, leading to systemic toxicity. For example, ammonia or phenol ingestion may lead to significant methemoglobinemia. Hemolysis and leukocytosis are occasionally seen. Disseminated intravascular coagulation may be seen in severe cases, but fibrinolysis is more common. Since corrosive ingestion may be an act of suicide, other substances may have been taken, and plasma acetaminophen (paracetamol) and salicylate levels should be determined.

The mainstay of investigation is endoscopy which should be performed as soon as is practicable after patient stabilization, ideally between 6 and 24 h after ingestion. Endoscopy should be performed by an experienced operator using a small-diameter flexible endoscope. The endoscope should be passed through damaged areas unless there is severe necrotizing damage. Reported series describing the use of early endoscopy show negligible risk of perforation. Burns are classified according to the criteria shown in Table,2. Assessment of burn severity and extent may be difficult as there are often concomitant burns of different stages present. The distinction between grade 2(b) and grade 3 burns may be particularly difficult.

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Table 2 Endoscopic grading of corrosive injury

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