Resuscitation begins with control of the airway. Stridor and hoarseness are suggestive of upper airway obstruction and early endotracheal intubation is essential. Since upper airway edema may progress over the first 24 h, all cases involving potentially significant corrosive ingestion and any patients with respiratory embarrassment should undergo fiber-optic laryngoscopy. Prophylactic endotracheal intubation should be undertaken if laryngeal edema is seen. Tracheobronchial involvement is seen in up to 10 per cent of cases of severe corrosive burns. Intravenous fluids should be administered and the patient kept nil by mouth. Patients with severe injury will lose large volumes of body fluids and require generous fluid resuscitation. Central venous pressure measurement and urinary catheterization will help guide replacement therapy.
The type of corrosive, the amount ingested, and the time of ingestion should be determined where possible, and the Regional Poisons Unit should be consulted. Any corrosive solids or crystals should be wiped from the mouth which may then be gently irrigated with water. Emetics are contraindicated as the friable esophagus may be re-exposed to the corrosive substance and there is a risk of pulmonary aspiration. Indeed, antiemetics should be administered if the patient is vomiting. Activated charcoal has no role and will coat the gut lining, making endoscopic assessment of tissue damage extremely difficult. Gastric lavage has traditionally been avoided but may be useful in diluting corrosives; however, only small aliquots of water (not more than 5 mg/kg) should be used to avoid inducing emesis ( DOWS.e.tL§n„d.,..L.!^d§D.. 19.96). The pH of the stomach contents should be measured. An alkaline aspirate is indicative of severe gastric injury. Water must be the only diluent used, and attempts to neutralize corrosives are liable to cause even further tissue damage due to the vigorous exothermic reaction that may ensue.
Antibiotics should be administered early. Necrotic burns are rapidly invaded by pathogenic organisms, particularly Escherichia coli and Klebsiella species, and sepsis is a major cause of death. In addition to anticipating sepsis and possibly reducing the risk of perforation, there is evidence that antibiotic administration may decrease the incidence of stricture formation.
Patients with grade 1 burns can usually be discharged after observation for 24 h. No specific treatment is needed, but patients should be reviewed at 4 weeks and undergo a barium study to exclude stricture formation, as initial endoscopy may have underestimated the grade of burn. Patients with grade 2 burns are at risk of perforation and careful hospital observation is needed. Most patients with grade 2a burns recover quickly and can be discharged within 2 weeks. Again, careful follow-up is needed as strictures may develop. Patients with grade 2b and grade 3 burns will require a prolonged stay in hospital; many will perforate or develop strictures that are resistant to dilatation. Surgery is essential for patients with perforation or extensive grade 3 burns, but the mortality is high and the surgery is technically difficult, involving dissection of necrotic and inflamed tissues. Surgery may also allow the placement of a gastrotomy tube or the fashioning of a feeding jejunostomy since the institution of early nutrition improves the overall prognosis.
Dilatation therapy should not be carried out before 4 weeks as it confers no benefit and is associated with perforation ( ShaL§l.§L§.L 1994). Severe and extensive stricturing should be treated surgically, where esophagectomy and colonic or jejunal interposition yield good results. Burns of the lips and mouth can lead to severe chronic disability, and the oral surgeon should be consulted at an early stage. Customized mouth protectors and extraoral splints may help to limit the extent of scar contracture.
The most controversial issue is the use of corticosteroids to prevent stricture formation. Patients with grade 1 burns do not develop strictures and so corticosteroids are not indicated. Corticosteroids may reduce the incidence of strictures in patients with second- and third-degree burns, although previous reports indicate that strictures develop in most patients with third-degree burns regardless of any therapy ( Hoow§1L§JLML 1992). Although evidence available at present is insufficient to recommend corticosteroid use, there appears to be no increase in morbidity or mortality from these drugs. Corticosteroids are absolutely contraindicated where there is perforation or hemorrhage.
Novel pharmacological approaches that have been used with good result to prevent stricture formation in animal models include D-penicillamine and b-aminoproprionitirile. More recently, the sequential use of epidermal growth factor and interferon-g has been shown to reduce the frequency of residual stenosis significantly in corrosive esophageal burns of rats ( Berthet.,,ei l al 1994). The applicability of such treatments to humans remains to be demonstrated.
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