OVERVIEW: What every practitioner needs to know

Are you sure your patient has a caustic chemical injury? What are the typical findings for this disease?

Exposure to caustic agents occur through the dermal, ocular, respiratory, and gastrointestinal routes. Ingestion of caustic agents result in the most significant degree of morbidity and mortality.

Ingestion of caustic chemicals occurs most frequently in children less than 6 years of age and are unintentional in nature. The ingestion of caustic agents by adolescents and adults are generally intentional and are associated with a higher degree of morbidity and mortality. The likelihood of significant injury depends on the characteristics of the substance ingested and the quantity ingested. Generally speaking, strong acids (those with a pH of <3) and strong alkalis (those with a pH >11) are the greatest risk for causing tissue injury. Hydrofluoric acid requires special consideration and will not be discussed in this chapter.

Multiple studies and case reports demonstrate that the presence or absence of symptoms after ingestion does not predict the likelihood that an injury occurred nor does it correlate with the severity of injury. The most common symptoms after a caustic ingestion include dysphagia, drooling, pain, and vomiting. Stridor is suggestive of significant airway compromise. Epigastric pain and hematemesis may also occur.

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Pathophysiology of Alkalis and Acids

The severity of injury after a caustic ingestion is due to multiple factors, including the pH of the agent and the titratable acid or alkaline reserve (TAR). The concentration of the substance and the quantity are also important factors.

In the emergency department (ED), the pH of the substance can be determined in a few ways. If the product is available, an effort to obtain the Material Safety Data Sheet (MSDS) should be made, as this can provide invaluable information.

Contact with the regional poison center is imperative; they can facilitate obtaining the MSDS and can have additional product-specific information. If the product is present in the ED, the pH can be tested using litmus paper.

The TAR is the amount of acid or base that is required to titrate a chemical’s pH to neutral (pH 8). The TAR is more reliable to predict the likely injury after a caustic exposure, although this information is much more difficult to obtain in real time.

Acids and alkalis produce different types of tissue injury.

Acids damage epithelial cells with a resultant eschar formation. This is histologically known as coagulative necrosis. Because of the eschar formation, there is often limited substance penetration and decreased depth of injury. This is particularly important after ocular exposure to acids. The extent of injury is often limited and is not as severe when compared with ocular exposures to alkalis.

Alkalis damage tissue surfaces and lead to protein dissolution, fat saponification, and cell death. This is known histologically as liquefactive necrosis or saponification. The mechanism of injury and deep penetration makes ocular alkali exposures a medical emergency.

In some reports, acids spare the esophagus of significant injury compared with the stomach. Alkalis characteristically cause more damage to the esophagus than the stomach. However, in significant exposures, both the esophagus and stomach are damaged from both acids and alkalis.

Grading/Classification of Injury

Esophageal burns, regardless of whether caused by an acid or an alkali, are classified based on endoscopic evaluation in a manner similar to the grading of burns of the skin. Grade I burns are first degree and described as hyperemia or edema in the absence of ulcer formation. Grade IIa burns are second degree and noncircumferential and are described as submucosal lesions and ulcerations. Grade IIb burns are second degree but are circumferential. Grade III burns are third-degree burns and are described as deep ulcers and necrosis.

Grade I and grade IIa burns carry no risk of stricture formation, whereas grade IIb burns result in stricture formation in about 75% of cases, and grade III burns invariably result in stricture formation.

The risk of esophageal carcinoma has been demonstrated to be 1000-fold higher in patients with stricture formation.

Differential Diagnosis

Because of the nature of the exposure, it is often well known that a patient was exposed to or ingested an acid or alkali. There is often not a broad differential diagnosis in this scenario because most of these ingestions occur in pediatric patients less than 6 years of age and are often quickly identified by the caregivers. Generally speaking, although the mechanism of injury differs between acids and alkalis, the clinical presentation is often similar.

Clinical Presentation

The clinical presentation may vary among patients. Some patients may be asymptomatic, whereas others may complain of nausea, vomiting, dysphagia, stridor, abdominal pain, or chest pain. Oral lesions/burns may also be present; however, the absence of oral lesions/burns does not exclude the possibility of injury to the esophagus or stomach.

Several studies have tried to evaluate whether the clinical symptoms, if any, can predict the severity of injury and thereby be used to triage patients based on the need for endoscopy. A retrospective case series by Crane et al evaluated children after ingestion of alkali and found that the presence of two or more symptoms (vomiting, drooling, stridor) was predictive of esophageal injury.

An additional study demonstrated that dysphagia and drooling alone were predictive of injury. There have been no studies evaluating the clinical symptoms and severity of injury secondary to acids. Because of this and the fact that acids are somewhat anesthetic and may not cause pain, one should approach these cases conservatively; endoscopy should be performed in all of these exposures.

What laboratory studies should you request to help confirm the diagnosis? How should you interpret the results?

Multiple unsuccessful attempts have been made to correlate laboratory values with the degree of injury.

Severe ingestion of acids or alkalis can cause perforation, peritonitis, mediastinitis, and hemodynamic instability. In these scenarios, clinical laboratory findings suggestive of hypoperfusion would be expected. Additionally, acids can be absorbed from the gastrointestinal tract and may result in either an anion gap or nonanion gap metabolic acidosis on a basic metabolic profile.

In unintentional exposures, it is not unreasonable to obtain baseline laboratory studies, including a basic metabolic profile. However, in an intentional exposure, it is imperative that a complete toxicologic work-up is performed—including acetaminophen and salicylates—as well as a basic metabolic profile and other laboratory studies, as indicated.

Would imaging studies be helpful? If so, which ones?

Classifying the degree of injury is imperative for further treatment. The gold standard for visualization and subsequent grading of injury is endoscopy. The decision for the need for endoscopy should be made on a case-by-case basis; however we provide the following criteria for guidance:

Endoscopy should be performed within the first 24 hours in all patients with an intentional ingestion of a caustic chemical.

Endoscopy should be performed within the first 24 hours in all patients with an unintentional ingestion of an acid.

Endoscopy should be performed within the first 24 hours in all patients with an unintentional ingestion of an alkali in the presence of pain or a combination of drooling, stridor, and vomiting.

Other diagnostic modalities have been evaluated to determine the esophageal injury. Most recently, chest and abdominal computed tomography (CT) was investigated. Chest and abdominal CT should be performed in patients in whom perforation or mediastinitis is suspected. However, the radiation exposure risk is far greater than any risk associated with esophagogastroduodenoscopy (EGD) in the pediatric population.

If you are able to confirm that the patient has a caustic chemical injury, what treatment should be initiated?

Initial treatment of these patients includes airway stabilization. In any patient with signs of airway compromise or upper airway edema, every attempt should be made for early endotracheal intubation. If there is significant airway edema, a single dose of dexamethasone before intubation is not unreasonable.

pH neutralization is not standard of care and presents the fear of the creation of an exothermic reaction, which can worsen the degree of injury.

Early dilution with water or milk should not be attempted.

There should be consultation with gastroenterologist for EGD.

If grade IIb or grade III burns are confirmed by EGD, early interventions aimed at minimizing stricture formation are imperative. In the past, in patients with grade IIb lesions, therapy with corticosteroids and antibiotics was used to minimize stricture formation. A recent meta-analysis of these data showed that there is no benefit from corticosteroids in preventing strictures, and the risk associated with their use (e,g., infection) outweigh any benefit.

Interventions aimed at preventing stricture include but are not limited to esophageal stent placement,endoscopic dilation, and intralesional corticosteroid injection. These interventions should be performed only by gastroenterologists; they are not ED interventions.

What are the possible outcomes of caustic chemical injuries?

By far, the most significant morbidity from caustic agents is after an ingestion. In patients with grade I or grade IIa lesions, there is little to no risk of complications. Oral intake can be advanced as tolerated by the child. For grade IIb lesions, however, there is a significantly increased risk of esophageal carcinoma of 1000-fold, and it appears that this is latent for up to 40 years. Patients with grade IIb lesions require close follow-up and monitoring by a gastroenterologist on a regular basis. In patients with grade III lesions, the risk of perforation, infection, and other complications is significantly elevated. These patients may require surgical intervention.

What is the evidence?

Crain, EF, Gershel, JC, Mezey, AP. “Caustic ingestions. Symptoms as predictors of esophageal injury”. Am J Dis Child. vol. 138. 1984. pp. 863-5.

Nuutinen, M, Uhari, M, Karvali, T. “Consequences of caustic ingestions in children”. Acta Paediatr. vol. 83. 1994. pp. 1200-5.

Gaudreault, P, Parent, M, McGuigan, MA. “Predictability of esophageal injury from signs and symptoms: a study of caustic ingestion in 378 children”. Pediatrics. vol. 71. 1983. pp. 767-70.

Salzman, M, O’ Malley, RN. “Updates on the evaluation and management of caustic exposures”. Emerg Med Clin North Am. vol. 25. 2007. pp. 459-76.

Fulton, JA, Hoffman, RS. “Steroids in second degree casutic burns of the esophagus: a systematic pooled analysis of fifty years of human data: 1956-2006”. Clin Toxicol. vol. 45. 2007. pp. 402-8.