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Caustic Esophageal Injury
A caustic esophageal ingestion involves damage to the wall of the esophagus, secondary to direct contact with an acid or base, through a well-described inflammatory response. Knowledge of the pathophysiology of caustic injuries guides complex management decisions through the multiple phases of these potentially life-threatening injuries.
Epidemiology
There are two etiologies of caustic ingestion: accidental and intentional. The age of the patient is predictive of the etiology. Accidental ingestions occur in pediatric patients younger than 5 years, whereas intentional ingestions occur in adults and adolescents as an act of self-harm.
The 2013 Annual Report of the American Association of Poison Control Centers' National Poison Data System found the majority of caustic ingestions occurred in children younger than 5 years, thus the majority of the epidemiologic data is published in the pediatric literature. Retrospective studies consistently report low social economic status, low parental education, residence in low-income countries, and crowded living conditions as risk factors for accidental ingestion. The majority of children ingest an alkaline substance, most commonly a household cleaning agent. Often the substance was not stored in a labeled container. Manufacturers in developing countries have poor compliance with the use of safety caps ; conversely, this injury appears to be declining in developed countries.
Pathophysiology
Chemical Factors
The pathophysiology of caustic injuries is different for ingestion of acidic and alkali substances. In addition to pH, the severity of the injury depends on the following factors: viscosity, concentration, amount ingested, contact time, and comorbidities. Most studies report the substances consumed; however, the volume is not reported because this information cannot be gathered reliably from the patient. One study estimated the minimum consumption at 50 to 200 mL and attempted to predict the grade of injury based on volume and concentration of alkali substance consumed, acknowledging this inherent difficulty. Not surprisingly, more severe esophageal injuries occur in adults attempting suicide compared with pediatric accidental ingestions, because larger quantities of the corrosive substance are ingested. Substances with a pH < 2 or pH > 12 are known to cause significant damage. Full-thickness injury to the esophagus occurs with 10 seconds of contact with 22.5% sodium hydroxide or 1 second with 30% sodium hydroxide. Animal studies have shown variable degrees of injury with 10% sodium hydroxide exposed for 60 seconds. The total alkalinity or acidity of a substance also appears to determine the depth of the injury.
Substances
The substances consumed are often household cleaners or hair products. In North America, alkalizing agents are more commonly used for cleaning, whereas in India strong acids are readily available and used for cleaning. Commercially available drain cleaners (e.g., Liquid Plumr [Clorox, Oakland, California] and Drano [S.C. Johnson & Son, Inc., Racine, Wisconsin]) and oven cleaners contain varying concentrations of sodium hydroxide. Dishwasher detergents contain phosphates. Hair relaxers contain sodium or calcium hydroxide or ammonium hydroxide. Lye is a generic term used to describe high concentrations of sodium hydroxide or potassium hydroxide used for cleaning. Bleach is an alkali made of various chemical compounds and thus the pH varies by brand. Mister Plumber and Lysol toilet cleaners are acids. The majority of swimming pool cleaners are acids.
Inflammatory Response
The pathophysiology differs for ingestion of acid (coagulation necrosis) and alkali (liquefaction necrosis).
There is a perception that acid injury is less severe. Acids cause instant burning when ingested, resulting in a lower quantity consumed compared with alkali substances. Esophageal mucosal exposure to acid also results in formation of a superficial and protective eschar; however, ingestion of a strong acid can still cause a transmural injury to the esophagus. One study reported more significant injuries and higher mortality with acid ingestion compared with alkali ingestion. Acids are also thought to cause more significant injury to the stomach compared with the esophagus because of gastric retention of the substance due to pyloric spasm. However, a study focusing only on acidic ingestions reported a significantly higher grade of injury to the esophagus compared with the stomach.
The pathophysiology resulting from an alkali ingestion is more complex than for acid ingestion. Animal studies in the 1950s and 1960s demonstrated that corrosive substances damage the esophagus through ischemia, thrombosis, and inflammation. Johnson studied 85 dogs after consumption of 10% sodium hydroxide and described three phases of injury based on the gross and histologic examination of the esophagus from the sacrificed dogs. Haller et al. exposed cats to 10% sodium hydroxide for 1 minute, documenting similar findings to Johnson. These phases of injury are described in Table 47.1 .
TABLE 47.1
Histopathologic Phases of Caustic Injury to the Esophagus
Data from Haller JA Jr, Andrews HG, White JJ, Tamer MA, Cleveland WW. Pathophysiology and management of acute corrosive burns of the esophagus: results of treatment in 285 children. J Pediatr Surg . 1971;6(5):578–584; and Johnson EE. A study of corrosive esophagitis. Laryngoscope. 1963;73:1651–1696.
| Phase | Timing | Histopathologic Findings |
|---|---|---|
| Acute necrotic | <72 h |
|
| Ulcerative granular | 3 days to 3 weeks |
|
| Cicatrization and stricturing | 3 weeks to 3 months |
|
The first phase, the acute necrotic phase, occurs during the first 72 hours of ingestion, featuring four findings: (1) death of cells through coagulation of proteins, (2) an intense inflammatory response, (3) thrombosis of vessels, and (4) infiltration of the esophagus wall and underlying tissues with hemorrhage and bacteria. Johnson's studies showed that the submucosal layer and occasionally the muscularis were liquefied through a process called liquefaction necrosis. Complete liquefaction of the esophagus and trachea and part of the lungs has been described with ingestion of a large quantity of alkaline substances. Johnson described an intense but variable inflammatory response. Interestingly, four decades later using a mouse model and intravital microscopy, Osman et al. reported minimal inflammatory cells in the early phases of the injury. However, the same study did confirm thrombosis of the microcirculation. Thrombosis inhibits blood flow contributing to necrosis in the compromised tissue and delays arrival of inflammatory cells. This concept is supported by a later study of esophageal injury in rats that showed increased free radicals after 24 hours and persisting for 72 hours. The fourth finding results from the first: with necrosis of the protective layers of the esophagus, the muscularis propria is exposed to the contents of the esophagus, allowing bacterial invasion into the esophageal wall and surrounding mediastinal tissues. Clinically, the majority of patients will present to medical attention in the first phase of the injury.
The second phase, the ulcerative/granular phase, spans 3 days to 3 weeks after ingestion. This phase begins with sloughing of the necrotic tissue produced in the first phase, resulting in ulcers throughout the damaged esophagus. Infiltration of fibroblasts and development of new blood vessels result in fresh granulation tissue and early collagen, producing very weak connective tissue. Clinically, it is at this time the healing esophagus is weakest and subject to hemorrhage or perforation.
The third phase, cicatrization and stricturing phase, occurs between 3 weeks to 3 months after ingestion. Acute inflammatory cells are no longer present, replaced by dense fibrotic bands throughout the muscularis and submucosa. There is also reepithelialization of the mucosa with squamous cells. Clinically, it is during this third phase of the injury that deposition of dense connective tissue leads to esophageal narrowing due to annular fibrosis (stricture).
The depth of injury is dependent on the pH of the substance and the duration of mucosal exposure. These factors ultimately determine the severity of the injury in all three phases, the patient's associated clinical condition, and risk of subsequent stricture formation. Therefore the degree of injury is an important predictor of long-term outcome, and attempts to improve outcomes have focused on interventions based on understanding the underlying pathophysiology. Despite the studies cited here describing separate pathophysiology for alkali and acid injuries, the initial clinical management of a patient with ingestion of a strong acid or alkali substance is similar.
Clinical Features
It is important to obtain an accurate history and carefully assess the patient with special attention to their clinical stability. A combination of history, physical findings, laboratory studies, imaging, and endoscopic exams will be used to make management decisions for a patient with a caustic injury.
On history, it is important to characterize the substance ingested, including the name of the substance, texture (solid or liquid), quantity ingested, and the timing of the ingestion relative to time of presentation. In accidental ingestions the time passed since ingestion and quantity consumed are usually less than in intentional ingestions in the adult population. Patients must be questioned regarding dysphagia, odynophagia, refusal to drink, chest pain, vomiting, and epigastric pain. Dysphagia, odynophagia, refusal to drink in pediatric patients, and chest pain may represent esophageal injury. Vomiting is concerning for recurrent exposure of the esophagus to the caustic substance and risk of aspiration. Epigastric pain is concerning for gastric injury or perforation.
On physical exam, special attention to the patient's vital signs is essential to allow for early aggressive interventions that can be lifesaving. The mouth should be inspected for signs of mucosal injury. Drooling, hoarseness, and stridor must also be noted. The presence of oral mucosal injury and drooling has been reported to increase the probability of significant esophageal injury. Hoarseness and stridor can indicate injury to the larynx and airways. The abdomen should be examined because tenderness can represent a gastric injury or even perforation.
It has been recognized that correlating signs and symptoms of patients presenting with caustic ingestion can be difficult to correlate with severity of injury. A detailed retrospective review of pediatric patients concluded no single or group of signs or symptoms can be used to determine the severity of the esophageal injury. However, they did report that all patients with grade 2 or 3 injury on endoscopic exam ( Table 47.2 ) were symptomatic. Another smaller retrospective review found that all patients with endoscopically proven injury were symptomatic, whereas all asymptomatic patients did not have endoscopic evidence of injury. A more recent study assessed prospectively a series of 148 patients (majority adults) to create a model to predict severity of esophageal injury. Drooling, buccal mucosal burn, and elevated white blood cell count were useful parameters to predict significant esophageal injury. Given these contradicting results, no single finding should be used to rule out a significant injury and all patients should undergo endoscopy for objective assessment.
TABLE 47.2
Endoscopic Grading of Caustic Injuries
From Zargar SA, Kochhar R, Mehta S, Mehta SK The role of fiberoptic endoscopy in the management of corrosive ingestion and modified endoscopic classification of burns. Gastrointest Endosc. 1991;37(2):165–169.
| Grade | Endoscopic Finding |
|---|---|
| Grade 0 | Normal |
| Grade 1 | Superficial mucosal edema and erythema |
| Grade 2 | Mucosal and submucosal ulcerations |
| Grade 2a | Superficial ulcerations, erosions, exudates |
| Grade 2b | Deep discrete or circumferential ulcerations |
| Grade 3 | Transmural ulcerations with necrosis |
| Grade 3a | Focal necrosis |
| Grade 3b | Extensive necrosis |
| Grade 4 | Perforations |
The three clinical phases may be described as follows: acute, intermediate, and chronic. In the acute phase the priority and purpose of the clinical assessment is to guide resuscitation, assess for necrosis or perforation of the esophagus or stomach, and determine disposition. In the intermediate phase, repeated assessment is done to assess for necrosis or delayed perforation. The chronic phase requires attention to three common consequences of caustic injuries, which include stricture formation, dysmotility, and development of cancer.
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