Acute corrosive injuries can result from the ingestion of acids, bases, oxidants, heavy metal salts, and other chemical substances, leading to varying degrees of damage to the upper gastrointestinal tract [1]. Early endoscopic examination within 48 h is reportedly useful for assessing the severity of mucosal injury and predicting prognosis [2]. The classification system proposed by Zargar et al. [3] in 1991 is used as an indicator of the severity and prognosis of corrosive injuries. The extent of injury depends on the type, concentration, duration of contact, and quantity of the ingested substance. Acids with a pH of <2 and alkalis with a pH of >12 generally cause the most extensive injury [2]. In particular, alkalis induce tissue damage through the saponification of fats, resulting in liquefaction necrosis, allowing deeper penetration and extending tissue destruction [2]. Sodium hypochlorite (chlorine bleach), a household cleaner, is one of the most commonly ingested alkaline caustics [2]. Here, a case of the natural progression of severe corrosive esophageal injury caused by chlorine bleach ingestion has been reported.

A 66-year-old female with no medical history presented to the emergency room approximately 2 h after ingesting 200 mL of chlorine bleach, without experiencing vomiting. Laboratory tests, endoscopic evaluation, and computed tomography (CT) scans were planned. Initial CT scan revealed diffuse swelling of the pharynx, larynx, and cervical esophagus (Fig. 1A-C) with narrowing of the airway at the glottic level (Fig. 1D); however, no evidence of esophageal or gastric perforation was observed. Endoscopy, performed 6 h after presentation, showed diffuse injury and necrosis of the esophageal and gastric walls (Fig. 2). Based on these findings, the patient’s corrosive injury was classified as severe, consistent with Zargar grade 3b, and a poor prognosis was anticipated. The treatment plan included prolonged fasting, total parenteral nutrition, and prophylactic antibiotic treatment until stabilization of vital signs and inflammatory markers. Although the patient remained afebrile with stable vital signs, empirical antibiotics (ceftriaxone) were administered based on the emergency physician’s assessment. During hospitalization, follow-up chest radiography revealed pneumonic infiltration, and antibiotic treatment was continued for 2 weeks until resolution of the pneumonia. Jejunostomy was performed after approximately 1 month of conservative treatment.

The patient underwent multiple hospitalizations and discharges while awaiting complete healing of the esophagus and stomach. Follow-up endoscopies were performed 2 months after the injury (to evaluate the feasibility of resuming an oral diet, following confirmation of mucosal injury improvement on a CT scan) (Fig. 3A) and 4 months after the injury (at the request of the thoracic surgeon before the reconstruction surgery) (Fig. 3B). Although the esophageal wall had healed, severe stenosis prevented oral intake, as passage of the endoscope was blocked at the proximal esophagus (approximately 20 cm from the incisor), and esophagography could not be performed due to failure in guidewire passage. Consequently, surgical treatment, including esophagectomy and esophagocolojejunostomy, was planned and performed approximately 7 months after the injury. Intraoperative endoscopy revealed chronic ulcerative changes in the stomach, accompanied by a severe pyloric stricture (Fig. 4A), necessitating a total gastrectomy. The surgical specimen showed an ulcer scar with severe esophageal stricture and chronic transmural inflammation (Fig. 4B).

Since the initial surgery, the patient underwent multiple surgical interventions due to complications associated with infection and dehiscence. These included wound exploration for infection 7 days after the initial surgery, coloesophagogastrostomy takedown for anastomotic dehiscence 10 days after the initial surgery, and four times of wound explorations with the application of a surgical vacuum for wound infection and abscess formation (over a period ranging from 2 weeks to 5 months after the initial surgery). Additionally, a reconstruction of the coloesophagogastrostomy was performed 8 months after the initial surgery. After the second reconstruction surgery, several esophageal bougienations were attempted to address anastomotic stenosis; however, these interventions were unsuccessful. The patient has continued to receive oral and jejunostomy tube feeding for approximately 2.5 years since the injury.

Caustic ingestion is a global public health concern, with cleaning substances being classified as caustic agents. In some Asian countries, it has been reported that women often use caustic substances in suicide attempts. Additionally, accidental ingestion is common among children [2]. Survivors of acute caustic ingestion might experience delayed and long-term complications, which occur in survivors of acute episodes, including esophageal strictures, which develop over weeks to months and are associated with chronic pain and malnutrition.

Endoscopy should be performed within the first 24–48 h after ingestion if the patient is hemodynamically stable, as delayed intervention increases the risk of perforation due to wound softening over time [2]. Classifying the extent of injury using the standardized terminology described by Zargar et al. [3] is useful for assessing severity. For patients who are unstable or at high risk for endoscopic evaluation, contrast-enhanced CT serves as an alternative diagnostic tool as it is rapid, noninvasive, and capable of detecting early signs of gastrointestinal perforation [4]. After initial assessment, 70%–90% of patients can be managed non-surgically [5]. However, patients with severe injuries (endoscopy grade 2b–3b) require close monitoring due to the risk of perforation and strictures formation in cases of extensive necrosis; perforation is often fatal [6]. Standard gastrointestinal decontamination methods, such as activated charcoal ingestion, dilution, or neutralization, are contraindicated in corrosive injury cases, as they can exacerbate the injury by causing gastric overdistension or heat damage [2].

Late sequelae of corrosive injury include hemorrhage, fistula formation (such as tracheobronchial and aortoenteric fistulas), pulmonary complications, strictures, and malignancy [7]. Among these, stricture formation is the most common, disabling, and resource-intensive complication [7,8]. Strictures typically develop within 2 months of ingestion, although the time frame varies from 3 weeks to 1 year [7]. The optimal timing for resuming oral intake following corrosive ingestion remains unclear, and the relationship between oral re-alimentation and the risk of perforation or delayed sequelae has not been established [8]. The use of glucocorticoids to prevent stenosis is generally not recommended [9], although some studies have reported that patients with grade 2b injuries, which carry a high risk of stricture and a low risk of perforation, might benefit from short-term glucocorticoid therapy [10]. Esophageal stenting for stricture prevention has been attempted; however, its effectiveness remains uncertain, and it is not widely adopted [7].

In cases of stricture formation, dilatation can be performed using various types of dilators, either with a combination of endoscopy and fluoroscopy or endoscopy alone. However, caustic strictures are often complex and difficult to dilate [11]. Bougie dilators are suitable for short and straight strictures, while pneumatic dilators are appropriate for tortuous, angulated, or long strictures [12]. For refractory strictures, which cannot be dilated to 14 mm over five sessions spaced at biweekly intervals [13], options such as electrocision, intralesional steroid injection, mitomycin-C injection, or esophageal stenting might be considered, though evidence supporting their efficacy is limited [12]. Esophageal dilatation for caustic-induced strictures has shown a lower success rate compared to esophageal strictures of other etiologies [14], with higher endoscopic grades and ingestion of strong acids or alkalis being significant risk factors [12]. Esophageal reconstruction is necessary to restore digestive continuity in patients who have undergone emergency esophagectomy or have strictures that are ineligible for or have failed dilation [8]. However, complications after esophageal reconstruction are common and often severe; for example, late morbidity occurs in approximately half of the patients after colon interposition, and stenosis of the cervical anastomosis is common (4%–59%) and often complicated by leakage [15]. When determining the appropriate treatment for caustic-induced esophageal strictures, factors such as the location and length of the stricture, its morphology (including tortuosity or angulation), associated complications (such as concealed perforation or diverticulum), and the coexistence of gastric stricture should be considered [12]. Surgical treatment should be considered for severe strictures with these accompanying conditions, but in less severe cases, endoscopic treatment might be prioritized due to the high morbidity associated with surgery.

In summary, severe corrosive injuries caused by alkaline substances showed a poor clinical prognosis, as anticipated based on initial endoscopic findings. From these results, it can be concluded that early endoscopy is useful for assessing the severity and predicting the prognosis of corrosive injury, and that caution is required in the diagnosis and treatment of this condition. Further research is needed to explore treatments that can alleviate the long-term sequelae of corrosive gastrointestinal injuries.