Caustic Ingestion and Foreign Bodies

Epidemiology

According to the most recent Annual Report from the American Association of Poison Control Centers there were 2,159,032 human exposures in the year 2016. Of these exposures, 46% of them occurred in children 5 years of age and under. While it is difficult to extrapolate how many of these exposures were true caustic ingestions, 12.8% of children less than 5 years of age sought medical attention for their exposure. The most frequently ingested substances in children under 5 years of age in the United States were cosmetics/personal care products (13.3%), household cleaning substances (11.1%), and analgesics (9.2%). Ingestion was more commonly reported in male children younger than 13 years of age, while a female predominance was found in teens greater than 13 years. In children under 12 years of age, most exposures are unintentional. In contrast, most exposures in teenagers older than 13 years occur with the intent of self-harm or suicide.

The unintentional ingestion of corrosive substances has been declining in Western countries with increased education and safety measures such as warning labels and child safety caps. In stark contrast, caustic ingestion remains a major problem in developing countries where it remains a significant cause of morbidity and mortality in children. The method by which known caustic agents are stored and handled may have a significant impact on the accessibility of these products by young children. Countries that have established national prevention programs targeted at parents of young children have experienced a decline in accidental exposures and esophageal injuries. For example, the Poison Prevention Packaging Act of 1970 stated that caustic agents should have “special packaging” that is designed to be difficult for children under 5 years of age to open, and that the amount of the caustic agent should be limited to 10% of the product. In developing countries where prevention campaigns are not as widespread, children continue to have higher rates of caustic ingestion and may come to medical attention later with more severe injuries. One of the mechanisms that contributes to increased risk of caustic exposure in developing countries is the use of secondary containers, which are typically unlabeled and sometimes unsecured containers that are used to store household products or are even sold in open marketplaces.

Alkaline agents account for most caustic ingestions in the Western world. Table 18.1 lists many of the common alkaline and acidic household agents that are implicated in caustic ingestions. In a published series evaluating 473 pediatric caustic ingestions, the most common agents consumed were household bleach (36.6% of patients) and oven cleaner (23% of patients). Other common agents include dishwashing liquids, drain cleaners, and cosmetic products.

Household bleach usually contains sodium hypochlorite at a concentration between 5% and 10% with a pH ranging from 10.8 to 11.4 when manufactured in the United States. Therefore, unintentional ingestion typically produces minimal injury to the gastrointestinal (GI) tract; however, ingestion of large quantities of bleach has been associated with serious damage. ^, Sodium hydroxide (NaOH) or lye is an alkaline substance found in drain and oven cleaners as well as dishwasher detergent. Lye can produce severe injury to the GI tract such as perforation and strictures ( Fig. 18.1 ). Hair relaxer is another common household liquid; the ingestion of hair relaxers, which are alkaline products, does not typically result in significant injury, although pain and minor erythema in the mouth may occur. ^,

Acid ingestion accounts for less than 5% of all caustic ingestions in the United States, but is much more common in countries like India and Surinam where hydrochloric acid, glacial acetic acid, and sulfuric acid are more easily accessible. ^{, ,} In the United States, acids are commonly found in toilet bowel cleaners (sulfuric, hydrochloric), anti-rust compounds (hydrochloric, oxalic, hydrofluoric), battery fluids (sulfuric), and swimming pool cleaners (hydrochloric).

Pathophysiology

The severity of injury to the GI tract is dependent on the agent’s pH, concentration, tissue contact time, ingested form of the agent (liquid, gel, or solid), and amount ingested. Acidic suspensions with a pH of less than 2 and alkaline suspensions with a pH greater than 12 are considered highly caustic agents. The solution concentration is a significant predictor of esophageal injury. In a rat model investigating the concentration and tissue contact time of lye or NaOH on a rat esophagus, concentrations of 1.83% were sufficient to cause epithelial necrosis, concentrations of 7.33% induced submucosal damage, and concentrations of 14.33% resulted in muscle and adventitial damage. In this same study, 10 minutes of contact time was sufficient to stimulate necrosis even at the lowest concentration of 1.83%. At higher concentrations, a 22.5% NaOH solution in contact with the esophagus for 10 seconds or 30% NaOH solution for 1 second can produce a full thickness injury.

The physical state of the ingested agent also plays a role in the type of tissue injury. Solid agents are more likely to affect the supraglottic and oropharyngeal areas. Powdered or crystallized particles are more likely to affect the airway, pharynx, and upper esophagus. Crystals tend to adhere to mucosa and thus may lead to more injury due to increased contact time. Liquid agents have increased surface area exposure leading to more circumferential injury. In addition, liquids can pass through the esophagus reaching the stomach and small bowel leading to more extensive injury. In animal studies of liquid alkaline ingestion, reflux of the agent back into the esophagus was found to occur and lead to more extensive damage of the esophagus and stomach prior to passage into the small bowel. The amount of caustic agent ingested also affects injury. Alkaline agents are tasteless which usually results in larger quantities ingested. In contrast, the unpleasant taste of acids tends to limit the amount of acid ingested in cases of unintentional exposure.

Acids produce tissue injury via coagulation necrosis. The formation of eschar has been hypothesized to limit further acid penetration and lessen depth of injury. The development of eschar may also lead to preferential damage of the stomach. These hypotheses have been questioned with recent reports of serious esophageal injury due to acid ingestion. ^, In addition, the low viscosity and specific gravity of acids results in rapid transit to the stomach, and thus gastric injury (especially to the prepyloric area) is more common than esophageal injury. On the other hand, alkaline agents bind with tissue proteins producing liquefactive necrosis and saponification, resulting in increased depth of tissue injury. Alkali ingestion produces thrombosis in blood vessels, impeding blood flow to already damaged tissue. ^, Free radical damage with consequent lipid peroxidation may also contribute to esophageal damage.

Esophageal injury begins within minutes of caustic ingestion and persists for hours afterwards. Initial tissue injury begins with eosinophilic necrosis with accompanied swelling and hemorrhagic congestion. Four to 7 days after ingestion, there is marked mucosal sloughing and ulceration of the esophagus, which leads to bacterial infiltration. Fibroblasts appear at injury sites around day 4 or 5, and this window of time is characterized by further inflammation and the initial appearance of granulation tissue. The ulcerated tissue develops a fibrinous layer. Deep ulceration into the muscle layer may lead to perforation around this time. By day 10 postingestion, esophageal repair begins. Epithelialization of denuded tissue begins 1 month after initial exposure. ^, The tensile strength of the injured tissue is low during the first 3 weeks after injury. Starting week 3, scar retraction occurs. The end result of this phase, which lasts for several months, is stricture formation and shortening of the involved segment of tissue. ^,

Clinical Presentation

Common features on presentation after caustic ingestion include drooling, vomiting, refusal of intake by mouth, and abdominal pain. The patient may also experience visible mouth lesions such as erythema or ulceration of the lips and oral mucosa. Hoarseness and stridor suggest upper airway and or epiglottic involvement; dysphagia and odynophagia point toward esophageal injury while epigastric pain and bleeding are suggestive of stomach involvement. ^,

The relationship between symptoms and severity of injury is uncertain. There have been conflicting studies in the literature correlating symptoms with extent of GI injury. Crain et al. demonstrated that the presence of two or more signs or symptoms, including vomiting, drooling, or stridor, predicted serious esophageal injury. Nuutinen et al. suggested that the combination of drooling and dysphagia correlated well with esophageal injury. A subsequent study by Chen et al. supported that children with three or more signs and symptoms tended to have severe esophageal injury ( P = .027) and esophageal stricture ( P = .05). These studies have been refuted by several others that have shown that the presence or absence of symptoms does not predict the likelihood or extent of esophageal or GI injury. In a review of 378 pediatric ingestions by Gaudreault et al., 12% of asymptomatic children had severe esophageal burns, whereas 82% of symptomatic children had no esophageal burns. Dogan et al. illustrated that the presence or absence of oral lesions is a poor indicator of esophageal injury. In this study of 473 pediatric caustic ingestions primarily of alkaline agents, 61% (240 out of 389) of the patients without oral cavity burns had esophageal lesions found at endoscopy. In that series 80% of patients had an esophageal injury and 17% had gastric injury. Additional studies have demonstrated the discordance between oral and esophageal injury. ^{, ,}

Clinical Assessment

The clinical assessment of a patient after a caustic ingestion involves a thorough physical examination and careful history. The physical exam should include an airway assessment and evaluating the mouth for oral lesions. The history should involve obtaining the identity of the ingested material, its pH, estimated volume, and approximate timing of the ingestion. It is also important to determine if the ingestion was accidental or intentional, since suicide attempts are more likely to involve larger volumes compared to patients who ingested the agent accidentally.

Patients with caustic ingestion are at risk for hemolysis, disseminated intravascular coagulation, renal failure, and liver failure. Laboratory studies may be useful in assessing for these risks and guiding patient management but are not useful in predicting morbidity or mortality. There have been attempts to correlate laboratory values with ingestion of severity; Rigo et al. found that a white blood cell count greater than 20,000 cells/mm ³ was a predictor of mortality, while a later study refuted this and found no correlation between C-reactive protein or white blood cell count with esophageal injury, morbidity, or mortality. ^,

A plain chest radiograph may reveal air in the mediastinum suggesting esophageal perforation, as well as free air under the diaphragm indicating possible gastric perforation. An upper GI contrast study is generally not indicated in the acute setting. If it is deemed necessary to do, then a water-soluble contrast agent is preferred over barium due to potential for extravasation of contrast out of the lumen if perforation has occurred. A computed tomography (CT) scan can be done in order to obtain detailed evaluation of the transmural damage of the esophageal and gastric walls as well as the extent of necrosis. It has been suggested that CT may be an equal or superior alternative to endoscopy to predict extent of injury and esophageal stricture. ^,

Role of Endoscopy

Esophagogastroduodenoscopy (EGD) is a vital tool in the initial evaluation of patients who have had a caustic ingestion. The recommended timing of endoscopy is 12 to 48 hours after caustic ingestion, although it has been reported to be safe to perform endoscopy up until 96 hours postingestion. ^{, ,} Endoscopy is generally avoided 5 to 15 days after caustic ingestion, since during this time period the esophagus is at its weakest integrity with the highest risk of perforation. EGD should be performed with anesthesia present to provide adequate airway protection via orotracheal or nasotracheal intubation. Once the degree of injury is known, treatment and prognosis can be determined. In the past, endoscopists usually stopped at the first evidence of severe injury, but some centers now consider it appropriate to identify the full extent of injury, at least to the level of the duodenum. Air insufflation should be minimized to decrease the risk of a perforation through a deeply ulcerated area. The procedure should be terminated if a perforation is suspected or encountered.

The object of endoscopy is to categorize the extent and grade of injury per Zargar classification ( Table 18.2 ). Grade 0 and 1 lesions usually do not develop delayed esophageal complication, such as strictures or gastric outlet obstruction. As lesion grade severity increases, the likelihood of stricture formation also increases. The incidence of stricture may be as high as 71% for grade 2b burns and anywhere from 75% to 100% for grade 3 caustic burns. ^, Furthermore, the degree of esophageal injury at endoscopy is an accurate predictor of systemic complications and death, with each increased injury grade correlated with a ninefold increase in morbidity and mortality. In a large study of 473 patients who underwent endoscopy after caustic ingestion, 379 patients sustained esophageal lesions (80%), whereas 81 children sustained gastric damage (17%). The majority of children were diagnosed with mild lesions, Zargar stage 1 to 2a.

Acute Management

The most important initial factors in management of caustic ingestion include determining the patient’s risk for respiratory compromise or impending shock. Initial management includes an airway assessment, with possible endotracheal, nasotracheal, or surgical airway performed when necessary. The presence of supraglottic or epiglottic burns with erythema and edema may be a sign of airway obstruction and is an indication for early endotracheal intubation. Fluid resuscitation should be started in patients who demonstrate hemodynamic instability.

A conservative observational approach can be taken after ingestion of certain lower risk products, in patients who are asymptomatic, and in patients without oral lesions. ^, It is important that patients discharged after observation have follow-up to ensure no long-term complications develop and to provide preventive teaching. Symptomatic patients and/or patients with oral lesions should be admitted to the hospital, made nil per os (NPO), and started on intravenous fluids.

If severe esophageal and gastric necrosis is found, antibiotics should be started and emergency esophagogastrectomy may be required to avoid extension of corrosion to nearby organs. The presence of shock, fever, or prostration indicates profound tissue damage and requires immediate surgical consultation. Gastric perforation is almost invariably fatal due to toxic and septic effects of acute hemorrhagic pancreatitis, multiple bowel perforations, and peritonitis. Urgent and aggressive surgical debridement of all necrotic tissue in the chest and abdomen has been shown to significantly improve survival. Endoscopy in the setting of a suspected perforation should only be performed in concert with the surgeon and only if required for planning the surgical approach.

Induced vomiting is contraindicated after caustic ingestion to avoid re-exposing the esophagus and airway to the caustic material. Charcoal administration is not recommended since it does not absorb caustic agents. Consuming either a weak acid or base to induce pH neutralization has been shown effective in animal studies, ^, but there is a concern of potentially compounding injury by inducing an exothermic reaction. ^, There is no human data to support pH neutralization and it is currently not recommended. Consuming milk or water as dilution therapy has been suggested for patients with caustic agents; an animal model demonstrated that the consumption of milk and water following 50% sodium hydrochloride ingestion decreased esophageal injury. However, due to the risk of vomiting with dilution therapy and the lack of human data supporting the practice there is no current recommendation to support dilution therapy in patients.

In order to minimize the reflux of gastric contents back into the esophagus and minimize esophageal re-injury, proton-pump inhibitors and H-2 blockers are generally recommended to be initiated 24 hours after caustic ingestion. This recommendation is based on one study that demonstrated increased gastric injury when H-2 blockers were administered immediately following corrosive ingestion. The study’s hypothesis was that decreased acid led to decreased neutralization of the caustic agent, leading to more injury. There has been no human data proving or disproving this theory. Once acid blocking therapy is instituted, it is generally recommended to continue treatment in order to reduce the risk of gastroesophageal reflux accelerating stricture formation.

Prevention of Strictures

A chronic long-term complication of caustic ingestions is stricture formation. The overall rate of stricture development after a caustic ingestion has been reported as anywhere between 26% and 55%. ^, The risk for stricture formation may be as high as 77% in patients with grade 2b burns and the risk may reach 100% in patients with grade 3 burns. ^, Stricture formation can occur as early as 3 weeks following ingestion and is confirmed in 80% of patients who develop stricture by 8 weeks.

Corticosteroids have been proposed as a treatment to reduce stricture formation. The rationale for using corticosteroids after caustic ingestion is attenuation of inflammation as well as promotion of granulation and fibrous tissue formation. Anderson et al. in a prospective study showed no benefit from systemic steroid administration in children post–caustic ingestion and that the development of strictures was related only to the severity of injury. Conversely, a study by Boukthir et al. found that high doses of methylprednisolone were beneficial in patients with grade 2b esophageal lesions, with a decreased incidence of stricture formation and decreased need for bougienage after stricture formation. An early meta-analysis by Howell et al. showed a benefit to steroids in stricture prevention. However, two more recent meta-analyses have shown corticosteroids are of no benefit and do not significantly decrease the incidence of strictures after corrosive ingestion and therefore recommend the abandonment of this practice. ^, Corticosteroids remain a controversial treatment for stricture prevention but in general are no longer recommended.

The use of antibiotics is recommended in the setting of caustic ingestion with associated signs of infection, peritonitis, or mediastinitis. Antibiotics are also warranted in patients with full-thickness injury since they are at a high risk for perforation as a result of the loss of the mucosal and muscular barriers. The role of antibiotics in stricture prevention is less clear. In theory, antibiotics reduce the bacterial count in the wound thus possibly decreasing inflammation and reducing scar tissue formation. Currently there are no sufficient human data to support the global use of antibiotics in patients with caustic ingestion. Patients treated with steroids should also be treated with antibiotics since steroids may mask signs of perforation and infection, but prophylactic antibiotics to prevent strictures, in the absence of steroid therapy, has not been advocated.

Stricture Management

First-line treatment for strictures is dilation. Balloon or mechanical (bougienage) dilators can both be used to dilate. The most common type of mechanical dilator used is the Savary-Gilliard dilator, which is passed over a guidewire and delivers both radial and longitudinal force to the stricture. Balloons deliver equal radial force simultaneously across the entire length of the stricture. Balloon dilation can be performed through the endoscope or over a guidewire. There is no clear difference in effectiveness and safety between balloon and mechanical dilation. The method of choice depends on operator experience and comfort with the equipment.

Timely evaluation and dilation of strictures are crucial to obtaining a good outcome. The late onset of treatment has been shown to be a strong predictor of future esophageal replacement. Dilation should be avoided from 7 to 21 days postingestion to minimize risk of perforation. Although early prophylactic dilation with bougienage has been reported to be safe and effective in this period, it is generally recommended to start dilations after 21 days postingestion. The interval between dilations varies from weekly to every 2 to 3 weeks. The total number of dilations required to keep lumen patency is highly variable. Intralesional corticosteroid (triamcinolone acetonide) injections into the stricture site have been shown to reduce the total number of dilations needed in small case studies. ^, However, intralesional steroid injections can be difficult to place and are less effective in long strictures. There is no standard dose or frequency of intralesional steroid used to treat strictures.

Mitomycin C is an antineoplastic agent that disrupts base pairing of DNA molecules. This agent inhibits fibroblast proliferation and induces apoptosis at higher doses. It has been proposed as an adjunct treatment to manage caustic strictures. Mitomycin C is usually placed topically ( Fig. 18.2 ); however, there are reports of injection of mitomycin C. The dose of mitomycin C is also variable, ranging from 0.004 mg/mL to 1 mg/mL. A systematic review of the literature suggested there might be promising long-term benefits of mitomycin C, but prospective studies are needed to determine the most effective concentration, duration, and frequency of application. There is a hypothetical risk of secondary malignancy with mitomycin C, which must be taken into account and discussed with the patient prior to use.

The use of self-expanding plastic stents (SEPS) and fully covered self-expanding metal stents (FCSEMS) have been reported as alternative or adjunctive means of preventing stricture formation by providing continuous dilation forces to the esophagus for prolonged periods of time. Broto et al. showed a 50% success rate with SEPS, and Zhang et al. reported a 75% success rate using FCSEMS. Both of these studies are limited by their small sample size and retrospective design. ^, The use of “dynamic stents,” which are custom silicon stents attached to a nasogastric tube, has been proposed to be a useful treatment for caustic strictures. In several published series, the reported healing of the strictures with intraluminal stents ranged from 69% to 96%. These authors hypothesize that the dynamic effect of food passage through the stent on the esophageal wall allows for the long-term improvement of esophageal patency.

Biodegradable stents (poly-L-lactide or polydioxanone) are a newer technology that are under evaluation for benign strictures. Currently available biodegradable stents remain intact and apply declining radial forces over approximately 8 weeks, after which the stents begin to degrade. ^, The largest multicenter, randomized, controlled trial to date compared the use of a polydioxanone biodegradable stent (32 patients) against standard dilation therapy (34 patients) in adults with benign refractory stricture. Patients randomized to receive the biodegradable stent had significantly longer time to first dilation and significantly fewer repeat dilations at 3 months, but there was no difference in the number of dilations by 6 months. Importantly, the number of total endoscopies was similar between the groups even at 3 months, which the authors attributed to the stent group requiring diagnostic endoscopy for new symptoms of retrosternal pain, nausea, and vomiting that have been previously described in patients with both biodegradable and FCSEM stents. ^, One group has had some modest success with sequential biodegradable stent placement in reducing dysphagia. Timing of stent placement in these studies has been limited to late in the natural history of refractory stricture; it is unclear if earlier prophylactic stent placement in certain populations might limit fibrotic remodeling and progression to refractory stricture. Moreover, the overwhelming majority of patients in these studies had anastomotic stricture or peptic stricture, and the response of caustic stricture to this type of therapy is less studied.

The evidence describing use of biodegradable stents in caustic ingestion is limited to small case series. One study of seven patients with caustic ingestion reported complete or partial benefit of biodegradable stent in three of seven patients. Another series of 13 patients found that while most patients experienced restenosis and recurrence of dysphagia by 3 months, the frequency of dilations at 3-year follow-up was reduced to once every 4 to 6 months. There was no control arm in this study to understand if the stent potentially had a beneficial effect on dilation frequency or if reduced dilation over time was part of the natural history of caustic stricture. A pediatric case series reported on four children (two of whom had caustic ingestion) found tissue hyperplasia requiring subsequent dilations or therapy with mitomycin C in three-quarters of cases, culminating in complete esophageal stenosis in one patient. The reported stent migration rate is approximately 10%, and with stent degradation there is also a significant hyperplastic tissue response. Biodegradable stents along with the other above-mentioned stents show promise but still require further investigation before they can go into more widespread use.

Strictures are common after caustic ingestion, and repeated dilations may be required over a period of years to maintain adequate esophageal diameter. Symptoms that indicate the need for stricture dilation include odynophagia, dysphagia, or decreased oral intake with weight loss. Strictures may require multiple dilations. Kukkady et al. described a case series of 10 patients with known esophageal stricture after caustic injuries that were followed over time; they reported that a total of 424 dilations were performed in these patients over the course of 9 months to 4 years, with esophageal perforation occurring in two patients. In developing countries, children may present later with caustic injury and esophageal strictures and consequently experience the development of more severe fibrotic esophageal stenotic lesions. Esophageal perforation rates at the time of endoscopy in these regions have been reported to be as high as 18%. Other severe complications, such as mediastinitis, pneumothorax, peritoneal soiling, or brain abscess, have been reported at the time of stricture dilation. ^,

In cases where dilation fails to produce an adequate lumen size to eliminate or significantly reduce dysphagia symptoms, surgery may be necessary. Surgical techniques performed include partial esophagectomy, local resection of the stricture, and esophageal replacement. Types of esophageal replacement include gastric pull-up, gastric tube, colon interposition, and jejunal interposition. The most common operations are gastric pull-up and colon interposition. In a study of 173 patients with gastric pull-up over a 21-year period, Spitz et al. overall reported good functional outcome with no graft failures. Post-operative complications included 9 deaths (5.2%), anastomotic leaks in 21 patients (12%)—of which 11 resolved spontaneously—and anastomotic strictures requiring dilatation in 19.6%. Long-term morbidities in another study included significant gastroesophageal reflux and delayed gastric emptying.

Colon interposition is a common esophageal replacement surgery. Accepted disadvantages with this approach include the need for three anastomoses, increased risk of anastomotic leak, and strictures at the proximal esophagocolic anastomosis due to poor vascularity. These complications have been outlined by Hamza et al. in their report of their 30-year experience with 775 patients with colonic interposition, mainly in patients with caustic strictures. Their reported complications included 10% with cervical leaks, 5% with proximal strictures, 2% with postoperative obstruction, and 1% mortality. Other studies have reported a cervical leak rate ranging from 30% to 60%. ^, In addition, there are long-term complications associated with colonic interpositions including redundancy, tortuosity, and dilation of the colonic conduit in 3% to 12% of patients. ^, These long-term complications can lead to dysphagia, early satiety, respiratory difficulties, and gastroesophageal reflux. The native esophagus can either be left in situ and bypassed or removed. It has been shown that resection of the affected esophagus can be performed without a substantial increase in morbidity and mortality compared to bypass. Given the 13% incidence of esophageal cancer after bypass, the risk of infected esophageal mucocele in 50% of the patients after 5 years, and the impossibility of endoscopic follow-up for cancer in the bypassed esophagus, the preferred option for children is esophageal resection. ^,

Dysmotility

Esophageal and gastric dysmotility can occur when the lower third of the esophagus is involved in the burn. Depending on the depth of the scar, the myenteric plexus may be damaged and the normal syncytium of smooth muscle cells may be interrupted. Dysmotility also occurs due to auto-vagotomy secondary to nerve entrapment from scar formation. Impaired vagal cholinergic transmission may also affect gallbladder and gastric emptying, especially in patients with caustic ingestion that affects the lower esophagus. ^,

Cancer Risk

A late complication of caustic ingestion is esophageal cancer. Both adenocarcinoma and squamous cell carcinoma have been reported at rates of 1000 to 3000 times higher than the general population. ^, The incidence of esophageal carcinoma in patients with caustic ingestion ranges from 2% to 30% in the literature. The time to presentation has been reported anywhere from 10 to 30 years after the time of caustic ingestion. The most common location for carcinoma is at an area of stenosis. The American Society for Gastrointestinal Endoscopy suggests periodic surveillance endoscopy every 2 to 3 years in patients starting 10 to 20 years after the initial ingestion. However, there are no prospective studies supporting this practice and no studies evaluating the cost-effectiveness of endoscopic screening in this population. ^,

Gastric Injury

Gastric outlet obstruction can occur after both alkali and acid ingestion. Early surgery has been reported to decrease mortality and morbidity. ^, Endoscopic gastric dilation has been considered an alternative to surgery, but such dilations have a less than 50% success rate in preventing surgery. In the setting of severe gastric adhesions and significant duodenal injury, gastrojejunostomy should be considered as an alternative to gastric resection. Partial gastric resection has been proposed as prophylaxis against gastric malignancy. ^, However, reports of gastric carcinomas after acid ingestion are limited. ^, Regular follow-up and surveillance endoscopy is currently the more preferred approach.