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| REVIEW ARTICLE |
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| Year : 2018 | Volume
: 16
| Issue : 3 | Page : 92-95 |
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Corrosive injuries of the upper gastrointestinal tract: A review of management practices
Sasank Kalipatnapu, Jonathan Sadhu Reddipogu, Sam Varghese George, Vijay Abraham, Inian Samarasam
Department of Surgery, Christian Medical College, Vellore, Tamil Nadu, India
| Date of Web Publication | 9-Nov-2018 |
Correspondence Address:
Dr. Sasank Kalipatnapu
Department of Upper GI and Bariatric Surgery, Division of Surgery, Paul Brand Building, Christian Medical College, Vellore - 632 004, Tamil Nadu
India
 Source of Support: None, Conflict of Interest: None  | Check |
DOI: 10.4103/cmi.cmi_34_18
Corrosive injuries to the upper gastrointestinal tract can occur by either acid or alkali ingestion. They can lead to significant morbidity and mortality, thus necessitating a rapid assessment and appropriate management. This article aims to provide an overview of corrosive injuries and to provide a management plan for corrosive injuries. Keywords: Acid, alkali, corrosive, gastric, esophagus
How to cite this article:
Kalipatnapu S, Reddipogu JS, George SV, Abraham V, Samarasam I. Corrosive injuries of the upper gastrointestinal tract: A review of management practices. Curr Med Issues 2018;16:92-5 |
How to cite this URL:
Kalipatnapu S, Reddipogu JS, George SV, Abraham V, Samarasam I. Corrosive injuries of the upper gastrointestinal tract: A review of management practices. Curr Med Issues [serial online] 2018 [cited 2023 Jun 7];16:92-5. Available from: https://www.cmijournal.org/text.asp?2018/16/3/92/245040 |
| Introduction | |  |
Caustic injury to the esophagus is defined as injury to the esophagus either by acid or alkali ingestion. Alkali ingestion is more common in Western countries, while in India, acid is generally the more common agent.[1]
| Epidemiology | | |
The true prevalence of esophageal caustic injury is unknown and is likely to be underreported. This is a significant problem worldwide and up to 80% of injuries occur in children. These injuries are mostly accidental and the volume ingested is small. Adults usually ingest much higher volumes of agents with suicidal or psychotic intent. Hence, the damage caused is much more, proportional to the volume of agent ingested.[2]
There were a total of 195 patients admitted in the upper gastrointestinal (GI) unit of general surgery with corrosive ingestion from 2003 to 2016. The mean age of patients was 30.2 years (range: 14–69 years). There was a female predominance with 114 (58.46%) females and 81 (41.53%) males. Acid was the most common agent ingested by 168 patients (86.15%). The other agents included 8 (4.1%) alkalis and 18 (9.23%) corrosive agents of unknown composition. Most of the patients, 114 (58.46%) ingested with suicidal intent. Forty-three (22%) patients were accidental and three (1.5%) patients were due to homicides.
| Pathophysiology | | |
The mechanism of injury is different for acids and alkalis. Acids cause coagulative necrosis and lead to eschar formation which limits spread of the agent. Alkalis cause liquefactive necrosis and saponification of the tissues associated with thrombosis of the vessels. This leads to higher penetration of the alkali and proportionally higher tissue damage.[3]
From the practical standpoint, both acids and alkalis can penetrate and damage the esophagus and stomach. However, acids may have a higher incidence of systemic complications such as renal failure, liver dysfunction, disseminated intravascular coagulation, and hemolysis.
Injury caused by alkalis can be divided into three phases based on their tissue histopathological response [Table 1]. These phases of injury are not as distinctly demarcated in acid injury. Acids cause an immediate burning sensation in the mouth and this by itself limits damage, as the person stops ingesting it.
| Clinical Presentation | | |
The clinical features of the injury depend on the physical form of the substance ingested (solids vs. liquids), substance, quantity and concentration, and duration of tissue contact. The symptomatology can be broadly divided into two phases – acute phase and chronic phase.
Acute phase includes the initial post-injury period, wherein the patient can present with oral and substernal pain, hypersalivation, odynophagia, dysphagia, vomiting, and hematemesis. These symptoms gradually resolve as injuries heal and fibrosis develops.
Symptoms may be used as an indicator of organ damage. Hoarseness or stridor indicates laryngeal or epiglottic involvement. Odynophagia or dysphagia signifies esophageal damage, while esophageal perforation presents with back pain. Epigastric pain or bleeding may point toward the involvement of the stomach. Symptoms of stridor and drooling are 100% specific for esophageal damage. However, no single symptom has been found to be predictive of the severity of injury. There is a role for screening for gastric injury in patients with esophageal injury, as a coexistent injury has been seen in 20%–62.5% of patients. However, 70% of patients with oropharyngeal burns may not have any esophageal injuries.[2]
Patients in the chronic phase of corrosive injury present with dysphagia secondary to either esophageal strictures or disruption of the swallowing mechanism.
| Evaluation | | |
Clinical examination
A patient presenting with acute corrosive ingestion requires a thorough examination of the mouth, airway, chest, and abdomen keeping in mind the possibility of concurrent injuries over the lips, palate, pharynx, and larynx. Auscultation of the lungs helps in ruling out aspiration and concomitant lung damage. Abdominal examination should be focused to rule out signs of perforation and peritonitis.
Endoscopic examination
An upper GI endoscopy is the single most important prognostic factor in caustic injuries of the esophagus. The current recommendations state that it should be performed within 12–48 h after the ingestion of the agent. Gentle insufflation, adequate sedation, and caution are mandatory to avoid an iatrogenic perforation of the friable esophagus. Endoscopy is contraindicated if there is any suspicion of perforation or if the airway is not secure. Third-degree burns of the hypopharynx or burns involving the supraglottic area and epiglottis are relative contraindications.[2] Endoscopic classification of caustic injuries proposed by Zargar has been shown to have prognostic significance.[1] [Table 2].
Imaging
Imaging options include plain films and computed tomography (CT) scans. Plain X-rays are indicated to rule out pneumoperitoneum. CT scan of the thorax/abdomen should be done in a patient with clinical suspicion of injury and inconclusive plain films.
CT scans of the thorax can provide detailed evaluation of the injuries. A grading system based on the CT findings [Table 3] has been proposed for caustic lesions of the esophagus.[4]
Endoscopic ultrasound is an emerging option to assess wall damage. Destruction of the muscle layers on the ultrasound is a reliable sign of the future stricture formation. However, this modality requires further evaluation before it becomes a part of the mainstream evaluation for acute corrosive injuries.[2]
Correlation of laboratory investigations to the severity of injury is poor. Arterial pH <7.22 and a base excess <−12 are two factors found to have predictive value for severity. High white blood cell count (>20,000 cells/cu.mm), elevated serum C-reactive protein, age of the patient, and presence of an esophageal ulcer have been found to have an association with mortality.[2]
Management
There are three broad phases during the management of a corrosive injury – early, intermediate, and chronic phase. The early phase of management includes immediate assessment of the extent of injury, resuscitation, and to plan on further care of the acute episode. The intermediate phase is concerned with managing the acute episode in hospital and deals with the issues of sepsis, aspiration, and nutrition. The chronic phase deals with the management of long-term sequelae of corrosive ingestion including strictures and swallowing dysfunction.
| Early or Acute Phase of Injury | | |
The aim of management is to limit the extent of injury. Immediate management includes airway, breathing, and circulation. Airway management requires early involvement from the ENT surgeons for a nasopharyngolaryngoscopy. In case of airway edema or upper airway damage, there may be need for advanced airways such as tracheostomy. Neutralization of the ingested compound has not been proven to be of significance and is not recommended. Gastric lavage and induced emesis are contraindicated. While the role of proton-pump inhibitors and corticosteroids remains controversial, steroids are usually reserved for patients with symptoms involving the airway.
| Intermediate Phase of Management | | |
The primary aim of this phase is to tide over the sepsis and optimize the nutrition of the patient. Modalities used depend on the severity and extent of injury of the upper GI tract. The findings of an early upper GI endoscopy can decide the further course of management.
Patients without signs of injury on the initial examination do not require further treatment. Patients with Grade 1 injuries require observation for 48 h along with acid suppression. Both these patients can be restarted on oral diet once they can swallow saliva painlessly.
Patients with Grade 2 and 3 injuries require admission to the intensive care unit (ICU) and aggressive resuscitation. Standard of care includes keeping the patient nil per oral with intravenous (IV) fluids, IV antibiotics, and proton-pump inhibitors. The management of airway in such patients takes precedence and securing the airway early with either fiberoptic intubation or a tracheostomy is of paramount importance. Maintenance of nutritional status in this group of patients is a challenging aspect. More often than not, they will require an enteral feeding tube in the form of a feeding gastrostomy or jejunostomy due to inability to give per oral enteral nutritional support.
Patients with Grade 4 injuries assume a special place in the management. They require emergency surgical intervention and debridement of organs which have undergone necrosis. These patients are usually very sick and require monitoring in the ICU, mandatory ventilation, and aggressive resuscitation.
| Chronic Phase | | |
The most common late sequel of corrosive ingestion is the formation of strictures. They usually develop within 8 weeks of ingestion, but they can develop as early as 3 weeks or as late as 1 year. Incidence of strictures is 71% after Grade 3B injuries and 100% after Grade 3 injuries.[1]
In the stomach, late sequelae include intractable pain, late achlorhydria, protein-losing enteropathy, gastric outlet obstruction due to antral/pyloric strictures, mucosal metaplasia, or carcinoma.
Reconstruction of strictures secondary to corrosive ingestion should be delayed till 6–12 months to allow for complete scar formation and for adequate recovery from the acute insult. Strictures can either be treated with resection or bypass operations. Options include gastric pull-up, jejunal interposition, or esophageal replacement graft with the colon.
| Surgical Interventions | | |
Patients with corrosive strictures most commonly present to the outpatient department with dysphagia. Due to the dynamic nature of strictures and evolution of the injury, patients are reevaluated with an upper GI endoscopy and barium studies. Barium studies are particularly helpful in assessing the dynamic nature of the swallowing process and the performance of the strictured part in relation to its normal counterparts.
Short-segment thoracic esophageal strictures can be attempted to be treated with endoscopic dilatation. However, the predominant mode of management of strictures is surgical. The choice of a particular type of surgery is made based on the extent of the injury, the symptomatology of the patient, nutritional status, and social condition of the patient. A debilitated patient with absolute dysphagia will initially undergo a feeding jejunostomy for nutritional rehabilitation, following which he would then be planned for a definitive procedure. Patients with short-segment strictures of the stomach, most commonly of the antropyloric region, are treated with a resection procedure with the reestablishment of continuity. Esophageal strictures require either a resection or more commonly, a bypass procedure. Resection procedures for the esophagus are technically challenging due to dissection of the esophagus from within the charred tissues of posterior mediastinum. They are associated with the risk of injury to great vessels, trachea, thoracic duct, or vagus nerve, thus significantly increasing morbidity. Hence, bypass procedures are usually preferred. They are usually done through the substernal route using either a colonic or gastric conduit. The proposed drawbacks include persistent acid reflux into the esophagus, cystic dilatation of the esophagus with risk of rupture, and increased risk of malignancy within the damaged esophagus. Bypass surgeries may also be accompanied by a resection procedure in case of involvement of short segments of the stomach.
A critical choice to be made for a bypass procedure is the conduit that is used as the interposition graft. Procedures have been described using both the stomach and the colon. Gastric pull-up is technically easier and requires only one anastomosis. Colon graft, on the other hand, requires three anastomoses and requires extensive dissection. However, in caustic injury where the stomach itself may be scarred, a colonic graft would be a better choice. The left colon is preferred to the right due to its smaller diameter, more constant, and reliable blood supply (from the left colic artery), adequate length for total esophageal replacement, and superior ability to propel a solid bolus.[5],[6] In rare cases when both the stomach and colon cannot be used, a jejunal graft could also be used, most often as a free flap of the jejunum.
Preoperative evaluation of a patient being planned for an esophageal bypass procedure includes:
- Upper GI endoscopy and barium study to assess the extent of injury and assess the stomach
- Nasopharygolaryngoscopy (NPL) scopy to assess the status of the larynx and pharynx
- Spirometry to assess lung function
- Assessment of the colon with CT abdomen/colonoscopy/barium enema.
High corrosive strictures or strictures involving the pharynx offer more challenges in their management due to the difficulty of restoring swallowing without creating intractable aspirations. Laryngeal involvement in this subset of patients presents with dysphonia and may require an elective tracheostomy.
At our center, depending on the organs involved, level of stricture, and previous operations done, resection, or bypass reconstructive operations were performed. Resection was done for 43 patients: 13 patients had transhiatal esophagectomy and 30 patients had gastric resections. Bypass operations were done for 74 patients: esophageal for 70 patients and gastric for four patients. Colon in 71 (84.52%) patients was the most common conduit used followed by the stomach in 12 patients (6.15%).
| Role of Tracheostomy and Laryngectomy | | |
Assessment and management of the airway remain an integral part of the management of patients with corrosive ingestion. In the acute phase, tracheostomy may be indicated in patients with respiratory distress due to corrosive induced laryngeal edema. In the chronic phase, it can be either temporary or permanent based on the location of the anastomosis and the need for a laryngectomy.
High strictures mandate an anastomosis in the pharynx or pyriform sinus. In such situations, there is a decision to be made by the patient's ability to speak versus being able to eat food. Laryngectomy and permanent tracheostomy is needed to avoid the recurring problem of aspiration.
| Stents and Their Role in the Management of Corrosive Strictures | | |
Stents are defined as devices used to maintain or restore the lumen of the hollow organs, vessels, and ducts. They have been found to be helpful in preventing strictures, but the efficacy is <50% with a high migration rate (25%). They can also be used to maintain the lumen of the esophagus following dilatation. Self-expanding plastic stents are preferred as they do not get embedded into the tissue and have been shown to be effective.[7]
Financial support and sponsorship
Nil.
Conflicts of interest
There are no conflicts of interest.
| References | | |
| 1. | Zargar SA, Kochhar R, Nagi B, Mehta S, Mehta SK. Ingestion of corrosive acids. Spectrum of injury to upper gastrointestinal tract and natural history. Gastroenterology 1989;97:702-7.  |
| 2. | Contini S, Scarpignato C. Caustic injury of the upper gastrointestinal tract: A comprehensive review. World J Gastroenterol 2013;19:3918-30. |
| 3. | Sabiston DC, Townsend CM. Sabiston Textbook of Surgery: The Biological Basis of Modern Surgical Practice. Philadelphia, PA: Elsevier Saunders; 2012. |
| 4. | Ryu HH, Jeung KW, Lee BK, Uhm JH, Park YH, Shin MH, et al. Caustic injury: Can CT grading system enable prediction of esophageal stricture? Clin Toxicol (Phila) 2010;48:137-42. |
| 5. | Agha FP, Orringer MB. Colonic interposition: Radiographic evaluation. AJR Am J Roentgenol 1984;142:703-8. |
| 6. | Postlethwait RW. Colonic interposition for esophageal substitution. Surg Gynecol Obstet 1983;156:377-83. |
| 7. | Evrard S, Le Moine O, Lazaraki G, Dormann A, El Nakadi I, Devière J, et al. Self-expanding plastic stents for benign esophageal lesions. Gastrointest Endosc 2004;60:894-900. |
[Table 1], [Table 2], [Table 3]
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