26
Endoscopic management of caustic ingestion

Erasmo Miele and Samy Cadranel

KEY POINTS

Mucosal injury begins within minutes of caustic ingestion.
Alkali ingestion has a greater risk of transmural damage.
Endoscopy should ideally occur within 6–12 hours of the ingestion and if performed more than 48 hours following ingestion, it increases the risk of perforation.
Various treatments have been proposed to prevent esophageal strictures, including ipecac, oral dilutions, neutralizing agents, antacids, antibiotics, and systemic corticosteroids, but the optimal management strategy remains controversial.
If a stricture develops then balloon or bougie dilation should occur.
If repeated dilation (more than two times) is needed then postdilation topical application of the antifibrotic mitomycin C is indicated.
Caustic ingestion increases the risk of carcinoma formation (both adenocarcinoma and squamous cell carcinoma) with an incidence of 2–8% and some suggest endoscopic surveillance after the age of 20 years.

Introduction

Ingestion of caustic agents can induce severe esophageal and gastric lesions, including necrosis, sometimes leading to life‐threatening acute complications [1]. In contrast with deliberate ingestion in adults and adolescents, in children younger than 6 years (with peak incidence at 2 years) the small amount of corrosive substances, usually ingested accidentally, causes mild and superficial lesions [2]. Preventive measures implemented in industrialized countries have significantly reduced caustic injuries whereas this objective has yet to be realized in many developing countries [3].

Epidemiology

Caustic ingestion in children remains a worldwide problem, with an incidence ranging from 5 to 518 per 100 000 children per year [3], with more than 40 000 cases reported yearly in England and Wales [4]. In 2014, the annual report of the American Association of Poison Control Centers documented more than 1 million substance exposures in children younger than 5 years, representing 50% of all exposures, with a male/female predominance of 1.3:1. However, only one out of the 25 fatalities was due to a caustic agent, sodium hypochlorite [5].

Pathophysiology

The severity of lesions depends on the type, quantity, concentration, and time of contact of the caustic substance with the mucosa [6]. Strong alkali (pH >11) causes tissue injury by liquefactive necrosis, a process that involves saponification of fats and solubilization of proteins. Cell death occurs from emulsification and disruption of cellular membranes. This leads to deeper penetration into tissues with a greater likelihood of transmural injury. Alkali absorption leads to thrombosis of blood vessels impeding blood flow to the already damaged tissue [7]. The higher surface tension of alkalis permits a longer contact time with esophageal tissues. In addition, the stomach and duodenum could be affected [8].

The mode of tissue injury with acids is coagulation necrosis. The coagulum prevents the corrosive agent from spreading transmurally, hence reducing the incidence of full‐thickness injury. Its lower surface tension and the formation of protective esophageal eschar allow acids to bypass the esophagus rapidly without much damage while affecting the stomach more severely [9]. Mucosal injury begins within minutes of caustic ingestion, characterized by necrosis and hemorrhagic congestion secondary to the formation of thrombosis in the small vessels. These events continue in the next several days until approximately 4–7 days, leading to mucosal sloughing, bacterial invasion, granulation tissue, and collagen deposition. The healing process typically begins three weeks after ingestion. By the third week, scar retraction occurs and may continue for a few more months until stricture formation occurs.

Clinical presentation

Corrosive ingestion may be deduced from oral burns, including lip or tongue erythema and edema, leukoplakia, or ulceration [10]. Most common symptoms are dysphagia, drooling, feeding refusal, retrosternal pain, abdominal pain, and vomiting. Minor symptoms do not rule out the presence of relevant injury, but increased number of symptoms correlates with a likelihood of significant injury [7]. Rarely, children develop airway symptoms, such as shortness of breath or hypoxia and, in severe cases, hemodynamic instability and/or circulatory collapse, although none of these symptoms is completely predictive of esophageal injury [11]. Beware of symptoms of sepsis, indicative of esophageal perforation which requires emergent surgical debridement and/or esophagectomy [10].

Assessment and management

Suspicion of caustic ingestion needs prompt evaluation in the closest emergency department and requires a detailed history, verification of the nature of the ingested product, ideally with the container brought by whoever brings the child. If the ingestion is doubtful, without oral lesions, and the patient is asymptomatic, observation by the physician can be sufficient, providing adequate follow‐up is ensured [12]. Symptomatic children should be kept nil by mouth on intravenous maintenance fluid until further investigations are performed; broad‐spectrum antibiotics are indicated if there are signs of perforation, and may be given empirically for patients with suspected bacteremia or aspiration pneumonia or pneumonitis [13]. Chest and abdominal radiographs and standard blood tests should be obtained to detect metabolic acidosis, leukocytosis, hemolysis or signs of coagulopathy [14]. Every child suspected of caustic ingestion and with symptoms/signs (e.g., oral lesions, vomiting, drooling, dysphagia, hematemesis, dyspnea, abdominal pain, etc.) needs an early upper GI endoscopy (UGE) to identify all digestive tract lesions [12].

Endoscopy

Endoscopy should be performed within the first 24 hours, preferably 6–12 hours after ingestion in order to observe any severe complications while stabilizing the child. A too early endoscopy may not show the extent of the burns whereas an endoscopy done after 48 hours increases the risk of perforation. UGE is performed in the operating room, under general anesthesia and a protected airway, with minimal air insufflations [10] and great caution taken to avoid advancing blindly. If an adequate view cannot be achieved or severe circumferential injury is detected, endoscopy should be terminated [3]. Careful examination of the esophagus, stomach, and duodenum determines the degree and extent of tissue damage (Table 26.1, Figures 26.1–26.4 ) and the necessity for nasogastric feeding tube placement to facilitate enteral feeding and patency of esophageal lumen in children with severe esophageal damage and high risk of stricture [10,12,14].

Table 26.1 Endoscopic classification of caustic injuries

Grade	Features
Grade 0	Normal
Grade I	Superficial mucosal edema and erythema
Grade II	Mucosal and submucosal ulcerations
Grade IIa	Superficial ulcerations, erosions, exudates
Grade IIb	Deep discrete or circumferential ulcerations
Grade III	Transmural ulcerations with necrosis
Grade IIIa	Focal necrosis
Grade IIIb	Extensive necrosis
Grade IV	Perforations

Photo depicts grade I corrosive esophagitis with diffuse erythema and minimal mucosal sloughing. — **Figure 26.1** Grade I corrosive esophagitis with diffuse erythema and minimal mucosal sloughing.

Photo depicts grade IIa corrosive esophagitis described by extensive mucosal sloughing. — **Figure 26.2** Grade IIa corrosive esophagitis: extensive mucosal sloughing.

Treatment

Most children affected by mild injuries (grade 0–IIa) need observation in hospital until full oral feeds are tolerated. Patients with more severe injuries (grade IIb and III) require accurate evaluation of probable development of strictures during initial hospitalization of 2–4 weeks. A liquid diet, orally or via nasogastric tube, may initially be necessary in as many as a quarter of patients [15] and efforts should be undertaken to prevent vomiting. Nothing should be given by mouth if perforation is suspected [12].

Photo depicts grade IIb of corrosive esophagitis described by multiple ulcerations. — **Figure 26.3** Grade IIb of corrosive esophagitis: multiple ulcerations.

Photo depicts corrosive gastritis. — **Figure 26.4** Corrosive gastritis.

Various treatments have been proposed to prevent esophageal strictures, including ipecac, oral dilutions, neutralizing agents, antacids, antibiotics, and systemic corticosteroids, but the optimal management strategy remains controversial [16,17].

Induction of emesis with syrup of ipecac or liquids used to dilute or neutralize the caustic agent are strongly contraindicated because vomiting further exposes the esophagus to the caustic agent [10]. Broad‐spectrum antibiotics are frequently prescribed in the acute phase, based on animal studies of increased granulation with bacterial invasion of disrupted mucosa [18], although clinical evidence does not support its routine use [19]. To prevent stricture formation, corticosteroids have been used to reduce fibroblast proliferation in children, adults, and rabbits with grade II or III lesions [10,19–21]. Although corticosteroids did not show any benefit in metaanalysis, recent guidelines recommend the use of high doses of intravenous dexamethasone (1 g/1.73 m² per day) administration for a short period (three days) in IIb esophagitis early after corrosive ingestion [12,22]. There is no evidence of benefit from the use of corticosteroids in other grades of esophagitis (I, IIa, III) [12]. Use of PPIs is a widespread practice although there is no evidence suggesting that it effectively protects the esophageal mucosa and reduces the formation of stricture [3].

Long‐term complications

The risk of esophageal stricture (Figure 26.5), the major complication following caustic ingestion, is as high as 77% in grade IIb lesions and may reach 100% in patients with grade III [1]. Stricture formation can occur as early as three weeks after ingestion, usually established in 80% of the patients who will develop stricture by eight weeks (Figure 26.6) [7].

Photo depicts esophageal stricture after lye ingestion. — **Figure 26.5** Esophageal stricture after lye ingestion.

Photo depicts multiple esophageal strictures two months after caustic ingestion. — **Figure 26.6** Multiple esophageal strictures two months after caustic ingestion.

Once strictures develop, repeated dilations are needed. Several methods can be used, including mercury‐filled bougies, antegrade Maloney or retrograde Tucker dilators and dilators passed over a guidewire or pulled through a string left in situ between dilations [1]. Balloon dilation under endoscopic control has been successfully used in children [23].

After the dilation session, topical application (four minutes of 0.4 mg of mitomycin in 1 mL of vehicle) of mitomycin, an antibiotic with antineoplastic and antiproliferative properties that also inhibits RNA and protein synthesis. seems a promising strategy in reducing the number of dilations needed and stabilizing the scarring of the esophagus at an acceptable diameter [24].

Unfortunately, in some children, surgery is needed. Extensive necrosis noted on endoscopy and patients with evidence of perforation are indications for immediate surgical intervention. Esophagectomy, esophagogastrectomy or gastrectomy may be indicated if wide necrosis is confirmed or in case of long and tight strictures. Esophageal reconstruction may be achieved by small bowel or colon interposition and gastric transposition [1].

Caustic ingestion increases the risk of carcinoma formation (both adenocarcinoma and squamous cell carcinoma) with an incidence of 2–8% [25]. However, periodic surveillance for the development of dysplasia following caustic ingestion is controversial. It has been suggested that after the initial ingestion, periodic endoscopy should be considered in patients 20 years of age or older [26].