Introduction

Corrosive (caustic) substances are chemical agents that cause tissue damage upon direct contact. Corrosive substance ingestion in children usually occurs by accident. Corrosive-related accidents continue to be a life-threatening problem, especially in children under 6 years of age, particularly in developing countries [1,2,3,4,5,6,7,8,9,10,11,12,13,14]. This review aims to investigate the epidemiology, clinical features, and current early and late treatment strategies for corrosive ingestion in children.

Corrosive substances

Corrosive substances are chemical substances that cause damage upon direct contact with the internal and external organs of the body. Although they are defined as caustic substances, referring to these chemicals as corrosive substances is more appropriate because caustic substances can imply only alkaline substances. Corrosive substances can damage the body in solid, liquid and gaseous forms. Most frequently, corrosive accidents occur due to the ingestion of liquid corrosives. Serious accidents may also occur due to the ingestion of solid forms of corrosives that are sold as powders, granules or tablets or due to inhalation of vapor from liquid corrosives (Table 1, Fig. 1). The amount, physical state, and especially the pH of corrosives greatly affect the location and severity of tissue damage [3, 7, 10]. For example, a pH > 12 or < 1.5 is directly related to serious damage. Highly alkaline (pH ≥ 12) substances (e.g., concentrated sodium hydroxide) sold in liquid or granular form under names such as degreasers, grease removers, or drain cleaners are the main causes of serious corrosive damage (Figs. 1a, d, 2, 3) [3, 5, 10]. Less corrosive forms, such as household bleach, dishwasher detergents and other cleaning agents, are other frequently used corrosives. However, the degree of damage from these corrosive liquids is usually limited to the oro-esophageal mucosa. Strong acids, however, can cause serious damage to the stomach after passing through the esophagus, especially if the stomach is empty. The duodenum and the rest of the small intestine are mostly protected due to pylorospasm [3, 10, 15]. However, in recent publications, highly acidic corrosives have been reported to cause serious damage to the esophagus. An example of such substances is clear pickle vinegar, which is used in the production of homemade pickles and contains concentrated acetic acid (pH = 1.5) (Fig. 1b). Bleach accounts for approximately one-third of corrosives ingested by children, highly alkaline grease cleaner accounts for another one-third, and other acidic and weak alkaline substances account for the remaining one-third (Table 1) [2,3,4, 7, 10, 14, 16, 17].

Table 1 Common corrosive substances ingested [3, 5]
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Fig. 1
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Some generic corrosive materials sold in ordinary bottles that can be ingested easily by children (The original photos taken by the authors over the past decade in Turkey) (a–e). a Cleaning agents sold in water bottles by a local store. b Pickling vinegars (concentrated acetic acid) (B1, B2) sold in containers similar to water bottles (B3) at the street market. c Battery acids (red labeled) and battery pure water (blue labeled) in ordinary bottles that can be easily opened by children. d An unlicensed grease cleaner. e Lime solvent (E1), bleach (E2), and detergent (E3) in water bottles stored together with foods

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Fig. 2
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Endoscopic images of a 5-year-old girl who was referred late at 26 days after grease remover ingestion (a–d). In her esophagus, a long severe stricture a exhibiting prolonged tissue healing with diffuse fibrin and an abscess b–d in the middle section of the esophagus were observed, and the stricture was dilated immediately with an 18-mm diameter balloon during the same anesthesia procedure. She completely recovered after 30 balloon sessions performed over 28 months

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Fig. 3
figure 3

A 14-month-old boy was admitted for ingestion of a granular drain opener (a–c), which was sold without a child-protective container at a renowned supermarket chain (b, black arrow). However, several hours after the accident, after removing his clothes, his mother had noticed that his belly had severe black-colored burns due to the corrosive beads (b, c). He had mild oral lesions without drooling and was not reluctant to eat (a). After treating oral and skin burns, he was discharged the next day without any swallowing symptoms. Upon follow-up, he had no swallowing symptoms, and no endoscopy procedure or barium study was needed. Unfortunately, his belly skin burns healed with a severe hypertrophic scar and loss of the umbilicus (his skin lesions, c at admission, d 12 days later, e six months later)

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Epidemiology

Despite training programs, warning labels, and childproof packaging, corrosive-related accidents continue to be a problem that threatens the lives and organs of children [3, 7, 10]. Preventive medicine has been inadequate at effectively reducing these accidents. Since living and health conditions vary greatly from country to country, it is difficult to define uniform measures. Governments should take the necessary measures according to the conditions in their own country to reduce corrosive ingestion accidents [3, 7, 10,11,12, 14, 18,19,20,21].

Corrosive ingestion mostly occurs in boys (57–66%), in children aged 3–4 years, in the summer (38–41%) and spring (25–31%) seasons, in children’s homes (71–80%), and in kitchens (36–51%). Notably, a significant portion of these accidents (20–23%) occurs during home visits (grandparents’ and relatives’ houses) [2, 4, 5, 7, 11, 14, 22, 23]. Most corrosive-related accidents are caused by substances that are not sold in their original containers but rather in bottles without a childproof cap (83–93%), bottles without a warning label (72–83%), or transparent 500-ml water bottles (38–40%) or plastic carbonated beverage bottles (23%). Corrosive substances are mostly ingested by children seeking drinking water (82%) and are rarely mistakenly given to them by their mothers, grandmothers or babysitters (3–5%) [5, 14]. In children, corrosion-related incidents are mostly unintentional. However, these events cannot always be considered accidents because of extensive negligence in developing countries [5, 7, 14, 23]. The education (mothers, 81–96%; fathers, 62–80%) and income levels of most families involved in corrosive-related accidents are low [4, 5, 7, 11, 14, 23].

Pathophysiology

Base and acid injuries differ from each other [7, 10]. After contact with strong bases and acids, mucosal damage begins immediately. Acid ingestion usually triggers coagulation necrosis and causes scarring that is limited to the mucosa. In contrast, alkali substances penetrate tissues and induce liquefaction necrosis. Tissue damage continues until the alkali is neutralized. Esophageal injury occurs mainly in three regions, including the crico-pharyngeal region (the upper part), the region where the aortic arch and left main bronchus intersect (the middle part) and the esophago-gastric junction (the lower part) [7, 10]. Hemorrhage, thrombosis and evident edema develop within the first 24 h. Depending on the degree of the burn, inflammation may extend to the muscle layers and perforation of the tissues may occur. After a few days, necrotic tissues disappear, edema decreases, and neovascularization begins. This repair phase starts at the end of the first week and continues during the second week. At approximately the third week, the proliferation of fibroblasts leads to the development of esophageal strictures and scar tissue in the submucosal and muscular layers. Subsequently, mucosal re-epithelialization begins and is usually completed in the sixth week (Fig. 2). This process may result in a shortened, tethered esophagus and fibrotic stenosis [7, 10]. If the damage is transmural, necrosis may extend to the mediastinum and cause mediastinitis. If the damage extends to the anterior side, tracheo-esophageal or aorto-esophageal fistulas may develop. Esophageal motility disorder may continue for several weeks or persist if the muscle layer heals with fibrosis [10].

The most affected organ after corrosive accidents is the esophagus [1, 7, 10]. In children, gastric injury is relatively rare compared with esophageal injury (3.9–8.2%) [15, 24]. Gastric outlet obstruction and pyloric stenosis are the most commonly reported gastric complications. Gastric perforation is very rare [15, 24,25,26]. Alkali substances may cause more damage in the esophagus, while acidic corrosives may cause more damage in the stomach. Neutralization of substances via gastric contents in these situations contributes to reducing damage. The extent of damage to the stomach caused by corrosives varies according to the amount of the ingested substance, its pH, and whether the stomach is full or empty [24, 25].

While corrosives can cause damage to internal organs as a result of ingestion, they can also cause damage to the skin with direct contact. More than half of these chemical skin burns occur as a result of strong bases, and a greater depth of damage results in a more difficult treatment process and a longer healing time (Fig. 3) [27].

Clinical manifestations and diagnosis

Patients may be asymptomatic or may present with various initial signs and symptoms after corrosive ingestion. These signs and symptoms can include the following: drooling/difficulty in swallowing saliva, reluctance to eat, dysphagia/odynophagia, oropharyngeal lesions/burns, retrosternal or abdominal pain, epigastric pain, abdominal or chest tenderness, hematemesis, vomiting, agitation, crying, dyspnea, tachycardia, fever, and leukocytosis. Most of these symptoms are mild and usually regress within hours. Children do not swallow their saliva, and their saliva therefore flows along the rim of the mouth until esophageal edema resolves, which is called drooling. Reluctance to eat is associated with an inability to swallow saliva and esophageal pain. After drooling stops, a child’s appetite may recover, but reluctance to eat may persist. Long durations of drooling (> 12 h) and reluctance to eat (> 24 h) may be signs of esophageal stricture development [5].

Symptoms of dyspnea, such as stridor, hoarseness, nasal flaring, or costal retraction evident on inhalation, are suggestive of airway involvement. Acute upper airway obstruction may occur due to laryngeal or posterior pharyngeal edema after spillage of corrosives into the upper airways. Airway symptoms may start immediately but may also develop several hours after inhalation, especially if an agent is inhaled in powder form. Emergency endotracheal intubation, cricothyroidotomy or tracheostomy may be required if the airway is severely compromised. Fever, chest pain and hypotension may be signs of necrosis and perforation [7, 10].

The management of corrosive injuries in children is based on signs and symptoms. Initial endoscopic grading within 48 h after corrosive ingestion is redundant, and this traditional approach should be abandoned [5,6,7], as it does not provide any significant contribution to the diagnosis, prediction, treatment, hospitalization or management. Endoscopy displays only the mucosa and not the muscle layer, where burns and necrosis trigger stricture formation.[3, 5, 10]. In addition, endoscopy is an invasive procedure and is concerning to parents. A new prognostic scoring system currently exists for all corrosive injury patients: the DROOL score (Table 2). The DROOL system, developed by Uygun et al., is a simple and noninvasive scoring (similar to the APGAR score) method based on the duration and severity of all symptoms (Table 2) [5,6,7]. A recent, detailed, clinico-epidemiological study of 202 patients revealed that a DROOL score ≤ 4 was highly predictive (100% sensitivity, 96.63% specificity, 85% positive predictive value, 100% negative predictive value) of esophageal stricture development (p < 0.001) [5]. The DROOL score should be preferred over endoscopic grading for all children who ingest corrosive substances (Table 2) [4,5,6,7].

Table 2 The five criteria of the DROOL score for the assessment of patients with corrosive ingestion [5]
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Management

The aim of the management is first to save the life of the child who ingested the corrosive and then to reduce the complications, especially esophageal stricture, which is a serious complication after corrosive ingestion (1.7–15%) [3,4,5,6,7, 11].

The primary assessment of corrosive ingestion patients should include taking a detailed medical history. A good history can reveal when the patient ingested a corrosive substance, the amount of the substance ingested, the chemical character and type, and whether the substance was in the original package or another container. Whether the corrosive substance was ingested voluntarily or for a suicide attempt should also be investigated. Regardless of the corrosive properties, the toxic effect of the substance should also be considered [7, 10].

A detailed physical examination should be performed for airway and hemodynamic stabilization. In some patients, emergency endotracheal intubation or surgical airway opening may be required [7, 10]. To remove corrosive substances that have entered/absorbed in the patient's clothes, all the clothes of the patient should be removed, and the whole body should be examined (Fig. 3). To avoid re-exposing the damaged tissue to the corrosive material, the patient should not be forced to vomit. If the patient has persistent nausea and vomiting, a nasogastric tube may be inserted carefully. Since activated charcoal does not absorb corrosives, it is not recommended for treatment [7, 10]. Although dilution of the ingested corrosives with water or milk has been recommended by some researchers, no evidence supports this practice [10].

Patients with mild cases of corrosive ingestion should be fed, and if they are asymptomatic after a few hours of observation, they may be discharged home after instructing the family to seek medical advice if dysphagia, fever, or a reluctance to eat develops [5, 10]. A standing chest radiograph may be required in symptomatic patients to detect the presence of free air in the mediastinum or abdomen. Contrast-enhanced esophagography is not required upon initial examination and is also contraindicated if perforation has not been excluded. If perforation is suspected, computed tomography should be performed [7, 10]. More attention should be directed towards those who ingest corrosives with suicidal intent; these patients may have ingested a much larger amount than those with accidental ingestion [10]. Additionally, patients with signs and symptoms of acute abdomen, mediastinitis, airway obstruction or perforation require a dynamic approach under intensive care conditions. If necessary, under life-threatening conditions, such as extensive esophageal, gastric or other organ necrosis or perforation, an urgent surgical intervention such as esophagostomy, gastrostomy, or jejunostomy should be attempted [5, 10].

Millar et al. recommend endoscopic grading for corrosive ingestion management. However, according to their protocol, endoscopy does not substantially guide the treatment approach and affects only the decision to use empirical antibiotics [8,9,10]. In contrast, we do not recommend endoscopic grading for any patients. The management of corrosive ingestion should be based entirely on signs and symptoms. All patients who ingest corrosives should be examined between 10 and 14 days after ingestion for dysphagia, vomiting and reluctance to eat. Those who do not have any complaints should be followed up in the outpatient clinic, and the patients with any complaints should immediately be hospitalized, and fluoro-endoscopic examination of the esophagus should be performed under general anesthesia. Thus, a highly probable stricture should be diagnosed early before the 14th day, and simultaneously, early treatment should be performed by balloon dilatation [5]. The treatment protocol that we recommend based on the results of the review is presented in Fig. 4.

Fig. 4
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The flowchart recommended by us for managing corrosive ingestion in children

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Various agents, such as ipecac syrup, oral dilution, neutralizing agents, corticosteroids and antacids, have been used in the treatment of corrosive ingestion. However, the efficacy of these therapies has not been fully demonstrated [5, 6, 10, 21]. The benefits of some substances, such as honey, sugar and garlic oil, have been shown in other studies [4].

Patients who can swallow their saliva and have no signs of perforation or sepsis should be fed, not starved. Many positive impacts of nutrition and saliva on wound healing have been shown. Oral feeding and consequently increased saliva secretion and esophageal motility may also help debridement of the burned esophagus and reduce the development of infection and adhesion/stenosis [3,4,5,6,7, 11]. In the past, some authors suggested without evidence that patients should not be fed for more than one week because of the chance that embedded foods in their esophagus may increase the risk of infection. However, contrary to this claim, we did not detect any embedded food during endoscopy at 10–14 days after corrosive ingestion in the esophagus of any symptomatic patient fed solid foods [4,5,6,7].

Corticosteroids should not be used after corrosive ingestion. A meta-analysis consisting of a 50-year follow-up of patients and the results of two other clinical studies showed that steroid use did not reduce the frequency of strictures after corrosive ingestion; therefore, steroid use was not recommended [28,29,30].

Routine antibiotic use remains a controversial issue. Antibiotics are indicated in patients with respiratory sepsis, persistent fever, suspected perforation, a poor general condition, pneumonia and mediastinitis. Prophylactic single-dose antibiotics should be used during dilatation because cerebral abscesses have been reported after repeated dilatations [7, 10, 31].

Esophageal balloon dilatation is the first treatment for esophageal strictures. Significant contributions of early dilation to the success and duration of treatment have been confirmed by recent studies. Esophageal stricture should be diagnosed earlier (10–14 days) by endoscopy only for patients with persistent dysphagia instead of relying on late classic barium studies (≥ 21 days) and treated with fluoroscopic balloon dilation earlier (during the same anesthesia procedure performed for endoscopy) (Fig. 5) [4,5,6,7, 10]. Routine barium esophagography in patients with persistent dysphagia and/or food intake reluctance after corrosive ingestion is not indicated because it may delay early diagnosis and treatment of esophageal strictures. Esophagography may be difficult in children, especially those with dysphagia; it can lead to misdiagnosis of mild-moderate strictures, such as esophageal peristalsis; it can require lengthy appointment and reporting times; estimating the length, severity, and number of strictures may be difficult due to hypomotility and an inadequate barium bolus below the probable first narrowed point; and most importantly, it does not eliminate the indication for a fluoro-endoscopic balloon-assisted scan in patients with dysphagia [5, 6]. Historically, esophagography was performed on the 21st day after corrosive ingestion, and the first dilatation was delayed until an average of 40 days in these patients [5].

Fig. 5
figure 5

A 5-year-old boy with Down syndrome and severe cardiac anomaly was admitted with a stricture due to grease cleaner ingestion. His stricture was found to be long and severe by fluoroscopic balloon-assisted esophageal screening (a). After six dilatations (a–e), his parents agreed to esophageal replacement. However, gastric pull-up was carried out after open heart surgery 1 year later (f–h). d, e endoscopic imaging of the stricture and its balloon dilatation, f after cardiac surgery, control esophagography was performed immediately before replacement, g, h no anastomotic stricture and good gastric emptying were observed on esophagography after gastric pull-up

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Esophageal stricture can be detected in the first endoscopic evaluation and fluoroscopic balloon-assisted esophageal examination (esophageal screening) under general anesthesia in every patient with persistent dysphagia between 10 and 14 days, and the treatment process can be started immediately with dilatation. With endoscopy, the esophagus, stomach and duodenum can be visualized directly, and the severity of corrosive burns, the healing phase of tissues, and the presence of foreign bodies and strictures can be detected. Then, via fluoroscopic balloon-assisted esophageal screening, all strictures and their features, such as their presence, location, number, shape, length, resistance, severity, and ability to be detected by endoscopy, and strictures that cannot otherwise be reached because they are distal to severe stenosis can be appropriately diagnosed and dilated at the same time [5, 6, 32].

Early initiation of balloon dilatation between 10 and 14 days greatly contributes to the effective treatment; this approach has been recommended for many years in textbooks and in many publications [5,6,7,8,9,10]. Interestingly, however, some centers traditionally call patients for esophagography after 3 weeks [2, 13, 33,34,35]. We showed that compared with late dilation (≥ 21 days), starting balloon dilation early (10–14 days) results in highly satisfactory treatment outcomes in patients with stricture who were referred late. In early treatment patients, the treatment duration and the number of dilations were significantly lower (p < 0.001) than those in later treatment patients [6]. Consequently, conventional management based on initial endoscopic grading, nothing by mouth, total parenteral nutrition, a late barium study after 21 days, later commencement of dilation for stricture, and gastrostomy should be avoided [5,6,7,8,9,10].

Modern balloon dilators, especially radially expandable balloons, have several advantages: they are safe, efficacious, lack the shearing longitudinal force associated with other techniques, and do not require gastrostomies, permanent tubes or nose ropes [5, 6, 10, 32, 34]. Fluoroscopic balloon dilatation is more effective and safer than endoscopic dilatation [5, 6, 32, 36] and has several advantages, especially in terms of better image control. Additionally, the time required for the procedure is short, and the success rate is very high (100%) [5, 6].

Esophageal dilatation should be performed regularly every two weeks for the first two months and then every three to four weeks in the following months. The frequency of dilatation may be reduced in the following months according to the patient’s needs. During the dilatation program, the patient’s diet is not restricted. The family is told to have meals together with the patient. Dilatation should be stopped for those who have not experienced repeated difficulty swallowing solid food for at least 3 months [5, 6].

Although esophageal perforation is a major complication of dilatation, the risk of perforation is very low (0.33–1.6%). Most perforations occur during the first dilatation [6, 32, 37]. However, this finding should not cause any delay in the treatment of a patient with stricture, and the patient's first dilatation should be performed between 10 and 14 days [5,6,7,8,9,10, 34]. In contrast to common knowledge, most perforations occurring in the first sessions are reported in patients receiving late dilatation (≥ 21 days) and not in patients receiving early dilatation [6, 32, 37]. Tiryaki et al. showed that early (7–14 days) dilatation did not increase the risk of perforation; in contrast, the perforation rate was 2.5-times higher in patients with late (≥ 21 days) dilatation than in those with early dilatation [34]. In our study, the risk of perforation in late-treatment (≥ 21 days) patients was 3 times higher than that in early treatment (10–14 days) patients for the first dilatation and 6 times higher during the total dilatation program [6]. Consequently, although the risk of perforation is higher during the first dilatation, this risk does not decrease with delayed dilatation; in contrast, the risk increases progressively [6, 32, 34]. The high rate of perforation in patients undergoing late dilatations may be proof that the tissue healing phases last longer in some patients. Therefore, in all patients with corrosive injury-related strictures, the first dilatations should be performed more carefully [5,6,7,8,9,10, 32, 37]. Indeed, in many esophagoscopic videos of patients undergoing late dilatations (≥ 21 days), continued inflammation is observed during the first balloon session (Fig. 2).

The treatment approach for perforations is mostly conservative, including nasojejunal nutrition, antibiotic treatment and tube thoracostomy, if necessary. With this treatment, the mortality rate has approached zero in the last decade. However, early diagnosis is important [7, 16, 21, 32, 36, 37]. Gentle and careful movements of the balloon and slow inflation of the balloon may prevent esophageal perforation [5, 6, 21, 32].

Although some successful results have been obtained with dilatation of esophageal stenosis with local steroid (triamcinolone acetate) or mitomycin-C (an inhibitor of fibroblast proliferation) application, these approaches have not been prospectively examined in large series [4, 21, 38].

Esophageal stents, partial esophagectomy (stricturotomy) and esophageal replacement surgery are other treatment options [5, 6, 10, 18, 39,40,41]. Esophageal stents are not generally used in children because they can cause tracheal or bronchial erosion, triggering gastroesophageal reflux and esophagitis [6, 40]. Partial esophagectomy should be considered for short-segment strictures [6, 7, 41]. However, before partial esophagectomy, the shape and location of the stenotic region should be examined with the aid of endoscopy and fluoroscopy, and the length of the stricture should be measured fluoroscopically by the balloon, which is inflated only slightly for the procedure. A histological fibrotic stricture may be longer than that observed radiologically. Notably, a burned esophagus may be a “shortened esophagus”, “tethered esophagus”, or “sclerosed esophagus”; therefore, partial esophagectomy can be very difficult to perform. Consequently, partial esophagectomy may only be a suitable option for patients with a true short-segment stricture [5, 6, 10]. Many authors recommend esophageal replacement surgery instead of long-term dilatation [10, 18, 39]. Millar et al. suggest switching to replacement surgery in cases of failure of 12-week dilatation therapy [10]. In children, colonic interposition and gastric pull-up operations are the most commonly used replacement surgery techniques, and gastric pull-up seems to be less complicated, easier and better tolerated [10, 39]. Open or laparoscopic transhiatal gastric pull-up with total esophagectomy is currently considered the best esophageal replacement surgery for children (Fig. 5) [7, 39]. The frequency and severity of gastroesophageal reflux should be investigated considering that gastroesophageal reflux may cause persistent strictures [42]. Reflux can generally be treated with surgical fundoplication; however, medical reflux therapy is preferred for gastric transposition candidates [7, 10, 39].

Other complications resulting from corrosive ingestion are dysphagia, esophageal motility disorders, gastric outlet obstruction, pancreatic and intestinal injury, orofacial and skin burns, and damage to the eyes and other organs (Fig. 3). Gastric outlet obstruction and pyloric stenosis can be successfully treated by balloon dilatation [7, 10, 26, 27, 43].

Esophageal carcinoma is a late-term complication of corrosive burns. This type of carcinoma has been reported to develop 1–3 decades after corrosive ingestion, with a frequency of 2–30% in corrosive patients, and this frequency is at least 1000 times higher than that in other patients in the same age group [3]. Unfortunately, fatal squamous cell esophageal carcinoma developed in a 14-year-old child only 1 year after corrosive ingestion according to a previous report [44]. Current publications indicate that this major problem has been ignored, and families may not be given sufficient information on this issue. Studies investigating long-term outcomes are urgently needed. Dilatation, stenting, or esophageal bypass surgery after corrosive ingestion cannot prevent the development of esophageal carcinoma [3, 10]. In previous editions of a pediatric surgery textbook, an example of esophageal replacement with colonic interposition without esophagectomy in a boy was presented, and in the most recent edition, the authors emphasized that he died due to squamous cell carcinoma that developed approximately 30 years after corrosive ingestion [8,9,10]. Therefore, if esophageal replacement is required, removal of the diseased esophagus is recommended [7].

Conclusion

Corrosive substance ingestion remains a major health issue, particularly in developing countries. The unacceptable incidence of these accidents can be reduced via legal sanctions and by selling corrosive materials in their original childproof containers. The management strategy after corrosive agent ingestion should be planned according to the signs and symptoms. A more dynamic approach should be implemented in patients who intentionally ingest corrosive substances in large amounts for suicide attempts.