Caustic injury of the aerodigestive tract is a problem, despite legislation to diminish the sale of hazardous and caustic household products (1,2). Development of esophageal strictures is closely related to the severity of the initial injury (1,3,4), and early endoscopy is widely recommended to assess the severity and extent of aerodigestive lesions and appropriate therapeutic regimens (1,2,5–9). Most caustic-substance ingestions by young children are accidental and, in developed countries, associated with a low risk of significant esophageal lesions and/or complications (10,11). The aim of this study was to determine the predictive value of clinical symptoms and ingested-substance types as markers of severe exogastric lesions and to define indications for endoscopy.
Between January 1989 and December 1995, 85 children underwent esophagogastroduodenoscopy as a result of accidental caustic ingestion. Commercial name, physical state (liquid, crystalline, solid), and chemical property (acid or basic) of the caustic substance were recorded, as were timing and modality of the accident, age and sex of the child, initial and actual symptoms, and data regarding the presence of oropharyngeal lesions, results of endoscopy, initial treatment, and late sequelae (and their treatment). The same operator performed all endoscopies and all patients were under general anesthesia. Mucosal lesions were scored as grade I (erythema or petechiae), grade II (noncircumferential [IIa] or circumferential [IIb] ulcerations), or grade III (mucosal necrosis) (7). Severe injury was defined as a near-circumferential ulceration or kissing ulcer with pseudomembranes or black-brown necrosis (grades IIb and III). Children with no or minimal lesions (group A) were discharged home with normal alimentation; treatment with aluminum phosphate when dysphagia was persistent. In children with severe lesions (group B), a central line was inserted for parenteral nutrition during the same anesthesia. Ranitidine and antibiotics were administered. Nasogastric tubes and corticosteroids (for the prevention of esophageal stricture) were not used. Endoscopy was repeated on day 10 to confirm healing without stricture and allow oral alimentation. In cases where severe lesions persisted, parenteral alimentation was maintained and a barium meal was performed on day 30 and on day 90, if necessary. Predictors, such as symptoms and signs (vomiting, drooling, hematemesis, respiratory distress, oropharyngeal burns), and ingested-substance types were tested for their diagnostic value in relation to severe lesions. Symptoms such as dysphagia and pain were excluded because most of the children were toddlers who were unable to give clear descriptions of these symptoms. Sensitivity, specificity, positive predictive value (PPV), and negative predictive value (NPV) were calculated for each parameter; 2 × 2 tables were compared by the two-side Fisher exact test.
Patients included 56 male (66%) and 29 female (34%) children, aged 11 months to 14 years (median, 24 months). Accidents occurred at home in 80 cases (94%), usually in the kitchen. The ingested substances included dishwater detergents, lye-containing detergents, drain cleaners, and bleach; 61% of the substances were basic and most were liquids (Table 1). The products were stored in and subsequently ingested from mineral-water bottles or glasses in 10 cases (lye-containing products in 7/10). Forty-eight children (57%) had no symptoms; the other 37 children (43%) presented with vomiting, hematemesis, drooling, respiratory distress (requiring intubation in 4/5 cases), and/or oropharyngeal lesions. Endoscopy was performed within 2 to 72 hours (median, 4 hours) after ingestion. Endoscopy showed no severe lesions in 63 cases (group A, 74%): normal endoscopy in 40 cases and minimal lesions in 23 cases (involving only the esophagus in 7, the stomach alone in 11, and both organs in 5). Severe digestive lesions were present in 22 cases (group B, 26%), which involved only the esophagus in 11, the stomach alone in 3, and both organs in 8. Most severe lesions were caused by ingestion of lye (14/22 group-B patients), but some were caused by ingestion of strong acids (Table 1). Severe lesions caused by ingestion of dishwater detergents or bleach were rare. All of the 10 children who drank caustic substances out of mineral-water bottles or glasses had severe lesions; 5 of these children, all of whom had ingested lye, had sequelae. Table 2 shows the predictive values of the ingested-substance types and the symptoms and signs for severe endoscopic lesions.
Vomiting, drooling, and oropharyngeal lesions were not predictors for severe lesions. Hematemesis, respiratory distress, or presence of at least three symptoms was always associated with severe lesions (PPV = 1). The absence of symptoms was always associated with no or minimal lesions (NPV = 1). There was no fatal case and no case of esophageal perforation or mediastinitis. Laparotomy was performed on day 3 in a child from group B who had peritoneal signs that revealed only a considerable inflammatory reaction involving the stomach without any perforation. Nine patients from group B (41%) developed esophageal stenosis, requiring dilations in two cases and esophagoplasty in seven cases (associated with antrectomy in two). Digestive lesions healed without sequelae in the other group-B patients, one of whom had a skin graft on day 20 after a third-degree caustic burn of the anterior thoracic wall. No digestive sequelae occurred in patients from group A; one child of this group who sucked on a solid form of lye had severe lip injury that led to microstomia and required several operations.
Severe digestive lesions resulting from accidental caustic ingestion occurred in 26% of the children studied; oesophageal stenosis occurred in half of them. These results are higher than those reported by other studies, which showed only a 1 to 5% rate of stenosis (9,12,13), although they are similar to the 19% stenosis rate reported by Christensen et al. (11). Prevention of stenosis with nasogastric tube insertion, stent, and corticosteroids is controversial (4,14–19) However, high doses of methylprednisolone (20) or dexamethasone (21) seem to decrease the risk of esophageal stricture. This emphasizes the need for early endoscopy to recognize severe esophageal lesions. Conversely, more than half of the children who accidentally ingest caustic substances do not have serious digestive lesions and do not require treatment or further examination. Clinical signs able to predict severe esophagogastric lesions would be useful for the practical management of disease in these children.
A product's pH primarily determines how caustic it is, but titratable alkalinity/acidity reserve, physical state (liquid/solid), viscosity, and concentration are also important. As reviewed in the literature (4,11,12), most significant caustic burns are caused by strong alkali (pH ≥12) substances. Liquid lye is the most dangerous substance that is ingested (11,13) and is responsible for 64% of the severe endoscopic lesions and 78% (7/9) of the esophageal stenosis in our study. Lye has not been sold in Finland without special authorization since 1969, resulting in a dramatic decrease in severe oesophageal burns (12). In spite of efforts to make child-resistant containers in France, the incidence of severe caustic lesions after lye ingestion did not decrease during the study period, because products decanted into mineral-water bottles and glasses led to the most severe burns. Nevertheless, alkali ingestion cannot be used as a reliable predictor for severe digestive lesions because endoscopy shows no or minimal lesions in 69% of these cases (suspicion of ingestion), and other substance types were involved in 36% of the cases with significant injury. Dishwater detergents, mostly in powder form, usually cause oropharyngeal injury with minor oesophageal lesions (11–13), although we observed two cases of severe lesions with one case of dilatable stenosis as previously reported (12). In the United States, ingestion of dishwater detergents resulted in major digestive or respiratory complications in 0.02 to 0.06% of cases (22–24). Bleach usually causes only minor lesions (25), but may lead to severe burns when concentrated (26). In contrast to Christensen et al. (11), we observed severe esophageal lesions after ingestion of strong acids, which led to extended strictures in two cases. Thus, significant digestive injury can also occur after ingestion of nonalkaline substances.
This study confirms that the absence of an oropharyngeal burn does not rule out the presence of severe esaphagogastric lesions (8,9,11–13,27). Respiratory distress is highly predictive of severe digestive lesions (11,13) and like hematemesis has a PPV of 1, although its sensitivity is low. None of the other symptoms was found to be a good predictor (11,12,27), including vomiting, which had been associated with a high incidence of severe lesions in previous studies (8,13). Of interest, the high NPV related to the absence of symptoms is consistent with results from other studies where patients with severe exogastric lesions were always symptomatic (4,8,11,13,27,28). Avoiding endoscopy in asymptomatic patients, as suggested by some authors (11,12,27), would have led to the sparing of this procedure in half of the children included in this study.
In conclusion, children with severe caustic lesions and subsequent risk of esophageal stenosis always presented with symptoms. We suggest that endoscopy is not recommended for children who are asymptomatic after accidental caustic ingestion. However, we do recommend that every child be evaluated by an experienced team in a referral center. The decision of whether to perform endoscopy should be promptly made by a trained pediatric gastroenterologist to avoid excessive delay in the treatment of severe caustic lesions. These recommendations do not apply to developing countries where hazardous caustic substances are more likely to be available for children and severe digestive lesions occur more frequently (15,26,29), which justifies systematic endoscopy.
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