children included in the review ingested chlorine bleach; 1.2% had mild oral
lesions, but others were asymptomatic at presentation.
Accidental or unintentional corrosive ingestion was encountered in all
children involved in the study. Corrosives were ingested either directly from
the bottle or diluted. Immediately after ingestion, parents tried to induce
emesis while others gave either milk or water for their children. All children
were hospitalized initially in the pediatric ward and kept nil per os till
upper gastrointestinal endoscopy was performed for them. None of our children
had severe respiratory symptoms or care in the PICU. Children with a history of
button battery or paint thinner ingestion were asymptomatic at presentation.
Symptoms and signs at presentation in children who ingested acid or
alkali (chlorine bleach, button batteries and paint thinner were excluded) were
vomiting either induced by parents or not in 47.9%, oral lesions in 34.2%,
drooling of saliva in 26%, strider in 12.3%, and abdominal pain or irritability
in 8.2%. Esophageal injuries were reported in 25% of children; 28% alkali
ingestion, 30.4% acid ingestion, 13.6% button battery ingestion and 20% paint
thinner ingestion. Gastric injuries were reported just in four (17.4% )
children who ingested acids.
Although vomiting was considered as a nonspecific symptom in our
patients, because in many cases it was induced by parents, there is a
significant association between vomiting and esophageal injury. Drooling of
saliva was also significantly associated with esophageal injuries, while oral
lesions, strider, and abdominal pain were not [table II].
Table II: Association between symptoms and development of
Esophageal injury present
Esophageal injury absent
Oral lesions were present in 78.6% of children who ingested pipe opener
granules, while esophageal injuries were present in 14.3% (P > 0.05). There
was no significant association between symptoms at presentation and grade of
the esophageal injury (P > 0.05), but children with grade 3 esophageal
injury had at least two or more symptoms [figure 1].
The esophageal stricture was
developed in 2% of children due to alkaline substances ingestion, while
esophageal strictures not developed in patients who ingested acids, button
batteries or paint thinner.
Esophageal injuries encountered
in this review include;4% grade 1, 64% grade 2, and 32% grade 3. Children with
grade 0 and 1 esophageal injuries were discharged home, while grade 2 and 3
were kept in the hospital for 7 to 14 days. Grade 2 and 3 esophageal injuries
were treated with intravenous antibiotics (Cefotaxime 100
mg/kg/day), H2 blocker (Ranitidine 2 mg/kg/day), and
steroid (Hydrocortisone 10 mg/kg/day) in the pediatric ward. Oral fluids and
soft diet were offered for all children in the first 3 days then regular diet
if tolerated till discharge.
In developing countries;
unintentional or accidental ingestion of caustic substances is relatively
common especially among people with poor socioeconomic status [7-9] while it is
declining in developed countries. According to the
American Association of Poison Control (AAPCC),
household cleaning substances are the second most frequently substance classes
which account for 7.54% of all human exposures .
In developing countries, a large number of cases are underreported and so in
In this review, alkaline
agents were ingested more than acids similar to studies in western countries
bleach or Sodium hypochlorite is largely found
in household bleaching agents. Children may expose to
chlorine bleach accidentally or intentionally, and poisoning related to
chlorine bleach usually results in a benign clinical course [12-15]. Severe
complications due to chlorine bleach were reported in a few studies such as
esophageal stenosis or perforation . In our study, chlorine bleach was the
most common corrosive agent ingested (62.4% children) and had a benign clinical
In this review, initial
endoscopy was performed for all children within 24 hours after ingestion except
in patients who ingested button batteries. Initial endoscopy after 48 h of
ingestion is not advised to avoid the risk of perforation . In this review,
2% of cases developed esophageal stricture. This low rate of esophageal
stricture development may be due to accidental or unintentional ingestion of
diluted and small amount of corrosives. In previous studies; the rates of
esophageal strictures were variable between 2% and 75% [17-19]
unintentional corrosives ingestion was encountered Recent
evidence concluded that acids in comparison to alkalis were more likely to
cause gastric injury (31 vs. 13 %, p =0.042), but similar damage to the
esophagus (14 vs. 12 %, p = 0.98) . In this study, the rates
of esophageal injuries were 28%, 30.4%, 13.6%, 20% in
children who ingested alkalis, acid, button battery and paint thinner
respectively, while gastric injuries were reported just in four children 17.4%
who ingested acids.
In this review, we found that vomiting and drooling
saliva had a significant association with the presence of esophageal injuries,
but oral lesions, abdominal pain, and strider were not. We found that the
presence of three or more symptoms was associated with grade 3 esophageal
injury. This data support the previous data in the literature .
In conclusion, most children ingest corrosives
accidentally or unintentionally. Vomiting was the most common complaint. The
esophageal stricture was developed in 2% of cases which was lower than some
studies. Early clinical and endoscopic evaluation is of great help in improving
the outcome for children with a history of corrosives ingestion.
Hospitalization and endoscopic evaluation for children with a history of
accidental chlorine ingestion are not necessary unless the patient is
symptomatic or there is a suspicion of suicidal attempt.
1 .Gumaste VV, Dave PB. Ingestion of corrosive substances by adults. Am Gastroenterol. 1992;87:1-5.
2 .Watson WA, Litovitz TL, Rodgers GC, Klein-Schwartz W, Reid N, Youniss J, et al. 2004 annual report of the American Association of poison control centers toxic exposure surveillance system. Am J Emerg Med. 2005;23:589-666.
3 .Dantas RO, Mamede RC. Esophageal motility in patients with esophageal caustic injury. Am Gastroentrol. 1996;91:1157-1161.
4 .Mamede RC, de Mello Filho FV. Ingestion of caustic substances and its complication. Soa Paulo Med J. 2001;119:10-15.
5 .Lahoti D, Broor SL. Corrosive injury to the upper gastrointestinal tract. Indian J Gastroenterol. 1993;12:135–41.
6 .Zargar SA, Kochhar R, Metha S, Metha SK. The role of fiberoptic endoscopy in the management of corrosive ingestion and modified endoscopic classification of burns. Gastrointest Endosc. 1991:37:165-169.
7 .Contini S, Swarray-Deen A, Scarpignato C. Oesophageal corrosive injuries in children: a forgotten social and health challenge in developing countries. Bull World Health Organ. 2009;87(12):950–954. doi:10.2471/BLT.08.058065
8 .Christesen HB. Epidemiology and prevention of caustic ingestion in children. ActaPaediatr. 1994; 83(2): 212-215.
9 .World Health Organization. Strengthening poison prevention and treatment programme. 1999. Kathmandu, Nepal. World Health Organization.
10 .Gummin DD, Mowry JB, Spyker DA, Brooks DE, Fraser MO, Banner W. 2016 Annual Report of the American Association of Poison Control Centers’ National Poison Data System (NPDS): 34th Annual Report. Clinical Toxicology, 55:10, 1072-1254,
11 .Lakshmi CP, Vijayahari R, Kate V, Ananthakrishnan N. A hospital-based epidemiological study of corrosive alimentary injuries with particular reference to the Indian experience. Natl Med J India. 2013;26:31-36.
12 .Park JS, Min JH, Kim H, Lee SW. Esophageal perforation and mediastinitis after suicidal ingestion of 4.5% sodium hydrochlorite bleach. Clin Toxicol 2011;49(8):765-6.
13 .Racioppi F, Daskaleros P, Besbelli N, Borges A, Deraemaeker C, Magalini S, et al. Household bleaches based on sodium hypochlorite: review of acute toxicology and poison control center experience. Food Chem Toxicol 1994;32(9):845- 61.
14 .Ross M, Spiller H. Fatal ingestion of sodium hypochlorite bleach with associated hypernatremia and hyperchloremic metabolic acidosis. Vet Hum Toxicol 1999;41(2):82-6.
15 .Karaman I, Koc O, Karaman A, Erdogan D, Cavusoglu YH, Afsarlar CE et al (2015) Evaluation of 968 children with corrosive substance ingestion. Indian J Crit Care Med 19(12):714–718
16 .Poley JW, Steyerberg EW, Kuipers EJ, Dees J, Hartmans R, Tilanus HW, Siersema PD. Ingestion of acid and alkaline agents: outcome and prognostic value of early upper endoscopy. Gastrointest Endosc. 2004;60:372-377.
17 .Dogan Y, Erkan T, Cokugras FC, Kutlu T. Caustic gastroesophageal lesions in childhood: an analysis of 473 cases. Clin Pediatr (Phila). 2006;45(5):435-8.
18 . Demiroren K, Kocamaz H, Dogan Y. Gastrointestinal system lesions in children due to the ingestion of alkali and acid corrosive substances. Turk J Med Sci. 2015;45(1):184-90.
19 .Mamede RC, de Mello Filho FV. Ingestion of caustic substances and its complications. Sao Paulo Med J. 2001;119(1):10-5.
20 .Ducoudray R, Mariani A, Corte H, Kraemer A, Munoz-Bongrand N, Sarfati E et al. The Damage Pattern to the Gastrointestinal Tract Depends on the Nature of the Ingested Caustic Agent. World J Surg. 2016;40:1638-1644.
21 .Crain EF, Gershel JC, Mezey AP. Caustic Ingestions: Symptoms as Predictors of Esophageal Injury. Am J Dis Child. 1984;138(9):863–865.