Caustic Injury of Upper Gastrointestinal Tract: 20 Year Experience at a Tertiary Referral Center

Hye-Kyung Song; Ki-Nam Shim; Hye-Won Yun; Chung Hyun Tae; Seong-Eun Kim; Hye-Kyung Jung; Sung-Ae Jung; Kwon Yoo

doi:10.4166/kjg.2015.65.1.12

Journal List > Korean J Gastroenterol > v.65(1) > 1007337

Go to TopGo to Top Go to BottomGo to Bottom

TOOLS

Song, Shim, Yun, Tae, Kim, Jung, Jung, and Yoo: Caustic Injury of Upper Gastrointestinal Tract: 20 Year Experience at a Tertiary Referral Center

Original Article

Korean J Gastroenterol 2015;65(1):12-20.

Published online: 4 October 2015

DOI: https://doi.org/10.4166/kjg.2015.65.1.12

Caustic Injury of Upper Gastrointestinal Tract: 20 Year Experience at a Tertiary Referral Center

Hye-Kyung Song, Ki-Nam Shim¹, Hye-Won Yun¹, Chung Hyun Tae¹, Seong-Eun Kim¹, Hye-Kyung Jung¹, Sung-Ae Jung¹, Kwon Yoo¹

Department of Health Promotion Medicine, Ewha Womans University Medical Center Mokdong Hospital, Seoul, Korea

¹Department of Internal Medicine, Ewha Medical Research Institute, Ewha Womans University School of Medicine, Seoul, Korea

Correspondence to: Ki-Nam Shim, Department of Internal Medicine, Ewha Womans University School of Medicine, 1071, Anyangcheon-ro, Yangcheon-gu, Seoul 158-710, Korea. Tel: +82-2-2650-2632, Fax: +82-2655-2076, E-mail: shimkn@ewha.ac.kr

Received 10 October 20141 November 2014 Accepted 17 November 2014

This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/3.0/) which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.

Abstract

Background/Aims

Caustic ingestion can cause severe injury to upper gastrointestinal tract. There were few studies about clinical characteristics and treatments of caustic injury in Korea. We investigated the changes in clinical features of caustic injury over the past 20 years including pattern of endoscopic mucosal injury and treatment modality.

Methods

This study was a retrospective review of medical records from patients with caustic injury from September 1993 through December 2012. Patients were classified into two groups based on the year when caustic ingestion occurred: patients who visited the hospital from 1993 to 2002 (early group) and patients who visited the hospital from 2003 to 2012 (late group).

Results

A total 140 patients were included (early group [n=50] vs. late group [n=90]). Annual number of caustic ingestions did not show decreasing tendency over the past 20 years. Alkali ingestion increased (20.0% vs. 65.6%, p<0.001) and cases with more than grade 2b of esophageal mucosal injury decreased (41.3% vs. 20.7%, p=0.012) in late group. There were no differences between two groups in sex, age, proportion of accidental ingestion, and systemic/gastrointestinal complications. Use of gastric lavage (p<0.01) and broad spectrum antibiotics (p=0.03) decreased in late group. However, there was no difference in use of steroid between two groups.

Conclusions

In this study, overall caustic ingestion did not decrease and ingestion of alkali agents increased over the past 20 years. Tighter legislation on caustic agents is required and we need to be alert to the best management of caustic injury.

Keywords: Caustics, Gastrointestinal tract, Clinical features

References

1. Ramasamy K, Gumaste VV. Corrosive ingestion in adults. J Clin Gastroenterol. 2003; 37:119–124.

2. Goldman LP, Weigert JM. Corrosive substance ingestion: a review. Am J Gastroenterol. 1984; 79:85–90.

3. Cello JP, Fogel RP, Boland CR. Liquid caustic ingestion. Spectrum of injury. Arch Intern Med. 1980; 140:501–504.

4. Wasserman RL, Ginsburg CM. Caustic substance injuries. J Pediatr. 1985; 107:169–174.

5. Bautista Casasnovas A, Estevez Martinez E, Varela Cives R, Villanueva Jeremias A, Tojo Sierra R, Cadranel S. A retrospective analysis of ingestion of caustic substances by children. Ten-year statistics in Galicia. Eur J Pediatr. 1997; 156:410–414.

6. Arévalo-Silva C, Eliashar R, Wohlgelernter J, Elidan J, Gross M. Ingestion of caustic substances: a 15-year experience. Laryngo-scope. 2006; 116:1422–1426.

7. Nuutinen M, Uhari M, Karvali T, Kouvalainen K. Consequences of caustic ingestions in children. Acta Paediatr. 1994; 83:1200–1205.

8. Poley JW, Steyerberg EW, Kuipers EJ, et al. Ingestion of acid and alkaline agents: outcome and prognostic value of early upper endoscopy. Gastrointest Endosc. 2004; 60:372–377.

9. Ertekin C, Alimoglu O, Akyildiz H, Guloglu R, Taviloglu K. The results of caustic ingestions. Hepatogastroenterology. 2004; 51:1397–1400.

10. Zargar SA, Kochhar R, Nagi B, Mehta S, Mehta SK. Ingestion of strong corrosive alkalis: spectrum of injury to upper gastrointestinal tract and natural history. Am J Gastroenterol. 1992; 87:337–341.

11. 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; 97:702–707.

12. Zargar SA, Kochhar R, Mehta S, Mehta SK. The role of fiberoptic endoscopy in the management of corrosive ingestion and modi-fied endoscopic classification of burns. Gastrointest Endosc. 1991; 37:165–169.

13. Cheng HT, Cheng CL, Lin CH, et al. Caustic ingestion in adults: the role of endoscopic classification in predicting outcome. BMC Gastroenterol. 2008; 8:31.

14. Salzman M, O'Malley RN. Updates on the evaluation and management of caustic exposures. Emerg Med Clin North Am. 2007; 25:459–476.

15. Chibishev A, Pereska Z, Chibisheva V, Simonovska N. Corrosive poisonings in adults. Mater Sociomed. 2012; 24:125–130.

16. Rao RB, Hoffman RS. Caustics and batteries. Goldfrank LR, Norwalk CT, editors. Goldfrank's toxicologic emergencies. 6th ed.Norwalk: Appleton & Lange;1998. p. 1399–1428.

17. Contini S, Scarpignato C. Caustic injury of the upper gastrointestinal tract: a comprehensive review. World J Gastroenterol. 2013; 19:3918–3930.

18. Pelclová D, Navrátil T. Do corticosteroids prevent oesophageal stricture after corrosive ingestion? Toxicol Rev. 2005; 24:125–129.

19. Yeom HJ, Shim KN, Kim SE, et al. Clinical characteristics and pre-disposing factors for complication of caustic injury of the upper digestive tract. Korean J Med. 2006; 70:371–377.

20. Yoon KW, Park MH, Park GS, et al. A clinical study on the upper gastrointestinal tract injury caused by corrosive agent. Korean J Gastrointest Endosc. 2001; 23:82–87.

21. Kim YS, Choi SM, Kim HM, Youn CS, Park KN. The clinical characteristics and risk factors of upper digestive lesions that are due to ingestion of caustic material. J Korean Soc Clin Toxicol. 2009; 7:113–120.

22. Gumaste VV, Dave PB. Ingestion of corrosive substances by adults. Am J Gastroenterol. 1992; 87:1–5.

23. Satar S, Topal M, Kozaci N. Ingestion of caustic substances by adults. Am J Ther. 2004; 11:258–261.

24. Kay M, Wyllie R. Caustic ingestions in children. Curr Opin Pediatr. 2009; 21:651–654.

25. Khi W, Kim JS, Baek KJ, et al. A retrospective review of patients who ingested liquid household bleach containing sodium hypochlorite. J Korean Soc Emerg Med. 2005; 16:298–303.

26. Kim GB, Cheon YJ, Choi YH. Is the emergent endoscopy necessary for the patients who ingested liquid household bleach containing sodium hypochlorite? J Korean Soc Emerg Med. 2006; 17:351–356.

27. Wason S. The emergency management of caustic ingestions. J Emerg Med. 1985; 2:175–182.

28. Watson WA, Litovitz TL, Rodgers GC Jr, et al. 2002 annual report of the American Association of Poison Control Centers Toxic Exposure Surveillance System. Am J Emerg Med. 2003; 21:353–421.

29. Racioppi F, Daskaleros PA, Besbelli N, et al. Household bleaches based on sodium hypochlorite: review of acute toxicology and poison control center experience. Food Chem Toxicol. 1994; 32:845–861.

30. Trabelsi M, Loukhil M, Boukthir S, Hammami A, Bennaceur B. Accidental ingestion of caustics in Tunisian children. Report of 125 cases. Pediatrie. 1990; 45:801–805.

31. Ross MP, Spiller HA. Fatal ingestion of sodium hypochlorite bleach with associated hypernatremia and hyperchloremic met-abolic acidosis. Vet Hum Toxicol. 1999; 41:82–86.

32. Park JS, Min JH, Kim H, Lee SW. Esophageal perforation and me-diastinitis after suicidal ingestion of 4.5% sodium hypochlorite [correction of hydrochlorite] bleach. Clin Toxicol (Phila). 2011; 49:765–766.

33. de Jong AL, Macdonald R, Ein S, Forte V, Turner A. Corrosive esophagitis in children: a 30-year review. Int J Pediatr Otorhinolaryngol. 2001; 57:203–211.

34. Penner GE. Acid ingestion: toxicology and treatment. Ann Emerg Med. 1980; 9:374–379.

35. Peter M, Loeb-Abram M. Caustic injury to the upper gastrointestinal tract. Sleisenger MH, Fordtran JS, Feldman M, Scharschmidt B, editors. Sleisenger & Fordtran's gastroincestinal and liver disease. 6th ed.Eisenstein: W.B. Saunders;1998. p. 335–342.

36. Heyerdahl F, Hovda KE, Bjornaas MA, et al. Pre-hospital treatment of acute poisonings in Oslo. BMC Emerg Med. 2008; 8:15.

37. Krey H. On the treatment of corrosive lesions in the oesophagus; an experimental study. Acta Otolaryngol Suppl. 1952; 102:1–49.

38. Boukthir S, Fetni I, Mrad SM, Mongalgi MA, Debbabi A, Barsaoui S. High doses of steroids in the management of caustic esophageal burns in children. Arch Pediatr. 2004; 11:13–17.

39. Gün F, Abbasoğ lu L, Celik A, Salman ET. Early and late term management in caustic ingestion in children: a 16-year experience. Acta Chir Belg. 2007; 107:49–52.

40. Riffat F, Cheng A. Pediatric caustic ingestion: 50 consecutive cases and a review of the literature. Dis Esophagus. 2009; 22:89–94.

41. Anderson KD, Rouse TM, Randolph JG. A controlled trial of corticosteroids in children with corrosive injury of the esophagus. N Engl J Med. 1990; 323:637–640.

42. Fulton JA, Hoffman RS. Steroids in second degree caustic burns of the esophagus: a systematic pooled analysis of fifty years of human data: 1956–2006. Clin Toxicol (Phila). 2007; 45:402–408.

43. Oh BJ, Kim W, Cho GC, et al. Research on poisoning data collection using toxic exposure surveillance system: retrospective preliminary survey. J Korean Soc Clin Toxicol. 2006; 4:32–43.

44. Mills LJ, Estrera AS, Platt MR. Avoidance of esophageal stricture following severe caustic burns by the use of an intraluminal stent. Ann Thorac Surg. 1979; 28:60–65.

Fig. 1.

Trend of caustic ingestion. Annual number of caustic ingestions didn't decrease and alkali ingestion significantly increased over the past 20 years (Linear-by-linear association; Acid, p=0.312; Alkali, p=0.017; Total N, p=0.213).

Table 1.

Clinical Characteristics of Patients

Characteristic	Total (n=140)	Early group (n=50)	Late group (n=90)	p-value
Age (yr)	43.7±17.4	43.6±15.8	43.8±18.2	0.959
Gender				0.898
Male	57 (40.7)	20 (40.0)	37 (41.1)
Female	83 (59.3)	30 (60.0)	53 (58.9)
Co-morbidity	48 (34.3)	15 (30)	33 (36.7)	0.426
Diabetes mellitus	7 (5.0)	2 (4.0)	5 (5.6)
Hypertension	7 (5.0)	4 (8.0)	3 (3.3)
Depression	19 (13.6)	4 (8.0)	15 (16.7)
Other psychiatric disorder ^a	12 (8.7)	5 (10.0)	7 (7.8)
Etc. ^b	3 (2.1)	0.0 (0.0)	3 (3.3)
Purpose of caustic ingestion (suicide/accident/unknown)	96/42/2	32/18/0	64/24/2	0.381
	(68.6/30.0/1.4)	(64/36/0)	(71.1/26.7/2.2)
Caustic agents (acid/alkali)	70/70 (50/50)	40/10 (80/20)	30/60 (33.3/66.7)	<0.001

Values are presented as mean±SD or n (%).

Early group, the years of diagnosis 1993–2002; Late group, the years of diagnosis 2003–2012.

^a Schizophrenia, atypical psychosis, adjustment disorder, dementia, alcoholism;

^b stroke, liver cirrhosis, chronic nephritis.

Table 2.

Changes of Caustic Agents according to Purpose

Caustic agent	Total (n=140)		Suicide (n=96)		Accident (n=42)
Caustic agent	Early group (n=50)	Late group (n=90)	Early group (n=32)	Late group (n=64) ^a	Early group (n=18)	Late group (n=24) ^a
Acid	40 (80.0)	30 (33.3)	23 (71.9)	24 (37.5)	17 (94.4)	6 (25.0)
Glacial acetic acid	21 (42.0)	18 (20.0)	10 (31.2)	14 (21.9)	11 (61.1)	4 (16.7)
Hydrochloric acid	13 (26.0)	9 (10.0)	10 (31.2)	8 (12.5)	3 (16.7)	1 (4.2)
Acid etc.	6 (12.0)	3 (3.3)	3 (9.4)	2 (3.1)	3 (16.7)	1 (4.2)
Alkali	10 (20.0)	60 (66.7)	9 (28.1)	40 (62.5)	1 (5.6)	18 (75.0)
Rox	4 (8.0)	37 (41.1)	3 (9.4)	27 (42.2)	1 (5.6)	10 (41.7)
Lye	5 (10.0)	5 (5.6)	5 (15.6)	3 (4.7)	0 (0)	2 (8.3)
Alkali etc.	1 (2.0)	18 (20.0)	1 (3.1)	10 (15.6)	0 (0)	6 (25.0)

Values are presented as n (%).

Early group, the years of diagnosis 1993–2002; Late group, the years of diagnosis 2003–2012.

Rox, 5% sodium hypochlorite solution; Lye, sodium or potassium hydroxide; Acid etc., hair dye, insecticide, furniture polish; Alkali etc., liquid detergent, cleaner, glue, oxygen bleach (sodium percarbonate), detergent powder, disinfectant.

^a Purpose of ingestion was unknown in two cases with alkali ingestion of late period group.

Table 3.

Changes in Endoscopic Grade of Caustic Injury

Endoscopic grade	Early group (n=46)^a	Late group (n=87)^a p-value
Esophagus		0.012
≤ Grade 2a	27 (58.7)	69 (79.3)
≥ Grade 2b	19 (41.3)	18 (20.7)
Grade 0	2 (4.3)	27 (30.0)
Grade 1	8 (17.4)	20 (21.1)
Grade 2a	17 (37.0)	22 (25.6)
Grade 2b	7 (15.2)	5 (6.7)
Grade 3a	7 (15.2)	4 (4.6)
Grade 3b	5 (10.9)	9 (10.3)
Stomach		0.101
≤ Grade 2a	29 (67.4)	70 (80.5)
≥ Grade 2b	14 (32.6)	17 (19.5)
Grade 0	0 (0)	26 (29.9)
Grade 1	11 (23.9)	24 (27.6)
Grade 2a	18 (39.1)	20 (23.0)
Grade 2b	6 (13.0)	7 (8.0)
Grade 3a	6 (13.0)	4 (4.6)
Grade 3b	2 (4.3)	6 (6.9)
Non-available	3 (6.5)	0 (0)
Duodenum		0.10
≤ Grade 2a	37 (94.9)	84 (92.2)
≥ Grade 2b	2 (5.1)	0 (7.8)
Grade 0	21 (45.7)	70 (80.5)
Grade 1	13 (28.3)	10 (11.5)
Grade 2a	3 (6.5)	3 (3.4)
Grade 2b	1 (2.2)	0 (0)
Grade 3a	0 (0)	0 (0)
Grade 3b	1 (2.2)	0 (0)
Non-available	7 (15.2)	4 (4.6)

Values are presented as n (%).

Early group, the years of diagnosis 1993–2002; Late group, the years of diagnosis 2003–2012.

^a Four patients of early group and three patients of late group did not perform endoscopy.

Table 4.

Changes in Treatment Modality of Caustic Injury

Treatment modality	Early group (n=50)^a	Late group (n=90)^a	p-value
Gastric lavage	7 (14)	2 (2.2)	0.010
NPO ^b	4 (8.7)	27 (31.0)	0.005
Antibiotics ^c	21 (45.7)	23 (26.4)	0.033
Steroid	19 (38)	46 (51.1)	0.159

Values are presented as n (%).

Early group, the years of diagnosis 1993–2002; Late group, the years of diagnosis 2003–2012; NPO, nulla per os (nothing by mouth).

^a Denominator of NPO and antibiotics was patients with endoscopic evaluation (early group, n=46; late group, n=87).

^b Use of NPO in patients with grade 0, 1 of mucosal injury of upper gastrointestinal tract.

^c Use of antibiotics in patients without grade 3 of mucosal injury or suspected perforation of upper gastrointestinal tract.

Table 5.

Complication of Caustic Injury

Complication	Early group (n=50)	Late group (n=90)	p-value
Transfer or voluntarily discharge	17 (34.0)	23 (25.6)	0.331
Hospital stay (day) ^a	14.0 (9.50-20.50)	5.0 (3.00-13.0)	<0.001
ICU admission (day) ^a	11 (22)	21 (23.3)	0.857
	0 (0.0-0.0/0-20)	0 (0.0-0.0/0-22)	0.385
Mortality	0 (0)	3 (3.3)	0.076
Acute complication	6 (12.0)	8 (8.9)	1.000
Stricture	7 (14.0)	9 (10.0)	0.581

Values are presented as n (%), median (interquatile range) or median (interquatile range/range).

Early group, the years of diagnosis 1993–2002; Late group, the years of diagnosis 2003–2012; ICU, intensive care unit.

^a Hospital stay and ICU admission were calculated after exclusion of patients with transfer or voluntary discharge.

Table 6.

Logistic Regression Analysis of the Esophageal Endoscopic Grade for Acute Complication and Stricture

Esophageal endoscopic grade	n (%)	OR ^b (95% CI)	p-value
Acute complication ^a
Grade 0–2a	4/96 (4.2)	1.0
Grade 2b-3a	3/23 (13.0)	2.41 (0.05-12.99)	0.306
Grade 3b	6/14 (42.9)	14.43 (3.21-64.81)	<0.001
Late sequelae-stricture
Grade 0–2a	2/96 (2.1)	1.0
Grade 2b-3a	2/23 (8.7)	1.0
Grade 3b	11/14 (78.6)	129.19 (21.44-778.16)	<0.001

^a One patient with acute complication did not take gastroendoscopy.

^b Adjusted for age and comorbidity.

TOOLS

Similar articles