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Journal of Indian Association of Pediatric Surgeons
     Journal of Indian Association of Pediatric Surgeons
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CASE REPORT
Year : 2007  |  Volume : 12  |  Issue : 1  |  Page : 47-49
 

Gastric outlet obstruction without esophageal involvement: A late sequelae of acid ingestion in children


Department of Ped. Surgery, SMS Medical College, & SPMCHI, Jaipur, India

Correspondence Address:
Shyam Sharma
M-30, Income Tax Colony, Tonk Road, Jaipur - 302 018
India
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/0971-9261.31094

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   Abstract 

Accidental corrosive ingestion is not a rare occurrence in children because of easy access to strong household cleansers. Gastric injury as a predominant finding following acid ingestion in pediatric age group is less widely known with a few cases being reported in Indian literature. We report two such cases of gastric outlet obstruction following accidental ingestion of dilute acid. Both children have typical clinical presentation just 4-6 weeks after the ingestion. Upper GI endoscopy and barium meal studies confirmed the diagnosis. Early surgical intervention resulted in a satisfactory recovery. Both patients are doing well on follow up.


Keywords: Acid Ingestion, gastric outlet obstruction


How to cite this article:
Sharma S, Debnath P R, Agrawal L D, Gupta V. Gastric outlet obstruction without esophageal involvement: A late sequelae of acid ingestion in children. J Indian Assoc Pediatr Surg 2007;12:47-9

How to cite this URL:
Sharma S, Debnath P R, Agrawal L D, Gupta V. Gastric outlet obstruction without esophageal involvement: A late sequelae of acid ingestion in children. J Indian Assoc Pediatr Surg [serial online] 2007 [cited 2019 May 24];12:47-9. Available from: http://www.jiaps.com/text.asp?2007/12/1/47/31094



   Introduction Top


Corrosive injury to stomach without esophageal involvement is rare entity in children. A review of recent literature suggests that acid and alkali ingestion should no longer be considered collectively as corrosive injury due to a significant dissimilarity in their mode of action, site of injury, sequelae, early, and late management.[1] The ingestion of alkali primarily results in oropharyngeal and esophageal injury whereas acids tend to spare the esophagus and primarily results in gastric injury.[1],[2],[3],[4] Absence of overt clinical and radiological signs at the time of acid ingestion usually results in a delayed diagnosis in such cases.[1],[2] Upper GI endoscopy thus remains the diagnostic modality of choice and is also useful in planning the time and the type of surgical intervention, which remains the treatment of choice in such children.[5],[6],[7] To the best of our knowledge, corrosive pyloric obstruction in children has been discussed rarely in Indian literature till date. Thus, we report to such cases with the aim to highlight the role of early upper GI evaluation and surgical intervention in the management of such children with acid ingestion.


   Case reports Top


Case 1

A 3-year-old boy was referred with complaint of persistent vomiting for the last 4 days. The vomiting used to occur 12-18 hour after taking meal and vomitus contained foul smelling undigested meal. There was a history of accidental ingestion of H 2 So 4 on full stomach by the child 40 days ago, when child had symptoms of increased salivation, vomiting, decreased oral intake, and abdominal pain. Patient was managed conservatively at a primary health center and was discharged after 7 days. Patient remained asymptomatic during the intervening period except for anorexia and weight loss noticed by the parents. On physical examination, patient was mildly dehydrated, poorly nourished, with a normal vital signs and mild anemia. Oropharyngeal, abdominal, and chest examination revealed no abnormality. Laboratory investigations revealed Hb of 9 gm%, TLC 6000 mm 3sub , serum albumin 3 gm%, mild hypokalemia and a normal coagulation profile. Upper GI endoscopy suggested pyloric stenosis with a normal esophagus [Figure - 1]. Patient was taken up for surgery after initial resuscitation aimed at the correction of fluid and electrolyte imbalance, nutritional support, antibiotic prophylaxis, and gastric lavage. Laparotomy revealed adhesions in the region of pylorus and pyloric antrum, a contracted and firm pylorus and distal pyloric antrum. The rest of the stomach was dilated and normal in consistency. There was partial obliteration of pyloric lumen with the presence of viable mucosa.  Heineke-Mikulicz pyloroplasty More Details was performed. Post-operatively, the recovery was uneventful. After eighth post-operative day, the patient started accepting orally and is doing well on follow up for the last 4 months.

Case 2

A 5-year-old girl presented with foul smelling vomitus of ingested food taken 12-18 hours before and decreased oral intake for the last 3 days. There was a history of accidental ingestion of dilute H 2 So 4 (battery fluid) 6 weeks back when patient got treatment from a local hospital and remained asymptomatic thereafter. On examination, patient appeared to be mildly dehydrated, moderately nourished, hemodynamically stable, and clinically anemic. Oropharyngeal, abdominal, and chest examination revealed no abnormality. On laboratory investigation, patient had Hb of 8 gm%, TLC 8000 mm 3sub , mild hypokalemia, albumin of 3 gm% and a normal liver function test. Chest X-ray revealed no abnormality. Barium studies of upper GI tract revealed gastric outlet obstruction with a normal esophagus [Figure - 2]. Upper GI endoscopy revealed stenosis in the region of pylorus and pyloric antrum. After pre-operative preparation patient was taken up for laparotomy. Intra-operative findings revealed fibrosis and contraction of pylorus and distal pyloric antrum. Rest of the stomach was dilated and normal in consistency. Duodenum and small gut were normal. Heineke-Mikulicz pyloroplasty was performed. Post-operative period remained uneventful and patient was discharged in a satisfactory condition. For the last 8 months, she is asymptomatic and gaining weight.


   Discussion Top


In 1828, Robert reported the first case of corrosive induced pyloric stenosis,[1] Ciftci et al . reported gastric outlet obstruction in 5% of cases following corrosive ingestion.[8] Gastric outlet obstruction is more common following acid ingestion although an incidence of 20% has been reported following ingestion of alkalis.[1]

Acids being commonly available in household items as toilet cleaners (sulfuric acid (H 2 So 4 ), hydrochloric acid (HCl)), antirust compounds (oxalic acid (H 2 C 2 O 4 ), HCl), battery fluid (sulfuric acid (H 2 So 4 )), etc. makes them easily accessible to the kids, thus resulting in high incidence of accidental ingestion by children.[1],[3] The clinical manifestations and thus the surgical implications of acid ingestion depends upon several factors including the surrounding circumstances, alike the nature, quantity and concentration of the agent, physical state, duration of exposures and post-prandial state of the child patient.[3] Due to contact burns and bitter taste, concentrated acids are usually vomited out thereby producing a little damage to esophagus and stomach.[2] Gastric injuries usually follows ingestion of dilute acids.[1] Once ingested the acids due to low viscosity and low specific gravity have a rapid transit which results in a superficial action on the resistant squamous epithelium of the esophagus.[1],[2],[8] The resulting pylorospasm induced by the presence of acid in stomach results in a maximum damage to pylorus and pyloric antrum.[3] A diffuse injury results following its ingestion in empty stomach.

The pathological changes vary widely. Grossly, stomach appears to be firm, contracted, and nodular. The lumen may be completely obliterated. In most of the cases, the only change is scarring of the pyloric antrum or the pyloric ring with surrounding adhesions. Microscopically, the acute phase is characterized by edema, inflammation, and thromosis of sub-mucosal vessels resulting in local necrosis and gangrene. Early reparative phase follows by the end of 1st week and is characterized by chronic inflammatory cell infiltration. Scar formation usually start from third week and is completed by sixth week.[1] The resulting fibrosis and adhesions formation during this phase results in obliteration of the lumen thus resulting in the characteristic manifestation of gastric outlet obstruction. More diffuse injury with resulting fibrosis and destruction of nerve plexus results in squamous metaplasia and altered motility of the stomach.[1]

Clinically patients presents with severe local burning of lips, mouth, and pharynx immediately following the ingestion.[1],[2] Nausea, vomiting, anorexia, and hematemesis usually continue for 24-48 hrs.[1],[2],[3],[8],[9] Patient usually responds to conservative treatment in the acute phase, although anorexia persists for one to two weeks. After a latent period of 4-6 weeks, patient again presents with complaints of persistent vomiting, early satiety and post-prandial fullness.[1],[2],[8],[10] Vomiting, rapid loss of weight, and decreased oral intake remain the most notable features in children. The latent period of even 5-6 years has been reported in literature.[1]

Evaluation of upper GI tract by endoscopy confirms the diagnosis, the extent and the severity of injury.[3],[5] Upper GI contrast studies too remains a useful diagnostic tool in patients with associated esophageal stricture.[9] Early surgical intervention remains the treatment of choice with the aim to restore normal passage for food from stomach to small intestine. The type of surgery depends upon the patient's character, ability, and judgment of the surgeon and above all, the findings at laparotomy.[1] As experienced in the present case partial obstruction with moderate mucosal injury usually responds to pyloroplasty. A number of complication reported with gastrojejunostomy makes partial gastrectomy with Billroth I reconstruction remains the procedure of choice in patients with complete luminal obstruction, deep ulceration, eschar formation, and non-viable mucosa.[6],[7] A recent review of literature suggests that endoscopic balloon dilatation with or without intra-lesional steroid injection proves to be useful in a few cases but the long-term results are still awaited.[3],[11]

In present cases, both patients presented with typical, clinical manifestations of gastric outlet obstruction, and had a normal esophagus on upper GI endoscopy and contrast studies. An early surgical intervention resulted in a satisfactory recovery in both the cases thus avoiding the repeated attempts at endoscopic dilatation, which is usually not feasible in developing countries like ours due to scarcity of resources, facilities and the low socio-economic status.

As antral-pyloric strictures and gastric outlet obstruction develops even in the absence of overt clinical and radiological signs of potentially severe upper GI tract pathology we recommend a thorough upper GI endoscopic evaluation in all children with acid ingestion with the aim to have satisfactory recovery by early surgical intervention.

 
   References Top

1.Howard KG, Holmes CL. Pyloric stenosis caused by ingestion of corrosive substances: Report of case. Surg Clin North Am 1948;28:1041-56.  Back to cited text no. 1    
2.Alastair J, Millar, Sidney C. Caustic stricture of the esophagus. O'-Neill Jr, et al , editors. Pediatric surgery. 5th ed. Mosby: St. Louis, Baltimore; 1998. p. 969-79.  Back to cited text no. 2    
3.Treem WR, Long WR, Friedman D, Watkins JB. Successful management of an acquired gastric outlet obstruction with endoscopic guided balloon dilatation. J Pediatr Gastroenterol Nutr 1987;6:992-6.   Back to cited text no. 3    
4.Zamir O, Hod G, Lemau OZ, Mogle P, Nissan S. Corrosive injury to the stomach due to acid ingestion. Am Surg 1985;51:170-2.  Back to cited text no. 4    
5.Lowe JE, Graham DY, Boisaubin EV Jr, Lanza FL. Corrosive injury to stomach: The natural history and role of fibro optic endoscopy. Am J Surg 1979;137:803-6.   Back to cited text no. 5    
6.Tekant G, Eroglu E, Erdogan E, Yesildag E, Emir H, Buyukunal C, et al . Corrosive injury induces gastric outlet obstruction: A changing spectrum of agents and treatment. J Pediatr Surg 2001;36:1004-7.  Back to cited text no. 6    
7.Subbarao KS, Kakar AK, Chandrasekhar V, Ananthakrishnan N, Banerjee A. Cicatrical gastric stenosis caused by corrosive ingestion. ANZ J Surg 1988;58:143-6.  Back to cited text no. 7    
8.Ciftci AO, Senocak ME, Buyukpamukcu N, Hicsonmez A. Gastric outlet obstruction due to corrosive ingestion: Incidence and outcome. Pediatr Surg Int 1999;15:88-91.  Back to cited text no. 8    
9.Beg MH, Reyazuddin, Ansari MM. Corrosive pyloric obstruction without oesophageal involvement in children-a report of two cases. Ann Trop Pediatr 1990;10:223-5.  Back to cited text no. 9    
10.Maull KI, Scher LA, Greenfileld LJ. Surgical implications of acid ingestion. Surg Gynecol Obstet 1979;148:895-8.   Back to cited text no. 10    
11.Kochhar R, Sriram PV, Ray JD, Kumar S, Nagi B, Singh K. Intralesional steroid injection for corrosive induced pyloric stenosis. Endoscopy 1998;30:734-6.  Back to cited text no. 11    


    Figures

[Figure - 1], [Figure - 2]


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