Alarming Incidence of Gastric Outlet Obstruction Related to NSAIDS and Synthetic Opioid in North West India.

BACKGROUND: In recent years, there has been an alarming increase in cases of gastric outlet obstruction (GOO) at our center due to drug abuse. So, we conducted this study to know the incidence of nonsteroidal anti-inflammatory drugs (NSAIDs) and synthetic opioid abuse in cases of GOO. METHODS: This was an observational study involving consecutive cases of GOO diagnosed from September 2017 to February 2019. A detailed history, including drug addiction history and clinical examination, was done. Investigations included routine biochemical and hematological tests, upper gastrointestinal endoscopy (UGIE), ultrasonography, rapid urease test (RUT), and histopathology of the diseased area. RESULTS: Among the 102 cases diagnosed with GOO, 62 (60.78%) cases had a history of drug addiction. The drug addiction history was as follows: NSAIDs and opioids in 56, opioids alone in four, and NSAIDs alone in two cases. The most common site of stricture was the second part of the duodenum. The features on histopathology were ulcerations of the mucosa infiltrated by eosinophils, plasma cells, and lymphocytes. CONCLUSION: There is an alarming increase in the incidence of GOO due to NSAIDs and opioid abuse at our center. Efforts should be made to control the indiscriminate use of these over-the-counter drugs to prevent dreaded complications.

Etiological spectrum and response to endoscopic balloon dilation in patients with benign gastric outlet obstruction.

BACKGROUND AND AIMS: Peptic ulcer disease (PUD)-related gastric outlet obstruction (GOO) is known to respond favorably to endoscopic balloon dilation (EBD). However, data on efficacy of EBD for other etiologies of benign GOO are sparse. We aimed to compare the response of EBD among different etiologies of GOO. METHODS: Records of all patients with benign GOO who underwent EBD at our tertiary-care center between January 1998 and December 2017 were analyzed. Dilation was done by using through-the-scope balloons. Procedural and clinical success of EBD was compared among different etiologies. RESULTS: A total of 306 patients were evaluated, of whom 264 (mean [± standard deviation] [SD] age 37.89 ± 17.49 years; men 183, women 81) underwent dilation. Etiologically, caustic ingestion was the commonest cause of GOO (53.8%) followed by PUD (26.1%) and medication-induced (8.3%). Overall procedural and clinical success was achieved in 200 (75.7%) and 243 (92.04%) patients, respectively, requiring a mean (± SD) of 2.55 (2.8) and 5.37 (3.9) sessions, respectively. Caustic-induced GOO responded less favorably, requiring a higher number of dilation sessions and having more refractory strictures than other etiologies. Medication-induced GOO performed worse than PUD-related GOO. Of the 264 patients, 9 (3.4%) had perforations during EBD, 3 had contained leaks and were managed conservatively, and 6 underwent successful surgery. CONCLUSION: EBD is successful in a majority of patients with benign GOO, with caustic-induced GOO and medication-induced GOO being more difficult than PUD-related GOO.

Endoscopic Treatment of Gastric Outlet Obstruction Secondary to Accidental Acid Ingestion in a Child.

Accidental corrosive ingestion is not rare in pediatric patients in developing countries. We report a case of gastric outlet obstruction after the accidental ingestion of an acidic substance by a child who was successfully treated with endoscopic balloon dilatation.

Complications of Long-Term Prostaglandin E1 Use in Newborns With Ductal-Dependent Critical Congenital Heart Disease.

Prostaglandin E1 (PGE1) has been used for decades in the medical treatment of ductal dependent critical congenital heart disease in neonates. The article is a report of a retrospective evaluation of the long-term effects of PGE1 in a neonatal intensive care unit in Saudi Arabia. There were 22 subjects with a wide spectrum of cardiac defects maintained on PGE1 for a mean of 38 days (range: 6-200 days). The majority of the complications included hypokalemia, hypotension, and apnea/bradycardia. Pseudo-Barett syndrome and gastric outlet obstruction were also found. While long-term administration of PGE1 is rare in North America, it is important to be aware of possible adverse effects of fluid and electrolyte imbalance, gastric outlet obstruction, and feeding difficulties.

An unusual presentation of hydrochloric acid ingestion: a mystery unraveled.

BACKGROUND: Unintentional acid ingestion is less commonly encountered than alkali ingestion. The injury develops for hours to days after ingestion and often results in progressively increasing difficulty in airway management. However, gastric perforation is rare. CASE: A 3-year-old boy presented to us with an orotonsillopharyngeal membrane and severe upper airway obstruction. Subsequently, he was diagnosed with a case of gastric perforation due to unintentional hydrochloric acid ingestion. He was treated with partial gastrectomy and feeding jejunostomy, and the recovery was good. CONCLUSIONS: Unintentional hydrochloric acid ingestion is rare in children. The manifestations masquerade many other clinical conditions, and the diagnosis is difficult in cases in which history of ingestion is not available. Treatment is symptomatic, and emergency surgery is indicated in case of gastrointestinal perforation.

Pneumatic pyloric dilatation for the treatment of gastric outlet obstruction in a child.

Acquired causes of gastric outlet obstruction (GOO) are rarely encountered in infancy, having an approximate incidence of 1 per 100,000 live births. Reports of short-term exposure to non-steroidal anti-inflammatory drugs having adverse events are few. We present the case of a previously healthy 3-year-old boy who developed severe chronic gastric outlet obstruction and antral stenosis after a short-term ingestion of liquid ibuprofen at a dosage not thought to be associated with unfavorable effects. Even though the optimal management of these cases remains to be determined, we report on a prompt and successful endoscopic treatment for this condition.

Can computed tomography-antral wall thickness predict response to endoscopic balloon dilation in patients with caustic-induced gastric outlet obstruction?

BACKGROUND: Caustic-induced gastric outlet obstruction (GOO) remains one of the important causes of long-term morbidity in patients with caustic ingestion. Though endoscopic balloon dilation is an effective modality, response to caustic GOO is poorer as compared to peptic stricture. Computed tomography (CT)-antral wall thickness (AWT) has not been previously explored to predict the procedural success in patients with caustic GOO. METHODS: In a retrospective single-center study of prospectively maintained database, all patients with symptomatic caustic GOO who underwent CT scan prior to endoscopic balloon dilation were included. Gastric AWT was measured at the site of maximum visible thickness on CT scan. Details regarding caustic ingestion and endoscopic dilation were retrieved. Patients were divided into two groups, based on CT-AWT (< or ≥9 mm) and compared for outcome measures. RESULTS: Mean age of included patients (n=35) was 33.51 ± 13.65 years and 22 were male. Procedural success was achieved in 29 (82.85%) patients. Number of mean dilation sessions required were 5.28 ± 2.96 for achieving procedural success. The mean CT-AWT was 10.73 ± 2.80 mm (range 4-18 mm). There was no significant association between the CT-AWT and the number of dilations and procedural success. On univariate analysis, size of the first balloon used was a predictor of refractory stricture (p=0.011). However, no other factors predicted either refractory stricture or procedural success. CONCLUSION: There is no additional role of CT-AWT in predicting response to endoscopic balloon dilation or to predict refractory stricture in patients with caustic GOO.

Endoscopic balloon dilation in caustic-induced chronic gastric outlet obstruction.

BACKGROUND: The standard treatment of caustic-induced gastric outlet obstruction (GOO) is surgery. There are only a few reports in the medical literature on endoscopic balloon dilation (EBD) for caustic-induced GOO. OBJECTIVE: To study the short-term and long-term response of EBD in patients with caustic-induced GOO. SETTING: Tertiary-care center in India. DESIGN: Retrospective analysis of data. PATIENTS: Of the 49 patients with caustic-induced GOO seen by us between January 1998 and December 2003, 41 were treated by EBD. Thirty-seven patients had consumed an acid and 4 had consumed an alkali a mean (SD) of 19.5 +/- 14.5 weeks earlier. EBD was performed every 3 weeks by using through-the-scope balloons under endoscopic guidance. INTERVENTION: The balloon was negotiated across the narrowed segment and inflated for 60 seconds by using a pressure gun. Balloons of incremental diameters, up to a maximum of 3 sizes, were used in each sitting. The end point of dilation was 15 mm, after which patients were assessed for recurrence. The patients were observed until August 2007. RESULTS: All 41 patients (23 men; mean [SD] age 29.6 +/- 8.5 years) could be successfully taken for EBD. Thirty-nine patients underwent successful repeated dilations, which required a mean (SD) of 5.8 +/- 2.6 dilations (range 2-13) to achieve the end point of 15 mm. All 39 patients were followed up for an average (SD) of 35.4 +/- 11.1 months (range 18-58 months). The mean (SD) size of the first dilator was 8.2 +/- 0.6 mm (range 8-10 mm). One patient had a perforation and was subjected to antrectomy; another patient had pain every time he received EBD; he also had surgery. Other complications were minor: self-limiting pain (n = 8) or bleeding (n = 7). CONCLUSIONS: EBD is a safe, effective, and long-lasting alternative to surgery for caustic-induced GOO.

Comparative evaluation of nasoenteral feeding and jejunostomy feeding in acute corrosive injury: a retrospective analysis.

BACKGROUND: Nutritional support in corrosive injury patients is traditionally achieved through total parenteral nutrition (TPN) or jejunostomy feeding (JF). There are no reports of nasoenteral tube feeding in patients with corrosive ingestion. OBJECTIVE: We report our experience with nasoenteral tube feeding (NETF) and compare the outcome of these patients with those undergoing JF. SETTING: Tertiary medical center in North India. DESIGN AND INTERVENTION: The records of 53 and 43 patients with severe acute corrosive injury who underwent NETF and JF, respectively, were reviewed. All had received a 50-kcal/kg, 2-g/kg protein homogenized liquid diet for 8 weeks. A contrast study was performed at 8 weeks, and body weight and serum albumin levels were recorded at hospitalization and at 8 weeks. MAIN OUTCOME MEASUREMENTS: Change in weight and serum albumin at 8 weeks and stricture development rate. RESULTS: Strictures developed in 41 (80.39%) and 36 (83.72%) patients in the NETF and JF groups, respectively. Development of esophageal stricture (P = .71) and gastric stenosis (P = .89) was comparable in the 2 groups. No significant changes in serum albumin and weight were noted at 8 weeks in either group. The complication rate was lower in the NETF group compared with the JF group. Although all of the patients in the NETF group had a patent lumen, 5 in the JF group had total obstruction precluding endoscopic intervention. LIMITATIONS: Retrospective study design. CONCLUSION: NETF is as effective as JF in maintaining nutrition in patients with severe corrosive injury. The stricture development rate is similar, but nasoenteral tube placement provides a lumen for dilatation should a tight stricture develop.

Gastric outlet obstruction due to an iatrogenic cause in a neonatal period - report of two cases.

Gastric mucosa hyperplasia is a rare cause of upper gastrointestinal obstruction in the neonatal period. One of the etiologic factors of this disorder is prolonged prostaglandin E1 (PGE1) therapy of neonates with congenital cyanotic heart diseases. Continuous PGE1 administration ensures patency of the ductus arteriosus, which is essential for stabilizing the general condition until cardiac surgery can be performed. The clinical symptoms of gastric mucosa foveolar hyperplasia due to long-term PGE1 therapy simulate hypertrophic pyloric stenosis. However, the characteristic ultrasound appearance of both pathologies facilitates determination of the final diagnosis and further treatment. We present two cases of neonates with gastric mucosa and submucosa hyperplasia revealed during ultrasound examination. The results of the ultrasound examination combined with clinical anamnesis allowed diagnosis of gastric mucosa foveolar hyperplasia due to prolonged PGE1 therapy.

Laparoscopic Diamond Antroduodenostomy for Postcorrosive Pyloric Cicatrization: A Novel Approach.

BACKGROUND: Traditionally, Billroth I procedure or bypass gastrojejunostomy were the recommended approaches for management of postcorrosive complete gastric outlet obstruction (GOO), whereas Heineke Mickulicz pyloroplasty was recommended for moderate mucosal injury with partial cicatrization. In this study, laparoscopic diamond antroduodenostomy was carried out as an alternative minimally invasive approach for cases with pyloric cicatricial obstruction. PATIENTS AND METHODS: Between January and December 2017, children who were referred to Pediatric Surgery Department, Cairo University Hospital, with GOO as a consequence of caustic liquid ingestions were included in this study. Laparoscopic diamond antroduodenostomy was performed for the presented cases. RESULTS: Through the year 2017, 5 cases were approached with laparoscopic diamond antroduodenostomy. Isolated pyloric cicatrization was evident in 4 cases, whereas synchronous insult to thoracic esophagus and pylorus was manifest in the fifth case. Laparoscopic feeding jejunostomy completed the procedure for the case with esophageal stricture. Contrast study-24 hour postoperatively-assured no radiological leaks in the presented cases, where enteral feeding was gradually commenced, and patients discharged home a day later. After a mean follow-up of 13.5 months, neither recurrence of obstructive symptoms nor dumping was displayed. Cosmetic outlook inherent to the minimally invasive approach was appreciated by the parents. CONCLUSION: Laparoscopic diamond antroduodenostomy is a feasible approach for management of postcorrosive pyloric obstruction. It allowed early enteral feeding, with no dumping symptoms, in addition to the fundamental advantages of minimally invasive surgery. A bigger series and longer follow-up is recommended to verify the reported results.

Gastric outlet obstruction after long-term prostaglandin administration mimicking hypertrophic pyloric stenosis.

Prostaglandin E1 (PGE1) is widely used in neonates with cyanotic congenital heart disease who depend on the patency of the ductus arteriosus for oxygenation. Side effects of prostaglandin therapy are common and include respiratory depression, generalized flushing, and cardiovascular and neurological effects. Little is known about the complex effects on the gastrointestinal tract. We report on an infant with gastric outlet obstruction after long-term prostaglandin administration. At the age of 1 month, feeding problems developed with projectile vomiting. Ultrasonography showed progressive elongation of the antropyloric channel without wall thickening, which was causing gastric outlet obstruction. Three days after cardiac surgery and cessation of prostaglandin therapy, the infant fed normally and rapidly gained weight. The clinical signs in such patients can mimic hypertrophic pyloric stenosis. Therefore, the sonographic findings should not be confused with pyloric wall thickening to avoid a false diagnosis and unnecessary surgery. The symptoms diminish with cessation of the prostaglandin therapy after a corrective cardiac operation.

A conscious mouse model of gastric ileus using clinically relevant endpoints.

BACKGROUND: Gastric ileus is an unsolved clinical problem and current treatment is limited to supportive measures. Models of ileus using anesthetized animals, muscle strips or isolated smooth muscle cells do not adequately reproduce the clinical situation. Thus, previous studies using these techniques have not led to a clear understanding of the pathophysiology of ileus. The feasibility of using food intake and fecal output as simple, clinically relevant endpoints for monitoring ileus in a conscious mouse model was evaluated by assessing the severity and time course of various insults known to cause ileus. METHODS: Delayed food intake and fecal output associated with ileus was monitored after intraperitoneal injection of endotoxin, laparotomy with bowel manipulation, thermal injury or cerulein induced acute pancreatitis. The correlation of decreased food intake after endotoxin injection with gastric ileus was validated by measuring gastric emptying. The effect of endotoxin on general activity level and feeding behavior was also determined. Small bowel transit was measured using a phenol red marker. RESULTS: Each insult resulted in a transient and comparable decrease in food intake and fecal output consistent with the clinical picture of ileus. The endpoints were highly sensitive to small changes in low doses of endotoxin, the extent of bowel manipulation, and cerulein dose. The delay in food intake directly correlated with delayed gastric emptying. Changes in general activity and feeding behavior were insufficient to explain decreased food intake. Intestinal transit remained unchanged at the times measured. CONCLUSION: Food intake and fecal output are sensitive markers of gastric dysfunction in four experimental models of ileus. In the mouse, delayed gastric emptying appears to be the major cause of the anorexic effect associated with ileus. Gastric dysfunction is more important than small bowel dysfunction in this model. Recovery of stomach function appears to be simultaneous to colonic recovery.

Corrosive-induced gastric outlet obstruction without oesphageal involvement: a case report.

BACKGROUND: The objective of this paper is to report an unusual case of isolated gastric outlet obstruction following corrosive ingestion. METHOD: A case report of a 28-year old female seen by the authors. The literature on gastric outlet obstruction following ingestion of corrosives is reviewed briefly. RESULTS: Features of worsening gastric outlet obstruction were found in this 28-year old female five months after ingestion of hydrochloric acid. There was an antecedent history of depressive illness. The upper gastrointestinal barium contrast radiographs showed a normal oesophagus and proximal stomach. The distal stomach was however scarred, contracted with severe antropyloric stenosis. She underwent nutritional rehabilitation with high protein diet and made an uneventful recovery after a gastrojejunostomy. CONCLUSION: This case suggests a relative resistance of the oesophagus to corrosive acids as reported in the literature. The stomach, however, is more susceptible to acids causing burns with subsequent cicatrisation around the antrum and pylorus.

Gastrointestinal system lesions in children due to the ingestion of alkali and acid corrosive substances.

BACKGROUND/AIM: TO examine esophageal and gastric lesions in children due to the ingestion of alkali and acid corrosive substances and to emphasize all related complications. MATERIALS AND METHODS: The reports of 103 children who ingested or were suspected to have ingested corrosive substances and who then underwent upper gastrointestinal endoscopic inspections were evaluated retrospectively. RESULTS: Of the patients, the mean age was 41 ± 3.6 months, and 57.3% were male. Vomiting was the most common symptom (44.7%). Eighteen different commercial products were defined as corrosive substances: 59.2% of them were alkali, 39.8% were acids, and 1% had a neutral pH. These corrosive agents most frequently contained sodium hydroxide, followed by hydrochloric acid, sodium hypochlorite, and sulfuric acid. Endoscopic inspections were abnormal in 68% of the cases. Esophageal lesions were observed in 56.3% of the patients, while gastric lesions were observed in 35%. During the follow-up period, esophageal strictures developed in 4.9% of patients, while gastric outlet obstructions developed in 1%. CONCLUSION: Of the patients, the mean age was 41 ± 3.6 months, and 57.3% were male. Vomiting was the most common symptom (44.7%). Eighteen different commercial products were defined as corrosive substances: 59.2% of them were alkali, 39.8% were acids, and 1% had a neutral pH. These corrosive agents most frequently contained sodium hydroxide, followed by hydrochloric acid, sodium hypochlorite, and sulfuric acid. Endoscopic inspections were abnormal in 68% of the cases. Esophageal lesions were observed in 56.3% of the patients, while gastric lesions were observed in 35%. During the follow-up period, esophageal strictures developed in 4.9% of patients, while gastric outlet obstructions developed in 1%.

Corrosive-induced gastric outlet obstruction.

Ten patients with gastric scarring and an outlet obstruction secondary to ingestion of corrosive substances were referred to our department for surgical management, between May 1999 and April 2003. Hydrochloric acid was the most common corrosive ingested (4 cases), although many were not aware of the nature of the ingested substance. An associated esophageal stricture was present in 5 cases (50%). All the patients initially underwent feeding jejunostomy, with definitive surgery performed at a later date. A partial gastrectomy was found to be the most satisfactory procedure, and was performed in 90% of the cases (9 patients).

Surgical management of corrosive strictures of stomach.

BACKGROUND: Corrosive injuries of the upper aero-digestive tract are a frequent cause of morbidity in India. We report here our institution's experience in managing patients with corrosive strictures of the stomach. METHODS: Records of 28 patients who underwent definitive surgery for corrosive strictures of the stomach in our institution over a 15-year period were reviewed. RESULTS: The main presenting complaints were vomiting (75%), dysphagia (46%) and significant weight loss (100%). Pre-operative evaluation included barium and endoscopic studies. Most patients had antro-pyloric strictures (n=22); in 6 patients, however, near-total or total gastric involvement was observed. Thirteen (46%) patients had associated strictures of the esophagus; of these, 7 responded to esophageal dilation. Strictures of the stomach were managed with resectional procedures like distal gastrectomy (n=16), subtotal gastrectomy (1) or total gastrectomy (3) and esophagogastrectomy (1) in 21 (75%) patients. The remaining 7 patients underwent bypass procedures like gastrojejunostomy (5), stricturoplasty (1), and colonic bypass of esophagus and stomach (1). Three patients had entero-cutaneous fistulae in the postoperative period. One patient died in hospital of septicemia and malnutrition. CONCLUSIONS: In patients with corrosive strictures of the stomach, surgery, tailored according to the extent of gastric involvement and presence of associated esophageal strictures, gives excellent results.

Predicting the progress of caustic injury to complicated gastric outlet obstruction and esophageal stricture, using modified endoscopic mucosal injury grading scale.

Severe caustic injury to the gastrointestinal tract carries a high risk of luminal strictures. The aim of this retrospective study was to identify predicting factors for progress of caustic injury to gastric outlet obstruction (GOO) and esophageal strictures (ES), using modified endoscopic mucosal injury grading scale. We retrospectively reviewed medical records of patients with caustic injuries to the gastrointestinal tract in our hospital in the past 7 years. We enrolled 108 patients (49 male, 59 female, mean age 50.1 years, range 18-86) after applying strict exclusion criteria. All patients received early upper gastrointestinal endoscopy within 24 hours of ingestion. Grade III stomach injuries were found in 58 patients (53.7%); 43 (39.8%) esophageal, and 13 (12%) duodenal. Of the 108 patients, 10 (9.3%) died during the acute stage. Age over 60 years (OR 4.725, P = 0.029) was an independent risk factor of mortality for patients after corrosive injury. Among the 98 survivors, 36 developed luminal strictures (37.1%): ES in 18 patients (18.6%), GOO in 7 (7.2%), and both ES and GOO in 11 (11.3%). Grade III esophageal (OR 3.079, P = 0.039) or stomach (OR 18.972, P = 0.007) injuries were independent risk factors for obstructions. Age ≥ 60 years was the independent risk factor for mortality after corrosive injury of GI tract. Grade III injury of esophagus was the independent risk factor for development of ES. Grade III injury of stomach was the independent risk factor for development of GOO.