The Indian Society of Gastroenterology has developed an evidence-based practice guideline for the management of caustic ingestion–related gastrointestinal (GI) injuries. A modified Delphi process was used to arrive at this consensus containing 41 statements. These statements were generated after two rounds of electronic voting, one round of physical meeting, and extensive review of the available literature. The exact prevalence of caustic injury and ingestion in developing countries is not known, though it appears to be of significant magnitude to pose a public health problem. The extent and severity of this preventable injury to the GI tract determine the short and long-term outcomes. Esophagogastroduodenoscopy is the preferred initial approach for the evaluation of injury and contrast-enhanced computed tomography is reserved only for specific situations. Low-grade injuries (Zargar grade ≤ 2a) have shown better outcomes with early oral feeding and discharge from hospital. However, patients with high-grade injury (Zargar grade ≥ 2b) require hospitalization as they are at a higher risk for both short and long-term complications, including luminal narrowing. These strictures can be managed endoscopically or surgically depending on the anatomy and extent of stricture, expertise available and patients’ preferences. Nutritional support all along is crucial for all these patients until nutritional autonomy is established.

Gastric cicatrization is a well recognized late sequela of corrosive gastric injury, but the optimum timing and type of surgery for this complication are still unclear. Over a 7-year period (1988-1994) 33 patients underwent elective surgery for gastric lesions secondary to corrosive ingestion. A total of 18 (53%) patients had an associated esophageal stricture and presented with dysphagia, 15 (41%) patients had features of gastric outlet obstruction, 6 (18%) had diffuse gastric injury, and 28 (82%) had a segmental lesion. A tube jejunostomy was done in 23 (68%) patients to improve nutrition and resulted in a significant increase in weight and in the serum protein level after 8 weeks of tube feeding. Elective surgery was performed 3 to 23 months (average 7 months) after ingestion of the corrosive substance. Gastric resection was done in 20 (59%) patients and gastrojejunostomy (without vagotomy) in 11 (32%); at follow-up the latter group did not exhibit development of a stomal ulcer. In patients with an associated esophageal stricture, endoscopic dilatation was successful in 89% patients and simplified the surgical approach. In conclusion, the success of surgery for corrosive-induced gastric injury depends on selecting the right procedure and intervening at the appropriate time.

Background: The problem of dysphagia in children and adolescents differs from that in adults, and therefore requires special consideration.Methods: Forty-one consecutive children and adolescents 16 years of age or younger (mean, 7.2 years), with benign esophageal strictures were evaluated in a prospective manner over a 7-year period. The most frequent causes of esophageal strictures were caustic ingestion and complications of endoscopic sclerotherapy of esophageal varices. Dilation was done on a weekly basis using bougies and was considered adequate if the esophageal lumen could be dilated to 15 mm diameter (11 mm in children less than 5 years old) with complete relief of dysphagia.Results: Of the 30 patients who could be adequately followed after initial dilation, 16 had corrosive strictures and 14 had strictures due to other causes. Patients with corrosive strictures required a significantly higher number of sessions for adequate initial dilation (7.8 +/- 2.5 sessions vs 1.86 +/- 0.48 sessions; p < 0.01). Patients with corrosive strictures had a higher number of mean symptomatic recurrences per patient month as compared to the noncorrosive stricture group (0.15 +/- 0.01 vs 0.087 +/- 0.03, p < 0.01). Six esophageal perforations occurred during a total of 327 dilation sessions (1.8%); there was one fatality.Conclusions: From our experience, we conclude that benign esophageal strictures in young patients can be treated effectively and with acceptable safety by means of endoscopic dilation.

Percutaneous balloon angioplasty was used to dilate inferior vena cava (IVC) stenosis in 12 patients with Budd Chiari syndrome. There were seven men and five women, aged 32.8 +/- 8.5 years. Angioplasty was performed using balloon 18-20 mm in diameter. In eleven (91.6%) patients, IVC could be successfully dilated. In these eleven patients, the caval diameter at the site of stenosis increased from 2.3 +/- 1.5 to 13.1 +/- 2.8 mm (p < 0.001), the mean IVC pressure decreased from 28.2 +/- 4.1 to 10.5 +/- 3.4 mmHg (p < 0.001) and the gradient across the stenosis decreased from 23.1 +/- 2.2 to 4.2 +/- 1.9 mmHg (p < 0.001). There was appreciable clinical improvement after angioplasty. On a mean followup of 10.8 (3-18) months four (36.4%) patients had restenosis which could be successfully dilated again. These results suggest that balloon dilatation of inferior vena cava stenosis is safe and effective, however, recurrence is common and needs redilatation.

Portal hypertension diffusely affects the gastrointestinal tract. The frequency and profile of distinct colonic mucosal lesions (portal colopathy) and rectal varices (RV; veins > 4 cm above the anal verge) is not well studied. Fifty consecutive patients with portal hypertension (25 with cirrhosis, 10 with noncirrhotic portal fibrosis [NCPF], and 15 with extrahepatic portal vein obstruction [EHPVO]) were assessed clinically and by upper and lower gastrointestinal (GI) endoscopy. Colorectal lesions were seen in 35 (70%) patients, significantly more often in bleeders than in nonbleeders. Rectal varices were detected in 22 (44%) patients; larger and more often seen in EHPVO (80%) than in cirrhosis (28%) and NCPF (30%) (P < .01) patients. Portal colopathy was seen in 26 (52%) patients, with nearly similar frequency in cirrhotics, NCPF, and EHPVO patients. Previous sclerotherapy or presence of gastric varices had little influence on the development of these lesions. An association (P < .01) was, however, seen between the presence of colopathy and portal gastropathy. Overt bleeding was seen in 8% and 4% of patients with RV and colopathy, respectively. In conclusion, our results demonstrate that colorectal lesions are present in about two thirds of patients with portal hypertension. Patients with portal hypertension and lower GI bleeding should be colonoscoped. Patients with extrahepatic portal vein obstruction may in turn benefit from baseline sigmoidoscopic examination to define the presence and size of rectal varices.

Twenty-one patients with corrosive esophageal strictures underwent contrast-enhanced CT of the chest to determine (1) the esophageal wall thickness at the stricture site and (2) its correlation with number of sessions required for adequate dilation. Average esophageal wall thickness was defined as the mean thickness of all four walls at the site of the stricture, whereas the size of the thickest wall was taken as maximal esophageal wall thickness. Average esophageal wall thickness (8.52 +/- 0.61 mm; range, 5.4 to 13.5 mm) and maximal esophageal wall thickness (11.63 +/- 0.83 mm; range, 5.4 to 20 mm) were significantly higher in patients with corrosive esophageal strictures than normal esophageal wall thickness (2.70 +/- 0.04 mm, p < .01). These patients required a mean of 5.70 +/- 1.42 sessions for achieving adequate dilation. Age, sex, grade of dysphagia, and cause and site of the stricture did not influence the number of sessions required for adequate dilation. On multivariate analysis, maximal esophageal wall thickness (p < .01) but not average esophageal wall thickness or stricture length was independently associated with the number of sessions required for adequate dilation. Patients with maximal esophageal wall thickness of 9 mm or more required a significantly higher number of sessions for adequate dilation than did those with wall thickness of less than 9 mm (7.57 +/- 1.80 versus 1.42 +/- 0.27, p < .05).(ABSTRACT TRUNCATED AT 250 WORDS)

Although dilatation is the treatment of choice for most patients with benign oesophageal strictures, there is little information on its efficacy and safety in corrosive oesophageal strictures. Of 123 adults with benign oesophageal strictures treated by endoscopic dilatation, 52 (42.3%) had strictures after corrosive ingestion and 39 (31.7%) had peptic strictures. Treatment was considered adequate if the oesophageal lumen could be dilated to 15 mm and there was complete relief of dysphagia. If dysphagia recurred after adequate initial dilatation, the stricture was dilated again up to 15 mm. Initial dilatation was adequate in 93.6% of patients with corrosive strictures and this success rate was comparable with that of the peptic stricture group (100%, p > 0.05). Long term success after adequate initial dilatation was studied in 36 patients with corrosive strictures (mean follow up 32.36 (17.12) months, range 6-60) and 33 patients with peptic strictures (mean follow up 36.32 (17.9) months, range 6-60). The mean (SEM) number of symptomatic recurrences per patient month during the total follow up period in the corrosive group was significantly higher than that in the peptic group (0.27 (0.04) v 0.07 (0.02), p < 0.001). The recurrence rate in the corrosive group, however, decreased over time, and after 12 months it was significantly (p < 0.001) lower than the recurrence rate in the first six months. After 36 months, the difference in the recurrence rate in the two groups was not significant (p > 0.05). Only nine oesophageal perforations occurred during a total of 1373 dilatation treatments (procedure related incidence 0.66%), and eight of these were in the corrosive stricture group. These patients were managed conservatively and subsequently strictures were dilated adequately in all. Endoscopic dilatation is safe and effective for short and long term relief of dysphagia in patients with corrosive oesophageal strictures.

Abnormalities of the autonomic nervous system function and cholecystokinin release have been described in patients with irritable bowel syndrome. Because the autonomic nervous system and cholecystokinin have an important role in the normal functioning of the gallbladder, we studied gallbladder contraction in response to a meal, using real time ultrasonography in irritable bowel syndrome patients (n = 20) and healthy controls (n =: 15). The following parameters were studied: 1) fasting gallbladder volume, 2) residual volume after maximal contraction and at the end of 2 h, 3) maximum percent of gallbladder emptied, and 4) the time taken for maximal contraction. Fasting gallbladder volume (26.21 +/- 1.81 ml vs. 15.21 +/- 1.63 ml, p < 0.001), and residual volume after maximal contraction (14.2 +/- 1.69 ml vs. 5.86 +/- 0.98 ml, p < 0.001) and at the end of 2 h (18.81 +/- 1.73 ml vs. 11.65 +/- 1.45 ml, p < 0.01) were significantly higher in the patient group, compared with controls. The maximum emptying was less (49.55 +/- 2.75% vs. 63.98 +/- 4.55%, p < 0.01) and the time taken for maximal contraction (59.25 +/- 3.8 min vs. 42.33 +/- 2.04 min, p < 0.001) was longer in the patient group than in the controls. Based on these observations, we conclude that patients with irritable bowel syndrome have significant abnormalities of gallbladder motor function.

Corrosive injury to the UGI tract is a common problem and has a wide spectrum of presentations. Unlike in the West, where lye ingestion is more frequent, corrosive injury in India is more commonly due to acids. Depth of the injury is the most important factor which determines the outcome. Endoscopy done soon after corrosive ingestion is safe and is very helpful in assessing the extent and severity of injury and in planning proper management of these patients. At present no therapy has been proven to be effective for prevention of stricture formation. Endoscopic dilatation seems to be the treatment of choice for management of most esophageal strictures with very good short and long term results. Surgery should be considered only when dilatation fails.

To determine the prevalence and natural history of gastric varices, we prospectively studied 568 patients (393 bleeders and 175 nonbleeders) with portal hypertension (cirrhosis in 301 patients, noncirrhotic portal fibrosis in 115 patients, extrahepatic portal vein obstruction in 117 patients and hepatic venous outflow obstruction in 35 patients). Primary (present at initial examination) gastric varices were seen in 114 (20%) patients; more were present in bleeders than in non-bleeders (27% vs. 4%, respectively; p < 0.001). Secondary (occurring after obliteration of esophageal varices) gastric varices developed in 33 (9%) patients during follow-up of 24.6 +/- 5.3 mo. Gastric varices (compared with esophageal varices) bled in significantly fewer patients (25% vs. 64%, respectively). Gastric varices had a lower bleeding risk factor than did esophageal varices (2.0 +/- 0.5 vs. 4.3 +/- 0.4, respectively) but bled more severely (4.8 +/- 0.6 vs. 2.9 +/- 0.3 transfusion units per patient, respectively). Once a varix bled, mortality was more likely (45%) in gastric varix patients. Gastric varices were classified as gastroesophageal or isolated gastric varices. Type 1 gastroesophageal varices (lesser curve varices) were the most common (75%). After obliteration of esophageal varices, type 1 gastroesophageal varices disappeared in 59% of patients and persisted in the remainder; bleeding from persistent gastroesophageal varices was more common than it was from gastroesophageal varices that were obliterated (28% vs. 2%, respectively; p < 0.001). Type 2 gastroesophageal varices, which extend to greater curvature, bled often (55%) and were associated with high mortality. Type 1 isolated gastric varices patients had only fundal varices, with a high (78%) incidence of bleeding.(ABSTRACT TRUNCATED AT 250 WORDS)

Portal hypertensive gastropathy (PGP) is an important cause of bleeding in portal hypertension patients. Although hyperdynamic congestion seems to be the underlying mechanism, the factors that influence the development of PGP are not understood. To investigate these, 107 patients [cirrhosis, 35; noncirrhotic portal fibrosis (NCPF), 24; extrahepatic portal vein obstruction (EHPVO), 46; Budd-Chiari syndrome, 2] were prospectively studied. Eighty-three patients had Child's A, 17 had Child's B, and 7 had Child's C liver disease. Before sclerotherapy, although intravariceal pressure was similar, 4 cirrhosis patients (3.7%) but no NCPF or EHPVO patients had PGP. After sclerotherapy, 21 additional patients (20.3%) developed PGP during a follow-up of 23.2 ± 3.4 months (range, 1–52). The incidence of PGP was higher in cirrhotic patients (37.1%) than in NCPF (16.7%; P < 0.05) or EHPVO (8.7%; P < 0.01) patients. The probability of developing PGP among all patients at the end of 52 months of follow-up was 30%, more in cirrhosis than in EHPVO (55% vs. 15%; P < 0.005). Only 2 patients bled from PGP during follow-up. Development of PGP correlated with severity of liver disease, being more common in Child's C than Child's A patients (87% vs. 13%; P < 0.001). PGP was seen more often in patients with gastroesophageal varices than in patients with esophageal varices alone (42% vs. 11%; P < 0.01). In conclusion, the results show that development of PGP is significantly influenced by sclerotherapy, severity of liver disease, etiology of portal hypertension and coexisting gastric varices and is not directly correlated with intravariceal pressure.

Gastric varices (GV) are a common (20%) accompaniment of portal hypertension; they are more often seen in those patients who bleed than in those who do not (27% versus 4%, p < 0.01). They can develop in both segmental and generalized portal hypertension. Depending on their location and relation with oesophageal varices, GVs can be classified as gastrooesophageal varices (GOV) and isolated gastric varices (IGV); each of these can be further subdivided as follows: GOV1 (extension of oesophageal varices along lesser curve) and GOV2 (extension of oesophageal varices towards fundus); and IGV1 (varices in the fundus) and IGV2 (isolated varices anywhere in the stomach). The common presentation of GVs is variceal bleeding and encephalopathy. In comparison with oesophageal varices, GVs bleed significantly less often (64% versus 25%, p < 0.01) but more severely (2.9 +/- 0.3 versus 4.8 +/- 0.6 transfusion units, p < 0.01). Patients with GOV2 and IGV1 bleed more often than patients with other types of GVs. Sclerotherapy for oesophageal varices can significantly influence the natural history of GVs. GOV1, or lesser curve varices, disappear in the majority of cases (59%) after obliteration of oesophageal varices. In those with persisting GOV1, the incidence of bleeding and mortality is high and these patients require gastric variceal sclerotherapy (GVS). During oesophageal variceal sclerotherapy, bleeding can occasionally be induced from GVs. After obliteration of oesophageal varices, recurrence as GVs (secondary GVs) can occur in about 9% of patients. Emergency GVS is quite effective in controlling acute bleeding from GVs, more so than balloon tamponade. Potent sclerosants like tetradecyl sulphate and alcohol and a glue, bucrylate, have been quite effective. Elective GVS can achieve obliteration of GVs in nearly 70% of patients. Rebleeding and ulceration are common complications of GVS; probably related to incomplete obliteration and mucosal injury respectively. Splenectomy is quite effective in treating GVs due to segmental protal hypertension. For GV bleeding due to generalized portal hypertension, a shunt operation is often effective. TIPS procedure appear to be a very promising therapy for GV bleeding. Liver transplantation may be a superior alternative to sclerotherapy and shunt surgery for gastric varices.

Histopathological changes in the esophagus and gastric antrum were studied in 47 patients with duodenal ulcer. Twenty three (49%) patients complained of heartburn. Esophagitis was present in 87% of the patients with heartburn and in 71% of the patients with no heartburn. In the majority, esophagitis was of mild to moderate severity. Gastritis was present in 83% (atrophic type in 22%) of patients with heartburn compared to 96% (25% atrophic type) of patients without heartburn. There was no statistical difference in the incidence of esophagitis and gastritis between the heartburn and no heartburn groups. This study suggests that histologic esophagitis and gastritis occur frequently in patients with duodenal ulcer and the presence of heartburn is not related to these histologic changes.