Tc-99m dextran: a new and sensitive general purpose scintigraphic agent for diagnosing intestinal inflammation.

PURPOSE: This feasibility study was undertaken to compare the sensitivity of Tc-99m dextran with that of Tc-99m human immunoglobulin G to diagnose ulcerative colitis, and to explore its possible role in disease follow-up. MATERIALS AND METHODS: Twenty-six patients with active disease and six patients in remission underwent serial Tc-99m dextran scanning for as long as 3 hours or more after injection. Eight of the patients with active disease also underwent Tc-99m human immunoglobulin G imaging. RESULTS: Twenty-four of 26 (92%) patients with active ulcerative colitis had a positive result of the Tc-99m dextran study, mainly within 1 hour. In comparison, Tc-99m human immunoglobulin G accumulated abnormally in four of eight (50%) patients and had a relatively poor target localization with high persisting background even after 6 hours. Four of the six patients in remission still had a positive result of the dextran scan, but the abnormal uptake was less than that in the patients with active disease. The disease has recurred already in one of these patients. A patient with pancolitis who was receiving steroid enema therapy had intense uptake of Tc-99m dextran in the ascending colon, probability because it was outside the range of the enema. CONCLUSIONS: Tc-99m dextran is a sensitive and cost-effective agent to diagnose ulcerative colitis, and it may have a role in disease follow-up.

Acute pancreatitis with cholestatic hepatitis: an unusual manifestation of hepatitis A.

Acute hepatitis A infection is an uncommon cause of pancreatitis in children. To date, only four cases have been reported in the paediatric literature. We report a 7-year-old girl with acute pancreatitis associated with hepatitis A infection who made a satisfactory recovery. The report highlights the CT findings including focal necrosis not previously reported. Because of the extreme rarity of the complication, the four previous reports have also been single case reports. This paper reviews all these cases with a view to elucidating the aetiopathogenesis of the pancreatitis.

Scintigraphic diagnosis of gastrointestinal bleeding with 99Tcm-dextran.

Intravenously administered dextran is used clinically as a plasma expander. The aim of this study was to assess the use of 99Tcm-dextran in the diagnosis of gastrointestinal (GI) blood leaks. Twenty-one patients with GI blood loss underwent 99Tcm-dextran scintigraphy, 17 of whom were found to be positive. Pathologic or 99Tcm-RBC (red blood cell) blood pool correlation was possible in 15 cases, while 2 were unconfirmed. No case had a positive 99Tcm-RBC blood pool study and a negative 99Tcm-dextran study. Images obtained with 99Tcm-dextran were generally better than those with 99Tcm-RBC. This agent may have several other advantages over 99Tcm-RBC blood pool and 99Tcm-sulphur colloid scintigraphy for detecting GI blood loss.

Elective surgery for corrosive-induced gastric injury.

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) 34 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 (44%) 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 24 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.

Balloon dilatation of inferior vena cava stenosis in Budd-Chiari syndrome.

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.

Benign esophageal strictures in children and adolescents: etiology, clinical profile, and results of endoscopic dilation.

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.

Technetium-99m dextran: a promising new protein-losing enteropathy imaging agent.

The purpose of this study was to evaluate technetium-99m dextran (99mTc-Dx; molecular weight 81000) as a prospective protein-losing enteropathy (PLE) imaging agent. Twenty-two patients with diseases commonly associated with PLE and 12 healthy control subjects underwent intravenous 99mTc-Dx scintigraphy. All of the 22 test patients showed significant radiotracer accumulation in the intestines within 3-4 h post injection. The focal, regional or generalised nature of the enteropathy and involvement of the large or small intestine could be identified in most cases. Four of the 12 apparently healthy subjects also showed minimal accumulation in the abdominal area occurring late in the study period. This could have been physiological, related to food habits or due to unsuspected intestinal worms. We attribute the high sensitivity of 99mTc-Dx to its relatively fast blood (background) clearance. The radiotracer may have several other advantages over 99mTc-labelled human serum albumin in imaging PLE.

Scintigraphic diagnosis of protein losing enteropathy using Tc-99m dextran.

The authors performed abdominal scintigraphy using intravenously administered Tc-99m dextran in a patient with protein losing enteropathy. The study revealed abnormal leakage of the radiotracer in the left lumber area that moved over time in a pattern suggestive of small intestinal transit. Besides being a nonprotein and having long stay in intravascular compartment, the macromolecule may have many advantages over Tc-99m human serum albumin, the current radiotracer of choice for imaging intestinal protein loss.

The prevalence and spectrum of colonic lesions in patients with cirrhotic and noncirrhotic portal hypertension.

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.

Corrosive esophageal strictures: predictors of response to endoscopic dilation.

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)

Long term results of endoscopic dilatation for corrosive oesophageal strictures.

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.

Corrosive injury to the upper gastrointestinal tract.

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.

Abnormal gallbladder function in patients with irritable bowel syndrome.

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.

Prevalence, classification and natural history of gastric varices: a long-term follow-up study in 568 portal hypertension patients.

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)

Management of gastric varices.

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.