Anatomical insight into tortuosity of the splenic artery: a case report

The splenic artery is known to be tortuous in its entire course. The tortuosity of the splenic artery has been, reported in various arteriographic and corrosion cast studies but there are less histological studies to corraborate this fact. The present case describes tortuosity of the splenic artery, observed in a 47 year female cadaver who died of meningitis. The splenic artery was thickened and the tortuosity was evident from the number of loops it formed throughout its course. The splenic artery further divided into two branches [i.e upper and lower branches] to enter the spleen. The left gastroepiploic artery originated from the lower branch. A detail histological study of the specimen revealed the presence of calcification and atheromatous plaques. Presence of tortuosity of the vessel may be linked to atheroma, as seen in the present case. The tortuosity of the splenic artery accompanied with atheromatous plaques and calcification may result in hypertrophy of the muscle wall of the vessel and may be responsible for altering the dynamics of blood flow. Prior anatomical knowledge of tortuosity, abnormal loopings of the splenic artery and its branching pattern may be clinically important before performing any abdominal surgeries and also important for correct interpretation of arteriograms

Esophageal and gastric dysmotility in non ulcer dyspepsia.

BACKGROUND: The pathophysiology of non ulcer dyspepsia is poorly understood. Data on gastrointestinal motility alterations in this condition in the Indian population are scanty. We studied esophageal and gastric motility in patients with non ulcer dyspepsia. METHODS: 58 consecutive patients with non ulcer dyspepsia (according to the Rome criteria) were studied; 10 healthy volunteers were studied as controls. Esophageal transit of solid and liquid boluses (in all patients) and solid-phase gastric emptying (in 20 patients) were studied using scintigraphic techniques. RESULTS: Delayed esophageal transit and delayed gastric emptying were observed in 32 (55%) and 9 (45%) patients, respectively. Delay of both esophageal and gastric transit was found in 5 patients. Mean (SD) esophageal transit for liquid bolus was significantly delayed in patients (9.3 [3.7] s) compared to controls (7.0 [2.0] s; p < 0.01). Mean (SD) gastric emptying time (T50) was significantly delayed in patients (61.6 [13.6] min) compared to controls (50.0 [5.0] min; p < 0.001). Esophageal and gastric delayed transit was found in about two thirds of patients with dysmotility-like dyspepsia, but there were no significant difference in these abnormalities among different subgroups of dyspepsia. CONCLUSION: High prevalence of esophageal and gastric transit delay was found in non ulcer dyspepsia, particularly in the dysmotility subgroup.

Natural history of severe duodenal ulcer disease.

BACKGROUND: A subset of patients with chronic duodenal ulcer has severe ulcer diathesis in the form of frequent relapses and complications like perforation and hemorrhage. We observed the effect of drug treatment on the natural history of this subset. METHODS: Of 526 patients diagnosed to have chronic duodenal ulcer by endoscopy, 23 patients with severe diathesis were available for long follow-up (mean period 36 months). Each patient was assessed clinically and endoscopically every 2 months for at least 12 months and then every 3 months or when symptomatic. Helicobacter pylori status was assessed during endoscopy. The effect of antisecretory drugs and anti-H. pylori therapy on natural history was determined. RESULTS: Thirteen of 23 patients (56%) had refractory ulcers; six responded to double dose of H2-receptor antagonists (H2RA) for 8 weeks and six to omeprazole 40 mg daily for 4-8 weeks. Of 20 patients (87%) who were H. pylori-positive, 15 completed triple-drug therapy; of these, 10 patients eradicated H. pylori. These 10 patients were followed up for 24 months; there were no ulcer relapses within the first 12 months but 8 of them relapsed between 12 and 24 months (total number of relapses 8). Reinfection with H. pylori occurred in 3 patients. In the other 10 patients who remained H. pylori-positive, there were 19 episodes of ulcer relapse in 7 patients over 24 months, in spite of maintenance therapy with H2RA (p < 0.05). CONCLUSIONS: Refractoriness in patients with severe ulcer disease is usually episodic and amenable to larger doses of omeprazole or H2RA. Anti-H. pylori therapy improves the natural history but its effect in preventing ulcer relapse is short lasting (less than 12 months). Recurrence of infection is a problem in our population.

Portal hypertensive gastropathy and gastric varices before esophageal variceal sclerotherapy and after obliteration.

OBJECTIVES: To evaluate the frequency and clinical importance of portal hypertensive gastropathy (PHG) and gastric varices (GV) before endoscopic sclerotherapy (EST) and after esophageal variceal obliteration. METHODS: Patients with portal hypertension (PHT) with variceal bleed were prospectively evaluated for PHG and GV before EST with intravariceal injection of absolute alcohol and after esophageal variceal obliteration. Gastric varices and PHG were characterized and graded according to previously established criteria. Patients were followed up for 12-48 (mean 37) months after variceal obliteration. RESULTS: Of 70 patients with PHT 26 had PHG before (severe in two) [18/37 in cirrhosis, 6/20 in non-cirrhotic portal fibrosis (NCPF), and 2/13 in extrahepatic portal vein obstruction (EHPVO)] and 50 had PHG after variceal obliteration (severe in 22) (27/37 in cirrhosis, p = 0.03 before versus after esophageal variceal obliteration; 16/20 in NCPF, p < 0.01; and 7/13 in EHPVO, p = ns). Type I GV (continuation of esophageal varix into the stomach) was found in 25/70 before and 5/70 after esophageal variceal obliteration (p < 0.001); in contrast, other types of GV were seen in 14/70 before and 29/70 after (p < 0.01). Overt bleeding from GV and PHG during follow-up after variceal obliteration occurred in 6 and 4 patients, respectively. CONCLUSIONS: Esophageal variceal obliteration by EST increases the frequency of PHG and GV (except type I GV which get obliterated); both PHG and GV have potential to cause rebleeding.

Study of portal hypertension in children with special reference to sclerotherapy.

Portal Hypertension (PH) is the commonest cause of upper gastrointestinal bleeding in children. Most Indian studies have highlighted extrahepatic portal venous obstruction (EHPVO) as the major cause of PH in children. As there is paucity of data from the eastern part of the country we decided to study the major causes of PH in children in this region and to ascertain the efficacy of sclerotherapy for its management. Fifty children aged 14 months to 10 years with PH were studied from April 1990 to April 1995. Thorough examination and relevant investigations showed non-cirrhotic portal fibrosis (NCPF) in 24 (48%), EHPVO in 18 (36%) and cirrhosis of liver in 8 (16%) children. Forty six children had hematemesis and melaena of whom endoscopic sclerotherapy (EST) was done in 45 cases. One child having type 2 gastric varices was referred for surgery. Following eradication of varices the patients were followed-up at 3 monthly intervals. Number of sittings of sclerotherapy required for obliteration of varices was 5.9 +/- 1.6. A variceal state was achieved in 35 (78%) cases and varices were reduced to Grade I in 6 cases (13%). Two cases underwent surgery for EST failure. One patient of cirrhosis died within two weeks of bleeding episode due to hepatic encephalpathy. Rebleeding (13%) and recurrences (13%) were noted during the follow-up period. Retrosternal discomfort (22%), dysphagia (22%), stricture (13%), oesophageal ulceration (13%) and fever (11%) were the complications noted but these could be managed conservatively. The present study highlights that NCPF is an important cause of PH in eastern India. EST is useful in controlling variceal bleeding in children irrespective of their aetiology.

A study of nosocomial diarrhea in Calcutta.

BACKGROUND: Nosocomial infection is a major problem in hospitalized patients, particularly those who are debilitated. These infections may manifest as diarrhea. The spectrum of infections agents causing nosocomial diarrhea in our country is not known. METHODS: Thirty-two patients, admitted to the hospital with various complaints, who developed diarrhea during their hospital stay, were studied to identify the causative agents of diarrhea. Hospital food samples were also processed for pathogens. RESULTS: The bacteria isolated from patients included established enteropathogens like Salmonella, enteropathogenic Escherichia coli, Campylobacter species and organisms with low pathogenicity like Serratia marsescens, Pseudomonas aeruginosa and Morganella morganii. The bacterial pathogens isolated were resistant to most antibiotics, suggesting their nosocomial character. Hospital food samples contained Salmonella typhimurium, Campylobacter jejuni (biotype 1) and enteropathogenic Escherichia coli, suggesting that food might have been the vehicle for these infections. CONCLUSION: Nosocomial infection was found to be an important cause of diarrhea (34%), EPEC and Salmonell being the predominant pathogens. Water, egg and milk were the source of infection in these cases. Special measures to obtain uneffected items will prevent occurrence of nosocomial diarrhea in our hospitals.

Prevalence of the type of hepatitis virus in hospitalized jaundiced individuals.

The prevalence of different types of hepatitis virus was estimated in 185 hospitalized jaundiced patients. It was found that 41.08% were positive for HBs Ag by ELISA method. The jaundiced group was also tested for IgM antibody and for total antibodies (IgG and IgM) to HAV infection by ELISA method and 5.40% were found to be positive. All patients in the jaundiced group had serum bilirubin above normal values. It was, therefore, assumed that the rest 52.92% were suffering from Non A Non B virus infection.