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Query: UMLS:C0023890 (cirrhosis)
 42,195 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Transient esophageal ulceration is a common finding after sclerotherapy of varices. A small proportion of these ulcers become chronic and resistant to conventional therapy. Such chronic ulcers have been associated with pain, stricture formation, and recurrent hemorrhage. The use of omeprazole, a proton pump inhibitor, was examined in the current study in the treatment of 10 patients (6 women, 4 men; age range, 27-86 years) with cirrhosis (PBC, 4; sclerosing cholangitis, 2; chronic active liver disease, 2; alcohol, 1; and cryptogenic, 1) who developed an esophageal ulcer after a mean of 13 (range, 8-21) sessions of sclerotherapy. The ulcers had been present for 3-54 months despite prolonged treatment with high-dose H2-receptor antagonists and sucralfate. In each case one or more complications had occurred: severe pain in 3, stricture formation in 4, and recurrent hemorrhage in 7 cases. After an 8-week course of omeprazole, 40 mg daily, endoscopy confirmed complete healing of the ulceration in all 10 cases with symptom resolution. In 2 cases the ulcer recurred, with associated bleeding within 6 weeks of discontinuing the treatment in 1 patient. Both cases responded to repeat therapy. These results confirm the efficacy of omeprazole for postsclerotherapy ulceration and imply that acid-pepsin has a role in perpetuating such ulcers.
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PMID:Omeprazole in the management of intractable esophageal ulceration following injection sclerotherapy. 222 99

Thirty children, aged 7 months to 13 years, with bleeding esophageal varices were managed by endoscopic sclerotherapy (EST). Of these children, 73.3% had extrahepatic portal vein obstruction (EHPVO), 16.6% had cirrhosis of the liver, and 10% had noncirrhotic portal fibrosis. EST was done with fiberoptic pediatric upper gastrointestinal endoscopes and a flexible sclerotherapy needle under sedation with intravenous diazepam and pentazocine. The sclerosants used were ethoxysclerol 1% and absolute alcohol. Ten injections were given to control active variceal bleeding, and 145 injections were given on planned basis at 2-3-week interval. An average of five injections was required to obliterate the esophageal varices. In 90% of cases, an avariceal state was achieved; 10% had decreased size and number of varices. Emergency EST was effective to control bleeding in all sessions. Complications, including retrosternal discomfort, esophageal ulceration, stricture formation, and aspiration pneumonia, occurred in 60, 20, 20, and 6.6% of cases, respectively; complications were managed conservatively. Strictures were dilated with Eder-Puestow's olive dilators. Recurrence of esophageal varices, gastric varices, and rebleeding was seen in 13.3, 13.3, and 10% of cases, respectively. Shunt surgery was performed in 13.3% cases, who had developed gastric varices and were having EHPVO.
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PMID:Endoscopic sclerotherapy of esophageal varices in infants and children. 235 74

Sixteen children (3.5-14.7 years) with portal hypertension and variceal hemorrhage were treated by direct endoscopic variceal sclerotherapy. Follow-up clinical and endoscopic evaluations have been carried out over a 1-6-year period (mean, 2.3 years). Prior to sclerotherapy, three patients had undergone unsuccessful surgical approaches, and the mean transfusional requirement from the time of the first hemorrhage was 12.3 units of blood per child per year for those with extrahepatic portal vein obstruction (n = 10) and 3.8 units for those with primary liver disease. Following sclerotherapy, transfusional requirements were significantly reduced in both groups, to 1.8 units and 2.2 units (85% and 43% reduction, respectively). Re-bleeding in four patients was due to the occurrence of gastric varices. One patient with extrahepatic portal hypertension has required subsequent shunt surgery for this complication, 5 years after sclerotherapy. Two patients have died, one with cystic fibrosis and hemorrhage from gastric varices and one from liver failure due to progressive biliary cirrhosis. Complications of sclerotherapy included transient retrosternal pain (eight occasions), esophageal ulceration with bleeding (n = 1) and esophageal stricture (n = 1). We conclude that sclerotherapy is an effective technique in obliterating esophageal varices and reducing the risk of hemorrhage in children with portal hypertension, with an acceptably low complication rate. We favor its use over more invasive surgical measures for control of acute and recurrent variceal hemorrhage, particularly for cases of extrahepatic portal hypertension in which a favorable natural history is likely.
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PMID:Evaluation of endoscopic sclerotherapy of esophageal varices in children. 348 30

Esophageal varices in 59 consecutive children with portal hypertension were treated by paravariceal injection sclerotherapy. Repeated injections were performed using a special rigid instrument under general anesthesia. In children older than 10 a flexible endoscope was used without general anesthesia. Using 0.5% Polidocanol, a fibrous layer protecting varices against the further bleeding was produced in 59 children. Complications during treatment included hemorrhage, esophageal ulceration and stricture, each in two children. 55 children have been followed for 6 months to 10 years after two phases of paravariceal injection following the first phase of treatment. Three rebleeds have occurred in this group. Sclerotherapy was repeated. Thereafter, using a regular endoscopic control every year, no rebleeding occurred. Four children with liver cirrhosis died of liver failure. All other children except four foreign ones could be followed. 51 of them (86%) are alive.
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PMID:Ten years experience with paravariceal injection sclerotherapy of esophageal varices in children. 387 76

Continued haemorrhage from oesophageal varices despite adequate injection sclerotherapy and tamponade has a high mortality rate. Such patients are usually referred for surgery. Over a 10-year period, 30 patients (21 men and nine women of median age 52 (range 21-70) years) with acute variceal haemorrhage uncontrolled by initial treatment underwent early emergency oesophageal transection. Portal hypertension was caused by alcoholic cirrhosis in 22 patients; other forms of cirrhosis were present in seven and portal vein thrombosis in one. Hepatic function immediately before operation was Pugh grade A in two patients, B in six and C in 22. Deterioration between admission and transection from grade A to B occurred in one patient and from B to C in five. Oesophageal transection stopped variceal haemorrhage in 29 of the 30 patients. Rebleeding from gastric varices within 35 days of surgery occurred in five patients. Postoperative haemorrhage also occurred from perioesophageal vessels (two patients), a gastrotomy (one) and oesophageal ulceration (two). Hepatic failure developed in seven patients, renal failure in five and both hepatic and renal failure in four. Mortality at 30 days occurred in neither of the two patients with liver function of grade A, in one of six of grade B and in 18 of 22 of grade C. The overall 30-day mortality rate was thus 63 per cent. Mortality was related to the preoperative Pugh grade (hazard ratio 3.95 per grade; P = 0.013) and preoperative blood transfusion (hazard ratio 1.37 per unit; P = 0.035). Four of six patients with grade B liver function died within 3 months and 21 of 22 with grade C disease within 1 year. Oesophageal transection is effective at stopping variceal bleeding but does not modify the underlying disease. Caution is urged for patients with grade C hepatocellular impairment proceeding to acute oesophageal transection after initial sclerotherapy. Such patients may benefit more from treatment with somatostatin or an intrahepatic porta-systemic stent shunt while awaiting definitive therapy.
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PMID:Emergency oesophageal transection for uncontrolled variceal haemorrhage. 792 95

Fifty consecutive patients presenting with upper gastrointestinal haemorrhage caused by oesophageal varices were subjected to endoscopic sclerotherapy during the period April 1989 to December 1991. Portal hypertension was caused by alcoholic liver cirrhosis in 22 (44pc), Hepatitis B induced liver cirrhosis in seven (14pc), cryptogenic liver cirrhosis in three (six pc), bilharzial portal fibrosis in 17 (34pc) and extrahepatic portal obstruction in one (two pc). Acute bleeding was controlled in 12 out of 13 patients, five of whom with a fresh bleed and eight who rebled while on the endoscopic sclerotherapy regimen. All patients were treated on a weekly sclerotherapy regimen. Reduction in variceal size of two or more grades was achieved in all 30 patients who had completed at least four or more endoscopic sclerotherapy courses with total eradication of varices in 27 (90pc). Three patients died. All deaths were caused by progressive hepatic encephalopathy. Complications usually seen were retrosternal pain, fever, dysphagia and oesophageal ulceration. There were no fatal complications. The study shows that endoscopic sclerotherapy is effective not only in controlling acute bleeding but also in preventing rebleeding. We recommend a weekly schedule for the early eradication of varices.
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PMID:Endoscopic sclerotherapy in Zimbabwe. 802 85

Injection sclerotherapy is now the accepted first line treatment for bleeding oesophageal varices, although it is associated with an impressive list of rare complications. The main problem concerns the strategy for uncontrollable or recurrent bleeding. Patients with uncontrolled bleeding may be referred for surgery after considerable blood loss and are then extremely difficult to assess. The effects of blood loss on liver function can lead to an unduly pessimistic assessment of liver status. An effective choice of emergency surgical procedure may require considerable surgical expertise. Oesophageal transection and devascularisation are satisfactory for many patients with oesophageal varices secondary to cirrhosis and should nearly always control bleeding. Difficulties arise in patients who are grossly obese and in those who have undergone extensive surgery in the upper abdomen. Problems may also be encountered in those treated by repeated sclerotherapy, which may have caused severe inflammatory change and thickening around the lower oesophagus and upper stomach. We believe that an emergency mesocaval shunt using either a vein graft or a synthetic material such as polytetrafluoroethylene is the procedure of choice for this difficult group of very sick patients. The surgical exposure is satisfactory and not unduly prolonged in even the largest patients and the technique does not interfere with any subsequent transplant operation. There is a greater choice in the management of the patient with less urgent bleeding from recurrent varices after sclerotherapy. Repeat sclerotherapy may be effective for small oesophageal varices while liver transplantation may be indicated in the patient with deteriorating liver function. A selective distal splenorenal shunt should be considered for patients with intact splenic and left renal veins and a mesocaval vein graft for the remainder. We would therefore suggest that surgery should still be considered for the management of portal hypertension, particularly in the following circumstances: (1) Uncontrollable bleeding during the initial course of sclerotherapy; (2) Life threatening haemorrhage from recurrent varices; (3) Bleeding from ectopic varices not accessible to sclerotherapy; (4) Uncontrollable bleeding from oesophageal ulceration secondary to injection sclerotherapy; (5) Severe, symptomatic hypersplenism; (6) For patients who live in communities remote from blood transfusion facilities and adequate medical care. The management of the complications of portal hypertension continues to pose problems. We believe that the best results should come from a combined management approach using injection sclerotherapy as primary treatment and surgery for complications and for haemorrhage from unusual anatomical sites.
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PMID:Complications and limitations of injection sclerotherapy in portal hypertension. 831 27

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.
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PMID:Study of portal hypertension in children with special reference to sclerotherapy. 938 57

We describe a patient diagnosed with AIDS and cirrhosis who had recently suffered a self-limited and non-specific esophageal ulceration. After this, he was hospitalized because of an oral bleeding with fatal evolution, and Cryptococcus neoformans was isolated from ascitic fluid during a routine paracenteses. We have reviewed the literature and, since 1963, only another 10 cases of cryptococcal peritonitis have been reported. A liver disease and not the AIDS (surprisingly, our case is the only report of cryptococcal peritonitis in a subject having both diseases) was the most common underlying disease (72.7%) and was associated with the worst prognosis (only one patient survived). An oral or upper gastrointestinal bleeding was the most common associated circumstance although recent steroid or antibiotic therapy has been also reported. Finally, diagnosis was delayed in many patients. The reasons for these delays are discussed.
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PMID:Cryptococcal peritonitis: report of a case and review of the literature. 1043 Mar 6