Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0022116 (ischemia)
 91,303 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A 33-year-old male patient with hepatitis B surface antigen positive cirrhosis, received 2 courses of endoscopic injection sclerotherapy for bleeding esophageal varices. A Streptococcus viridans brain abscess developed 2 weeks after the first sclerotherapy (or 1 week after the second sclerotherapy). In cirrhotic patients, an increase in pulmonary vasodilatation and pulmonary arteriovenous shunting has been well recognized. Sclerosant as well as bacteria may pass through a pulmonary arteriovenous shunt and reach the brain, directly after an infection of esophageal varices. Brain ischemia and a bacterial infection may occur at the same time, this can accelerate the development of a pyogenic brain abscess. Careful observation for the early detection and treatment of infection following endoscopic sclerotherapy is essential.
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PMID:Brain abscess following endoscopic injection sclerotherapy: report of a case. 168 87

We report a 33-year-old man who developed cutaneous necrosis of the lower extremities with extensive bulla formation after i.v. administration of vasopressin for the treatment of bleeding esophageal varices. Due to its potent nonselective vasoconstrictive action, vasopressin not only may induce cardiac and gastrointestinal ischemia, but cutaneous ischemia as well. As in our patient, this may lead to extensive necrotic skin lesions at sites distant from the infusion.
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PMID:Vasopressin-related bullous disease of the legs. 200 55

In four patients who underwent liver transplantation, portal vein thrombosis was associated with esophageal varices and significant gastrointestinal bleeding. In a fifth liver transplant patient, portal vein stenosis was suspected when evidence of hepatic ischemia was revealed at liver biopsy. Four patients were treated with percutaneous transhepatic portal vein angioplasty. Percutaneous recanalization was precluded by technical factors in the remaining patient. Early in the series, one patient required surgical excision of what proved to be a thick cuff of fibrous tissue and lymph nodes after angioplasty failed to widen the stenosis significantly. Later, a patient with residual stenosis was treated successfully by means of intravascular stent placement. Of the four patients treated, three eventually died secondary to multiple problems unrelated to the percutaneous procedure. This early experience suggests that transhepatic portal vein interventions are feasible in patients who have received liver transplants and may prove useful at least in the early postprocedure period.
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PMID:Percutaneous transhepatic portal vein angioplasty and stent placement after liver transplantation: early experience. 215 69

Endoscopic variceal ligation (EVL) was performed in 14 consecutive patients who had recently bled from esophageal varices. None was actively bleeding at initial treatment. Ligations were accomplished using an endoscopic ligating device and an overtube. There were no procedural complications. 132 varix ligations were performed during 44 separate EVL sessions. Two patients were lost to follow-up and two died; neither death resulted from hemorrhage or treatment complications. Variceal rebleeding occurred in 2 noncompliant patients (14.3%) and was successfully controlled with emergent EVL. Ten patients achieved complete variceal eradication with from 1 to 6 (mean, 3.9) EVL sessions. No major complications (perforation, secondary bleeding, deep ulceration) resulted and there were no treatment failures. Follow-up of 10 surviving patients ranged from 240 to 370 (mean, 280) days. Endoscopic observation suggested that varices were obliterated by a process of mechanical strangulation, ischemia, superficial ulceration, and scar formation. Preliminary data indicate that EVL is a safe and effective treatment for esophageal varices.
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PMID:Endoscopic esophageal varix ligation: preliminary clinical experience. 325 95

Endoscopic reflectance spectrophotometry was used to compare the effect of vasopressin and propranolol on gastric mucosal hemodynamics in dogs with surgically induced esophageal varices and prehepatic portal hypertension. Reflectance spectrophotometry provides indices of mucosal hemoglobin concentration (IHB) and oxygen saturation (ISO2). Hyperemia (increased IHB, normal ISO2), ischemia without congestion (decreased IHB, decreased ISO2), and ischemia with congestion (increased IHB, decreased ISO2) are accompanied by characteristic patterns of IHB and ISO2. Under anesthesia, measurements were obtained on separate days from the gastric corpus mucosa of eight dogs before and 2 to 10 min after either 1 to 5 units of intravenous vasopressin or 1 mg of propranolol. Results revealed that vasopressin (in doses that significantly reduced variceal and portal venous pressure in this animal model) produced a reduction in both IHB and ISO2, indicating gastric mucosal ischemia secondary to splanchnic vasoconstriction. On the other hand, propranolol in a dose that significantly reduced pulse rate by 27 +/- 2% had no effect on IHB or ISO2, suggesting that this dose of propranolol has no direct vasoactive effect on the gastric (splanchnic) circulation.
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PMID:Endoscopic demonstration that vasopressin but not propranolol produces gastric mucosal ischemia in dogs with portal hypertension. 326 2

In 25 years, from 1959 to 1984, esophageal substitution was performed in 32 patients. In most, the transverse colon was used, brought through the left chest on a vascular pedicle of the left colic artery. Indications for operation included: 21, esophageal atresia; 5, caustic injury; 3, peptic stricture; 2, esophageal varices with previous splenectomy; and 1, cartilagenous hamartoma of the esophagus. Six patients had failed prior reconstructions (1, gastric tube; 2, intrathoracic stomach; 1, presternal jejunum; 1, sloughed colon segment, 1, extensive stricture after primary repair). There was one postoperative death from fluid overload early in the series. Two patients had a localized leak at the upper anastomosis in the neck; neither resulted in stricture. One patient had a side leak in the lower intrathoracic colon, probably from an anchoring suture placed too deeply. Most patients had pyloroplasty with their operation. Four who did not required one later. Four patients required late reoperation for redundancy of the lower colon segment which emptied poorly; one lower colon was revised for stricture from exstrinsic compression at the substernal hiatus and another one for an inflammatory pseudopolyp with bleeding. There was no loss of a colon segment from ischemia. There is follow-up on all but one patient. Nineteen are more than ten years postoperative (mean of 18 years). Growth was assessed in that group. In atresia patients growth correlated with weight preoperatively and the presence or absence of associated anomalies. In the others growth was excellent in all but one patient. In our experience the colon conduit provides an excellent substitute esophagus for pediatric patients. The operation should have relatively low rate of major complications, most of which are avoidable, and most of which can be corrected to give a satisfactory long-term result.
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PMID:Colon interposition for esophagus in children. 408 10

Portal hypertension is defined as an increase of the portal venous pressure over 20 cm H2O or 7 mm Hg, respectively. It may be induced by different types of portal venous stenosis or obstruction, primarily by cirrhosis and fibrosis of the liver and, less frequent by posthepatic disorders such as the Budd-Chiari-syndrome or congestive heart failure. Portal hypertension is followed by ectasia and phlebosclerosis of the portal vein, by splenomegaly, ascites and by various types of collateral circulation. Among these, oesophageal varices, are most important since they often lead to acute upper gastrointestinal haemorrhage, the major complication of portal hypertension. Bleeding from oesophaeal varices is essentially based on atrophy of the squamous epithelium, caused by ischemia from local hypoxia and venous stasis. Portal hypertension and the frequently compromised blood clotting mechanism due to reduced synthesis of clotting factors in the liver aggravate the bleeding. Atrophy of the esophageal mucosa presents an area of decreased resistance likely to ulcerate with easy erosion of the varices--usually lying very superficially--; with mechanical irritation by food or peptic erosion from gastroesophageal reflux being frequent inducers of hemorrhage.
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PMID:[Pathologic-anatomic reflections on portal hypertension (author's transl)]. 624 21

In a randomized controlled trial, the effect of continuous intravenous administration of vasopressin was compared with Sengstaken-Blakemore balloon tamponade in 37 episodes of bleeding esophageal varices in patients with cirrhosis. The majority were Group A and B of Child's classification. Bleeding was controlled in 11 of 17 (65%) patients on vasopressin and in 14 of 20 (70%) patients on tamponade. The patients who failed to respond initially (6 episodes on vasopressin and 5 on tamponade) were treated successfully with the alternative method. Overall mortality was similar in both groups: 3 patients in the vasopressin group and 4 in the tamponade group died. Only one patient died of uncontrolled bleeding; 4 patients probably died of complications of treatment, 2 of cardiac ischemia after vasopressin and 2 of pulmonary infection after tamponade. The vasopressin group required significantly fewer blood transfusions than did the tamponade group.
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PMID:Controlled trial of vasopressin and balloon tamponade in bleeding esophageal varices. 638 98

Reflux esophagitis and anastomotic ulcer are potential complications associated with surgery for esophagogastric lesions. This study compared 10 cases following terminal esophagoproximal gastrectomy (TEPG) for esophageal varices and 20 cases following esophageal transection (ET) for esophageal varices with respect to postoperative motor function and mucosal blood supply, to ascertain the reason for the development of anastomotic ulcer. Endoscopic findings showed that anastomotic ulcers were detected more often after TEPG than after TR. Maximum swallowing pressure, high pressure zone pressure, and length did not differ between the two groups. However, maximum swallowing pressure in the lower esophagus after both procedures was significantly lower than in the control group (20 cases; p < 0.01). The results, measured by reflectance spectrophotometry, showed that the index of esophageal mucosal blood volume following TEPG is significantly lower than that following ET and in non-operated esophageal varices (10 cases; p < 0.01). Yet the index of oxygen saturation of hemoglobin was similar in the three groups. This study has demonstrated that patients undergoing TEPG have mucosal ischemia of the lower esophagus, causing the development of anastomotic ulcers.
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PMID:Postoperative motor function and mucosal blood flow of lower esophagus: comparison between terminal esophagoproximal gastrectomy and esophageal transection for esophageal varices. 831 7

Bleeding from esophageal varices presents a considerable challenge to clinicians. Adequate fluid resuscitation must be undertaken before urgent endoscopy. Pharmacotherapy of acute variceal hemorrhage consists of either vasopressin plus nitroglycerin or intravenous octreotide. Vasopressin should not be used alone because of a high incidence of side effects such as cardiac and/or visceral ischemia. Band ligation appears superior to sclerotherapy primarily because of decreased rebleeding from varices and decreased esophageal stricture formation among patients undergoing band ligation. Future trials with newer sclerosant agents, such as cyanoacrylate, are anxiously awaited.
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PMID:Endoscopic management of esophageal variceal hemorrhage: injection, banding, glue, octreotide, or a combination? 936 Feb 82


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