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1/61. Massive esophageal variceal hemorrhage triggered by complicated endotracheal intubation.

    Esophageal variceal hemorrhage is frequently a catastrophic event. The specific events that trigger variceal rupture are not well understood. Acute elevations in systemic blood pressure and increased splanchnic blood flow, however, may lead to increased intravariceal pressure followed by variceal rupture and hemorrhage. This report describes a strong temporal association between complicated endotracheal intubation and abrupt onset of life-threatening variceal hemorrhage. A 52-year-old man with a history of portal hypertension was intubated emergently for airway protection because of respiratory insufficiency due to sepsis. intubation was complicated by initial inadvertent esophageal intubation and by a peak mean arterial blood pressure of 155 mmHg. At the conclusion of the procedure, the patient sustained large volume hematemesis due to esophageal variceal rupture. This case suggests a risk of triggering variceal hemorrhage as a result of intubation-induced increase in blood pressure. A number of agents, including fentanyl, have been shown to be effective in attenuating the cardiovascular response to intubation. This case report provides strong evidence in support of administering fentanyl, or a suitable alternative adjunctive medication, before intubation of patients with documented portal hypertension and a history of esophageal variceal hemorrhage.
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2/61. Recurrent variceal hemorrhage following successful Warren shunt.

    Recurrent variceal hemorrhages are demonstrated following a technically successful Warren shunt. Serial barium esophagrams show the progressive enlargement of distal esophageal varices. Results of celiac arteriograms and direct examination confirmed the patency of the distal splenorenal shunt. hemorrhage from varices was shown by fiberoptic esophagoscopy; end-to-side portacaval anastomosis reduced portal pressure and stopped the bleeding.
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3/61. Stent recanalization of chronic portal vein occlusion in a child.

    An 8-year-old boy with a 21/2 year history of portal hypertension and repeated bleedings from esophageal varices, was referred for treatment. The 3.5-cm-long occlusion of the portal vein was passed and the channel created was stabilized with a balloon-expandable stent; a portosystemic stent-shunt was also created. The portosystemic shunt closed spontaneously within 1 month, while the recanalized segment of the portal vein remained open. The pressure gradient between the intrahepatic and extrahepatic portal vein branches dropped from 17 mmHg to 0 mmHg. The pressure in the portal vein dropped from 30 mmHg to 17 mmHg and the bleedings stopped. The next dilation of the stent was performed 12 months later due to an increased pressure gradient; the gastroesophageal varices disappeared completely. Further dilation of the stent was planned after 2, 4, and 6 years.
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4/61. Idiopathic splenic vein stenosis: a cause of gastric variceal hemorrhage.

    We report the case of a patient with isolated gastric variceal bleeding. obesity precluded the use of noninvasive means for assessing splenic vein patency. splenic vein stenosis was diagnosed by transhepatic portal and splenic venography with pressure measurements. A cause for the stenosis could not be found. splenectomy was used as a curative measure.
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5/61. Successful treatment of TIPS-induced hepatic failure with an hourglass stent-graft: a simple new technique for reducing shunt flow.

    A simple new technique for creating an hourglass reducing stent-graft by means of targeted balloon expansion of each end of a commercially available device is presented. A 67-year-old man with progressive hepatic failure after TIPS creation was treated. A 48-mm-long Jostent stent-graft was placed inside the TIPS through a 10-F introducer and fully expanded only at the proximal and distal ends, resulting in an hourglass shape. Immediate increase of portal pressure was achieved, followed by complete clinical recovery. Advantages of covered versus bare reducing stents are discussed.
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6/61. Restoration of liver function and portosystemic pressure gradient after TIPSS and late TIPSS occlusion.

    TIPSS (transjugular intrahepatic portosystemic shunt) may be indicated to control bleeding from esophageal and gastric varicose veins, to reduce ascites, and to treat patients with budd-chiari syndrome and veno-occlusive disease. Numerous measures to improve the safety and methodology of the procedure have helped to increase the technical and clinical success. Follow-up of TIPSS patients has revealed shunt stenosis to occur more often in patients with preserved liver function (child A, child B). In addition, the extent of liver cirrhosis is the main factor that determines prognosis in the long term. Little is known about the effects of TIPSS with respect to portosystemic hemodynamics. This report deals with a cirrhotic patient who stopped drinking 7 months prior to admission. He received TIPSS to control ascites and recurrent esophageal bleeding. Two years later remarkable hypertrophy of the left liver lobe and shunt occlusion was observed. The portosystemic pressure gradient dropped from 24 mmHg before TIPSS to 11 mmHg and remained stable after shunt occlusion. The child's B cirrhosis prior to TIPSS turned into child's A cirrhosis and remained stable during the follow-up period of 32 months. This indicates that liver function of TIPSS patients may recover due to hypertrophy of the remaining non-cirrhotic liver tissue. In addition the hepatic hemodynamics may return to normal. In conclusion, TIPSS cannot cure cirrhosis but its progress may be halted if the cause can be removed. This may result in a normal portosystemic gradient, leading consequently to shunt occlusion.
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7/61. Bleeding portal-hypertensive gastropathy managed successfully by partial splenic embolization.

    The use of partial splenic embolization to decrease portal pressure and reduce gastric bleeding from portal-hypertensive gastropathy, a complication of liver cirrhosis, is described. A 62-year-old man with hepatic cirrhosis secondary to hepatitis c and documented portal hypertension was admitted with hypersplenism and bleeding esophageal varices. Endoscopic ligation successfully controlled acute bleeding, but blood loss continued over the next 45 days. Bleeding secondary to portal-hypertensive gastropathy was diagnosed endoscopically. The patient's poor surgical status precluded a portosystemic shunt procedure, so partial splenic embolization was performed radiologically by the injection of Gelfoam squares. Splenic volume decreased 50% following partial embolization. Over 3 weeks, the hemoglobin concentration increased from 8.5 g/dL to 9.8 g/dL, and the platelet count increased from 41,000 to 90,000/microL. Repeat endoscopy found no gastric bleeding 18 days post-procedure. Partial splenic embolization is a radiologic procedure which can be performed safely in patients too ill to undergo portosystemic shunt. This report documents its successful use to manage hypersplenism and reduce portal pressure in a cirrhotic patient with portal-hypertensive gastropathy and hypersplenism.
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8/61. Appearance of rectal varices in extrahepatic portal obstruction after treatment for esophago-gastric varices: a case report.

    We report a case of rectal varices that developed after endoscopic injection sclerotherapy (EIS) and Hassab's operation for esophageal varices with extrahepatic portal obstruction. A 54-year-old woman was admitted to our hospital in September 1997 for treatment of hematochezia. Emergent colonoscopy revealed tortuous rectal varices with a white plug. angiography revealed that rectal varices were provided with backward blood flow by the inferior mesenteric vein due to extrahepatic portal obstruction. In this case, previous treatment, EIS and Hassab's operation, for esophago-gastric varices might have inhibited the development of collaterals apart from surface of gastrointestinal tract, such as para-esophageal collateral veins or spleno-renal shunt. Since the thrombus in the extrahepatic portal vein causes strong pressure on inferior mesenteric vein which is connected to the inferior vena cava via the inferior rectal vein, rectal varices might be developed. In this case, it was considered that rectal varices were not treated enough by endoscopic therapy because of regurgitant hyper blood flow against portal venous pressure. Therefore, rectal transection was performed. After the treatment, the patient suffered no further episodes of bleeding from rectal varices.
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9/61. The critically ill liver patient: the variceal bleeder.

    Esophageal varices develop in patients with cirrhosis once portal pressure, measured by hepatic venous pressure gradient, and exceeds 10 mm Hg. At a portal pressure of 12 mm Hg, variceal bleeding may develop that is associated with a mortality of 30% to 50% per episode. In addition to an elevated portal pressure, other risk factors for the development of variceal hemorrhage include: variceal size, endoscopic features on the variceal wall (i.e., red wales), and child-Pugh class. In patients with suspected variceal hemorrhage, the treatment of the acute episode includes intravascular volume expansion, hemostasis through the use of pharmacological agents and endoscopy, and the prevention and treatment of potential complications associated with variceal hemorrhage such as aspiration pneumonia, spontaneous bacterial peritonitis and hepatic encephalopathy. Given a high rate of rebleeding, long-term prevention through secondary prophylaxis should be instituted in all patients who have survived an episode of variceal bleeding. Current prophylactic options include: non-selective beta-blockers alone (first line) or in combination with long-acting nitrates (isosorbide mononitrate) and/or endoscopic variceal obliteration achieved through sclerotherapy or preferably, band ligation.
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10/61. Acute visual loss in a child with autosomal recessive polycystic kidney disease: case report and review of the literature.

    Acute visual loss secondary to ischemic optic neuropathy in children is extremely rare. The causes are usually hypotension or anemia. We describe the clinical course of a 9-year-old boy with a functional renal transplant who presented to the emergency room hemodynamically stable after waking up with complete bilateral loss of vision (no light perception). Examination showed that he had suffered massive nocturnal blood loss from esophageal varices secondary to portal hypertension. The patient's end-stage renal disease was secondary to autosomal recessive polycystic kidney disease (ARPKD), an entity comprised of renal cysts and hepatic fibrosis. Ophthalmologic findings in ARPKD are rarely cited in the literature. A literature search revealed 3 other cases of sudden visual loss reported in nonophthalmologic journals in patients with ARPKD. Funduscopic examination showed bilateral optic nerve head pallor and swelling with associated flame hemorrhages. The fact that this patient already had mildly pale nerves on presentation, along with hemodynamically compensated blood pressure and pulse, suggested chronic as well as acute ischemia. Based on our findings and other reported cases in the literature, ophthalmologic examinations may be indicated in all patients with ARPKD.
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