Non-bleeding Esophageal Varices Research Articles

Have the metabolic support pendulums in the intensive care unit stopped swinging?

Have the metabolic support pendulums in the intensive care unit stopped swinging?

Using Capsule Endoscopy to Identify GI Tract Lesions in Cirrhotic Patients With Portal Hypertension and Chronic Anemia

We aimed to evaluate the ability of capsule endoscopy (CE) to detect small intestine (SI) lesions, especially SI varices, in patients with intrahepatic cirrhosis, portal hypertension (PHTN), and chronic anemia. Gastroesophageal variceal bleeding is a well-recognized complication of cirrhosis and PHTN, yet methods of identifying lesions in the SI that may contribute to covert bleeding and anemia, such as small bowel enteroscopy and angiography, are invasive and may be inadequate. In this observational pilot study, 19 consecutive patients presenting to a tertiary care, liver transplantation referral center with cirrhosis, PHTN, and chronic anemia after obliterative esophageal variceal therapy were evaluated with wireless CE using the GIVEN Pillcam SB M2A capsule. Two independent and blinded examiners reviewed the CE examinations. SI varices were identified in 15.8% (3/19) of patients. Other PHTN-related findings included portal hypertensive gastropathy (13/19, 68.4%), portal hypertensive enteropathy (12/19, 63.1%), and portal hypertensive colopathy (3/19, 15.8%). Two patients had nonbleeding esophageal varices (2/19, 10.5%). A potential source of gastrointestinal blood loss was identified in 89.5% (17/19) of patients. Active bleeding sites were identified in 15.8% (3/19). CE can identify potential bleeding sources and could have diagnostic utility in patients with end-stage liver disease and chronic anemia after obliterative esophageal variceal therapy.

Clinical Challenges and Images in GI

Question: A 52-year-old woman with alcoholic cirrhosis (MELD score 12) developed massive hematemesis and melena requiring tracheal intubation and balloon tamponade with a Sengstaken-Blakemore tube (SBT). At endoscopy, nonbleeding esophageal varices and a gastroesophageal varix (GOV type 2, extending to the greater curve) were identified; the former were banded. Massive rebleeding occurred 24 hours later, and at re-endoscopy the GOV was seen to be actively bleeding. Eight milliliters of a 1:2 mixture of N-butyl-2-cyanoacrylate (histoacryl “glue”) and lipiodol was injected into the GOV.

Hepatic Artery Pseudoaneurysm—A Rare Complication of Liver Biopsy

Hepatic artery pseudoaneurysms are rare. Potential causes include blunt or penetrating trauma, liver surgery and far less common, percutaneous interventional procedures, such as biopsy or percutaneous transhepatic cholangiography. We report a case of a hepatic artery pseudoaneurysm secondary to percutaneous liver biopsy with subsequent hemobilia. Case Presentation: A 68 year old man with chronic Hepatitis C infection was found to have a liver mass on CT scan. The patient had a percutaneous liver biopsy done with pathology revealing moderately differentiated hepatocellular carcinoma. He was subsequently admitted 2 weeks later with complaints of melena and coffee-ground emesis. On admission the patient was found to have a hematocrit of 17% and was transfused with packed red cells. Upper endoscopy revealed grade 2 non-bleeding esophageal varices and a large amount of red blood in the second portion of the duodenum. Celiac and hepatic angiogram revealed a pseudoaneurysm supplied by a branch of the artery supplying the posterior segment of the right lobe of the liver. Also noted was filling of a bile duct adjacent to the pseudoaneurysm consistent with an arterial-biliary fistula. The hepatic artery was embolized using polyvinyl alcohol particles and the follow-up angiogram showed no visualization of the pseudoaneurysm or bile ducts. The patient's hematocrit subsequently stabilized and the bleeding ceased. Summary: Hemobilia can present acutely after simultaneous perforation of intrahepatic bile ducts and blood vessels such as in hepatoma; or, more commonly from gradual erosion of a biopsy-induced hematoma or pseudoaneurysm into a bile duct presenting as massive gastrointestinal bleeding. The diagnostic test of choice is angiography, which offers the advantage of therapeutic embolization at the same time. Surgery is the definitive treatment if nonoperative management fails. [figure 1]Figure

Portal Venous Flow Pattern as a Useful Tool for Predicting Esophageal Varix Bleeding in Cirrhotic Patients

This study aimed to evaluate whether (1) the portal venous flow pattern determined by color Doppler sonography could be related to the clinical severity of liver cirrhosis and (2) whether the flow patterns differ between patients with bleeding and nonbleeding esophageal varices. One hundred twenty-nine cirrhotic patients and 60 noncirrhotic healthy controls were enrolled after endoscopic survey for the presence of esophageal varices. Each patient received color Doppler echography to define the pattern of blood flow direction as hepatopetal or nonhepatopetal (hepatofugal, turbulence, and bidirection) in type. The patients with esophageal varices were further categorized into two groups: with recent bleeding (BEV; n = 99) and without recent bleeding (NBEV; n = 30). More patients in the BEV group (72.7%) had a nonhepatopetal Doppler flow pattern than in the control group (1.7%) and NBEV group (13.3%) (P < 0.001). Among the 129 cirrhotic patients, the nonhepatopetal flow pattern of the portal vein was higher in 96% of Child-Pugh grade C patients than in 41.8% of grade A patients and 57.6% of grade B patients (P < 0.05). Moreover, for those cirrhotic patients with Child-Pugh grades A and B, the nonhepatopetal Doppler flow pattern was more commonly found in the BEV group than in the NBEV group (63.0 vs. 13.8%; odds ratio, 10.64; 95% CI, 0.03-0.299; P < 0.001). Portal venous blood flow pattern is related to severity of cirrhosis. The presence of a nonhepatopetal flow pattern implicates an increased risk of esophageal varices bleeding, especially for those cirrhotic patients with Child-Pugh grades A and B.

Cases from the Osler Medical Service at Johns Hopkins University

Presenting features A 47-year-old African American man was admitted to the Osler Medical Service with a chief complaint of light-headedness. He was a heavy drinker and consumed 2 pints of fortified wine every day. On the day of admission, he had been at home consuming alcohol when he stood up, became lightheaded, and immediately had to sit down. He denied any loss of consciousness, dyspnea, hematemesis, coffee-ground emesis, lower abdominal pain, bright red blood per rectum, or melena, but he recalled a burning epigastric discomfort. The patient's medical history was notable only for a 20-year history of hypertension and recently diagnosed type 2 diabetes mellitus. He was not taking any medications. He had a normal hematocrit of 43% 6 months prior to admission. Physical examination showed a supine heart rate of 115 beats per minute and blood pressure of 165/90 mm Hg, without orthostatic changes. There was scleral icterus and a jaundiced palate, but no other stigmata of end-stage liver disease. His abdominal examination was unremarkable; there were no masses, tenderness, or hepatosplenomegaly. Rectal examination revealed guaiac-negative stool. The chest radiograph and electrocardiogram were unremarkable. On admission, the laboratory examination was notable for the following values: hematocrit, 22.8% with a mean corpuscular volume of 86.7 fL and a red cell distribution width of 25.7%; absolute reticulocyte count, 177,500/mm 3; total bilirubin, 4.2 mg/dL; direct bilirubin, 2.3 mg/dL; albumin, 3.3 g/dL; lactate dehydrogenase, 481 U/L; aspartate aminotransferase, 106 U/L; and alanine aminotransferase, 44 U/L. The prothrombin and activated partial prothrombin times were normal. There was no evidence of iron, vitamin B 12, or folate deficiency. The patient's haptoglobin level was severely depressed (<6 mg/dL) with a negative direct Coomb test and normal glucose-6-phosphate dehydrogenase activity. A peripheral blood smear was compatible with hemolysis and demonstrated normocytic, normochromic erythrocytes with moderate poikilocytosis, as well as rare spherocytes and target cells Figure 1). On the second day of hospitalization, a lipid panel revealed hypercholesterolemia with a total cholesterol level of 300 mg/dL. Due to the patient's complaint of burning epigastric pain and long history of alcohol consumption, esophagogastroduodenoscopy was performed and revealed grade 1 nonbleeding esophageal varices. What is the diagnosis?

The Influence of Liver Disease and Portal Hypertension on Bleeding in Mallory-Weiss Syndrome

The records of 79 patients admitted to the hospital from January 1985 through December 1990 for acute esophageal hemorrhage were analyzed to determine the influence of liver disease and/or portal hypertension on the severity of bleeding from Mallory-Weiss syndrome. Forty-two patients had bled from Mallory-Weiss syndrome; 8 had liver disease and nonbleeding esophageal varices, 6 had liver disease without varices, and 28 had no evidence of liver disease. The severity of bleeding was determined by the transfusion requirement for each group. The number of units of blood needed for patients with liver disease was significantly increased (p < 0.005) over the number of units necessary for patients without liver disease. There was no statistically significant difference in the transfusion requirement between liver disease patients with and without varices (i.e., portal hypertension). The transfusion requirement was also unrelated to the Child classification of hepatic functional reserve. We conclude that the severity of bleeding from Mallory-Weiss syndrome is primarily related to the status of liver function and that portal hypertension does not make an additive contribution.

Ultrasonic Diagnosis of Cruveilhier-Baumgarten Syndrome

History A 46-year-old alcoholic man was hospitalized because of mild hematemesis. Clinical examination revealed the presence of hepatomegaly and evidence of a moderately extensive abdominal collateral circulation. Findings from abdominal auscultation were normal. Endoscopy of the upper gastrointestinal tract demonstrated small, nonbleeding esophageal varices and hemorrhagic gastritis. Serum bilirubin level was 1.3 mg/dL. The SGPT value was 47 IU. The alkaline phosphatase was 185 IU (normal, less than 170 IU). The albumin level was 3.2 g/dL and the γ-globulin level was 1.8 g/dL. The prothrombin time was 75% of the control. A gray-scale ultrasonogram was obtained. The liver appeared normal, and the portal axis was patent. A tubular channel (Fig 1) (small arrows) was observed transversing the area from the portal vein (large arrow) to the umbilical area (asterisk). Diagnosis Cruveilhier-Baumgarten syndrome. Comment The tubular channel noted in the ultrasonogram in Fig 1 was interpreted as a probable umbilical vein.