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Skin: Resilience
Published in Philip Berry, Necessary Scars, 2021
Valerie, 79 years old, was admitted with bleeding oesophageal varices (complicating a previously undiagnosed liver disorder). Varices are swollen veins, as thick as your little finger, that run up the inside of the oesophagus. Their walls become thin over time, and often they rupture. The blood pours out, filling the stomach. Patients vomit pure, dark blood; it is one of the most frightening experiences imaginable. They can die within hours. That’s what happened to Sarah, in ‘Comfort’.
Gastrointestinal Bleeding
Published in Stephen M. Cohn, Alan Lisbon, Stephen Heard, 50 Landmark Papers, 2021
Endoscopy is beneficial in UGI bleeds because it can be simultaneously diagnostic and, occasionally, therapeutic. Ulcer bleeding can be stopped or reduced with medical treatment as discussed previously, but studies have shown that endoscopy prevents re-bleeding. Endoscopic findings of active bleeding or a visible vessel require treatment due to their high rates of re-bleeding. While endoscopy is used for the treatment of ulcer disease, it can be used for both the treatment of active bleeding and prophylaxis in patients with varices. Options for endoscopic management of varices include injection sclerotherapy and banding ligation. Both techniques have been used for the control of acute hemorrhage: multiple studies, however, have found that ligation is superior to sclerotherapy. Regardless of cause, patients admitted with an UGIB benefit from endoscopic intervention within the first 24 hours of admission.
The patient with acute gastrointestinal problems
Published in Peate Ian, Dutton Helen, Acute Nursing Care, 2020
Rebecca Maindonald, Adrian Jugdoyal
The portal vein carries approximately 1500mL/min of blood from the intestines, spleen and stomach to the liver. Obstruction to this blood flow (whatever the aetiology) will result in elevated portal venous pressure. This, in turn, causes distension of the proximal veins and an increase in the intracapillary pressure in the organs drained by the obstructed veins. Particularly vulnerable to this increase in pressure is the gastro-oesophageal junction, where varices can develop and sometimes rupture, resulting in haemorrhage and haematemesis. Varices are portosystemic anastomoses, or a connection between the veins of the portal system and the systemic circulation. These communications between the two systems are formed when the direct drainage routes are blocked. The typical site of varices is the lower third of the oesophagus, between the lower oesophageal veins and the short gastric veins.
Hepatic blood volume is decreased in patients with cirrhosis and does not decrease further after a meal like in healthy persons
Published in Scandinavian Journal of Gastroenterology, 2021
One of the limitations of the study is that the hepatic venous pressure gradient was not measured during the second PET study because the subjects were placed in the PET/CT-camera. Reliable postprandial measurements of HVPG could not be obtained because the subject had to be moved out of the scanner which interfered with the measurements and sometimes caused displacement of the hepatic venous catheter into the vena cava. A postprandial increase in HVPG of up to 33% and a decrease in hepatic vascular resistance of 31% in patients with cirrhosis has been demonstrated by others [9]. The present results are in accordance with those observations since an increased blood flow would increase the vascular pressure. A compensatory decrease in vascular resistance would allow blood to be mobilized from the liver and seek to counteract the increased pressure. This is further supported by the vascular resistance across the liver primarily being post-sinusoidal [17]. The present findings in conjunction with other studies could thus indicate that normal hemodynamic changes caused by a meal could induce a risk for patients with cirrhosis and portal hypertension as the liver’s ability to adjust is ameliorated and the meal itself may increase the portal pressure. This could potentially increase the risk of gastric and esophageal varices and thus bleeding.
Massive gastrointestinal bleeding due to ectopic varix in distal duodenum: a case report
Published in Journal of Community Hospital Internal Medicine Perspectives, 2021
Patrick Mallea, Aaron Allen, Maureen Kim Lynch, Elsbeth Jensen-Otsu, David Tompkins
Gastrointestinal bleeding (GIB) is a significant cause of morbidity and mortality worldwide. Gastrointestinal bleeding from proximal sources (esophagus, stomach and duodenum) has an incidence of 47/100,000 and lower gastrointestinal bleeding has an incidence of 33/100,000 [1]. Ectopic varices are an uncommon source of gastrointestinal bleeding, accounting for only 2–5% of variceal bleeding [2]. Ectopic varices are defined as large portosystemic collateral veins occurring anywhere in the gastrointestinal tract other than the esophagogastric region [3]. Though ectopic varices can occur at numerous sites in the GI tract, 17% of the ectopic varices are located in the duodenum [2]. Duodenal varices are generally associated with portal hypertension, which can be secondary to cirrhosis or extrahepatic venous obstruction [2]. Despite the uncommon occurrence of ectopic varices, they have a four-times higher risk of bleeding than gastroesophageal varices [4], and mortality is as high as 40% [5]. We report a case of massive gastrointestinal bleeding due to distal duodenal ectopic varix successfully treated with interventional radiology guided transcatheter embolization and transjugular intrahepatic portosystemic shunt (TIPS) procedure.
Modified ‘sandwich’ injection with or without ligation for variceal bleeding in patients with both esophageal and gastric varices: a retrospective cohort study
Published in Scandinavian Journal of Gastroenterology, 2020
Tingting Hu, Simon Stock, Wandong Hong, Yongping Chen
Failure to control bleeding was based on Baveno V consensus. It required that the time frame for the acute bleeding episode should be 120 h (5 days) and defined failure as death or the need to change therapy according to one of the following criteria: (1) Fresh hematemesis or nasogastric aspiration of ≥100 mL of fresh blood ≥2 h after the start of a specific drug treatment or therapeutic endoscopy. (2) Development of hypovolemic shock. (3) A 3 g drop in Hb (equivalent to a 9% drop in hematocrit) within any 24 h period if no blood transfusion is administered [19]. Rebleeding was defined as occurrence of one or more times clinically significant rebleeding (example: melena or/and hematemesis) from portal hypertensive sources after day 5 [20]. As proposed by Baveno VI consensus, 6 weeks should be the primary endpoint for studies for treatment of acute variceal bleeding. Therefore, we analyzed 6-week rebleeding rate [4]. The 1-year rebleeding rate was defined as cumulative rebleeding rate within 1-year after day 5.