Endoscopic Therapy for Esophageal Variceal Hemorrhage

2011 ◽  
pp. 313-315
Author(s):  
Gregory V. Stiegmann
Hepatology ◽  
1999 ◽  
Vol 29 (1) ◽  
pp. 44-50 ◽  
Author(s):  
Ian M. Gralnek ◽  
Dennis M. Jensen ◽  
Thomas O. Kovacs ◽  
Rome Jutabha ◽  
Gustavo A. Machicado ◽  
...  

2000 ◽  
Vol 118 (4) ◽  
pp. A964
Author(s):  
W.R. Kim ◽  
P.S. Kamath ◽  
Mayo Clin

Author(s):  
Christos Sotiropoulos, MD, MSc ◽  
Eftichia Sakka, MD ◽  
Georgios Theocharis, MD, PhD ◽  
Konstantinos Thomopoulos, MD, PhD

Liver cirrhosis is a defined liver disease with a wide range of clinical manifestations. Variceal bleeding is the main source of gastrointestinal hemorrhage among cirrhotic patients induced by several factors, such as alcohol consumption or infections. This is a report of a cirrhotic patient presenting with esophageal variceal bleeding in the context of COVID-19 infection. We report the case of a 53-year-old patient with liver cirrhosis and multifocal hepatocellular carcinoma presenting with upper gastrointestinal bleeding as the first manifestation of COVID-19 infection. Upon admission, the patient had no symptoms suggestive of a respiratory tract infection or any contact with positive SARS-CoV-2 individual and upper gastrointestinal endoscopy revealed variceal hemorrhage. After a few hours the patient manifested with fever, cough and dyspnea and a SARS-CoV-2 polymerase chain reaction test obtained was positive. The patient was initially treated with endoscopic band ligation and transferred in the COVID-19 infection clinic, where after a few days of hospitalization he passed away. The devastating pandemic of coronavirus disease 2019 had altered the pathophysiology and clinical presentation of several chronic diseases. This case report suggests that coronavirus disease as a potential triggering factor of variceal bleeding.


2015 ◽  
Vol 148 (4) ◽  
pp. S-646
Author(s):  
Bradley Confer ◽  
Mohannad Dugum ◽  
Thimmaiah G. Theethira ◽  
Ibrahim A. Hanouneh ◽  
Rocio Lopez ◽  
...  

2002 ◽  
Vol 126 (10) ◽  
pp. 1197-1200 ◽  
Author(s):  
M. Tsokos ◽  
E. E. Türk

Abstract Context.—Some autopsy studies have dealt with histologic features of esophageal varices after different therapeutic procedures. However, to the best of our knowledge, no reports have been published describing outpatient characteristics that are associated with fatal esophageal variceal hemorrhage in a medicolegal autopsy population. Objectives.—To (1) assess the incidence of sudden deaths from esophageal variceal hemorrhage in an unselected medicolegal autopsy population and (2) determine demographics of outpatients dying from esophageal variceal hemorrhage with special reference to blood alcohol concentrations at the time of death. Design.—We performed a retrospective study of all autopsy cases of sudden death from esophageal variceal hemorrhage from a total of 6038 medicolegal autopsies performed over a 5-year period (1997–2001). We analyzed individual cases to determine gender, age, location and histology of bleeding esophageal varices, pathogenic mechanism for esophageal varices, concomitant underlying diseases contributing to fatal outcome, body mass index, circumstances at the death scene, and blood alcohol levels at the time of death. We reviewed the results of toxicologic analyses of alcohol concentrations in samples of femoral venous blood and urine obtained at autopsy; concentrations had been determined by gas chromatography with mass spectroscopy and enzymatic assays. Results.—We identified 45 cases of fatal esophageal variceal hemorrhage that occurred out of hospital and presented as sudden death; the corresponding 5-year incidence in this autopsy population was 0.75%. All of the deceased were white; the male-female ratio was 1.6:1, and the mean age was 50.6 years. Ruptured esophageal varices were located in the lower third of the esophagus in 44 cases. Cirrhosis of the liver was present in all cases (alcoholic cirrhosis of the liver in 42 cases), and a hepatocellular carcinoma was present in 3 cases. Alcohol-induced pancreatic tissue alterations were frequently found. The results of toxicologic analysis were positive for alcohol in femoral venous blood and urine in 30 cases. Blood alcohol levels at the time of death were less than 100 mg/dL (21.7 mmol/L) in 15 cases, between 100 and 200 mg/dL (21.7 and 43.4 mmol/L) in 8 cases, and greater than 200 mg/dL (43.4 mmol/L) in the remaining 7 cases. Conclusions.—Apart from abnormalities in coagulation due to poor liver function in long-term alcohol users, acute alcohol intake may represent an important factor influencing mortality in individuals with esophageal variceal hemorrhage. Acute alcohol intake has transient effects on blood clotting time caused by ethanol and its main metabolites. In the present study, bloodstains at the death scene and unusual body positions of the deceased that aroused suspicion of a violent death were leading reasons for conducting a medicolegal autopsy. Apart from aspects of forensic pathology, the demographics of our study population are also noteworthy from the viewpoint of social medicine. The data we present stress the importance of fatal esophageal variceal hemorrhage as a relevant cause of sudden death occurring outside the hospital in socially isolated, alcohol-addicted individuals.


2020 ◽  
Vol 45 (8) ◽  
pp. 2305-2314
Author(s):  
Faeze Salahshour ◽  
Mohammad-Mehdi Mehrabinejad ◽  
Mohammad-Hossein Rashidi Shahpasandi ◽  
Maede Salahshour ◽  
Nastaran Shahsavari ◽  
...  

2004 ◽  
Vol 18 (2) ◽  
pp. 109-113 ◽  
Author(s):  
Juan G Abraldes ◽  
Alessandra Dell'Era ◽  
Jaime Bosch

Bleeding from gastroesophageal varices is a frequent and often deadly complication of cirrhosis. The key factor in the natural history of esophageal varices is increased portal pressure, which in cirrhosis is due to the combination of increased hepatic vascular resistance and increased portal collateral blood flow. The maintenance and aggravation of this situation leads to the progressive dilation of the varices and thinning of the variceal wall, until the tension exerted by the variceal wall exceeds the elastic limit of the vessel, leading to variceal hemorrhage. Mortality from a variceal bleeding episode has decreased in the last two decades from 40% to 20% due to the implementation of effective treatments and improvement in the general medical care. Initial treatment should include adequate fluid resuscitation and transfusion to maintain the hematocrit at 25% to 30%, and prophylactic antibiotics (norfloxacin or amoxicillin-clavulanic acid). It is currently recommended that a vasoactive drug be started at the time of admission. Drug therapy may be started during transferal to hospital by medical or paramedical personnel and maintained for up to five days to prevent early rebleeding. Terlipressin, a vasopressin derivative, is the preferred agent because of its safety profile and proven efficacy in improving survival. Somatostatin is as effective as terlipressin, but may require higher than the usually recommended dosage. Octreotide is effective in conjunction with endoscopic therapy, but is the second choice because it has not been shown to reduce mortality. Vasopressin may be used where terlipressin is not available, but should be given in combination with transdermal nitroglycerin. Endoscopic elastic band ligation is the recommended endoscopic treatment, but injection sclerotherapy is still employed in many centres for active variceal bleeding. Failures of medical therapy (drugs plus endoscopic therapy) should undergo a second course of endoscopic therapy before proceeding to transjugular intrahepatic portosystemic shunt or, in rare occasions, to portosystemic shunt surgery. Administration of recombinant activated factor VII may decrease the number of treatment failures among patients with advanced liver failure (Child-Pugh class B and C).


2011 ◽  
Vol 2011 ◽  
pp. 1-6 ◽  
Author(s):  
Àngels Escorsell ◽  
Jaime Bosch

Acute variceal bleeding (AVB) is a life-threatening complication in patients with cirrhosis. Hemostatic therapy of AVB includes early administration of vasoactive drugs that should be combined with endoscopic therapy, preferably banding ligation. However, failure to control bleeding or early rebleed within 5 days still occurs in 15–20% of patients with AVB. In these cases, a second endoscopic therapy may be attempted (mild bleeding in a hemodynamically stable patient) or we can use a balloon tamponade as a bridge to definitive derivative treatment (i.e., a transjugular intrahepatic portosystemic shunt). Esophageal balloon tamponade provides initial control in up to 80% of AVB, but it carries a high risk of major complications, especially in cases of long duration of tamponade (>24 h) and when tubes are inserted by inexperienced staff. Preliminary reports suggest that self-expandable covered esophageal metallic stents effectively control refractory AVB (i.e., ongoing bleeding despite pharmacological and endoscopic therapy or massive bleeding precluding endoscopic therapy) with a low incidence of complications. Thus, covered self-expanding metal stents may represent an alternative to the Sengstaken-Blakemore balloon for the temporary control of bleeding in treatment failures. Further studies are required to determine the role of this new device in AVB.


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