The management of upper gastrointestinal haemorrhage in a tropical country.

Rao, Tanushree; Pande, Girish; Sahni, Peush; Nundy, Samiran

doi:10.1136/emj.8.3.169

Cited by 9 publications

(24 citation statements)

References 11 publications

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“…The etiology of these presinusoidal causes of PHT has remained obscure, and these diseases are also not prevalent in the West (<10% of PHT cases) [1,3,4]. In our country, EHPVO affects the young (age of onset <20 years) with the first bleeding episode occurring before puberty in most patients [7][8][9]. Patients with EHPVO have good liver function, which remains preserved over the long term; amoderately enlarged spleen; tolerate variceal bleeding episodes well; rarely develop ascites (except during an acute bleed or in children <5 years); and do not show signs of liver decompensation such as encephalopathy.…”

Section: Natural History Of Phtmentioning

confidence: 95%

“…Extrahepatic portal venous obstruction (EHPVO) and noncirrhotic portal fibrosis (NCPF) together account for 40-50% of acute variceal hemorrhage (AVH) presenting to the emergency services in our country [7]. The etiology of these presinusoidal causes of PHT has remained obscure, and these diseases are also not prevalent in the West (<10% of PHT cases) [1,3,4].…”

Section: Natural History Of Phtmentioning

confidence: 99%

“…In a previously diagnosed patient with cirrhosis, variceal bleeding would be the likely cause of upper gastrointestinal hemorrhage (GIH) in 70% of the cases, whereas in patients with EHPVO/NCPF the source of bleeding should be considered variceal unless proved otherwise [3,4,7,8,14]. In addition, hyperactive bowel sounds on abdominal auscultation indicate upper gastrointestinal source of bleeding, and splenomegaly is an important clinical indicator toward the presence of PHT.…”

Section: Surgery For Acute Variceal Hemorrhage (Avh)mentioning

confidence: 99%

“…In addition, hyperactive bowel sounds on abdominal auscultation indicate upper gastrointestinal source of bleeding, and splenomegaly is an important clinical indicator toward the presence of PHT. The diagnosis of AVH is dependent on upper gastrointestinal endoscopy that allows direct visualization of bleeding esophageal/gastric varix, or signs of recent bleeding such as (white nipple or overlying clot) or red signs associated with blood in the stomach [3,4,7,8,14].…”

Section: Surgery For Acute Variceal Hemorrhage (Avh)mentioning

confidence: 99%

“…At surgery, a gastrotomy is often required to directly under run the esophagogastric varices with interlocking nonabsorbable sutures to arrest the hemorrhage before constructing the decompressive portosystemic shunt [7,9,26]. In centers where expertise is available, surgical shunt should be considered in patients with Child's A status and patients with noncirrhotic portal hypertension (NCPH) once the other modalities have failed to arrest the variceal bleeding.…”

Section: Surgery For Acute Variceal Hemorrhage (Avh)mentioning

confidence: 99%

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Current Role of Surgery in Portal Hypertension

Pal

2011

Indian J Surg

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Treatment for portal hypertension (PHT) has evolved from surgery being the only option during the 1970s to the wide range of options currently available. Surgery has not vanished from the therapeutic armamentarium, but its role has changed and is constantly evolving. The present review primarily focuses on the role of surgery in tackling patients with PHT and varices with regard to the Indian scenario and also looks at its relevance, given the availability of a host of other therapeutic options.Keywords Portal hypertension . Portosystemic shunt . Surgery . Variceal haemorrhage Pathophysiology of PHTFor understanding how surgery can help modify the natural course in patients with PHT, it is necessary to understand its pathophysiology and the natural history of varices in such patients. PHT is usually the consequence of increased resistance to portal blood flow coupled with increased blood flow through the splanchnic circulation because of a hyperdynamic circulatory state that exists both in cirrhotics and to some extent in noncirrhotic etiologies (large congested splenomegaly) as well. Traditionally, at the ultrastructural level, PHT has been classified into presinusoidal, sinusoidal, and postsinusoidal. It is for the sinusoidal and postsinusoidal blocks that there is an accurate but invasive way of monitoring the portal pressure by using the method to estimate the hepatic venous pressure gradient (HVPG) in the vascular/hemodynamic lab [1][2][3]. In cirrhotic patients, as about a third to half of them will actually have PHT; HVPG >5 mmHg indicates PHT. PHT becomes clinically significant when the HVPG is ≥10 mmHg [1][2][3]. This is the pressure threshold when PHT leads to the formation of esophagogastric varices, retroperitoneal and periportal collaterals, hypersplenism, low serum albuminascitic albumin gradient ascites, spontaneous bacterial peritonitis, etc. Varices rupture and bleed only when the HVPG >12 mmHg [1][2][3]. Natural History of PHTIt has been estimated that varices are present in about 30-40% of compensated cirrhotics and nearly two-thirds of the decompensated patients. In cirrhotic patients without varices on the first endoscopy, the annual incidence of new varices is between 5% and 10% [1,4]. Once developed, the progression of varices from small to large depends on the deterioration of liver function and continued hepatic insult (virus-, alcohol-, metabolic-, drug-induced, etc.). The overall annual incidence of bleeding is about 4% and this increases to 15% per year in those with large varices, red signs, and poor Child's status [1,[4][5][6]. About a third of the cirrhotic patients with varices will bleed and the mortality following each episode of bleeding is about 20% (maybe higher) in experienced tertiary health centers. Early mortality (within 6 weeks) following an acute episode of variceal bleeding depends on the etiology of PHT, the severity of underlying liver disease (Child's C, model for end-stage liver disease [MELD] >18), actively bleeding varices, bleeding gastric varices (GV...

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