Surgical management of portal hypertension.

Portal hypertension is frequently complicated by upper gastrointestinal tract bleeding and ascites. Hemorrhage from esophageal varices is the most common cause of death from portal hypertension. Medical treatment, including resuscitation, vasoactive drugs, and endoscopic sclerosis, is the preferred initial therapy. Patients with refractory hemorrhage frequently are referred for immediate surgical intervention (usually emergency portacaval shunt). An additional cohort of patients with a history of at least 1 episode of variceal hemorrhage is likely to benefit from elective shunt operations. Shunt operations are classified as total, partial, or selective shunts based on their hemodynamic characteristics. Angiographically created shunts have been introduced recently as an alternative to operative shunts in certain circumstances. Devascularization of the esophagus or splenectomy is done for specific indications. Medically intractable ascites is a separate indication for surgical intervention. Liver transplantation has been advocated for patients whose portal hypertension is a consequence of end-stage liver disease. In the context of an increasingly complex set of treatment options, we present an overview of surgical therapy for complications of portal hypertension.     

Animal models of portal hypertension

Chronic liver diseases ultimately lead to cirrhosis and portal hypertension (PHT). Indeed, PHT is a major cause of severe complications, while medical treatment is limited to non-selective beta blockers. Sophisticated animal models are needed to investigate novel treatment options for different etiologies of liver disease, effective anti-fibrotic agents as well as vasoactive drugs against PHT. In this review, we present some of the most common animal models of liver disease and PHT – including pre-hepatic, intra-hepatic and post-hepatic PHT in rodents. Methodology for induction, considerations for disease etiology, advantages and limitations and practical issues of these animal models are discussed. The appropriate and sensible use of animal models in preclinical research supporting the 3R concept of replacement, reduction and refinement is highlighted.     

Discussion on the surgery of portal hypertension

IN THE SURGICAL TREATMENT OF PORTAL HYPERTENSION, THREE PROBLEMS PRESENT: (1) mesenteric venous thrombosis, (2) haemorrhage from the alimentary tract, and (3) ascites.     

Angioarchitecture of the esophagogastric veins in portal hypertension

Based on our previous studies on the human normal venous angioarchitecture of the esophagogastric transition segment, we performed a similar analysis in 25 postmortem specimens obtained from subjects with a diagnosis of portal hypertension. The specimens were injected with India ink or barium sulfate and sectioned for histological examination. A 'weak' zone (point of lesser resistance) was described as being the most probable site of origin for the development of varicosities in the complex venous system of the esophagogastric junction. Such a system can be considered to be a physiological hemodynamic venous blockade mechanism interposed between the portal system and the systemic veins. The 'weak' zone is made up by the scarce submucous veins (shunt veins), by the submucous confluent and final confluent trunks, and by the true perforating veins of the tunica muscularis which compose a venous unity located about 3-5.5 cm above the Z (epithelioglandular) line.