Other causes include:Prehepatic causes

Portal vein thrombosis
Splenic vein thrombosis
Arteriovenous fistula (increased portal blood flow)
Splenomegaly and/or hypersplenism (increased portal blood flow)Hepatic causes

Cirrhosis of any cause. alcohol use disorder
chronic viral hepatitis
biliary atresia
Primary biliary cirrhosis
Primary sclerosing cholangitis
Chronic pancreatitis
Hereditary haemorrhagic telangiectasia
Schistosomiasis
Congenital hepatic fibrosis
Nodular regenerative hyperplasia
Fibrosis of space of Disse
Granulomatous or infiltrative liver diseases (Gaucher disease, mucopolysaccharidosis, sarcoidosis, lymphoproliferative malignancies, amyloidosis, etc.) Toxicity (from arsenic, copper, vinyl chloride monomers, mineral oil, vitamin A, azathioprine, dacarbazine, methotrexate, amiodarone, etc.) Viral hepatitis
Fatty liver disease
Veno-occlusive diseasePosthepatic causes

Inferior vena cava obstruction
Right-sided heart failure, e.g. from constrictive pericarditis
Budd–Chiari syndrome also known as hepatic vein thrombosis

Pathophysiology
The pathophysiology of portal hypertension is indicated by increased vascular resistance via different causes; additionally, hepatic stellate cells and myofibroblasts are activated. Increased endogenous vasodilators in turn promote more blood flow in the portal veins.Nitric oxide is an endogenous vasodilator and it regulates intrahepatic vascular tone (it is produced from L-arginine). Nitric oxide inhibition has been shown in some studies to increase portal hypertension and hepatic response to norepinephrine. Diagnosis
Ultrasonography (US) is the first-line imaging technique for the diagnosis and follow-up of portal hypertension because it is non-invasive, low-cost and can be performed on-site.A dilated portal vein (diameter of greater than 13 or 15 mm) is a sign of portal hypertension, with a sensitivity estimated at 12.5% or 40%. On Doppler ultrasonography, a slow velocity of <16 cm/s in addition to dilatation in the main portal vein are diagnostic of portal hypertension.
This enhanced form of the disease led to 80% hospitalization in the recipients of FIRSV compared to 5% in the control group. Additionally, 2 fatalities occurred among the vaccine recipients upon reinfection in subsequent years. Subsequent attempts to develop an attenuated live virus vaccine with optimal immune response and minimal reactogenicity have been unsuccessful. Further research on animal subjects suggested that intravenously administered immunoglobulin with high RSV neutralizing activity can protect against RSV infection. In 1995, the U.S. Food and Drug Administration (FDA) approved the use of RespiGam (RSV-IGIV) for the prevention of serious lower respiratory tract infection caused by RSV in children younger than 24 months of age with bronchopulmonary dysplasia or a history of premature birth. The success of the RSV-IGIV demonstrated efficacy in immunoprophylaxis and prompted research into further technologies. Thus, Palivizumab was developed as an antibody that was found to be fifty times more potent than its predecessor. This antibody has been widely used for RSV since 1998 when it was approved. Palivizumab, originally known as MEDI-493, was developed as an RSV immune prophylaxis tool that was easier to administer and more effective than the current tools of that time (the 1990s). It was developed over a 10-year period by MedImmune Inc. by combining human and mouse DNA. Specifically, antibody production was stimulated in a mouse model following immunization with RSV. The antibody-producing B cells were isolated from the mouses spleen and fused with mouse myeloma cell lines.