SLIDE ON PORTAL HYPERTENSION (GASTROENTEROLOGY )

Slide on types of portal hypertension

1. P O R T A L H Y P E R T E NSION D r O k u b i k e Adaobi

2. I N T R O D U C TION P o r tal hypertension is defined by a pathologic increase in the pressure of the portal venous system. I t is the result of resistance to portal blood flow and may lead to complications such as variceal bleeding and ascites. Cirrhosis is the most common cause of portal hypertension, but it can also be present in the absence of cirrhosis, a condition referred to as "noncirrhotic portal hypertension."

3. Normal portal pressure is generally considered to be between 5 and 10 mm Hg. Once the portal pressure rises to 12 mm Hg or greater, complications can arise, such as varices and ascites. E sophageal varices are responsible for the main complication of portal hypertension

4. Pathophysiology Portal hypertension develops when there is resistance to portal blood flow and is aggravated by increased portal collateral blood flow • The resistance most often occurs within the liver (as is the case in cirrhosis), but it can also be prehepatic (eg, portal vein thrombosis) or posthepatic (eg, Budd-Chiari syndrome)

5. There are two components to the increased resistance, structural changes and dynamic changes . Structural changes occur when there is distortion of the liver microcirculation by fibrosis, nodules, angiogenesis, and vascular occlusion . Dynamic changes occur when there is contraction of activated hepatic stellate cells and myofibroblasts that surround hepatic sinusoids and are in the fibrous septa and vascular smooth muscle cells of the hepatic vasculature .

6. The dynamic changes are thought to be due to increased production of vasoconstrictors (eg, endothelins, angiotensin-II, norepinephrine, thromboxane A2) and reduced release of endothelial vasodilators (eg, nitric oxide). As portal hypertension worsens, splanchnic blood flow is increased because of local release of vascular endothelial growth factor, nitric oxide, and other splanchnic vasodilators that cause splanchnic arteriolar vasodilation and angiogenesis

7. In addition to worsening the portal hypertension, these changes also lead to systemic hypotension, vascular underfilling, stimulation of endogenous vasoactive systems, plasma volume expansion, and increased cardiac output, factors that are important in the development of ascites.

8. E t i o l o g y I t c o u l d be pre h e p a t i c , h e p a t i c o r p o s t hepatic .

9. P r e h e p a t i c Portal vein thrombosis Splenic vein thrombosis Congenital atresia or stenosis of portal vein Extrinsic compression (tumors) Splanchnic arteriovenous fistula

10. Hepatic P r e s i n u s o d i a l Schistosomiasis (early stage) Primary biliary cirrhosis (early stage) Idiopathic portal hypertension (early stage) Nodular regenerative hyperplasia Myeloproliferative d i s e a s e Polycystic disease Hepatic metastasis Granulomatous diseases (sarcoidosis, tuberculosis)

11. S i n u s o d i a l Hepatic cirrhosis Acute alcoholic hepatitis Schistosomiasis (advanced stage) Primary biliary cirrhosis (advanced stage) Idiopathic portal hypertension (advanced stage) Acute and fulminant hepatitis

12. Congenital hepatic fibrosis Peliosis hepatitis Veno-occlusive disease Vitamin A toxicity Sclerosing cholangitis Hepatitis B virus–related and hepatitis C virus–related cirrhosis Wilson disease Hemochromatosis Alpha-1 antitrypsin deficiency Chronic active hepatitis

13. P o s t s i n u s o d a l Sinusoidal obstruction syndrome (previously called veno-occlusive disease) Phlebosclerosis of hepatic veins (eg, due to alcohol-associated liver disease, chronic radiation injury, hypervitaminosis A) Primary vascular malignancies (eg, epithelioid hemangioendothelioma, angiosarcoma) Granulomatous phlebitis (eg, from sarcoidosis, Mycobacterium avium or M. intracellulare infection) Lipogranulomas (eg, mineral oil granuloma)

14. P o s t h e p a t i c Thrombosis of the inferior vena cava (IVC) Right-sided heart failure Constrictive pericarditis Severe tricuspid regurgitation Budd-Chiari syndrome Arterial-portal venous fistula

15. Clinical M a n i f e s t a t i o n s Portal hypertension is often asymptomatic until complications develop

16. Diagnosis

17. U l t r a s o n o g r a p h y Findings on transabdominal ultrasound with Doppler imaging may support a diagnosis of portal hypertension, but lack sensitivity . Ascites Splenomegaly Nodular liver Portal flow mean velocity <12 cm/second I nversion of flow in the portal vein, Portosystemic collaterals (patent-paraumbilical vein, splenorenal

18. collaterals, dilated left and short gastric veins) Portal vein diameter >13 mm Decreased or no respiratory variation in splenic and superior mesenteric vein diameter Portal/splenic/superior mesenteric vein thrombosis

19. Transient elastography Transient elastography using ultrasound is a noninvasive method for detecting hepatic fibrosis . It has been suggested that a value <13.6 kPa can be used to rule out portal hypertension, whereas a value ≥21.1 kPa can be used to rule it in .

20. C o m p l i c a t i on Variceal hemorrhage ●Portal hypertensive gastropathy ●Ascites ●Spontaneous bacterial peritonitis ●Hepatorenal syndrome ●Hepatic hydrothorax ●Hepatopulmonary syndrome ●Portopulmonary hypertension ●Cirrhotic cardiomyopathy ●Portal cholangiopathy

21. Treatment I t is directed at the cause of portal hypertension.