1. SEMINAR No 8. Portal hypertension
By Susanna Sebastianpillai

2. ANATOMY OF PORTAL CIRCULATION
The portal system, includes all the veins which drain the blood from the abdominal part of the digestive tube (with the exception of the lower part of the rectum) and from the spleen, pancreas, and gall-bladder. 
From these viscera the blood is conveyed to the liver by the portal vein. 

3.  In the liver this vein ramifies like an artery and ends in capillary-like vessels termed sinusoids, from which the blood is conveyed to the inferior vena cava by the hepatic veins.
From this it will be seen that the blood of the portal system passes through two sets of vessels, (a) the capillaries of the digestive tube, spleen, pancreas, and gall- bladder; and (b) the sinusoids of the liver.

4. THE PORTAL VEIN
Is 8 cm. It originates behind head of pancreas by the confluence of superior, inferior mesenteric veinc and splenic vein. The portal vein receives cystic vein, right and left gastric veins and prepyloric vein and Paraumbilical veins  In the lesser omentum it is placed behind and between the common bile duct and the hepatic artery.
The right branch of the portal vein enters the right lobe of the liver, but before doing so generally receives the cystic vein.
The left branch gives branches to the caudate lobe, and then enters the left lobe of the liver.

5. THE SPLENIC VEIN
Commences by five or six large branches which return the blood from the spleen.
Tributaries:
 The short gastric veins, four or five in number, drain the fundus and left part of the greater curvature of the stomach.
  The left gastroepiploic vein receives branches from the antero-superior and postero-inferior surfaces of the stomach and from the greater omentum.
 The pancreatic vein consist of several small vessels which drain the body and tail of the pancreas.
 The inferior mesenteric vein returns blood from the rectum and the sigmoid, and descending parts of the colon.

6. THE SUPERIOR MESENTERIC VEIN
Returns the blood from the small intestine, from the cecum, and from the ascending and transverse portions of the colon. (Besides the tributaries which correspond with the branches of the superior mesenteric artery, the jejunal, ileal, ileocolic, right colic, and middle colic veins)
The right gastroepiploic vein receives branches from the greater omentum and from the lower parts of the antero-superior and posteroinferior surfaces of the stomach.
 The pancreaticoduodenal veins drains blood from the pancreas and duodenum.
 The Coronary Vein derives tributaries from both surfaces of the stomach.
The Pyloric Vein is of small size, and runs from left to right along the pyloric portion of the lesser curvature of the stomach
  The Cystic Vein drains the blood from the gall- bladder.

7. Pathophysiology of portal hypertension
Is elevated pressure in the portal vein. It is caused most often by cirrhosis (in developed countries), schistosomiasis (in endemic areas), or hepatic vascular abnormalities.
Normal portal pressure is 5 to 10 mm Hg (7 to 14 cm H 2 O), which exceeds inferior vena caval pressure by 4 to 5 mm Hg (portal venous gradient). Higher values are defined as portal hypertension.
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. 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).

8. There are many causes of portal hypertension including etiologies above the liver, within the liver, and below the liver;
Prehepatic: Suprahepatic abnormalities leading to portal hypertension include cardiac disease, hepatic vein etiology, and inferior vena cava thrombosis or webs. Hepatic vein thrombosis, or Budd-Chiari syndrome, has multiple etiologies but is generally related to a hypercoagulable state. Liver fibrosis and cirrhosis can also develop late in the disease course.
Intrahepatic: Cirrhosis is the most common cause of portal hypertension, and chronic viral hepatitis C is the most common cause of cirrhosis in the United States. Alcohol-induced liver disease and cholestatic liver diseases are other common causes of cirrhosis.
Posthepatic: Alterations of portal venous blood flow can also lead to portal hypertension. Arteriovenous malformation of the splenic vasculature, splenomegaly and portal vein thrombosis are examples of infrahepatic causes of portal hypertension.

9. DIAGNOSTIC OPTIONS
Imaging studies: Duplex doppler ultrasonography is a noninvasive, low-cost method of diagnosis that provides sophisticated information. It is often the initial procedure performed and provides specifics regarding the direction and velocity of portal flow. Findings of increased hepatic echogenicity , splenomegaly, portal vein dilation, thrombotic occlusion, collaterals, and gallbladder wall thickening are indicative of portal hypertension.

10. Pressure Measurement Studies
Portal pressure measurement is not generally indicated. It is most often performed in setting of therapeutic or hemodynamic research studies. Clinically it is used to assess the efficacy of pharmacological agents or shunting procedures. The most commonly used and preferred method for measuring the portal pressure is by indirectly calculating this pressure after occlusion of the hepatic vein. This is an invasive procedure, typically performed by interventional radiologists. It involves passing a catether via the jugular vein.

11. ENDOSCOPIC DIAGNOSIS
standard diagnostic approach in patients with acute gastrointestinal hemorrhage after initial resuscitation.
In most patients with cirrhosis (60–80%) bleeding is related to esophageal varices. In addition to making a definitive diagnosis, endoscopic therapy may be indicated for bleeding.

12. BLEEDING FROM ESOPHAGEAL VARICES
Bleeding esophageal varices are enlarged veins in the walls of the lower part of the esophagus that bleed. The esophagus is the tube that connects your throat to your stomach.
Cause:
Scarring (cirrhosis) of the liver is the most common cause of esophageal varices. This scarring cuts down on blood flowing through the liver. As a result, more blood flows through the veins of the esophagus.
The extra blood flow causes the veins in the esophagus to balloon outward. Heavy bleeding can occur if the veins break open.
Any type of chronic liver disease can cause esophageal varices.

13. SYMPTOMS
People with chronic liver disease and esophageal varices may have no symptoms.
If there is only a small amount of bleeding, the only symptom may be dark or black streaks in the stools.
If larger amounts of bleeding occur, symptoms may include:
Black, tarry stools
Bloody stools
Light-headedness
Paleness
Symptoms of chronic liver disease
Vomiting
Vomiting blood

14. EXAMS AND TESTS
May show:
Bloody or black stool (in a rectal exam)
Low blood pressure
Rapid heart rate
Signs of chronic liver disease or cirrhosis
Tests to find the source of the bleeding and determine if there is active bleeding include:
Esophagogastroduodenoscopy (EGD), which involves-the use of a camera on a flexible tube to examine the upper gastrointestinal system
Insertion of a tube through the nose into the stomach (nasogastric tube) to look for signs of bleeding

15. Medicines and medical procedures
To prevent future bleeding including:
Drugs called beta blockers, such as propranolol and nadolol that reduce the risk of bleeding.
A rubber band can be placed around the bleeding veins during an EGD procedure.
Transjugular intrahepatic portosystemic shunt (TIPS). This is a procedure to create new connections between two blood vessels in your liver. This can decrease pressure in the veins and prevent bleeding episodes from happening again.

16. Prognosis and complications
Bleeding often comes back with or without treatment. Bleeding esophageal varices are a serious complication of liver disease and have a poor outcome.
Encephalopathy (sometimes called hepatic encephalopathy)
Esophageal stricture after surgery or endoscopic therapy
Hypovolemic shock
Infection (pneumonia, bloodstream infection, peritonitis)
Return of bleeding after treatment

17. Portal gastropathy
Portal hypertensive gastropathy (PHG) is an important cause of bleeding in patients with cirrhosis associated with portal hypertension.
In portal hypertension, chronic portal venous congestion leads to dilatation and ectasia of the submucosal vessels in the stomach. This may result in upper or lower gastrointestinal bleeding, even in the absence of varices. The bleeding may be acute or chronic but is most commonly chronic low-grade GI blood loss associated with an iron-deficiency anaemia.

18. CLINICAL FINDINGS and diagnosis
Worsening Portal Hypertensive Gastropathy ( increased portal venous pressure gradient and decreased hepatic blood flow)
Ectactic blood vessels
Bleedings
Edema of stomach wall
The diagnosis of portal hypertensive gastropathy is usually made on endoscopy.
The normal mucosa of the stomach wall develop a mosaic like appearance that looks like snake-skin.

19. THERAPY
The most effective specific treatments in patients with PHG are those aimed at reducing portal pressure. The main pharmacological agent that has been investigated in this setting is the nonselective beta-blocker propranolol.
In the most frequent context of chronic blood loss, iron supplementation should be provided in order to counteract the continuous depletion of iron deposits.

20. TREATMENT AND PROCEDURES
Argon Plasma Coagulation: is performed during endoscopy. This procedure involves using argon gas and electrical current to seal irregular or bleeding tissue without any direct contact.
Transjugular intrahepatic portosystemic shunt (TIPS): is a procedure to create new connections between two blood vessels in your liver.
The doctor inserts a catheter (a flexible tube) through your skin into the jugular vein. On the end of the catheter is a tiny balloon and a metal mesh stent (tube).
Using an x-ray machine, the doctor guides the catheter into a vein in your liver.
Dye (contract material) is then injected into the vein so that it can be seen more clearly.
The balloon is inflated to place the stent.
The doctor uses the stent to connect the portal vein to one of the hepatic veins.
At the end of the procedure, your portal vein pressure is measured to make sure it has gone down.
The catheter with the balloon is then removed.
The procedure takes about 60 to 90 minutes to complete.

21. BUDD-CHIARI SYNDROME
Hepatic vein obstruction is a blockage of the hepatic vein, which carries blood away from the liver.
Hepatic vein obstruction prevents blood from flowing out of the liver and back to the heart. This blockage can cause liver damage. Obstruction of this vein can be caused by a tumor or growth pressing on the vessel, or by a clot in the vessel (hepatic vein thrombosis).

22. Causes and symptoms Symptoms: Abdominal swelling or stretching
Pain in the right upper abdomen
Vomiting blood
Yellowing of the skin (jaundice)
Abnormal growth of cells in the bone marrow (myeloproliferative disorders)
Cancers
Chronic inflammatory or autoimmune diseases
Infections
Inherited (hereditary) or acquired problems with blood clotting
Oral contraceptives
Pregnancy

23. tests and treatment Diagnosis: CT scan or MRI of the abdomen
Doppler ultrasound of the liver veins
Liver biopsy
Liver function tests
Ultrasound of the liver
Medicines:
Blood thinners (anticoagulants)
Clot-busting drugs (thrombolytic treatment)
Surgery:
Angioplasty and stent placement
Liver transplant
Transjugular intrahepatic portosystemic shunt (TIPS)
Venous shunt surgery

24. ASCITES
Ascites is the build-up of fluid in the space between the lining of the abdomen and abdominal organs.
Causes:
Ascites results from high pressure in the blood vessels of the liver (portal hypertension) and low levels of a protein called albumin.
Diseases that can cause severe liver damage can lead to ascites. These include long-term hepatitis C or B infection and alcohol abuse over many years.
People with certain cancers in the abdomen may develop ascites. These include cancer of the colon, ovaries, uterus, pancreas, and liver.
Other conditions:
Clots in the veins of the liver (portal vein thrombosis)
Congestive heart failure
Pancreatitis
Thickening and scarring of the sac-like covering of the heart.

25. TESTS 24-hour urine collection Electrolyte levels
Kidney function tests
Liver function tests
Tests to measure the risk of bleeding and protein levels in the blood
Urinalysis
Abdominal ultrasound

26. TREATMENT
The condition that causes ascites will be treated, if possible.
Avoiding alcohol
Lowering salt in your diet (no more than 1,500 mg/day of sodium)
Limiting fluid intake
Medications:
Diuretics - to get rid of extra fluid
Antibiotics for infections
Procedures that you may have are:
Procedures:
Inserting a tube into the belly to remove large volumes of fluid (called a paracentesis)
Placing a special tube or shunt inside your belly (TIPS) to repair blood flow to the liver
People with end-stage liver disease may need a liver transplant.

27. COMPLICATIONS
Spontaneous bacterial peritonitis (a life- threatening infection of the ascites fluid)
Hepatorenal syndrome (kidney failure)
Weight loss and protein malnutrition
Mental confusion, change in the level of alertness, or coma (hepatic encephalopathy)
Other complications of liver cirrhosis
When to Contact a Medical Professional:
Fever above 100.5°F (38.05°C), or a fever that does not go away
Belly pain
Blood in your stool or black, tarry stools
Blood in your vomit
Bruising or bleeding that occurs more easily
Build-up of fluid in your belly
Swollen legs or ankles
Breathing problems
Confusion or problems staying awake
Yellow color in your skin and whites of your eyes (jaundice)

28. THANK YOU FOR YOUR ATTENTION