Symptoms and Manifestations of Portal Hypertension

Name: Seyedsaeid Seyedraoufi Subject: Internal disease 2

Lecturer: Prof. Konstantine Liluashvili

• http://www.healthline.com/health/copd/understandingchronic-bronchitis
• http://www.medicinenet.com/chronic_bronchitis/article.htm

Jan 2022
 What is Portal Hypertension?

 Portal hypertension is elevated pressure in the portal

vein. The portal vein is a major vein that leads to the
liver It is caused most often by cirrhosis (in
developed countries), schistosomiasis (in endemic
areas), or hepatic vascular abnormalities.
 Consequences include esophageal varices and
portosystemic encephalopathy. Diagnosis is based on
clinical criteria, often in conjunction with imaging
tests and endoscopy.
 Treatment involves prevention of gastrointestinal
bleeding (GI) bleeding with endoscopy, drugs, or both
and sometimes with portacaval shunting or liver
transplantation.
 Etiology of Portal Hypertension

 Portal hypertension results mainly from increased resistance to blood flow in

the portal vein.
 A common cause of this resistance is disease within the liver.
 Uncommon causes include blockage of the splenic or portal vein and
impaired hepatic venous outflow Increased flow volume is a rare cause,
although it often contributes to portal hypertension in cirrhosis and in
hematologic disorders that cause massive splenomegaly.
 Pathophysiology of Portal Hypertension

 In Cirrhosis, tissue fibrosis and regeneration increase resistance in the

sinusoids and terminal portal venules. However, other potentially reversible
factors contribute; they include contractility of sinusoidal lining cells,
production of vasoactive substances (eg, endothelins, nitric oxide), various
systemic mediators of arteriolar resistance, and possibly swelling of
hepatocytes. Over time, Portal hypertension creates portosystemic venous
collaterals.
 They may slightly decrease portal vein pressure but can cause
complications. Engorged serpentine submucosal vessels (varices) in the
distal esophagus and sometimes in the gastric fundus can rupture, causing
sudden, catastrophic gastrointestinal bleeding Bleeding. rarely occurs unless
the portal pressure gradient is > 12 mm Hg. Gastric mucosal vascular
congestion (portal hypertensive gastropathy) can cause acute or chronic
bleeding independent of varices. Visible abdominal wall collaterals are
common; veins radiating from the umbilicus (caput medusae) are much rarer
and indicate extensive flow in the umbilical and periumbilical veins.
Collaterals around the rectum can cause rectal varices that can bleed.
 Pathophysiology of Portal Hypertension
 Portosystemic collaterals shunt blood away from the liver. Thus, less blood
reaches the liver when portal flow increases (diminished hepatic reserve). In
addition, toxic substances from the intestine are shunted directly to the systemic
circulation, contributing to Portosystemic encephalopathy .Venous congestion
within visceral organs due to portal hypertension contributes to ascites via
altered Starling forces. Splenomegaly and hypersplenism commonly occur as a
result of increased splenic vein pressure.
 Thrombocytopenia, leukopenia, and, less commonly, hemolytic anemia
may result.
 Portal hypertension is often associated with a hyperdynamic circulation.
Mechanisms are complex and seem to involve altered sympathetic tone,
production of nitric oxide and other endogenous vasodilators, and enhanced
activity of humoral factors (eg, glucagon).
 Symptoms and Signs of Portal Hypertension

 Portal hypertension is asymptomatic; symptoms and signs result

from its complications. The most dangerous is acute variceal
bleeding. Patients typically present with sudden painless upper
gastrointestinal bleeding, often massive. Bleeding from portal
hypertensive gastropathy is often subacute or
chronic Ascites, splenomegaly, or portosystemic
encephalopathy may be present.
 Diagnosis of Portal Hypertension

 Usually clinical evaluation

Portal hypertension is assumed to be present when a patient with chronic liver
disease has collateral circulation, splenomegaly, ascites, or portosystemic
encephalopathy.
 Proof requires measurement of the hepatic venous pressure gradient, which
approximates portal pressure, by a trans jugular catheter; however, this procedure
is invasive and usually not done. Imaging may help when cirrhosis is suspected.
Ultrasonography or CT often reveals dilated intra-abdominal collaterals, and
Doppler ultrasonography can determine portal vein patency and flow.

 Esophagogastric varices and portal hypertensive gastropathy are best diagnosed

by endoscopy, which may also identify predictors of esophagogastric variceal
bleeding (eg, red markings on a varix).
 Prognosis for Portal Hypertension

 Mortality during acute variceal hemorrhage may exceed 50%.

Prognosis is predicted by the degree of hepatic reserve and the
degree of bleeding. For survivors, the bleeding risk within the next
1 to 2 years is 50 to 75%. Ongoing endoscopic or drug therapy
lowers the bleeding risk but decreases long-term mortality only
marginally. For treatment of acute bleeding.
 Treatment of Portal Hypertension

• Ongoing endoscopic therapy and surveillance

• Nonselective beta-blockers with or without isosorbide mononitrate
• Sometimes portal vein shunting

 When possible, the underlying disorder is treated.

In patients with esophagogastric varices that have bled, combined endoscopic and drug
treatment decreases mortality and reduces risk of rebleeding better than either therapy used
alone.
A series of endoscopic banding sessions are done to obliterate residual varices, then periodic
endoscopic surveillance is done to identify and treat recurrent varices. Long-term drug
therapy usually involves nonselective beta-blockers; these drugs lower portal pressure
primarily by diminishing portal flow, although the effects vary.
 Agents include propranolol (40 to 80 mg orally twice a day), nadolol (40 to 160 mg orally
once a day), timolol (10 to 20 mg orally twice a day), and carvedilol (6.25 to 12.5 mg orally
twice a day), with dosage titrated to decrease heart rate by about 25%. Adding isosorbide
mononitrate 10 to 20 mg orally twice a day may further reduce portal pressure.
In patients with esophagogastric varices that have not yet bled (ie, for primary prophylaxis),
outcomes are similar with beta blocker therapy or endoscopic therapy.
 Treatment of Portal Hypertension

 Patients who do not adequately respond to either treatment should be considered

for trans jugular intrahepatic portosystemic shunting (TIPS) or, less
frequently, a surgical portacaval shunt. In TIPS, the shunt is created by placing a
stent between the portal and hepatic venous circulation within the liver.
 Although TIPS may result in fewer immediate deaths than surgical shunting,
particularly during acute bleeding, maintenance of patency may require repeat
procedures because the stent may become stenosed or occluded over time. Long-
term benefits are unknown. Liver transplantation may be indicated for some
patients.
 For bleeding due to portal hypertensive gastropathy, beta blockers can be used to
decrease portal pressure.
 A shunt should be considered if drugs are ineffective, but results may be less
successful than for esophagogastric variceal bleeding.
 Because it rarely causes clinical problems, hypersplenism requires no specific
treatment, and splenectomy should be avoided.