Portal Hypotension: Clinical Assignment

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PORTAL HYPOTENSION

CLINICAL ASSIGNMENT

Hijab Zehra
Hamna Khaleel
Alishba Khan
Syeda Khansa Saboor

8th Semester
Pharm-D

0|Page
Definition:
Portal hypertension is a term used to describe elevated pressures in the portal venous system (a
major vein that leads to the liver). or
PHT is a pathologic increase in port
al pressure in which the pressure gradient between the portal vein and the Inferior vena cava
(Portal pressure gradient or PPG) is increased above the upper limit of 5 mm of Hg. 
Normal portal vein pressures range from 5–10 mm Hg.
Portal hypertension may be caused by intrinsic liver disease, obstruction, or structural changes
that result in increased portal venous flow or increased hepatic resistance.
 PPG > 10 mmHg(varices)
 PPG > 12mmHg (variceal bleed, ascites)
 PPG > 6 to 10 mmHg (subclinical PHT)

Normally, vascular channels are smooth, but liver cirrhosis can cause them to become irregular
and tortuous with accompanying increased resistance to flow. This resistance causes increased
pressure, resulting in varices or dilations of the veins and tributaries. Pressure within the portal
system is dependent upon both input from blood flow in the portal vein, and hepatic resistance to
outflow. Normally, portal vein pressure ranges between 1–4 mm Hg higher than the hepatic vein
free pressure, and not more than 6 mm Hg higher than right atrial pressure. Pressures that exceed
these limits define portal hypertension.

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Symptoms:
 Gastrointestinal hemorrhage may be the initial presenting symptom.
 Ascites.
 Jaundice.
 Coagulopathy.
 Spider angioma.
 Patients who are hemodynamically stable may have;
 Warm skin.
 Hyperdynamic pulses.
 Low systolic blood pressures
The clinical manifestations of portal hypertension may include;
Caput medusae, splenomegaly, edema of the legs, and gynecomastia (less commonly).

Pathophysiology:
The fundamental haemodynamic abnormality is an increased resistance to portal blood flow.
Increased portal vascular resistance leads to gradual reduction in the flow of portal blood to the
liver and simultaneously to the development of collateral vessels, allowing portal blood to bypass
the liver and enter the systemic circulation directly.
Collaterals develop when the pressure gradient between the portal and hepatic vein rises above a
certain threshold, a process involves angiogenic factors.
At the same time portal flow increases in the splanchnic bed due to splanchnic vasodilatation
and increased cardiac output
Portal vascular resistance is increased in chronic liver disease. Liver cell injury Stellate cell
activation Stellate cells transform into myofibroblast De novo expression of specific smooth
muscle protein alpha-actin Endothelin, NO Prostaglandins Contraction of activated cells
Abnormal blood flow pattern causing increased resistance fibrogenesis Increased resistance leads
to portal hypertension

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Causes:
Any condition that interferes with blood flow or vascular resistance in the portal venous system
can lead to portal hypertension. Cirrhosis remains the most common cause in western countries,
and all other etiologies account for less than 10% of cases.
The causes of portal hypertension can be classified according to their anatomical location:
1. Prehepatic.
2. Intrahepatic.
3. Post hepatic.

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Prehepatic:
Although cirrhosis and portal hypertension are the most common causes of portal vein
thrombosis (PVT), isolated PVT may result in prehepatic portal hypertension due to impaired
blood flow in the portal venous system. In the absence of cirrhosis, PVT is often a consequence
of prothrombotic conditions (congenital or acquired), local complications (neonatal omphalitis,
pancreatitis, abdominal trauma, surgery), or both. Despite extensive investigation, the etiology of
PVT cannot be identified in approximately 15% to 30% of patients.

Intrahepatic:
Intrahepatic portal hypertension is driven by high vascular resistance at the presinusoidal,
postsinusoidal, or sinusoidal capillaries. The main causes of presinusoidal portal hypertension
include nodular regenerative hyperplasia, schistosomiasis, sarcoidosis, primary biliary
cholangitis, autoimmune cholangiopathy, congenital hepatic fibrosis, and adult polycystic
disease. Cirrhosis is the most common cause of sinusoidal portal hypertension, which can also be
caused by infiltrative conditions such as amyloidosis, mastocytosis, and Gaucher disease.
Finally, postsinusoidal portal hypertension is usually caused by veno-occlusive disease or
sinusoidal obstruction syndrome.

Post hepatic:
Post hepatic portal hypertension is generally caused by venous outflow impairment resulting in
increased vascular resistance to hepatic blood flow. The most common causes are Budd-Chiari
syndrome and right-sided heart failure resulting from conditions such as constrictive pericarditis,
restrictive cardiomyopathy, complex congenital heart diseases, and Fontan physiology.

Diagnostic Evalution:

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♦ Blood Count
♦ Liver Function Tests
♦ Esophagogastroduodenoscopy
♦ USG (ultrasound sonography test)
♦ MRI (Magnetic resonance imaging)
♦ Liver Angiography
♦ Coeliac-mesenteric Arteriography
♦ Splenic Portogram

Treatment:
Lifestyle changes such as these can help treat portal hypertension.

1. improving your diet

2. avoiding alcohol consumption

3. exercising regularly

4. quitting smoking 
Medications:
Beta-blockers:
Beta-blockers are also important to help reduce your blood pressure and relax your blood
vessels.
Propranolol and isosorbide:
Propranolol and isosorbide, may help lower the pressure in the portal vein, too. They can also
reduce the risk of more internal bleeding.
Diuretics:
If you’re experiencing ascites, your doctor may prescribe a diuretic to help reduce fluid levels in
your body. Sodium must also be severely restricted to help reduce fluid retention.

Therapy Treatment:
 Sclerotherapy.
 Nonsurgical trans jugular intrahepatic portal-systemic shunt (TIPSS)
 Distal splenorenal shunt (DSRS)
 Devascularization
 Paracentesis

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Sclerotherapy or banding:
A treatment called sclerotherapy or banding uses a solution that can help stop bleeding in the
blood vessels of your liver. Banding involves the placement of rubber bands to block unhealthy
blood flow to enlarged veins, known as varices or varicose veins, in your digestive system.

Nonsurgical trans jugular intrahepatic portal-systemic shunt (TIPSS):


This therapy helps control acute bleeding. It creates new pathways for blood to flow from the
portal vein into other blood vessels.
This procedure involves placing a stent (a tubular device) in the middle of the liver.  The stent connects the
hepatic vein with the portal vein, which reroutes blood flow in the liver and helps relieve pressure in abnormal
veins.

Distal splenorenal shunt (DSRS):


This procedure connects the vein from your spleen to the vein from the left kidney in order to reduce pressure
in the varices and control bleeding.

Devascularization.:
A surgical procedure that removes the bleeding varices; this procedure is done when a TIPS or a surgical shunt
is not possible or is unsuccessful in controlling the bleeding.

Paracentesis:
This is a procedure in which the accumulation of fluid in the abdomen (ascites) is directly removed. The results
are usually temporary and the procedure will need to be repeated as needed.

References:

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https://www.hopkinsmedicine.org/gastroenterology_hepatology/_pdfs/liver/portal_hypertension.
pdf
https://www.mayoclinicproceedings.org/article/S0025-6196(18)31008-5/pdf
https://www.google.com/url?sa=i&url=https%3A%2F%2Ffanyv88.com%3A443%2Fhttps%2Fwww.researchgate.net%2Ffigure
%2FDiagram-of-pathophysiology-of-portal-hypertension-The-increase-in-portal-pressure-
is_fig2_49671797&psig=AOvVaw0tQOz2kGC8v9_e9KZ_0Z7P&ust=1639578675929000&sou
rce=images&cd=vfe&ved=0CAkQjhxqFwoTCIDvuNzA4_QCFQAAAAAdAAAAABAD
https://www.lecturio.com/concepts/portal-hypertension/

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