1. PORTAL HYPERTENSION Prepared by: Lubabah

2. WHAT IS PORTAL HYPERTENSION?
Portal hypertension is a term used to describe elevated
pressures in the portal venous system (a major vein
that leads to the liver). Portal hypertension may be
caused by intrinsic liver disease, obstruction, or
structural changes that result in increased portal
venous flow or increased hepatic resistance.

3. WHAT IS PORTAL HYPERTENSION?
Portal hypertension is a term used to
describe elevated pressures in the
portal venous system (a major vein
that leads to the liver). Portal
hypertension may be caused by
intrinsic liver disease, obstruction, or
structural changes that result in
increased portal venous flow or
increased hepatic resistance.
Most commonly it is caused be hepatic
cirrhosis. Which is when the liver

4. EPIDEMIOLOGY
Population-based prevalence data for portal hypertension in the
United States are not available, but portal hypertension is a frequent
manifestation of liver cirrhosis. According to the National Institute on
Alcohol Abuse and Alcoholism (NIAAA), liver cirrhosis accounted for
almost 30,000 deaths in the United States in 2007, making it the
12th leading cause of US deaths.
In Western countries, alcoholic and viral cirrhosis are the leading
causes of portal hypertension and esophageal varices; 30% of patients
with compensated cirrhosis and 60-70% of patients with

5. SEX- AND AGE-RELATED
DEMOGRAPHICS
Liver disease demonstrates a sex predilection, with
males making up more than 60% of patients with
chronic liver disease and cirrhosis.
In general, alcoholic liver disease and viral hepatitis
are the most common causes for esophageal varices in
both sexes.

6. MECHANISM
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.

7. HOW THE PORTAL SYSTEM WORKS
The portal venous system consists of
the portal vein and its tributaries, this
blood contains all the nutrients
absorbed by the gi tract but it also
carries toxins that the liver metabolizes
so that they can be safely excreted by
the kidney. Once the liver processes all
these substances it sends the blood to
the heart through IVC to enter the
systemic circulation

8. PORTAL HYPERTENSION
In portal hypertension the venous
blood accumulates in the portal
system because of an obstruction
which can be caused by various
reasons and this ultimately causes
pressure to rise above 12mmHg.
Portal hypertension leads to the
formation of portosystemic shunts (
which is when blood is diverted away
from the portal system and backs up

9. SYMPTOMS
Gastrointestinal haemorrhage may be the initial presenting
symptom of patients with portal hypertension. Those patients
with more advanced liver disease often present with ascites,
hepatic encephalopathy , jaundice, coagulopathy, or spider
angiomata. Patients who are hemodynamically stable may
have warm skin, hyper dynamic pulses, and low systolic blood
pressures in the range of 100–110 mm Hg.

10. 1.Caput medusae is a network of dilated veins
surrounding the umbilicus. It is caused by
increased blood flow in the umbilical and
periumbilical veins and is often accompanied
by an audible venous hum over the umbilical
vein
2.Gynecomastia refers to the abnormal
enlargement of breast tissue behind the
areola in males.
3.Ascites is the presence of excess fluid in the
peritoneal cavity.
4.Edema, or swelling of the legs, is seen in
portal hypertensive patients because of

11. CLINICAL CONSEQUENCES OF
PORTAL HYPERTENSION
Hepatic encephalopathy:
Less blood gets to the liver
leading to diminished liver
function and less blood
detoxification. This leads to
build up of toxic metabolites
like ammonia un the blood,
ammonia and other toxins can
pass through the blood brain
Hepatic
encephalopathy

12. CLINICAL CONSEQUENCES OF
PORTAL HYPERTENSION
Portosystemic shunts:
which happens in the three points where the systemic
and the portal system are connected
1.Esophageal varices
2.Haemorrhoids
3.Caput medusa

13. CLINICAL CONSEQUENCES OF
PORTAL HYPERTENSION
Increased intrahepatic
resistance and portal
blood flow
Increased portal
pressure
Increased varix size
and decreased
thickness
Increased variceal wall
tension and ultimately
bleeding
Esophageal varices: Portal hypertension is
the most common causes of esophageal
varices and these extremely fragile and can
easily rupture causing massive upper GI
bleeding.

14. CLINICAL CONSEQUENCES OF
PORTAL HYPERTENSION
Rectal varices:
Portosystemic shunts in the rectum
or the anal canal causes
haemorrhoids which are basically
enlarged veins that can bleed.

15. CLINICAL CONSEQUENCES OF
PORTAL HYPERTENSION
Caput medusae:
Round ligament re-channelling
ultimately allows blood from the
portal system into the systemic
veins of the abdomen which then
dilated making the abdomen look
like the head of the Greek
mythological creature “medusa”,

16. CLINICAL CONSEQUENCES OF
PORTAL HYPERTENSION
Splenomegaly
Results from the increased flow of blood from the hepatic
vein. Spleen size increases to approximately 400mg.

17. CLINICAL CONSEQUENCES OF
PORTAL HYPERTENSION
Ascites:
Another consequence of portal hypertension is that
the endothelial cells lining the blood vessels release
more nitric oxide the reason behind this is unclear.
NO makes peripheral arteries dilate so BP drops, drop
in BP stimulates the release of aldosterone which tells
the kidneys to bring BP back to normal bt retaining
more sodium and water.
Plasma volume expands so much that fluid and blood
vessels is more likely to be pushed into tissues and
across tissues into large open spaces like peritoneal
cavity.
This accumulation of fluids in the peritoneal cavity is
called ascites.

18. PATHOPHYSIOLOGY
Liver is injured, stellate cells activated
and converted into myofibroblasts.
Abnormal blood flow patterns and
increased resistance to blood flow
Increased resistance leading to portal
hypertension
Increased
resistance to
portal flow “R”
Increased blood
inflow “Q”
Portal
hypertension

19. ETIOLOGY
With regard to the liver itself, causes of portal
hypertension usually are classified as the following
depending on where the obstruction is:
1.Prehepatic causes
2.Intrahepatic causes
3.Posthepatic causes

20. SUPRAHEPATIC CAUSES
Suprahepatic abnormalities leading to portal
hypertension include cardiac disease, hepatic vein
etiology, and inferior vena cava thrombosis or webs.
Liver fibrosis can result from suprahepatic disease, and
cirrhosis can also develop late in the disease course

21. HEPATIC CAUSES
Cirrhosis is the most common cause of portal
hypertension, and chronic viral hepatitis C is the most
common cause of cirrhosis.
Schistosomiasis which is when flatworms invade the
liver.
Sarcoidosis which is the inflammatory cells from

22. PREHEPATIC CAUSE
The most common Prehepatic cause is portal vein
obstruction, when there is a thrombus occluding the
portal vein and blocking blood flow

23. DIAGNOSIS
Hepatic venous pressure gradient measurement:
where a catheter is inserted inside the inferior vena
cava and inside the portal vein to measure the
difference between both pressures.
Liver ultrasounds can help detect nodules in cirrhosis.
CT scan or MRI help diagnose ascites, cirrhosis,
splenomegaly or vascular alterations like inferior vena
cava dilatations.
Lab tests including full blood count, liver enzymes can
be used to identify the causes.

24. TREATMENT
Treatment is directed at the cause of portal hypertension.
Pharmacologic therapy for portal hypertension includes the
use of beta-blockers, most commonly propranolol and
nadolol.
Investigators have suggested that the use of some statins
(e.g. simvastatin) may lower portal pressure and potentially
improve the liver function.
Management of patients with liver cirrhosis and ascites but
without variceal hemorrhage includes a low-sodium diet
and diuretics.

25. TREATMENT
If esophageal varices bleed a medication called
“octreotide” is used which basically reduces the portal
blood pressure and can prevent re-bleeding the
patent's hospitalization.
Octreotide act by mesenteric arterial vasoconstriction.

26. TREATMENT
In esophageal varices techniques such as balloon
tamponade, sclerotherapy, and variceal ligation are
used to prevent and stop re-bleeding of the varices.

27. BALLOON TAMPONADE
When inserted into the
esophagus or stomach,
balloon catheters are
intended to stop bleeding
such as from vascular
structure including
esophageal varices and
gastric varices in the
upper gastrointestinal
tract.

28. SCLEROTHERAPY
Sclerotherapy is a medical procedure used to eliminate varicose
veins and spider veins. Sclerotherapy involves an injection of a
solution (generally a salt solution) directly into the vein. The
solution irritates the lining of the blood vessel, causing it to
collapse and stick together and the blood to clot. Over time, the
vessel turns into scar tissue that fades from view.
This forces the blood to use another route.

29. VARICEAL LIGATION
Using an endoscope, the doctor uses suction to pull
the varices into a chamber at the end of the scope and
wraps them with an elastic band, which essentially
"strangles" the veins so they can't bleed.