2. DEFINITION
• Portal Hypertension (PH) – the elevation of Hepatic
Venous Pressure Gradient (HVPG) above 5 mm Hg
• Normal condition – the Portal Pressure Gradient (PPG)
ranges between 1 and 5 mmHg
• PH is considered to be clinically significant when HVPG
exceeds 10 to 12 mmHg, since this is the threshold for the
clinical complications of PH to appear
3.
4. SITES OF PORTA –SYSTEMIC
COLLATERALIZATION
1. Lower end of esophagus: It is located between left gastric and
short gastric veins.
2. Umbilicus: It is between paraumbilical vein and anterior abdominal
vein resulting in caput medusae.
3. Lower end of rectum: It is between superior hemorrhoidal vein
and inferior, middle hemorrhoidal vein resulting in piles.
4. Retro peritoneum: It is vein of retzius, these are various veins in
the dorsal wall of the abdomen forming anastomoses between the
inferior vena cava and the superior and inferior mesenteric veins.
5. Bare area of the liver: The veins of the bare area of the liver also
communicate with those of the diaphragm, as well as the right internal
thoracic vein.
6. CAUSES OF PORTAL HYPERTENSION
Portal hypertension caused by a combination of two simultaneous
occurring hemodynamic processes
• Increased intrahepatic resistance to passage of blood flow through the
liver due to cirrhosis
• Increased splanchnic blood flow secondary to vasodilatation within
the splanchnic vascular bed
Portal hypertension can be caused by
• Prehepatic
• Intrahepatic
• Posthepatic
7. CAUSES OF PORTAL HYPERTENSION
Prehepatic:
– Wedged Hepatic Venous Pressure (WHVP): Normal
– Free Hepatic Venous Pressure (FHVP): Normal
– Normal Hepatic Venous Pressure Gradient (HVPG): Normal
Causes:
• Hyper-reactive Malarious Splenomegaly (HMS)
• Portal vein thrombosis
• Splenic vein thrombosis
• Arteriovenous fistula
• Congestive splenomegaly (Banti’s syndrome)
13. CLINICAL PRESENTATIONS
Triad of portal hypertension:
The triad comprises of oesophageal varices, splenomegaly and ascites.
Oesophageal varices:
• Present with hematemesis or malaena or as recurrent bleeding
• Varices begin to bleed when portal pressure exceeds 12 mm Hg
• Severe hematemesis associated with shock
Types of varices:
– Esophageal: It is present in the lower 1/3rd of the esophagus, usually
3 or more in number based on gastroscopic findings that is graded
as I,II, III, Iv (80%)
– Gastric: It is fundal or in upper part of the stomach (20%)
14. CLINICAL PRESENTATIONS
Splenomegaly:
• Common in patients with portal hypertension and there is a poor
correlation between spleen size and portal venous pressure
• Usually asymptomatic but causes hypersplenism, which may be
associated with
o Thrombocytopenia
o Leucopenia or
o Combination of these two
Ascites:
It is a frequent complication of sinusoidal and postsinusoidal or
posthepatic forms of portal hypertension
15. CLINICAL PRESENTATIONS
Jaundice
Previous jaundice suggests the possibility of a
• Previous acute hepatitis
• Hepatobiliary disorder
• Drug-induced liver disease
Recurrence of jaundice suggests the
• Possibility of reactivation
• Infection with another virus
• Onset of hepatic decompensation
16. CLINICAL PRESENTATIONS
Hepatic Encephalopathy
Ammonia bypasses the liver through portosystemic shunt and reaches
the astrocytes in the brain.
Within the astrocyte, ammonia
Direct ammonia toxicity triggers nitrosative and oxidative stress, which
lead to astrocyte mitochondrial dysfunction
Metabolized
Glutamine
Acts as an osmole to attract water
causes
Cerebral edema
17. CLINICAL PRESENTATIONS
West Haven Criteria of Severity of Hepatic Encephalopathy
Grade 0 Impaired driving ability
minimally impaired psychometric tests
Decreased global functioning
Increased risk of falls
Grade 1 Trivial lack of awareness
Euphoria or anxiety
Shortened attention span
Impaired performance of addition
Grade 2 Lethargy or apathy
Minimal disorientation for time and place
Subtle personality change
Inappropriate behavior
Impaired performance of subtraction
Grade 3 Somnolence to semistupor, but responsive to verbal stimuli
Confusion
Gross disorientation
Grade 4 Coma (unresponsive to verbal or noxious stimuli)
18. INVESTIGATION
Liver Function Tests
• Postprandial total serum bile acid concentrations may be the most
sensitive test for detection of MAPSS
• Hyperbilirubinemia and decreases in serum albumin, urea nitrogen,
and cholesterol concentrations
Multiple Acquired Portosystemic
Shunts (MAPSS) or
functional hepatic failure
Blood ammonia or
total serum bile acid
in the
Presence of
Abnormal liver function tests can be used to infer the presence of PH
19. INVESTIGATION
Ultrasound
The ultrasound techniques are the modalities of choice, because they are
noninvasive, rapid, reliable and highly sensitive and specific.
Ultrasound techniques
• Duplex Doppler ultrasonography
• Color doppler ultrasonography
Duplex Doppler ultrasonography (dDU)
• It can be utilized repeatedly in assessing the hemodynamics of the
portal system
• Measures the main portal vein flow velocity and volume
20. INVESTIGATION
Color Doppler Ultrasonography (CDUS)
• Very accurate in the detection of portal flow direction
• Useful in the evaluation of portal vein thrombosis and cavernous
transformation
• Detects portosystemic collaterals, especially the gastroesophageal, the
paraumbilical, the splenorenal and the gastrorenal veins
Transient elastography
• It is a new technique used as a noninvasive method to study portal
hypertension in chronic liver disease with variable results
• Study revealed that TE could be used as a good screening tool for
significant portal hypertension
21. INVESTIGATION
Alpha fetoprotein
Patients with clinically significant portal hypertension with Alpha
fetoprotein ≥10 ng/ml were at highest risk for development
Hepatocellular Carcinoma (HCC).
GI scopy
Identifies varices
Splenoportography
Allows an accurate depiction of the portal vein and its afferent flow areas.
It is importance in clarifying the causes of portal hypertension.
22. INVESTIGATION
Liver biopsy
• key role in the differential of intrahepatic causes of portal
hypertension
• Indicated in patients with portal vein thrombosis only when
concomitant cirrhosis or nodular regenerative hyperplasia is
suspected
Splenoportography
• Provides a useful method for the evaluation of circulatory
disturbances in portalhypertension
• It is safe technique for visualizing the portal vein without surgical
intervention
23. INVESTIGATION
Endoscopy
Endoscopic appearance of portal hypertensive gastric mucosa includes
• Several lesions fine pink speckling
• Scarlatina-type rash petechia
• Multiple bleeding spots, papules
• Superficial reddening, snake-skin pattern
• Cherry red spots and mosaic-like pattern
26. MANAGEMENT
General measures
In acute variceal bleeding
• General resuscitation measures
• Start pharmcotherapy
o Octreotide 50 µg intravenous bolus, followed by 50 µg/h
intravenous for 3–5 days (or terlipressin)
o Third generation cepaholsporine
• Endoscopic therapy in case of early (within 5 days of index-bleed)
rebleeding
• Consider Transjugular Intrahepatic Portosystemic Shunt (TIPS) in
recurrent or uncontrolled bleeding or endoscopic treatment failure
27. MANAGEMENT
Specific measures
Treatment of oesophageal varices
Pharmacological therapy for the management of varices include
• Splanchnic vasoconstrictors: Vasopressin and analogues, somatostatin
and analogues, nonselective β-blockers
• Venodilators: Nitrates
• Endoscopic therapies: Sclerotherapy or endoscopic variceal ligation
• Shunting therapy : Radiological or surgical
28. MANAGEMENT
Treatment of oesophageal varices
Effect of therapies on portal flow, resistance and pressure
Therapy Portal Flow Portal Resistance Portal Pressure
Vasoconstrictors
(e.g. βblockers)
↓↓ ↑ ↓
Venodilators (e.g.
nitrates)
↓ ↓* ↓
Endoscopic therapy - - -
TIPS/Shunt therapy ↑ ↓↓↓ ↓↓↓
*Although theoretically nitrates act by decreasing resistance, they actually act by decreasing portal flow through a decrease in mean arterial pressure
TIPS: Transjugular intrahepatic portosystemic shunt
29.
30. MANAGEMENT
Treatment of Ascites
• It is treated in the first instance with sodium restriction and correction
of serum proteins
o Na+ diet (88 mEq/day) or 5 g salt (1 teaspoon) diet (85 mEq)
o No restriction of water unless patient has hyponatremia
• Ascitic tap to be placed below the umbilicus, lateral to the rectus
muscle. Bladder should be empty before tapping.
• Diuretics such as spironolactone and furosemide
• Transjugular intrahepatic portosystemic shunt (TIPS) may be
considered as an alternative to repeated Large-volume Paracentesis
(LVP).
31.
32. MANAGEMENT
Measures to reduce portal pressure
Transjugular intrahepatic portosystemic shunt (TIPS)
It is stent placed via the jugular vein to create a shunt from the portal
vein to the systemic circulation
Following should be performed before TIPS
• Routine blood tests: To assess liver and kidney function and clotting
• Echocardiography: For suspicion of cardiac or respiratory distress
• Cross-sectional liver imaging: To assess patency of vessels and rule
out the presence of hepatoma or cysts that may contraindicate TIPS
33. MANAGEMENT
Transjugular intrahepatic portosystemic shunt (TIPS)
TIPS inserted under aseptic condition with guidance of ultrasonography
almost via the right jugular vein and other approaches described in the
figure.
A) Portal hypertension, HVPG
20 mm Hg;
B) insertion of guide wire via
jugular artery, advanced to a
branch of hepatic vein;
C) passage of a collapsed stent;
D) expansion of stent to create an
artificial shunt between
portal and systemic venous
system.
HPVG: Hepatic Venous Pressure Gradient
34.
35. MANAGEMENT
Prevention of hepatic encephalopathy
Identification of site of bleeding by fibroscopy maintenance of fluid and
electrolyte balance
To reduce the entry of nitrogenous products and toxic products from gut
into the circulation
• Restriction of dietary protein
• Removal of blood from bowel by purgation or enemas
• Oral lactulose 30-50 ml 4 times a day
• Oral neomycin to reduce bacterial load inside the bowel lumen 1 gm 4-
6 hours or metroniadazole 250 mg every 8 hours
