This document provides information on portal hypertension, including its definition, causes, presentations, investigations, and management. Some key points: - Portal hypertension is defined as a sustained elevation of portal pressure above 12 mm Hg. It can be caused by conditions affecting blood flow pre-sinusoidally (e.g. portal vein thrombosis), sinusoidally (e.g. cirrhosis), or post-sinusoidally (e.g. Budd-Chiari syndrome). - Common presentations include esophageal varices, splenomegaly, ascites, and features of hepatic encephalopathy. Investigations include liver function tests, ultrasound, and endoscopy to identify varices. -

1. PORTAL HYPERTENSION
Dr. HIREN PATOLIYA
Seth Nandlal Dhoot Hospital
Aurangabad

2. PORTAL HYPERTENSION
• Defi nition: Sustained elevation of portal pressure more than
• 12 mm Hg (normal 8-12 mmHg)
• Left sided portal hypertension (sinistral) can be caused by
isolated splenic vein thrombosis, which is often caused by
adjacent pancreatitis.
• A rise in portal pressure stimulates portasystemic circulation.
• Portal vein carries 75% of blood flow to liver with all nutrients
to maintain its integrity and gives 50% oxygen supply
to liver. 25% hepatic arterial blood flow gives remaining
50% of oxygen supply to liver.

3. • Portal hypertension causes compensatory
portosystemic venous collateral formation,
altered intrahepatic circulation and increased
splanchnic blood flow. High pressure portal
blood is diverted via coronary (left gastric vein),
short gastric and esophageal veins into azygos
venous system.
• There is increased portal resistance and altered
portal blood flow. Increased resistance may be
presinusoidal, sinusoidal and postsinusoidal.

4. • Presinusoidal
– Extrahepatic—portal vein/splenic vein thrombosis.
– Intrahepatic—schistosomiasis, sarcoidosis
• Sinusoidal – cirrhosis, haemochromatosis, Wilson’s
disease, congenital hepatic fibrosis.
• Postsinusoidal – Budd-Chiari syndrome, conges-tive
heart failure, veno-occlusive disease.

5. • 30% of varices patients will bleed; 30% of
them will die of bleed; 30% of patients with
cirrhosis will develop portal hypertension;
30% of them have variceal bleed in 2 years.
• 70% of patients who had bleeding once, will
rebleed later.
• Variceal bleed accounts for 7% of upper GI
bleed.

6. Sites of Portosystemic
Collateralisation
1. Lower end of oesophagus :-between left gastric
and short gastric veins with azygos vein resulting
in oesophageal varices—commonest
2. Umbilicus:- between paraumbilical vein and
anterior abdominal vein resulting in caput
medusae.
3. Lower end of rectum:-between superior haemor
rhoidal vein and inferior, middle haemorrhoidal
vein resulting in piles.
4. Retroperitoneum (vein of Retzius).
5. Bare area of the liver.

8. Causes of portal hypertension
• PREHEPATIC
– PORTAL VEIN OR SPLENIC VEIN THROMBOSIS
– HYPERCOAGULABLE STATE
– PERIPORTAL INFLAMMATION
• HEPATIC(80%)
– ALCOHOLIC CIRRHOSIS
– PRIMARY BILIARY CIRRHOSIS
– SCHISTOSOMIASIS
– WILSON DISEASE
– CENGENITAL HEPATIC FIBROSIS
• POSTHEPATIC
– BUD-CHIARI SYNDROME
– CONSTRUCTIVE PERICARDITIS
– CONGESTIVE CARDIAC FAILURE
– VENO-OCCULASIVE DISEASE

9. Presentations
• Triad of portal hypertension
i. Oesophageal varices.
ii. Splenomegaly.
iii. Ascites.
• Jaundice.
• Features of encephalopathy.
• Coagulopathy.
• Hepatorenal syndrome.

10. Investigations
• Liver function tests.
• Ultrasound.
• Alfa-feto protein.
• CT/MRI to look for cause
• MELD scoring is Model for End-stage Liver Disease
• Doppler imaging to see vascular pattern :-direction of blood flow,
size of the vein.
• Hepatic venous pressure gradient (HVPG): It is done using a balloon
catheter. Difference between free hepatic vein pressure and
wedged hepatic vein pressure is HVPG. Normal HVPG is 8 mm Hg. It
is more than 10 mm Hg in cirrhosis.
• GI scopy—to identify varices.
• Liver biopsy(confirm the cause for the portal hypertension)
• Endosonography.

11. Management of Portal Hypertension
• General measures:
– Anaemia to be corrected.
– Nutrition supplementation.
– Inj. vitamin K—10 mg IM for 5 days.
• Specific measures:
– Treatment of oesophageal varices.
– Prevention of hepatic encephalopathy.
– Treatment of ascites.
• Measures to reduce portal pressure:
– Surgeries—Portosystemic shunt.
Nonselective.
Selective.
– TIPSS.
– Drugs to reduce the portal pressure like pro pranolol, nadolol,
isosorbide-5-mono nitrate.
• Liver transplantation.

12. OESOPHAGEAL VARICES
• May be asymptomatic.
• May present with haematemesis or melaena or as
recurrent bleeding. Varices begin to bleed when
portal pressure exceeds 12 mmHg.
• When present with severe haematemesis, patient
shows features of shock.
• Mortality in bleeding varices is 25-30%.
• Factors related to variceal bleed are—portal venous
pressure; gastro-oesophageal reflux causing
ulceration; variceal size; variceal wall tension.

13. Types of Varices
1. Oesophageal which is in the lower 1/3rd of the
oesophagus,usually 3 or more in number, graded as I, II,
III, IV (based on gastroscopic findings) (80%).
2. Gastric which is fundal or in upper part of the stomach
– A. Extension of oesophageal varices
• I. Into lesser curve
• II. Into fundus
– B. Isolated gastric varices
• I. In fundus common
• II. In other parts—stomach, duodenum—rare
• Gastric varices are treated by endoscopic N butyl
cyanacrylate glueing, sclerotherapy. Banding is usually
not done.

14. Grading of varices
I. Minimal varices without luminal prolapse
II. Moderate varices, with luminal prolapse and
with minimal obscuring of O-G junction
III. Large varices, with luminal prolapse and with
moderate obscuring of O-G junction
IV. Very large varices, with luminal prolapse and
with complete obscuring of O-G junction

15. Treatment of Oesophageal Varices
• PRIOR TO BLEED
– Drugs—propranolol (reduces the portal pressure by
20% with pulse rate below 55/minute or 25% of
resting pulse); nadolol (long acting, less lipophilic, not
metabolised by liver); isosorbide mononitrate. Drugs
reduce bleeding by 40%.
– Endotherapy.
• AFTER ONE OR MORE EPISODE OF BLEEDING.
– Endotherapy.
– Shunt surgeries.
– Drugs.

16. EMERGENCY MANAGEMENT IN SEVERE
HAEMORRHAGE
Initial important measures
– Volume and electrolyte corrections; volume replacement using crystalloids with central line (CVP line
placement with CVP maintained at 5 cm of water, sudden overload should be avoided which may precipitate
pulmonary oedema/ascites/hyponatraemia)
– Blood and blood products transfusion
– Antibiotics, nutrition (TPN)/Vitamin K injection
– – Catheterisation and hourly urine output monitoring
– – Prevention of encephalopathy
– – Rest/sedation only if needed with care
• Pharmacotherapy
– Inj. Vasopressin (constricts the splanchnic vessels thus lowers the portal pressure)
– Somatostatin (reduces the splanchnic and hepatic blood fl ow.)
– Propranolol (decreases the portal pressure)
– Ranitidine(Acid inhibiting drugs)
– tranexamic acid(antifi brinolysins )
• Endoscopic banding/sclerotherapy (Banding/band ligation has become gold standard and ideal for
oesophageal varices.) glue therapy(Butyl cyanoacrylate :-tissue adhesive)
• Balloon tamponade(If bleeding does not stop by banding/sclerotherapy/gluing, balloon
tamponade should be tried)
• TIPSS
• Devascularisation surgical procedures

17. DEFINITIVE MANAGEMENT OF
VARICES
• Sclerotherapy
• Shunt surgery (Shunt surgeries should not be
done if the varices have not bleed before.)
• Splenectomy(Left sided portal hypertension
also called as segmental portal hypertension is
due to splenic vein thrombosis)
• TIPSS (Transjugular Intrahepatic
portosystemic Stenting / Shunt)

19. PORTAL HYPERTENSIVE
GASTROPATHY
• Portal hypertension causes vascular dilatation and ectasia
in the stomach which appears pink, speckled, with red
mosaic pattern in the gastric mucosa. It occasionally causes
upper GI bleed
• Endoscopy is diagnostic.
• Portal gastropathy is more common in cirrhotic patients.
• Commonly presents with chronic bleed causing anaemia;
bu acute bleed with haematemesis and melaena also can
occur.
• Treatment is mainly to reduce the portal pressure using
• propranolol.

20. ASCITES
• It is pathological collection of fl uid in the
peritoneal cavity.
• Ascites is the most common complication of
cirrhosis.
• It is a poor prognostic factor.
• Portal hypertension, renin angiotensin
aldosterone pathway causing renal sodium
retention, increased hydrostatic pressure in
hepatic sinusoids and splanchnic vessels cause
ascites.

21. Types of ascites
• Mild — Up to 150 ml amount required to demonstrate radiologically
• Moderate — 1500-2000 ml causes clinical dullness in flanks.
• Severe — > 2000 ml.
Classification of ascites
– Transudate (Protein < 2.5 gm/ dl).
• CCF—Commonest (SAAG > 1.1).
• Hypoproteinaemia.
• Anaemia.
• Nephrotic syndrome.
• Portal hypertension.
– Exudate (Protein > 2.5 gm/dl) (SAAG < 1.1).
• Peritoneal diseases.
– Tuberculosis.
– Neoplasm.
• Collagen disorder.

22. ASCITES IN PORTAL HYPERTENSION
CAUSES
• Hypoproteinaemia.
• Increased hydrostatic pressure.
• Decreased colloidal osmotic pressure.
• Lymphatic blockage.
• Altered aldosterone mechanism.
Treatment
• Medical—spironolactone, salt restriction
• Abdominal paracentesis(below the umbilicus, lateral to the rectus
muscle. Bladder should be empty before tapping. Slow gradual
tapping is important, otherwise patient goes in for fluid and
electrolyte imbalance.)
• TIPS as a bridge to liver transplant
• Liver transplantation

23. Thank you