This document discusses portal hypertension and its management. It defines portal hypertension as increased portal pressure and describes how hepatic venous pressure gradient (HVPG) is used to measure it noninvasively. The main causes of portal hypertension are discussed as pre-hepatic, intra-hepatic, and post-hepatic. Clinical features include gastroesophageal varices, ascites, and splenomegaly. Management involves screening and treatment of varices, diuretics for ascites, and splenectomy in rare cases. Transjugular intrahepatic portosystemic shunt (TIPS) or surgical shunts are considered if medication fails or is not available.

1. Dr. Ankur
PGIMS, Rohtak
PORTAL HYPERTENSION

2. PORTAL HYPERTENSION
• Portal Hypertension - clinical syndrome with ↑ Portal Pressure (PP).
• Direct measurement:
➢ Invasive
➢Inconvenient
➢Clinically impractical
• Other parameter used - HVPG (represents pressure gradient between PV
and intraabdominal IVC.
• HVPG – Simple, Safe, Reproducible.

3. HEPATIC VENOUS PRESSURE GRADIENT (HVPG)
1.5-6
mmHg
• Normal
>5-6
mmHg
• Portal
Hypertension
>10
mmHg
• Predicts
complication
>12
mmHg
• Threshold for Vx
bleeding

4. PATHOLOGY
• Pressure gradient is due to ↑
resistance to blood flow in
➢Pre-sinusoidal
➢Sinusoidal
➢Post-sinusoidal circulation
• (Rarely portal flow ↑ without
resistance eg. Splanchnic AV fistula)

5. Portal Hypertension
PRE-HEPATIC INTRA-HEPATIC POST- HEPATIC
- Thrombosis of PV,SV -Cirrhosis -Constrictive pericarditis
(Umblical Vein Catheterization) - Schistosomiasis -Budd chiari syndrome
- Invasion by malig. Tm. -Congenital Hepatic -IVC web
- Extrinsic press. by L.N. Fibrosis
or other mass

6. PREHEPATIC
• Accounts for 5-10%
• Incidence may be high in India
• Sometimes splenic vein thrombosis is seen with normal PV
- Acute pancreatitis
- Ca body and tail of pancreas
-Presents only with splenomegaly
-Tackled by splenectomy

7. INTRA-HEPATIC
• Accounts for 90%
• Cirrhosis- Alcoholic and Hepatitis C
Hepatic vascular resistance in hepatic sinusoids is due to
fibrosis, scarring and distribution of microvasculature &
Dysregulation of contractile elements including hepatic
myofibroblast.
• Schistosomiasis- seen in middle and Far East and South Africa.

8. POST -HEPATIC
• Accounts for 1-2%
• Outflow block leads to
-Increased sinusoidal pressure
- Centrilobular hepatocyte injury
- Fibrosis, scarring and cirrhosis

9. • Portal vein - lies behind neck of pancreas, formed by joining of
SMV and splenic vein.
• Divide into Rt. and Lt. branches (tributary).
• Feeding tributaries of SMV/SV/PV may have some variations.

10. IMPORTANT VENOUS ANATOMY ( VARIX)
4 Zones identified
➢ Gastric Zone – 2-3 cm below GE Jn.
Veins run longitudinally
➢ Palisade Zone – 2 – 3 cm above Gastric Zone
Parallel palisade run longitudinally & Correspond to
oesophageal mucosal folds
➢ Perforating Zone – 2-3 cm superior to palisade zone
Veins perforate oesophageal wall linking external to
internal veins
➢ Truncal Zone – Extends 8 – 10 cm up the oesophagus, having 4 – 5
longitudinal veins
Irregular perforating veins from submucosa to external
oesophageal plexus

11. CLINICAL FEATURES OF PORTAL HYPERTENSION
• Portal hypertension presents with mainly 3
primary complications
1. Gastro-esophageal Varices with or without
bleed
2. Ascites
3. Splenomegaly and Hypersplenism

12. OESOPHAGEAL VARICES
• 1/3rd cases of portal hypertension will have it
• 1/3rd cases of varices will eventually bleed
❖Predictors of risk of bleeding:
➢ Severe cirrhosis ( Child-Pugh criteria & MELD score )
➢Height of hepatic venous pressure
➢Size of varices
➢Location of varices
➢Tense ascites
Contd…..

13. Endoscopic stigmata
➢Red wale sign
➢Hematocystic spot
➢Diffuse erythema
➢Bluish discoloration
➢Cherry red spots
➢White nipple spots Cherry red spots Hematocystic spot Red wale sign

14. ASCITES
• Late sign of portal hypertension
• Diagnosed by physical examination and paracentesis
• Serum Ascites albumin gradient (SAAG) – Replaced exudate/transudate concept
• If gradient (serum albumin:ascitic fluid albumin is > 1.1 g/dL - Portal hypertension
• If gradient (serum albumin:ascitic fluid albumin is < 1.1 g/dL - Malignant/Infectious
➢Small amount – Restrict salts
➢Moderate amount – Add diuretics
➢Refractory – Repeated large volume paracentesis & TIPS ( Increased
Encephalopathy)
• <50 % survive 2 years after onset of ascites .
• So, Consider Liver transplantation at onset of ascites

15. SPLENOMEGALY & HYPERSPLENISM
• Thrombocytopenia – diagnostic of portal hypertension
• Leukopenia
• Splenectomy is treatment under very special circumstances

16. OTHER UNCOMMON PRESENTATIONS
• LIVER FAILURE & ENCEPHALOCEPATHY Due to progressive underlying liver disease
• HEPATOCELLULAR CARCINOMA
➢High prevalence of hepatitis C in cirrhosis
➢Transplantation in carefully selected patients who are otherwise NOT candidates for resection
• HEPATO PORTO PULMONARY SYNDROME – a triad of
➢Liver disease
➢Arterial hypoxemia
➢Intrapulmonary vascular dilatation
Medical treatment has limited success
Transplantation specially in Paediatric patients

17. WORK UP
Multidisciplinary approach
• Diagnostic and prognostic priorities vary for each patient depending on
➢Etiology
➢Presentation
➢Severity of disease
• But essential component of work up are :-
a. Endoscopy
b. Imaging
c. Liver function

18. ENDOSCOPY
➢Done for finding out
• Size of varices
• Extent of varices
• Risk factors of bleeding
• Portal gastropathy ( Changes in mucosa
of stomach like friability and presence of
ectatic blood vessels at the surface) Endoscopic view of Portal Gastropathy

19. IMAGING
• Doppler Ultrasound 1. Size & flow through PV & tributaries
2. Define morphology in Cirrhosis
• CT for Morphological assessment of liver parenchyma & liver tumour
• HVPG Transhepatic/Transvenous catheterization of Hepatic veins ( Gold
standard in diagnosis of PH) & measure Wedge hepatic venous
pressure(WHVP) and Free hepatic venous pressure(FHVP) .
WHVP-FHVP = HVPG ( reducing it to <10 mm Hg will reduce risk of variceal bleeding )
• Angiography – CT /MR angiography to evaluate arterial & venous flow of liver
( replaced the need of variceal angiography)

20. ASSESSMENT OF LIVER FUNCTIONS
Done by several ways
1. Clinical
2. Lab data
3. Child-Pugh criteria
4. MELD Score
There is a scoring system for Oesophageal varices and Portal Gastropathy

21. 1. CLINICAL ASSESSMENT OF LIVER FUNCTIONS
Presence of
• Ascites
• Encephalopathy
• Clinical Jaundice
• Muscle wasting
Indicate impairment of liver functions and actually advanced liver disease

22. 2. LAB DATA FOR ASSESSMENT OF LIVER FUNCTIONS
a. Serum Bilirubin
❑ Serum Albumin
❑ Prothrombin Time
❑ SGOT/SGPT
❑ Serum Alkaline phosphate
b. Haematological parameters
❑ Haemoglobin
❑ Platelet Count - <1 lakh indicate significant Portal Hypertension
❑ White blood cell count
c. PT:INR ratio of 1:5 indicate poor liver function
contd…..

23. LAB DATA FOR ASSESSMENT OF LIVER FUNCTIONS
d. Specific Liver disease markers ( Hepatic panel )
❑ Antinuclear antibody
❑ Antimitochondrial antibody
e. Metabolic markers
❑ Iron
❑ Copper
❑ Alfa 1 antitrypsin
f. Risk of hepatoma by screening through
❑ estimation of Alfa fetoprotein

24. 3. CHILD –PUGH SCORE FOR SEVERITY OF LIVER DISEASE
Parameter Score 1 Score 2 Score 3
Encephalopathy None 1 or 2 3 or more
Ascites None Mild Moderate
Bilirubin(mg/dL) 1 - 2 2.1 - 3 Equal to or >3.1
Albumin(g/dL) Equal to or >3.5 2.8 – 3.5 Equal to or <2.7
PT increase (in seconds) 1 - 4 4.1 - 6 Equal to or > 6.1

25. SCORING SYSTEM FOR SEVERITY OF LIVER DISEASE
# CHILD – PUGH SCORE
> Grade A severity = 5 – 6 points
> Grade B severity = 7 – 9 points
> Grade C severity = 10 – 15 points
# MELD SCORE (Model for End stage Liver disease )
Score = 0.957x log e Creatinine(mg/dL) + 0.378 x log e Bilirubin ( mg/dL)+1.20 log e INR
@ MELD Score 19 = Refer for liver transplantation evaluation
@ MELD Score 12 = Initiate prophylaxis for Spontaneous bacterial peritonitis
@ MELD Score 10 = Continue follow up and Repeat MELD at 1 month
@ MELD Score 8 = Continue follow up and Repeat MELD at 3 months
MELD routinely used in patients awaiting Transplantation.

26. MANAGEMENT
Clinical reality- Address advanced stage complications of PH
1. Prophylaxis for oesophageal varices
2. Management of acutely bleeding varices/Prevention of re-bleed
3. Management of Ascites
4. Management of Splenomegaly /Hypersplenism

27. OESOPHAGEAL VARICES
Past century – seen a shift in treatment paradigm From Expectant treatment to
➢ Screening
➢ Pharmacologic treatment
➢ Endoscopic prophylaxis
All patients with signs/symptoms of Cirrhosis are screened for
➢ Oesophageal varices at the time of diagnosis
➢ Every 2 – 3 years thereafter
➢ Every year if progresses to Child B or beyond

28. OESOPHAGEAL VARICES
• Small Varices – No intervention
• Moderate to large varices ( 5 – 10 mm ) Prophylactic pharmacological intervention
• Presence of risk factors of bleeding
• Child C Score Non selective β blockers
Non responders –Carvedilol ( α1 receptor
blocker besides being nonselective β blocker)
-PLUS EVL

29. ENDOSCOPIC BAND LIGATION

30. MANAGEMENT OF ACUTE BLEED
Mortality of acute bleeding 15 – 20%
➢ Splanchnic vasoconstrictors e.g. Somatostatin / Octreotide ( Vasopressin almost
obsolete ), followed by
➢ Endoscopy therapy ( mostly variceal band ligation: Sclerotherapy not the choice of
Gastroenterologist now)
➢ If Endoscopic treatment not available- SENGSTAKEN – BLACKMORE TUBE
➢ If varices extend into proximal stomach , endoscopic therapy fails
➢ Consider TIPS ( Expandable metallic stent to create P-S shunt)
➢ If TIPS is also not available, Surgical oesophageal transection – Rarely used as the
outcome very poor

31. RECENT BLEED
• Repeated variceal ligation until all varices are obliterated
• Beta blockers as adjunct and stop after all varices obliterated
• Take all supportive measures for achieving
Hemoglobin – 8 g/dL
Hematocrritt – 24 %
• EVL- came in 1988 and virtually replaced sclerotherapy
- Complete obliteration of varices achieved in fewer
sessions than sclerotherapy
- Each session of EVL interspaced by 7 – 10 days

32. IF ENDOSCOPIC TREATMENT NOT AVAILABLE
SENGSTAKEN – BLACKMORE TUBE
❖ Principle: BALLOON TEMPONADE
➢Gastric Balloon – 200 ml
➢Oesophageal Balloon – 40 mm Hg
➢After control of bleeding with Balloon – it is mandatory to decompress
varices within 24 hours

34. IF VARICES EXTEND INTO PROXIMAL STOMACH , ENDOSCOPIC THERAPY FAILS
THEN, RESORT TO BALLOON OCCLUDED OBLITERATION OF VEINS
• Gastric varices often associated with
➢Compensatory gastro-renal and Gastro-caval shunts which are
less amenable to portal decompression
• Such cases managed by Balloon occluded obliteration of veins.
• 2 techniques
➢BRTO ( Balloon occluded retrograde obliteration )
➢BATO ( Balloon occluded antegrade obliteration )
depending upon vascular anatomy of problematic varices
• Balloon catheter can be introduced via femoral vein or IJV approach

35. DECOMPRESSION OF VEINS
• Achieved by
a. TIPS
b. Surgical Shunts

36. TRANS JUGULAR INTRAHEPATIC PORTOSYSTEMIC SHUNT(TIPS)
• EVALUATE PATIENTS FOR
✓ Cardio-pulmonary function
✓ Portal vein patency
✓ Liver functions
contd…

37. TIPS ( IMPORTANT STEPS)
• Trans jugular, to
• Right or Middle hepatic vein, to
• Substance of liver traversed and needle punctures portal vein
• Catheter placed over guide wire into vein
• Pressure taken and portogram done
• Trans parenchymal tract dilated and stent placed
• Stent dilated to bring pressure gradient to < 10 mm Hg
• Success rate 95%
• 1 Year patency rate 90%

38. TIPS

39. TIPS ( INDICATIONS)
• Indications
➢Failed endoscopic treatment
➢Failed medical treatment
➢Poor surgical risk
➢Bridge to transplantation

40. TIPS ( CONTRA-INDICATIONS)
ABSOLUTE RELATIVE
Primary prevention of variceal bleeding Hepatoma, particularly if central
Severe congestive heart failure Obstruction of all hepatic veins
Tricuspid regurgitation Hepatic encephalopathy
Multiple hepatic cysts Significant portal vein thrombosis
Uncontrolled systemic infection or sepsis Severe uncorrectable coagulopathy (INR > 5)
Unrelieved biliary obstruction Thrombocytopenia (< 20,000 platelets/mm3)
Severe pulmonary hypertension Moderate pulmonary hypertension
Contraindications to placement of a TIPS

41. SURGICAL SHUNTS
• Porta-systemic shunts viable option for;
➢Patient optimum for methods but the facilities not available
➢Long term bridge to transplantation in carefully selected patients
➢3 types of shunts
• Total
• Partial
• Selective

42. SURGICAL SHUNTS
➢Total shunts
➢ Complete/Near total diversion of portal flow to IVC via
1. Porto caval shunt
2. Mesenterico-caval shunt
3. Proximal Spleno-renal shunt
➢Partial shunts
• Small diameter shunt e.g. H shunt or graft shunt
• Maintain some flow to liver
• Thrombosis is a problem
H Shunt or graft shunt

43. SURGICAL SHUNTS
• Selective shunts
➢Distal Spleno-renal shunt (DSR)
➢Currently used commonly
➢Selectively decompresses oesophageal
varices
➢While maintaining portal flow and pressure
➢Success rate – 85% ( Child A) & 75% ( Child
B )

44. DISTAL SPLENO –RENAL SHUNT(DSR)
➢Explore left renal vein and Splenic vein
➢Splenic vein isolated & divided near Spleno-SMV
junction
➢Brought down and anastomosed end to side
with left renal vein
➢Complete operation by interrupting left gastric
vein both at portal vein and above pancreas

45. OESOPHAGEAL DEVASCULARIZATION
SIGUIRA’S PROCEDURE
❑ 2 stage procedure of Esophago-gastric devascularization + sutured
anastomosis with Splenectomy, vagotomy & pyloroplasty
MODIFIED SIGUIRA’S PROCEDURE
❑ 1 stage procedure of oesophageal devascularization with stapled
anastomosis without vagotomy and pyloroplasty