The document summarizes portal hypertension and portal vein system. It describes that the portal vein is formed by the union of the splenic and superior mesenteric veins, running within the lesser omentum and posterior to the common bile duct and hepatic artery. Portal hypertension is defined as a hepatic venous pressure gradient greater than 5 mmHg and can be caused by pre-hepatic, intra-hepatic, or post-hepatic issues. Complications of portal hypertension include splenomegaly, ascites, and esophageal varices. Treatment involves pharmacological therapy, endoscopic procedures like band ligation, and transjugular intrahepatic portosystemic shunt placement.

1. PORTAL SYSTEM
and
PORTAL HYPERTENSION
Dr. A. Bharath

2.  The portal vein is formed in
front of IVC and behind the
neck of the pancreas ( at the
level of 2nd lumber vertebra )
by union of the splenic & SMV.
 About 5-8cm in length and
1cm in diameter in adults and
devoid of valves
 It runs with in the free border
of lesser omentum as a part of
Porta hepatis posterior to CBD
and Hepatic artery

3. Tributaries
Its main tributaries are :
The coronary (Lt gastric) vein.
Pyloric vein.
Cystic vein.
Pancreaticodudenal vein.
Ligamentum teres (umbilical
vein)

4. Branches

5. Site Portal Vein tributaries Systemic veins
Gastroesophage
al junction
Left Gastric (Coronary)
Vein
And Short Gastric Veins
(Submucosal veins)
Lower esophageal veins that
drain into Azygos and
Accessory Hemiazygos veins
Rectum Superior rectal veins that
drain into Inferior
mesenteric vein
Middle and Inferior rectal veins
that drain into Internal Iliac and
pudendal veins
Umbilicus Persistant small branches
of Left Portal vein running
thrugh ligamentum teres
Periumbilical branches of
superior and inferior epigastric
veins
Bare area of
liver
Intraparenchymal branches
of Right Portal vein
Veins of Sappey
Retroperitoneal veind draining
into Azygos and Hemiazygos
veins
Retroperitoneum Colonic veins near hepatic
and spleenic flexures
Retroperitoneal veins of
Retzius
Porto Systemic Anastamoses

6. Portal Hypertension
 Normal Portal venous pressure 5-10 mm Hg
 Defined as Increase in portal venous pressure above the
normal limit
 Defined as a Hepatic venous pressure gradient > 5mm Hg

7.  Hepatic Venous Pressure Gradient(HVPG) = Wedged Hepatic
Venous Pressure(WHVP) – Free Hepatic Venous
Pressure(FHVP)
 It is a measure of portal sinusoidal pressure and is obtained by
catheterization of a hepatic vein via the jugular or femoral vein.
 Normal HVPG value is 3-5 mm Hg
HVPG

8. Measurement of HVPG

10. Etiology
 Pre hepatic
» Portal vein Thrombosis
» Splenic vein thrombosis
» Compression of Portal vein
 Intra Hepatic
» Pre sinusoidal – Schistosomiasis
» Sinusoidal – Cirrhosis
» Post sinusoidal – Veno occlusive Disease

11. Post Hepatic – Budd Chiari syndrome, Venacaval webs,
Constrictive Pericarditis

12. Portal hypertension in cirrhosis results from
 increased resistance to portal flow at the level of the sinusoids
(Sinusoidal)
 compression of central veins by perivenular fibrosis and
expanded parenchymal nodules (Post Sinusoidal)

13. Pathophysiology
 Block to portal flow leads to increased portal pressure
 Splanchnic vascular bed response
 Initial increased vasoconstrictor response
 Seondarily vasodilator response dominates which
increases splanchnic blood flow
 Development of collaterals b/w portal and systemic circulations
 Plasma volume expansion occurs with development of
systemic hyperdynamic circulation

14. Clinical features
and
Complications

15. Important presenting features of Portal HTN are
 Spleenomegaly
 Esophageal Varices
 Ascites
In severe cases, can progress to Hepatorenal Syndrome,
Hepatopulmonary syndrome and Hepatic encephalopathy.

16. Spleenomegaly
 Congestive splenomegaly is common and most consistent
finding in patients with portal hypertension.
 It is Congestive Spleenomegaly
 Patients may develop thrombocytopenia and Leukopenia
 Splenomegaly itself usually requires no specific treatment

17. Ascites
 Increased movement of intravascular fluid into the space of
Disse, caused by sinusoidal hypertension and
hypoalbuminemia.
 Leakage of fluid from the hepatic interstitium into the peritoneal
cavity.(blockage of lymph radicles)
 Renal retention of sodium and water due to secondary
hyperaldosteronism

18.  Present with distended abdomen or breathlessness in massive
ascites
 Careful differentiation of other causes of ascites is needed
 Diagnostic paracentesis
 Serum Ascites to Albumin Gradient (SAAG) > 1.1gm/dl, If
<1gm/dl then other causes are considered

19.  Treatment of Ascites is mainly by Diuretics and dietary Sodium
restriction(<2gm/day)
 In Ascites refractory to medical therapy therapeutic large
volume paracentesis is done
 If ascites progresses despite LVP, TIPS is considered

20. Esophageal varices
Engorged submucosal veins in lower esophagus and proximal
stomach
 Thirty percent of patients with cirrhosis develop varices
 The rate of development of varices in cirrhotics is approximately
5-15% per year.
 One third of patients with varices present with bleeding varices
Screening EsophagoGastroDuodenoscopy (EGD)

21. Risk of developing bleeding from varices depends on
 Severity of liver disease
 Patients with HVPG >12 mmHg
 Previous episodes of variceal bleeding
 Size of varices
 Red wale signs

22. Assessment of patient
• Assessment of the liver disease
• Assessment of the portal circulation
• Upper gastrointestinal (GI) endoscopy

23.  Evaluation of liver disease is based on clinical findings and
laboratory studies
 T. Bilirubin and liver enzymes increases, Albumin decreased
and Prothrombin time increased
 Viral serology to rule out viral hepatitis
The two important scoring systems for liver disease severity are
the Child-Pugh score and the Model for End-stage Liver
Disease (MELD) score

25. Model for End-Stage Liver Disease (MELD) Score
9.57 Ln(S.Cr) + 3.78 Ln(T.bil) + 11.2Ln(INR) + 6.43
<10 – safely undergo elective surgery,
10 - 15 – may undergo surgery with caution,
>15 – should not be subjected to elective
surgical procedures

26. Assessment of Portal Circulation and vascular anatomy of
liver is by Imaging techniques
 USG and Doppler
 CT and MR Angiography

27.  Doppler ultrasound can assess size, directional flow, velocities
and wave-form patterns of the portal and hepatic veins
especially patency (or thrombosis) of the portal vein.
 CT or MR angiography helps when doppler findings are
inconclusive or of any doubt

28. Upper GI Endoscopy
 All patients diagnosed as cirrhotics have to undergo upper gi
endoscopy
 Varices are classified depending on their endoscopic
appearance

29. Grading of Varices
Size of varix 2 size classification 3 size classification
Small < 5 mm Minimally elevated
veins above the
mucosal surface
Medium Tortuous veins
occupying <1/3rd of
the lumen
Large > 5 mm Occupying >1/3rd of
the lumen
Red signs/Red wale signs denote impending bleeding from the
varices

30. Grade 1

31. Grade 2

32. Grade 3

33. Red Signs

34. Treatment
 Treatment of complications
 TIPS and Shunt procedures
 Liver transplant

35. Treatment of Varices
 Primary prophylaxis
 Treatment of Acute bleeding
 Prevention of rebleeding

36. Primary prophylaxis
Screening Esophagogastroduodenoscopy
Prophylaxis depends on
 Grade of varices
 Cirrhosis Compensated or Decompensated (Child’s class A or
B/C)
Pharmacological and Endoscopic therapies

37. Pharmacological therapy consists of
 Non selective β bolcker therapy – Propranolol, Nadolol
 Cost effective
 Reduce the risk of first hemorrhage by 45% and assoscuated
mortality by 50%
 Have significant side effects – Impotence
 Non responders(20%) and not tolerated(20%)

38. Endoscopic therapy consists of
 Endoscopic Variceal ligation(EVL) or Sclerotherapy
 Performed for 1-2 weeks untill obliteration followed by EGD 1-3
months following the procedure
 Controls variceal bleeding in >90% patients
 Reduces the risk and has minimal side effects when compared
to β blocker therapy
 But is more costly and not easily available in developing
countries

39. 1. Patients with Compensated cirrhosis and No varices
No prophylaxis, Screening EGD every 3 years
2. Patients with Small varices and
 No Increased risk – β blockers can be used but benifit not
established
 Having increased risk – β blocker therapy and repeat EGD every
2 years

40. 3. Patients with cirrhosis and medium or large varices
 No Increased risk – β blocker therapy is considered with annual
screening EGD
In case of contraindication or non compliance, EVL or
sclerotherapy
 Has Increased risk – prophylactic EVL or sclerotherapy is
considered

41. Acute variceal bleeding
 Recussitation
 Admission to ICU
 Blood transfusion (Target Hb-8gm)
 Correction of Coagulopathy (FFP, Platelets)
 Prophylactic Antibiotics
 Combined Pharmacologic and endoscopic treatment
 Tracheal intubation may be needed in cases of massive bleed
to secure airway and prevent aspiration

42. Pharmacological therapy consists of
 Vasopressin and analogues
 Somatostatin and analogues
 β blocker therapy

45.  When medical and endoscopic measures fail to control
variceal hemorrhage, balloon tamponade using a Sengstaken-
Blakemore tube will control refractory bleeding in up to 90% of
patients.
 However, its application is limited due to the potential for
complications, which include aspiration, airway obstruction,
and esophageal perforation due to overinflation or pressure
necrosis
Luminal Tamponade

46.  The gastric balloon is inflated
first by 200 ml of air, and
pulled upwards to press the
gastric fundus.
 If bleeding continues, the
oesophageal balloon is inflated.
 The pressure in the
oesophageal balloon should
be 30-40 mm Hg.
 This therapy is effective in
controlling bleeding in 80-90%
of cases.

48. Secondary Prophylaxis
Combined endoscopic and pharmacologic therapies are used
 Long term endoscopic control with banding or sclerotherapy of
recurrent varices every 3-6 months
 Non selective β blocker therapy starting at low dose and
increasing until resting HR decreases by 25% but not below
55bpm
If combined therapy fails / patient is not compliant, TIPS or other
shunt procedure is considered especially if patient is a
transplant candidate

49. Transjugular Intrahepatic Portocaval Shunt

50.  TIPS procedure involves implantation of a metallic stent
between an intrahepatic branch of the portal vein and a hepatic
vein radicle
 The needle track is dilated until a portal pressure gradient of
≤12 mmHg is achieved
 Controls variceal bleeding in >90% of cases refractory to
medical treatment,

51.  The major advantage of TIPS is that it is nonoperative
approach
 Portal vein patency must be established conclusively before
procedure
Disadvantages
 Shunt Occlusion(50% at 1yr) – Thrombosis or Neointimal
hyperplasia
 High incidence of Hepatic Encephalopathy(30-35%)
 Severe hemorrhage in case of puncture of extra hepatic portal
vein

52.  TIPS is best suited to provide short term portal system
decompression
 Patients most suitable for TIPS are Liver transplant
candidates who fail endoscopic or pharmacologic
therapies

53. Surgical therapy
 Porto systemic shunt procedures
 Devascularisation procedures
 Liver transplant

54. Porto Systemic Shunts
 Porto systemic shunt procedures aim to decompress the
portal system to varying degrees by shunting portal blood
to systemic vessels
 Most of the shunt procedures today are only historically
significant

55. Surgical shunt procedures today are considered only if the patient
has
Severe liver disease
Not a transplant candidate
Does not have access to TIPSS
Prognosis mainly depends on hepatic reserve

56. Surgical shunt procedures are classified as
 Non Selective Shunts
 Selective Shunts
 Partial Shunts

57. Non Selective shunts
 Aim to decompress the portal system by completely
diverting the portal blood flow
 Hence also called Total shunts

59. End to Side Anastomosis (Eck’s fistula)
 In classic end-to-side portocaval shunt the portal vein is divided
close to the hilum of the liver and the splanchnic end
anastomosed to the side of the vena cava.
 This decompresses the portal hypertension but leaves the
obstructed sinusoids under high pressure.
 It will not relieve ascites but will control variceal bleeding.

61. Side to side Anastamosis
 Side to side shunts are either direct vein to vein anastamoses
or wide interposition grafts
 Intact upper end of the portal vein serves as a decompressive
outflow from the high-pressure–obstructed liver sinusoids.
 Hence, in addition to controlling variceal bleeding, these shunts
also control ascites.

63. Proximal Splenorenal shunt
 Conventional Splenorenal shunt involves splenectomy and end
on side anastamosis of proximal end of the splenic vein to left
renal vein
 Major disadvantage is Shunt stenosis and thrombosis

64. Controls variceal bleeding effectively
Major drawbacks of Total shunts
Loss of Portal Circulation to liver (Portoprivial Syndrome)
Accelerated Hepatic failure
High incidence of Hepatic Encephalopathy

65. Selective Shunts
Selective shunts aim to
decompress the esophagogastric varices and
preserve the portal blood flow to liver
Maintain residual portal HTN
Distal Splenorenal shunt

66. Distal Spleno Renal Shunt (DSRS)

67. Distal Spleno Renal Shunt
 Distal part of splenic vein is anastomosed to left renal vein
 Introduced by Warren
 Decompresses the gastro splenic circulations but high pressure
in mesenteric and portal veins persist
 Doesnot relieve / rather aggravates Ascites

68.  Control of variceal bleeding in 90-95%
 Portal perfusion maintained in >90% in nonalcoholic liver
disease but only 50% in alcoholic liver disease
 Incidence of encephalopathy reduced to 15%
 Technically more difficult than total shunts

69. Partial shunt

70. Partial shunts
 Objectives are same as selective shunts
 Different from selective shunt in that splenic and mesenteric
blood flows are not divided from one another
 Previously narrow vein to vein side on anastamosis was done
 Either thrombosed or dilated to become total shunt

71.  Recently small calibre interposition grafts are being used
 Controlled variceal bleeding in 90%
 Maintained Portal perfusion in 80%

72. Devascularisation procedures
Devascularisation procedures aim to interrupt the inflow to
varices
Sugiura Approach
Modified Sugiura approach
Esophageal devascularisation without Splenectomy (EDWS)

73. The Sugiura procedure is a 2 step procedure, consists of
Extensive devascularization of the stomach and distal esophagus
Splenectomy
Transection of the esophagus
Truncal vagotomy
Pyloroplasty.
Modified Sugiura approach differs from original in that it spares
vagal branches to pylorus so that pyloroplasty is not required

74. Modifications for Sugiura-Futagawa procedure
 Sparing of Vagal branches to pylorus of stomach and eliminating
need for pyloroplasty
 Esophageal Devascularisation without Splenectomy – by
Orozco recommends Splenectomy only in cases of
hyperspleenism and Spleenic vein thrombosis

75. Liver Transplant
 Definitive treatment for any End Stage Liver Disease
 Only therapy that addresses underlying liver disease
 Very expensive and Donor organs are not readily available

76. THANK YOU

77. References
 Sabiston Text book of Surgery 20th ed.
 Bailey and Love Short Practice of Surgery 26th ed.
 Schwartz Principles of Surgery 10th ed.
 Maingot’s Abdominal Operations 12th ed.
 Harrisons principles of Internal Medicine 19th ed.
 Robins Textbook of Pathology 10th ed.
 Internet