slides on the complete surgical management of the portal hypertention

1. PORTAL
HYPERTENSION
BY
DR NIKHIL AMEERCHETTY
MS (general surgery ) RESIDENT
E – MAIL nikhilameerchetty@gmail.com

2. ANATOMY
• The portal vein arises from the post duodenal plexus of the embryonic viltelline
veins.
In the adult the portal vein and its tributaries have no valves
• It provides -75% of hepatic blood flow and 50% of the oxygen delivery
• 'Ihe portal vein trunk is 4.8 to 8.8 Cm long with an average length of 6.4 cm and
o.6 to 1.2 cm wide. with an average width of 0.9 cm.
• It is formed behind the neck of the pancreas at the level of the second lumbar
vertebra by the confluence of the superior mesenteric vein (SMV) and the splenic
vein

5. PORTAL HYPERTENSION
• Portal hypertension is defined by a portal pressure higher
than 5 mm Hg. However, higher pressures (8 to 10 mm Hg)
are typically required to begin stimulating the development
of portosystemic collateralization.
• If pressure >12 mmHg chances of variceal bleeding
• Pressure >15mmHg brisk bleeding
• Pressure > 20mmHg continuous bleeding

6. PATHOPHYSIOLOGY
• Block to portal flow leads to increased portal pressure.
• Splanchnic vascular bed response.
(a) Initial increased vasoconstrictor and decreased vasodilator response increases
intrahepatic resistance.
(b) Secondarily, the vasodilator response dominates, with increase in splanchnic
inflow. Collaterals develop between the portal circulation and the systemic
circulation.
(c) Plasma volume expansion occurs with the development of a systemic
hyperdynamic circulation.

7. PORTOSYSTEMIC ANASTOMOSIS
• It is important to know the points of communication between the portal and
systemic (caval, azygous, and hemiazygous) venous systems
• Most important portosystemic anastomoses are the veins of the proximal
stomach and distal esophagus. which receive flow from the coronary and
short gastric veins and drain into the superior venacava via the azygous
system.

8. • 'Ihe submucosal venous plexus in the rectum between the superior hemorrhoidal
veins (the portal system) and the middle and inferior hemorrhoidal veins (the
cavalsystem)
• The paraumbilical veins, connect the left portal vein to the epigastric venous
network ‘This plexus can become the variceal "caput Medusae· in patients with
portal hypertension and produce the Cruveilhier-Baumgarten syndrome.
• Relzlus veins: a group of small but numerous retroperitoneal veins that connect
abdominal viscera. both tubular and solid. with the caval system via
intercostals.phrenic, hunbat and renal veins

10. CAUSES
• PRE-HEPATIC
• HEPATIC
1) PRESINUSOIDAL
2) SINUSOIDAL
3) POST SINUSOIDAL
• POST HEPATIC

11. 1. Portal vein thrombosis
2. Malignant occlusion
a) Congenital
b) Sepsis
c) Trauma
3. Splenic vein
thrombosis
Extrahepatic
1. Schistosomiasis
2. Congentital
hepatic fibrosis
1.Cirrhosis 1. Budd-Chiari
2. Veno-occlusive
disease
Sinusoid Hepatic
vein
Pre sinusoidal

12. PRE HEPATIC
1.)Extrahepatic portal hypertension is the most common cause of portal hypertension
• ” cavernomatous transformation of the portal vein” Centripetal distribution of the
collaterals .
2.)Isolated splenic vein thrombosis (left-sided portal hypertension) is usually secondary
to pancreatic inflammation or neoplasm.
• gastrosplenic venous hypertension, with superior mesenteric and portal venous
pressures remaining normal.
• Importance - Easily reversed by splenectomy alone

13. INTRAHEPATIC
• The most common cause of Intrahepatic presinusoidal hypertension is
schistosomiasis.
• Most common cause of portal hypertension at the sinusoidal is “Alcoholic cirrhosis”
1)Vasodilators produced in the body such as cytokines and TNF alpha stimulate the
endothelial vasodilators (NO) and prostacyclins causing splanchnic hypertension
2) secondary to deposition of collagen in the space of Disse.
• Centrifugal distribution of the collaterals.

14. EVALUATION
(1) Diagnosis Of The Underlying Liver Disease
(2) Estimation Of Functional Hepatic Reserve
(3) Definition Of Portal Venous Anatomy And Hepatic Hemodynamic Evaluation
(4)Identification Of The Site Of Upper Gastrointestinal Hemorrhage.

15. ASSESSMENT
• Jaundice, Ascites, Encephalopathy, And Malnutrition - End-stage Liver Disease.
• Specific Serologic Markers - Viral Hepatitis,
• Antimitochondrial Antibody – Primary Biliary Cirrohosis
• Iron Studies - Heamocromatosis
• 1-antitrypsin – Cirrhosis Of Liver
• Ceruloplasmin Levels – Wilson’s Disease
• Alpha-fetoprotein (AFP) should be measured in all such patients as a screening test
for hepatoma.

16. SCROING SYSTEMS
• Child-Turcotte-Pugh score .
• Useful to assess the prognosis
• Model for End-stage Liver Disease (MELD) score .
• Useful to predict the mortality
Score = 0.957 × loge creatinine (mg/dL) + 0.378 ×
logebilirubin (mg/dL) + 1.120 loge INR

17. CHILD-TURCOTTE-PUGH SCORE
• Parameter 1 Point 2 Points 3 Points
• Serum bilirubin (mg/dL) <2 2–3 <3
• Albumin (g/dL) >3.5 2.8–3.5 <2.8
• Prothrombin time ( S) 1–3 4–6 >6
• Ascites None Slight Moderate
• Encephalopathy None 1–2 3–4
• Grades: A 5–6 points B 7–9 points C 10–15 points

18. • Ultrasound to show overall liver morphology to pick up focal lesions suggestive of
hepatoma.
• Contrast-enhanced computed tomography (CT) scan or magnetic resonance imaging
(MRI) alone or in combination with CT, MRI angiography for morphologic
assessment.
• Liver biopsy may be required to confirm cirrhosis, and in focal lesions, to differentiate
hepatocellular carcinoma from regenerative nodules.
• Doppler ultrasound can assess the hepatic artery, portal and hepatic veins

19. • Quantitative liver testing with studies such as
• Indocyanine green clearance
• Galactose elimination capacity
• Monoethylglycinexylidide (MEGX)

20. ANGIOGRAPHY
• Portal pressure is measured indirectly from the hepatic veins by measuring
wedged and free hepatic vein pressures, difference is hepatic venous pressure
gradient(HVPG).
• Done using a balloon occlusion technique akin to a Swan-Ganz catheter
measurement in the pulmonary circulation.
• Normal HVPG is 6–8 mm Hg, and in cirrhosis it will be greater than 10
mm Hg.

21. UPPER GI ENDOSCOPY
• All patients with cirrhosis should have an upper endoscopy.
1. 30% patients with cirrhosis develop portal hypertension.
2. 30% patients with portal hypertension will bleed from varices within 2
years.
3. The rate of development of varices in patients with cirrhosis
approximately 8% per year.

22. TREATMENT
1. PHARMACOTHERAPY
2. VARICEAL TAMPONADE
3. ENDOSCOPIC THERAPY
4. DECOMPRESSIVE SHUNTS—RADIOLOGIC
TIPS
SURGICAL
TOTAL
PARTIAL
SELECTIVE
4. DEVASCULARIZATION OPERATIONS
5 LIVER TRANSPLANTATION

23. PHARMACOTHERAPY
• Antibiotic Prophylactic Should Be Initiated.
• Somatostatin, And Its Longer Acting Analogue Octreotide, Are As Efficacious As Endoscopic
Treatment For Control Of Acute Variceal Bleeding.
• Combination Of Octreotide And Endoscopic Therapy Is More Effective In Controlling
Bleeding Than Octreotide Alone And Is The Preferred Treatment For Most Patients.
• In Severe Cases Of Hemorrhage, Vasopressin Can Be Used To Diminish Splanchnic Blood
Flow.
• The Target For Treatment Is Less Than 12 Mm Hg Reduction In Hvpg. If This Is Achieved,
Patients Will Not Bleed.
• Other Pharmacologic Agents Such As Nitrates, Serotonin Antagonists, And Calcium
Channel Blocker, Non selective beta blockers.

24. VARICEAL TAMPONADE
• Sengstaken- Blakemore tube is used
Advantage :
• Immediate cessation of bleeding in more than 85% of patients
• widespread availability of this device
Disadvantages
• Cannot be used in the gastric varices
• Recurrent hemorrhage in up to 50% of patients after balloon deflation
• Discomfort for the patient
• High incidence of serious complications when used incorrectly by an inexperienced
health care provider.

25. Modified sengstaken-Blakemore tube

26. ENDOSCOPIC THERAPY
• ENDOSCOPIC BANDING
• The current standard for endoscopic therapy for esophageal varices is endoscopic
banding.
ADVANTAGES: fewer side effects, obliterates varices faster, and can be easily applied.
Multiband ligators allow the firing of six to eight bands in a spiral fashion
• A course of banding—usually two to three sessions—is then applied over the next
month to 6 weeks
• ENDOSCOPIC SCLEROTHERAPY
• Endoscopic sclerotherapy with injection of a sclerosing solution may be a useful
adjunct to complete the obliteration of smaller varices that cannot be banded.

28. Decompressive Shunts
• Decompression is considered second-line treatment
• Reserved for patients who rebleed through pharmacologic therapy and
endoscopic banding or whose varices remain “high risk.”
1. Radiologically placed shunt—TIPS.
2. Surgical shunts
Total, Partial, and Selective shunts.

29. TRANSJUGULAR INTRAHEPATIC
PORTOSYSTEMIC SHUNT (TIPS)
• Direct puncture of the internal jugular vein (IJV),
• passage of a catheter through the right atrium into one of the major hepatic veins followed
by a trans-parenchymal puncture of the liver to cannulate the portal vein.
• The catheter is passed into the portal vein
• The intraparenchymal track is then dilated and the track stented with an expandable metal
stent in the 10- to 12-mm-diameter range.
• The technical success rate is high (>90%) with a low procedural morbidity and mortality
(<10%).
• Patients are usually in the hospital for 1–2 days and the shunt patency should be
documented the day after the procedure with a Doppler ultrasound.

30. TIPS
• It is a temporary procedure
• Advantages:
• Useful in patients waiting for the transplant
• Useful in advanced hepatic functional decompensation who are unlikely to
survive for longer duration
• Useful for the treatment of medically intractable ascites.

31. TIPS
• DISADVANTAGES
• Shunt stenosis
• Shunt thrombosis
• Seen within the first year.
• Covered TIPS stents have reduced thrombosis and stenosis rates.
• Reintervention rates to maintain patency are high with uncovered stents, ranging from 40 to
80% and 20% with covered stents.
• Rebleeding rates for TIPS are around 20%, and this was reduced to 13% in the covered stent
• Shunt stenosis, which is usually secondary to neointimal hyperplasia, is more common than
thrombosis and can often be resolved by balloon dilation of the TIPS or, in some cases, by
placement of a second shunt.

33. Shunts
Total Shunts
1. End-to-side portacaval shunt
2. Side to side portocaval shunt (diameter >10mm)
Partial shunts
1. Side to side portocaval shunt(diameter <8mm)
Selective shunts
1. Distal splenorenal shunt

34. End-to-side portacaval shunt
• In end to side portocaval shunt (Eck fistula) portal vein is divided close to
the hilus of the liver and the splanchnic end anastomosed to the side of the
vena cava.
• It does not relieve ascites but will control variceal bleeding.
• Complications : portosystemic encephalopathy and accelerated hepatic
failure.

36. Side to side portocaval shunt
• side-to-side portacaval shunts with direct vein-to-vein or a short interposition
graft, or the other inter- position shunts such as mesocaval or mesorenal
• These shunts need to be at least 10 mm in diameter, usually being 12–15 mm, to
fully decompress portal hypertension.
• shunts differ from the end-to-side portacaval shunt in that the 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.

38. Splenorenal shunt
• The conventional splenorenal shunt consists of anastomosis of the proximal
splenic vein to the renal vein.
• Splenectomy is performed.
• Complications : shunt thrombosis

40. • The only indication for a total portal systemic
shunt at present is for patients with acute Budd-
Chiari syndrome

41. Partial Shunts
• Partial shunts are side-to-side shunts whose diameter is reduced to 8 mm.
• 90% control of variceal bleeding
• polytetrafluoroethylene (PTFE) graft is approximately 2–3 cm long, and
beveled at each end to give a larger anastomosis.

43. Selective Shunts
• Selective shunts are most commonly the distal splenorenal shunt (DSRS)
• Divide the splenic vein at its junction with the superior mesenteric vein, and
anastomoses the splenic vein to the left renal vein.
• This selectively decompresses gastroesophageal varices.
• Control of bleeding has been at 94%, with good portal perfusion maintained in
90% of patients initially.
• The overall incidence of encephalopathy has been around 15% following this
operation.

45. Devascularization Procedures
• Sugiura operation
• These operations approach the problem of variceal bleeding by interrupting inflow to the varices.
• The components are splenectomy, gastric and esophageal devascularization, and possibly
esophageal transaction
• The effectiveness of these procedures appears to depend on the aggressiveness of the operation.
• The advantage of these procedures is that portal hypertension is maintained with portal flow to
the cirrhotic liver.
• Devascularization can be useful when patients have extensive portal and splenic venous
thrombosis and there are no other operative or radiologic options.

46. Meso-Rex bypass
• Direct portal revascularization can be achieved by interposing a vascular graft
between the SMV and the Rex recessus (left portal vein system)
• MRB achieves a very successful physiologic cure of chronic portal
hypertension and restores the portal flow into and through the liver graft.
• Primary revascularization of liver grafts
• Managing early acute portal vein thrombosis episodes.

47. Liver transplant
• Liver transplant is the most commonly used operation for patients with
portal hypertension at the present time.
• The major issues are
1. Patient Selection
2. Timing Of Transplant,
3. Expanding The Donor Pool
4. Outcomes.

48. Patient selection
• Standards for patient listing have been set by the United Network for Organ
Sharing (UNOS)
• The indication for transplant is end-stage liver disease
• Variceal bleeding ,ascites and encephalopathy are clinical indicators of end-stage
liver disease.
• comorbid medical conditions and a psychosocial suitability for transplant
particularly in the alcoholic and other chemical dependency patient populations.
• Hepatitis C population with hepatoma

49. Timing
• The timing of transplant is dictated by the severity of the underlying liver
disease.
• Prioritization for organs occurs on the basis of MELD scores
• Sickest patients receiving cadaveric organs first based on bilirubin,
prothrombin time, and serum creatinine.
• Timing is dictated by these objective criteria rather than individual physician
decisions in day-to- day patient management

50. outcomes
Hospital mortality remains at less than 10%,
80+% 1-year survival
60–65% 5-year survival

53. THE MULTIDISCIPLINARY TEAM
Hepatologists are in the front line for diagnosing and directing the
management for many of the clinical presentations.
Endoscopists play an important role diagnostically and in primary therapy for
managing variceal bleeding. Endoscopic banding requires significant expertise.
Radiologists, both imaging and interventional, play roles in diagnosis, directed
biopsy, and procedural (TIPS) manage- ment of these patients.
Surgeons play a major role in liver transplant but may also have a role in
shunting good-risk patients with refractory variceal bleeding.

54. • Pathologists with an interest in liver pathology are important in the accurate
diagnosis and staging of disease severity.
• Critical care physicians and anesthesiologists are vital team members when
patients with portal hypertension have acute events and in their perioperative
management.
• Nephrologists, cardiologists, and pulmonologists all play a role in the
management

55. Finally, who coordinates? In a complex
multidisciplinary team
• coordinators are the ones to whom the patients
turn for help in navigating their way through
management in this complex field

56. • Thank you