This document provides information on portal hypertension and its surgical management. It begins with the history of portal hypertension, describing early anatomists who studied the portal venous system. It then covers the anatomy of the portal system and pathophysiology of portal hypertension. Etiologies of portal hypertension including pre-hepatic, hepatic, and post-hepatic causes are discussed. Clinical presentation, diagnosis, evaluation, and general management approaches are summarized. The document concludes by focusing on surgical options for treating portal hypertension including devascularization procedures and liver transplantation.

1. PORTAL HYPERTENSION
SURGICAL MANAGEMENT
DR. ZAHID IQBAL MIR
MBBS,MS,DNB

2.  HISTORY
 ANATOMY
 PATHOPHYSIOLOGY
 ETIOLOGY
 CLINICAL
PRESENTATION
 DIAGNOSIS
 EVALUATION &
ASSESSMENT
 MANAGEMENT
 SURGERY IN PATIENT
WITH PORTAL
HYPERTENSION

3. HISTORY
 Porta – Latin ( gate / passage)
 Babylonians – liver as seat of soul –
sacrificed animal liver were
interpreted to predict future
Explanation of the portal venous
system in human
Herophilos
a Greek physician
IV century B.C.
Presentation of liver vascular
anatomy
Mondino de Liuzzi
Italian surgeon
1319

4. First description of portal hypertension
Leonardo da Vinci
Italian Renaissance polymath, 1511
"De humanis corpore".
..the artery and the vein which go from the spleen to
the liver become so large, to block the blood coming from
the mesentric vein the latter vein dilates and
becomes torturous like a snake, that the liver dries and
become like frozen bran, in colour and consistency..
First description of portal system accurately
Andreas van Wesel
Flemish anatomist, 1543

5. First demonstration of portal
circulation
Francis Glisson
British physician, 1650
First introduction of the term "portal hypertension"
Augustin Gilbert
French physician, 1902

6. ANATOMY
 post duodenal plexus of the
embryonic viltelline veins
 No valves
 75% of hepatic blood flow and 50%
of the oxygen delivery
 4.8 to 8.8 cm long (average 6.4 cm)
and o.6 to 1.2 cm wide (average 0.9
cm)

7. Major changes of clinical significance is around GEJ
Morphometry & corrosion casting
 Gastric Zone
2-3 cms below GEJ. Veins run longitudinally in
SM & LP to short gastric & left gastric veins
 Palisade Zone
multiple communication between the veins in
LP but no perforating veins
 Perforating Zone
Vessels perforate through the esophageal
wall linking the internal & external veins
 Truncal Zone
8-10 cms up the esophagus, irregular
perforating veins from submucosa to external
esophageal plexus.

8. PATHOPHYSIOLOGY
Hepatic Venous Pressure Gradient (gradient in pressure between
the PV and IVC >5 mmHg

9.  Obstruction to portal venous flow is usually secondary to an
intrahepatic block with cirrhosis (etiologic causes of portal
hypertension)
 Functional increase in resistance occurs secondary to activated
hepatic stellate cells and myofibroblasts in the fibrous septa of the
sinusoid - reversible component to intrahepatic resistance
 Imbalanced production of vasoconstrictors, endothelin,
norepinephrine, and angiotensin, with an insufficient release of
hepatic vasodilators, such as nitric oxide and prostaglandins

10.  Splanchnic vasodilation occurs with increased splanchnic flow
aggravating and contributing to the portal hypertensive syndrome
• This is multifactorial, with neurogenic, humoral, and local mediators
 Portosystemic collaterals develop not only at the gas-trosophageal
junction but also in the abdominal wall and retroperitoneum.
 Increase in plasma volume secondary to the vascular changes.
Systemic hyperdynamic circulation
-increased cardiac output
-low total systemic vascular resistance
 further aggravation of the splanchnic hyperemia and overall
hyperdynamic state

11. OBSTRUCTION TO PORTAL FLOW ( Cirrhosis, PVT)
INCREASED PORTAL VENOUS PRESSURE
INCREASED PRODUCTION OF
VASOCONSTRICTORS INCREASED PRODUCTION OF VASODILATORS
INCREASED HEPATIC VASCULAR RESISTANCE
Systemic BP
Increased
collateral flow
Increased CO
INCREASED HEPATIC VASCULAR TONE
Splanchnic hyperemia
Neurohumoral activation
PORTAL
HYPERTENSION
Na+ & H20 retention

12. Porto Systemic Anastamosis

13. ETIOLOGY
 Pre hepatic
 Hepatic
• Pre sinusoidal
• Sinusoidal
• Post sinusoidal
 Post hepatic
MCC - Cirrhosis & schistosomiasis
 Western countries – Cirrhosis
 Rest of world - Non cirrhotic
(Schistosomiasis & Portal vein
thrombosis)

14. PRE HEPATIC CAUSES
Portal vein thrombosis
Splenic vein thrombosis
Sinistral L sided portal hypertension
Splanchnic arteriovenous fistula
Splenomegaly
(lymphoma, Gaucher's disease)
NON CIRRHOTIC CAUSES

15. PRE SINUSOIDAL
Schistosomiasis
Idiopathic noncirrhotic portal hypertension
Primary biliary cholangitis
Sarcoidosis
Congenital hepatic fibrosis
primary sclerosing cholangitis
Hepatic arteriopetal fistula
Adult polycystic liver disease
Arteriovenous fistulas
Autoimmune cholangiopathy
Vinyl chloride toxicity
Neoplastic occlusion of the intrahepatic portal vein
Mineral oil granuloma
H
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16. SINUSOIDAL
Arsenic poisoning, Vinyl chloride toxicity
Drugs (eg, amiodarone, methotrexate)
ALD, NAFLD
Gaucher's disease
Zellweger syndrome
Viral hepatitis
Chronic Q fever
Schistosomiasis
Amyloid or light chain deposition in space of Disse
Acute hepatic injury
Mastocytosis
Agnogenic myeloid metaplasia
Acute fatty liver of pregnancy
H
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17. POST SINUSOIDAL
Sinusoidal obstruction syndrome
(venoocclusive disease)
Budd-Chiari syndrome
Alcoholic liver disease
Chronic radiation injury
Vitamin A toxicity
Epithelioid hemangioendothelioma
Angiosarcoma
Sarcoidosis
Mycobacterium avium or M. intracellulare infection
Mineral oil granuloma
H
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18. POST HEPATIC CAUSES
IVC obstruction
Budd-Chiari syndrome
Cardiac disease
Constrictive pericarditis, restrictive cardiomyopathy

19. CLINICAL MANIFESTATIONS
 Often asymptomatic until complications develop
 Clinical manifestations
 Splenomegaly
 Abdominal wall collateral vessels
 Thrombocytopenia
 Other clinical manifestations - related to the
underlying cause
 spider angiomata & gynecomastia (cirrhosis)
 Complications of portal hypertension.

20. Complications of portal hypertension
 Variceal hemorrhage
 Portal hypertensive gastropathy
 Liver failure
 Ascites
 Spontaneous bacterial peritonitis
 Hepatorenal syndrome
 Hepatic hydrothorax
 Hepatopulmonary syndrome
 Portopulmonary hypertension
 Cirrhotic cardiomyopathy
 Portal cholangiopathy

21. DIAGNOSIS
 Patient with a known risk factor for portal
hypertension (eg, cirrhosis) + clinical
manifestations of portal hypertension -
Additional testing not needed
 Diagnosis in doubt -HVPG
 Patients with portal hypertension ( No
previously identified risk factor) – Additional
testing

22. Hepatic venous pressure gradient
 HVPG = WHVP-FHVP
 Qantify degree of portal hypertension due to sinusoidal
resistance to blood flow
 Normal = 1 to 5 mmHg
 Portal hypertension ≥6 mmHg
 Subclinical = 6 to 9 mmHg
 Clinical ≥ 10 mmHg
 ≥12 mmHg - risk for variceal bleeding & ascites.
 Direct measurement of the pressure in the portal vein and IVC -
more invasive - intraperitoneal bleeding

23. Prognostic implications of HVPG thresholds
 Compensated cirrhosis
 10 mmHg: Varices, HCC, decompensation after HCC surgery
 12 mmHg: Variceal bleeding
 16 mmHg: First clinical decompensation in varices, mortality
 Decompensated cirrhosis
 16 mmHg: Variceal rebleeding, mortality
 20 mmHg (active bleed): Failure to control, low 1 year survival
 22 mmHg: Mortality (alcoholic cirrhosis & acute alcoholic hepatitis)
 30 mmHg: Spontaneous bacterial peritonitis

24. Non invasive tests - USG
 Ascites
 Splenomegaly
 Nodular liver
 Portal flow mean velocity <12 cm/second
 Inversion of flow in the portal vein,
 Portosystemic collaterals
 Portal vein diameter >13 mm
 Decreased or no respiratory variation in splenic and
superior mesenteric vein diameter
 Portal/splenic/superior mesenteric vein thrombosis

25. TRANSIENT ELASTOGRAPHY
• Under the receiver operating
characteristic curve of 0.77 to 0.99
for transient elastography
predicting portal hypertension,
with variable optimal liver stiffness
cutoff values (13.6 to 34.9 kPa)
• <13.6 kPa — rule out portal
hypertension, whereas a value
≥21.1 kPa can be used to rule it in
• 13.6 - 21.1 kP—indeterminant.

26. Evaluation for an underlying cause
 If portal hypertension is diagnosed in a patient who does
not have a known risk factor for portal hypertension, the
evaluation should first determine whether cirrhosis is
present. If cirrhosis is present, additional testing to
determine the cause is indicated
When to suspect cirrhosis?
 Stigmata of chronic liver disease discovered on physical examination
 Evidence of cirrhosis on laboratory or radiologic testing
 Direct visualization while undergoing a surgical procedure
 Evidence of decompensated cirrhosis - Variceal hemorrhage - Ascites
-Spontaneous bacterial peritonitis- hepatic encephalopathy

27.  Anorexia, Weight loss
 Weakness, Fatigue, Muscle cramps
 Easy bruising
 Amenorrhea/oligomenorrhea/metrorrhagia (women);
Impotence (men), Infertiliy, decreased libido (men)
 Jaundice,Dark or "cola-colored“ urine, Pruritus
 Hematemesis/melena/hematochezia
 Abdominal distension
 Lower extremity edema
 Confusion or sleep disturbances

28.  Hepatomegaly, Splenomegaly
 Spider angiomata/spider telangiectasias
 Palmar erythema
 Digital clubbing
 Hypertrophic osteoarthropathy, Dupuytren's
contracture
 Muehrcke nails, Terry nails
 Parotid gland enlargement (alcohol)
 Gynecomastia , Loss of chest or axillary hair, Testicular
atrophy
 Caput medusa, Cruveilhier-Baumgarten murmur
 Jaundice, Ascites, Asterixis, Fetor hepaticus

29.  Moderately elevated aminotransferases (often with
an AST:ALT ratio >1)
 Elevated alkaline phosphatase (2 to 3 times the
ULN)
 Elevated gamma-glutamyl transpeptidase
 Thrombocytopenia, Leukopenia/neutropenia,
Anemia
 Low serum albumin
 Prolonged prothrombin time/elevated INR
 Hyperbilirubinemia
 Hyponatremia

30.  Surface nodularity
 Increased echogenicity (ultrasound)
 Atrophy of the right lobe
 Hypertrophy of the caudate or left lobe
 Small, nodular liver
 Ascites
 Hepatocellular carcinoma
 Portal/splenic/superior mesenteric vein
 Portosystemic collaterals

31.  Computed tomography – Not routinely used, similar
information to USG, but at the expense of radiation and
contrast exposure.
• CT findings of hepatic nodularity, atrophy of the right
lobe and hypertrophy of the caudate or left lobes,
ascites, or varices suggest the presence of cirrhosis, but
they are not diagnostic.
• Patency of the portal vein - CT portal phase imaging,
but direction of blood flow cannot be determined.
 Magnetic resonance imaging –role unclear.
• Expensive , poor tolerance

32.  Nuclear studies
• 99mTc sulfur colloid is normally taken up by cells of the
reticuloendothelial system.
• seldom performed in clinical practice.
 Liver biopsy — Gold standard for diagnosing cirrhosis -
percutaneous, transjugular, laparoscopic, or radiographically-
guided fine-needle approach
• Sensitivity - 80 to 100 % - not necessary if the clinical,
laboratory, and radiologic data strongly suggest the presence of
cirrhosis and if the results would not alter the patient's
management
• Cause - hereditary hemochromatosis, nonalcoholic
steatohepatitis, Wilson disease, and alpha-1 antitrypsin
deficiency.

33. UGIE
 All patients with cirrhosis should have an upper
endoscopy
 30% patients with cirrhosis develop portal hypertension
 30% patients with portal hypertension will bleed from
varices within 2 years
 The rate of development of varices in patients with
cirrhosis approximately 8% per year.

34. DETERMINING THE CAUSE OF CIRRHOSIS

35. DETERMINING THE CAUSE OF CIRRHOSIS

36. SCORE

37. SCORE

38. SCORE

39. ?
 Diagnosis Of The Underlying Liver Disease
 Estimation Of Functional Hepatic Reserve
 Definition Of Portal Venous Anatomy And Hepatic
Hemodynamic Evaluation
 Identification Of The Site Of Upper Gastrointestinal
Hemorrhage.

40. Differential diagnosis
 Hematemesis / melena: PUD, Dieulafoy's lesion, Mallory-Weiss tear
 Ascites: Malignant ascites, nephrogenic ascites, tuberculosis
 Splenomegaly: Hematologic malignancy, infections, inflammation
 Bacterial peritonitis: Secondary bacterial peritonitis
 Hydrothorax: Malignancy, sarcoidosis, nephrotic syndrome
 Hypoxemia: Heart failure, CNS depression, muscular weakness
 Pulmonary hypertension: Idiopathic PAH , valvular heart disease,
connective tissue diseases

41. MANAGEMENT
prevention & treatment of complications
 PHARMACOTHERAPY
 VARICEAL TAMPONADE
 ENDOSCOPIC THERAPY
 DECOMPRESSIVE SHUNTS
 RADIOLOGIC – TIPS
 SURGICAL
 SURGICALTREATMENT
 DEVASCULARISATION
 LIVER TRANSPLANT

42. VARICES INCREASE IN DIAMETER PROGRESSIVELY

43. Cirrhosis

44. TREATMENT OF VARICES / VARICEAL HEMORRHAGE
No varices
Varices
No hemorrhage
Variceal
hemorrhage
Recurrent
hemorrhage
Prevention of
variceal
development

45. Treatment of Varices / Variceal
Hemorrhage
No varices
Varices
No hemorrhage
Variceal
hemorrhage
Recurrent
hemorrhage
No specific therapy
Repeat endoscopy in every
2-3 yrs

46. Treatment of Varices / Variceal
Hemorrhage
No varices
Varices
No hemorrhage
Variceal
hemorrhage
Recurrent
hemorrhage
Prevention of first
variceal
hemorrhage

47. Treatment of Varices / Variceal
Hemorrhage
Variceal
hemorrhage
Recurrent
hemorrhage
Varices
No hemorrhage
No varices
Management depends on
the size of varices

48. Treatment of Varices / Variceal Hemorrhage
Medium/ large varices
No hemorrhage
Variceal
hemorrhage
Recurrent
hemorrhage
Small varices
No hemorrhage
No varices
? Prevention of variceal
growth

49. Treatment of Varices / Variceal Hemorrhage
Small varices
No hemorrhage
No varices
Repeat endoscopy in 1-2
years
Beta-blockers?
Medium/ large varices
No hemorrhage
Variceal
hemorrhage
Recurrent
hemorrhage

50. Treatment of Varices / Variceal Hemorrhage
Recurrent
hemorrhage
Variceal
hemorrhage
Medium/ large varices
No hemorrhage
No varices
Small varices
No hemorrhage
1) -blockers (propranolol 1-2
mg/kg/day) indefinitely
2) Endoscopic variceal
ligation/Sclerotherapy in
patients intolerant to -
blockers

51. PROPRANOLOL
DECREASES CARDIAC OUTPUT
RESULTING IN DECREASED PORTAL
PRESSURE AND VARICEAL SIZE.
REDUCES THE INTRAHEPATIC PORTAL
VASCULAR RESISTANCE.
PRODUCES SPLANCHNIC
VASOCONSTRICTION WHICH LEASD
TO DECREASE IN PORTAL BLOOD
FLOW.
USED ALONG WITH
SCLEROTHERAPY.
BENIFICIAL RESULTS IN TERMS OF LOWER
REBLEEDING RATES & LOWER VARICEAL
RECURRENCE.
MOST WIDELY
USED β
BLOCKER.

52. ENDOSCOPY
 ENDOSCOPIC BANDING
 ENDOSCOPIC
SCLEROTHERAPY

53. Treatment of Varices / Variceal Hemorrhage
Control of
hemorrhage
Recurrent
hemorrhage
Variceal
hemorrhage
No varices
Small varices
No hemorrhage
Medium/ large varices
No hemorrhage

54. Recurrent
hemorrhage
No varices
Small varices
No hemorrhage
Medium/ large varices
No hemorrhage
Treatment of Varices / Variceal Hemorrhage
Variceal
hemorrhage
1) Safe vasoactive drug +
endoscopic therapy + balloon
tamponade + antibiotic
prophylaxis
2) TIPS / Shunt (rescue therapy)

55. Treatment of Varices / Variceal Hemorrhage
No varices
Varices
No hemorrhage
Variceal
hemorrhage
Recurrent
hemorrhage
1) -blockers + EVL
2)TIPS / shunt surgery

56. Repeat endoscopy in 2-3 years No
specific therapy
 Small varices
 Repeat endoscopy in 1-2 years No specific
therapy
 ? beta-blocker to prevent
 enlargement
 Medium/Large varices
 Non-selective beta-blockers
 EVL in those intolerant to drugs
 Endoscopic/pharmacologic therapy Antibiotics in all
patients
 TIPS or shunt surgery as rescue therapy
 Beta-blockers + EVL
 TIPS or shunt surgery as rescue
therapy

57. PHARMACOTHERAPY
 Antibiotic Prophylaxis
 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 Severe Cases Of Hemorrhage, Vasopressin Can Be Used To Diminish
Splanchnic Blood Flow
 Target For Treatment Is Less Than 12 Mm Hg Reduction In Hvpg.
 Other Pharmacologic Agents Such As Nitrates, Serotonin Antagonists,
And Calcium Channel Blocker, Non selective beta blockers.

59. VARICEAL TAMPONADE
 Sengstaken- Blakemore tube
 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.

62. MANAGEMENT OF ASCITES
• SODIUM RESTRICTION AND PROMOTION OF SODIUM
EXCRETION ARE THE CORNER STONES OF ASCITES
MANAGEMENT.
• SODIUM RESTRICTION TO 1 TO 2 meq/Kg/day.
• FLUID RESTRICTION.
• SPIRONOLACTONE IS THE DIURETIC OF CHOICE BECAUSE
OF ITS ADDITIONAL ANTI ALDOSTERONE ACTIVITY.
• INITIATE AT 2-3mg/kg/day IN DIVIDED DOSES. CAN BE
SAFELY DOUBLED IF NO INCREASE IN URINE OUTPUT
OCCOURS IN 3-4 DAYS.
• FUROSEMIDE CAN BE ADDED IF THERE IS NO RESPONSE
TO HIGH DOSES OF SPIRONOLACTONE.

63. • HYPONATREMIA ASSOCIATED WITH FUROSEMIDE
ADMINISTRATION SHOULD BE CORRECTED.
• INTRAVENOUS ALBUMIN 1g/kg WITH FUROSEMIDE
CAN BE GIVEN TO PREVENT RECOLLECTION OF
ASCITIC FLUID.
• IN VERY LARGE ASCITES PARACENTESIS MAY BE
DONE.

65. DENVER AND LEVEEN SHUNTS
• SUBCUTANEOUS SHUNTS
THAT DRAIN ASCITIC FLUID
FROM THE ABDOMEN INTO
THE CENTRAL VENOUS
SYSTEM.
• DIC IS A KNOWN
COMPLICATION OF
PERITONEOVENOUS SHUNTING
OF ASCITIC FLUID.

66. TREATMENT FOR HYPER SPLEENISM
• SELECTIVE SPLEENIC INFARCTION EFFECTIVELY
CONTROLS HYPERSPLEENISM, REDUCES INCIDENCES
OF REBLEEDING & CONSERVES SPLEENIC IMMUNE
FUNCTION
• MUST BE DONE IN CONJUNCTION WITH PNEUMOCOCCAL
VACCINATION AND LONG TERM ANTIBIOTIC PROPHYLAXIS
TO THE AGE OF 6 YEARS.

67. TIPS - transjugular intrahepatic portosystemic shunt

68. Indications
 Bleeding related to portal hypertension
 Esophageal varices
 Active bleeding – failed initial therapy , rebleed within 120 hours of
initial hemorrhage
 Preventing recurrent bleeding - < 72 hours of initial endoscopic
hemostasis (Child-Pugh C, HVPG= 20 mmHg)
 Gastric varices – failed initial therapy
 Ectopic varices - duodenal, rectal, or peristomal varices
 Portal hypertensive gastropathy – failed treatment
 Refractory ascites
 Other uses
 Budd Chiari Syndrome, Hepatic hydrothorax, Investigational uses

69.  Absolute contraindications
 Congestive heart failure
 Severe tricuspid regurgitation
 Severe PAH (mean pulmonary pressure >45 mmHg)
 Polycystic liver disease
 Active systemic infection or sepsis
 Unrelieved biliary obstruction
 Relative contraindications
 Hepatic tumors - centrally located
 Obstruction of all hepatic veins
 Hepatic encephalopathy
 Portal vein thrombosis
 Thrombocytopenia (<20,000)
 Moderate PAH

70. Portal venogram - pre-TIPS portosystemic venous pressure gradient
Obtain vascular access through the right internal jugular vein
Catheter into right or middle hepatic veins - perform venogram
Sheath and cannula into proximal hepatic vein and CO2 portovenogram - localize
and target the intrahepatic segment of the portal vein
Balloon dilation of the intrahepatic tract between HV & PV
Shunt by deploying a covered stent
post-TIPS portosystemic gradient

71. NON SELECTIVE SHUNTS

72.  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.
Total Shunts
End-to-side portacaval shunt

73. Side to side portacaval shunts
 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.

74. Splenorenal shunt
 The conventional splenorenal shunt consists of anastomosis
of the proximal splenic vein to the renal vein - Splenectomy is
performed
 Complications : shunt thrombosis
 The only indication for a total portal systemic shunt at
present is for patients with acute Budd- Chiari syndrome
 TIPS ?

75. SELECTIVE SHUNTS

76. 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 in90% of patients initially
 The overall incidence of encephalopathy has been around 15%
following this operation.

77. Partial shunts

78. 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.

79. 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.

80.  These procedure have been more extensively used in Japan & Egypt than
USA
 Non shunting procedures include devascularization, splenectomy &
esophageal transection
 It is disconnection of esophagogastric veins from hypertensive portal
tributaries
 Spence & colleagues showed that large vessels in lamina propria
communicate directly with dilated intraepithelial blood channels
 These intraepithelial channels seen histologically represent the cherry red
spots viewed endoscopically
 Ideal technique to control bleeding varices - obliteration of varices in lower
periesophageal vessels & intraepithelial dilated vessels.
Devascularisation

81. HASSAB
 HASSAB (1967) proposed a method for Gastroesophageal
decongestion & splenectomy (GEDS) for management of
bleeding varices
 Splenectomy
 Perihiatal devascularization of the lower lower 3-4 inches of
esophagus
 Ligation of left gastric artery branches to stomach
 Devascularization of proximal half of stomach & to
reperitonealize it
 Complication of Hassab procedure - GOO d/t vagus trunk
transection w/o pyloroplasty.

82. Sugiura operation
 The components are splenectomy, gastric and esophageal
devascularization, and possibly esophageal transaction
 Effectiveness depend on the aggressiveness of the operation
 Advantage - portal hypertension is maintained with portal flow to the
cirrhotic liver
 Specific complication of Sugiura is esophageal leak & stenosis from
transection
 Devascularization can be useful when patients have extensive portal
and splenic venous thrombosis and there are no other operative or
radiologic options

83. LIVER TRANSPLANT
 Liver transplant is the most commonly used operation for patients
with portal hypertension at the present time
 The major issues are – patient Selection - Timing Of Transplant, -
Expanding The Donor Pool - Outcomes.

84. 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 morbid
 Comedical conditions and a psychosocial suitability for transplant particularly in
the alcoholic and other chemical dependency patient populations
 Hepatitis C population with hepatoma

85. 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
 Hospital mortality remains at less than 10%, 80+% 1-year survival60–
65% 5-year survival

86. Who coordinates?
MULTIDISCIPLINARY
APPROACH
coordinators are the ones to whom the patients turn for help in
navigating their way through management in this complex field
 Hepatologists, Endoscopists, Radiologists (imaging and interventional)
 Surgeons play a major role in liver transplant but may also have a role in
shunting good-risk patients with refractory variceal bleeding
 Pathologist, Critical care physicians and anesthesiologists,
 Nephrologists, cardiologists, and pulmonologists

87. ?
SURGERY IN PATIENT WITH PORTAL HYPERTENSION ?

88. SURGERY IN PATIENT WITH PORTAL HYPERTENSION ?
 Patients with liver disease and portal hypertension usually as a
result of advanced fibrosis or cirrhosis, are at increased risk of
complications when undergoing surgery
 Acute or fulminant liver failure and acute viral and alcoholic
hepatitis are contraindications to elective surgery
 Model for ESLD score is likely more accurate than the Child-
Turcotte-Pugh score in predicting perioperative morbidity and
mortality

89.  Improved assessment of surgical risk can improve
informed consent as well as surgical decision making and
thus lead to the implementation of medical and surgical
strategies, including preoperative transjugular intrahepatic
portosystemic shunt, to mitigate risks
 Preoperative liver assessment checklist (POLA)
There is no such thing as a good cirrhotic patient

90. TIMING OF SURGERY
 Emergent surgeries performed in patients with cirrhosis have
poorer outcomes than those with normal liver function and
compared with elective surgery
 This consensus is likely related to the effect of life threatening
presentations in sicker cirrhotic patients and the paucity of time
to optimize patients before surgery

91. Laparoscopic Versus Open Cholecystectomy
 Prevalence of gallstones in patients with cirrhosis is 29.4% ( 2 X general population )
 Most of these patients are asymptomatic, and should not be operated
 Cholecystectomy is safe in patients with Child A and B cirrhosis and MELD scores of
up to 11 to 13, with mortalities of 0% to 6% and laparoscopy the preferred method
 When the risks of surgery are prohibitive, alternative treatments should be
considered, such as prolonged antibiotic treatment, percutaneous cholecystostomy
(not preferred if ascites is present), and transpapillary cystic duct stenting

92. PREOPERATIVE STRATEGY
 Preoperative liver assessment (POLA) checklist
 Optimizing medical therapy: compensate the decompensated

96. INTRAOPERATIVE STRATEGY
 Anesthesia team has an important role — liver disease oriented team
 Administration of anesthesia invariably reduces blood flow to the liver, which is well
tolerated by patients with normal liver function, but can precipitate liver
decompensation in cirrhotic patients.
 Alterations in liver perfusion during surgery should therefore be minimized, and
avoidance of hypotension is crucial.
 Normovolemia should be maintained, especially in circumstances of potential large-
volume losses
 Ascites should be replaced by albumin, usually at a ratio of 12.5 g of 25% albumin for
every 1 L of ascites removed during surgery.

97.  The surgeon should attempt to avoid significant blood loss during
surgery
 Extreme care should be taken when handling varices, because these
vessels have a thin wall and high pressure, which can result in
massive bleeding if injured
 Meticulous hemostasis is important, because postoperative
coagulopathy and thrombocytopenia can precipitate significant
bleeding from even minor potential sources
 When performing emergent hernia repairs – prefer to perform
primary repair of the fascial defect, to avoid possible mesh infection
– Drain – controversial

98. POST OPERATIVE STRATEGIES
 If oral or enteral nutrition is inadequate after surgery, patients with cirrhosis
should receive early postoperative parenteral nutrition — low complication
rates
 Maintenance fluids should be based on 5% albumin to increase oncotic
pressure
 In the event of ascites leaking from a wound or wound dehiscence - early
large-volume paracentesis and the subsequent use of short-term 25%
intravenous albumin infusions and diuresis with furosemide and
spironolactone - Meticulous wound care

99.  If drains – no longer than 5 to 7 days after surgery in order to
reduce the risk of infection (alternative interval, preemptive,
large volume paracentesis)
 Prophylactic measures against venous thromboembolism
 Antiviral medications for patients with HIV or chronic hep. B
should be restarted immediately after surgery with attention to
dosing for any renal impairment that may occur
 Patients on hepatitis C virus treatment going into surgery
usually stop treatment after surgery to allow for recovery

100. SUMMARY
 Patients with liver disease and portal hypertension, usually as a result
of advanced fibrosis or cirrhosis, are at increased risk of complications
when undergoing surgery
 MELD is likely more accurate than the CTP score in predicting
perioperative morbidity and mortality, although there is still value in
calculation of CTP
 Improved assessment of surgical risk can improve informed consent
as well as surgical decision making and implementation of medical
and surgical strategies to mitigate risks
 A POLA checklist Surgery

101. REFERENCES