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.
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.
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
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
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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
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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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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
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.
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.
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.
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.
58.
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.
60.
61.
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.
64.
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.
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
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 ?
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.
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
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
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
The portal vein is formed behind the neck of the pancreas by the joining of the superior mesenteric and splenic veins.
It courses along the free edge of the gastrohepatic ligament to the liver hilus, where it divides into right and left branches
Its feeding tributaries have some variability, with theinferior mesenteric vein entering the splenic vein in approximately two-thirds of persons and superior mesen-teric vein in one-third. Similarly the left gastric or coronary vein enters the portal vein in approximately two-thirds and the splenic vein in one-third. The latter may vary considerably in size in portal hypertension and is often one of the major veins feeding into gastrosophageal varices. The umbilical vein is remarkably constant in its communication with the left branch of the portal vein, and in portal hypertension when recanalized this may be quite large.
This sequence of pathophysiologic changes in the hepatic, splanchnic, and finally systemic circulation offers an opportunity for pharmacologic