Portal Hypertension

By: J. Neale MD
Date: 7/12/07
Pathophysiology
 Superiormesenteric + Splenic vein =
Portal vein

Portal Vein carries outflow from:

1.) Spleen
2.) Oesophagus
3.) Stomach
4.) Pancreas
5.) Small and large intestine
Pathophysiology
 Collateral routes
1.) Veins of Retzes: Retroperitoneal

2.) Caput Medusa: Umbilical vein

3.) Hemorrhoidal veins:

a.) Superior hemorrhoidal vein = Portal
b.) Inferior hemorrhoidal vein = Systemic

4.) Adhesions

5.) Oesophageal varices: ( coronary vein and azygous)

Etiology= Portal outflow obstruction
 Prehepatic:
Portal vein, Splenic vein thrombosis, Congenital
portal vein thrombosis
(cavernous transformation)

 Intrahepatic:
Cirrhosis

 PostHepatic:
Budd Chiari Syndrome
Importance for Surgeons
1.) Ascites

2.) Hepatic encephalopathy

3.) Variceal bleeding

Ascites
Origin:
1.) Hepatic sinusoidal pressure >Colloid oncotic
pressure = leakage of fluid into parenchyma, and
overwhelms lymphatic system

2.) Aldosterone = Salt retention by the kidney due to

high levels ( pre-renal state)
Induced by:
1.) Stress: ( variceal hemorrhage, OR, infection)
2.) IVF:
Complication:
1.) SBP: Monomicrobial= high M and M
2.) Hepatorenal syndrome = Pre-renal azotemia to
extreme
Controlling Ascites
A.) Sodium and H20 restriction:
B.) Diuretics:
1.) Start with spironolactone,
2.) Watch K+
3.) Start Loop diuretics
4.) Hepatorenal syndrome: Iatorgenic
(over diuresis)
Controlling Ascites
C.) Large volume paracentesis:
Replace with albumin????

D.) Peritoneal venous shunt

Effective in short term problems

E.) TIPS:
Extreme cases, trading ascites for
encephalopathy
Encephalopathy
Etiology:
1.) Cause unclear, Nitrogen compounds contribute to it.
Symptoms:
1.) Asterixis 2.) coma

Induced by:
A.) Advanced liver disease

B.) Moderate liver disease and…

1.) Infection ( sepsis)
2.) Constipation
3.) Dehydration
4.) Blood within the gut
Encephalopathy
Diagnosis
1.) No diagnostic test
2.) Serum ammonia levels often high
3.) EEG abnormalities
4.) Neuropsych testing

CLINICAL DIAGNOSIS
Encephalopathy
Treatment:
1.) Limit protein: ( Limit intake and
maximize gut cleansing)
2.) Tx and find possible causes, ie sepsis
Variceal Bleeding
1.) Resuscitation
2.) Initial treatment
3.) Diagnosis
4.) Further therapy
a.) Endoscopic
b.) Surgical
5.) Supportive therapy and evaluation
Resuscitation
Tx hemorrhagic shock
a.) Volume repletion: blood ideal, until it arrives use
crystalloid and colloid, ( try to keep limited) also use FFP.

b.) Plts ususally low:

Transfuse
1.) Prolonged bleeding time
2.) Count less than 50, 000

GOAL: INCREASE TISSUE PERFUSION = URINE OUTPUT

REMEMBER: MONITOR CVP, (central pressure

correlates with variceal pressure
Initial treatment
IF suspected on clinical hx and px
a.) VASOPRESSIN
b.) SOMATOSTATIN
Vasopressin
1.) Intense constrictor of arterial beds
2.) Acts to decrease mesenteric flow =
decrease in portal pressure.
3.) Stops bleed 80% of time.
4.) Must add nitroglycerin to combat side
effects of peripheral and myocardial
ischemia.
Somatostatin
1.) Efficacy mirrors Vasopressin

2.) No side effects with respect to

myocardial or peripheral ischemia

3.) Pharmacologic agent of choice

Diagnosis
1.) Even with cirrhotics 50% bleeds from
other sources
a.) Mallory Weiss tears
b.) Gastritis
c.) Ulcer disease
THEREFORE = NEEDS EGD ASAP !!!!!
Why? Various etiologies = Various
therapies
Variceal hemorrhage
VARICES and……

1.) Active bleeding from varices

2.) Stigmata of bleeding varices ( cherry red

spots, wheals)

3.) Absence of any other bleeding source

Further therapy
1.) Sclerotherapy
2.) Banding
3.) Balloon Tamponade
Sclerotherapy
1.) Inject an agent into or adjacent to varix
Goal: Arrest bleeding and obliterate lumen

Variceal ligation or banding

1.) Fewer complications vs. sclerotherapy
Procedure: suction varix and deploy rubber band

Balloon Tamponade, (Sengstaken- Blakemore tube)

1.) Arrests bleed in 90% patients
2.) Can have fatal complications
3.) Can only be used for 24 hrs

IF ALL ABOVE FAIL PT NEEDS A TIPS

Supportive Therapy and Evaluation
1.) Address coagulopathy
a.) Vit K infusion
b.) Plts
c.) FFP

2.) Aspiration
a.) Aggressive pulm toilet
b.) Protect airway

3.) Immunosuppression
a.) Infections other than pneumonia occur

4.) Treat encephalopathy and poor nutrition

a.) Purge gut with lactose and neomycin
b.) Begin TPN
 Supportive Therapy and Evaluation
5.) Assess functional reserve of the liver
a.) Childs classification
b.) Hepatitis profile
c.) Further history ( Alcohol, IVDA, Hepatitis)

6.) Candidate for liver transplant

7.) Angiography:
a.) Portal venous anatomy, ( smv, splenic, portal, hepatic and L
renal )
b.) Hepatic venous pressures ( free and wedged) allows eval of
sinusoidal pressures
Child’s Classification
Definitive Therapy
1.) Designed to prevent re-bleeding

Categories
A.) Medical
B.) Endoscopic
C.) Surgical
D.) Radiological
Medical Therapy
1.) Beta blockade
a.) Decrease bleeding by decreasing
variceal flow / pressure

b.) Decreases bleeding, but has no effect

on long term survival
c.) Use as an adjunct to endoscopic
therapy
Endoscopic Therapy
1.) Long term prevention of variceal bleeding
a.) obliteration of all variceal channels with sclerotherapy
and banding
b.) Multiple sessions required
c.) Surveillance endoscopy

Sclerotherapy complications
Local
1.) ulceration, 2.) stricture, 3.) perforation
Systemic
1.) fever, pneumonitis, mediastinitis
Surgical therapy
1.) Total shunts
2.) Selective shunts
3.) Partial shunts
4.) Non shunt operations
Total Shunts
1.) Divert most or all flow form portal to systemic
circulation
2.) All prevent rebleeding in 90% patients
3.) All divert portal flow= liver atrophy
4.) Encephalopathy = 40% patients

Types:
1.) Portocaval ( end-side and side-side +/- graft
material
2.) Mesocaval shunts ( created with or without graft
material
3.) Central Splenorenal shunts
Selective Shunts
Goal
1.) Prevent variceal bleeding
2.) Prevent horrible encephalopathy

Mechanism
1.) Decompress gastrosplenic compartment
2.) Maintains portal htn in the portal bed = nutrients to liver = no
atrophy
3.) Technically difficult

Types
1.) Distal Splenorenal shunt = splenic vein divided from portal
and anastomosed to renal
2.) Coronal caval shunt = Not used in usa
Selective Shunts
Results
1.) Re-bleeding rates = those of total
shunts
2.) Long term mortality = those of total
shunts
3.) Encephalopathy decreased vs Total
shunts
Partial Shunts
Design
1.) Ease of construction like portocaval shunts
2.) Decreased encephalopathy like selective
shunts
3.) Side to side portacaval shunts ( 8-10mm)
4.) Short and straight= decrease shunt
thrombosis
5.) Similar to portocaval to prevent rebleed,
BUT decreased encephalopathy
 Transjugular intrahepatic portocaval shunt
(TIPS)
1.) What is it?

2.) Complications
A.) Intraperitoneal hemorrhage
B.) Subcapsular hematoma
C.) Hemobilia
D.) Infection
E.) Chf and Acute renal failure

3.) Procedure Mortality ( 30 day )

a.) 3-13%, ( most are done under emergent conditions in the
critically ill)
 Problems with TIPS
Hepatic encephalopathy
1.) Total shunt= large amt portal flow to systemic circulation
2.) Approx 30-40%

Occlusion
1.) Neointimal hyperplasia= 33-73% occlusion yearly
2.) Needs surveillance= Increase cost, and time

Rebleeding
18 % yearly
Indications for TIPS
1.) Refractory bleeding
2.) Provision as a bridge to transplant
3.) Child C cirrhosis
Liver Transplant
1.) Not indicated for variceal bleeding

2.) Indicated for liver failure

Therefore counsel liver transplant team

Special Cases for portal
Hypertension
1.) Splenic vein thrombosis

2.) Extrahepatic portal vein thrombosis

3.) Budd Chiari syndrome

Splenic Vein thrombosis
Causes:
1.) Pancreatitis
2.) Pancreatic carcinoma

Mechanism:
1.) Submucosal veins in the stomach act as a porto-porto
collateral around thrombosis

Hallmarks:
1.) ISOLATED GASTRIC VARICES
2.) NORMAL LIVER FUNCTION
Extrahepatic Portal Vein
Thrombosis
Etiologies
1.) Trauma
2.) Low flow states
3.) hypercoagulable states
4.) Congenital portal vein thrombosis
a.) Umbilical artery catheterization
Congenital Portal vein thrombosis
Most common cause of extrahepatic portal vein
thrombosis
Pathophysiology
2.) Mass of porto-portal collateral passing along porta
hepatis to nl liver.
3.) Collaterals= cavernous transformation of portal vein

Hallmarks:
1.) Normal liver function, 2.) Gastroesophageal varices,
Tx:
Endoscopic therapy or selective shunt, ( nl perfusion to
nl liver)
Budd-Chiari Syndrome
1.) Hepatic venous outflow obstruction in the liver
Causes
1.) Hypercoagulable states
a.) Exogenous and endogenous estrogen
b.) Radiation therapy
c.) Myeloproliferative disorders
d.) Paroxysmal nocturnal Hemoglobinuria
e.) Mxyoma ( R atrium presses on IVC)
f.) Pericarditis
g.) Congenital caval webs or membranes
h.) Liver masses
i.) High dose chemo ( occludes hepatic venules)
Budd- Chiari Syndrome
Triad of presentation
1.) New onset abdominal pain
2.) Ascites
3.) Hepatomegaly

Diagnosis
1.) Angiography ( inferred by Ct scan / MRI )

Treatment
1.) IF biopsy shows zone 3 necrosis =
a.) Portocaval shunt, if IVC patent
b.) Mesoatrial shunt, if IVC is occluded