AAK[1].VaricealBleeding.VivaLaVida.March2008.ppt

8/14/2019 AAK[1].VaricealBleeding.VivaLaVida.March2008.ppt

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Portal vein - 5-9 cmHepatic blood flow - 1500 ml/min

30% from HA and 70% PVLow outflow resistance in hepatic sinusoidsClose relationship between portal and HA flow

PV flow cause HA flow (even Tx liver)Converse not true

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Definition of PHTNPorto-venous gradient > 5 mm Hg =Portal HTN

Complications when gradient > 10-12 mm Hg

Normal PV pressure: 5-10 mm Hg

Normal porto-venous (IVC) gradient:1-5mmHg

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Causes of Portal Hypertension

Obstruction of portal vein (presinusoidal) or splenic vein

Obstruction within the liver

(sinusoidal) Obstruction of hepatic veins and

beyond (post sinusoidal)

Cirrhosis is the most common (>90%)cause of portal hypertension

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Resistance toPortal Flow

Portal Bloodinflow

Varices

Splanchnic

arteriolar Rce

PortalPressure

CIRRHOSIS

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Portal Bloodinflow

Varices

Splanchnic

arteriolar Rce

PortalPressure

CIRRHOSIS

Variceal

growth 6


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8/65Fundal varix: large 8


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Prevalence & Size of Esophageal VaricesIn Patients with Newly Diagnosed Cirrhosis

ALL cirrhotics: 40% have varices

Patients w ascites: 60% have varices

Childs C cirrhosis: 80% w/ varices

& 25-30% have large varices

Pagliaro et al, In: Portal HTN: Pathophysiology and Management, 1994:729


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Varices


Portal Bloodinflow

Splanchnicarteriolar Rce

PortalPressure

CIRRHOSIS

Varicealrupture

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Variceal Bleeding

Predictors of Variceal Hemorrhage:- Size- Red Signs- CPT

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Red spots(2mm)

Wale signs HematocysticSpots (4mm)

Red signs

NIEC. NEJM 1988; 319:98312


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Large Varices Are More Likely to Rupture

Merli et al, J Hepatol 2003; 38(3):266-72, Conn et al. Hepatology 1991; 13:902

%Pa

tientsw/o

Bleeding

Time (months)

No VaricesSmall Varices

2 yr Probability of 1stbleed:Small varices: 7%Large varices: 30%

Large Varices

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No Varices

VaricesNo Hemorrhage

VaricealHemorrhage

Recurrent

Hemorrhage

Prevention of VaricealDevelopment

Treatment of Varices/Variceal Hemorrhage

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No Varices


VaricealHemorrhage

recurrent

Hemorrhage

No RxRepeat EGD in 2-3 yrs*


*EGD sooner in decompensated cirrhosis

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No Varices


Variceal

Hemorrhage

recurrent

Hemorrhage

Prevent 1stVaricealBleeding


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Propranolol

Nadolol

Atenolol

Timolol

Which of the following is not indicated

for primary prophylaxis:

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Propranolol

Nadolol

Atenolol

Timolol

Which of the following is not indicated

for primary prophylaxis:

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Primary Prophylaxis:b-blockers prevent a 1stbleed

Bleeding Rate Cpntrol b-blocker Absolute rate(~2yr) difference

All Varices 25% 15% -10%

(11 trials) (n=600) (n=590) (-16 to -5)

Large Varices 30% 14% -16%

(8 trials) (n=411) (n=400) (-24 to -8)

Small Varices 7% 2% -5%

(3 trials) (n=100) (n=91) (-11 to 2)

DAmico et al. Sem Liv Dis 1999; 19:47519


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No Varices

Varices

No Hemorrhage

Variceal

Hemorrhage

recurrent

Hemorrhage

Size of Varix matters


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No Varices

Small Varices

No Hemorrhage

Variceal

Hemorrhage

recurrent

Hemorrhage

Prevent Variceal

Growth?


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Merkel et al, Gastroenterol 2004; 127:476

Nadolol May Prevent Growth of SmallVarices

%p

robabilityofgrowth Nadolol

Placebo

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No Varices

Small Varices

No Hemorrhage

Variceal

Hemorrhage

recurrent

Hemorrhage

1. Repeat EGD in 1-2 yrs

2. Consider b-blockers ?


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*EGD sooner in decompensated cirrhosis


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No Varices

Medium/Large


Variceal

Hemorrhage

recurrent

Hemorrhage

1 b-blockers indefinitely2. EGD w/ ligation if intolerant tob-blockers


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h l f l h


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Prophylaxis of Variceal Hemorrhage

Cirrhosis

EGD

No Varices

F/U EGD in 2-3 yrs*

*EGD yearly in decompensated cirrhosis

Small Varices

F/U EGD in 1-2 yrs*

Med/LargeVarices

b-blockers

EVL

Contraindic

ation

or

b-blocker

into

lerance

Stepwise increase to maximal doseContinue life-long

No Contraindications

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No Varices

Varices

No Hemorrhage

Variceal

Hemorrhage

Recurrent

Hemorrhage

Control of Variceal

Bleeding


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Mortality: Acute Variceal Bleeding

The Current Mortality from Acute Variceal Bleeding is:

A. 10%

B. 20%C. 30%

D. 40%

E. 50%

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Mortality: Acute Variceal Bleeding

The Current Mortality from Acute Variceal Bleeding is:

A. 10%

B. 20%C. 30%

D. 40%

E. 50%

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Treatment of Acute Variceal Bleeding

General Management:

IV access and fluid resuscitation

AVOID overtransfusion (Hb~8 g/dl or Hct~24%)

Antibiotic prophylaxis (Norflox 40 bid or Levo if IV needed)Variceal Specific Therapy:

Pharmacologic Rx: Terlipressin,

Somatostatin & analogues, VP + Nitroglycerin

Endoscopic Rx: ligation; scleroRxy

Shunt Rx: TIPS; surgical 29


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Endoscopic Variceal Band Ligation

Bleeding controlled in 90% Rebleeding rate 30%

Compared w/ sclerotherapy:

Less rebleeding

Lower mortality

Fewer complicationsFewer treatment sessions

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T f V i /V i l H h


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No Varices

Varices

No Hemorrhage

Variceal

Hemorrhage

Recurrent

Hemorrhage

1) Safe vasoactive drug +EGD-Rx + ANTIBIOTIC

2) TIPS / Shunt(rescue Rx)


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Management of Acute Variceal Bleeding

Initial Management

Variceal Hemorrhage Suspected

Bleeding controlled

TIPS/?shunt surgery

NoBalloon Tamponade(Bridging Therapy)

Yes

Early rebleed

2nd EGD

Yes

Further bleeding

Prophylaxis Rx

No

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Early PharmacoRxy,..

T t t f V i /V i l H h


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No Varices

Varices

No Hemorrhage

Variceal

Hemorrhage

Recurrent

Hemorrhage

Preventing recurrent

Hemorrhage


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C mpared t End sc pic Rxy TIPS


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0 More w/TIPS

More w/Endoscopic Rxy

RiskDifference

Compared to Endoscopic Rxy, TIPSReduces Rebleeding but Increases

Encephalopathy Risk w/o clear Survival Benefit

Recurrent Variceal Bleeding

Hepatic Encephalopathy

Mortality

Death from Recurrent Bleeding

Luca A et al., Radiology 1999; 212:41135

T t t f V i /V i l H h


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No Varices


VaricealHemorrhage

RecurrentHemorrhage

1 b-blockers + ISMN or EVL2 b-blockers + EVL preferable3) TIPS / shunt surgery


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h l f l l d


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Prophylaxis of Recurrent Variceal Bleeding

Prophylactic PharmacoRxyand/or EVL

Control of Acute Variceal Hemorrhage

Recurrent Bleeding

Surveillance EGDand/or Life-long

PharmacoRxy

No

Yes

Is pt on EVL + PharmacoRxy ?

Initiate combination

No Yes

Further bleeding

TIPS

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G i V i


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Gastric Varices

20% of cirrhotics

Up to 65% bleed in 2 years; Bleeding more profound

Banding not favorable

Two Classes:

1- GOV: a- GOV-I

b- GOV-II

2- IGV: a- IGV-I

b- IGV-II

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IGV-I

IGV-II

GOV-I GOV-II

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G st i V i s


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Gastric Varices

10-15% of total variceal bleeding episodes

Limited controlled trials; hence, limied data

Optimal therapy not known

Vasoactive drugs used; yet, not studied

Endoscopic Cyanoacrylate injection

90% control of bleeding Balloon tamponade w/ Linton-Nachlas tube

TIPS: 90% control of bleeding 40

M t f G t i V i


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Management of Gastric Varices

Gastric varices extending along lesser curvature

(GOV-1) are to be treated as esophageal varices

Isolated fundal gastric varices (IGV-1),splenic vein thrombosis should be investigated

Cirrhotics bleeding from fundal varicesrequire specific therapy

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Management of Acute Gastric (Fundal)


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Management of Acute Gastric (Fundal)Variceal Bleeding

Variceal Bleeding Suspected

Initial Management

Variceal obliterationpossible?

TIPS

No

Yes

Variceal obliteration +b-blockers

Not possible or rebleed

Controlled?

YesNo

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T j l I t h ti


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Transjugular IntrahepaticPorto-Systemic Shunt (TIPS)

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TIPS: Complications


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TIPS: Complications

Occlusion / Stenosis 10-15%

Encephalopathy (any grade) 10-45%

Malposition 10-20%Transcapsular Perf. 1-2%

Hemobilia


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Gl


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GlueN-butyl Cyanoacrylate or 2-Octyl Cyanoacrylate:

greater experience w/ former. Yet, latter has more

prolongued time -to polymerization hence dereased

risk of embolization?

Optimal mix: Lipidol, saline, water).

Injection technique / timing not standardized:

() per-expertise,..49

Ever Expanding Experience


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Ever Expanding Experience

92 pts @ UVA w/ gastric varices (80 w/ portal HTN & 12 w/ SVT)

injected w/ Cyanoacrylate:Ethiodol (1:1)

Rebleeding in portal HTN: 5% @ 0-72 hrs; 6.5% @ 72hrs-3 mos,

17% @ 3 mos-1 yr

Embolization (serious) susected in 2%

Offers an important intervention in gastric variceal bleeding

Most common reported SE => Pulmonary Emboli: 6/140 (4.3%)

Risks: 1- volume (if > 1.8 ml; PE developed post-injection of ~ 4.2ml)

2- size of varix

Huang, YH et al., W, et al., GIE; 2000; 52: 16067

Caldwell SH et al., 2007; 26: 49-59

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Clinical success in these studies typically has

been higher than in prospective studies, with hemostasis

rates ranging from 60% to 100%. Cyanoacrylate-based

compounds have not been approved by the FDA for usein the US. Injection of cyanoacrylate-based compounds

is associated with the development of bacteremia, and

thus antibiotic prophylaxis should be considered in high-risk patients

Qureshi W, et al., GIE; 62, (5) : 2005

ASGE Guidelines

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EUS Doppler Stratifies Gastric Varices ?


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EUS w/ color Doppler provides hemodynamic data:

-Stratify severity of portal HTN

- Monitor response post-Therapy(pharmacologic vs endoscopic)

- Quatify risk of recurrence / rebleeding

(diffuse type >> localized type)

Iwase H et al., GIE 53, NO. 6, 2001

EUS Doppler Stratifies Gastric Varices ?

Better Risk Stratification pre-Glue ?

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Adverse Events


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needle adhesion to the varix, embolization,

abscess formation, esophageal perforation,

peritoneal cavity extravasation,

and splenic infarction.

Adverse Events

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rFactor VII: What is the Verdict?


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rFactor VII immediately normalizes PT amongst bleeding cirrhotics.

Case reports prompted larger studies

No overall effect found; though analysis of CPT B & C indicated that

rF-VII significantly decreased proportion of patients who failed

to control varices

Dosing appeared safeBosch J et al., Gastroenterol 2004; 127(4):1123-30

Case series of 8 pts w/ severe hemorhage from esophageal varices ..

h in our experience rFactor VII achieves hemostasis in bleeding

esophageal varices unresponsive to standard treatment.

Romero-Castro R et al., Clin Gastr Hepatol 2004 2(1):78-84

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F t VII: Wh t is th V di t?


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Akyildiz M. et al., CVA event after a single dose

administration of rF-VII in a patient w/ esophageal

variceal bleeding

DDS 2006; 51(9):1647-9

Dangerous remedy

Baltimore Sun

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CAPSULE ENDOSCOPY


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SI varices: 15.8% (3/19).

Other PHTN-related findings: portal HTN gastropathy (13/19, 68.4%),portal HTN enteropathy (12/19, 63.1%), portal HTN colopathy (3/19, 15.8%),

nonbleeding esophageal varices (2/19, 10.5%).

Potential source of GI blood loss identified in 89.5% (17/19).Active bleeding sites identified in 15.8% (3/19).

CONCLUSIONS:

CE can identify potential bleeding sources and could have

diagnostic utility in patients with ESLD and chronic anemia

after obliterative esophageal variceal therapy.

Canlas KR et al, J Clin Gastroenterol Feb 2008

CAPSULE ENDOSCOPY

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Imaging of Portal Vein & Hepatic Veins


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Imaging of Portal Vein & Hepatic Veins

Ultrasound with duplex

3D-CT scan

MRI

Venous phase of splenic or mesentericarteriogram

HVW carbon dioxide venography

EUS w/ Doppler

FLOW easily measuredvs. RESISTANCE?

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Variceal Bleeding: Summary


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Variceal Bleeding: Summary

1ryProphylaxis: b-blockers or EVL

Vasoactive drug, EVL & Antibioticsfor acute bleed

Secondary Prophylaxis: b-blockers & EVL

CE: will be in the algorithm of portal-HTN w/u ?

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Variceal Bleeding: Pearls


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Glue in experienced hands for GOV-2/IGV: useful !

Having Hepatologists go interventional: priceless!!

EUS (w/ Doppler)-guided glue injection: optimal !

Variceal Bleeding: Pearls


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For ALL other procedures/perforations, ()

Theres


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DR KANTSEVOY


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Thank [email protected]

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AAK[1].VaricealBleeding.VivaLaVida.March2008.ppt

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