portal hypertension

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Page 1: Portal Hypertension

Dr Saeed Al-ShomimiKFHU

Khobar

Page 2: Portal Hypertension

Anatomy6 – 8 cm Splenic + s. mesenteric (behind neck of the pancreas )i. mesenteric , Lt gastric

Page 3: Portal Hypertension

Blood Supply of the Liver

Hepatic Arterial Autoregularity Vasodilatation

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Pathophysiology

Pressure = Flow X ResistancePortal pressure : 3 – 6 mm HgNormal elevation:

EatingExerciseValsalva

Page 5: Portal Hypertension

10 mmHg (prolonged) → ShuntingLt Gastric → esophagealShort Gastric → Gastric Submucosal

Lt portal → epigastricRetroperetoneal and anorectal collateral

12 mm Hg → Bleeding

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Causes of Portal HypertensionCauses of Portal Hypertension

Pre-sinusoidal

Sinusoidal

Post Sinusoidal

BLOOD FLOW

LIVER

Page 7: Portal Hypertension

Pre-sinusoidalExtra-hepatic:

Portal vein thrombosisSplenic vein Thrombosis

Intra-hepatic:Congenital hepatic fibrosisPrimary biliary cirrhosisSarcidosisSchistosomaisis

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SinusoidalSteatohepatitsWilson disease

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Post SinusoidalExtra-hepatic:

Budd Chiari syndromeR heart Failure

Intra-hepatic:HeamochromatosisAlcoholic cirrhosisPost-hepatitic cirrhosis

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Variceal BleedingMortality associated with 1st episode:

Cirrhotic patient : 40% - 70%Non cirrhotic : 5% - 10%

If bleeding resolved spontaneously30% re-bleed , 6 weeks70% re-bleed , 1 year

(30% of the initial bleeding episodes are fatal)

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Acute Variceal Bleeding

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Initial evaluation & stabilization

Assessment of intravascular volume statusFluid resuscitationEndotracheal intubation prior to endoscopy for: • Uncontrolled bleeding• Altered mental status, severe agitation• Respiratory distress or depression

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Treatment for Treatment for Acute Variceal BleedingAcute Variceal Bleeding

Pharmacologic

Radiologic shuntTIPSS

Surgical Shunt

Balloon Tamponade

Pharmacologic and endoscopic

therapyare the usual 1st

and 2nd interventions

Endoscopic

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Pharmacologic TherapyOctreotide• Synthetic analogue of somatostatin• Decreases portal pressure and azygos

blood flow• Stops variceal bleed in 80% of the cases• Efficacy is similar to endoscopic

sclerotherapy and better than vasopressin

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• 5-day course reduces bleeding after endoscopic therapy

• Can cause mild hyperglycemia and abdominal cramping

• 250 µg Iv Bolus – followed by infusion 25 – 50 µg/h (2-4 days)

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Vasopressin

• Reduces portal pressure but causes myocardial and mesenteric ischemia (more side effects)

• 20 u IV bolus (over 20 min) – infusion 0.2 – 0.4 u/min

• Control approximately 50% of acute episodes

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Terlipressin

• Efficacy similar to endoscopic sclerotherapy and as effective as balloon tamponade when used with nitroglycerin

• Not approved for use in U.S.

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Endoscopic TherapySclerosant injectionBand ligation

Became a standard form of therapy in acute variceal bleeding

Initial control of hge in 70 – 95% Re-bleeding 20 – 50%

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sclerotherapy5% sodium morrhuate5% ethanolamine oleate

Intravariceally : to obliterate the varix

Paravariceally : induce submucus fibrosis

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3 prospective randomized controlled trials studies comparing sclerotherapy and balloon temponade:Sclerotherapy achieved better initial hge control

Fewer episodes of rebleedingImproved long-term survival

(furthermore, routine use of balloon temponade after sclerotherapy confer no additional benefit)

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Complications:Pulmonary complicationsTransient chest painEsophageal stricturePortal vein thrombosisEsophageal perforationBacteremia

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Band Ligation

Alternative to sclerotherapy

Fewer rebleeding episodes

Fewer endoscopic interventions

Lower procedure related mortality and over all mortality

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Pharmacologic versus Endoscopic Therapy

2 meta-analysis compared medical pharmacotherapy with emergency sclerotherapy as 1st line treatment for acute bleeding:No significant difference regarding initial hge

control or mortalityAdministration of somatostatin before and after sclerotherapy : Improve treatment efficacyReduce blood transfusion

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Balloon TemponadeApplication of direct

upward pressure against varices at G-E junction

Should be intubated:Prevent aspirationPrevent airway

occlusion

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Balloon positioning

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Tube Positioning and Gastric Balloon Inflation

1. Tube inserted to 50 cm2. Auscultate in stomach 3. Inflate gastric balloon with

50 cc4. Stat portable film

1. Re-confirm proximal position

2. Inflate GB 300-400 cc air3. Pull to insure anchorage4. Recheck film 5. 1-2 lbs of pully traction

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Gastric and Esophageal Balloon Inflation

Esophageal Balloon inflated

to 35 - 40 mmHg

1. Last resort2. Deflate

periodically3. Use minimum

effective pressure4. Complication

- ulcer- perforation- stricture

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Direct temponade therapy is 90% effective in controlling the bleeding

50% rebleeding after removalSerious potential complications

(mortality 20%)Bridge therapy

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TIPS(Transjagular Intrahepatic Portosystemic Shunting)

Creating an intrahepatic portosystemic fistula to decompress the portal hypertension

First performed in 1982(non- selective side to

side portosystemic shunt)

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1 -Cannulating the Rt hepatic vein via internal jagular vein2 – passing needle through liver parenchyma to portal vein

branch3- guide wire4 balloon dilatation

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5 – stenting the tract

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Page 33: Portal Hypertension

Meta-analysis comparing TIPS with endoscopy in acute hge:

Significant improvement in controlling the hge

Coast : ↑rate of hepatic encephalopathy

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Contraindications:

R side heart failurePolycystic liverPortal vein thrombosis

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Complications:

•Intraperitoneal bleeding due to perforation of the hepatic capsule, hepatic, or portal veins

•TIPS embolization

•Acute right heart failure due to increased venous return to right heart

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•Late:

•recurrent bleeding due to TIPS stenosis or thrombosis

•Infection•hepatic encephalopathy.

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Surgical Therapy

Operative intervention is reserved for cases refractory to other modalities

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Esophageal transection EEA stapler

Operative mortality 75%Complications 25%:

PerforationStrictureEsophagitis→ not useful in acute state

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Portosystemic Shunt (side-to-side)Non-selective shuntManipulation and dissection in porta hepatica →

Scaring and fibrosis → complicate future liver transplant

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DSRSSelective shuntSome cases un accompanied

by refractory ascitis

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Prevention of Recurrent Variceal Bleeding

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Pharmacotherapy:

Rebleeding without treatment 70% in 1 year

Non-selective B blockers (propranalol)↓portal pressureEffect is variable and unpredictableLess benefit with decompesated liver

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Endoscopic therapy:

Advocated as a means for complete eradication of esophageal varices

Once eliminated routine endoscopy 6-12 months

Fewer rebleeding episodes than medical treatment

50 % rebleding in 1 year30% need conversionReserved for complaint patients

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TIPS:

Bridge therapy → liver transplant

Advantiges over surgery:No risk of general anesthesiaNo post-operative complications

LimitationsStenosis (50% in 1st year)Encephalopathy (1/3)

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Surgical Therapy:

Most effective method in controlling portal hypertension and recurrent bleeding

1 Portosystemic shunt procedures2 Esophagogastric devascularization

3 Orthotopic liver transplantation

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Portosystemic Shunt

Decompressing the hypertensive portal Venus system into the low pressure systemic venous circulation

Toxins → systemic circulation → encephalopathy

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To minimize these effects shunting operations have evolved:Non-selectiveSelectivepartial

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1 – Non selective ShuntsEnd to side portocaval

(Eck fistula):Higher rate of

encephalopathy among operative shunting groups

Better control of rebleeding than medical treatment

Eck fistula – medical therapy → same incidence of encephalopathy

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Side to Side portocaval shunt:

Maintain the anatomic continuity of the portal vein

Encephalopathy rate : no differenceDecompress the sinusoidal pressure → better ascitis control

Recommended for Budd Chiari Syndrome

More difficult than end to side

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Interposition Mesocaval Shunt:Prosthetic – autogennous vienAvoid hilar dissection (future transplant)

Shunt ligation in refractory post-op encephalopathy

Drawback → thrombosis (35%)

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Proximal Spleno-Renal Shunt:

Splenectomy + anastomosing proximal Splenic vein to Lt Renal vein

Divert all portal flow into renal vein → non selective

Shunt occlusion 18%

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2 – Selective ShuntsIn response to post-op

complications of non-selective procedures

1967 DSRSDistal Splenic vein to Lt

renal VeinSelectively decompress the

esophagogastric veins

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Contraindications:Refractory ascitisSplenic vein thrombosisPreviously underwent splenectomySplenic vein diameter < 7 mm

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Coronary – Caval Shunt:Described in Japan in 1984

Interposition graft between L Gastric and inferior vena cava

Little experience with this procedure

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3 – Partial Shunts

Small diameter interposition graftsMaintaining a degree of hepatopedal

portal flow to the liver

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Esophagogastric DevascularizationThe most effective non-shunt

operation for preventing variceal bleeding:Devascularization + transection + splenectomy

Sugiura procedure

Page 57: Portal Hypertension

Orthotopic Liver TransplantationThe most definitive form of therapy

for complications of portal hypertension

Selective patients:CoastUnavailability Immunosuppresion

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Child A – mild B → non-transplant surgery

Child C – advanced B → transplant

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Prophylaxis

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Likehood of variceal bleeding:

Alcoholic cirrhosisActive alcohol consumptionSever hepatic dysfunctionEndoscopy:

Variceal wall thinningVariceal tortuositySuperimposition of varices on otherGastric varicose

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Non selective B blockers

Prophylactic shunts showed no benefit , ↑morbidity

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Portal hypertension in north Indian children

Arora NK, Lodha R, Gulati S, Gupta AK, Mathur P, Joshi MS, Arora N, Mitra DK

Department of PaediatricsAll India Institute of Medical Sciences

New Delhi.

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cross-sectional observational studyTertiary care centre in northern

IndiaJanuary, 1990 to December, 1994Children below the age of 14 years

with suspected portal hypertension To determine the etiology and

clinical profile of portal hypertension

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115 patients with portal hypertension76.5% had extrahepatic portal hypertension (EHPH)

23.5% had intrahepatic causes of portal hypertension

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Results:

Children with EHPH had a significantly earlier onset of symptoms as compared to those with intrahepatic portal hypertension (p = 0.002)

And bled significantly more frequently (p = 0.00).

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History suggestive of potential etiological factors could be elicited in only 7% of EHPH patients.

The commonest site of block in splenoportal axis was at the formation of the portal vein.

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An inverse relation of bleeding rates with duration of illness was seen in EHPH

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Conclusion:

Understanding the natural history of EHPH and portal hypertension due to other etiologies may have significant implications in choosing the appropriate intervention and predicting the outcome.

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References

ACS Surgery : Principles and Practice 2004 Web,MD

Schwartz Principles of Surgery 7th EditionIndian J Pediatr. 1998 Jul-Aug;65(4):585-91.Johns Hopkins Gastroenterology & Hepatology

Resource Center http://hopkins-gi.nts.jhu.edu

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Thank You