gastroenterology and hepatology - portal hypertension and bleeding

8/22/2019 Gastroenterology and Hepatology - Portal Hypertension and Bleeding

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Portal hypertension: Bleeding

Warren Schmidt MD, PhD

Professor

Division GI/Hepatology

Department of Internal Medicine

University of Iowa

Carver College of Medicine


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Anatomy

Krige, J E J et al. BMJ 2001;322:348-351


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Causes of portal hypertension

Increased resistance to flow

Prehepat ic (po rtal vein ob struct io n)Congenital atresia or stenosis

Thrombosis of portal vein

Thrombosis of splenic vein

Extrinsic compression (eg. tumors)

Hepatic

Cirrhosis

Acute alcoholic liver disease

Congenital hepatic fibrosis

Idiopathic portal hypertension

Schistosomiasis

Posthepat icBudd-Chiari syndrome

Constrictive pericarditis

Increased portal blood flow

Arterial-portal venous fistula

Increased splenic flow


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Pathophysiology of portal hypertension in cirrhosis


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Why do varices bleed?

Degree of portal HTN: larger varices from higherpressure head tend to bleed more often.

History: patients who have bled are more likely to bleedagain.

Factors that increase portal hypertension increasebleeding: Progressive/more severe liver disease

Alcohol intake

Physical exercise

Increased intra-abdominal pressure

Morphologic signs Red spots Weals or Wheals

Fibrin plugs


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Variceal Bleeding.

A serious problem : 20-30 % mortality

Therapy: to correct hypovolemic shock and achieve

hemostasis at the bleeding site;

resus, resus, resus, resus, ----- then Scope. H/H correct to 10/30.

Correct coagulopathy

tap ascites

treat encephalopathy

Antibiotic prophylaxis in all patients.

Patients with stage 3-4 encephalopathy need intubation.


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Medical Therapies for acute variceal

hemorrhage. Vasoconstrictive agents. [reduce hepatic venous pressure, variceal

pressure and azygos blood flow]

Vasopressin (or analogs) and nitroglycerin

Nitroglycerinmustbe used with vasopressin to reduce thevasoconstrictive side effects of vasopressin.

Not widely employed in US. Terlipressin

Somatostatin and analogs (octreotide). [same hemodynamictransient effects]

Octreotide is a synthetic, long acting analog of somatostatin.

Agent of choice here.

Dosing: 50-100 ug bolus IV, then 25-50 ug/hr infusion. Duration 1-5 days.

Few side effects. Nearly equal efficacy with sclerotherapy


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Endoscopic therapy for acute esophageal

variceal hemorrhage. Variceal band ligation.

Success rates better than sclerotherapy.

Lower complication rate:

esophageal perforation, ulceration, pneumonia,peritonitis known complications

Sclerotherapy.

Passe at many centers

70-90% success rate for initial control of bleeding.

High complication rate, more repeat sessions thanbanding.

Ulcerations, strictures, pleural effusion, bacteremia,fever, peritonitis, chest pain.


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Gastric Varices

Cause of serious/exsanguinating bleeding in up to 36% Korula et al. Dig Dis Sci 36:303, 1991.

-blocker therapy recommended if no contraindication.

Emerging role of cyanoacrylate injection with acute

bleed. Cyanoacrylate injection appears better than ligation

Lo et al Hepatology 33:1060, 2001.

Prophylactic banding not universally recommended

Bleeding from GV frequently leads to necessity forballoon tamponade and TIPS.


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TIPSS

Recommendations:

For Patients who fail medical and variceal interventions.Very effective at reducing portal hypertension, deflating

varices and decreasing bleeding.

One third of patients develop increased encephalopathy.


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Sengsten-Blakemore/Minnesota tube

Recommendations:Acute, emergent control of variceal bleeding until TIPS or

surgical shunt can be arranged.

Temporary solution only and definitive plan should be in place

by 24 hr after placement


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Prophylaxis of variceal bleeding in cirrhosis

Dib, N. et al. CMAJ 2006;174:1433-1443


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Prophylactic management of

varices

Primary prophylaxis

Endo screen for all patients with new diagnosis of cirrhosis

Repeat at 1-3 yr intervals if no varices

If varices, start nonselective -blocker therapy

80-160 mg/day or

Nadolol 80 mg/day

Target is 20-25% reduction in HR or less than 60 beats/min.

Secondary prophylaxis

Both pharmacologic and endo treatments used to preventrecurrence

Eradication of varices is now indicated

Band ligation is preferred to sclerotherapy


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Failure of Prophylaxis

If banding + -blocker therapy fail to

prevent recurrent bleed:

TIPS is initial treatment of choice

High success rate to prevent bleeding, but TIPS

complicated with encephalopathy, early occlusion,

and bleeding.

Surgical shunts still an option for early Childs

class patients


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Portal Hypertensive Gastropathy,

Vascular ectasia

Krige, J E J et al. BMJ 2001;322:348-351


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Vascular ectasias Portal hypertensive gastropathy (PHG)

Always associated with portal hypertension

When severe can be associated with oozing vascular ectasiasand IDA.

Ectasias (red spots) chiefly in fundus and proximal body

Bleeding responds to -blocker

Gastric Antral Vascular Ectasia (GAVE) Occurs in cirrhotic and non-cirrhotic patients

Ectasias in stripped antral pattern

Chronic bleeding and IDA more common than PHG

May not respond to -blocker

Does not respond to TIPS or decompression Treat with AP laser or surgical antrectomy

gastroenterology and hepatology - portal hypertension and bleeding

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