Portal Hypertension

Dr. Ravi Gadani

MS, FMAS
Anatomy- portal circulation
• Superior mesenteric + Splenic vein = Portal vein
Portal Vein carries outflow from:
1.) Spleen
2.) Oesophagus
3.) Stomach
4.) Pancreas
5.) Small and large intestine
Anatomy
PV-portal vein
LG-left gastric vein
RG-right gastric vein
S-splenic vein
SM-superior mesenteric vein
IM-inferior mesenteric vein
RGE-right gastroepiploic
LGE-left gastroepiploic
Definition
• Increased portal venous pressure
• Normal pressure- 5-7 mm of Hg
• Pressure>10mm of Hg (14cm of H2O)
• When pressure exceeds 10 mm Hg, a collateral circulation may
develop to maintain venous return from structures drained by the
portal vein
• Engorgement of collateral veins can lead to esophageal varices and,
less often, caput medusae.
Collateral routes- porto-systemic
connections
• Oesophageal varices: coronary vein(left gastric vein) and azygous
vein
• Veins of Retzius: Retroperitoneal veins
• Caput Medusa: Umbilical vein– veins of anterior abdominal wall
• Hemorrhoidal veins:
• Superior hemorrhoidal vein = Portal
• Inferior hemorrhoidal vein = Systemic
• Adhesions
• Stomal sites
Causes -Classification A/C to site of
obstruction
Pre- hepatic Presinusoidal Extrahepatic portal vein
obstruction
Intra-hepatic a)Presinusoidal Non cirrhotic portal
fibrosis (NCPF)
Schistosomiasis
b)Sinusoidal Cirrhosis

Post -hepatic Post sinusoidal Hepatic vein outflow

obstructioin (Budd Chiari
syndrome)
Constrictive pericarditis
Etiology= Portal outflow obstruction
• Prehepatic:
• Portal vein thrombosis , Splenic vein thrombosis, Congenital portal vein
thrombosis, tumors compressing the portal vein
• Intrahepatic:
• NCPF- non cirrhotic portal fibrosis
• Cirrhosis
• Post Hepatic:
• Budd Chiari Syndrome
Clinical presentation
• GI Bleeding – most common presentation, once bleeding occurs –
70% chances of re-bleed
• Hematemesis or melena or hematochezia
• Bleeding- spontaneous , profuse, painless
• Most commonly- esophageal varices
• Less commonly from gastric varices (2-10%)
• 30 % cirrhotics – develop variceal bleed
• 50% will re-bleed within 6 weeeks most commonly within 48 to 72 hrs
• Mortality increases with increase in the no. of bleeds and severity of liver
disease ( child C ) patients
Clinical presentation
• Splenomegaly :
• present in all cases of PHT
• Hypersplenism :
• Leucopenia -WBC <4000/mm3
• Thrombocytopenia < 100000
• Low haemoglobin
• Ascitis:
• Suggests hepatic decompensation
• Encephalopathy :
• Sign of hepatic decompensation
• Range grade 1 to grade 4
• Euphoria to coma
Caput meduse
Ascites
Oesophageal varices
Investigations
• Hematological : complete hemogram- see for hypersplenism
• Liver function tests :
• To differentiate between cirrhosis from non cirrhotic portal hypertension
• Abnormal liver function tests -- cirrhosis or active liver parenchymal disease
• Renal function tests
• Coagulation profile- PT, APTT, BT CT
Investigations
• Viral markers- Hepatitis B antigen and anti HCV antibodies
• Liver biopsy
• USG Abdomen along with color doppler-
• liver parenchyma- cirrhotic or non cirrhotic
• Differentiates between intrahepatic and EHPVO
• Status of splenic and portal vein
• Direction of blood flow- hepatopetal or hepatofugal
Investigations
• Upper GI scopy- to see for oesophageal and gastric varices and rule
out other cause of bleeding
• Portovenography
• CT angiography
• MR angiography
Effects of PHT
• Ascites

• Hepatic encephalopathy

• Variceal bleeding
Ascites
Origin:
• Hepatic sinusoidal pressure >Colloid oncotic pressure = leakage of
fluid into parenchyma, and overwhelms lymphatic system
• Aldosterone secretion :Salt retention by the kidney due to high levels
( pre-renal state)
Controlling Ascites
Treatment:
• Sodium and H20 restriction
• Diuretics
• Large volume paracentesis:
• Replace with albumin
• Peritoneal venous shunt
• Effective in short term problems
• TIPS:
• Extreme cases, of ascites with encephalopathy
Encephalopathy
• Etiology:
• Cause unclear, Nitrogen compounds contribute to it.
• Symptoms:
• Altered sensorium, coma
• Induced by:
• Advanced liver disease
• Moderate liver disease
• Infection ( sepsis)
• Constipation
• Dehydration
• Blood within the gut
Encephalopathy
Diagnosis
• No diagnostic test
• Serum ammonia levels often high
• EEG abnormalities
• Neuropsych testing
• Clinical Diagnosis
Treatment:
• Limit protein: ( Limit intake and maximize gut cleansing)
• Treatment of the possible causes, i.e. sepsis
Variceal Bleeding
• Resuscitation
• Initial treatment with drugs
• Diagnosis
• Intervention
• Endoscopic
• Surgical
• Supportive therapy and evaluation
Resuscitation
Treatment of hemorrhagic shock
• Volume repletion:
• Blood ideal, until it arrives use crystalloid and colloid
• Platelets usually low: Transfuse, Fresh frozen plasma
• Prolonged bleeding time
• Count less than 50, 000
• Goal: Increase Tissue Perfusion = Urine Output
• Monitor CVP (central venous pressure), hourly urine output, oxygen
saturation
Initial treatment with drugs
Drugs
• Vasopressin
• Somatostatin
Diagnosis
• Even with cirrhotics 50% bleeds from other sources
• Mallory Weiss tears
• Gastritis
• Ulcer disease
• Therefore = Needs Upper GI Scopy
Intervention - Endoscopic
• Indication for intervention for variceal bleed
• Active bleeding from varices
• Stigmata of bleeding varices ( cherry red spots, wheals)
• Absence of any other bleeding source
Intervention - Endoscopic
• Sclerotherapy
• Inject an agent into or adjacent to varix
• Goal: Arrest bleeding and obliterate lumen
• Variceal ligation or banding
• Fewer complications vs. sclerotherapy
• Procedure: suction varix and deploy rubber band
• Balloon Tamponade, (Sengstaken- Blakemore tube)
• Arrests bleed in 90% patients
• Can have fatal complications
• Can only be used for 24 hrs
• If all above fail pt needs a TIPSS (Transjugular intrahepatic portosystemic shunt)
Endoscopic sclerotherapy
Oesophageal banding
Sengstaken blackmore tube
Supportive Therapy and Evaluation
• Address coagulopathy
• Vit K infusion
• Platelet infusion
• FFP
• Aspiration
• Aggressive pulmonary toilet
• Protect airway
• Antibiotics
• Infections other than pneumonia occur
• Treat encephalopathy and poor nutrition
• Purge gut with lactose and neomycin
• Begin TPN
Definitive Therapy
Designed to prevent re-bleeding
Categories
• Medical
• Endoscopic
• Surgical
• Radiological
Medical Therapy
• Beta blockade –propanalol
• Decrease bleeding by decreasing variceal flow / pressure
• Decreases bleeding, but has no effect on long term survival
• Use as an adjunct to endoscopic therapy
Endoscopic Therapy
• Long term prevention of variceal bleeding
• Obliteration of all variceal channels with sclerotherapy and banding
• Multiple sessions required
• Sclerotherapy complications
• Local
• Ulceration, stricture, perforation
• Systemic
• Fever, pneumonitis, mediastinitis
Surgical therapy
Three procedures
• Portal decompressive procedure- porto systemic shunts
• Non decompressive procedures
• Liver transplantation
Porto systemic shunts
• Aim:
• Diversion of blood from portal system to systemic circulation by anastomosing
• Anatomy:
• Portal vein or its tributaries (spleenic or superior mesenteric vein) to Renal
vein or inferior vena cava
• Mech:
• In order to reduce the portal pressure
 Types of shunts
Total shunt Selective shunt Partial shunt

Portocaval End to side Distal spenorenal Small diameter

Side to side shunt portocaval shunt

Central splenorenal Proximal side to Coronocaval shunt

side
Mesocaval Cavo-mesenterico
Mesocaval – “H”
graft
Total Shunts
• Divert most or all flow form portal to systemic circulation
• All prevent rebleeding in 90% patients
• All divert portal flow= liver atrophy
• Encephalopathy = 40% patients
• Types:
• Portocaval ( end-side and side-side +/- graft material
• Mesocaval shunts ( created with or without graft material
• Central Splenorenal shunts
Total shunt
• A- portocaval
shunt

• B- central
splenorenal shunt
Selective Shunts
• Goal
• Prevent variceal bleeding
• Prevent encephalopathy
• Mechanism
• Decompress gastrosplenic compartment
• Maintains portal htn in the portal bed = nutrients to liver = no atrophy
• Types
• Distal Splenorenal shunt = splenic vein divided from portal and anastomosed to
renal
• Proximal spleenorenal shunt with spleenectomy
• Coronal caval shunt ( less commonly used)
Selective shunt- DSRS
Selective Shunts
• Advantage
• Prevents liver atrophy as blood flow to liver maintained
• Prevents encephalopathy
• Results similar to total shunts with regard to bleeding varices and mortality

• Disadvantage
• Technically difficult
• Can cause or even aggravate ascitis
Partial Shunts
• Design
• Ease of construction like portocaval shunts
• Decreased encephalopathy like selective shunts
• Side to side portacaval shunts ( 8mm graft) used
• Short and straight= decrease shunt thrombosis
• Similar to portocaval to prevent rebleed, BUT decreased encephalopathy
• Can be done in emergency to control bleeding
Non decompressive procedures
• Devascularization surgery with or without lower end of oesophageal
transection & spleenectomy
• Aim – control gastroesophageal varices by direct ligation of the
oesophageal and gastric varices or indirectly by ligation of the feeding
vein ( left gastric, short gastrics)
• Used in cirrhotics and emergency uncontrolable bleeding
Liver Transplant
• Not indicated for variceal bleeding
• Indicated for liver failure- cirrhosis
• Therefore counsel liver transplant team
Transjugular intrahepatic portocaval
shunt (TIPSS)
• Image guided radiological procedure
• Expandable metallic stent –kept via tranjugular route to create
intrahepatic communication between hepatic and portal vein to
reduce portal venous pressure
TIPSS
Indications for TIPS
• Refractory bleeding
• Provision as a bridge to transplant
• Child C cirrhosis
• Budd chiari syndrome
• Refractory ascites in cirrhosis
Complications
• Intraperitoneal hemorrhage
• Subcapsular hematoma
• Hemobilia
• Infection
• CHF and Acute renal failure

Procedure Mortality ( 30 day )

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

• Occlusion
• Neointimal hyperplasia= 33-73% occlusion yearly
• Needs surveillance= Increase cost, and time

• Rebleeding
• 18 % yearly
Special Cases for portal
Hypertension
• Splenic vein thrombosis

• Extrahepatic portal vein thrombosis

• Budd Chiari syndrome

Splenic Vein thrombosis
• Causes:
• Pancreatitis
• Pancreatic carcinoma
• Mechanism:
• Submucosal veins in the stomach act as a porto-porto collateral around thrombosis
• Hallmarks:
• Isolated gastric varices
• Normal liver function
• Treatment :
• Splenectomy
Extrahepatic Portal Vein Thrombosis
• Etiologies
• Trauma
• Low flow states
• hypercoagulable states
• Congenital portal vein thrombosis
• Umbilical artery catheterization
Congenital Portal vein thrombosis
• Most common cause of extrahepatic portal vein thrombosis
• Pathophysiology
• Mass of porto-portal collateral passing along porta hepatis to nl liver.
• Collaterals= cavernous transformation of portal vein
• Hallmarks:
• Normal liver function
• Gastroesophageal varices,
• Treatment:
• Endoscopic therapy or selective shunt
Budd-Chiari Syndrome
Hepatic venous outflow obstruction in the liver
• Causes
• Hypercoagulable states
• Exogenous and endogenous estrogen
• Radiation therapy
• Myeloproliferative disorders
• Paroxysmal nocturnal Hemoglobinuria
• Mxyoma ( R atrium presses on IVC)
• Pericarditis
• Congenital caval webs or membranes
• Liver masses
• High dose chemo ( occludes hepatic venules)
Budd-Chiari Syndrome
• Triad of presentation
• New onset abdominal pain
• Ascites
• Hepatomegaly
• Diagnosis
• Angiography ( inferred by Ct scan / MRI )
• Treatment
• Portocaval shunt, if IVC patent
• Mesoatrial shunt, if IVC is occluded
Thank you