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Portal hypertension
Usually caused by increased resistance to portal venous blood flow
The obstruction is prehepatic, hepatic or posthepatic
The normal pressure in the portal vein varies from 5 to 15 cmH2O.
When the portal venous pressure is consistently raised above 25 cmH2O may → serious clinical consequences
Portal hypertension
Portal hypertension
Anatomy of the portal venous system
Causes of portal hypertension
Obstruction to portal flow Increased blood flow (rare)
Prehepatic Congenital atresia of the portal vein
Portal vein thrombosis Neonatal sepsis Pyelophlebitis Trauma, Tumour
Extrinsic compression of the portal vein Pancreatic disease Lymphadenopathy Biliary tract tumours
Intrahepatic Cirrhosis Schistosomiasis
Posthepatic Budd-Chiari syndrome Constrictive pericarditis
Arteriovenous fistula Increased splenic blood flow in hypersplenism
Portal hypertensionPrehepatic
Portal vein thrombosis Rare cause
Commonly due to neonatal umbilical sepsis, though the effects may manifest after many years
Portal hypertension
Portal hypertensionHepatic - Liver cirrhosis
Cirrhosis of the liver The commonest cause Results from chronic liver disease
Characterized by liver cell damage, fibrosis & nodular regeneration
Micronodular cirrhosis even distribution of nodules a few millimeters in diameter
Macronodular cirrhosis the nodules vary in size usual in end-stage cirrhosis
The fibrosis obstructs portal venous return & → portal hypertension
Portal hypertension
Portal hypertension Hepatic - Liver cirrhosis
Alcohol The commonest etiological factor in western countries
Abnormal resistance is predominantly postsinusoidal (increase in wedge hepatic venous pressure)
The hepatic veins become distorted by regenerative nodules, there is narrowing of the central veins by centrilobular collagen deposition, and swelling of the hepatocytes encroaches on the sinusoidal lumen
Schistosomiasis Due to Bilharzia mansonii is a common cause in North Africa, Middle East
Granulomas from parasitic involvement are seen in the portal triads
Hypertension is presinusoidal
Portal hypertension
Portal hypertensionHepatic - Liver cirrhosis
Other causes Chronic active hepatitis
Primary & secondary biliary cirrhosis
Cryptogenic cirrhosis (obscure cause)
Portal hypertension
Portal hypertensionPosthepatic
Rare
Due to spontaneous thrombosis of the hepatic veins
Associated with Neoplasia Oral contraceptive agents Polycythaemia Presence of abnormal coagulants in the blood
The resulting Budd-Chiari syndrome is characterized by portal hypertension, liver failure & gross ascites
Portal hypertension
Abdominal radiograph demonstrating calcified & thrombosed portal & splenic veins
Effects of portal hypertension
Gradual chronic occlusion of the portal venous system → Collateral develop between the portal & systemic venous circulations The most important consequence of shunting is the development of varices in
the submucosal plexus of veins in lower esophagus & gastric fundus. The esophageal varices may then rupture → acute massive gastrointestinal bleeding
(occurs in 40% of patients with cirrhosis). Initial episode of variceal hemorrhage is fatal in ⅓ of patients.
Bleeding from retroperitoneal & periumbilical collaterals.
Collaterals may develop & → bleeding at site of stomas.
Anorectal varices are found at proctoscopy but rarely cause bleeding.
Progressive enlargement of the spleen due to vascular engorgement & associated hypertrophy
Portal hypertension
Sites of portosystemic shunting
Effects of portal hypertension
Hematological consequences Anemia, thrombocytopenia & leukopenia (hypersplenism)
Ascites Increased formation of hepatic & splanchnic lymph Hypoalbuminaemia Retention of salt & water Increased aldosterone & antidiuretic hormone
Portosystemic encephalopathy due to Increased level of toxins (ammonia) in systemic circulation Develop where there are large spontaneous or surgically created
portosystemic shunts Gastrointestinal hemorrhage increases absorption of nitrogenous products
→ encephalopathy
Portal hypertension
Clinical presentation
Patients with cirrhosis Anorexia Generalized malaise Weight loss
Clinical manifestations of liver disease Hepatosplenomegaly Ascites Jaundice Spider naevi
Serum bilirubin may ↑ Serum albumin ↓ Anaemia Leukocyte count ↑ or ↓ (hypersplenism) Prothrombin time & other indices of clotting may be abnormal
Portal hypertension
Gross splenomegaly secondary to portal hypertension
Modified Child's grading system (Clinical & biochemical parameters)
Points scored
Criterion 1 2 3
Encephalopathy
Ascites
Bilirubin (µmol/L)
Albumin (g/L)
Prothrombin ratio
None
None
< 35
> 35
< 1.4
Minimal
Slight
35-50
28-35
1.4-2.0
Marked
Moderate
> 50
<28
> 2.0
Portal hypertensionAcute variceal bleeding
Patients presenting with acute upper gastrointestinal bleeding are carefully examined for evidence of chronic liver disease.
Distended collateral veins around the umbilicus ('caput medusae‘).
Slurring of speech, a flapping tremor or dysarthria may point to encephalopathy may be precipitated or intensified by accumulation of blood in gastrointestinal
tract
The key investigation during an episode of active bleeding is endoscopy
Allows detection of varices & defines whether they are or have been site of bleeding.
Peptic ulcer & gastritis are common complaints (in 20% of patients with varices).
Portal hypertension
Management of bleeding esophageal varices
Active resuscitation Group & cross-match blood
Assessment of coagulation status Prothrombin time Platelet count
Establish i.v. infusion line(s)
Monitor pulse , blood pressure hourly urine output , central venous pressure
Urgent endoscopy
Management of bleeding esophageal varices
Control of bleeding Tamponade (Minnesota tube) or injection sclerotherapy
Pharmacological measures (e.g. vasopressin/somatostatin)
Treatment of hepatocellular decompensation
Treatment/prevention of portosystemic encephalopathy
Portal hypertension
Management of bleeding esophageal varices
Prevention of further bleeding from varices Injection sclerotherapy
Stapled esophagogastric junction
Portosystemic shunting/TIPSS
Liver transplantation
Portal hypertension
Active resuscitation
Large volumes of blood may be lost rapidly and the aim is to replace blood loss quickly.
Fresh blood is preferred for transfusion purposes
Fresh-frozen plasma (FFP)
Platelet transfusion
Portal hypertension
Endoscopy
Performed at the earliest opportunity, and in patients threatened by massive bleeding, active resuscitation is instituted and continued in the endoscopy suite.
The tortuous varices are usually in three columns & most prominent in the lower third of the esophagus.
If varices are the source of blood loss, this usually occurs from the lowest few centimeters of esophagus.
Rarely, bleeding occurs from varices in gastric fundus.
Portal hypertension
Control of bleeding
Medical agents to lower portal venous pressure & arrest bleeding synthetic form of somatostatin, octreotide
If variceal hemorrhage is apparent at the endoscopy injection of a sclerosant (ethanolamine) application of bands
If hemorrhage is torrential & prevents direct injection, balloon tamponade may be used to stop the bleeding. Minnesota tube (four-lumen) Sengstaken-Blakemore tube (three-lumen)
Portal hypertension
Control of bleedingMinnesota tube (four lumen)
Aspiration of gastric contents Inflation of a gastric balloon with 150 ml of water with radio-opaque dye
(Hypaque) to be checked radiologically compresses the gastric fundus & EGJ → reducing flow of blood into
esophageal varices Inflation of esophageal balloon with air to a pressure of 40 mmHg (direct
pressure to the esophageal varices) Aspiration of esophagus & pharynx above esophageal balloon, reducing the
risk of aspiration pneumonitis Traction is applied to the Minnesota tube by pulling the gastric balloon up
against EGJ & taping the tube as it emerges from the angle of the mouth. Pharynx & stomach are aspirated every 15-30 minute. Arrests bleeding from varices in over 90% of patients The tube is not left in place for more than 24-36 hours for fear of causing
esophageal necrosis.
Esophageal tamponade using a Minnesota tube
Control of bleeding
Tamponade should be regarded as a holding measure
Further resuscitation & treatment of hepatic decompensation.
More definitive measures are used to prevent further variceal bleeding two-thirds rebleed while still in hospital 90% rebleed within a year
Portal hypertension
Resuscitation & treatment of hepatocellular decompensation
Control of variceal bleeding allows blood loss to be made good & permits a full assessment of coagulopathy.
Blood may be evacuated from the gut by a bowel washout to reduce the risk of portosystemic encephalopathy.
Lactulose (15-30 ml tid) to reduce bacterial degradation of blood in the gut lumen & further reduce risk of encephalopathy.
Esophageal varices due to liver disease frequently have major defects in intrinsic & extrinsic clotting systems.
Vitamin K to aid restoration of the extrinsic system
FFP, factor concentrates & platelet transfusion may all be required to cover specific procedures such as sclerotherapy.
Transfusion measures have transient effects on blood coagulation
Ultimate coagulation status depends upon restoration of hepatic function.
Portal hypertension
Prevention of further bleedingInjection sclerotherapy
Carried out by fibreoptic endoscopy.
Injection is repeated at weekly or fortnightly intervals until the varices are completely sclerosed.
Following complete ablation, fibreoptic examination is repeated periodically & any recurrent varices are injected.
Excessive or too frequent injection may be complicated by ulceration & necrosis, sometimes with a fatal result.
Sclerosant can be injected directly into the varix or into the surrounding mucosa.
Reduced the number of patients undergoing surgery
Most successful in patients with well-preserved liver function.
Improves long-term survival?.
Portal hypertension
Prevention of further bleedingEndoscopic banding
Used to occlude varices at esophagogastric junction.
The reduced risk of esophageal ulceration & perforation has resulted in this technique being favoured in many centres.
Portal hypertension
Prevention of further bleedingSurgical disconnection
Rarely used in management of variceal hemorrhage.
The gastric veins & short gastric veins are ligated and the distal esophagus is transected & reanastomosed just above the cardia using a stapling gun.
Stapled esophageal transection occludes flow into varices.
Technically difficult in patients who have been submitted to repeated injection sclerotherapy.
Considerable morbidity & mortality when employed as a last resort in the emergency situation.
Esophageal stapling
Prevention of further bleedingEmergency portosystemic shunting
High mortality.
Elective portosystemic shunting is still used to decompress portal system & reduce risk of further variceal hemorrhage, but portosystemic encephalopathy can be troublesome.
Operation is rarely considered in patients whose condition is complicated by jaundice, ascites or encephalopathy, and where there is a clear indication for liver transplantation.
Portal hypertension
Types of shunt procedureThe distal splenorenal (Warren) shunt
Selectively decompresses lower esophagus & upper stomach
Maintains liver blood flow
The incidence of encephalopathy is lower than after other shunt procedures
Portal hypertension
Types of shunt procedureTransjugular intra hepatic portosystemic stent shunting (TIPSS)
In this procedure a metal stent is inserted via the transjugular route using a guide-wire passed through the hepatic vein to the intrahepatic branches of the portal vein.
Relatively safe (no GA & no laparotomy).
The risk of encephalopathy is similar to that of a surgical portosystemic shunt.
Now considered routinely before surgical intervention in both the acute and the elective setting.
Portal hypertension
Types of portosystemic shunt
Ascites
Ascites can be controlled by bed rest, salt & water restriction & a diuretic such as the aldosterone-inhibitor spironolactone.
If refractory, ascites can be treated by inserting a peritoneojugular (LeVeen) shunt, which allows one-way flow between the peritoneum & jugular vein.
Portal hypertension
Peritoneovenous (Le Veen) shunt to relieve ascites