Portal Hypertension Causes, Treatment and Complications

 Control Of Ascites In Portal Hypertension

Ascites in portal hypertension is a slow, insidious accumulation of free peritoneal fluid, an occurrence in advanced liver disease. It can be troublesome and refractory to commonly available treatment. Diagnosis is confirmed by ultrasound and aspiration.

When there is a doubt regarding the diagnosis, laparoscopy is advisable which not only detects and confirms cirrhosis but also rules out other intra-abdominal pathologies (malignancy, tuberculosis, etc.).

Ascites in Portal Hypertension Causes

• Reduction in plasma albumin
• Central hypovolaemia
• Retention of salt and water by kidneys
• Portal hypertension

Ascites in Portal Hypertension Treatment

1. Diuretics: K⁺ sparing diuretics such as spironolactone or frusemide can be given. However, hyponatraemia and hypokalaemia should be monitored.
   • Salt restriction
   • Abdominal paracentesis
   • Liver transplantation
   • TIPSS
   • Intake of diuretics
   • SHunt—peritoneovenous
   • Remember as SALTISH
2. Restriction of salt intake: 20 mg/day is advised.
3. Peritoneovenous shunt: Le Veen shunt
   • Le Veen shunt is done by using a silastic tube to insert into ascites. It is then tunnelled subcutaneously to the neck and inserted under vision into internal jugular veins.
   • Mode of action: Ascitic fluid is drawn into the systemic circulation with each respiration because of the presence of a one-way valve.

Ascites in Portal Hypertension Complications

• Occlusion
• Displacement
• Infection

Other causes of hypoalbuminaemia are given.

Ascites in Portal Hypertension Causes of Hypoalbuminaemia

• Sepsis
• Enteropathy—protein-losing
• Poor nutrition—malnutrition
• Syndrome—nephrotic
• Injury—trauma
• Sick Liver—chronic liver disease
• Remember as SEPSIS

Ascites in Portal Hypertension Miscellaneous: Ten Commandments Of Bleeding Varices

1. All cases of cirrhosis should undergo upper gastro-intestinal endoscopy to rule out varices.
2. Almost all cases of varices should receive propranolol prophylaxis. Propranolol prophylaxis reduces the risk of bleeding in varices by at least 10%.
3. Acutely bleeding oesophageal varices should be first treated with octreotide and endoscopic treatment.
4. Endoscopic sclerotherapy, and variceal banding should be tried in all patients with variceal bleeding. Banding is safer than sclerotherapy.
5. One should consider TIPSS if available, when pharmacotherapy and endoscopic therapy fail.
6. One should consider the Sengstaken-Blakemore tube if endoscopic facilities and TIPSS are not available although it is associated with a high rate of recurrent bleeding.
7. Inexperienced surgeon should consider oesophageal transection to tide over bleeding varices resistant to octreotide and endoscopic treatment.
8. One should consider Child’s score before planning measures to prevent rebleeding.
9. Surgical shunts should be considered for the Child’s A and B categories.
10. In Child’s C category, one should consider TIPSS followed by liver transplant.

Portal Hypertensive Gastropathy

Due to increased portal pressure and collaterals, vascular dilatation and ectasia occur in the stomach. Endoscopically they appear pink speckled with red mosaic-like pattern in the gastric mucosa. Lesions are diffuse. They are responsible for about 3.5% of cases of upper GI bleeds and 15% in portal hypertension cases.

They can present as acute bleeding with needs to be managed conservatively. Chronic bleeds present as anaemia. Propranolol is used to reduce portal pressure which in turn reduces bleeding.

Portal Biliopathy (Pseudosclerosing Cholangitis)

It refers to bile duct changes due to portal hypertension. More common in extrahepatic portal hypertension. Portal cavernosa, ischaemic injury to the bile duct are the causes. Infection is also one of the causes.

Changes in the bile duct include strictures and dilatation of both extra and intrahepatic bile ducts secondary to varices encircling CBD and gallbladder wall. Choledocholithiasis is common.

• Can present with bile duct obstruction, cholangitis and bleeding into the CBD.
• Prolonged obstruction leads to secondary biliary cirrhosis.
• Investigation: U/S, CT scan, colour Doppler to image varices.
• Treatments: Endoscopic sphincterotomy, clear the CBD, stenting.
• Portosystemic shunt in failed endoscopic extraction of stone.

Budd Chiari Syndrome

It occurs due to obstruction to the hepatic vein.

Budd-Chiari Syndrome Causes

1. Congenital: It is a potentially curable condition where in a web exists in the suprahepatic portion of inferior vena cava.
2. Clotting disorders—polycythaemia
3. Contraceptive pills
4. Cancerous infiltration of hepatic veins (hepatocellular carcinoma).
5. Crotalaria is a plant extract used in the tea.

Budd-Chiari Syndrome Clinical features

1. Acute form is dangerous, resulting in rapid enlargement of liver, severe abdominal pain, vomiting and hypotension.
2. Chronic form resembles cirrhosis: Hepatomegaly— firm, can be irregular, dilated veins over the abdominal wall. Bilateral pedal oedema which can be irritating, signs of liver cell failure are seen. Haematemesis occurs later.

Budd-Chiari Syndrome Treatment: In congenital cases, if web can be proved by vena-cacography, it can be excised by transatrial meatotomy. However, in general, prognosis is very poor. The peritoneo-venous shunt has to be considered as an alternate method to drain the ascitic fluid into one of the veins in the neck (internal jugular vein).

Role Of Octreotide In Surgery

1. Variceal bleeding:
   • Acute—50 mg IV stat followed by 50 mg/h infusion for 120 hours.
   • Long-term prophylaxis is 100 mg s/c tds for 15 days.
2. Pancreatic disorders
   • ERCP-induced pancreatitis
   • Acute pancreatitis
   • Relapsing pancreatitis
   • Chronic pancreatitis
   • Pancreatic surgery—100 mg s/c 1 h prior to surgery and to continue 100 pg tds for 7 days.
3. Bowel dysfunction—AIDS-related diarrhoea, short bowel syndrome, dumping syndrome, chemotherapy-induced diarrhoea.
4. Gastrointestinal fistulae.
5. Carcinoid and other neuroendocrine tumours.
6. Advanced malignancies: Hepatocellular carcinoma, metastatic breast cancer, colonic cancer, pancreatic cancer.
7. Acromegaly.

Liver Transplantation

Liver Transplantation Indications

• Decompensated cirrhosis: Chronic hepatitis C, primary biliary cirrhosis, etc.
• Acute fulminant hepatic failure (FHF): Causes are paracetamol overdosage, acute hepatitis B infection, Wilson’s disease, drugs.

Signs and Symptoms of Decompensated Liver

• Hepatic encephalopathy
• Ascites
• Spontaneous bacterial peritonitis
• Hepatorenal syndrome
• Hyperbilirubinaemia, coagulopathy

Decompensated Liver Types 

1. Living donor transplant: Easily available, no waiting period but potential risk to donor (normal person) is present.
2. Cadaveric: Preserving organ by hypothermia
   • Waiting period
   • No risk to donor
   • To be done within 12 hours, ideally within 6 hours.

Liver Transplantation Organ Preservation:

• Hypothermia and by cold storage solutions o University of Wisconsin solution is commonly used. It contains:
  • Lactobionate: Prevents intracellular swelling
  • Hydroxyethyl startch: Decreased interstitial oedema, decreased hypothermia-induced damage to cells.

Liver Transplantation Types 

• Partial hepatectomy: Usually right lobe (60% of total liver)
• Split liver transplant: Divide into two functioning units and transplant into two patients.

Liver Transplantation Procedure

• Mobilise the diseased liver and isolate vena cava, portal vein, hepatic artery and bile duct.
• Remove the diseased liver.
• Donor liver is transplanted and anastomosis of various structures done.

Liver Transplantation Complications

• Thrombosis of hepatic artery
• Thrombosis of portal vein
• Bile leak
• Nonfunctioning of hepatic allograft
• Infections

Haemobilia

Haemobilia Definition: Bleeding from liver into the biliary tree. There is usually a communication between a blood vessel and the bile duct or any other part of the biliary tree.

• Accidental trauma
• Malignant liver disease
• Portal hypertension
• Percutaneous diagnostic and therapeutic procedures
• Vascular disease of hepatic artery
• Gallstones may get impacted, erode the hepatic artery and cause life-threatening haemobilia.

Haemobilia Clinical Features

• Triad of Sandblom—jaundice, pain and melaena
• Pain abdomen—colicky
• Obstructive jaundice
• Haematemesis or melaena

Haemobilia Investigation: LFT, USG abdomen, selective arteriography, upper GI endoscopy.

Haemobilia Treatment

• Selective arterial embolisation (angiographic, under fluoroscopic guidance)
• Blood transfusions and antibiotics to prevent cholangitis.