- Normal portal pressure = 5 - 10 mmHg
- Portal hypertension is defined as a pressure > 12 mmHg
Aetiology
| Prehepatic |
Intrahepatic |
Posthepatic |
| Portal vein thrombosis |
Presinusoidal |
Caval abnormality |
| Splenic vein thrombosis |
Schistosomiasis |
Constrictive
pericarditis |
| Tropical splenomegaly |
Primary biliary
cirrhosis |
|
| Arterio-venous fistula |
Chronic active hepatitis |
|
|
Sarcoidosis |
|
|
Sinusoidal |
|
|
Cirrhosis - post
hepatitic, alcohol, cryptogenic, metabolic (e.g. Wilson's,
haemochromotosis) |
|
|
Non-cirrhotic -
cytotoxic drugs, Vitamin A intoxication |
|
|
Postsinusoidal |
|
|
Budd-Chiari syndrome |
|
|
Veno-occlusive disease |
|
Pathophysiology
- Increased portal pressure reduces portal venous flow
- Encourages development of porto-systemic anastomoses
- Develop at site of connections between portal and systemic
circulation
- Gastro-oesophageal junction
- Lower rectum
- Peri-umbilical veins
- Retroperitoneal veins of Retzius
- Peri-hepatic veins of Sappey
Clinical features
- Cirrhosis is commonest cause of portal hypertension in the UK
- Cirrhosis produces features of:
- Hepatocellular failure
- Portal hypertension
- Variceal bleeding
- Ascites
- 90% patients with cirrhosis will develop oesophageal varices
- Bleeding will occur in 30% of these patients
Severity of Cirrhosis
- Severity can be assessed using Child-Pugh classification
- Score 5-6 = Class A
- Score 7-9 = Class B
- Score > 10 = Class C
| Variable |
Score |
|
1 point |
2
points |
3 points |
| Encephalopathy |
Absent |
Mild
/ moderate |
Severe or coma |
| Bilirubin (μ
mol/l) |
<34 |
34-51 |
>51 |
| Albumin (g/l) |
>3.5 |
2.8-3.5 |
<2.8 |
| Prothrombin time (secs above normal) |
1-4 |
4-6 |
>6 |
Management
- In patients with known varices bleeding can be prevented by
β blockers
- Sclerotherapy does not prevent variceal bleeding
- The role of TIPS in primary prevention is at present unknown
Surgical shunts
- Portocaval shunts were commonly performed until the mid 1980s
- Aim is to reduce portal pressure
- Their use has decreased due to:
- The introduction of TIPS
- Liver transplantation in end stage liver disease
- Shunts can be total, partial or selective
- Role of shunts is to:
- Emergency control of variceal bleeding when no access to TIPS
- Reduce portal hypertension in patients awaiting transplantation
- Relieve intractable ascites
- Reduce bleeding from rectal, colonic or stomal varices
Total shunts
- Have wide diameter and decompress all of portal circulation
- There is no portal vein flow to the liver
- Over 90% long-term patency can be achieved
- 30-40% of patients will develop encephalopathy
- Examples of total shunts are:
- End-to-side portocaval shunt
- Side-to-side portocaval shunt
- Mesocaval C-graft
- Central splenorenal shunt
Partial shunts
- Have narrow diameter and partially decompress portal circulation
- Some portal vein flow is maintained
- Lesser procedure than total shunt
- 20% will either stenose or occlude
- 10% of patients will develop encephalopathy
- Examples of partial shunts are:
- Small bore portocaval H-graft
Selective shunts
- Decompress part of portal circulation
- Portal vein flow is maintained
- Examples of selective shunts are:
- Distal splenorenal shunt
- Distal splenocaval shunt
Bibliography
Henderson J M. Surgical treatment of portal hypertension.
Ballieres Best Pract Res Clin Gastroenterol 2000; 14:
911-925.
Menon K V, Kamath P S. Managing the complications of
cirrhosis. Mayo Clin Proc 2000; 75: 501-509.
Patel N H, Chalasani N, Jindal R M. Current status of
transjugular intrahepatic portosystemic shunt. Postgrad Med J
1998; 74: 716-720.
Samonakis D N, Triantos C K, Thalheimer U et al.
Management of portal hypertension. Postgrad Med J 2004;
80: 634-641. |