Budd-Chiari Syndrome
The eponymous name for hepatic vein occlusion. Typically caused by a thrombus but can also be secondary to infiltration by a tumour.
The classic triad includes right upper quadrant pain, ascites and hepatomegaly. The clinical features are summarised in Table 3.
| Clinical feature | Additional notes |
|---|---|
| Abdominal pain | Typically sudden onset and severe. Usually in the right upper quadrant but can be epigastric. |
| Liver enlargement | The hepatomegaly is usually tender. The differential for tender hepatomegaly includes right-sided heart failure and constrictive pericarditis, which similarly lead to hepatic congestion. |
| Ascites | May present as abdominal distension. Serum-ascites albumin gradient (SAAG) would reveal a transudate (>11g/L). |
| Portal hypertension | If left unchecked, can lead to complications such as acute variceal bleeding. |
| Hepatocyte damage | Leads to a transaminitis, with raised ALT and AST. Can rarely lead to fulminant, acute, subacute or chronic liver failure, or can cause decompensation of existing chronic liver disease. Liver cirrhosis is a possibility with ongoing hepatocyte destruction and subsequent fibrosis. |
Table 3: Features of Budd-Chiari syndrome
Budd-Chiari syndrome is exceptionally rare in the absence of a procoagulant condition, and its presence should trigger investigation for the cause of hypercoagulability. A rarer alternative is the direct extension of a tumour mass into the hepatic vein. The causes are shown in Table 2.
| Hypercoagulable state | Tumour infiltration |
|---|---|
| Polycythaemia rubra vera or other primary myeloproliferative disorders | Kidney tumour |
| Thrombophilia: factor V Leiden, protein C or S deficiency, antithrombin III deficiency | Hepatic tumour |
| Pregnancy | Adrenal tumour |
| Combined oral contraceptive pill | |
| Paroxysmal nocturnal haemoglobinuria | |
| Antiphospholipid syndrome |
Table 4: Causes of Budd-Chiari syndrome
If Budd-Chiari syndrome is suspected, the initial radiological investigation is typically ultrasound with doppler flow studies, which is highly sensitive for hepatic vein occlusion. An alternative is a CT with contrast, for which hypertrophy of the caudate lobe is a characteristic sign (highly specific but only seen in ~50% of cases).
The management is variable and will typically be made by the hepatology team. Lifelong anticoagulation is often required, though this may be contraindicated with concurrent oesophageal varices. The occlusion may need to be bypassed with a surgical shunt or a transjugular intrahepatic portosystemic shunt (TIPSS). If fulminant liver failure is present, the patient may be eligible for a liver transplant.
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