Venoocclusive disease

Presents clinically early post-transplant (usually within the first 14d). Pathophysiology poorly understood. Risk factors for severe VOD include: intensive conditioning regimens, pre-transplant hepatitis and second transplants. VOD is characterised by a triad of hepatomegaly, jaundice and ascites (resulting in rapid post-transplant weight gain) as a result of this. Commoner in allografts than autografts.

Diagnosis is largely clinical but may be supported by typical findings on Doppler ultrasound study of hepatic arterial and venous flows, or by elevated plasminogen activator inhibitor (PAI 1) levels. However, the only definitive diagnostic investigation is transjugular liver biopsy, the risks of which must be weighed against the importance of the information obtained.

There is no treatment currently universally accepted as effective prophylaxis.

Strategies include

• Heparin 100u/kg/d by continuous IVI.

328 • LMWH SC od or a prostaglandin E1 (PGE1) infusion.

No universally accepted effective treatment. The key is supportive therapy with management of fluid overload with spironolactone and frusemide while maintaining intravascular volume with albumin or plasma substitute. In severe VOD, infusion of TPA or PGE1 may be considered.

If thrombolysis required

• Ensure no active bleeding is occurring and keep platelets >20 x109/L.

• Give tissue-type plasminogen activator (Altaplase™).

- 10mg IV into central line over 30 minutes

- Then 40mg as IVI over next 60 minutes i.e. total dose of 50mg over 90 minutes

(5 doses proportionally for patients weighing <than 60kg).

• Give daily for 3 days minimum and assess against VOD parameters.

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