A horse can live with laminitis for many years, and although a single episode of laminitis predisposes to further episodes, with good management and prompt treatment it is by no means the catastrophe sometimes supposed: most horses suffering an acute episode without pedal bone displacement make a complete functional recovery. Some countermeasures can be adopted for pasture based animals. Discovery of laminitis, either active or relatively stabilized, on an equine prepurchase exam typically downgrades the horses value, as the possibility of recurrence is a significant risk factor for the future performance of the horse. Several radiographic abnormalities can be judged to correlate with a worsened prognosis:

Increased degree of rotation of P3 relative to the dorsal hoof wall (rotation greater than 11.5 degrees has a poorer prognosis)
Increased founder distance, the vertical distance from the coronary band (seen with a radio-opaque marker) to the dorsoproximal aspect of P3 (distance greater than 15.2mm has a poorer prognosis)
Decreased sole depth
Sole penetration by P3

Treatment
In laminitis cases, a clear distinction must be made between the acute onset of a laminitis attack and a chronic situation. A chronic situation can be either stable or unstable. The difference between acute, chronic, stable, and unstable is of vital importance when choosing a treatment protocol. There is no cure for a laminitic episode and many go undetected. Initial treatment with cryotherapy and anti-inflammatory drugs may prevent mechanical breakdown if instituted immediately, but many cases are only detected after the initial microscopic damage has been done.
However, the majority of patients require further intervention. Milder forms of Budd–Chiari may be treated with surgical shunts to divert blood flow around the obstruction or the liver itself. Shunts must be placed early after diagnosis for best results. The TIPS is similar to a surgical shunt: it accomplishes the same goal but has a lower procedure-related mortality, a factor that has led to a growth in its popularity. If all the hepatic veins are blocked, the portal vein can be approached via the intrahepatic part of inferior vena cava, a procedure called DIPS (direct intrahepatic portocaval shunt). Patients with stenosis or vena caval obstruction may benefit from angioplasty. Limited studies on thrombolysis with direct infusion of urokinase and tissue plasminogen activator into the obstructed vein have shown moderate success in treating Budd–Chiari syndrome; however, it is not routinely attempted.Liver transplantation is an effective treatment for Budd–Chiari. It is generally reserved for patients with fulminant liver failure, failure of shunts, or progression of cirrhosis that reduces the life expectancy to one year. Long-term survival after a transplant ranges from 69 to 87%. The most common complications of transplants are rejection, arterial or venous thromboses, and bleeding due to the need for anticoagulants. Up to 10% of patients may have a recurrence of Budd–Chiari syndrome after the transplant. Prognosis
Several studies have attempted to predict the survival of patients with Budd–Chiari syndrome. In general, nearly 2/3 of patients with Budd–Chiari are alive at 10 years.