The heart and vessels are accessed via median sternotomy, and a cardiopulmonary bypass machine is used; as this machine needs its "circulation" to be filled with blood, a child will require a blood transfusion for this surgery. The procedure involves transecting both the aorta and pulmonary artery; the coronary arteries are then detached from the aorta and reattached to the neo-aorta, before "swapping" the upper portion of the aorta and pulmonary artery to the opposite arterial root. Including the anaesthesia and immediate post operative recovery, this surgery takes an average of approximately six to eight hours to complete. Some arterial switch recipients may present with post-operative pulmonary stenosis, which would then be repaired with angioplasty, pulmonary stenting via heart cath or median sternotomy, and/or xenograft. Atrial switch
In some cases, it is not possible to perform an arterial switch, either because of late diagnosis, sepsis, or a contraindicative coronary artery pattern. In the case of sepsis or late diagnosis, a delayed Arterial Switch can sometimes be made possible by PAB, which may also require a concomitant construction of an aortic-to-pulmonary artery shunt.When an arterial switch is impossible, an atrial switch will be attempted using either the Senning or Mustard procedure. Both methods involve creating a baffle to redirect red and blue blood flow to the appropriate artery. Since the late 1970s the Mustard procedure has been preferred.
Budd–Chiari syndrome is a very rare condition, affecting one in a million adults. The condition is caused by occlusion of the hepatic veins that drain the liver. It presents with the classical triad of abdominal pain, ascites, and liver enlargement. The formation of a blood clot within the hepatic veins can lead to Budd–Chiari syndrome. The syndrome can be fulminant, acute, chronic, or asymptomatic. Subacute presentation is the most common form. Signs and symptoms
The acute syndrome presents with rapidly progressive severe upper abdominal pain, yellow discoloration of the skin and whites of the eyes, liver enlargement, enlargement of the spleen, fluid accumulation within the peritoneal cavity, elevated liver enzymes, and eventually encephalopathy. The fulminant syndrome presents early with encephalopathy and ascites. Liver cell death and severe lactic acidosis may be present as well. Caudate lobe enlargement is often present. The majority of patients have a slower-onset form of Budd–Chiari syndrome. This can be painless. A system of venous collaterals may form around the occlusion which may be seen on imaging as a "spiders web". Patients may progress to cirrhosis and show the signs of liver failure.On the other hand, incidental finding of a silent, asymptomatic form may not be a cause for concern. Causes
The cause can be found in more than 80% of patients.