Bullous keratopathy, also known as pseudophakic bullous keratopathy (PBK), is a pathological condition in which small vesicles, or bullae, are formed in the cornea due to endothelial dysfunction. In a healthy cornea, endothelial cells keeps the tissue from excess fluid absorption, pumping it back into the aqueous humor. When affected by some reason, such as Fuchs dystrophy or a trauma during cataract removal, endothelial cells suffer mortality or damage. The corneal endothelial cells normally do not undergo mitotic cell division, and cell loss results in permanent loss of function. When endothelial cell counts drop too low, the pump starts failing to function and fluid moves anterior into the stroma and epithelium. The excess fluid precipitates swelling of the cornea. As fluid accumulates between the basal epithelium cells, blister like formations form (bullae) and they undergo painful ruptures releasing their fluid content to the surface. These characteristic malformations disrupt vision and create pain sensations. Symptoms
Disease begins with vesicles that coalesce. There is severe progressing edema and rupture may occur in 24 hours or less. Bullous keratopathy

Treatment
Treatment can include hyperosmotic eye drops to reduce swelling (5% sodium chloride), bandage contact lenses to reduce discomfort, glaucoma medications to reduce the flow of fluid into the cornea, and surgical procedures . The most common types of surgical treatment are Descemets stripping automated endothelial keratoplasty (DSAEK) and Descemets membrane endothelial keratoplasty (DMEK). Prognosis
Keratopathy is common in older people. Keratopathy occurs after cataract surgery, its incidence has decreased since the advent of intraoperative viscoelastic agents that protect the endothelium.
Transplanting hepatocytes was ineffective, but liver endothelial cells were effective.In the blood, it mainly circulates in a stable 
noncovalent complex with von Willebrand factor. Upon activation by thrombin (factor IIa), it dissociates from the complex to interact with factor IXa in the coagulation cascade. It is a cofactor to factor IXa in the activation of factor X, which, in turn, with its cofactor factor Va, activates more thrombin. Thrombin cleaves fibrinogen into fibrin which polymerizes and crosslinks (using factor XIII) into a blood clot. The factor VIII protein has a half-life of 12 hours in the blood stream when stabilized by the von Willebrand factor. No longer protected by vWF, activated FVIII is proteolytically inactivated in the process (most prominently by activated protein C and factor IXa) and quickly cleared from the blood stream. Factor VIII is not affected by liver disease. In fact, levels usually are elevated in such instances. Medical use
FVIII concentrated from donated blood plasma, or alternatively recombinant FVIIa can be given to hemophiliacs to restore hemostasis. Antibody formation to factor VIII can also be a major concern for patients receiving therapy against bleeding; the incidence of these inhibitors is dependent of various factors, including the factor VIII product itself. Immunostain target
Factor VIII related antigen is used as a target for immunohistochemistry, where endothelial cells, megakaryocytes, platelets and mast cells normally stain positive. Contamination scandal
In the 1980s, some pharmaceutical companies such as Baxter International and Bayer sparked controversy by continuing to sell contaminated factor VIII after new heat-treated versions were available.