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An 89-year-old man with acute vision loss in the right eye
Digital Journal of Ophthalmology 2007
Volume 13, Number 6
February 10, 2007
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Annette Sims | University of South Florida Burton Goldstein | University of South Florida
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| Diagnosis and Discussion | Spontaneous choroidal hemorrhage has been described in patients using systemic anticoagulation such as coumadin, heparin and tissue plasminogen activator.(1) It can be assumed that a bleeding diathesis such as DIC, where bleeding is the predominant clinical manifestation, may result in choroidal hemorrhage as well. Although documented cases of spontaneous choroidal hemorrhage are rare, it has recently been reported by Yang et al. that other risk factors may include hypertension, advanced age, age related macular degeneration and generalized atherosclerosis.(2) Final vision in those patients was poor despite surgical choroidal drainage. The patient presented has met the profile of risk factors, and in addition he had a predisposing consumption coagulopathy that served as an inciting factor in frank choroidal bleeding. We cannot, however, rule out a choroidal neovascular membrane as a cause of the bleeding although extensive choroidal hemorrhage is often seen in the setting of anticoagulation.
DIC is caused by the excessive generation of thrombin leading to a cascade of reactions that occur in an unregulated fashion. Thrombin activates platelets and induces platelet aggregation. It also induces the release of tissue plasminogen activator (t-PA). Plasminogen is cleaved to release plasmin resulting in fibrinolysis in the normal coagulation cascade. In DIC, the excess thrombin subsequently results in vigorous fibrinolysis by excess plasmin activity, thereby resulting in concurrent excess of thrombosis and bleeding.(3)
Case reports in the literature have described histopathological descriptions of patients with known DIC having serous retinal detachment, thrombotic occlusion of choriocapillary vessels and hemorrhage within the choroid at time of autopsy. Cogan described the histopathological effects of DIC upon the choroids.(4) Characteristic similarities among the cases include thrombosis within the smaller choroidal vessels, organization over time by hyaline formation and endothelial proliferation, and hemorrhage into the choroid but not extending through Bruch’s membrane. The thromboses within the choriocapillaris result in hemorrhage into the choroid and serous exudation into the subretinal space. Endothelial proliferation described in one case suggested neovascularization as a result of a chronic process. These findings indicate that DIC compromises the structural integrity of the choroid and results in microscopic evidence of choroidal hemorrhage. Long term follow up of the above mentioned cases was impossible as they each died from their underlying disorder. We suggest that a patient with DIC for a prolonged period of time can have microscopic signs of DIC that may progress to gross hemorrhage over time.
A few underlying disorders known to initiate DIC include sepsis, malignancy, and mechanical tissue injury. Any of these disease entities may trigger the excess production of thrombin and plasmin resulting in a consumption coagulopathy. In the patient presented, this may include urinary tract infection, history of cancer and aortic aneurysm.(5) The clinical expression of DIC may vary from fulminant to subacute or chronic. Our patient did not present with the characteristic systemic presentation of fulminant DIC. Although the presentation can be variable, he did not present with common clinical findings such as petechiae and purpura, hypotension, or frank bleeding from unrelated sites prior to the choroidal hemorrhage. Based on clinical presentation our patient was thought to have had a subacute or chronic form of DIC, also known as compensated DIC. He responded to the recommended vitamin K as evidenced by the normalization of follow up serial labs. The blood tracking down his face and neck also resolved over time following vitamin K administration. We suggest that in the presence of a spontaneous choroidal hemorrhage, even in the absence of other end organ damage, it may be advantageous to consider a bleeding diathesis such as DIC as a potential etiology of the bleeding.
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