A 55-year-old patient came to the emergency department with visual acuity deficit (VA) in the right eye (OD).
The VA was 0.1 in RE and 1 in left eye with correction.
His personal history included right deep vein thrombosis 5 years ago and hypertension under treatment.
She had no known thrombotic family history.
Intraocular pressure, biomycosis and ocular motility were normal.
Hemorrhage of the right eye revealed peripapular flame, vascular tortuosity, cotton-wool exudate and macular edema.
Fluorescein angiography confirmed the presence of edematous central venous thrombosis.
The basic coagulation study showed high levels of tissue prothrombin (1.55 Uml), so a thrombophilia study was requested, which revealed increased resistance to activated protein c (1.5).
In the genetic analysis DNA fragments were amplified by PCR that included the nucleotides 1691 of the factor V gene and 20210 of factor II, subsequently performing an electrophoresis that identified the 1691 G mutation.
The rest of the study included complete blood count, sedimentation rate, general biochemistry and other causes of hypercoagulability (proteins S and C, antithrombin III, fibrinogen, antinuclear antibodies, homocysteinemia) and antibodies.
It was decided to anticoagulation the patient with acenocoumarol (sintrom®).
Photocoagulation was not required because the patient did not develop ischemia.
The VA of the OD was equal to or equal to 50 cm.
