A 55-year-old patient attended the emergency department with a visual acuity (VA) deficit in the right eye (RA). The VA was 0.1 in the OD and 1 in the left eye with correction.
His personal history included a deep vein thrombosis in the right leg 5 years earlier and arterial hypertension under treatment.
He had no known family history of thrombophilia.
Intraocular pressure, biomicroscopy and ocular motility were normal.
Ophthalmoscopy of the OD showed peripapillary flame haemorrhages, vascular tortuosity, cotton wool exudates and macular oedema. Fluorescein angiography confirmed the existence of an oedematous central venous thrombosis.
The basic coagulation study showed elevated tissue prothrombin levels (1.55 Uml) and a thrombophilia study was requested, which revealed increased resistance to activated protein c (1.5).
In the genetic analysis, DNA fragments including nucleotides 1691 of the factor V gene and 20210 of factor II were amplified by PCR, and electrophoresis subsequently identified the mutation 1691 G-A of factor V and 20210 G-A of factor II.
The rest of the study included haemogram, sedimentation rate, general biochemistry and other causes of hypercoagulability (proteins S and C, antithrombin III, fibrinogen, antinuclear antibodies, homocysteinemia and antiphospholipid antibodies) with no significant findings.
It was decided to anticoagulate the patient with acenocoumarol (sintrom®). From the ophthalmological point of view, he did not require photocoagulation, as he did not develop retinal ischaemia. The VA of the eye remained stabilised on finger counts at 50 cm.
