Terson Syndrome Treatment & Management

Spontaneously clearing vitreous hemorrhage or small intraocular hemorrhage is most common. Elevated head positioning with bed rest and avoidance of anticoagulation medications (eg, aspirin, nonsteroidal anti-inflammatory drugs [NSAIDs], warfarin) may be helpful. Resolution of symptoms may take months. One study demonstrated an average of 9 months for the clearance of such hemorrhages.

A large vitreous hemorrhage may not clear spontaneously and may require a vitrectomy to facilitate clearing. In pediatric cases, the development of amblyopia is a consideration for early vitrectomy. A vitrectomy with possible epiretinal membrane peeling may be necessary for late complications (eg, macular pucker).

Perform a B-scan ultrasound examination.

Consult with a neurologist to approve of the patient's neurologic stability for surgery.

Intervention with a vitrectomy is rarely needed in most patients with Terson syndrome because of the spontaneous clearing of both the vitreous and the preretinal or subhyaloidal hemorrhage. Special consideration should be made for early intervention in those patients where amblyopia is concerned.

For long-standing vitreous hemorrhages of over 4- to 6-month duration without signs of progressive clearing, a core vitrectomy can be performed using the standard 3-port vitrectomy technique. In patients with loculated, nonclearing preretinal or subhyaloidal hemorrhage, the posterior hyaloid face can be incised and stripped away from the retinal surface with a bent microvitreoretinal (MVR) blade following a core vitrectomy.

The use of YAG laser photodisruption of the preretinal or posterior hyaloid membrane has been used for the treatment of subhyaloidal hemorrhages due to other mechanisms, but it is not recommended for patients with Terson syndrome because of the potential for the development of late-stage macular pucker or epiretinal membrane formation. This late complication of Terson syndrome is best addressed by posterior hyaloid membrane stripping using a bent MVR blade and excision of the peeled membrane with the vitrectomy instrument.

Avoid anticoagulation therapy.

Coordinate postoperative care with a neurologist.

The most common complication is the formation of epiretinal membranes, observed in 27-78% of patients with Terson syndrome. The subhyaloidal or subinternal limiting membrane space created by the intraocular hemorrhage may result in fibroblast or glial cell proliferation. The resulting macular pucker or epiretinal membrane formation may severely affect vision after the resolution of the hemorrhage and may become visually significant as late as 4 years after the resolution of the hemorrhage.

Other reported long-term complications include retinal pigment epithelium mottling, optic atrophy, macular holes, retinal folds, cystoid retinal changes, proliferative vitreoretinopathy, retinal detachment, and cataract formation.

Terson syndrome has been correlated significantly in several studies with elevated morbidity and mortality when compared with subarachnoid hemorrhage without intraocular bleeding. Vitreous hemorrhage is associated with a 3- to 9-fold higher rate of mortality in comparison to other sites of intraocular bleeding in Terson syndrome.

Patients able to survive the neurologic complications usually have a favorable visual prognosis. In a study of 30 patients with Terson syndrome, over 83% of patients achieved a long-term visual acuity better than 20/50 following observation or a vitrectomy.^[5] No statistical difference in final visual acuity was found between patients treated with observation or a vitrectomy.

The most common cause of persistent visual loss is epiretinal membrane formation as a late complication of Terson syndrome. A nonclearing vitreous hemorrhage in an infant may lead to amblyopia and warrants early vitrectomy.

Observation usually results in a favorable visual outcome for patients with Terson syndrome. Ophthalmic surgical intervention may be necessary to treat late complications (eg, macular epiretinal membranes). Immediate vitrectomy for intraocular hemorrhages is not recommended, except for patients with submacular hemorrhage, patients who are monocular with severe visual loss, or pediatric patients at risk for amblyopia.

The exact etiology of the mechanism of the intraocular blood remains to be elucidated definitively through histologic or experimental models.