Woman experiences acute eye redness and dark vision

The slit lamp showed 360° conjunctival injection in the left eye and a 1.5-mm layered hyphema in the left anterior chamber.

Mark E. Patron

Andre J. Witkin

A 62-year-old woman with a history of Graves’ disease and thyroid ophthalmopathy noted an acute onset of left eye redness upon waking. During the day, the redness continued to get worse and was accompanied by pressure pain behind the left eye. She also noted that her left eye appeared larger than previously when looking in a mirror. While working later that night, she bent down to pick up an object and noted an acute darkness come over her left eye upon standing. The dark vision lasted a few minutes before slowly becoming lighter; however, her left eye vision did not return to normal, and she presented to the emergency room shortly after.

The patient’s medical history was significant for hypercholesterolemia and a 10-year history of deep vein thrombosis, for which she was on Coumadin (warfarin, Bristol-Myers Squibb) 5 mg daily.

Examination

On examination, the patient’s best corrected visual acuity in both eyes was 20/25. Her left pupil measured 2 mm compared with 3 mm in her right pupil, but both eyes reacted equally, and there was no afferent pupillary defect. Her extraocular movements were full with no diplopia in all cardinal gazes. IOPs were 10 mm Hg in the right eye and 18 mm Hg in the left eye. There was 4-mm proptosis on the left side, and lid lag was elicited on the left upper eyelid.

Figure 1. Acute onset of left-sided proptosis (above). Spontaneous hyphema and conjunctival injection of the left eye (below). Images: Chen J, Krishnan C

Slit lamp examination showed 360° conjunctival injection of the left eye and a 1.5-mm layered hyphema in the left anterior chamber with 3+ pigmented cells (Figure 1). No iris abnormalities were present, and no abnormal iris vessels were seen. Gonioscopy was unremarkable, and dilated fundus examination demonstrated normal vessels, maculae and optic discs.

Blood work revealed an INR of 2.7. The patient reported that she had recent fluctuations in her INR level; prior to presentation, her last INR 2 weeks before was 4.5, prompting her primary care physician to reduce her Coumadin dose from 7 mg to 5 mg daily.

What is your diagnosis?

Spontaneous hyphema on anticoagulation therapy

Coumadin and other anticoagulants have been reported in the literature to be linked to spontaneous bleeding into the anterior chamber. Most of these cases involve anticoagulation accompanied by abnormal iris vessels such as neovascular tufts, although there are reports of cases involving normal, non-operated eyes. It is possible that this patient may have had subclinical neovascularization, which could have been demonstrated by iris fluorescein angiography, but the patient did not show any evidence of diabetes in her blood work or vessel occlusive disease, nor did the patient show any structural iris abnormalities on exam.

A discussion was generated with the primary care doctor as to how best to proceed. Given that the patient’s INR level was within the targeted range (INR 2 to 3), a decision was made to watch the patient overnight, without adjusting the Coumadin dose. The patient was placed on prednisolone, cyclopentolate and timolol to the left eye. Hyphema precautions were discussed, and an eye shield was placed. CT scan of the orbits with contrast was ordered and showed rectus muscle thickening and left-sided proptosis consistent with thyroid ophthalmopathy (Figure 2).

Figure 2. Coronal CT image showing enlarged rectus muscles of the left eye with an enlarged superior ophthalmic vein.

The following day, the layered hyphema was no longer present, although a microhyphema was still present. The IOP was 10 mm Hg in the left eye. Over the course of the next 10 days, the patient was seen daily, and the drops were tapered accordingly. A week later, her vision improved to 20/20 in the left eye, the anterior chamber cell and conjunctival injection were no longer present, and the IOP in her left eye remained normal after timolol was discontinued.

Discussion

The most common causes for spontaneous hyphema are iris abnormalities such as neovascular tufts, microhemangiomas, tumors and persistent pupillary membranes. Other ocular causes such as pseudoexfoliation syndrome, uveitis-glaucoma-hyphema syndrome and acute angle-closure glaucoma as well as systemic conditions such as lymphoma and juvenile xanthogranuloma have also been implicated in nontraumatic hyphemas.

Anticoagulants such as Coumadin, aspirin and even ginkgo have been linked with spontaneous hyphemas. Cases involving Coumadin therapy are usually associated with an INR of 5 or greater. It is interesting that the patient’s INR was 2.7, putting her at a lower risk for bleeding. However, increased venous pressure from straining, coughing or bending over, as well as increased episcleral venous pressure from such conditions as thyroid eye disease and dural shunts, can increase the chance of hemorrhages. It is possible that the anticoagulation, combined with elevated episcleral venous pressure induced by the thyroid ophthalmopathy and the patient’s bending, caused spontaneous bleeding into the anterior chamber.

Although spontaneous hyphemas are still a rare occurrence in patients on Coumadin therapy, they are not benign conditions, and patients on anticoagulation should be seen immediately by an ophthalmologist if they notice any acute change in their vision.

References:

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• John Chen, MD, and Chandrasekharan Krishnan, MD, can be reached at New England Eye Center, Tufts University School of Medicine, 750 Washington St., Box 450, Boston, MA 02111; 617-636-4219; fax: 617-636-4866; Web site: www.neec.com.

• Edited by Mark E. Patron, MD, and Andre J. Witkin, MD. Drs. Patron and Witkin can be reached at New England Eye Center, Tufts University School of Medicine, 750 Washington St., Box 450, Boston, MA 02111; 617-636-4219; fax: 617-636-4866; Web site: www.neec.com.