Elizabeth Chiang

Acute retinal necrosis secondary to varicella zoster virus in an immunosuppressed post-kidney transplant patient.

A woman, aged 42 years, presented to the ophthalmologist complaining of right eye redness, tearing, photosensitivity, and blurred vision of a 1-month duration. Her past medical history was significant for a kidney transplant for which she was immunosuppressed with mycophenolate mofetil 750 mg twice a day and prednisone 10 mg daily. Ophthalmologic examination of the right eye revealed visual acuity of 20/60, intraocular pressure of 16 mmHg, scleral injection, and a significant inflammatory reaction in the anterior chamber. Funduscopy revealed vitreous haze, optic nerve edema, arteriolar sheathing and attenuation, and peripheral 360° of retinal whitening – a clinical picture consistent with retinitis (figure 1). The left eye examination was entirely normal. Figure 1 (A) Examination of the fundus on day of presentation shows peripheral whitening and vasculitis as evidenced by optic nerve edema, vitreous haze, and retinal arteriolar narrowing. The decrease in clarity of the photograph is secondary to the vitreous haze, ... The differential diagnosis for retinitis in an immunocompromised host includes acute retinal necrosis (ARN), progressive outer retinal necrosis, cytomegalovirus (CMV) retinitis, and toxoplasmosis. Less common causes of acute retinitis include syphilis,1 Bechets disease, and lymphoma. Aqueous fluid obtained from the anterior chamber was sent for polymerase chain reaction (PCR) viral DNA analysis, and the patient was treated with 2 mg of ganciclovir injected intravitreally on the day of presentation. A 2-week course of renal-dose adjusted intravenous (IV) acyclovir was started with subsequent regression of the retinal whitening (figure 2). Varicella zoster virus (VZV) infection with a viral load of 6.5 × 107 IU was later confirmed with PCR of the aqueous fluid. The vision initially improved to 20/40 in the right eye. She was transitioned from IV acyclovir to oral valacyclovir. Figure 2 (A) After treatment with anti-viral medication, there is regression of retinal whitening and atrophic retinal tissue. (B) Areas of regression are indicated by white asterisks. The arterioles that previously were narrowed, indicated by the white arrows, ... Seven weeks later, the patient developed a rhegmatogenous retinal detachment that was diagnosed after she complained of an abrupt decrease in vision. Despite successful surgical reattachment of the retina with pars plana vitrectomy, scleral buckle, and silicon oil, the patients vision remained at light perception level only. Necrotizing herpetic retinopathies are caused by VZV, herpes simplex virus 1 and 2, CMV, and rarely, Epstein Barr virus. A spectrum of clinical presentations may occur depending on the virus and the hosts immunity.2 Immunosuppressed patients are at risk for development of necrotizing retinopathies typically associated with immunocompromised states, such as CMV retinitis and progressive outer retinal necrosis. They may also develop syndromes that are typically seen in immunocompetent hosts, such as ARN. Acute unilateral decrease in vision, photophobia, and eye pain are the usual presentations of ARN.3 The key feature seen on examination is white-yellow, multifocal, peripheral patches that later coalesce into diffuse areas of full-thickness, peripheral retinal necrosis.4 Other signs of ocular inflammation including vitritis, vasculitis, optic disc edema, keratic precipitates, and posterior synechiae may also be seen. Untreated ARN results in blindness from retinal scarring, retinal detachment, or optic atrophy; therefore, ARN is an ophthalmic emergency. One-third of patients develop the disease in the fellow eye within one month of presentation, if left untreated.5 The diagnosis of ARN is made on the basis of clinical appearance, and antiviral treatment should be initiated promptly. Timely referral to a uveitis or retina specialist experienced in the care of such patients and collaboration with an infectious disease specialist are essential.

Branch Retinal Artery Occlusion Caused by Toxoplasmosis in an Adolescent

Purpose: Branch retinal artery occlusion (BRAO), while not uncommon in elderly patient populations, is rare in children and adolescents. We report a case of a BRAO secondary to toxoplasmosis in this demographic. Case: A previously healthy 17-year-old male developed a unilateral BRAO in conjunction with inflammation and increased intraocular pressure. Family history was positive for cerebrovascular accidents in multiple family members at relatively young ages. The patient had a hypercoagulable workup as well as a cardiovascular workup which were both normal. A rheumatologic workup was unremarkable. By 3 weeks, a patch of retinitis was more easily distinguished from the BRAO and the diagnosis of ocular toxoplasmosis was made. Treatment was started with prednisone and azithromycin with subsequent improvement in vision. Toxoplasma antibody levels were elevated for IgG and negative for IgM, IgA, and IgE. The etiology of the BRAO was attributed to ocular toxoplasmosis. Conclusions: Vascular occlusions are rare in toxoplasmosis. This is the third case report of a BRAO in a patient in the pediatric population. The diagnosis of ocular toxoplasmosis should be considered in young patients with retinal artery occlusions associated with inflammation.

Does delayed repair of eyelid lacerations compromise outcome

We designed a study to determine if the repair of traumatic eyelid lacerations can be delayed to allow for the most appropriate setting and surgeon without increasing complications. We conducted a retrospective chart review of all eyelid lacerations treated by the Ophthalmology service at the Medical College of Wisconsin over a 38-month period and identified 143 patients. Of these, 92 (64.3%) were adults and 51 (35.7%) were children under 18 years of age. Males accounted for 92 of 143 patients (64.3%). One hundred eight cases (75.5%) were repaired in an operating room. Seventy-seven cases (53.8%) had canalicular system involvement. The median time from injury-to-repair was 16.5 h (mean, 33.1 h; range, 2–584 h). Ninety-five patients (66.4%) underwent repair b24 h after injury; 48 (33.6%) were repaired after 24 h. Patients repaired b24 h after injury were more likely to be younger (24.5 years vs. 32.0 years, p = 0.02), children under the age of 18 (45.2% vs. 16.7%, p b 0.01), less likely to have canalicular involvement (36.8% vs. 87.5%, p b 0.01) and less likely to be repaired in the operating room (64.2% vs. 98.0%, p b 0.01). There were 9 complications noted in follow up care, with 6 occurring in patients repaired within 24 h of injury (6.3%) and 3 occurring in patients repaired after 24 h (2.0%), which did not reach the level of statistical significance (p = 0.14). Complications included: ptosis (4), lid retraction (2), epithelial cyst (1), pyogenic granuloma (1) and eyelid deformity (1). No patient developed infection, chronic epiphora, or slit canaliculus. Three of the 4 cases

Unusual presentation of xanthogranuloma on the eyelid of an adult.

A 46-year-old man presented with an unusual papillary eyelid lesion in which histopathological study revealed a cutaneous xanthogranuloma. The clinical appearance was distinctively different from juvenile xanthogranuloma. There was no evidence of an infiltrative and orbital process consistent with adult orbital xanthogranulomatous disease. The histopathologic examination of the lesion revealed well-differentiated histiocytes with foamy cytoplasm. Immunohistochemistry stains were positive for CD163 and Factor XIIIa and negative for CD34, CD1A, CD117, and S100. The final histopathologic diagnosis was cutaneous xanthogranuloma.

Etiology of orbital fractures at a level I trauma center in a large metropolitan city

Background/Purpose: Orbital fractures are a common facial fracture managed by multiple surgical specialties. Methods: A retrospective review of the electronic medical records of patients (age, 18–85 years) presenting to Northwestern Memorial Hospital and Northwestern Medical Faculty Foundation in Chicago, IL, USA with International Classification of Diseases, Ninth Revision codes for facial fractures or CPT (Current Procedural Terminology) codes for orbital fracture repair. Results: A review of the electronic medical records identified 504 individual incidents of orbital fractures with available imaging for review. The most common location for an orbital fracture was a floor fracture (48.0%) followed by a medial wall fracture (25.2%). Left-sided orbital fractures were statistically significantly more common than right-sided orbital fractures (99% confidence interval). Orbital fractures were more prevalent in younger age groups. The mean patient age was 39.3 years. The most common cause of all orbital fractures was assault followed by falls. However, falls were the most common cause of orbital fractures in women and in patients aged 50 years and older. Evaluation by an ophthalmologist occurred in 62.8% of orbital fracture patients, and evaluation by a team comprising the facial trauma service (Otolar-yngology, Plastic Surgery, and Oral and Maxillofacial Surgery) occurred in 81.9% of orbital fracture patients. Conclusion: Assault was the largest cause of all orbital fractures, and occurred most commonly in young males. Assaulted patients were more likely to have left-sided fractures compared to nonassaulted patients. In patients aged 50 years and older, falls were the most common cause of orbital fractures.