Description: When viewing this fundus image (Fig 7.1), I see many noticeable microaneurysms, intraretinal hemorrhages, and several cotton-wool spots. This is concerning for ocular manifestations of an underlying systemic disease.

Differential Diagnosis: My working diagnosis for this patient is severe diabetic retinopathy with macular edema. My differential diagnosis would also include HIV retinopathy, hypertensive retinopathy, radiation retinopathy, central retinal vein occlusion, branch retinal vein occlusions, and cancer-associated retinopathy. If neovascularization is present, I would consider hypercoagulable states, inflammatory diseases, and sickle cell disease sequelae.

History: Given that this patient is obese, I would ask about a history of HTN, DM, and elevated lipids/cholesterol as well as how well controlled these diseases have been, if present. I would ask about his decline in vision and about symptoms associated with cataracts, presbyopia, and diabetic retinopathy.

Exam: I would initially check the patient’s blood pressure and blood sugar in my clinic. I expect to find the patient’s blood glucose to be elevated. On examination, I would look for any associated ocular manifestations of diabetes such as dry eyes, iris neovascularization, and early cataract formation. Because the patient’s findings are consistent with severe nonPDR, I expect to find similar findings in the contralateral eye.

Workup: The first test that I would perform is optical coherence tomography because it may reveal some form of diabetic macular edema. I would perform an intravenous fluorescein angiography to look for areas of capillary nonperfusion and neovascularization that may not have been obvious on dilated fundus examination. In addition, I would look for areas of leakage within the central macula. Based on the DRS and ETDRS, treatment for diabetic retinopathy depends on the presence of high-risk PDR or CSME.

Treatment: The treatment of PDR includes panretinal photocoagulation. The treatment for CSME includes grid or focal laser treatment. Recently, clinical trials have provided evidence that FDA-approved ranibizumab and aflibercept can treat diabetic macular edema and improve vision. I would also look at the DRCR.net studies to look for the most recent data on the treatment of diabetic retinopathy and diabetic macular edema to treat my patient accordingly. I would prefer treatments that are FDA approved and treatments that have better safety profiles for my patient.

Advice: I would discuss with this patient the natural history of diabetic retinopathy based on the diabetic control and complications trial (DCCT), which showed that patients with a HbA1c > 7.0% were 50% more likely to experience severe vision loss in 2 years than those with HbA1c below 7% with intensive insulin therapy. I would encourage such patients to aggressively manage their blood sugar, blood pressure, and cholesterol with their endocrinologist. A 1% reduction in HbA1c was associated with a 37% decrease in microvascular complications. I would also discuss the importance of regular exercise, a healthy diet, and medication compliance. Lastly, I would inform him that he is not a candidate for LASIK.

Follow-up: Because the patient has nonproliferative changes with macular, I would follow this patient closely in 1 month and begin treatment if patient reaches thresholds for treatment. When the patient’s condition stabilizes, I would follow the patient in 4- to 6-month intervals.

Description: Figures 7.2A and 7.2B reveal a fundus photograph and an optical coherence tomography of the right eye. My attention is drawn to a large red lesion temporal to the fovea. I see what appears to be retinal thickening, subretinal hemorrhage, and an associated gray to dark green lesion, most likely a choroidal neovascular membrane. Importantly, I also see drusen and areas of retinal pigment epithelial hyperpigmentation. On the OCT, I note the obvious submacular hemorrhage with retinal pigment abnormalities and subretinal fluid.

Differential Diagnosis: Given this presentation, my most likely diagnosis for this patient is proliferative age-related macular degeneration (ARMD). My differential diagnosis for a choroidal neovascularization membrane (CNVM) also includes macroaneurysm, old trauma with choroidal rupture, myopic degeneration, ocular histoplasmosis, macular dystrophies, and central serous chorioretinopathy (CSCR).

History: I would ask historical questions regarding the visual disturbance such as the following: Was it sudden or associated with any pain? Is it in a consistent location or does it move? I would also ask about a family history of blindness, age-related macular degeneration, smoking, and ocular trauma.

Exam: I would perform a complete dilated examination of both eyes. On funduscopy, I would look for elevation, thickening, and hemorrhages near the suspicious area. The slit lamp biomicroscopy with fundus contact lens would assist me to detect CNVM. The contralateral examination would also help me to determine the etiology. For example, the finding of drusen would add evidence to support my initial diagnosis.

Workup: I would also perform a fluorescein angiogram to look for evidence of a choroidal neovascular membrane with late hyperfluorescence and associated leakage. An OCT would also be helpful to identify fluid that may be under the retinal pigment epithelium (RPE), within the subretinal space, and/or within the retina.

Treatment: Treatment for proliferative ARMD has advanced significantly since the 1990s, and I would discuss the historical usage of photocoagulation therapy based on the macular photocoagulation study and the use of Visudyne with photodynamic therapy. Most importantly, I would state that intravitreal injections of anti-vascular endothelial growth factor (VEGF) agents such as ranibizumab have resulted in visual improvements in all angiographic subtypes of neovascular ARMD according to the Minimally classic/occult trial of the Anti-VEGF antibody Ranibizumab In the treatment of Neovascular AMD (MARINA) and ANti-VEGF antibody for the treatment of predominantly classic CHoroidal Neovascularization in AMD (ANCHOR) studies. From these studies, over 90% of patients lost <15 letters and about a third gained 15 letters of vision. Bevacizumab may be equally effective according to the Comparison of Age-related Macular Degeneration Treatment Trials study, but it is not an FDA-approved treatment of proliferative ARMD at the time of this writing. I would encourage initiation of treatments that are FDA approved in attempt to prevent progression into his central vision. In addition, I would encourage taking Age-Related Eye Disease Study 2 formula vitamins. This is a high-dose vitamin supplement, which was shown to slow the progression of ARMD in approximately one-third of patients with moderate or severe ARMD.

Advice: The major drawback to this treatment is the need for ongoing monthly clinical visits and intravitreal injections. I would discuss the natural history of proliferative ARMD. I would advise maintaining a nonsmoking lifestyle. Most importantly, close follow-up for life is indicated.

Follow-up: I would follow this patient closely in 3-4 weeks and, at each visit, measure the amount of retinal edema.

Description: This image (Fig 7.3) displays corneal edema, hypopyon, and exudative reaction over the implant surface in a patient 6 days post cataract surgery.

Differential Diagnosis: For this presentation, the number one differential diagnosis is an infectious postoperative endophthalmitis. Other causes of endophthalmitis in the postoperative period include postop uveitis and toxic anterior segment syndrome (TASS).

History: The most significant component of this history is the recent intraocular surgery. I would ask whether there were any complications of which she was aware. Does she have any underlying conditions increasing risk of infection such as blepharitis?

Exam: I would perform a complete ophthalmologic examination including a visual acuity assessment. In particular, I would be looking for any blepharitis as it is a nidus for infection. I would also be looking for any leaking wounds by performing a Seidel test. I would check intraocular pressure (IOP), and I would measure the amount of hypopyon and degree of anterior chamber inflammation.

Workup: Because my view is limited, I would perform B-scan to view the posterior fundus. I would perform anterior chamber paracentesis and vitreous aspiration and send them for cultures and sensitivities. In particular, I would consider the most common postoperative pathogenic organisms such as Staphylococcus epidermidis and S aureus. The culprit organism is frequently the patient’s own lid flora.

Treatment: In this case, I would start the patient on intravitreal broad-spectrum antibiotic such as vancomycin along with ceftazidime. I would also include topical fortified antibiotics, topical steroids, and atropine. I would also hospitalize the patient for close monitoring and daily follow-up visits. In addition, I would also plan for immediate pars plana vitrectomy if the patient’s condition worsens.

Follow-up: I would evaluate the patient every 12 hours, looking for pain relief as a sign of improvement. After discharge, I would have the patient follow up within 2-4 days and then weekly until resolution of endophthalmitis is certain.

Description: My attention is drawn in Figure 7.4 to the dark lesion located in the superior peripapillary region. The lesion appears to be deep under the vessels, and I note no evidence of elevation in this photograph. Also, I do not see breaks in Bruch membrane, orange pigment, or a sentinel vessel.