Hypoperfusion Retinopathy

Case in Point Hypoperfusion Retinopathy Gopita Patel, OD; and Andreea Chih, OD By identifying ocular manifestations of cardiovascular conditions, physicians can avoid potentially serious outcomes in patients. ardiovascular diseases are CASE REPORT lid apposition and mild cataracts in some of the most common A 71-year-old white male was re- both eyes but were otherwise unre- conditions found in the ge- ferred by his primary care physician markable (Figure 1). Dilated fun- C riatric population. Ocular (PCP) to the eye clinic for a routine dus examination revealed extensive manifestations of systemic cardiovas- comprehensive eye exam. The pa- hemorrhaging in the midperipheral cular conditions often are the initial tient reported that his current pro- retina of the right eye only (Figure presentation of the systemic disease. gressive lenses, prescribed 2 years 2). The left eye retina showed no Identifying these findings help reveal prior, were not strong enough at abnormalities. the underlying disease and prevent both distance and near, and that his At this point the patient declined more serious visual and systemic eyes often felt dry. The symptoms any additional symptoms, including complications or even death. were gradual in onset since his prior eye pain, headache, transient vision Hypoperfusion retinopathy can exam with no reported flashes, float- loss, jaw claudication, and stroke occur as an early manifestation of ers, loss of vision, headaches, or ocu- signs. A complete blood count and carotid occlusive disease. It results lar irritations. hemoglobin A1c (HbA1c) was ordered, from poor arterial perfusion pressure The patient’s medical history was and all findings were unremarkable secondary to significant or complete significant for morbid obesity, hyper- with no evidence of blood dyscrasia carotid artery blockage resulting in tension, borderline diabetes mellitus, and with a HbA1c of 6.0. A carotid ul- retinal changes. Atherosclerotic dis- and obstructive sleep apnea. His ocu- trasound (CUS) was also performed ease is generally the main culprit. lar history included recurrent con- and revealed severe narrowing of Early manifestations can be seen as junctivitis. At the time of the visit, the proximal section of the right in- midperipheral retinal hemorrhages, the patient’s medications included ternal carotid artery (ICA) with a dilated often nontortuous veins, and 81 mg aspirin, 10 mg benazepril, trickle flow (Figure 3). The peak sys- retinal neovascularization. Untreated 1,000 mg fish oil, 80 mg simvastatin, tolic velocity (PSV) at this level was or advanced cases of carotid occlu- and use of a continuous positive air- 508 cm/s. There also was severe nar- sive disease can lead to a more serious way pressure machine. rowing and turbulent flow in both ocular ischemic syndrome, which en- Best-corrected Snellen visual acu- the mid and distal portions of the compasses a panocular ischemia and ity was stable to his last eye exam right ICA. The patient was sent for a can result in severe vision loss and at 20/25+2 right eye and 20/25-1 left vascular evaluation 2 days following neovascular glaucoma. Restoration of eye with a manifest refraction of the CUS. arterial perfusion pressure is the main +2.25-0.75 × 077, and +2.75-1.25 × Based on the ocular findings and goal for managing this condition. 096 in the right and left eye, respec- CUS results, the diagnosis of hypo- tively. Pupils were equally round and perfusion retinopathy secondary to Dr. Patel was a primary care and ocular disease resident at the time this article was submitted, reactive to light with no afferent pu- carotid occlusive disease was made. and Dr. Chih is the residency in primary eye care pillary defect. Extraocular motility Because the patient was asymptom- program coordinator, both at William V. Chappell, and finger counting fields were unre- atic with no additional ocular se- Jr. VA Satellite Outpatient Clinic in Daytona Beach, Florida. Dr. Patel currently is an optometrist at the markable. Anterior segment evalu- quelae, he was scheduled for an eye Magruder Eye Institute in Orlando, Florida. ation revealed lax bilateral upper clinic follow-up in 2 months. The 42 • FEDERAL PRACTITIONER • APRIL 2017 www.fedprac.com electrocardiogram, chest X-ray, and Figure 1. Anterior Segment Photography Postdilation exercise stress test results were nega- tive for acute cardiopulmonary disease, ischemia, or arrhythmias. A computed tomography angiography was performed and confirmed a high-grade lesion of the right ICA of > 95%. The vascular surgeon reported an 11% risk of stroke within 5 years and a 1% risk of stroke with surgery. Based on these results the patient underwent a right carotid Left Right endarterectomy (CEA) 2 weeks later. A follow-up CUS was performed 1 month post-CEA and revealed no Figure 2. Right Eye Fundus Photograph abnormal fluid or significant plaque with a PSV of 92 cm/s (prior to sur- A B gery PSV was 508 cm/s) (Figure 3). The patient returned to the eye clinic 1 month after the CEA. Go- nioscopy revealed no neovascularization of the iris or angle and the dilated eye exam showed resolution of the midperipheral blot hemorrhages in his right eye with no evidence of retinal neovascularization. DISCUSSION Hypoperfusion retinopathy is char- acterized by posterior retinal changes A, Posterior pole. B, Midperipheral blot hemorrhages. secondary to chronic ocular ischemia from decreased arterial perfusion re- lated to significant or complete ca- presents before the age of 50 years, loss can occur from severe hypoper- rotid artery stenosis.1-5 Early literature with the average age of onset around fusion, creating an acute inner layer referred to this condition as venous 65 years.7 The exact rate of occur- retinal ischemia. This type of vision stasis retinopathy; however, this term rence is unknown as this condition loss often is accompanied by a cherry is misleading as the condition results often is underdiagnosed because it red spot in the macula and can be from a reduction in arterial perfusion mimics other vascular conditions, caused by an embolic plaque.1,8 Tran- pressure and the term describes ve- such as venous occlusive disease and sient vision loss (TVL) also can be nous outflow obstruction.6 The terms diabetic retinopathy.1,7 Patients can secondary to a plaque emboli or light carotid ischemic retinopathy, ischemic present asymptomatically where find- induced. Patients with light-induced oculopathy, and hypotensive retinopa- ings are incidental on a dilated eye TVL report poor to blurry vision or thy also have been used interchange- exam, or they may present with vi- prolonged after image when exposed ably when describing hypoperfusion sion loss that can be gradual, sudden, to bright lights. In theory when the retinopathy.6 or transient in nature.5,6,8 retina is exposed to light, there is an Incidence of hypoperfusion reti- Gradual vision loss can follow a increase in metabolic demand that is nopathy is twice as high in males as period of weeks to months and can unmet in those with choroidal vas- it is in females due to a higher prev- occur secondary to posterior isch- cular insufficiency from significant alence of cardiovascular disease.7 emia, macular edema, or choroidal carotid stenosis.3,8,10 Hypoperfusion retinopathy rarely hypoperfusion.1,3,8,9 Sudden vision The clinical presentation most www.fedprac.com APRIL 2017 • FEDERAL PRACTITIONER • 43 HYPOPERFUSION RETINOPATHY Figure 3. Carotid Ultrasound Doppler Image of the Proximal Right giography is commonly used to di- agnose and manage OIS, because it Internal Carotid Artery allows for the visualization of retinal A B and choroidal circulation and the de- tection of neovascular proliferation and ischemic areas. Diagnostic Imaging Several diagnostic testing strat- egies are available to evaluate for carotid occlusive disease. Carotid ultrasonography is a noninvasive, safe, and inexpensive screening tool to evaluate for high-grade stenosis. However, it can sometimes overestimate the degree of stenosis A, Before surgery with a peak systolic velocity of 508 cm/s. B, After surgery with a peak systolic and is not reliable with severe cal- velocity of 92 cm/s (left). cifications.8 Computed tomography angiography and magnetic reso- often is unilateral. Early stages of the genic factor release eventually leads nance angiography are minimally disease generally affect the midpe- to posterior neovascularization.1,2,5 invasive tools that can be used to ripheral retina but can be found in Further chronicity of carotid occlu- screen or confirm the degree of the posterior pole with chronicity. sive disease can create a panocular stenosis.8 These can be used in ad- Early findings include microaneu- ischemia that also involves anterior dition or instead of ultrasonogra- rysms, nerve fiber layer and inner ret- structures, including iris, conjunctiva, phy, especially in instances where inal layer hemorrhages, and dilated, episclera, or cornea. At this point, hy- patients have a short neck or high but generally not tortuous, veins.5 poperfusion retinopathy progresses to carotid bifurcation that may affect Chronic stage findings include arte- a more severe condition called ocular reliability. Both are contraindicated riolar narrowing, extreme venous di- ischemic syndrome (OIS).2,5 in those with renal failure as both lation, occasionally macular edema, Ocular ischemic syndrome can be modalities require the use of a con- and neovascularization of the disc associated with a 40% mortality rate trast dye. Magnetic resonance an- and or retina.5 Disc edema or collat- within 5 years of onset as it is gener- giography is far more expensive, erals usually are not present.5 ally found in those with overall poor time consuming, and not readily The mechanism behind hypoper- health.5 Along with posterior neo- available.8 Carotid angiography is fusion retinopathy results from an vascularization, anterior structures considered the gold standard for overall ischemic cascade and starts also are involved.

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