CMV Retinitis Clinical Presentation

  • Author: Michael Altaweel, MD, FRCS(C); Chief Editor: Hampton Roy Sr, MD   more...
 
Updated: Jan 28, 2010
 

History

Presenting symptoms vary depending on the location of retinal involvement. Posterior lesions present with diminished visual acuity. More peripheral lesions initially can be asymptomatic. Floaters often are noted if significant vitreitis is present. The eye usually is white and quiet.

  • Active CMV retinitis usually is found in conjunction with immunosuppression, whether from AIDS, leukemia, or use of chemotherapy. These points are important in evaluating the patient history. Rarely, CMV retinitis is the first presenting manifestation of AIDS.
  • Natural history
    • CMV retinitis is a slowly progressive disease, requiring weeks to months to involve the entire retina.[21, 22] Vision is lost with involvement of the posterior pole (macula or optic nerve) or retinal detachment.[23]
    • Initial reports described CMV retinitis as an end-stage disease, which indicated a life expectancy of 6 weeks. With the use of antiviral medications, the average survival after diagnosis ranged from 5.5-8 months. The advent of HAART has prolonged survival to years in some instances, and it has allowed discontinuation of medications targeted against CMV retinitis if clinical resolution occurs and the immune status recovers (reflected by a CD4 count of >100 cells/mL).
  • After initiation of therapy, some advance of the leading edge of retinitis may be noted. This usually is not a treatment failure but rather the revealing of an area of subclinical infection that was not previously evident.
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Physical

Patients with suspected CMV retinitis should have a complete ocular examination of both eyes. A careful examination should include the following:

  • Carefully check and record the patient's best corrected visual acuity as a baseline. Check for visual field defects that could represent optic nerve damage, retinal detachment (RD), or CNS disease from AIDS-related brain diseases (eg, encephalitis, stroke, CNS lymphoma).[24, 25] Ocular motility should be assessed as part of a cranial nerve examination. Pupils should be checked for a relative afferent pupillary defect indicating optic nerve involvement.
  • External examination of the lids and adnexa should be performed for other AIDS-associated findings, such as Kaposi sarcoma or lymphoma.
  • A thorough slit lamp examination should show a white and quiet conjunctiva. A red hot eye in an immunocompromised patient should alert the clinician to another possible diagnosis. Fine, stellate keratitic precipitates (KP) characteristic of CMV may be seen on the corneal endothelium.[26] Uveitis may be present in the anterior chamber and, if severe, may require treatment. The level of vitreitis can be assessed in the anterior vitreous and may be important for monitoring response to treatment or the occurrence of IRU.
  • A dilated fundus examination with indirect ophthalmoscopy is essential for assessing the location and extent of retinal involvement as well as for evaluating for retinal breaks or detachment. Retinal lesions have several characteristics,[27, 28] as follows:
    • Initial examination typically reveals 1 or 2 foci of disease. Multifocal disease at time of presentation is uncommon.
    • Most early lesions occur in a perivascular distribution, likely reflecting the hematogenous spread of the virus.
    • Lesions that present posteriorly appear along retinal vessels as large areas of thick white infiltrate accompanied by retinal hemorrhage described as "pizza pie" or "cheese pizza" in appearance.
    • The peripheral type of lesion demonstrates a more granular appearance with satellite lesions and less hemorrhage. Behind the advancing border is necrotic retina with mottled pigmentation from hyperplasia of the retinal pigment epithelium (RPE).
    • Lesions usually begin peripherally and spread posteriorly in a contiguous fashion (see image below). However, multiple unconnected lesions are frequent, and involvement of the posterior pole with minimal peripheral disease is possible (5-10%). Retinitis typically starts in the midperiphery andRetinitis typically starts in the midperiphery and can progress in a "brush fire" pattern.
    • Retinitis follows the nerve fiber layer.
    • Retinitis produces wide areas of necrosis, scarring, and atrophy (see image below). Early necrosis at periphery. Early necrosis at periphery.
    • Even severe retinitis is usually accompanied by minimal vitreitis in the immunocompromised patient. If HAART is instituted and immune reconstitution occurs, then IRU with severe anterior and posterior uveitis may occur.
    • Extensive vascular sheathing, often described as frosted branch angiitis, is a known but uncommon appearance (see image below).[29, 30] Frosted branch angiitis. Frosted branch angiitis.
    • Retinal vascular occlusion/nonperfusion can be seen on fluorescein angiogram.[31]
  • Peripheral holes and tears frequently occur in areas of necrosis (see image below). Retinal detachment due to peripheral tear in area Retinal detachment due to peripheral tear in area of necrosis.
  • Rate of progression of untreated retinitis is 250-350 µm per week. Skip lesions can occur.
  • Serial examinations may be necessary at early stages to distinguish CMV retinitis from HIV retinopathy with multiple cotton-wool spots.
  • Optic neuritis can develop without apparent retinitis.[32]
  • Most patients with CMV retinitis will initially present with unilateral disease. Untreated, the immunocompromised patient has a 50% risk of developing disease in the contralateral eye within 6 months.[33, 34] This is reduced to 20% with antiviral treatment and further reduced with HAART.
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Causes

Any immunosuppression due to disease or medication may allow clinical CMV infection to develop.

  • Acquired immune deficiency syndrome[35]
  • Leukemia, lymphoma, and aplastic anemia[36]
  • Use of immunosuppressive chemotherapy
  • Organ transplant recipients

Congenital CMV retinitis is acquired from vertical transmission during pregnancy. When primary maternal infection occurs during pregnancy, the risk of transmission to the fetus ranges between 30% and 40%. Transmission during the first half of pregnancy generally causes more severe disease.

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Contributor Information and Disclosures
Author

Michael Altaweel, MD, FRCS(C)  Associate Professor, Department of Ophthalmology and Visual Sciences, University of Wisconsin School of Medicine and Public Health

Michael Altaweel, MD, FRCS(C) is a member of the following medical societies: American Academy of Ophthalmology and Association for Research in Vision and Ophthalmology

Disclosure: Nothing to disclose.

Coauthor(s)

Peter N Youssef, MD  Vitreoretinal Fellow, Department of Ophthalmology and Visual Sciences, University of Wisconsin School of Medicine and Public Health

Disclosure: Nothing to disclose.

Matthew D Reed, MD  Fellow, Department of Ophthalmology and Visual Sciences, University of Wisconsin Clinical Science Center

Disclosure: Nothing to disclose.

Specialty Editor Board

V Al Pakalnis, MD, PhD  Professor of Ophthalmology, University of South Carolina School of Medicine; Chief of Ophthalmology, Dorn Veterans Affairs Medical Center

V Al Pakalnis, MD, PhD is a member of the following medical societies: American Academy of Ophthalmology, American College of Surgeons, and South Carolina Medical Association

Disclosure: Nothing to disclose.

Simon K Law, MD, PharmD  Associate Professor of Ophthalmology, Jules Stein Eye Institute, University of California, Los Angeles, David Geffen School of Medicine

Simon K Law, MD, PharmD is a member of the following medical societies: American Academy of Ophthalmology, American Glaucoma Society, and Association for Research in Vision and Ophthalmology

Disclosure: Nothing to disclose.

Steve Charles, MD  Director of Charles Retina Institute; Clinical Professor, Department of Ophthalmology, University of Tennessee College of Medicine; Adjunct Professor of Ophthalmology, Columbia College of Physicians and Surgeons; Clinical Professor Ophthalmology, Chinese University of Hong Kong

Steve Charles, MD is a member of the following medical societies: American Academy of Ophthalmology, American Society of Retina Specialists, Club Jules Gonin, Macula Society, and Retina Society

Disclosure: Alcon Laboratories Consulting fee Consulting; OptiMedica Ownership interest Other; Topcon Medical Lasers Consulting fee Consulting

Lance L Brown, OD, MD  Ophthalmologist, Affiliated With Freeman Hospital and St John's Hospital, Regional Eye Center, Joplin, Missouri

Disclosure: Nothing to disclose.

Chief Editor

Hampton Roy Sr, MD  Associate Clinical Professor, Department of Ophthalmology, University of Arkansas for Medical Sciences

Hampton Roy Sr, MD is a member of the following medical societies: American Academy of Ophthalmology, American College of Surgeons, and Pan-American Association of Ophthalmology

Disclosure: Nothing to disclose.

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White granular retinitis with intraretinal hemorrhage.
Early necrosis at periphery.
Attenuation of vessels in area affected by retinitis.
Retinitis typically starts in the midperiphery and can progress in a "brush fire" pattern.
Progression of retinitis toward the optic nerve.
Frosted branch angiitis.
Inactive cytomegalovirus retinitis.
Cytomegalovirus papillitis.
Intranuclear inclusions (arrows) found in cytomegalovirus retinitis. Referred to as owl's eye because of the dark intranuclear inclusion surrounded by a clear halo.
Retinal detachment due to peripheral tear in area of necrosis.
 
 
 
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