Floaters, while often benign, can also be a symptom of posterior uveitis
It happens to all of us every once in a while: During reading, watching television, viewing a concert, sporting event or something else, suddenly, an amorphous speck, commonly called a floater, slowly moves across our field of vision. And just as fast as it appears, it’s gone. The scenario described typically indicates the floater is benign. That said, floaters can be pathological, leading to such diagnoses as vitreous detachment, vitreous hemorrhage, retinal tears/detachments and, the subject of this month’s column, posterior uveitis.
To briefly review, posterior uveitis, also known as choroiditis, chorioretinitis and retinitis, is the inflammation of the choroid, retina and optic nerve, which can cause vision-threatening complications, such as glaucoma, cataract or retinal detachment and blindness. Posterior uveitis affects males and females in equal numbers, and most patients are between the ages of 20 and 60.
Here, I discuss, specifically, the broad spectrum of posterior uveitis, its diagnosis and treatment considerations, so we can increase the likelihood that these patients’ vision remains stable.
To arrive at a definitive diagnosis, optometrists should:
1. Take a detailed case history. The symptoms of posterior uveitis are floaters (as mentioned above), blurry vision or scotomas and photophobia. Additionally, posterior uveitis can be painless.
The causes of the condition are:
- Inflammatory: ankylosing spondylitis; Behcet’s syndrome; Kawasaki disease; lupus; multiple sclerosis; psoriasis; reactive arthritis; rheumatoid arthritis; sarcoidosis; ulcerative colitis; and Vogt-Koyanagi-Harada syndrome.
- Infectious: AIDS/HIV; Bartonella infection; cat-scratch disease; cytomegalovirus retinitis; endogenous endophthalmitis; herpetic disease; Lyme disease; Mycobacterium tuberculosis; syphilis and Toxoplasma gondii infection. One acronym O.D.s can use to remember the infectious causes of posterior uveitis is SSTTEEVE, with each letter representing Sarcoidosis, Syphilis, Toxoplasmosis, Tuberculosis, Endogenous Endophthalmitis, Virus and the final “E” for “et cetera.”
Of note: The most common cause (30% to 50%) of infectious choroiditis is Toxoplasma gondii, a single-cell, obligate, intracellular protozoan, reports the American Journal of Ophthalmology. Clinical findings include a focal necrotizing retinochoroiditis with intense vitreous haze, known as “headlight in the fog,” overlying the lesion. The lesion typically occurs at the border of a prior scar, however, it can occur de novo.
As the number of cases of syphilis is on the rise, according to the CDC, it should be considered high on the differential diagnosis of posterior uveitis. Typical presentations of syphilis are acute syphilitic posterior placoid chorioretinitis (yellowish placoid outer retinal lesions with varying degrees of vitreous inflammation) and syphilitic punctate inner retinitis (yellowish dewdrop-like inner retinal precipitates).
- Non-infectious: Acute posterior multifocal placoid pigment epitheliopathy; birdshot chorioretinopathy; geographic helicoid peripapillary choroidopathy; multifocal choroiditis; multiple evanescent white dot syndrome; ocular histoplasmosis; punctate inner choroidopathy; and serpiginous chorioretinopathy.
- Others: Leukemia; parasites/worms and prior episodes of ocular trauma (e.g. surgery).
2. Utilize diagnostic devices. Via dilated fundus examination, O.D.s should look for these signs of posterior uveitis: vitritis, snowballs (especially suggestive of sarcoidosis); retinal necrosis; focal, multiple or diffuse choroiditis; subretinal fibrosis; optic nerve head edema; retinal vasculitis; macular edema or choroidal neovascular membrane and optic nerve edema.
As a brief, yet related, aside, optometrists should document retinal and/or choroidal lesions, and monitor progression or regression of the disease with fundus photography. Also, because posterior uveitis can cause significant peripheral retina changes, ultra-widefield imaging is especially useful in capturing and monitoring peripheral retinal lesions.
B-scan ultrasound is useful in cases of posterior uveitis that have significant media haze (cataracts, severe vitritis or vitreous hemorrhage), precluding the adequate view of the posterior segment.
SD-OCT is an indispensable tool in aiding in establishing the diagnosis, localization of the lesions and monitoring the therapeutic response of posterior uveitis. Active vitritis can be detected as hyper reflective inflammatory cells in the vitreous. This is useful in detecting common posterior uveitis complications, including cystoid macular edema (CME), epiretinal membranes, subretinal fluid, secondary choroidal neovascularization (CNV) and inner/outer retinal and retinal pigment epithelium disruptions.
Enhanced-depth imaging (EDI)-OCT helps in the evaluation of choroidal lesions. Increased choroidal thickness has been noted in eyes that have posterior anterior uveitis. OCTA is valuable in aiding in the detection of abnormal vascular changes, including CNV and capillary non-perfusion that can occur in posterior uveitis.
Fundus autofluorescence is a great tool in confirming the activity of inflammation in cases, such as choroiditis, vasculitis, etc. HyperFAF is seen with the CME of active lesions, while retinal atrophy or atrophic, inactive lesion, and pigmented scars are observed as hypoFAF.
If the cause of the posterior uveitis is deemed infectious, based on the detailed case history and laboratory testing (blood work) for viruses, bacterias or syphilis, anti-infective medications must be prescribed along with a topical steroid and cycloplegic agents. A low-dose oral steroid should be started at least 48 hours to 72 hours after the start of anti-infective therapy.
Non-infectious posterior uveitis typically involves a course of oral steroids, which should be tapered over 4 weeks to 6 weeks, or based on clinical response to minimize rebound inflammation. In vision-threatening lesions, local steroid injections, implants and inserts may be needed to be effective or intravenous (IV) treatment in cases of optic nerve head involvement. Patients should be monitored closely (weekly or every three to four weeks) for resolution of inflammation and monitored for elevated IOP, due to prolonged steroid use. Patients with CNV should be treated with anti-VEGF therapy.
In patients with repeated recurrences, intolerance to systemic steroids or recalcitrant to therapy, immunosuppressives can be added with/without systemic steroids. Immunosuppressive options include antimetabolites, such as azathioprine, methotrexate or cyclosporine. Further, the immunomodulatory agent Humira (AbbVie), often referred to as a biologic, recently received FDA approval for the treatment of non-infectious posterior uveitis.
Given all the causes of posterior uveitis, it is imperative to manage it with the patient’s healthcare team, including the treating physician and retinal specialist. Additionally, O.D.s should educate patients about the disease and the importance of compliance to the prescribed treatment and related follow-up appointments. Finally, optometrists should advise patients on the recurrence of symptoms, such as possible worsening pain, decreased vision, floaters and/or photophobia.
A SPECK ISN’T ALWAYS JUST A SPECK
As is the case with cataracts, diabetes and retinal tears/detachments, among other vision-threatening conditions, floaters can be a sign of posterior uveitis as well. As a result, a careful history, examination and use of advanced diagnostic modalities are critical for accurate diagnosis. Timely treatment may greatly reduce the risk of long-term sight-threatening complications. OM