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Uveitis Case Reviews

This case review summarizes 3 uveitis cases: 1. A man with acute eye pain and decreased vision was found to have acute retinal necrosis (ARN) caused by HSV based on positive anterior chamber PCR. He was treated with antivirals. 2. A woman with recurrent eye pain, redness and decreased vision was diagnosed with toxoplasmosis chorioretinitis based on the appearance of her retina. 3. A woman with sudden vision loss after flu-like symptoms was found to have optic disc edema and a macular star exudate. Testing confirmed Bartonella henselae infection.

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0% found this document useful (0 votes)
13 views8 pages

Uveitis Case Reviews

This case review summarizes 3 uveitis cases: 1. A man with acute eye pain and decreased vision was found to have acute retinal necrosis (ARN) caused by HSV based on positive anterior chamber PCR. He was treated with antivirals. 2. A woman with recurrent eye pain, redness and decreased vision was diagnosed with toxoplasmosis chorioretinitis based on the appearance of her retina. 3. A woman with sudden vision loss after flu-like symptoms was found to have optic disc edema and a macular star exudate. Testing confirmed Bartonella henselae infection.

Uploaded by

Toma Babic
Copyright
© © All Rights Reserved
We take content rights seriously. If you suspect this is your content, claim it here.
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Download as PPTX, PDF, TXT or read online on Scribd
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Uveitis Case Reviews

Case # 1
A 49-year-old man complains of acute eye pain with decreased vision and photophobia.

1. What does the photo demonstrate?

2. What is the differential diagnosis?

3. What other findings would you look for on exam?

1. A well-defined area of retinal necrosis with retinal whitening and intraretinal


hemorrhages.

2. ARN, PORN, syphilis, CMV retinitis, toxoplasmosis, sclopoteria, lymphoma, sarcoidosis,


HORV; associated with intraocular vancomycin, and aminoglycoside toxicity.

3. Evidence of granulomatous anterior uveitis, vitritis, and retinal vasculitis.


4. What laboratory tests would be helpful?
Additional information: the anterior chamber PCR is positive for HSV, and the HIV test is negative.

5. What is the diagnosis?


6. What is the treatment?
7. What are the potential complications?

4. PCR testing of intraocular fluid is the most precise method to determine the cause of the viral retinitis: VZV, HSV, or, rarely, CMV, or EBV. Alternatively, blood testing for VZV and
HSV (type 1 and 2) immunoglobulin G and M (IgG and IgM) titers can be performed. The immune status should be obtained to verify whether the patient is immunocompetent because
it is important to differentiate ARN from PORN, which occurs in immunocompromised patients with minimal inflammation and vasculitis.
5. ARN

6. Immediately treat with antivirals since any delay in therapy can cause a dramatic increase in the retinitis. Typically, systemic acyclovir (IV until resolution of the retinitis, then oral
for 1–2 months); alternatively, if the lesions are more peripheral, then use oral therapy with valacyclovir instead of IV therapy. Ganciclovir is an alternative. It is important to follow
blood urea nitrogen and creatinine levels for nephrotoxicity. Both oral and topical steroids can be started after the patient begins to respond to prevent inflammatory complications.
Also treat with intravitreal foscarnet, follow closely for signs of regression, and if none seen additional injections may be required.

atients with ARN are at high risk of developing RRD with numerous holes and giant tears due to retinal necrosis. In addition, very careful observation of the fellow eye is important to rule out involvem
Case # 2
A 42-year-old woman reports pain, photophobia, redness, and decreased vision for 4 days. She recalls
having had a similar episode several years ago.

1. What finding is shown, and what is the diagnosis?

2. What is the differential diagnosis?


3. What other findings may be present?
4. How would you work up a patient with granulomatous uveitis?

1. This patient has large mutton-fat KP, which is a sign of granulomatous uveitis.

2. Syphilis, tuberculosis, leprosy, brucellosis, toxoplasmosis, Propionibacterium acnes chronic endophthalmitis, fungal
infection (Cryptococcus, Aspergillus), HIV, sarcoidosis, VKH syndrome, sympathetic ophthalmia, and a
phacoanaphylactic reaction.

3. Ciliary injection, anterior chamber cells and flare, hypopyon, iris nodules, rubeosis, synechiae, increased
or decreased IOP, cataract, pars planitis, optic nerve hyperemia, chorioretinitis, periphlebitis, and cystoid
macular edema.

mended to determine the cause of granulomatous uveitis in a patient with a negative history, review of systems, and medical examination. This includes CBC with differential, ESR, VDRL or RPR (syph
or indirect IFA for toxoplasma IgM and IgG titers, ACE (sarcoidosis), lysozyme.

rding to the patient's history including ANA, RF; juvenile idiopathic arthritis, ELISA for Lyme IgM and IgG, HIV antibody test, chest radiographs or CT scan (sarcoidosis, tuberculosis), sacroiliac radio

also be considered if the diagnosis is still unclear including HLA typing (HLA-A29: Birdshot chorioretinopathy), in the presence of vasculitis: ANCA (granulomatosis with polyarteritis, polyarteritis nod
circulating immune complexes (SLE, systemic vasculitides), complement proteins: C3, C4, total complement (SLE, cryoglobulinemia, glomerulonephritis), and soluble IL-2 receptor.
Additional information: the appearance of her retina is shown.

5. What is the diagnosis?

6. What is the treatment?

5. Toxoplasmosis chorioretinitis.

6. Topical steroids and cycloplegic are prescribed to treat the anterior inflammation. Systemic steroids are added for posterior pole lesions or those with intense inflammation.

Small peripheral lesions may be observed since they often heal spontaneously, especially in immunocompetent individuals. If a patient has decreased vision, moderate to severe vitreous
inflammation, or lesions that threaten the macula, papillomacular bundle, or optic nerve, he/she should be treated for 4–6 weeks with antibiotics that kill tachyzoites in the retina (note: they do
not affect cysts). Most patients respond well to trimethoprim–sulfamethoxazole (Bactrim). For aggressive lesions or posterior pole lesions, triple therapy can be considered with
pyrimethamine (Daraprim), folinic acid (leucovorin), and one of the following: sulfadiazine, clindamycin, clarithromycin, azithromycin, or atovaquone. Immunocompromised patients and
high-risk patients may require prophylactic treatment.
Case #3
A 28-year-old woman reports sudden vision loss in her left eye after having flu-like symptoms the week
before.
1. What findings are shown?
2. What is the differential diagnosis?
3. How would you work up this patient?

Additional information: laboratory testing is positive for B. henselae.

4. What is the diagnosis?

5. How would you treat this patient?

6. What is the prognosis?


1. Marked optic disc edema with disc hemorrhage and lipid exudation in a star shape.

2. The patient has a macular star exudate. Infectious etiologies to consider and rule out include B. henselae,
syphillis, Lyme disease, tuberculosis, tularemia, toxoplasmosis, viral retinitis (HSV, VZV, EBV), DUSN, and
toxocariasis. Noninfectious etiologies to consider include hypertensive retinopathy, diabetic retinopathy, AION,
retinal vein occlusion, acute macular neuroretinopathy, sarcoidosis, and papilledema.
3. Check blood pressure. Laboratory testing for VDRL or RPR, FTA-ABS or MHA-TP, PPD, and IFA for B. henselae.

initis, also known as Leber idiopathic stellate neuroretinitis, is due to a pleomorphic, Gram-negative bacillus called B. henselae (formerly known as Rochalimaea), which is associated with cat-scratch

guidelines given the self-limited nature of the disease and good prognosis. The use of systemic antibiotics (doxycycline, rifampin, tetracycline, ciprofloxacin, trimethoprim [Bactrim]) and steroids is co
immunocompetent patient is doxycycline for 2–4 weeks. For severe infections, IV doxycycline can be given along with rifampin.

≥ 20/20 vision, and 97% regaining > 20/40 vision. The disc edema resolves over 8–12 weeks, whereas the macular star takes longer, resolving over 6–12 months. Optic atrophy and retinal pigment epith
Case #4
A 50-year-old man presents with a recurrence of acute anterior uveitis and reports multiple episodes over the past
15 years. He denies any eye injury or surgery. Exam of the involved eye shows 20/40 vision, ciliary flush, 2+
anterior chamber cells and flare, hypopyon, fine keratic precipitates, and no vitreous cells.

1. What additional history would be helpful?

2. What other findings would you look for on exam?

3. What is the differential diagnosis?


Additional information: the patient has no significant past medical history. He denies ocular herpes. He has
eczema and occasional back pain, and he takes NSAIDs as needed. He travels internationally several times a year.
IOP and gonioscopy are normal.
4. What targeted workup would you order?
5. What disorders are associated with HLA-B27 iritis?
6. What is the treatment for this patient’s acute iritis?
7. What are the possible complications of iritis?

Past medical history, medication history, and review of systems with attention to joint pain, skin changes/rashes, infections, oral lesions, urethritis, genital ulcers, diarrhea, foreign travel, and conjunctivi

2. Increased IOP, corneal edema, corneal scarring, synechiae, iris color, iris atrophy, cataract, and CME.

is of nongranulomatous iritis is idiopathic, HLA-B27 associated, Fuchs heterochromic iridocyclitis, HSV, glaucomatocyclitic crisis (Posner–Schlossman syndrome), Lyme disease, Behçet disease, drug

is patient most likely has iritis associated with HLA-B27, so a targeted approach would be to order HLA-B27, sacroiliac X-ray, CBC with differential, urinalysis, VDRL or RPR, and FTA-ABS or MHA

5. Ankylosing spondylitis, reactive arthritis syndrome, psoriatic arthritis, inflammatory bowel disease, and Whipple disease.

6. Frequent topical steroids and cycloplegia. 7. Cataract, glaucoma, synechiae, band keratopathy, iris atrophy, CME.
Case # 5
A 68-year-old woman sees you 5 days after uncomplicated cataract surgery because her eye has become progressively
red and painful with blurry vision.

1. What is the diagnosis?

2. What are the most common organisms?

3. What are the risk factors?

4. What steps have been shown to reduce the risk of endophthalmitis?

5. What are the characteristic findings?

6. What are the EVS (Endophthalmitis Vitrectomy Study) treatment recommendations?

1. Acute postoperative endophthalmitis

of acute postoperative endophthalmitis is caused by Gram-positive bacteria: coagulase-negative staphylococci (70%), Staphylococcus aureus (10%), Streptococcus species (11%). Only 6% is due to Gra

3. Complicated surgery (prolonged surgical time, disrupted posterior capsule, vitreous loss, wound leak, iris prolapse), blepharitis, diabetes, immunosuppression.

on the ocular surface, barrier draping the eyelashes.Intraoperative: preservative-free antibiotics in irrigating solution (ie, vancomycin) or injected intracamerally at the conclusion of surgery (ie, cefurox

lid edema, proptosis, conjunctival injection, chemosis, wound abscess, corneal edema, keratic precipitates, anterior chamber cells and flare, hypopyon, vitritis, poor red reflex, and may have positive Se

d vitreous tap to collect specimens for culture, and intravitreal antibiotics (vancomycin and ceftazidime or amikacin). Also treat with subconjunctival (vancomycin and ceftazidime or gentamicin) and to
antibiotics and steroids, and a topical cycloplegic. Intravitreal steroids were not evaluated, and systemic antibiotics were not found to be beneficial.

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