ACUTE RETINAL NECROSIS AFTER INTRAVITREAL DEXAMETHASONE IMPLANT. A CASE REPORT.

INTRODUCTION: Ozurdex® (Allergan Pharmaceuticals, Castlebar Road, Westport, Ireland) is an intravitreal implant containing 0.7 mg of dexamethasone. It is indicated in adult patients for the treatment of diabetic macular edema, cystoid macular edema due to central retinal vein occlusion, and in patients with non-infectious uveitis. Common complications after Ozurdex® administration include an increase in intraocular pressure, cataract progression or conjunctival suffusion. Acute retinal necrosis after Ozurdex® administration is a very rare and serious complication. According to our current research, this is the fourth published case. Extreme caution must be exercised when treating immunosuppressed patients with Ozurdex®. CASE REPORT: This is case report about an immunosuppressed 68-year-old patient with diabetic macular edema, who developed acute retinal necrosis 74 days after Ozurdex® implantation. He suffers from chronic myeloid leukemia and takes the cytostatic imatinib 400 mg once per day. Urgent pars plana vitrectomy (PPV) with silicone oil instillation was performed and antiherpetic drugs were initiated intravenously. Serological examination confirmed an active infection of cytomegalovirus etiology (CMV). CONCLUSION: Acute retinal necrosis is a rare necrotizing retinitis. Corticosteroids administered intravitreally reduce the local immune response, which may cause a primary infection or reactivation of a latent viral infection.

Acute Retinal Necrosis from Reactivation of Varicella Zoster Virus following BNT162b2 mRNA COVID-19 Vaccination.

PURPOSE: To report a case of acute retinal necrosis (ARN) due to varicella zoster virus (VZV) after COVID-19 vaccine administration. DESIGN/METHODS: Observational case report. RESULT: A 62-year-old immunocompetent African American male presented with left eye redness, decreased vision, and floaters after receiving a COVID-19 vaccine seven days prior. Slit-lamp examination revealed diffuse fine endothelial keratic precipitates. Funduscopic examination was notable for vitreous cells, occlusive retinal vasculitis, large retinal hemorrhages, and three quadrants of peripheral areas of retinal whitening. Quantitative polymerase chain reaction testing was positive for varicella zoster virus in the vitreous humor. Treatment with intravitreal and intravenous antiviral therapy resulted in symptomatic improvement. CONCLUSION: COVID-19 mRNA vaccination may cause an immunomodulatory response that leads to reactivation of dormant VZV. Early recognition and treatment can improve visual outcomes.

Bilateral acute retinal necrosis during treatment with alemtuzumab for multiple sclerosis.

INTRODUCTION: Alemtuzumab is a humanized monoclonal antibody used as a treatment of multiple sclerosis (MS) and chronic lymphocytic leukemia. It decreases T cell count leading to significant immunosuppression, with increased risk of systemic and ocular infections. Herein, we report a unique case of bilateral acute retinal necrosis (ARN) caused by varicella-zoster virus (VZV) in a patient affected by MS under treatment with alemtuzumab. CASE DESCRIPTION: A 36-year-old man with a relapsing-remitting MS under treatment with alemtuzumab developed bilateral visual loss. Anterior segment examination displayed granulomatous keratic precipitates and 3+ cells in the anterior chamber, while fundoscopy showed bilateral 1+ vitritis and peripheral retinal necrosis, complicated by retinal detachment in the left eye. The high viral load for VZV in aqueous humor samples had a univocal interpretation for viral reactivation. In addition to systemic therapy with acyclovir, the patient was treated with bilateral intravitreal injections of foscarnet and underwent pars-plana vitrectomy and silicone oil tamponade for retinal detachment in the left eye. CONCLUSION: This report shows a unique case of bilateral ARN caused by VZV associated with alemtuzumab. Any visual loss in MS patients under biologic therapy should not be underestimated, performing an accurate differential diagnosis with optic neuritis.

Acute retinal necrosis caused by co-infection with multiple viruses in a natalizumab-treated patient: a case report and brief review of literature.

BACKGROUND: Acute retinal necrosis is considered a rare infectious uveitis. This condition is usually caused by varicella-zoster virus or herpes simplex virus. Acute retinal necrosis caused by co-infection with multiple viruses is extremely rare. Herein, we report a case of acute retinal necrosis caused by co-infection with herpes simplex virus (type I and II) and varicella-zoster virus (VZV) in a natalizumab-treated patient due to multiple sclerosis. CASE PRESENTATION: An adult man presented with a complaint of decreased vision of the right eye from 12 days ago. He was a known case of multiple sclerosis receiving natalizumab. Examination of the right eye revealed severe conjunctival injection, fine diffuse keratic precipitates, 3 + anterior chamber and vitreous cells, elevated intraocular pressure (26 mmHg), a blurred optic disk with hemorrhagic patches, and occlusive vasculitis plus confluent necrotizing patches in the peripheral retina compatible with diagnosis of acute retinal necrosis. He underwent anterior chamber and vitreous tap, and real-time PCR detected HSV I & II and VZV on the vitreous specimen. A second PCR showed the same result. After neurological consultation, natalizumab was discontinued and intravenous acyclovir was started followed by oral acyclovir and oral prednisolone to control the disease, which was successful. CONCLUSIONS: Although rare, multiple-viral infection should be considered in the physiopathology of acute retinal necrosis, especially in immunosuppressed patients.

Varicella zoster-associated acute retinal necrosis and central nervous system complications in natalizumab treated MS patients.

There is not much awareness of varicella zoster virus (VZV) associated central nervous system (CNS) infections under treatment with natalizumab. Here we describe two natalizumab treated MS patients who developed acute retinal necrosis combined with CNS vasculitis caused by VZV. In natalizumab treated patients, visual symptoms atypical of optic neuritis should be promptly evaluated by an ophthalmologist. Currently, a total of 12 cases of natalizumab-associated VZV CNS or retinal infections are reported in literature. Our two cases and overview of currently available data provide information on prognosis and treatment decisions of this rare but devastating complication.

Acute retinal necrosis following dexamethasone intravitreal implant (Ozurdex®) administration in an immunocompetent adult with a history of HSV encephalitis: a case report.

BACKGROUND: Dexamethasone intravitreal implants (0.7 mg) (Ozurdex®, Allergan Inc., Madison, NJ) are FDA approved for managing macular oedema (ME) of retinal vein occlusion (RVO). The major complications associated with intravitreal Ozurdex® implant include increased intraocular pressure and cataract progression. In regard to the occurrence of retinal complications, we report an unusual intravitreal Ozurdex® implantation-related acute retinal necrosis (ARN). CASE PRESENTATION: A 45-year-old immunocompetent woman with a history of encephalitis presented with photophobia, redness, floaters, and rapidly decreased vision in her left eye. Three and six months ago, she received two doses of intravitreal Ozurdex® implant for ME of RVO. Clinical evaluation, including slit-lamp biomicroscopy, retinal photography, and fluorescein angiography, revealed anterior chamber cells, granulomatous keratic precipitates, cells in the vitreous, optic disc oedema, occlusive retinal vasculitis, scattered retinal haemorrhages, one quadrant of peripheral white areas with retinal necrosis, optic disc and vessels fluorescein staining, and retinal nonperfusion zones. All the above clinical manifestations showed an ARN. Herpes simplex virus was detected in the aqueous and vitreous humour by quantitative polymerase chain reaction testing. Intravenous acyclovir 500 mg tid for 7 days followed by oral valcyclovir was immediately performed for ARN. At 4 months, the patient's condition improved without retinal detachment, and the best-corrected visual acuity remained stable at 0.3. CONCLUSIONS: ARN might represent a risk of Ozurdex® administration.

Acute retinal necrosis (ARN) following chickenpox in a patient of Vogt-Koyanagi-Harada (VKH) syndrome using immunosuppressants.

A 36-year-old woman presented with diminution of vision and floaters in both the eyes. Both eyes had disc oedema, multiple pockets of neurosensory detachments along with vitritis. Fluorescein angiography and optical coherence tomography showed characteristic features of Vogt-Koyanagi-Harada (VKH) syndrome (figure 1). She was started on corticosteroid pulse therapy and immunosuppressants following which her VKH lesions resolved. However, she developed chickenpox after 2 weeks and after 1 month she developed discrete yellowish white retinitis patches in the periphery of the right eye which were consistent with a diagnosis of acute retinal necrosis. She was started on oral antivirals for the same and immunosuppressants were withheld in view of immunocompromised state potentially acting as a trigger for reactivation of latent virus. Retinitis patches started to resolve and showed a favourable response to the treatment.

Progressive outer retinal necrosis after rituximab and cyclophosphamide therapy.

We report a case of progressive outer retinal necrosis (PORN) in a patient of microscopic polyangitis (MPA), being treated with immunosuppressive drugs such as cyclophosphamide and rituximab. Her aqueous tap was positive for Varicella Zoster virus and she was treated with oral and intravitreal antivirals, along with discontinuation of one of the immunosuppressive agents, i.e. rituximab, which might have led to reactivation of the virus causing necrotizing retinitis lesions. Rituximab and cyclophosphamide are extremely potent drugs, which are necessary to manage immunological disorders such as MPA. However, they may predispose the patient to serious complications like viral infections, including PORN.

ACUTE RETINAL NECROSIS AFTER ADMINISTRATION OF ADALIMUMAB, A SYSTEMIC ANTITUMOR NECROSIS FACTOR ANTIBODY.

PURPOSE: To report a case of acute retinal necrosis in a patient on anti-tumor necrosis factor α immunosuppressive therapy. METHODS: Case report. RESULTS: A 47-year-old man with psoriasis presented with blurred vision and floaters in the left eye 4 days after receiving his fourth dose of adalimumab, a tumor necrosis factor α antagonist. He was diagnosed with acute retinal necrosis and was treated with intravenous acyclovir as well as prophylactic laser barricade. Seven years later, he is 20/20 with no history of a retinal detachment. CONCLUSION: Physicians prescribing tumor necrosis factor α antagonist immunosuppressive therapy should be aware of the potential of developing acute retinal necrosis.

Development of Retinal Infarct Due to Intracameral Cefuroxime Injection Following Complicated Cataract Surgery

We present the case of a 60-year-old patient who underwent a complicated cataract surgery with cefuroxime injection (1 mg/0.1 mL) into the anterior chamber at the end of surgery. The patient presented to our hospital due to decrease in visual acuity (VA) after surgery. VA was counting fingers (CF) from 4 meters. There was extensive retinal hemorrhages and edema in addition to retinal vascular leakage detected with fluorescein angiography (FA). After negative microbiologic tests, the patient was treated with intravenous pulse and oral corticosteroids. Rheumatologic investigation was also negative. At month 5, VA was CF from 1 meter in addition to disseminated capillary loss in FA and optic nerve atrophy despite corticosteroid treatment. The patient developed retinal infarction due to cefuroxime injection following a complicated cataract surgery. Surgeons and surgical staff should be aware of the possibility of retinal toxicity while using cefuroxime, particularly in complicated cases.

Acute retinal necrosis and immune reconstitution inflammatory syndrome in a natalizumab-treated patient with multiple sclerosis.

PURPOSE: To describe a case of acute retinal necrosis and subsequent immune reconstitution inflammatory syndrome in a patient with multiple sclerosis treated with natalizumab. METHODS: Case report. RESULTS: A 51-year-old man with multiple sclerosis developed acute retinal necrosis during treatment with natalizumab. The patient was successfully managed with natalizumab discontinuation, oral valacyclovir, and prophylactic laser retinal photocoagulation. A few months after natalizumab interruption and 1 month after valacyclovir completion, the patient presented with an episode of presumed noninfectious anterior and intermediate uveitis, which responded well to oral steroid mini-pulse therapy. CONCLUSION: Natalizumab is a potent immune suppressor used in the treatment of multiple sclerosis and Crohn disease. It has already been linked to herpetic infections and immune reconstitution inflammatory syndrome in the central nervous system. These complications may also affect ocular tissues.

Presumed necrotizing viral retinitis after intravitreal triamcinolone injection: case report.

A 56-year-old man presented with anterior chamber inflammation, increased intraocular pressure, peripheral retinal infiltration, and generalized retinal arterial obstruction suggesting acute retinal necrosis five months after intravitreal triamcinolone acetonide injection (IVTA). He was treated with intravenous antiviral agents and aspirin. Shortly after treatment, retinal infiltrations were resolved, and partial recanalization of the obstructed vessel was observed. Viral retinitis may occur as an opportunistic infection following IVTA due to the local immune modulatory effect of the steroid; hence, close observation following IVTA is necessary.

Herpes simplex encephalitis presenting after steroid treatment of panuveitis.

A 62-year-old woman with an autoimmune disease presented with panuveitis and was treated with immune suppression. She subsequently developed herpetic acute retinal necrosis and later died of herpes simplex encephalitis. Acute retinal necrosis usually occurs months to years after herpes simplex encephalitis. In our case, the ocular findings were present for 5 weeks before the encephalitis presented. To our knowledge, this is the first Australian case of acute retinal necrosis preceding herpes simplex encephalitis.

Presumed Necrotizing Viral Retinitis after Intravitreal Triamcinolone Injection: Case Report

A 56-year-old man presented with anterior chamber inflammation, increased intraocular pressure, peripheral retinal infiltration, and generalized retinal arterial obstruction suggesting acute retinal necrosis five months after intravitreal triamcinolone acetonide injection (IVTA). He was treated with intravenous antiviral agents and aspirin. Shortly after treatment, retinal infiltrations were resolved, and partial recanalization of the obstructed vessel was observed. Viral retinitis may occur as an opportunistic infection following IVTA due to the local immune modulatory effect of the steroid; hence, close observation following IVTA is necessary.

Unilateral acute retinal necrosis in a multiple sclerosis patient treated with high-dose systemic steroids.

A 50-year-old man with multiple sclerosis developed unilateral acute retinal necrosis following a long-term systemic corticosteroid administration for treatment of an attack of paraparesis. The patient was treated with systemic acyclovir, aspirin, oral steroids and topical cyclopentolate and prednisolone acetate for almost 3 months. Pars plana vitrectomy and 360° endolaser photocoagulation posterior to necrotic retinal areas were performed a week after the initial diagnosis. Varicella zoster DNA was confirmed by PCR analysis in the vitreous sample. Two months later, pars plana vitrectomy with silicone oil injection was performed successfully to treat complicated retinal detachment. Careful peripheral fundus examination is essential when acute unexplained visual loss is noted in patients receiving systemic corticosteroids to exclude acute retinal necrosis syndrome.

[The intervention of tetrandrine in the acute renal injury induced by streptomycin sulfate in puinea pigs].

The article investigated the intervention and the protective mechanism of tetrandrine (Tet) on acute renal injury induced by streptomycin (SM). The experimental healthy albinoa pigs of each sex with both ears' threshold of auditory brainstem response (ABR) < or = 5dB were divided into 4 groups by randomized blocks, including group 1 (control), group 2 (tetradrine), group 3 (SM) and group 4(Tet+SM). After 10 days, the urinary specimen were set apart for the determination of NAG activity, renal specimen were reserved for observing the renal histology. The renal histology shows that the injury of group 3 is most grievous, the injury of group 4 is lighter than that of group 3, in addition, the apoptosis is obviously less than that of group 3. The activity of urine of NAG in group 4 is lower than that of group 3 (P < 0.01). The results suggested that tetrandrine has obvious antagonism action upon renal toxic effect induced by SM. Therefore, the tetrandrine has potential application prospect in protection against pharmaceutical organ injury.