scholarly journals Pyogenic Granuloma of the Retina: A Case Series

2018 ◽  
Vol 5 (3) ◽  
pp. 176-181
Author(s):  
Samera Ahmad ◽  
Daniel Capiz-Correa ◽  
Hans E. Grossniklaus

Aim: To describe the clinicopathologic features of pyogenic granuloma (granulation tissue proliferation) extending from the retina. Methods: We describe 3 patients who underwent enucleation for endophthalmitis. The eyes were processed routinely for histopathologic examination. Results: All 3 enucleated eyes contained granulation tissue with reactive vascular channels and intervening stroma infiltrated with inflammatory cells. The vascular channels were arranged in a fan-like configuration and the tissue was classified as representing pyogenic granulomas. Conclusions: Pyogenic granulomas (granulation tissue) may emanate from the retina in cases of endophthalmitis. This is distinct from neovascularization that may occur in proliferative diabetic retinopathy, central retinal vein occlusion, or other etiologies.

2014 ◽  
Vol 2014 ◽  
pp. 1-6 ◽  
Author(s):  
Christina L. Ryu ◽  
Adrian Elfersy ◽  
Uday Desai ◽  
Thomas Hessburg ◽  
Paul Edwards ◽  
...  

Purpose. Ischemic central retinal vein occlusion (CRVO) eyes are at high risk of developing neovascular glaucoma (NVG). Our purpose is to investigate the effect of anti-VEGF therapy for macular edema after CRVO on the development of neovascular glaucoma (NVG) in ischemic CRVO eyes.Methods. This is a retrospective case series of 44 eyes from 44 patients with CRVO treated with anti-VEGF therapy for macular edema. The primary outcome was the development of NVG.Results. Of the 44 eyes, 14 eyes had ischemic CRVO, and 30 eyes had nonischemic CRVO. Nonischemic eyes received a mean of 8.4 anti-VEGF doses, over mean follow-up of 24 months. One nonischemic eye (3.3%) developed NVD but not NVG. The 14 ischemic eyes received a mean of 5.6 anti-VEGF doses, with mean follow-up of 23 months. Of these 14 ischemic eyes, two eyes (14%) developed iris neovascularization and 3 eyes (21%) developed posterior neovascularization. Three of these 5 eyes with neovascularization progressed to NVG, at 19.7 months after symptom onset, on average.Conclusion. Anti-VEGF therapy for macular edema may delay, but does not prevent, the development of ocular NV in ischemic CRVO. Significant risk of NVG still exists for ischemic CRVO eyes.


2019 ◽  
Vol 6 (3) ◽  
pp. 159-163
Author(s):  
Jasmine H. Francis ◽  
Eli L. Diamond ◽  
Ping Chi ◽  
Korey Jaben ◽  
David M. Hyman ◽  
...  

Background: Central retinal vein occlusion (CRVO) is a visually threatening event that has rarely been observed in patients taking MEK1/2 inhibitors and that may necessitate permanent discontinuation of a potentially efficacious therapy. We investigated the clinical characteristics of CRVO in patients on mitogen-activated protein kinase kinase (MEK) inhibition to better understand their predisposing factors and clinical course. Case Series: This was a single-center, retrospective cohort study (between December 2006 and September 2018). Three of 546 patients enrolled in 46 prospective trials involving treatment with MEK inhibitors at Memorial Sloan Kettering Cancer Center were identified as having CRVO. Clinical examination and course, multimodal ophthalmic imaging, and serum laboratory results (including homocysteine levels and genetic variants of methylene tetrahydrofolate reductase [MTHFR]) were reviewed for the 3 affected patients. All 3 patients with MEK inhibitor-associated CRVO had elevated serum homocysteine and gene variants of MTHFR (1 homozygous for A1298C, 1 heterozygous for A1298C, and 1 homozygous for C677T). Following intravitreous injections of anti-VEGF and discontinuation of drug, all patients regained vision to their baseline. Discussion: MEK inhibitor-associated CRVO is a rare event which can exhibit visual recovery after drug cessation and intravitreous anti-VEGF injections. In this cohort, it was associated with hyperhomocysteinemia and genetic mutations in MTHFR, suggesting a potential role for hyperhomocysteinemia screening prior to initiation of MEK inhibitor therapy.


2021 ◽  
pp. 248-253
Author(s):  
Kamal Kishore ◽  
Daniel S. McGowan ◽  
Kurt A. Hanebrink

We present 2 cases of iatrogenic retinal penetration from intravitreal (IVT) injections in a retrospective noncomparative case series of 2 patients. The first patient, an 81-year-old Caucasian male, developed dense vitreous hemorrhage soon after receiving an IVT bevacizumab injection for macular edema from central retinal vein occlusion. A 25-g vitrectomy 1 week later showed a retinal hole surrounded by fresh hemorrhages in the same quadrant as the IVT injection. The second patient, an 87-years-old male, developed a retinal detachment after 28 injections of anti-VEGF medications for neovascular AMD. A peripheral round hole was observed during vitrectomy without any lattice degeneration in the same quadrant as prior IVT injections. Both eyes were pseudophakic, had normal axial lengths, and received injections without measuring the injection site. Retinal penetration from IVT injections can result in serious sight-threatening complications. Measuring the injection site from the limbus should be part of safe IVT injection technique.


2019 ◽  
Vol 25 (9) ◽  
pp. e110-e111 ◽  
Author(s):  
Harry Choi ◽  
Carine Bou-Abboud Matta ◽  
Gregory Fu ◽  
Georgios Trichonas ◽  
Michael L Morgan ◽  
...  

2020 ◽  
Vol 12 (24) ◽  
pp. 85-95
Author(s):  
Sreekala Nelliakkattu Parameswaran ◽  
Manjusree Radhakrishnan Parappurathu ◽  
Aravind Kumar ◽  
Krishnendu Sukumaran

1994 ◽  
Vol 72 (01) ◽  
pp. 039-043 ◽  
Author(s):  
Francesco Bandello ◽  
Silvana Vigano’ D’Angelo ◽  
Mariella Parlavecchia ◽  
Alessandra Tavola ◽  
Patrizia Della Valle ◽  
...  

SummaryA series of coagulation parameters and lipoprotein(a) (Lp(a)) were explored in plasma from 40 patients with central retinal vein occlusion (CRVO, non-ischemic type n = 12; ischemic type n = 28) free of local and systemic predisposing factors, 1 to 12 months after the acute event. Forty age- and sex-matched patients with cataract served as controls. Prothrombin fragment 1.2 (FI.2), D-dimer, FVII:C - but not FVII: Ag - were higher and fibrinogen was lower in CRVO patients than in controls. Patients with non-ischemic CRVO had higher FI .2 and FVII:C and lower heparin cofactor II than patients with ischemic CRVO. Lp(a) levels greater than 300 mg/1 were observed in 12 patients with CRVO and in 4 controls (30% vs 10%, p <0.025). Patients with high Lp(a) - consistently associated with the S2 phenotype - had higher FVII:C, FVII:C/Ag ratio, and fibrinogen than the remaining CRVO patients. Plasma FI.2 and D-dimer correlated fairly in controls (r = 0.41) and patients with normal Lp(a) levels (r = 0.55), but they did not in the group of patients with high Lp(a) (r = 0.19), where the latter parameter was negatively related to D-dimer (r = −0.55). There was no dependence of the abnormalities observed on the time elapsed from vein occlusion. The findings of activated FVII and high FI.2, D-dimer, and Lp(a) are not uncommon in patients with CRVO. Increased thrombin formation with fibrin deposition and impaired fibrinolysis may play a role in the pathophysiology of CRVO and require specific treatment


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