Review article
MR imaging findings of endophthalmitis Rupa Radhakrishnan1, Rebecca Cornelius2, Mary Beth Cunnane3, Karl Golnik4 and Humberto Morales2
The Neuroradiology Journal 0(00) 1–8 ! The Author(s) 2016 Reprints and permissions: sagepub.co.uk/journalsPermissions.nav DOI: 10.1177/1971400916633480 neu.sagepub.com
Abstract Endophthalmitis is a sight-threatening ophthalmologic emergency. The clinical diagnosis is often challenging, and delayed diagnosis may exacerbate the poor visual prognosis. B-scan ultrasonography or spectral domain optical coherence tomography are imaging aids at the clinician’s office. Cross-sectional imaging such as CT and particularly MRI can also help in the assessment of disease extent or complications. MR imaging findings are rarely described in the literature. Here, we discuss the spectrum of imaging findings of endophthalmitis and correlate them with key anatomic and pathophysiologic details of the globe. Early disease is often subtle on MR imaging with thick uveal enhancement, while advanced disease demonstrates retinal/choroidal detachment, vitreal exudates and peribulbar inflammation. Other noninfectious inflammatory diseases of the globe can show similar findings; however, MR diffusion-weighted images help identify infectious exudates and evaluate response to therapy. Knowledge of the spectrum of imaging findings of this disease is important for radiologists and help in the management decision process.
Keywords Endophthalmitis, magnetic resonance imaging, computed tomography, globe infection, ocular infection, diffusion-weighted images
Introduction Endophthalmitis refers to the infection of the inner tissues of the eye, which can progress to involve the vitreous cavity or anterior chamber. The terms uveitis or scleritis are broader in meaning and commonly used to refer to inflammatory changes within the coats of the eye, either noninfectious or infectious in etiology.1,2 Endophthalmitis is a serious condition with poor visual outcome despite aggressive therapy in most instances.3 Although diagnosis of endophthalmitis is made clinically, imaging modalities, especially postcontrast computed tomography (CT) and magnetic resonance imaging (MRI) with diffusion-weighted imaging (DWI) help in assessment of disease extent, complications, and response to therapy, especially when ophthalmoscopic visualization is hindered by lens opacification.
Anatomy The globe is composed of three main layers that from the outside in include: the sclera, choroid, and retina. The outer sclera is a tough layer of collagen and elastic tissue that is continuous with the cornea anteriorly and is perforated by the optic nerve and ciliary vessels posteriorly. The uveal tract forms the middle layer, and is made up of the iris anteriorly, the ring-shaped ciliary body at the periphery of the iris, and the highly vascular
and pigmented choroid posteriorly (Figure 1).3 The lens lies immediately posterior to the iris, held in place by the lens capsule and ciliary body. The iris separates the anterior and posterior portions of the aqueous chamber. The large vitreous chamber is posterior to the lens. The globe is surrounded by a fascial sheath called Tenon’s capsule, which is closely applied to the sclera and blends with the sclera at the corneoscleral junction and is also continuous with the muscle sheaths of the extraocular muscles3 (Figure 1). There are three potential spaces within the globe: the subhyaloid space between the posterior hyaloid membrane of the vitreous and the retina, the subretinal space between the two retinal layers (the inner sensory retina and the outer pigment epithelium), and the suprachoroidal space between the choroid and sclera. Ocular membrane detachments may have certain characteristic 1
Department USA 2 Department 3 Department 4 Department USA
of Radiology, Cincinnati Children’s Hospital Medical Center, of Radiology, University of Cincinnati Medical Center, USA of Radiology, Massachusetts Eye and Ear Infirmary, USA of Ophthalmology, University of Cincinnati Medical Center,
Corresponding author: Humberto Morales, Department of Radiology, University of Cincinnati, 234 Goodman St., Cincinnati, OH 45219, USA. Email: [email protected]
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Figure 1. Normal cross-sectional anatomy and MR imaging of the globe. (a) Diagrammatic representation of the eye. Key: 1, cornea; 2, anterior chamber; 3, sclera; 4, iris; 5, ciliary body; 6, choroid; 7, retina; 8, posterior chamber (vitreous); 9, lens; 10, Tenon’s capsule; 11, optic nerve; 12, extraocular muscle. Note the uvea is composed of the iris, ciliary body, and choroid. (b) Axial T2-weighted MR image of the eye demonstrates the normal hyperintense vitreous and aqueous chambers. The sclera demonstrates low signal (arrow) and is difficult to separate from the uvea. (c) Contrast-enhanced axial fat-sat T1-weighted MR image demonstrates the normal thin layer of uveal enhancement (arrow). The sclera can be seen as hypointense outer layer (asterisk). MR: magnetic resonance; fat-sat: fat saturation.
appearances on imaging depending on the compromised spaces.3 In addition to the intraocular spaces, there is a potential sub-Tenon space between the sclera and Tenon capsule (Figure 1).
Normal cross-sectional imaging of the globe Both CT and MRI evaluation of the globes are an adjunct to clinical ophthalmological and ocular ultrasound examination.4 CT imaging is quick and is useful for identification of radiopaque foreign bodies or displaced ocular prosthesis. MRI on the other hand has superior soft tissue resolution, and is without radiation. Intravenous contrast is useful for evaluation of inflammatory conditions. On CT, the aqueous and vitreous humor demonstrate uniform low attenuation. The sclera, uvea, and retina are not separately distinguishable and demonstrate high attenuation. On MRI, conventional head coils are used for evaluation of the orbits. Additional surface coils can provide improved evaluation of the globe with high spatial resolution and adequate signal-to-noise ratio.5 Recently, promising results have been shown with the use of two surface coils in addition to a conventional head coil to obtain fine detail of the globe as well as simultaneous evaluation of the bilateral orbits.6 In general, an orbital MRI protocol should include high-resolution images with 2–3 mm and 512 matrix slices, and at least one fat saturation (fat-sat) T2-weighted imaging (WI) and one fatsat post-contrast T1-WI in either axial or coronal planes. DWI should also be included as discussed later. Alternatively, heavily T2-WI sequences (constructive interference in steady state (CISS), fast
imaging employing steady-state acquisition (FIESTA), or driven equilibrium (DRIVE)) and post-contrast three-dimensional Fourier transformation (3DFT) T1WI sequences (volumetric interpolated breath-hold examination (VIBE) or T1 high-resolution isotropic volume excitation (THRIVE)) might be of additional value.7 The aqueous and vitreous humor, being nearly completely water, demonstrate hyperintense T2 and hypointense T1 signal on MRI (Figure 1). The uveal tract is difficult to separate from the adjacent bright signal in the vitreous on T2-WI. On T1-WI the uvea may be appreciated as a very thin, slightly hyperintense layer.5 The sclera, being fibrous, is hypointense on T1and T2-WI4 (Figure 1). In normal circumstances, the highly vascular uveal layer enhances intensely following contrast administration, better appreciated on MR than CT images (Figure 1(c)). Abnormal thick enhancement is sometimes difficult to assess; comparison with a normal contralateral eye is usually helpful.
Pathophysiology Organisms responsible for endophthalmitis are varied and reflect the origin of the infectious process (exogenous vs. endogenous), geographical location, and the patient case mix of the reporting group. Bacterial, fungal, viral or parasitic organisms can be involved. Infection is often exogenous secondary to cataract surgery.1,8 Trauma or corneal ulcers may also be responsible. In endogenous endophthalmitis, there is hematogeneous spread of organisms into the eye from an infectious focus elsewhere in the body.3 In endogenous endophthalmitis, the patients are often immunocompromised (e.g. diabetes mellitus,
Radhakrishnan et al. liver disease, malignancy) or intravenous drug abusers. Coagulase-negative staphylococci and Streptococcus viridans are common causes of endophthalmitis post-cataract surgery or intravitreal therapy.1,3,8,9 Bacillus cereus is often seen in post-traumatic endophthalmitis.1 Klebsiella pneumoniae is a common cause of endogenous endophthalmitis reported in the Asian population,1,10,11 while fungal organisms (particularly Candida albicans) are the most common cause in Western populations.12,13 Cytomegalovirus (CMV) retinitis is relatively common in immunosuppressed patients, particularly those with acquired immunodeficiency syndrome (AIDS), in whom it is a recognized cause of blindness.14 Although the incidence of neonatal endophthalmitis in the United States is declining,15 it deserves a special mention. Unlike endophthalmitis in adults, neonatal disease is frequently the result of an endogenous source of infection. Neonates with low birth weight, bacteremia, candidemia, and retinopathy of prematurity are at increased risk for endogenous endophthalmitis.13 The proposed mechanism of ocular infection in endogenous endophthalmitis is bacteremic seeding of the capillaries of the highly vascular choroid.16 Intraocular inflammation results in increased permeability of the blood-ocular barrier and extension of pro-inflammatory substances into the retina and vitreous.3,16 Fulminant inflammation causes degeneration of retinal architecture and death of the non-regenerating retinal photoreceptors.16 Inflammation can also involve all layers of the globe (referred to as pan-ophthalmitis) and extend outside the globe resulting in frank orbital cellulitis.
Clinical presentation The presenting symptom is often relatively rapid onset of loss of visual acuity, eye pain, and progressive eyelid swelling and conjunctival redness. Slit lamp examination may demonstrate corneal edema, increased leukocytes in the anterior chamber, and flare in the anterior chamber (reflection of light from protein in the aqueous humor). There may be layering pus in the anterior chamber, also called hypopyon (Figure 2). Culture of fluid aspirated from the anterior or posterior chamber confirms the presence of microorganisms.
Imaging findings Imaging is helpful in providing information in confounding cases of endophthalmitis, and in identifying disease extent and complications, by demonstrating the presence of ocular membrane detachment, intraocular abscess, and extraocular involvement. Clinically, numerous attempts have been made to classify the severity of the disease. Currently, there is no unifying classification.13 Hence, the appearance of endophthalmitis on imaging may be arbitrarily divided as early disease, advanced disease, and late stage, to reflect the previously described pathophysiology17 (Figure 3, Table 1).
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Figure 2. Clinical image of the eye in a patient with endophthalmitis. There is marked conjunctival injection, mild corneal haziness, and a layered collection (arrow) of white (hypopyon) and red (hyphema) blood cells in the inferior anterior chamber.
Early disease Identification of early endophthalmitis on imaging is challenging as the globe can appear normal or in some cases, particularly on CT imaging, only mild preseptal swelling can be seen (Figure 4).10 Similarly, mild smooth or irregular thickening and enhancement of the uveoscleral layer may be the only finding on contrastenhanced CT or MRI in early disease. This thickened appearance of the uveoscleral layer may be more easily visualized if one eye is involved and the other is normal. Occasionally, both eyes are involved, and this finding can be difficult to appreciate. Hyperdensity of the vitreous on CT or mild increased vitreous signal intensity on fluid-attenuated inversion recovery (FLAIR) and T1W MRI, also described as part of early disease, is thought to be due to proteinaceous exudates into the vitreous.10
Advanced disease Advanced endophthalmitis may result in ocular abscesses and focal exudates in conjunction with retinal or choroidal detachment. Exudates and abscesses may collect in the vitreous, subhyaloid space, subretinal space or suprachoroidal space. Focal exudates and ocular membrane detachment can be subtle on noncontrast CT; they are better appreciated on contrast enhanced CT and are readily seen with MRI (Figure 5). These focal exudates can be mildly hyperintense on T1 and FLAIR sequences, due to proteinaceous material or associated hemorrhage, easily identified against a background of relatively dark normal vitreous (Figure 5(c)).18,19 Exudates within the avascular vitreous demonstrate enhancement only after development of vitreal neovascularization.17 These proteinaceous/purulent exudates are more easily identified with DWI because of presence of diffusion restriction (Figures 5, 6 and 7).10,18,20
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Figure 3. Pathophysiologic evolution of endophthalmitis (compare with normal representation on Figure 1(a)). (a) Early disease. Key: 1, uveal involvement with thickening and inflammatory changes (thick enhancement is seen on imaging); 2, infection extends to the vitreous (abnormal density or signal is depicted on CT or MRI). (b) Fulminant/advanced disease. Key: 3, scleral involvement; 4, inflammatory changes to Tenon’s capsule; 5, retinal detachment (subhyaloid, subretinal and suprachorodial effusions with detachment are seen as the disease progress); 6, hypopyon. (c) Late stage. Shrunken globe with calcifications (phthisis bulbi) and vision loss is seen in some cases. CT: computed tomography; MRI: magnetic resonance imaging.
Table 1. Key clinical, pathophysiologic and imaging findings in endophthalmitis. Clinical Exogenous endophthalmitis after cataract surgery is the most common form of the disease. Endogenous endophthalmitis is a less common presentation after hematogenous spread of the infectious agent, usually in immunocompromised or iv-drug abuser patients. Pathophysiology Disease initiates in the highly vascular choroid, then spread to the retina and vitreous chamber. Eventually all layers of the globe are involved with associated ocular membrane detachment and focal exudates. Late, phthisis bulbi with shrunken and calcified globe is seen in some cases. Imaging Early disease demonstrates diffuse thick enhancement of the uveal layer. Progress to increased attenuation or increased signal intensity within the vitreous as seen on CT or T1/FLAIR MR images, respectively. Advanced endophthalmitis involves all layers of the globe with retinal or choroidal detachment, exudates, globe deformity and peribulbar inflammation. MRI better depicts the imaging findings. MRI is particularly useful in the definition of retrobulbar or extraocular extension. Restricted diffusion on DWI allows distinction of exudates/abscess within the globe and helps in the diagnosis and response to therapy. CT: computed tomography; FLAIR: fluid-attenuated inversion recovery; MR: magnetic resonance; MRI: magnetic resonance imaging; DWI: diffusionweighted imaging.
Figure 4. Pseudomonas endophthalmitis. A 45-year-old diabetic female with endogenous left eye endophthalmitis. (a) Non-contrast CT shows thickening of the preseptal soft tissues (asterisk). However, there is no obvious bulbar inflammatory change. (b) Non-contrast CT from one year prior (when patient had no infection) shows similar appearance of the left globe (elongation is due to degenerative myopia). There was significant visual deterioration on current presentation resulting in enucleation of the left globe and subsequent diagnosis of endophthalmitis. CT: computed tomography.
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Figure 5. Staphylococcus aureus endophthalmitis. A 25-year-old female IV drug abuser with endogenous MRSA endophthalmitis. (a) Axial non-contrast CT image shows thickening of the uve-oscleral layer and subtle increased density in the lateral and posterior aspect of the vitreous chamber of the right globe (arrow). (b) Axial fat-sat T2-WI better defines crescentic areas of abnormal mixed hypointensity in the vitreous chamber. There is episcleral inflammation that corresponds to Tenon’s capsule (arrow). (c) Axial FLAIR image demonstrates hyperintensity of a crescentic area, suspicious for focal exudate or abscess in the subretinal or suprachoroidal space. (d) DWI and (e) ADC maps demonstrate diffusion restriction (arrows) corresponding to signal abnormality noted on (c). Note normal DWI and ADC maps in the left globe. The patient underwent surgery with vitrectomy and debridement. The crescentic areas of abnormal signal on MRI correspond to retinal detachment with subretinal abscess. IV: intravenous; MRSA: methicillin-resistant Staphylococcus aureus; CT: computed tomography; T2-WI: T2-weighted imaging; fat-sat: fat saturation; FLAIR: fluid-attenuated inversion recovery; DWI: diffusion-weighted imaging; ADC: apparent diffusion coefficient; MRI: magnetic resonance imaging.
Figure 6. Bilateral endophthalmitis. (a) Axial T2-WI shows bilateral diffuse peribulbar edema. Subtle areas of intermediate to low signal intensity are present in the vitreous chamber of the right globe, particularly in the anterior portion (arrow), suspicious for focal exudates. There is also thickening of the ciliary bodies bilaterally. (b) Non-contrast T1-WI shows subtle hyperintensity layering posteriorly within the vitreous chamber (arrow). Abnormality in the anterior portion of the vitreous chamber is difficult to define. (c) Contrast enhanced T1-WI shows diffuse smooth thickening and enhancement of the uvea bilaterally (finding difficult to visualize with bilateral involvement; compare with thin normal uveal enhancement on Figure 1(c)). There is no enhancement within the vitreous chamber. (d) Diffusionweighted MR image and (e) ADC map show diffusion restriction in the anterior portion of the vitreal chamber of the right globe (arrow) consistent with focal exudate or abscess. There is also rim-like diffusion restriction, likely involving the sub-hyaloid space or uveal coat bilaterally. T2-WI: T2-weighted imaging; MR: magnetic resonance; ADC: apparent diffusion coefficient.
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Figure 7. Endogenous endophthalmitis. A 63-year-old diabetic female with pancreatic cancer and endogenous left endophthalmitis. (a) On fat-sat T2-WI, the left globe is enlarged and deformed with irregular rim-like intermediate to low signal intensity in the vitreous chamber (arrow). (b) Axial fat-sat post-contrast T1-WI shows thick irregular uveal enhancement (compare with normal thin uveal enhancement in the right globe). The globe is proptotic and there is extensive peribulbar stranding and enhancement; abnormal enhancement of the extraocular muscles is also noted. Findings are consistent with associated orbital cellulitis. (c) DWI shows welldefined rim-like diffusion restriction in the vitreous chamber consistent with exudate/abscess, most likely in the subhyaloid space or uveal coat. fat-sat: fat saturation; T2-WI: T2-weighted imaging; DWI: diffusion-weighted imaging.
phthisis bulbi, with a shrunken, often calcified globe, similar to the end stage of other ocular pathologies (Figure 8).10 At this stage, active infection has most likely healed and extraocular inflammation has resolved. There is often complete vision loss in such cases.
Management
Figure 8. Late-stage endophthalmitis. Bilateral shrunken deformed globes (phthisis bulbi) in a patient nine months after bilateral acute endophthalmitis.
Thus, FLAIR T2-WI images and particularly DWI are helpful in defining purulent exudates with respect to the suppressed (FLAIR) and non-restricted (DWI) normal vitreous fluid. Moreover, DWI can be helpful for the evaluation of the globe after treatment (an increase in the apparent diffusion coefficient (ADC) values has been associated with favorable treatment response).18 Infection can extend to involve all layers of the globe and result in panophthalmitis. Edema or exudates may present within the periscleral tissues, in the potential subTenon space (Figure 5(b)). There might be extensive extraocular inflammation as well, with lacrimal gland enlargement and enhancement, subconjunctival abscess, and preseptal and post-septal stranding that can result in frank orbital cellulitis (Figures 6 and 7).10 Severe intraocular inflammation can result in globe deformity (Figure 7) and ultimately rupture.
Late stage Most individuals with post-surgical, exogenous endophthalmitis recover useful vision. However, prognosis for endogenous endophthalmitis is generally poor. Severe fulminant endophthalmitis can end in
Acute bacterial endophthalmitis needs to be managed emergently because of the high risk of poor visual outcome. Vitreous aspiration is performed to identify causative organism. Intravitreal antibiotics are the mainstay of therapy. Severe disease may require surgery with vitrectomy and vitreous debridement.21
Differential diagnosis Imaging appearance of endophthalmitis should always be correlated with clinical presentation, as the imaging features may mimic other conditions including neoplasms, trauma, and noninfectious uveitis.22 Common intraocular malignancy in adults such as choroidal melanoma and metastasis are often nodular or focal with mass-like enhancement on post-contrast images (Figure 9), rather than the more common diffuse involvement of endophthalmitis.23 However, when complicated with retinal/choroidal detachment and subretinal hemorrhage, the differentiation of malignant processes can be difficult.24 For instance, retinoblastomas might resemble endophthalmitis and a high index of suspicion should be maintained in the pediatric population (Figure 9). Inflammatory scleritis or uveitis can mimic infection and can involve the anterior and/or posterior chambers of the globe.25 Often inflammation is related to systemic autoimmune or rheumatologic diseases; idiopathic cases are not uncommon. Rheumatoid arthritis is the most common cause of scleritis. Common causes of intermediate or posterior uveitis are sarcoidosis or Beh&et’s disease. Posterior
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Figure 9. Ocular neoplastic processes. Choroidal melanoma ((a), (b)) and retinoblastoma ((c), (d)). (a) Axial fat-sat T2-WI shows focal area of hypo intensity in the posterior aspect of the globe. (b) Axial fat-sat post-contrast T1-WI demonstrate focal homogeneous enhancement in the posterior uveal region. (c) Axial T2-WI and (d) axial fat-sat post-contrast T1-WI show significant mass-like enhancement in the temporal aspect of the posterior globe with retinal detachment (better visualized on T2-WI). Note the focal nature of both lesions described here and the relative absence of exudates within the globe or inflammatory orbital findings. fat-sat: fat saturation; T2-WI: T2-weighted imaging.
granulomatous panuveitis, has been reported to cause subretinal effusions with associated restricted diffusion.2 Though the restricted diffusion appears to be caused by bilateral symmetric increased uveal ‘‘cellularity,’’ the disease should be entertained in the differential diagnosis in the adequate clinical scenario.
Conclusion
Figure 10. Ocular inflammatory process. A 16-year-old with atypical Cogen’s syndrome and bilateral posterior scleritis. Axial contrast-enhanced fat-sat T1-WI shows abnormal enhancement superficial to the posterior sclera bilaterally (arrows). Compare to normal enhancement of the globe in Figure 1(c). fat-sat: fat saturation; T2-WI: T2-weighted imaging.
scleritis can show mild diffuse uveal/scleral thickening and enhancement (Figure 10). Restricted diffusion within the globe might represent hemorrhagic changes rather than infectious exudates; gradient-echo or susceptibility weighted imaging can help with identification of blooming areas in cases of hemorrhage. VogtKoyanagi-Harada (VKH) disease, an inflammatory condition resulting from autoimmune targeting of melanocytes and characterized by bilateral
Endophthalmitis is a highly morbid condition with imaging playing a useful role in identification of disease extent, complications, and response to therapy. MRI can be useful in early diagnosis of clinically questionable cases and particularly useful in the definition of retrobulbar or extraocular extension. The use of surface coils improves resolution and has shown promising results in other globe pathologies such as retinoblastoma; it might be stressed when available. Diffuse thickened enhancing uvea is a feature of early disease, which can progress to vitreous opacities, ocular membrane detachment (retinal/choroidal), exudates (vitreous or choroid/retinal), peribulbar inflammation (sub-Tenon fluid), and globe deformity. Radiologists should be aware of the described imaging findings. Particular attention to areas of restricted diffusion on DWI images is recommended, not only for evaluation of response to therapy but also in the initial diagnosis of infectious exudates.
8 Acknowledgments The authors thank Dr Angelo Rutty, Perea Hospital, Puerto Rico, for his contribution of wonderful art images. This work was previously presented as an exhibit at the annual meeting of the American Society of Neuroradiology, 2013, San Diego, CA, USA.
Funding This research received no specific grant from any funding agency in the public, commercial, or not-for-profit sectors.
Conflict of interest The authors declared no potential conflicts of interest with respect to the research, authorship, and/or publication of this article.
References 1. Durand ML. Endophthalmitis. Clin Microbiol Infect 2013; 19: 227–234. 2. Li CQ, Cho AA, Edward NJ, et al. Magnetic resonance imaging of uveitis. Neuroradiology 2015; 57: 825–832. 3. Mafee MF, Karimi A, Shah JD, et al. Anatomy and pathology of the eye: Role of MR imaging and CT. Magn Reson Imaging Clin N Am 2006; 14: 249–270. 4. Malhotra A, Minja FJ, Crum A, et al. Ocular anatomy and cross-sectional imaging of the eye. Semin Ultrasound CT MR 2011; 32: 2–13. 5. Georgouli T, Chang B, Nelson M, et al. Use of highresolution microscopy coil MRI for depicting orbital anatomy. Orbit 2008; 27: 107–114. 6. Sirin S, Schlamann M, Metz KA, et al. High-resolution MRI using orbit surface coils for the evaluation of metastatic risk factors in 143 children with retinoblastoma: Part 2: New vs. old imaging concept. Neuroradiology 2015; 57: 815–824. 7. de Graaf P, Go¨ricke S, Rodjan F, et al. Guidelines for imaging retinoblastoma: Imaging principles and MRI standardization. Pediatr Radiol 2012; 42: 2–14. 8. Wong TY and Chee SP. The epidemiology of acute endophthalmitis after cataract surgery in an Asian population. Ophthalmology 2004; 111: 699–705. 9. Sadaka A, Durand ML and Gilmore MS. Bacterial endophthalmitis in the age of outpatient intravitreal therapies and cataract surgeries: Host-microbe interactions in intraocular infection. Prog Retin Eye Res 2012; 31: 316–331. 10. Lee CC, Chen CY, Chen FH, et al. Septic metastatic endophthalmitis from Klebsiella pneumoniae liver abscess: CT and MR imaging characteristics—report of three cases. Radiology 1998; 207: 411–416.
The Neuroradiology Journal 0(00) 11. Wong JS, Chan TK, Lee HM, et al. Endogenous bacterial endophthalmitis: An east Asian experience and a reappraisal of a severe ocular affliction. Ophthalmology 2000; 107: 1483–1491. 12. Connell PP, O’Neill EC, Fabinyi D, et al. Endogenous endophthalmitis: 10-year experience at a tertiary referral centre. Eye (Lond) 2011; 25: 66–72. 13. Sadiq MA, Hassan M, Agarwal A, et al. Endogenous endophthalmitis: Diagnosis, management, and prognosis. J Ophthalmic Inflamm Infect 2015; 5: 32. 14. LeBedis CA and Sakai O. Nontraumatic orbital conditions: Diagnosis with CT and MR imaging in the emergent setting. Radiographics 2008; 28: 1741–1753. 15. Moshfeghi AA, Charalel RA, Hernandez-Boussard T, et al. Declining incidence of neonatal endophthalmitis in the United States. Am J Ophthalmol 2011; 151: 59–65.e1. 16. Callegan MC, Engelbert M, Parke DW 2nd, et al. Bacterial endophthalmitis: Epidemiology, therapeutics, and bacterium-host interactions. Clin Microbiol Rev 2002; 15: 111–124. 17. Seale M, Lee WK, Daffy J, et al. Fulminant endogenous Klebsiella pneumoniae endophthalmitis: Imaging findings. Emerg Radiol 2007; 13: 209–212. 18. Rumboldt Z, Moses C, Wieczerzynski U, et al. Diffusionweighted imaging, apparent diffusion coefficients, and fluid-attenuated inversion recovery MR imaging in endophthalmitis. AJNR Am J Neuroradiol 2005; 26: 1869–1872. 19. Platnick J, Crum AV, Soohoo S, et al. The globe: Infection, inflammation, and systemic disease. Semin Ultrasound CT MR 2011; 32: 38–50. 20. Yu E, Laughlin S, Kassel EE, et al. Nocardial endophthalmitis and subretinal abscess: CT and MR imaging features with pathologic correlation: A case report. AJNR Am J Neuroradiol 2005; 26: 1220–1222. 21. Durand ML. Bacterial endophthalmitis. Curr Infect Dis Rep 2009; 11: 283–288. 22. Mu¨ller-Forell W and Pitz S. Orbital pathology. In: Baert AL, Sartor K, Wibke S, et al. (eds) Imaging of orbital and visual pathway pathology. Mainz, Germany: SpringerVerlag, 2002, pp.147–340. 23. Roy AA, Davagnanam I and Evanson J. Abnormalities of the globe. Clin Radiol 2012; 67: 1011–1022. 24. Cunnane ME, Sepahadari AR, Gardiner M, et al. Pathology of the eye and orbit. In: Som PM and Curtin HD (eds) Head and neck imaging, 5th ed. St. Louis, MO: Elsevier Mosby, 2011, pp.591–756. 25. Jackson TL, Eykyn SJ, Graham EM, et al. Endogenous bacterial endophthalmitis: A 17-year prospective series and review of 267 reported cases. Surv Ophthalmol 2003; 48: 403–423.
MR imaging findings of endophthalmitis Rupa Radhakrishnan1, Rebecca Cornelius2, Mary Beth Cunnane3, Karl Golnik4 and Humberto Morales2
The Neuroradiology Journal 0(00) 1–8 ! The Author(s) 2016 Reprints and permissions: sagepub.co.uk/journalsPermissions.nav DOI: 10.1177/1971400916633480 neu.sagepub.com
Abstract Endophthalmitis is a sight-threatening ophthalmologic emergency. The clinical diagnosis is often challenging, and delayed diagnosis may exacerbate the poor visual prognosis. B-scan ultrasonography or spectral domain optical coherence tomography are imaging aids at the clinician’s office. Cross-sectional imaging such as CT and particularly MRI can also help in the assessment of disease extent or complications. MR imaging findings are rarely described in the literature. Here, we discuss the spectrum of imaging findings of endophthalmitis and correlate them with key anatomic and pathophysiologic details of the globe. Early disease is often subtle on MR imaging with thick uveal enhancement, while advanced disease demonstrates retinal/choroidal detachment, vitreal exudates and peribulbar inflammation. Other noninfectious inflammatory diseases of the globe can show similar findings; however, MR diffusion-weighted images help identify infectious exudates and evaluate response to therapy. Knowledge of the spectrum of imaging findings of this disease is important for radiologists and help in the management decision process.
Keywords Endophthalmitis, magnetic resonance imaging, computed tomography, globe infection, ocular infection, diffusion-weighted images
Introduction Endophthalmitis refers to the infection of the inner tissues of the eye, which can progress to involve the vitreous cavity or anterior chamber. The terms uveitis or scleritis are broader in meaning and commonly used to refer to inflammatory changes within the coats of the eye, either noninfectious or infectious in etiology.1,2 Endophthalmitis is a serious condition with poor visual outcome despite aggressive therapy in most instances.3 Although diagnosis of endophthalmitis is made clinically, imaging modalities, especially postcontrast computed tomography (CT) and magnetic resonance imaging (MRI) with diffusion-weighted imaging (DWI) help in assessment of disease extent, complications, and response to therapy, especially when ophthalmoscopic visualization is hindered by lens opacification.
Anatomy The globe is composed of three main layers that from the outside in include: the sclera, choroid, and retina. The outer sclera is a tough layer of collagen and elastic tissue that is continuous with the cornea anteriorly and is perforated by the optic nerve and ciliary vessels posteriorly. The uveal tract forms the middle layer, and is made up of the iris anteriorly, the ring-shaped ciliary body at the periphery of the iris, and the highly vascular
and pigmented choroid posteriorly (Figure 1).3 The lens lies immediately posterior to the iris, held in place by the lens capsule and ciliary body. The iris separates the anterior and posterior portions of the aqueous chamber. The large vitreous chamber is posterior to the lens. The globe is surrounded by a fascial sheath called Tenon’s capsule, which is closely applied to the sclera and blends with the sclera at the corneoscleral junction and is also continuous with the muscle sheaths of the extraocular muscles3 (Figure 1). There are three potential spaces within the globe: the subhyaloid space between the posterior hyaloid membrane of the vitreous and the retina, the subretinal space between the two retinal layers (the inner sensory retina and the outer pigment epithelium), and the suprachoroidal space between the choroid and sclera. Ocular membrane detachments may have certain characteristic 1
Department USA 2 Department 3 Department 4 Department USA
of Radiology, Cincinnati Children’s Hospital Medical Center, of Radiology, University of Cincinnati Medical Center, USA of Radiology, Massachusetts Eye and Ear Infirmary, USA of Ophthalmology, University of Cincinnati Medical Center,
Corresponding author: Humberto Morales, Department of Radiology, University of Cincinnati, 234 Goodman St., Cincinnati, OH 45219, USA. Email: [email protected]
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Figure 1. Normal cross-sectional anatomy and MR imaging of the globe. (a) Diagrammatic representation of the eye. Key: 1, cornea; 2, anterior chamber; 3, sclera; 4, iris; 5, ciliary body; 6, choroid; 7, retina; 8, posterior chamber (vitreous); 9, lens; 10, Tenon’s capsule; 11, optic nerve; 12, extraocular muscle. Note the uvea is composed of the iris, ciliary body, and choroid. (b) Axial T2-weighted MR image of the eye demonstrates the normal hyperintense vitreous and aqueous chambers. The sclera demonstrates low signal (arrow) and is difficult to separate from the uvea. (c) Contrast-enhanced axial fat-sat T1-weighted MR image demonstrates the normal thin layer of uveal enhancement (arrow). The sclera can be seen as hypointense outer layer (asterisk). MR: magnetic resonance; fat-sat: fat saturation.
appearances on imaging depending on the compromised spaces.3 In addition to the intraocular spaces, there is a potential sub-Tenon space between the sclera and Tenon capsule (Figure 1).
Normal cross-sectional imaging of the globe Both CT and MRI evaluation of the globes are an adjunct to clinical ophthalmological and ocular ultrasound examination.4 CT imaging is quick and is useful for identification of radiopaque foreign bodies or displaced ocular prosthesis. MRI on the other hand has superior soft tissue resolution, and is without radiation. Intravenous contrast is useful for evaluation of inflammatory conditions. On CT, the aqueous and vitreous humor demonstrate uniform low attenuation. The sclera, uvea, and retina are not separately distinguishable and demonstrate high attenuation. On MRI, conventional head coils are used for evaluation of the orbits. Additional surface coils can provide improved evaluation of the globe with high spatial resolution and adequate signal-to-noise ratio.5 Recently, promising results have been shown with the use of two surface coils in addition to a conventional head coil to obtain fine detail of the globe as well as simultaneous evaluation of the bilateral orbits.6 In general, an orbital MRI protocol should include high-resolution images with 2–3 mm and 512 matrix slices, and at least one fat saturation (fat-sat) T2-weighted imaging (WI) and one fatsat post-contrast T1-WI in either axial or coronal planes. DWI should also be included as discussed later. Alternatively, heavily T2-WI sequences (constructive interference in steady state (CISS), fast
imaging employing steady-state acquisition (FIESTA), or driven equilibrium (DRIVE)) and post-contrast three-dimensional Fourier transformation (3DFT) T1WI sequences (volumetric interpolated breath-hold examination (VIBE) or T1 high-resolution isotropic volume excitation (THRIVE)) might be of additional value.7 The aqueous and vitreous humor, being nearly completely water, demonstrate hyperintense T2 and hypointense T1 signal on MRI (Figure 1). The uveal tract is difficult to separate from the adjacent bright signal in the vitreous on T2-WI. On T1-WI the uvea may be appreciated as a very thin, slightly hyperintense layer.5 The sclera, being fibrous, is hypointense on T1and T2-WI4 (Figure 1). In normal circumstances, the highly vascular uveal layer enhances intensely following contrast administration, better appreciated on MR than CT images (Figure 1(c)). Abnormal thick enhancement is sometimes difficult to assess; comparison with a normal contralateral eye is usually helpful.
Pathophysiology Organisms responsible for endophthalmitis are varied and reflect the origin of the infectious process (exogenous vs. endogenous), geographical location, and the patient case mix of the reporting group. Bacterial, fungal, viral or parasitic organisms can be involved. Infection is often exogenous secondary to cataract surgery.1,8 Trauma or corneal ulcers may also be responsible. In endogenous endophthalmitis, there is hematogeneous spread of organisms into the eye from an infectious focus elsewhere in the body.3 In endogenous endophthalmitis, the patients are often immunocompromised (e.g. diabetes mellitus,
Radhakrishnan et al. liver disease, malignancy) or intravenous drug abusers. Coagulase-negative staphylococci and Streptococcus viridans are common causes of endophthalmitis post-cataract surgery or intravitreal therapy.1,3,8,9 Bacillus cereus is often seen in post-traumatic endophthalmitis.1 Klebsiella pneumoniae is a common cause of endogenous endophthalmitis reported in the Asian population,1,10,11 while fungal organisms (particularly Candida albicans) are the most common cause in Western populations.12,13 Cytomegalovirus (CMV) retinitis is relatively common in immunosuppressed patients, particularly those with acquired immunodeficiency syndrome (AIDS), in whom it is a recognized cause of blindness.14 Although the incidence of neonatal endophthalmitis in the United States is declining,15 it deserves a special mention. Unlike endophthalmitis in adults, neonatal disease is frequently the result of an endogenous source of infection. Neonates with low birth weight, bacteremia, candidemia, and retinopathy of prematurity are at increased risk for endogenous endophthalmitis.13 The proposed mechanism of ocular infection in endogenous endophthalmitis is bacteremic seeding of the capillaries of the highly vascular choroid.16 Intraocular inflammation results in increased permeability of the blood-ocular barrier and extension of pro-inflammatory substances into the retina and vitreous.3,16 Fulminant inflammation causes degeneration of retinal architecture and death of the non-regenerating retinal photoreceptors.16 Inflammation can also involve all layers of the globe (referred to as pan-ophthalmitis) and extend outside the globe resulting in frank orbital cellulitis.
Clinical presentation The presenting symptom is often relatively rapid onset of loss of visual acuity, eye pain, and progressive eyelid swelling and conjunctival redness. Slit lamp examination may demonstrate corneal edema, increased leukocytes in the anterior chamber, and flare in the anterior chamber (reflection of light from protein in the aqueous humor). There may be layering pus in the anterior chamber, also called hypopyon (Figure 2). Culture of fluid aspirated from the anterior or posterior chamber confirms the presence of microorganisms.
Imaging findings Imaging is helpful in providing information in confounding cases of endophthalmitis, and in identifying disease extent and complications, by demonstrating the presence of ocular membrane detachment, intraocular abscess, and extraocular involvement. Clinically, numerous attempts have been made to classify the severity of the disease. Currently, there is no unifying classification.13 Hence, the appearance of endophthalmitis on imaging may be arbitrarily divided as early disease, advanced disease, and late stage, to reflect the previously described pathophysiology17 (Figure 3, Table 1).
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Figure 2. Clinical image of the eye in a patient with endophthalmitis. There is marked conjunctival injection, mild corneal haziness, and a layered collection (arrow) of white (hypopyon) and red (hyphema) blood cells in the inferior anterior chamber.
Early disease Identification of early endophthalmitis on imaging is challenging as the globe can appear normal or in some cases, particularly on CT imaging, only mild preseptal swelling can be seen (Figure 4).10 Similarly, mild smooth or irregular thickening and enhancement of the uveoscleral layer may be the only finding on contrastenhanced CT or MRI in early disease. This thickened appearance of the uveoscleral layer may be more easily visualized if one eye is involved and the other is normal. Occasionally, both eyes are involved, and this finding can be difficult to appreciate. Hyperdensity of the vitreous on CT or mild increased vitreous signal intensity on fluid-attenuated inversion recovery (FLAIR) and T1W MRI, also described as part of early disease, is thought to be due to proteinaceous exudates into the vitreous.10
Advanced disease Advanced endophthalmitis may result in ocular abscesses and focal exudates in conjunction with retinal or choroidal detachment. Exudates and abscesses may collect in the vitreous, subhyaloid space, subretinal space or suprachoroidal space. Focal exudates and ocular membrane detachment can be subtle on noncontrast CT; they are better appreciated on contrast enhanced CT and are readily seen with MRI (Figure 5). These focal exudates can be mildly hyperintense on T1 and FLAIR sequences, due to proteinaceous material or associated hemorrhage, easily identified against a background of relatively dark normal vitreous (Figure 5(c)).18,19 Exudates within the avascular vitreous demonstrate enhancement only after development of vitreal neovascularization.17 These proteinaceous/purulent exudates are more easily identified with DWI because of presence of diffusion restriction (Figures 5, 6 and 7).10,18,20
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Figure 3. Pathophysiologic evolution of endophthalmitis (compare with normal representation on Figure 1(a)). (a) Early disease. Key: 1, uveal involvement with thickening and inflammatory changes (thick enhancement is seen on imaging); 2, infection extends to the vitreous (abnormal density or signal is depicted on CT or MRI). (b) Fulminant/advanced disease. Key: 3, scleral involvement; 4, inflammatory changes to Tenon’s capsule; 5, retinal detachment (subhyaloid, subretinal and suprachorodial effusions with detachment are seen as the disease progress); 6, hypopyon. (c) Late stage. Shrunken globe with calcifications (phthisis bulbi) and vision loss is seen in some cases. CT: computed tomography; MRI: magnetic resonance imaging.
Table 1. Key clinical, pathophysiologic and imaging findings in endophthalmitis. Clinical Exogenous endophthalmitis after cataract surgery is the most common form of the disease. Endogenous endophthalmitis is a less common presentation after hematogenous spread of the infectious agent, usually in immunocompromised or iv-drug abuser patients. Pathophysiology Disease initiates in the highly vascular choroid, then spread to the retina and vitreous chamber. Eventually all layers of the globe are involved with associated ocular membrane detachment and focal exudates. Late, phthisis bulbi with shrunken and calcified globe is seen in some cases. Imaging Early disease demonstrates diffuse thick enhancement of the uveal layer. Progress to increased attenuation or increased signal intensity within the vitreous as seen on CT or T1/FLAIR MR images, respectively. Advanced endophthalmitis involves all layers of the globe with retinal or choroidal detachment, exudates, globe deformity and peribulbar inflammation. MRI better depicts the imaging findings. MRI is particularly useful in the definition of retrobulbar or extraocular extension. Restricted diffusion on DWI allows distinction of exudates/abscess within the globe and helps in the diagnosis and response to therapy. CT: computed tomography; FLAIR: fluid-attenuated inversion recovery; MR: magnetic resonance; MRI: magnetic resonance imaging; DWI: diffusionweighted imaging.
Figure 4. Pseudomonas endophthalmitis. A 45-year-old diabetic female with endogenous left eye endophthalmitis. (a) Non-contrast CT shows thickening of the preseptal soft tissues (asterisk). However, there is no obvious bulbar inflammatory change. (b) Non-contrast CT from one year prior (when patient had no infection) shows similar appearance of the left globe (elongation is due to degenerative myopia). There was significant visual deterioration on current presentation resulting in enucleation of the left globe and subsequent diagnosis of endophthalmitis. CT: computed tomography.
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Figure 5. Staphylococcus aureus endophthalmitis. A 25-year-old female IV drug abuser with endogenous MRSA endophthalmitis. (a) Axial non-contrast CT image shows thickening of the uve-oscleral layer and subtle increased density in the lateral and posterior aspect of the vitreous chamber of the right globe (arrow). (b) Axial fat-sat T2-WI better defines crescentic areas of abnormal mixed hypointensity in the vitreous chamber. There is episcleral inflammation that corresponds to Tenon’s capsule (arrow). (c) Axial FLAIR image demonstrates hyperintensity of a crescentic area, suspicious for focal exudate or abscess in the subretinal or suprachoroidal space. (d) DWI and (e) ADC maps demonstrate diffusion restriction (arrows) corresponding to signal abnormality noted on (c). Note normal DWI and ADC maps in the left globe. The patient underwent surgery with vitrectomy and debridement. The crescentic areas of abnormal signal on MRI correspond to retinal detachment with subretinal abscess. IV: intravenous; MRSA: methicillin-resistant Staphylococcus aureus; CT: computed tomography; T2-WI: T2-weighted imaging; fat-sat: fat saturation; FLAIR: fluid-attenuated inversion recovery; DWI: diffusion-weighted imaging; ADC: apparent diffusion coefficient; MRI: magnetic resonance imaging.
Figure 6. Bilateral endophthalmitis. (a) Axial T2-WI shows bilateral diffuse peribulbar edema. Subtle areas of intermediate to low signal intensity are present in the vitreous chamber of the right globe, particularly in the anterior portion (arrow), suspicious for focal exudates. There is also thickening of the ciliary bodies bilaterally. (b) Non-contrast T1-WI shows subtle hyperintensity layering posteriorly within the vitreous chamber (arrow). Abnormality in the anterior portion of the vitreous chamber is difficult to define. (c) Contrast enhanced T1-WI shows diffuse smooth thickening and enhancement of the uvea bilaterally (finding difficult to visualize with bilateral involvement; compare with thin normal uveal enhancement on Figure 1(c)). There is no enhancement within the vitreous chamber. (d) Diffusionweighted MR image and (e) ADC map show diffusion restriction in the anterior portion of the vitreal chamber of the right globe (arrow) consistent with focal exudate or abscess. There is also rim-like diffusion restriction, likely involving the sub-hyaloid space or uveal coat bilaterally. T2-WI: T2-weighted imaging; MR: magnetic resonance; ADC: apparent diffusion coefficient.
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Figure 7. Endogenous endophthalmitis. A 63-year-old diabetic female with pancreatic cancer and endogenous left endophthalmitis. (a) On fat-sat T2-WI, the left globe is enlarged and deformed with irregular rim-like intermediate to low signal intensity in the vitreous chamber (arrow). (b) Axial fat-sat post-contrast T1-WI shows thick irregular uveal enhancement (compare with normal thin uveal enhancement in the right globe). The globe is proptotic and there is extensive peribulbar stranding and enhancement; abnormal enhancement of the extraocular muscles is also noted. Findings are consistent with associated orbital cellulitis. (c) DWI shows welldefined rim-like diffusion restriction in the vitreous chamber consistent with exudate/abscess, most likely in the subhyaloid space or uveal coat. fat-sat: fat saturation; T2-WI: T2-weighted imaging; DWI: diffusion-weighted imaging.
phthisis bulbi, with a shrunken, often calcified globe, similar to the end stage of other ocular pathologies (Figure 8).10 At this stage, active infection has most likely healed and extraocular inflammation has resolved. There is often complete vision loss in such cases.
Management
Figure 8. Late-stage endophthalmitis. Bilateral shrunken deformed globes (phthisis bulbi) in a patient nine months after bilateral acute endophthalmitis.
Thus, FLAIR T2-WI images and particularly DWI are helpful in defining purulent exudates with respect to the suppressed (FLAIR) and non-restricted (DWI) normal vitreous fluid. Moreover, DWI can be helpful for the evaluation of the globe after treatment (an increase in the apparent diffusion coefficient (ADC) values has been associated with favorable treatment response).18 Infection can extend to involve all layers of the globe and result in panophthalmitis. Edema or exudates may present within the periscleral tissues, in the potential subTenon space (Figure 5(b)). There might be extensive extraocular inflammation as well, with lacrimal gland enlargement and enhancement, subconjunctival abscess, and preseptal and post-septal stranding that can result in frank orbital cellulitis (Figures 6 and 7).10 Severe intraocular inflammation can result in globe deformity (Figure 7) and ultimately rupture.
Late stage Most individuals with post-surgical, exogenous endophthalmitis recover useful vision. However, prognosis for endogenous endophthalmitis is generally poor. Severe fulminant endophthalmitis can end in
Acute bacterial endophthalmitis needs to be managed emergently because of the high risk of poor visual outcome. Vitreous aspiration is performed to identify causative organism. Intravitreal antibiotics are the mainstay of therapy. Severe disease may require surgery with vitrectomy and vitreous debridement.21
Differential diagnosis Imaging appearance of endophthalmitis should always be correlated with clinical presentation, as the imaging features may mimic other conditions including neoplasms, trauma, and noninfectious uveitis.22 Common intraocular malignancy in adults such as choroidal melanoma and metastasis are often nodular or focal with mass-like enhancement on post-contrast images (Figure 9), rather than the more common diffuse involvement of endophthalmitis.23 However, when complicated with retinal/choroidal detachment and subretinal hemorrhage, the differentiation of malignant processes can be difficult.24 For instance, retinoblastomas might resemble endophthalmitis and a high index of suspicion should be maintained in the pediatric population (Figure 9). Inflammatory scleritis or uveitis can mimic infection and can involve the anterior and/or posterior chambers of the globe.25 Often inflammation is related to systemic autoimmune or rheumatologic diseases; idiopathic cases are not uncommon. Rheumatoid arthritis is the most common cause of scleritis. Common causes of intermediate or posterior uveitis are sarcoidosis or Beh&et’s disease. Posterior
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Figure 9. Ocular neoplastic processes. Choroidal melanoma ((a), (b)) and retinoblastoma ((c), (d)). (a) Axial fat-sat T2-WI shows focal area of hypo intensity in the posterior aspect of the globe. (b) Axial fat-sat post-contrast T1-WI demonstrate focal homogeneous enhancement in the posterior uveal region. (c) Axial T2-WI and (d) axial fat-sat post-contrast T1-WI show significant mass-like enhancement in the temporal aspect of the posterior globe with retinal detachment (better visualized on T2-WI). Note the focal nature of both lesions described here and the relative absence of exudates within the globe or inflammatory orbital findings. fat-sat: fat saturation; T2-WI: T2-weighted imaging.
granulomatous panuveitis, has been reported to cause subretinal effusions with associated restricted diffusion.2 Though the restricted diffusion appears to be caused by bilateral symmetric increased uveal ‘‘cellularity,’’ the disease should be entertained in the differential diagnosis in the adequate clinical scenario.
Conclusion
Figure 10. Ocular inflammatory process. A 16-year-old with atypical Cogen’s syndrome and bilateral posterior scleritis. Axial contrast-enhanced fat-sat T1-WI shows abnormal enhancement superficial to the posterior sclera bilaterally (arrows). Compare to normal enhancement of the globe in Figure 1(c). fat-sat: fat saturation; T2-WI: T2-weighted imaging.
scleritis can show mild diffuse uveal/scleral thickening and enhancement (Figure 10). Restricted diffusion within the globe might represent hemorrhagic changes rather than infectious exudates; gradient-echo or susceptibility weighted imaging can help with identification of blooming areas in cases of hemorrhage. VogtKoyanagi-Harada (VKH) disease, an inflammatory condition resulting from autoimmune targeting of melanocytes and characterized by bilateral
Endophthalmitis is a highly morbid condition with imaging playing a useful role in identification of disease extent, complications, and response to therapy. MRI can be useful in early diagnosis of clinically questionable cases and particularly useful in the definition of retrobulbar or extraocular extension. The use of surface coils improves resolution and has shown promising results in other globe pathologies such as retinoblastoma; it might be stressed when available. Diffuse thickened enhancing uvea is a feature of early disease, which can progress to vitreous opacities, ocular membrane detachment (retinal/choroidal), exudates (vitreous or choroid/retinal), peribulbar inflammation (sub-Tenon fluid), and globe deformity. Radiologists should be aware of the described imaging findings. Particular attention to areas of restricted diffusion on DWI images is recommended, not only for evaluation of response to therapy but also in the initial diagnosis of infectious exudates.
8 Acknowledgments The authors thank Dr Angelo Rutty, Perea Hospital, Puerto Rico, for his contribution of wonderful art images. This work was previously presented as an exhibit at the annual meeting of the American Society of Neuroradiology, 2013, San Diego, CA, USA.
Funding This research received no specific grant from any funding agency in the public, commercial, or not-for-profit sectors.
Conflict of interest The authors declared no potential conflicts of interest with respect to the research, authorship, and/or publication of this article.
References 1. Durand ML. Endophthalmitis. Clin Microbiol Infect 2013; 19: 227–234. 2. Li CQ, Cho AA, Edward NJ, et al. Magnetic resonance imaging of uveitis. Neuroradiology 2015; 57: 825–832. 3. Mafee MF, Karimi A, Shah JD, et al. Anatomy and pathology of the eye: Role of MR imaging and CT. Magn Reson Imaging Clin N Am 2006; 14: 249–270. 4. Malhotra A, Minja FJ, Crum A, et al. Ocular anatomy and cross-sectional imaging of the eye. Semin Ultrasound CT MR 2011; 32: 2–13. 5. Georgouli T, Chang B, Nelson M, et al. Use of highresolution microscopy coil MRI for depicting orbital anatomy. Orbit 2008; 27: 107–114. 6. Sirin S, Schlamann M, Metz KA, et al. High-resolution MRI using orbit surface coils for the evaluation of metastatic risk factors in 143 children with retinoblastoma: Part 2: New vs. old imaging concept. Neuroradiology 2015; 57: 815–824. 7. de Graaf P, Go¨ricke S, Rodjan F, et al. Guidelines for imaging retinoblastoma: Imaging principles and MRI standardization. Pediatr Radiol 2012; 42: 2–14. 8. Wong TY and Chee SP. The epidemiology of acute endophthalmitis after cataract surgery in an Asian population. Ophthalmology 2004; 111: 699–705. 9. Sadaka A, Durand ML and Gilmore MS. Bacterial endophthalmitis in the age of outpatient intravitreal therapies and cataract surgeries: Host-microbe interactions in intraocular infection. Prog Retin Eye Res 2012; 31: 316–331. 10. Lee CC, Chen CY, Chen FH, et al. Septic metastatic endophthalmitis from Klebsiella pneumoniae liver abscess: CT and MR imaging characteristics—report of three cases. Radiology 1998; 207: 411–416.
The Neuroradiology Journal 0(00) 11. Wong JS, Chan TK, Lee HM, et al. Endogenous bacterial endophthalmitis: An east Asian experience and a reappraisal of a severe ocular affliction. Ophthalmology 2000; 107: 1483–1491. 12. Connell PP, O’Neill EC, Fabinyi D, et al. Endogenous endophthalmitis: 10-year experience at a tertiary referral centre. Eye (Lond) 2011; 25: 66–72. 13. Sadiq MA, Hassan M, Agarwal A, et al. Endogenous endophthalmitis: Diagnosis, management, and prognosis. J Ophthalmic Inflamm Infect 2015; 5: 32. 14. LeBedis CA and Sakai O. Nontraumatic orbital conditions: Diagnosis with CT and MR imaging in the emergent setting. Radiographics 2008; 28: 1741–1753. 15. Moshfeghi AA, Charalel RA, Hernandez-Boussard T, et al. Declining incidence of neonatal endophthalmitis in the United States. Am J Ophthalmol 2011; 151: 59–65.e1. 16. Callegan MC, Engelbert M, Parke DW 2nd, et al. Bacterial endophthalmitis: Epidemiology, therapeutics, and bacterium-host interactions. Clin Microbiol Rev 2002; 15: 111–124. 17. Seale M, Lee WK, Daffy J, et al. Fulminant endogenous Klebsiella pneumoniae endophthalmitis: Imaging findings. Emerg Radiol 2007; 13: 209–212. 18. Rumboldt Z, Moses C, Wieczerzynski U, et al. Diffusionweighted imaging, apparent diffusion coefficients, and fluid-attenuated inversion recovery MR imaging in endophthalmitis. AJNR Am J Neuroradiol 2005; 26: 1869–1872. 19. Platnick J, Crum AV, Soohoo S, et al. The globe: Infection, inflammation, and systemic disease. Semin Ultrasound CT MR 2011; 32: 38–50. 20. Yu E, Laughlin S, Kassel EE, et al. Nocardial endophthalmitis and subretinal abscess: CT and MR imaging features with pathologic correlation: A case report. AJNR Am J Neuroradiol 2005; 26: 1220–1222. 21. Durand ML. Bacterial endophthalmitis. Curr Infect Dis Rep 2009; 11: 283–288. 22. Mu¨ller-Forell W and Pitz S. Orbital pathology. In: Baert AL, Sartor K, Wibke S, et al. (eds) Imaging of orbital and visual pathway pathology. Mainz, Germany: SpringerVerlag, 2002, pp.147–340. 23. Roy AA, Davagnanam I and Evanson J. Abnormalities of the globe. Clin Radiol 2012; 67: 1011–1022. 24. Cunnane ME, Sepahadari AR, Gardiner M, et al. Pathology of the eye and orbit. In: Som PM and Curtin HD (eds) Head and neck imaging, 5th ed. St. Louis, MO: Elsevier Mosby, 2011, pp.591–756. 25. Jackson TL, Eykyn SJ, Graham EM, et al. Endogenous bacterial endophthalmitis: A 17-year prospective series and review of 267 reported cases. Surv Ophthalmol 2003; 48: 403–423.
