Radiologic imaging is less sensitive and specific for determining the diffuse infiltrative pattern of disease, but this may show an anterior plaque without a discrete mass or calcifications. Ophthalmic imaging.
RADIOLOGIC TECHNOLOGY PROGRAM MT. SAC 1100 N. Grand Ave Walnut, CA 91789 Page 2 Program Overview The course of study in Radiologic Technology offered at Mt. SAC and its affiliated hospitals will prepare students to be. The Program The Radiologic Technology Program leads to an Associate in Science degree and has been accredited since 1970. Training includes operation of X-ray equipment, exposing and processing images, utilizing radiation. 2 rules and regulations pertaining to the radiologic technology licensure table of contents section i. authority.. 2 section ii. purpose. Identify the clinical and radiologic findings in tuberculosis affecting the respiratory, cardiac, central nervous, musculoskeletal, gastrointestinal, and genitourinary systems. •. Describe the differential diagnosis and.
Supplemental Admissions Process The Radiologic Technology program is designed as a 1 + 1 program, where Phase I includes your general education and related courses, which may be taken at Greenville Technical College or any. 2 Diagnostic Radiology Residents Physics Curriculum Prepared by Imaging Physics Curricula Subcommittee AAPM Subcommittee of the Medical Physics Education of Physicians Committee UPDATED – JUNE 2016 Supported by: AAPM. The Thyroid: Review of Imaging Features and Biopsy Techniques with Radiologic-Pathologic Correlation.
A Clinical Update and Radiologic Review of Pediatric Orbital and Ocular Tumors. Department of Radiology, University of California- San Diego, 2. West Arbor Drive, San Diego, CA 9. USA2. Department of Radiology, Rady Children’s Hospital San Diego, San Diego, CA 9.
USA3. Department of Radiology, San Diego VA Medical Center, La Jolla, CA 9. USA4. Department of Ophthalmology, Ratner Children's Eye Center, University of California- San Diego, San Diego, CA 9. USA5. Department of Ophthalmology, Shiley Eye Center, University of California- San Diego, San Diego, CA 9. USAAcademic Editor: A. J. M.Â Balm Copyright Â© 2. Ajay A. Rao et al.
This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. While pediatric orbital tumors are most often managed in tertiary care centers, clinicians should be aware of the signs of intraocular and orbital neoplasms. In the pediatric population, a delay in diagnosis of orbital and intraocular lesions, even if benign, can lead to vision loss and deformity. Intraocular lesions reviewed are retinoblastoma, medulloepithelioma, and retinal astrocytic hamartoma. Orbital neoplasms reviewed are rhabdomyosarcoma, neuroblastoma metastases, optic pathway glioma, plexiform neurofibroma, leukemia, lymphoprolipherative disease, orbital inflammatory syndrome, dermoid and epidermoid inclusion cysts, and Langerhans’ cell histiocytosis. Vascular lesions reviewed are infantile hemangioma and venous lymphatic malformation. In conjunction with clinical examination, high- resolution ophthalmic imaging and radiologic imaging play an important role in making a diagnosis and differentiating between benign and likely malignant processes.
The radiologic imaging characteristics of these lesions will be discussed to facilitate prompt diagnosis and treatment. The current treatment modalities and management of tumors will also be reviewed.
Introduction. The wide varieties of rare intraocular and orbital neoplasms differ in presentation in the pediatric population when compared to these same lesions in adults. While most pediatric ophthalmic tumors are benign, they may have a significant impact on vision and may result in significant morbidity and mortality. We categorize these diseases according to etiologies as neoplastic and vascular. Some congenital tumors may present in the first year of life, while others typically present later in childhood. Clinical examination signs that should raise concern include leukocoria (white pupil), strabismus, restriction of ocular motility, asymmetric eye position within the orbit, decreased vision, high pressure in the eye, inflammation of the eyelids or conjunctiva, pseudohypopyon (inferior whitish layer in the anterior chamber of tumor cells), vitreous hemorrhage or inflammation, and an afferent pupillary defect.
However, these are often late findings. Clinical presentation combined with the characteristic imaging features of the disease can narrow differential diagnoses. Imaging modalities most often used to evaluate these lesions include orbital ultrasonography (US), computed tomography (CT), and most importantly magnetic resonance imaging (MRI). Ophthalmic pathology is also critical to come to a diagnosis. In this paper, we review the epidemiology, clinical manifestations, current treatment modalities, and the imaging features that differentiate pediatric ocular and orbital lesions. Intraocular Neoplasms.
Retinoblastoma. Retinoblastoma is the most common intraocular malignancy in the pediatric population. The incidence of retinoblastoma is approximately one case per 1. There is no gender or racial predilection, and 9.
Biallelic mutations of the RB1 tumor suppressor gene likely predispose retinal progenitor cells to tumor growth . In the heritable form, the first mutation is constitutional, and the second is somatic, which causes bilateral disease in the majority of patients.
In the nonheritable form, both allelic mutations are somatic, limiting disease to one eye with delayed presentation compared to those with the heritable form . Very rarely, the heritable form of retinoblastoma can develop from primitive neuroectodermal cells in the suprasellar and pineal regions with resultant tri/tetralateral disease .
The most common initial sign of retinoblastoma is leukocoria, where the light emanating through the pupil is white light reflecting off the tumor instead of red light reflecting off the retina. Other signs of retinoblastoma may include decreased vision, strabismus, redness, pain, high pressure in the eye, cellulitic- like periocular inflammation, pseudohypopyon, and proptosis in late disease . Young children rarely complain of changes in their vision making nonvisual presenting signs of retinoblastoma more commonly observed. Additionally, measuring vision in young children can be difficult to assess accurately.
On fundoscopic exam, four patterns of growth can be seen. In the endophytic growth pattern, tumors are well visualized and extend from the deep retinal layer into the vitreous with vessels coursing into the mass. With exophytic growth, tumors extend from the retina outward into the subretinal space, with vessels coursing over the tumor. This growth pattern can be associated with retinal detachment, and total tumor extent may be underestimated. The third pattern is the most common, representing a mix of exophytic and endophytic growth. Extensive retinoblastoma can metastasize into the CNS and present with symptoms of meningitis.
The fourth pattern, diffuse infiltrating retinoblastoma, accounts for 1- 2% of retinoblastomas and usually arises from the anterior retina in older children. This form usually does not form a mass or contain calcium. The resultant pseudohypopyon and floating vitreal tumor cells can be easily mistaken for uveitis or endophthalmitis and has thus been termed a masquerade disease.
The absence of pain, conjunctival hyperemia, synechia (anatomic adhesions), cataract, and vitreous fibrosis suggests retinoblastoma rather than inflammation. Diffuse retinoblastomas start anteriorly and may enter the anterior chamber and fill the vitreous cavity but usually do not extend to the optic nerve. Spontaneous regression of tumor results in a shrunken, nonfunctioning globe .
The diagnosis of retinoblastoma is made noninvasively by exam under anesthesia with ophthalmoscopy, orbital ultrasound, and fluorescein angiography. Lumbar puncture and bone marrow biopsies are only performed in patients at high risk for having extraocular disease. Biopsies are not performed because of the risk of extraocular spread. Typically, neoplastic cells spread through the optic pathways via the optic nerve and can breach the pia to extend into the subarachnoid space. Direct extension through the choroid and sclera can occur with subsequent orbital extension.
Finally, hematogenous metastases can spread to the lungs, bones, brain, and other viscera . Historically, retinoblastoma was grouped into categories based on the Reese- Ellsworth classification system (groups I–V). The International Intraocular Retinoblastoma Classification System (IIRC) separates retinoblastomas into groups (A–E) based on prognosis, which is related to the extent of intraocular disease at diagnosis (Supplemental Table 1 will be available online at http: //dx.
More recently, the International Retinoblastoma Staging System (IRSS), proposed by a consensus of clinicians to separate retinoblastomas into stages based on management approach, has become popular . Based on the IRSS classification, Stage 0 eyes can be treated conservatively. Stage I eyes are enucleated with complete histologic resection, and Stage II eyes are enucleated with residual microscopic tumor. Stage III eyes have regional extension, including local lymph nodes, while Stage IV patients have metastatic disease (hematogenous, CNS, multiple lesions) . The Tumor, Node, and Metastasis (TNM) classification system is generally used for extension of retinoblastoma beyond the eye. Radiologic imaging can be used to help confirm the diagnosis and determine staging. The vast majority of nondiffuse type retinoblastomas appears nodular with calcifications, and presence of these calcifications distinguishes retinoblastoma from other intraocular lesions.
CT evaluation of retinoblastoma (Figure 1(a)) typically demonstrates a hyperattenuating mass in the posterior globe with calcifications. On ultrasound, retinoblastomas are irregular masses that are more echogenic than vitreous and contain shadowing calcifications.
Orbital ultrasound can detect calcifications in up to 9. Conventional 1. 5 T MR has not been considered as sensitive for detection of calcifications, but higher field- strength MR units and newer susceptibility- weighted sequences have increased its sensitivity. Galluzzi et al. found that when MR, ophthalmoscopy, and ultrasound were combined, none of the calcifications detected on CT were missed . MR evaluation avoids the ionizing radiation of CT and is more sensitive for detection of extraocular extension of disease, perineural spread into the optic nerve (Figure 1), and involvement of the subarachnoid space; therefore, CT is no longer the preferred modality.
Figure 1: 1. 7 months old diagnosed with bilateral retinoblastoma requiring systemic chemotherapy. Axial contrast- enhanced CT through the orbits (a) demonstrates bilateral intraocular masses with coarse calcifications (arrows) and mild- to- moderate enhancement, diagnostic of retinoblastoma.
MR axial T2- weighted image with fat- saturation (b) demonstrates curvilinear hypointensities in both globes, best visualized on the right, consistent with retinal detachment (arrows).