Persistent Hyperplastic Primary Vitreous

Persistent hyperplastic primary vitreous is caused by persistence of various portions of the primary vitreous (embryonic hyaloid vascular system) with hyperplasia of the associated embryonic connective tissue and may present as leukokoria in the neonate. The eye usually is microphthalmic, although the degree of microphthalmia can be minimal, and the lens can be small with flattening of the anterior chamber. Initially, a funnel-shaped mass of fibrovascular tissue (including the persistent hyaloid artery) is present in the retrolental space and runs in an S-shaped course (termed Cloquet’s canal) between the back of the lens and the optic nerve head. PHPV is vascular and prone to repeated hemorrhages and may vary in size. CT demonstrates generalized increased density in the globe and enhancement of the intravitreal tissue after intravenous contrast. Unlike retinoblastoma, PHPV does not calcify (this is key!). The CT diagnosis is facilitated by observing the S-shaped tubular fetal tissue between the lens and the optic nerve head (Fig. 10-2). A blood-vitreous layer may be seen as a result of posterior hyaloid detachment. On MR, vitreal intensity is variable; however, the visualization of Cloquet’s canal makes the diagnosis. This is an entity that may lead to high signal on T1WI in the vitreous, possibly from hemorrhage or high protein, with low or high signal on T2WI.

Figure 10-2 Persistent hyperplastic primary vitreous. Note the presence of Cloquet’s canal in the right globe (arrow). There is a calcified retinal detachment (chronic) in the small left globe.

Coats Disease

Coats disease is a vascular anomaly of the retina that may be clinically difficult to distinguish from retinoblastoma. This lesion is usually unilateral. Telangiectatic vessels leak serum and lipid into the retina (lipoproteinaceous effusion) and subretinal space, often producing a retinal detachment. Patients are usually seen when they develop strabismus and are noted to have leukokoria. It is common for patients to become symptomatic in the first 2 years of life, although the age at discovery is usually 6 to 8 years, with approximately two thirds of cases in boys. The CT appearance is of high density in the vitreous related to the exudate. Calcification is rare, again potentially distinguishing this condition from retinoblastoma; however, it cannot be distinguished from the noncalcifying variant of retinoblastoma or, when there is calcification, from calcified retinoblastoma. On MR, Coats disease is hyperintense on T1WI and T2WI, whereas retinoblastoma tends to be high intensity on T1WI but low intensity on T2WI. Coats disease enhances along the leaves of the detached retina and at the sites where the retina reinserts, whereas retinoblastoma enhances in a masslike fashion. MR spectroscopy (MRS) has been reported to show a large peak at 1 to 1.6 ppm that is thought to correspond to lipids or complex proteolipids.

Choroidal Hemangioma

This is a vascular hamartoma detected in middle-aged and elderly individuals. There are two varieties: a circumscribed or solitary form, unassociated with other abnormalities, and a diffuse angiomatous lesion associated with Sturge-Weber syndrome or facial nevus flammeus. The solitary lesion has been mistaken for choroidal melanoma. On MR, these lesions are isointense to slightly hyperintense on T2WI. They enhance avidly.

Toxocara canis Infection

Toxocara canis infection begins when a child ingests soil contaminated with dog feces containing the ova of the nematode T. canis. The ova hatch in the gastrointestinal tract and then migrate throughout the body. The ocular T. canis infection results when larvae of T. canis within the eye die, producing an inflammatory reaction (just like cysticercosis in the brain) with vitreous opacification and retinal detachment. Antibody titers for Toxocara are helpful in confirming the diagnosis and should be drawn when there is any suspicion of pica. The ocular lesions of Toxocara occur months to years after initial infection. This chronic granulomatous endophthalmitis causes unilateral leukokoria. On CT, diffuse high density is identified within the globe without calcification. Thick enhancement of the sclera has been observed. On MR, these lesions are reported to be high intensity on T1WI and T2WI. This, again, is somewhat different from the appearance of retinoblastoma, which is generally of lower intensity on T2WI. The intensity patterns are related to the protein content or associated hemorrhage in the globes. The globe size is normal, differentiating this condition from PHPV, which usually is associated with microphthalmia.

Cytomegalovirus

Cytomegalovirus (CMV) is the most common opportunistic infection of the retina and choroid. Up to one fourth of patients with AIDS have CMV infection. It is hemorrhagic and can produce high density on CT or various MR appearances depending on the stage of blood (Fig. 10-3). CMV retinitis can result in retinal detachment, the treatment of which may require intraocular injections of silicone oil or other high-density substances. Thus, ocular infection by CMV can lead to a myriad of imaging findings. Other less common infectious pathogens affecting the retina, choroid, or both in AIDS include Toxoplasma gondii, Mycobacterium tuberculosis, Pneumocystis carinii, and the herpesviruses.

Figure 10-3 Hemorrhagic cytomegalovirus infection. Computed tomography (CT) reveals bilateral hemorrhages in a patient with AIDS.

Posterior Scleritis

This can be infectious (bacterial, fungal, or viral) or autoimmune (collagen vascular diseases versus sarcoidosis) in origin. It is separated into acute and chronic categories. Findings include thickening and enhancement of the posterior sclera and uvea (Fig. 10-4). The thickening may be nodular or diffuse. The nodular variety can be mistaken for melanoma; the diffuse type can mimic lymphoma in its uniform thickening. The disease may be associated with retinal or choroidal detachments and uveitis.

Figure 10-4 Posterior scleritis. A, Computed tomography (CT) with bilateral posterior enhancement of episcleral region (arrows). B, T1- weighted image with shaggy posterior margins of both globes representing episcleritis.

Staphyloma

A staphyloma is an area of thinning of the cornea or sclera that usually is lined by uveal tissue. Most staphylomas are congenital and/or associated with high myopia, but a staphyloma may result from infections, inflammation, or trauma. Staphylomas can occur anywhere on the sclera or cornea and appear on imaging as an area of nonenhancing outward bulging of the eye wall.

Uveitis

Inflammation of the uveal tract may affect the choroid, ciliary body, iris, or a combination of these structures. Most cases of uveitis are idiopathic. When an etiology can be identified, viruses, particularly herpesviruses, are the usual pathogens; however, some cases are caused by bacteria (e.g., tuberculosis), fungi and parasites (e.g., T. gondii). In addition, the most common ocular manifestation of sarcoidosis is uveitis. Collagen vascular (connective tissue) diseases, such as ankylosing spondylitis, Reiter syndrome, (juvenile) rheumatoid arthritis, inflammatory bowel disease, psoriasis, and lupus also are causes of uveitis. Trauma is a common cause. A really omniscient neuroradiologist may see enhancement of the uveal tract on high-resolution MR to make the diagnosis.

Idiopathic Orbital Inflammation (Orbital Pseudotumor)

Pseudotumor (idiopathic nongranulomatous orbital inflammation) of the orbit occasionally is associated with intraocular inflammation, including uveitis, keratitis, and retinitis. It may also cause scleritis or episcleritis. It is diagnosed clinically by the preponderance of pain and excellent response to steroids, but may be seen as thickening and enhancement of any or all ocular structures.

Periorbital Cellulitis

Periorbital cellulitis is an inflammation of the anterior tissues of the orbit and is characterized by swelling and erythema of the eyelids and conjunctivitis, without visual loss, proptosis, or limitation of eye movement. The orbital septum is the main barrier preventing spread of infection from the anterior orbit and soft tissues to the retrobulbar space, where it becomes orbital cellulitis. Patients with periorbital cellulitis most often are treated as outpatients with oral antibiotics, whereas patients with orbital cellulitis have the potential to develop permanent visual loss and thus usually require treatment as inpatients with systemic antibiotics, surgical decompression, or both, particularly if the infection results from contiguous disease in the ethmoid or sphenoid sinuses. Patients with orbital cellulitis in whom a subperiosteal or orbital abscess develops may require not only systemic antibiotics but also urgent surgical intervention to incise and drain the lesion.

Ocular Hypotony and Choroidal Detachments

Ocular hypotony is defined as low intraocular pressure secondary to surgery, trauma, or glaucoma therapy and may be observed on CT as uveoscleral infolding, also referred to as the “flat tire” or “umbrella” sign (Fig. 10-7). This is most often seen after globe perforation and can be reversed by instillation of saline, silicone oil, or sodium hyaluronate (Healon), which expands the globe. Just two more words: double perforation. This term is used by ophthalmologists and means a perforation through the anterior and posterior portions of the globe. Suspected posterior perforation is one reason to perform an imaging study; it usually cannot be repaired (poor outcome). The most common cause of a double perforation is BB-sized shot.

Figure 10-7 Ocular hypotony. Computed tomography following perforation of the right globe. The globe has the appearance of an umbrella or a flat tire, which is characteristic of this condition.

Globe rupture may refer to perforation of the anterior chamber only, diagnosed on emergency department (ED) CT as flattening of the space anterior to the lens. It is important to compare the depth of the anterior chamber from left to right in all ocular trauma cases. It’s a common mistake to argue that there is no ruptured globe because the radiologist has looked only at the vitreous humor for flattening or blood rather than including the anterior chamber in the search pattern.

Ocular hypotonia, from inflammatory diseases (uveitis or scleritis), medication, or traumatic perforation of the globe, is the cause of serous choroidal detachments. Table 10-1 compares the various ocular detachments radiologists commonly encounter (see Fig. 10-7). Hemorrhagic choroidal detachment may be observed after penetrating injury or intraocular surgery and has a lenticular morphology. This is bad news because it means that you have had a rupture of a choroidal vessel, which has an associated poor prognosis. Serous choroidal detachment (benign prognosis) is crescentic or ring-shaped, and the curvilinear choroid can be identified. Serous choroidal effusions beneath the detached choroid appear as convex regions of low density outlined by the detached choroid. Hemorrhagic choroidal effusions are high density and do not change with position. Inflammatory choroidal effusions secondary to uveitis and posterior scleritis are high density but may change in location with changes in head position. Uveoscleral thickening and enhancement can be seen in inflammatory choroidal detachment. MR is beneficial in distinguishing hemorrhagic choroidal detachment from serous choroidal detachments. On MR, hemorrhagic choroidal detachment can display a variety of intensity patterns related to age of the hemorrhage (see Chapter 4). Serous choroidal detachment has been noted to be high intensity on T1WI and T2WI.

Table 10-1 Types of Ocular Detachments

An acute traumatic cataract differs from a senescent cataract in that the lens is usually less dense rather than more dense from acute edema. Look to see whether it is centered in the anterior chamber—it may also be subluxated. It may have fuzzy borders on CT. Rarely, the lens may be completely dislocated into the anterior chamber or the vitreous cavity. If dislocated anteriorly, it may interfere with aqueous humor flow and cause acute glaucoma.

Drusen

The most common calcifications in the globe are drusen. Optic nerve head (optic disk) drusen are composed of a mucoprotein matrix with significant quantities of acid mucopolysaccharides together with small quantities of ribonucleic acid and, occasionally, iron. They are laminated calcareous deposits located in the substance of the optic nerve anterior to the lamina cribrosa. This condition has an incidence of up to 2% of the population. Drusen may be familial (typically bilateral) or may be associated with other conditions, such as retinitis pigmentosa. They may be unilateral or bilateral and are located just anterior to the junction of the optic nerve and globe. CT demonstrates punctate calcifications in this region (see Fig. 10-1C). MR has difficulty detecting this condition because of its relative insensitivity to calcium. The clinical issue for the radiologist is that if the drusen are buried below the surface of the nerve head, they may not be seen by the ophthalmologist, and the patient may be referred for a workup of what appears to be papilledema (hence, drusen are a cause of pseudopapilledema). Rarely one might consider a differential diagnosis of retinoblastoma or astrocytic hamartoma in a child or adult with extensive optic disk calcification; however, drusen have no enhancement or soft-tissue mass on enhanced MR, as opposed to retinoblastoma.

Senile/Senescent Calcifications

As part of the aging process, fine pinpoint calcifications may develop at or just anterior to the insertion sites of the extraocular muscles on the globe within the sclerochoroidal layers. These areas can be appreciated on CT (see Fig. 10-1A). Hyperparathyroidism and hypomagnesemia predispose to these calcifications. Trochlear calcification may be symptomatic with pain and restricted movement as a tenosynovitis known as Brown syndrome, but it is more commonly asymptomatic and associated with diabetes mellitus.

Retinoblastoma

Retinoblastoma is the most common intraocular tumor of childhood. It usually presents before age 3 years with leukokoria, strabismus, decreased vision (particularly in bilateral lesions), retinal detachment, glaucoma, ocular pain, or signs of ocular inflammation. Ninety-eight percent occur in children younger than age 3 years. Accurate radiologic diagnosis is crucial for timely treatment and survival. The vast majority of lesions occur as sporadic mutations (90%), whereas approximately 10% are familial (autosomal dominant). Of the familial forms, more than one third are bilateral and associated with genes that predispose to other malignancies. The retinoblastoma gene (RB1) has been localized on chromosome 13 at the q14 locus. Absence or inactivation of both alleles of this suppressor gene within immature retinal cells is required for retinoblastoma to develop. Retinoblastoma may also occur sporadically as a somatic mutation; these lesions are unilateral, occurring later in life than the inherited form.

Although ophthalmoscopy is usually able to visualize retinoblastoma, imaging is of critical importance in revealing retrobulbar extension of the tumor and invasion of the optic nerve posterior to the lamina cribrosa, where the meninges surround the optic nerve and are contiguous with the subarachnoid spaces of the central nervous system (associated with a poor prognosis) (Box 10-2).

Retinoblastoma may spread directly into the subarachnoid space via the optic nerve (occasionally producing spinal implants), hematogenously, or via lymphatics and has a propensity to hemorrhage. Metastases from retinoblastoma occur within the first 2 years after treatment. There is a high incidence of nonocular malignant tumors in patients with the hereditary form of retinoblastoma, leading to a 59% 35-year mortality rate. These include midline, primitive neuroectodermal tumors (PNETs), pineal tumors, osteogenic sarcoma, soft-tissue sarcoma, malignant melanoma, basal cell carcinoma, and rhabdomyosarcoma (Fig. 10-8). The pineal gland in lower animals contains photoreceptors and has been termed the “third eye,” so that the triad of a pineal tumor (usually a pineoblastoma) and bilateral retinoblastoma has been termed trilateral retinoblastoma (Fig. 10-9). The pineoblastoma may be detected simultaneously with, after, or even before the ocular lesion. Ectopic retinoblastoma has also been reported in the parasellar or suprasellar regions.

Figure 10-8 Bilateral retinoblastoma. Postcontrast scan through the orbits shows bilateral enhancing ocular masses (arrowheads) with an associated mass infiltrating the left temporalis muscle (arrow) in this child. Can only be one thing: congenital retinoblastoma with sarcoma of facial soft tissues.

Figure 10-9 Trilateral retinoblastoma. Note the pineoblastoma in a patient with bilateral retinoblastoma.

The CT findings of retinoblastoma are calcifications in the posterior portion of the globe with extension into the vitreous (Fig. 10-10). The calcification may be homogeneous or irregular and occurs in 95% of patients. Noncalcified retinoblastoma has been reported in infants with a family history, under close observation. In children younger than age 3 years, ocular calcification is highly suggestive of retinoblastoma; conversely, its absence in this same group makes the diagnosis of retinoblastoma highly unlikely. These lesions minimally enhance; however, contrast is useful to appreciate intracranial extension. With orbital involvement, proptosis may be seen. Coronal imaging is useful in assessing enlargement of the optic nerve secondary to invasion by the tumor.

Figure 10-10 Retinoblastoma. A, On computed tomography retinoblastoma calcifications are noted extending from the posterior retina into the vitreous on the left. B, TI-weighted image of bilateral retinoblastoma. Notice that one cannot discern evidence of calcification, thus making the diagnosis of retinoblastoma problematic in this situation. Also, observe the bilateral retinal detachments.

Magnetic resonance findings in retinoblastoma include moderately high intensity on T1WI (Fig. 10-10B) and hypointensity on T2WI, with the noncalcified portion of the lesion less hypointense than the calcification. We speculate that the high intensity on T1WI may be caused by calcium or by some coexistent paramagnetic, tumor protein, or hemorrhagic component. Associated retinal detachment may be high intensity on T1WI and of variable intensity on T2WI, depending on the protein content and whether there is associated hemorrhage in the subretinal fluid. Enhancement is often present and may be the only indicator of spread to the retrobulbar compartment or along the subarachnoid space surrounding the optic nerve, intracranial, or intraspinal spaces. In patients with suspected retinoblastoma CT and MR are complementary examinations. CT detects calcification better than MR, whereas MR is more sensitive than CT for tumoral extension into the nerve and intracranial space, and for detecting secondary lesions.

Melanoma

Melanomas of the uveal tract are the most common intraocular malignancy in adults and have a characteristic intensity pattern on MR. They are rare in African Americans but when they occur tend to be larger, more pigmented, and more necrotic. Conditions predisposing to uveal melanoma include congenital melanosis, ocular melanocytosis, oculodermal melanocytosis, and uveal nevi. Unlike most other tumors, melanotic melanomas are hyperintense on T1WI and hypointense on T2WI. Free radicals known to exist in melanin are responsible for the associated T1- and T2-shortening by the proton-electron dipole-dipole proton relaxation enhancement mechanism (Fig. 10-11). The degree of T1- and T2-shortening appears to be related to the melanin content. Amelanotic melanomas have MR characteristics similar to those of other tumors (hypointense on T1WI and hyperintense on PDWI/T2WI). Other lesions with similar intensity patterns that could be confused with melanotic melanoma include fat and subacute hemorrhage in the intracellular methemoglobin state. Use of fat saturation images can easily separate fat from melanotic tumor. There have been reports of mucin-secreting adenocarcinoma metastatic to the choroid and other carcinomas having similar signal characteristics to a choroidal melanotic melanoma. Associated with the melanoma may be a retinal detachment, with a subretinal proteinaceous effusion that appears as high intensity on T2WI. To differentiate melanoma from other lesions, T1WI, T2WI, and enhanced scans must be used.

Figure 10-11 Ocular melanoma. A, T1-weighted image (T1WI) of enucleated globe with melanotic melanoma. Note the high intensity of the tumor (paramagnetic effect of melanin) and the episcleral extension (arrows). B, T2WI with marked hypointensity. C, Computed tomography of melanoma with posterior episcleral/orbital extension.

On CT, uveal melanomas are high density on noncontrast images and enhance. MR is superior to CT in visualizing retinal detachment, for noting associated vitreous changes, and for differentiating uveal melanoma from choroidal hemangioma (based on intensity characteristics) and choroidal detachment (based on enhancement). Extraocular invasion is important to detect as it is associated with a poorer prognosis and has different therapeutic implications. Ocular ultrasound and CT may be particularly useful here. Choroidal melanoma has a propensity for metastasis to the liver and lung.

Melanoma may also arise in the orbit from native orbital melanocytes located along ciliary nerves, optic nerve leptomeninges, and scleral emissary vessels. These lesions tend to be associated with pigmentary disorders, including nevus of Ota, ocular melanocytosis, and blue nevi. Melanocytomas occur most commonly in African Americans and also involve the uvea and optic nerve.

Medulloepithelioma

This tumor, formally termed dictyoma, arises from the primitive nonpigmented epithelial lining of the ciliary body. It occurs in children as well as adults. Its MR appearance is similar to melanoma, but it calcifies 25% of the time. In children, it is in the differential diagnosis of retinoblastoma, whereas in adults, think melanoma. These tumors are benign or locally invasive. Rarely, distant metastasis occurs. It may rarely involve the retina.

Metastases

Metastatic breast and lung cancer, lymphoma, and leukemia are common ocular malignancies in adults. Many metastatic neoplasms of the globe produce eccentric thickening of the uveoscleral rim and retrobulbar extension that may not be clinically apparent but that can be detected on CT and MR (Fig. 10-12). Choroidal lymphoma and leukemia can appear similar to uveal melanoma on MR, may cause retinal detachment, and may be bilateral (rare for melanoma) (Fig. 10-13).

Figure 10-12 Computed tomography of ocular spread of lymphoma. Note the uveoscleral thickening in the left globe (arrows) representing lymphoma.

Figure 10-13 Uveal tract (ciliary body) lymphoma. A, T2-weighted image (T2WI) with thickening of ciliary body of right globe (arrows). B, T1WI with enhancement in the ciliary body (open arrows) and choroid (black arrows).

Choroidal Osteoma

Choroidal osteoma is a benign tumor, usually seen in young women. These lesions are usually unifocal, demonstrate ossification, and are juxtapapillary in location. CT is the imaging modality of choice in this situation. Punctate calcification in the posterior pole of the globe, usually on the temporal side of the optic nerve, may be easily identified. The differential diagnosis of choroidal osteoma includes amelanotic melanoma and choroidal hemangioma (which do not ossify), metastatic carcinoma, mucinous adenocarcinoma, leukemic or lymphomatous infiltrates, macular choroidal scars, and resolving subretinal hemorrhage, but none of these ossify. An astrocytic hamartoma, retinoblastoma, or medulloepithelioma could look identical.

Persistent Hyperplastic Primary Vitreous

Persistent hyperplastic primary vitreous (PHPV) was previously described as a vascular lesion associated with microphthalmia, retinal-vitreal hemorrhages and detachments, and the persistence of Cloquet’s canal. Norrie disease is an inherited form of PHPV with similar ocular findings associated with seizures, mental retardation, and cataracts.

Coloboma

A coloboma of the eye is a congenital defect in any ocular structure. It is classified as typical or atypical depending on location and derivation. Atypical colobomas occur in the iris. The typical coloboma is a cone-shaped or notch deformity that occurs in the inferior medial portion of the globe. It is caused by incomplete closure of the choroidal fissure, which can result in an abnormal elongated or malformed globe or ocular cyst at the site of the fetal optic fissure closure. It may be associated with orbital cysts, midline craniocerebrofacial clefting, including sphenoidal encephalocele, agenesis of the corpus callosum, and olfactory hypoplasia, as well as cardiac abnormalities, retardation, genital hypoplasia, and ear anomalies. It is a part of the CHARGE syndrome (Coloboma, Heart defects, Atresia of the choana, Retarded Growth and development, and Ear anomalies). Other syndromes having coloboma include Lenz microphthalmia syndrome, Meckel syndrome, trisomy 13, Goldenhar syndrome, Rubinstein-Taybi syndrome, Aicardi syndrome, and Waardenburg anophthalmia syndrome.

On imaging, there is a cone- or notch-shaped deformity, usually of the posterior globe, that may involve the optic nerve, with eversion of a portion of the posterior globe (Fig. 10-14). Other structures, including retina, choroid, iris, and lens, can be affected. The sclera is normal. Colobomas usually arise sporadically and are unilateral, although rarely an autosomal dominant form can exist, with about 60% of those affected having bilateral coloboma.

Figure 10-14 A, Coloboma. Bilateral cone-shaped deformities at the junction of the optic nerve head and globe (open arrows). Bilateral orbital cysts (c) on B, coronal T2-weighted image (T2WI) and C, axial enhanced T1WI in a patient with coloboma.

Phakomatoses

Retinal astrocytic (glial) hamartomas are observed in cases of tuberous sclerosis, neurofibromatosis and, rarely, von Hippel-Lindau disease (see Chapters 3 and 9). On CT, a focal region of calcification is noted in the retina that is much more extensive than that of optic disc drusen and can potentially be confused with retinoblastoma. These hamartomas grow slowly and do not metastasize. A hallmark of von Hippel-Lindau disease is retinal hemangioblastoma (which cannot be identified angiographically). Hemangioblastomas of the retrobulbar optic nerve and orbit have also been reported in von Hippel-Lindau disease. The primary differential diagnosis of such optic nerve lesions is angioblastic meningioma and optic nerve glioma. Half the patients with optic nerve hemangioblastoma have other associated lesions of von Hippel-Lindau disease. Choroidal hemangiomas are reported in Sturge-Weber syndrome (tomato ketchup retina).

Lisch nodules are hamartomas of the iris that produce a focal discoloration and are one of the seven primary criteria of neurofibromatosis type 1 (NF-1). They are not visible on imaging, but the ophthalmologist sees a brown nodule on direct globe visualization or slit-lamp examination of the iris. Lisch nodules usually do not become evident until after age 6, but are present in more than 95% of patients with NF-1 by the early teens.

Retinopathy of Prematurity

Retinopathy of prematury is the result of prolonged oxygen therapy in premature infants. The severity of the condition is related to the birth weight, amount of oxygen used, and extent of prematurity. ROP can, in extreme cases, present as bilateral leukokoria because of traction retinal detachments. CT findings are of increased density in the posterior portion of the globe that may represent calcification. Occasionally, a thin line representing the detached retina can be identified beneath the high density.

Hydroxyapatite Orbital Implants

These are placed in the orbit after enucleation to take up the space once occupied by the eye and to permit movement of an ocular prosthesis. Their porous nature enables fibrovascular ingrowth. The implant has intermediate intensity on all MR pulse sequences and enhances variably. Enhancement is hypothesized to represent vascularization of the implant. Fibrovascular ingrowth (weeks to months) is a prerequisite for drilling and pegging of the hydroxyapatite sphere required to translate the ocular motion to the prosthesis. Nodular or infiltrating areas of enhancement around the implant may suggest recurrent tumor or inflammation.

Prosthetic Intraocular Lens

Contemporary cataract surgery usually includes placement of an intraocular lens. These lenses can be identified on CT or T2WI. This becomes an issue in orbital trauma when concern is raised regarding the position of the lens or about whether the patient has one. The crystalline lens can be dislocated in a variety of different medical conditions. Box 10-3 provides a list of these conditions as well as the common position of these dislocations.

Globe Tenting

Globe tenting occurs when the posterior globe configuration changes so that it appears as a conical or tented structure. It is caused by an intraorbital mass lesion, either acute or subacute, producing proptosis with tethering of the globe by the stretched optic nerve. Ocular tenting has been reported in acute trauma, inflammatory processes, carotid-cavernous fistula, subperiosteal abscess, hemorrhage into lymphangioma, and varix. Tenting with acute proptosis is an indication for emergent surgical decompression.