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Imaging of Intracranial and Orbital Complications of Sinusitis and Atypical Sinus Infection: What the Radiologist Needs to Know
Author’s Accepted Manuscript Imaging of Intracranial and Orbital Complications of Sinusitis and Atypical Sinus Infection: What the Radiologist Needs to Know Vinodkumar Velayudhan, Zeshan A. Chaudhry, Wendy R.K. Smoker, Roman Shinder, Deborah Reede www.elsevier.com/locate/enganabound
PII: DOI: Reference:
S0363-0188(16)30113-X http://dx.doi.org/10.1067/j.cpradiol.2017.01.006 YMDR492
To appear in: Current Problems in Diagnostic Radiology Cite this article as: Vinodkumar Velayudhan, Zeshan A. Chaudhry, Wendy R.K. Smoker, Roman Shinder and Deborah Reede, Imaging of Intracranial and Orbital Complications of Sinusitis and Atypical Sinus Infection: What the Radiologist Needs to Know, Current Problems in Diagnostic Radiology, http://dx.doi.org/10.1067/j.cpradiol.2017.01.006 This is a PDF file of an unedited manuscript that has been accepted for publication. As a service to our customers we are providing this early version of the manuscript. The manuscript will undergo copyediting, typesetting, and review of the resulting galley proof before it is published in its final citable form. Please note that during the production process errors may be discovered which could affect the content, and all legal disclaimers that apply to the journal pertain.
TITLE: Imaging of Intracranial and Orbital Complications of Sinusitis and Atypical Sinus Infection: What the Radiologist Needs to Know Vinodkumar Velayudhan, DO*a, Zeshan A. Chaudhry, MBBS*a, Wendy RK Smoker, MDb, Roman Shinder, MDc, Deborah Reede, MDa a
Department of Radiology, State University of New York Downstate Medical Center Department of Radiology, University of Iowa Hospitals and Clinics c Department of Opthalmology, State University of New York Downstate Medical Center *co-first authors. V.V and Z.A.C contributed equally to this work AUTHORS: 1. Dr. Vinodkumar Velayudhan b
Clinical Assistant Professor of Radiology and Neurology Divisions of Neuroradiology and Emergency Radiology State University of New York Downstate Medical Center Associate Director of Neuroradiology Kings County Hospital Center Brooklyn, NY Mobile: 516 473 4265 Office: 718 245 5103 (9 a.m. to 5 pm, Mon-Fri) Email: [email protected], [email protected] 2.
Dr. Zeshan A. Chaudhry PGY-5 Resident Physician Department of Radiology State University of New York Downstate Medical Center 450 Clarkson Avenue Brooklyn, NY 11203 Kings County Hospital Center Brooklyn, NY Office: 718-245-2682 Email: [email protected], [email protected]
3.
Dr. Wendy RK Smoker Professor Emeritus, Neuroradiology and Neurosurgery Department of Radiology University of Iowa Hospitals and Clinics 200 Hawkins Dr, Iowa City, IA 52246 [email protected]
4.
Dr. Roman Shinder Associate Professor of Clinical Ophthalmology Director of Oculoplastics State University of New York Downstate Medical Center 450 Clarkson Avenue Brooklyn, NY 11203 [email protected]
5.
Dr. Deborah Reede Professor and Chair Department of Radiology State University of New York Downstate Medical Center
450 Clarkson Avenue Brooklyn, NY 11203 Phone: 718-270-1603 Fax: 718-270-2667 Email: [email protected]
Abstract Sinusitis is a common disease. Complications, however, are less common and can be life threatening. Major complications occur from extension of disease into the orbit and intracranial compartment and often require emergent treatment with intravenous antibiotics or operative intervention. Immunocompromised patients with acute sinusitis are susceptible to atypical infections, such as invasive fungal sinusitis, which is a surgical emergency. Therefore, it is important to accurately and promptly identify potentional complications of acute sinusitis to ensure appropriate treatment and minimize negative outcomes. This article reviews the imaging features of a spectrum of complications associated with acute sinusitis and atypical infections. Introduction Rhinosinusitis is defined as inflammation of the paranasal sinus and nasal cavity mucosa. It is a common disease frequently encountered by primary care physicians in both adults and pediatric patients. It affects an estimated 35 million people per year and results in substantial morbidity1. The annual direct medical costs of treatment are approximately $5.8 billion2. This results in nearly 16 million office visits, over 500,000 surgical procedures and is reported to be the fifth leading indication for antibiotic prescriptions by primary care providers1,2,3. The majority of sinus infections are viral in origin and in the acute setting, are usually secondary to viral upper respiratory tract infections. Bacterial infection is the cause in only 2-10 % of cases4; an even smaller number are fungal in origin. Other etiologies include allergic and non-allergic rhinitis, chemical irritation (such as cigarette smoke) and anatomic variants that predispose to obstruction5. Isolated infection of the maxillary sinuses may be odontogenic in origin in up to 20% of cases6. In general, children are more prone to develop sinusitis and suffer complications due to anatomic, immunologic and environmental factors7,8. Most cases resolve with symptomatic treatments without antibiotics, even if bacterial in origin9. Viral and bacterial sinusitis often cannot be differentiated based on symptoms, although certain symptoms, such as purulent nasal discharge and pain, suggest a bacterial origin. A consensus statement published in Otolaryngology-Head and Neck Surgery in 2007 suggests a presumptive diagnosis of bacterial infection if symptoms last greater than ten days following an upper respiratory infection or worsen within ten days after initially improving10.
Pathophysiology and Anatomy The paranasal sinuses are normally sterile. Mucosal edema can cause narrowing and obstruction of the sinus ostia (Figure 1), which leads to stasis of secretions and subsequent infection. The periorbita and orbital septum are major barriers that limit spread of infection into the orbit (Figure 2). The periorbita is the periosteum of the bones that form the orbit. It is contiguous with the periosteum on the inner surface of the skull and dura at the optic foramen, superior orbital fissures, and ethmoid canals. The periorbita is tightly attached to bone at the anterior margin of the orbit and near openings for neurovascular fissures, foramina, and canals11. Elsewhere, the periorbita is loosely connected and creates a potential space for subperiosteal collections. Anteriorly, the periorbita extends into the eyelids and forms the orbital septum12,13. The orbital septum is located deep to the orbicularis oculi muscle and attaches to the levator aponeurosis in the upper eyelid and the tarsal plate in the lower eyelid. Infection may breach the orbital septum through perforations for neurovascular structures. The largest perforation is in the superomedial aspect of the orbital septum for passage of the infratrochlear neurovascular bundle and supraorbital vein to the eyelid12,13. The periorbita appears low in signal on MRI and is difficult to distinguish from the underlying cortical bone14. It is also difficult to visualize the orbital septum on imaging. Its location, however, can be approximated as the area just anterior to the orbital fat or near where the extraocular muscles insert on the anterior globe15. The orbit is bounded by frontal, ethmoid and maxillary sinuses. The parameningeal and periorbital location of the sinuses facilitates development of intracranial and orbital complications of sinusitis. Spread of infection may be either direct or indirect. Direct extension is often through neurovascular foramina, or congenital and acquired osseous defects (Figure 3), which are commonly seen in the lamina papyracea that forms the medial orbital walls and contains foramina for the anterior and posterior ethmoidal arteries. Occasionally, no osseous defect is found. Hematogenous spread is a form of indirect spread via a network of valveless veins that drain the soft tissues of the face and orbits (Figure 4). Thrombophlebitis of the veins that drain the face, sinuses and orbits are thought to be the major route for the spread of infection to adjacent structures7. Emissary veins located in the loose connective tissue layer of the scalp communicate with the intracranial compartment. Bidirectional flow of blood in these veins promotes spread of infection anteriorly into the scalp or intracranially. Infection commonly spreads retrograde into the orbits due to thrombophlebitis of ophthalmic veins and smaller venous tributaries that drain into the cavernous sinuses. Infection of specific sinuses demonstrates a predilection for certain complications (See Table 1) . Orbital complications are most commonly due to ethmoid
followed by frontal sinusitis. Intracranial complications typically occur with frontal, ethmoid and sphenoid sinus disease. Sphenoid sinusitis may result in cavernous sinus thrombosis.
Imaging Protocols: Plain radiography can detect and confirm the clinical diagnosis of sinusitis. However, radiography has shown poor interobserver agreement, a high false negative rate and has been supplanted by CT16. CT is the initial test of choice for evaluating complications of sinusitis as it is widely available and more accurate in depicting sinus pathology, bony detail and anatomic relationships. For orbital complications of sinusitis, helical CT should be performed ideally with intravenous contrast in the axial plane with submillimeter collimation to produce isotropic voxels. These data can then be reconstructed into high-quality sagittal and coronal images. Though less sensitive than MRI, contrast-enhanced CT can be used to quickly assess for intracranial complications, such as large extra-axial collections, brain lesions, mass effect and hydrocephalus. The patient may then be triaged appropriately for emergent neurosurgical intervention and for MRI7. MRI is more sensitive in the evaluation of orbital and intracranial complications of sinusitis6,17. Orbital imaging should be performed using a field of view that includes the nose and orbital soft tissues anteriorly and extends posteriorly through the sella to include the cavernous sinuses. T1-weighted images (T1WI) in the axial and coronal planes can depict orbital anatomy and the stranding and soft tissue thickening that occur with inflammation and infection. Short tau inversion recovery (STIR) or fat suppressed T2 weighted images (FST2) are useful in demonstrating edema and fluid collections. Unless contraindicated, IV contrast should be administered to differentiate abscess from phlegmon, evaluate for venous thrombosis and for intracranial collections and meningitis. Dedicated images of the brain should be obtained with any sinus or orbit MRI to screen for these complications and others, including cerebral infarction. The utility of specific MRI pulse sequences is discussed as they relate to different disease entities later in this article.
Imaging Findings of Sinustis Acute sinusitis is usually clinically evident. Cross-sectional imaging is typically indicated if intracranial or orbital complications are suspected or when evaluating immunocompromised patients18,19. An acutely infected sinus may demonstrate an airfluid level or aerosolized (frothy) secretions (Figure 5A). Mucosal thickening is a nonspecific finding, commonly encountered on imaging, and found incidentally in 20-40% of MR exams6. It is usually indicative of chronic sinusitis, especially with polypoid mucosal thickening, but may also occur with acute sinusitis. Bone thickening and sclerosis are usually associated with chronic sinusitis (Figure 5B and 5C). Inspissated secretions in chronic sinusitis may appear hyperdense or calcified on CT in bacterial and fungal
disease. On MR, secretions demonstrate progressively increased signal on T1WIs and low T2 signal as the ratio of protein to water content increases20. Complications of Sinusitis Orbital involvement is the most common complication of acute sinusitis. It is more common in children, and may be the first presenting symptom of acute sinusitis in this population. Orbital extension of sinus infection is the most common cause of unilateral proptosis in children and the third most common cause of proptosis in adults following thyroid eye disease and orbital pseudotumor7. Orbital infection is divided into two major categories: Preseptal (periorbital/superficial to the orbital septum) and postseptal (deep to the orbital septum). In 1970, Chandler and colleagues developed a classification system of sinusitis complications, based on orbital anatomy (Table 2)21. Following the advent of cross-sectional imaging, modifications to this classification system were made22,23. The current classification divides orbital complications into five groups. Note that these do not represent progression of disease as each complication can have different causes and occur exclusive of the others.
Preseptal Cellulitis Preseptal cellulitis is an infectious, inflammatory edema in the soft tissues anterior to the orbital septum. Patients present with swelling of the eyelid and surrounding soft tissues. Because the inflammation does not involve soft tissues deep to the orbital septum, there should be no vision loss, restricted extraocular movement or other findings associated with postseptal involvement (Table 3). Comprehensive clinical assessment is difficult when there is significant swelling of the eyelids. The etiology is most often due to a local skin infection (e.g. insect bite, trauma or retained foreign body) in both adults and children and may also be due to sinusitis in children24. Most patients respond to treatment with antibiotics (oral or intravenous). Surgery is indicated when there is an associated eyelid abscess or progression to orbital abscess. On imaging, preseptal cellulitis appears as swelling of the eyelid (Figure 6). Periorbital soft tissue swelling may also be present. The postseptal region, including the extraocular muscles, postseptal fat and lacrimal glands should be normal. Imaging findings of edema on CT consist of eyelid soft tissue thickening and increased density and stranding of the surrounding tissues. On MRI, eyelid edema may be present and appear as low signal reticulation on T1WI and hyperintense on FST2/STIR images with corresponding enhancement.
Orbital Cellulitis Orbital cellulitis represents inflammatory edema posterior to the septum without abscess formation. It is usually due to acute sinusitis. The vast majority of cases are secondary
to acute ethmoid sinusitis, typically involving the medial orbit. Patients can present with eyelid edema, erythema, ptosis, chemosis, and proptosis. There may be limited or no restriction of extraocular movement, depending on the degree of inflammation. Visual acuity is usually normal. Patients are typically febrile and have leukocytosis. Orbital cellulitis can lead to serious neurologic and visual deficits. Treatment consists of intravenous broad-spectrum antibiotics and sinus and orbital drainage if indicated. On imaging, orbital edema, diffuse or localized, is present posterior to the orbital septum, with or without periorbital soft tissue swelling (Figure 7). Inflammatory changes may involve extraconal structures, intraconal structures or both. Imaging shows edema and enhancement, without a rim-enhancing fluid collection to indicate a discrete abscess. It is important to differentiate between orbital and preseptal cellulitis because orbital cellulitis generally requires hospital admission for IV antibiotics and possible surgical intervention.
Subperiosteal Abscess A subperiosteal abscess (SPA) is a collection of purulent material between the bone and periorbita. The most common location is along the medial orbital wall, in association with ethmoid sinusitis. It can also occur in the superior aspect of the orbit, in association with frontal sinusitis, or rarely along the orbital floor, associated with maxillary sinusitis. A trial of IV antibiotics may be sufficient in children if the collection is small and visual function is not impaired. Drainage of the abscess and sinuses is performed in adults, older children, immunocompromised patients, and those who fail to respond to antibiotics. Urgent drainage is indicated when visual or neurologic complications are suspected. An abscess is best demonstrated on post-contrast CT and MR where a rim-enhancing fluid collection is identified (Figure 8). A collection along the medial orbital wall is readily identified on axial images. However, a collection along the roof and floor is best demonstrated in the coronal and sagittal planes. Diffusion-weighted MR demonstrates restricted diffusion. A medial SPA can displace extraocular structures and result in lateral dystopia and/or proptosis. If proptosis is severe, tension develops, and the posterior margin of the globe becomes tethered, which results in stretching of the optic nerve, which may lead to ischemic necrosis of the nerve, which is an ophthalmologic emergency (Figure 9B). Extraocular muscles may be enlarged due to myositis and result in diminished ocular movement.
Orbital Abscess An orbital abscess is a collection of pus that is not subperiosteal in location, less common than SPA, and may be intraconal or extraconal. Extraconal abscess is usually
secondary to orbital cellulitis or rupture of an SPA6. Intraconal abscess is typically due to penetrating trauma or surgical complications25. Clinical symptoms are similar to those of orbital cellulitis. Stretching of the optic nerve with ischemic necrosis, optic neuritis, or compression of the optic nerve at the orbital apex can result in loss of visual acuity and eventual blindness. Mass effect on cranial nerves as they exit the superior orbital fissure may result in ophthalmoplegia and diplopia. Treatment consists of medical therapy and surgical drainage of the orbital abscess and infected sinuses. Imaging shows a rim-enhancing fluid collection with surrounding inflammatory changes. The collection should be clearly separate from osseous structures to diagnose an orbital abscess (Figure 9).
Cavernous Sinus and Ophthalmic Vein Thrombosis: Preseptal soft tissues drain primarily into the systemic venous circulation. Venous drainage of the midface, sinuses, and orbits is via a rich network of valveless veins. These structures drain via the superior and inferior ophthalmic veins into the cavernous sinuses. The infraorbital and deep facial veins drain into the pterygoid venous plexus, which communicates with the cavernous sinuses via emissary veins within the foramen ovale and a tributary of the inferior ophthalmic vein that courses through the inferior orbital fissure (Figure 4)26. Cavernous sinus and ophthalmic vein thrombosis/thrombophlebitis are commonly due to infections in the areas they drain. Patients with cavernous sinus thrombosis are usually very ill and may have multiple cranial nerve palsies, headache, fever and signs of meningitis. Ophthalmologic findings, due to venous congestion, include periorbital edema, proptosis, chemosis and engorgement of retinal veins with papilledema on fundoscopy. Restricted movement or paralysis of extraocular muscles occurs because of involvement of cranial nerves (CN) III, IV, V1 and V2 that course in the lateral wall of the cavernous sinus and cranial nerve VI within the cavernous sinus proper (Figure 10). Cavernous sinus thrombosis due to sinus infection is usually treated with sinus drainage and high-dose intravenous antibiotics. Unlike other forms of cerebral venous and systemic deep vein thrombosis, the use of anticoagulants is controversial because of the risk of intracranial and orbital hemorrhage. On imaging, the normal cavernous sinus should demonstrate lateral margins that are either straight or concave. Convex bulging of the lateral wall is abnormal and should prompt further investigation to exclude pathologies such as, thrombosis, neoplasm, carotid cavernous fistula, aneurysm or tortuous ICA. Non-contrast CT (NCCT) may be normal. Abnormal findings include cavernous sinus and sometimes superior ophthalmic vein enlargement, infiltration of the intraorbital fat, proptosis and enlargement of extraocular muscles. On contrast-enhanced CT (CECT), the lateral dural wall of the cavernous sinus should enhance. After a sufficient delay of at least 45 seconds, venous structures of the cavernous sinus enhance homogeneously
and the cavernous ICA will not be visualized separately27. Thrombus may appear as a localized filling defect or non-enhancement of the entire cavernous sinus. MRI and contrast-enhanced MRV are considered superior to CT venography in evaluating cavernous sinus thrombosis28. MRI demonstrates variable signal in the cavernous sinus, often with high signal on FLAIR images. Filling defects or lack of enhancement may be seen. On routine post-contrast images, the only flow void present in the cavernous sinus is the ICA and should not be confused with thrombus. On both CECT and MRI, the cavernous sinus may be enlarged, with dilatation and thrombosis of the superior ophthalmic vein (Figure 11). Pott’s Puffy Tumor: In addition to orbital and intracranial complications, osteomyelitis may occur, most often associated with frontal sinusitis29. Frontal bone osteomyelitis with an associated subperiosteal/subgaleal abscess involving the overlying scalp is termed the Pott’s Puffy tumor. It can also be seen in the post-traumatic setting. This infection may spread intracranially resulting in meningitis, brain abscess, and extra-axial empyemas. Intracranial spread of infection can occur via three major pathways: 1) along valveless emissary veins that cross the calvarium and allow for bi-directional spread into the scalp or intracranially (Figure 12); 2) along nerves extending through the meninges; 3) through congenital or acquired osseous defects. Clinical presentation includes forehead swelling with pitting edema and tenderness. Headache, fever, and nasal drainage may also be present. Meningeal signs, altered mental status, and focal neurologic findings strongly suggest intracranial involvement. MRI is best for evaluation and should be performed if neurologic complications are clinically suspected. CT is highly sensitive in demonstrating sinusitis and associated subgaleal abscesses in Pott’s Puffy tumor and is often associated with bone destruction involving the inner and outer tables of the frontal sinus. MRI demonstrates marrow edema and enhancement due to osteomyelitis. A subgaleal abscess appears as a rim-enhancing fluid collection, closely adherent to the outer table of the frontal bone, with surrounding inflammatory changes on both CT and MRI, as well as with restricted diffusion on DWI (Figure 13).
Intracranial Complication of Sinusitis Potential intracranial complications include epidural and subdural abscess/empyema, meningitis, cerebritis, brain abscess, and dural sinus thrombosis. Although intracranial complications of sinusitis are rare, they can cause serious neurological deficits and other morbidity and mortality. Thirty to 45% of patients have residual long-term neurologic deficits7,30,31. The true incidence is difficult to determine because most cases of sinusitis are uncomplicated, treated in outpatient settings, and the literature often
contains only case reports and series of complicated cases. Three to 6% of patients hospitalized with sinusitis develop intracranial complications32,33,34,35. Up to 45% of patients exhibit more than one focus of infection: intracranial and/or orbital31,36. Therefore, it is important to maintain a high index of suspicion for intracranial involvement in patients with orbital extension. However, those with intracranial complications tend to have a longer duration of symptoms with more complicated and protracted hospital stays. They typically occur in older patients. The most common symptoms in both adult and pediatric populations are fever and headache30,36. Other symptoms include seizures, altered mental status, focal neurological deficits, meningeal signs and ocular complaints32,33,36,37. However, some patients with intracranial spread may be asymptomatic and detected only on imaging performed to evaluate the sinuses. Extracranial complications, particularly intraorbital, usually dominate the clinical presentation. This results in patients with extracranial complications presenting earlier since intracranial complications often have indolent, nonspecific or clinically silent features.
Extra-axial Collections (Epidural Abscess and Subdural Empyema) Spread of infections from the frontal sinus to the anterior cranial fossa results in the development of epidural abscess (EDA) and subdural empyema (SDE). Older studies report SDE as the most common complication; recent studies show EDA to predominate30,34,37. EDA occurs between the outer layer of the dura and the inner table of the calvarium. Initially, EDA are clinically occult or present with nonspecific symptoms such as headaches. This is likely due to the restricted space in which they develop, which slows progression until they either penetrate the dura resulting in a SDE or become large enough to cause significant mass effect and elevated ICP. SDE, however, can rapidly spread over the convexities and therefore can present more acutely with worrisome neurological findings, including neurological deficits and altered mental status30. EDA seems to be more commonly associated with intraorbital involvement30. Treatment requires surgical intervention. Imaging findings of EDA include a low-density, lenticular-shaped, extra-axial fluid collection on CT with an enhancing rim. An epidural collection does not cross sutures, although they can cross the midline. Adjacent mass effect and parenchymal edema can be present. The appearance on MRI includes T2 hyperintensity with variable T1 signal (depending on the relative proteinaceous/hemorrhagic content) with surrounding rim enhancement (Figure 14). Similar to other abscesses, there is often restricted diffusion on DWI. SDE often appears as a crescent-shaped, hypodense, rim-enhancing collection that can cross sutures, but not the midline. CT is often the first imaging study and may be negative in early cases when collections are small. CECT is often sensitive enough to
visualize SDEs; however, it is not as sensitive as MRI, and may fail to detect smaller collections6,30. Mass effect is often secondary to edema and ischemia, not necessarily from the extra-axial collection36. This can cause effacement of the basilar cisterns and cortical sulci. On MRI, T2WI demonstrate a hyperintense collection with mass effect. The rim is often T1 hyperintense on the non-contrast sequence. Diffusion-weighted imaging may aid in differentiating between SDE and EDA. Tsuchiya et al. noted that, while SDE demonstrated restricted diffusion, EDA had variable signal patterns, often low or mixed, on the diffusion trace images38,39. Reactive subdural effusions are a common complication of meningitis, especially in infants, and can occur in cases of complicated sinusitis. These effusions usually resolve without treatment. Therefore, subdural effusion should be differentiated from SDE. Both are hyperintense on T2 and show enhancement along the cerebral surface of the lesion on post-contrast images; however, SDE will demonstrate restricted diffusion39,40. SDE is a neurosurgical emergency with mortality rates ranging from 10%-70%6. SDE progresses rapidly, spreading over the convexities and often localizing in the supratentorial compartment. If untreated, this will result in increased intracranial pressure, development of focal neurological deficits, seizures, and coma within 1-2 days, thus underscoring the need for prompt diagnosis and aggressive management, including urgent surgical intervention6,36.
Meningitis Meningitis occurs most often in association with extra-axial suppuration rather than in isolation. While many studies report either EDA or SDE as the most common complication of sinusitis, others have found meningitis to be more common41. It is frequently secondary to sphenoid or ethmoid sinusitis. The most common sequelae are seizure and hearing loss. MR is more sensitive than CT for diagnosis. Leptomeningeal enhancement occurs in cisterns and sulci and pachymeningeal enhancement occurs along cerebral convexities and dural reflections (Figures 13, 14 and 15). Associated imaging findings include hydrocephalus and adjacent cerebral edema. Purulent exudate can form in the subarachnoid space, with increased attenuation on CT and incomplete suppression of CSF signal on FLAIR and restricted diffusion on MRI40.
Cerebritis and Cerebral Abscess Spread from the extra-axial space to the parenchyma results in focal cerebritis and abscess formation, which is a rare complication of intracranial spread of sinus disease. The frontal and parietal lobes are most often affected41.
Initially cerebritis may develop with focal brain edema manifesting as low attenuation on noncontrast CT. MRI is more sensitive for detection, particularly in the initial stages with increased signal on T2 and FLAIR sequences. Patchy enhancement on postcontrast sequences may or may not be seen in cerebritis. Frank abscess formation will have the characteristic imaging features of a well-defined, rim-enhancing fluid collection that demonstrates restricted diffusion, with surrounding mass effect and vasogenic edema (Figure 15). Rim enhancement is often thicker along the cortical aspect of the abscess. Treatment should include surgical drainage of the abscess, parenteral antibiotics and definitive management of the sinus disease.
Fungal Sinusitis Fungal sinusitis is classified as non-invasive or invasive. Among noninvasive disease, there are two subtypes: allergic fungal sinusitis and mycetoma. Invasive fungal sinusitis is subdivided into three groups: Acute fulminant, chronic invasive, and granulomatous42. The primary fungal pathogens are Zygomycetes (Mucor spp) and Ascomycetes (Aspergillus spp). A diagnosis of invasive fungal sinusitis requires histopathologic evidence of hyphae penetrating the mucosa, submucosa or bone with invasion of blood vessels and prominent tissue necrosis7,42,43.
Noninvasive Fungal Sinusitis Allergic fungal sinusitis is the most common form of fungal sinusitis19,44. It occurs in patients with a history of atopy (e.g. asthma and allergic rhinitis) and is often found in association with sinonasal polyposis6. It is felt to represent a hypersensitivity reaction to fungal pathogens, rather than an infection. The sinuses contain material referred to as “allergic mucin,” inspissated secretions that contain eosinophils, Charcot-Leyden crystals and eosinophilic degradation products. Mycetomas occur when these secretions become superinfected with fungus and form a ball6,19. Allergic fungal sinusitis is typically bilateral and involves multiple sinuses. Sinuses may be expanded with varying degrees of opacification and central high attenuation on CT corresponding to allergic mucin, desiccated secretions, and fungal concretions (Figure 16)6,45,46. Areas of low density along the margins of the sinus lumen are due to mucosal thickening. Co-existing polyps may be present and result in nodular mucosal thickening with expansion of the sinuses and sinus ostia. Sclerosis of the sinus walls may be seen due to chronic inflammation. Advanced cases of chronic allergic fungal sinusitis may result in marked thinning and erosion of sinus walls with intraorbital and intracranial extension. On MRI, T1 signal is variable and may be high, intermediate or low signal. Metallic ions, including zinc and manganese, can produce high T1 signal. Inflammatory mucosal thickening has high T2 signal. Central markedly diminished signal or signal voids are due to metallic ions, high protein and low water content of inspissated
secretions (Figure 16)6,19. This can mimic an aerated sinus. Polyposis and chronic allergic fungal sinusitis often coexist and there is considerable overlap in the imaging appearances, especially on CT. However, polyposis and inflammatory mucosal thickening demonstrate high T2 signal and enhancement, while fungal elements and desiccated secretions have low T2 signal and little, if any, enhancement. Mycetomas (fungus balls) typically involve one sinus, usually the maxillary sinus, and are hyperdense on CT due to matted hyphae that may contain calcifications (Figure 17). The sinus walls may be thickened due to chronic inflammation or thinned and eroded from expansion or pressure necrosis from the mycetoma. On MRI, the fungal elements in the center of the sinus demonstrate markedly diminished or no signal on T2WI and variable T1 signal (Figure 17). Mycetomas do not enhance; inflammatory changes along the walls of the sinus may enhance and appear hyperintense on T2WI. Treatment of chronic allergic fungal sinusitis is surgical removal of the allergic mucin and restoration of sinus drainage. Topical steroids are used postoperatively to suppress the immune response and prevent recurrence. Since this is a hypersensitivity reaction, antifungal medication is not required. For mycetomas, surgical removal of the fungal material and restoration of sinus drainage are usually curative19,44.
Invasive Fungal Sinusitis Acute (fulminant) invasive sinusitis is the most lethal form of fungal sinusitis with a mortality rate of 50-80%. It typically occurs in diabetics and immunocompromised and severely neutropenic patients. Disease typically progresses rapidly over days to a few weeks with fungal invasion of the mucosa, submucosa, blood vessels and bones of the nasal cavity and sinuses. Skull base invasion, intracranial and orbital extension are common. Angioinvasion may involve the cavernous sinus, ICA, and its branches. Invasive fungal sinusitis initially produces significant unilateral inflammatory changes and mucosal edema in the nasal cavity, though this finding is nonspecific19,47. Disease progresses from the nasal cavity to the sinuses, orbits and intracranially to involve the cavernous sinuses, brain, and meninges (Figure 18). The ethmoid and sphenoid sinuses are more commonly involved19. Sinus mucosal thickening may be subtle or mild. As the disease progresses, sinus opacification increases and bone destruction occurs. Premaxillary or retromaxillary fat inflammation are important indicators of invasive disease and can be seen in acute and chronic forms19 (Figure 19). Invasive disease tends to extend along vasculature. Specifically, sphenoid sinus disease may result in cavernous sinus thrombosis and compromise the ICA and can lead to cerebral infarction with restricted diffusion on DWI (Figure 20). Invasive fungal sinus disease should be considered whenever there is concurrent involvement of the nasal cavity, sinuses, and orbits6, particularly in the immunocompromised.
Chronic invasive sinusitis occurs in immunocompetent or mildly immunocompromised patients with a history of chronic rhinosinusitis. It has a similar pattern of disease to fulminant sinusitis but progresses over a longer time course, typically months. Granulomatous invasive sinusitis occurs primarily in North Africa (in the Sudan) and Southeast Asia. It is rare in the United States. This disease produces noncaseating granulomas with a similar pattern of involvement as chronic invasive sinusitis. Chronic and granulomatous invasive fungal sinusitis may be indistinguishable on imaging and can present with similar findings as advanced fulminant invasive disease. CT may demonstrate high attenuation material within the sinus (much less commonly seen in acute invasive disease) that appears iso to hypointense on T1WI and markedly hypointense on T2WI19,48 (Figure 19). Bony destruction or sclerosis may be present with extension beyond the sinus that can exceed the amount of disease within the sinus48. Sclerosis due to chronic inflammation helps differentiate chronic and granulomatous invasive forms from acute invasive disease19. The mass-like appearance, bone destruction and transpatial involvement of chronic and granulomatous invasive fungal sinusitis may mimic a neoplasm. While it may not always be possible to differentiate the two, the presence of calcifications, markedly diminished T2 signal and lack of enhancement of the non-inflammatory components favor the diagnosis of fungal sinus disease over tumor. For all forms of invasive fungal sinus disease, treatment is aggressive surgical debridement and administration of systemic antifungal medication. Reversal of diabetic ketoacidosis and neutropenia improve mortality19.
Summary Intracranial and orbital complications of sinusitis can have significant morbidity, including vision loss and other serious neurologic impairment and death. Radiologists should have a high index of suspicion when interpreting sinus imaging and closely examine the brain and orbits, particularly in patients with visual or neurologic symptoms. Becoming familiar with common and uncommon complications of sinusitis and patterns of spread of disease will facilitate prompt and accurate diagnosis. In addition, fungal sinusitis can have highly characteristic features and its fulminant invasive forms need to be recognized in immunocompromised patients as disease can progress rapidly and result in fatality. CT is the initial examination of choice and should be supplemented with contrast enhanced MRI to better characterize orbital and intracranial complications seen on CT or if CT is nonrevealing and clinical suspicion remains high.
FIGURE CAPTIONS: Figure 1: Maxillary sinus ostia. Coronal CT demonstrates the maxillary sinus ostia (white arrows), the opening for the drainage pathway of each maxillary sinus.
Figure 2: Periorbita and orbital septum. A) Sagittal illustration shows the location of the periorbita. B) The periorbita continues anteriorly as the orbital septum (arrow) in the upper eyelid, as demonstrated on the sagittal T1WI. Figure 3: Direct spread of infection. Axial CT image demonstrates a defect in the left medial orbital wall (lamina papyracea), a common location for dehiscence. Direct spread of infection occurs through neurovascular foramina or via congenital and acquired defects in bone. Figure 4: Indirect Spread of Infection. Lateral illustration demonstrates the network of communicating veins draining the face, sinuses and orbits. • Superior and inferior ophthalmic veins drain directly into the cavernous sinus (CS). • Infra-orbital vein can drain into the CS via the inferior ophthalmic vein and pterygoid plexus. • The deep facial vein drains into the pterygoid plexus and into the CS. Figure 5. Acute vs. chronic sinusitis. A) Axial T2WI demonstrates right maxillary sinus air fluid level (white arrow), suggestive of acute sinusitis. B) Axial CT demonstrates opacification of left sphenoid sinus with diffuse sclerosis and thickening of its walls (black arrow), indicating chronicity. C) Axial CT demonstrates partial opacification of left maxillary sinus with high density material centrally (white arrow) and wall thickening (black outlined arrow) due to chronic sinusitis. Calcifications can be seen in desiccated secretions from chronic sinusitis and in fungal sinusitis. Figure 6. Preseptal and postseptal cellulitis. Axial noncontrast CT in a patient with preseptal and orbital cellulitis. Soft tissue swelling involving the left eyelid (white arrows) consistent with preseptal cellulitis. Mild infiltration of the left retrobulbar fat is also seen (black outlined arrow) consistent with orbital cellulitis. Figure 7. Orbital cellulitis. Contrast enhanced axial CT scan demonstrates maxillary and ethmoid sinusitis with left orbital cellulitis. There is left preseptal soft tissue swelling (white arrow) and postseptal extension (black arrow) consistent with orbital cellulitis. Figure 8. Subperiosteal abscess. A) Illustration demonstrates the location of a subperiosteal abscess (black arrow) along the medial orbital wall beneath the periorbita (white outlined arrow). B) CECT shows a large peripherally enhancing subperiosteal abscess (asterisk) along the left medial orbital wall and anterior to the maxillary sinus with proptosis. Left maxillary and ethmoid sinus opacification with a dehiscence (white arrow) in the anterior wall of the maxillary sinus. C) Clinical image (same patient) demonstrates downward gaze restriction of the left eye consistent with postseptal involvement. Figure 9. Orbital abscess. Axial (A) and coronal (B) CECT images in a patient with frontal sinusitis and orbital abscess. There is a fusiform extraconal collection (large white arrow) with faint peripheral enhancement in the superior right orbit displacing the
globe inferiorly. The collection is an orbital abscess and not subperiosteal as there is fat plane (small white arrows) separating it from the orbital roof. There is tension on the right globe and optic nerve with tethering at the nerve insertion (white arrowhead). Figure 10. Anatomic basis of cranial neuropathies in CS thrombosis and sphenoid sinusitis. A) Coronal illustration demonstrates the location of the CN III, IV, V1 and V2 in the lateral dural wall of the CS and CN VI coursing within the sinus inferolateral to the cavernous ICA. Gaze palsy is related to involvement of these nerves, which supply the EOM. B) Coronal CT shows the relationship of the optic nerve canal (white arrow) coursing superior to the anterior aspect of the sphenoid sinus (asterisk). Optic neuropathy and afferent pupillary defect are likely secondary to encroachment on or irritation of the optic nerve (CN II) in the optic canal above the sphenoid sinus. Figure 11. Cavernous sinus and superior ophthalmic vein (SOV) thrombosis. A) Axial CE T1WI demonstrates filling defects in the right cavernous sinus (white arrow) consistent with thrombosis in this patient with ethmoid and sphenoid sinusitis (black arrows). B) Axial CECT in the same patient demonstrates the absence of enhancement of the right CS (black arrow) and a thrombosed SOV. Figure 12. Anatomic basis for bidirectional spread of infection via emissary veins. Illustration demonstrates emissary veins traversing the calvarium allowing for spread of infection anteriorly into the overlying subgaleal layer of the scalp or posteriorly into the intracranial compartment. Figure 13. Pott’s puffy tumor. Axial CE T1WI (A) demonstrates a rim enhancing epidural fluid collection (white asterisk) with restricted diffusion on DWI (black arrow, B) consistent with an abscess. There is adjacent dural enhancement in the interhemispheric fissure (outlined white arrows, A) and leptomeningeal enhancement in the sulci (outlined black arrows, B) consistent with meningitis. This process extends anteriorly into the scalp with a subgaleal abscess, also demonstrating peripheral enhancement (white arrow, A) and restricted diffusion (white arrow, B). Figure 14. Intracranial complications of sinusitis: Empyema. Axial CE T1WI demonstrates ethmoid and sphenoid sinusitis (small white arrows), thrombosis of the right superior ophthalmic vein (large white arrow) and cavernous sinuses (not shown) and bilateral extra-axial peripherally enhancing fluid collections (black arrows) consistent with subdural empyemas anterior to the temporal lobes. Figure 15. Intracerebral abscess. Coronal CE T1WI demonstrates a left supraorbital mucopyocele filling and expanding a left supraorbital ethmoid air cell (asterisk) and displacing the left globe (small white arrows). There is an intra-axial rim enhancing lesion in the left frontal lobe consistent with a brain abscess (large white arrow). Linear dural-based enhancement over the superior left frontal lobe is consistent with meningitis (black arrow).
Figure 16. Allergic Fungal Sinusitis (AFS). CT (images A and B) demonstrate complete sinus opacification (with central high and peripheral low attenuation) in the frontal, maxillary and sphenoid sinuses (black arrows) with expansion of the ethmoid air cells (white arrows, B) and widening of the accessory maxillary sinus ostia (white arrow, A). This is the classic appearance of AFS. Sinonasal polyposis often coexists and can have a similar appearance on CT. (C) Axial FLAIR image demonstrates markedly diminished areas of signal (white arrows) with surrounding mucosal thickening in the frontal sinuses. (D) Axial CT scan in the same patient demonstrates corresponding areas of high density material within, and expansion of, the frontal sinuses (black arrows) with marked thinning and dehiscence of the posterior wall (white arrow). Figure 17. Mycetoma. Coronal CT (A) demonstrates opacification of the right ethmoid and maxillary sinuses with a hyperdense, calcified lesion in the region of the medial wall of the right maxillary sinus and ostiomeatal unit (black arrow). The lesion has markedly diminished signal on the coronal T2WI (B, white arrow). Inflammatory mucosal thickening (B, black arrow) and intermediate signal secretions are also noted (B, asterisk). Figure 18. Invasive mucormycosis in a patient with acute myelogenous leukemia, neutropenia and necrotic nasal ulcer. Coronal T2 images demonstrates right sided pansinusitis (black arrows), opacification of the right nasal cavity (white arrows) and inflammatory changes in the right orbital fat (large white arrow, B) and masticator space (circle, B). Figure 19. Chronic invasive fungal sinusitis. (A) Axial CT using soft tissue window demonstrates bilateral maxillary sinus opacification with high density material on the left (black arrow) and marked infiltration of the fat anterior to the sinus (white arrow) in a patient with symptomatology for months. (B) Bone window image demonstrates destruction of the anterior and medial walls of the left maxillary sinus (arrows). Axial T1WI without (C) and with contrast (D) in another patient with chronic symptoms demonstrates effacement of the right pterygopalatine fossa and retromaxillary fat with enhancement (large white arrows). There is involvement of the cavernous sinuses with lack of enhancement and enlargement on the right (small arrows, D). Figure 20. Invasive fungal sinusitis with angioinvasion and cerebral infarction. Coronal CE T1WI (A) demonstrates absent enhancement of the left cavernous sinus (white arrow) consistent with thrombosis and narrowing of the left cavernous ICA. Axial DWI (B) demonstrates multiple left-sided watershed infarcts (white arrows) due to compromise of the left ICA. REFERENCES: 1. Lucas JW, Schiller JS, Benson V. Summary health statistics for U.S. adults: National Health Interview Survey, 2001. Vital health stat 10. 2004. 1-134.
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21. Chandler JR, Langenbrunner DJ, Stevens ER. The pathogenesis of Orbital complications in acute sinusitis. Laryngoscope 1970; 80(9), 1414-28. 22. Schramm VL Jr, Curtin HD, Kennerdell JS. Evaluation of orbital cellulitis and results of treatment. Laryngoscope. 1982; 92(7 Pt 1):732-8. 23. Moloney JR, Badham NJ, McRae A. The acute orbit. Preseptal (periorbital) cellulitis, subperiosteal abscess and orbital cellulitis due to sinusitis. J Laryngol Otol Suppl. 1987; 12:1-18. 24. Botting AM, McIntosh D, Mahadevan M. Paediatric pre- and post-septal periorbital infections are different diseases. A retrospective review of 262 cases. Int J Pediatr Otorhinolaryngol 2008; 72(3): 377-83. 25. LeBedis CA, Sakai O. Nontraumatic orbital conditions: diagnosis with CT and MR imaging in the emergent setting. Radiographics. 2008; 28(6):1741-53. 26. Weisman RA. Surgical anatomy of the orbit. Otolaryngol Clin North Am. 1988 Feb; 21(1):1-12. 27. Rodallec MH, Krainik A, Feydy A, Hélias A, Colombani JM, Jullès MC. Cerebral venous thrombosis and multidetector CT angiography: tips and tricks. Radiographics. 2006; 26 Suppl 1:S5-18. 28. Igarashi H, Igarashi S, Fujio N, Fukui K, Yoshida A. Magnetic resonance imaging in the early diagnosis of cavernous sinus thrombosis. Ophthalmologica. 1995; 209(5):292-6. 29. Bambakidis NC, Cohen AR. Intracranial complications of frontal sinusitis in children: Pott’s puffy tumor revisited. Pediatr Neurosurg 2001; 35:82–9. 30. Germiller JA, Monin DL, Sparano AM, Tom LW. Intracranial complications of sinusitis in children and adolescents and their outcomes. Arch Otolaryngol Head Neck Surg. 2006; 132(9):969-76. 31. Jones NS, Walker JL, Bassi S, Jones T, Punt J. The intracranial complications of rhinosinusitis: can they be prevented? Laryngoscope. 2002; 112(1):59-63. 32. Giannoni CM, Stewart MG, Alford EL. Intracranial complications of sinusitis. Laryngoscope. 1997; 107(7):863-7 33. Clayman GL, Adams GL Paugh DR, Koopmann CF Jr. Intracranial complications of paranasal sinusitis: a combined institutional review. Laryngoscope. 1991; 101(3):234-9. 34. Herrman BW, Forsen JW Jr. Simultaneous intracranial and orbital complications of acute rhinosinusitis in children. Int J Pediatr Otorhinolaryngol. 2004; 68(5):61925. 35. Lerner DN, Choi SS, Zalzal GH, Johnson DL. Intracranial complications of sinusitis in childhood. Ann Otol Rhinol Laryngol. 1995; 104(4 Pt 1):288-93. 36. Osborn MK, Steinberg JP. Subdural empyema and other suppurative complications of paranasal sinusitis. Lancet Infect Dis. 2007; 7(1):62-7. 37. Gallagher RM, Gross CW, Philips CD. Suppurative intracranial complications of sinusitis. Laryngoscope. 1998; 108(11 Pt 1):1635-42. 38. Tsuchiya K, Osawa A, Katase S, Fujikawa A, Hachiya J, Aoki S. Diffusionweighted MRI of subdural and epidural empyemas.Neuroradiology. 2003; 45(4):220-3.
39. Wong AM, Zimmerman RA, Simon EM, Pollock AN, Bilaniuk LT. Diffusionweighted MR imaging of subdural empyemas in children. AJNR Am J Neuroradiol. 2004; 25(6):1016-21. 40. Dankbaar JW, van Bemmel AJ, Pameijer FA. Imaging findings of the orbital and intracranial complications of acute bacterial rhinosinusitis. Insights imaging. 2015; 6(5):509-18. 41. Younis RT, Lazar RH, Anand VK. Intracranial complications of sinusitis: a 15year review of 39 cases. Ear Nose Throat J. 2002; 81(9):636-8, 640-2, 644. 42. deShazo RD, Chapin K, Swain RE. Fungal Sinusitis. N Engl J Med 1997; 337:254-259. 43. deShazo RD. Syndromes of invasive fungal sinusitis. Medical Mycology. 2009; 47(supplement 1):S309–314. 44. Schubert MS. Allergic fungal sinusitis. Otolaryngol Clin North Am 2004; 37(2):301–326. 45. Mukherji SK, Figueroa RE, Ginsberg LE, Zeifer BA, Marple BF, Alley JG. Allergic fungal sinusitis: CT findings. Radiology. 1998; 207(2):417–422. 46. Manning SC, Merkel M, Kriesel K, Vuitch F, Marple B. Computed tomography and magnetic resonance diagnosis of allergic fungal sinusitis. Laryngoscope 1997; 107(2):170–176. 47. DelGaudio JM, Swain RE Jr, Kingdom TT, Muller S, Hudgins PA. Computed tomographic findings in patients with invasive fungal sinusitis. Arch Otolaryngol Head Neck Surg 2003; 129(2):236–240. 48. Reddy CE, Gupta AK, Singh P, Mann SB. Imaging of granulomatous and chronic invasive fungal sinusitis: comparison with allergic fungal sinusitis. Otolaryngol Head Neck Surg. 2010; 143(2):294-300.
• • • • • • •
COMPLICATIONS ASSOCIATED WITH INFECTIONS OF SPECIFIC SINUSES FRONTAL AND ETHMOID SINUSITIS SPHENOID SINUSITIS Orbital cellulitis and abscess and • Cavernous sinus thrombosis subperiosteal abscess • Meningitis Meningitis • Temporal lobe and epidural abscess Epidural abscess • Superior orbital fissure syndrome: Subdural empyema proptosis, orbital pain, and Frontal lobe abscess ophthalmoplegia (CN III, IV, VI) + Superior sagittal sinus thrombosis numbness in ophthalmic division of Pott’s Puffy tumor (frontal) trigeminal nerve Direct extension from the maxillary sinus to critical structures is rare.
Table 1. Infection of specific sinuses have a predilection for certain complications
Chandler Classification
Group I: Preseptal Cellulitis
Group II: Orbital Cellulitis
Group III: Subperiosteal Abscess
Group IV: Orbital Abscess
Group V: Cavernous Sinus Thrombosis
Table 2. The Chandler classification system of orbital complications of sinusitis. These classifications do not represent a progression of disease since each category can have various underlying causes.
Clinical Signs of Postseptal Involvement of Orbit Infections
Proptosis Limitation of gaze/extraocular movement Decreased visual acuity Color vision defects Afferent pupillary defect
Table 3. Clinical Signs of Postseptal Involvement of Orbital Infections
PII: DOI: Reference:
S0363-0188(16)30113-X http://dx.doi.org/10.1067/j.cpradiol.2017.01.006 YMDR492
To appear in: Current Problems in Diagnostic Radiology Cite this article as: Vinodkumar Velayudhan, Zeshan A. Chaudhry, Wendy R.K. Smoker, Roman Shinder and Deborah Reede, Imaging of Intracranial and Orbital Complications of Sinusitis and Atypical Sinus Infection: What the Radiologist Needs to Know, Current Problems in Diagnostic Radiology, http://dx.doi.org/10.1067/j.cpradiol.2017.01.006 This is a PDF file of an unedited manuscript that has been accepted for publication. As a service to our customers we are providing this early version of the manuscript. The manuscript will undergo copyediting, typesetting, and review of the resulting galley proof before it is published in its final citable form. Please note that during the production process errors may be discovered which could affect the content, and all legal disclaimers that apply to the journal pertain.
TITLE: Imaging of Intracranial and Orbital Complications of Sinusitis and Atypical Sinus Infection: What the Radiologist Needs to Know Vinodkumar Velayudhan, DO*a, Zeshan A. Chaudhry, MBBS*a, Wendy RK Smoker, MDb, Roman Shinder, MDc, Deborah Reede, MDa a
Department of Radiology, State University of New York Downstate Medical Center Department of Radiology, University of Iowa Hospitals and Clinics c Department of Opthalmology, State University of New York Downstate Medical Center *co-first authors. V.V and Z.A.C contributed equally to this work AUTHORS: 1. Dr. Vinodkumar Velayudhan b
Clinical Assistant Professor of Radiology and Neurology Divisions of Neuroradiology and Emergency Radiology State University of New York Downstate Medical Center Associate Director of Neuroradiology Kings County Hospital Center Brooklyn, NY Mobile: 516 473 4265 Office: 718 245 5103 (9 a.m. to 5 pm, Mon-Fri) Email: [email protected], [email protected] 2.
Dr. Zeshan A. Chaudhry PGY-5 Resident Physician Department of Radiology State University of New York Downstate Medical Center 450 Clarkson Avenue Brooklyn, NY 11203 Kings County Hospital Center Brooklyn, NY Office: 718-245-2682 Email: [email protected], [email protected]
3.
Dr. Wendy RK Smoker Professor Emeritus, Neuroradiology and Neurosurgery Department of Radiology University of Iowa Hospitals and Clinics 200 Hawkins Dr, Iowa City, IA 52246 [email protected]
4.
Dr. Roman Shinder Associate Professor of Clinical Ophthalmology Director of Oculoplastics State University of New York Downstate Medical Center 450 Clarkson Avenue Brooklyn, NY 11203 [email protected]
5.
Dr. Deborah Reede Professor and Chair Department of Radiology State University of New York Downstate Medical Center
450 Clarkson Avenue Brooklyn, NY 11203 Phone: 718-270-1603 Fax: 718-270-2667 Email: [email protected]
Abstract Sinusitis is a common disease. Complications, however, are less common and can be life threatening. Major complications occur from extension of disease into the orbit and intracranial compartment and often require emergent treatment with intravenous antibiotics or operative intervention. Immunocompromised patients with acute sinusitis are susceptible to atypical infections, such as invasive fungal sinusitis, which is a surgical emergency. Therefore, it is important to accurately and promptly identify potentional complications of acute sinusitis to ensure appropriate treatment and minimize negative outcomes. This article reviews the imaging features of a spectrum of complications associated with acute sinusitis and atypical infections. Introduction Rhinosinusitis is defined as inflammation of the paranasal sinus and nasal cavity mucosa. It is a common disease frequently encountered by primary care physicians in both adults and pediatric patients. It affects an estimated 35 million people per year and results in substantial morbidity1. The annual direct medical costs of treatment are approximately $5.8 billion2. This results in nearly 16 million office visits, over 500,000 surgical procedures and is reported to be the fifth leading indication for antibiotic prescriptions by primary care providers1,2,3. The majority of sinus infections are viral in origin and in the acute setting, are usually secondary to viral upper respiratory tract infections. Bacterial infection is the cause in only 2-10 % of cases4; an even smaller number are fungal in origin. Other etiologies include allergic and non-allergic rhinitis, chemical irritation (such as cigarette smoke) and anatomic variants that predispose to obstruction5. Isolated infection of the maxillary sinuses may be odontogenic in origin in up to 20% of cases6. In general, children are more prone to develop sinusitis and suffer complications due to anatomic, immunologic and environmental factors7,8. Most cases resolve with symptomatic treatments without antibiotics, even if bacterial in origin9. Viral and bacterial sinusitis often cannot be differentiated based on symptoms, although certain symptoms, such as purulent nasal discharge and pain, suggest a bacterial origin. A consensus statement published in Otolaryngology-Head and Neck Surgery in 2007 suggests a presumptive diagnosis of bacterial infection if symptoms last greater than ten days following an upper respiratory infection or worsen within ten days after initially improving10.
Pathophysiology and Anatomy The paranasal sinuses are normally sterile. Mucosal edema can cause narrowing and obstruction of the sinus ostia (Figure 1), which leads to stasis of secretions and subsequent infection. The periorbita and orbital septum are major barriers that limit spread of infection into the orbit (Figure 2). The periorbita is the periosteum of the bones that form the orbit. It is contiguous with the periosteum on the inner surface of the skull and dura at the optic foramen, superior orbital fissures, and ethmoid canals. The periorbita is tightly attached to bone at the anterior margin of the orbit and near openings for neurovascular fissures, foramina, and canals11. Elsewhere, the periorbita is loosely connected and creates a potential space for subperiosteal collections. Anteriorly, the periorbita extends into the eyelids and forms the orbital septum12,13. The orbital septum is located deep to the orbicularis oculi muscle and attaches to the levator aponeurosis in the upper eyelid and the tarsal plate in the lower eyelid. Infection may breach the orbital septum through perforations for neurovascular structures. The largest perforation is in the superomedial aspect of the orbital septum for passage of the infratrochlear neurovascular bundle and supraorbital vein to the eyelid12,13. The periorbita appears low in signal on MRI and is difficult to distinguish from the underlying cortical bone14. It is also difficult to visualize the orbital septum on imaging. Its location, however, can be approximated as the area just anterior to the orbital fat or near where the extraocular muscles insert on the anterior globe15. The orbit is bounded by frontal, ethmoid and maxillary sinuses. The parameningeal and periorbital location of the sinuses facilitates development of intracranial and orbital complications of sinusitis. Spread of infection may be either direct or indirect. Direct extension is often through neurovascular foramina, or congenital and acquired osseous defects (Figure 3), which are commonly seen in the lamina papyracea that forms the medial orbital walls and contains foramina for the anterior and posterior ethmoidal arteries. Occasionally, no osseous defect is found. Hematogenous spread is a form of indirect spread via a network of valveless veins that drain the soft tissues of the face and orbits (Figure 4). Thrombophlebitis of the veins that drain the face, sinuses and orbits are thought to be the major route for the spread of infection to adjacent structures7. Emissary veins located in the loose connective tissue layer of the scalp communicate with the intracranial compartment. Bidirectional flow of blood in these veins promotes spread of infection anteriorly into the scalp or intracranially. Infection commonly spreads retrograde into the orbits due to thrombophlebitis of ophthalmic veins and smaller venous tributaries that drain into the cavernous sinuses. Infection of specific sinuses demonstrates a predilection for certain complications (See Table 1) . Orbital complications are most commonly due to ethmoid
followed by frontal sinusitis. Intracranial complications typically occur with frontal, ethmoid and sphenoid sinus disease. Sphenoid sinusitis may result in cavernous sinus thrombosis.
Imaging Protocols: Plain radiography can detect and confirm the clinical diagnosis of sinusitis. However, radiography has shown poor interobserver agreement, a high false negative rate and has been supplanted by CT16. CT is the initial test of choice for evaluating complications of sinusitis as it is widely available and more accurate in depicting sinus pathology, bony detail and anatomic relationships. For orbital complications of sinusitis, helical CT should be performed ideally with intravenous contrast in the axial plane with submillimeter collimation to produce isotropic voxels. These data can then be reconstructed into high-quality sagittal and coronal images. Though less sensitive than MRI, contrast-enhanced CT can be used to quickly assess for intracranial complications, such as large extra-axial collections, brain lesions, mass effect and hydrocephalus. The patient may then be triaged appropriately for emergent neurosurgical intervention and for MRI7. MRI is more sensitive in the evaluation of orbital and intracranial complications of sinusitis6,17. Orbital imaging should be performed using a field of view that includes the nose and orbital soft tissues anteriorly and extends posteriorly through the sella to include the cavernous sinuses. T1-weighted images (T1WI) in the axial and coronal planes can depict orbital anatomy and the stranding and soft tissue thickening that occur with inflammation and infection. Short tau inversion recovery (STIR) or fat suppressed T2 weighted images (FST2) are useful in demonstrating edema and fluid collections. Unless contraindicated, IV contrast should be administered to differentiate abscess from phlegmon, evaluate for venous thrombosis and for intracranial collections and meningitis. Dedicated images of the brain should be obtained with any sinus or orbit MRI to screen for these complications and others, including cerebral infarction. The utility of specific MRI pulse sequences is discussed as they relate to different disease entities later in this article.
Imaging Findings of Sinustis Acute sinusitis is usually clinically evident. Cross-sectional imaging is typically indicated if intracranial or orbital complications are suspected or when evaluating immunocompromised patients18,19. An acutely infected sinus may demonstrate an airfluid level or aerosolized (frothy) secretions (Figure 5A). Mucosal thickening is a nonspecific finding, commonly encountered on imaging, and found incidentally in 20-40% of MR exams6. It is usually indicative of chronic sinusitis, especially with polypoid mucosal thickening, but may also occur with acute sinusitis. Bone thickening and sclerosis are usually associated with chronic sinusitis (Figure 5B and 5C). Inspissated secretions in chronic sinusitis may appear hyperdense or calcified on CT in bacterial and fungal
disease. On MR, secretions demonstrate progressively increased signal on T1WIs and low T2 signal as the ratio of protein to water content increases20. Complications of Sinusitis Orbital involvement is the most common complication of acute sinusitis. It is more common in children, and may be the first presenting symptom of acute sinusitis in this population. Orbital extension of sinus infection is the most common cause of unilateral proptosis in children and the third most common cause of proptosis in adults following thyroid eye disease and orbital pseudotumor7. Orbital infection is divided into two major categories: Preseptal (periorbital/superficial to the orbital septum) and postseptal (deep to the orbital septum). In 1970, Chandler and colleagues developed a classification system of sinusitis complications, based on orbital anatomy (Table 2)21. Following the advent of cross-sectional imaging, modifications to this classification system were made22,23. The current classification divides orbital complications into five groups. Note that these do not represent progression of disease as each complication can have different causes and occur exclusive of the others.
Preseptal Cellulitis Preseptal cellulitis is an infectious, inflammatory edema in the soft tissues anterior to the orbital septum. Patients present with swelling of the eyelid and surrounding soft tissues. Because the inflammation does not involve soft tissues deep to the orbital septum, there should be no vision loss, restricted extraocular movement or other findings associated with postseptal involvement (Table 3). Comprehensive clinical assessment is difficult when there is significant swelling of the eyelids. The etiology is most often due to a local skin infection (e.g. insect bite, trauma or retained foreign body) in both adults and children and may also be due to sinusitis in children24. Most patients respond to treatment with antibiotics (oral or intravenous). Surgery is indicated when there is an associated eyelid abscess or progression to orbital abscess. On imaging, preseptal cellulitis appears as swelling of the eyelid (Figure 6). Periorbital soft tissue swelling may also be present. The postseptal region, including the extraocular muscles, postseptal fat and lacrimal glands should be normal. Imaging findings of edema on CT consist of eyelid soft tissue thickening and increased density and stranding of the surrounding tissues. On MRI, eyelid edema may be present and appear as low signal reticulation on T1WI and hyperintense on FST2/STIR images with corresponding enhancement.
Orbital Cellulitis Orbital cellulitis represents inflammatory edema posterior to the septum without abscess formation. It is usually due to acute sinusitis. The vast majority of cases are secondary
to acute ethmoid sinusitis, typically involving the medial orbit. Patients can present with eyelid edema, erythema, ptosis, chemosis, and proptosis. There may be limited or no restriction of extraocular movement, depending on the degree of inflammation. Visual acuity is usually normal. Patients are typically febrile and have leukocytosis. Orbital cellulitis can lead to serious neurologic and visual deficits. Treatment consists of intravenous broad-spectrum antibiotics and sinus and orbital drainage if indicated. On imaging, orbital edema, diffuse or localized, is present posterior to the orbital septum, with or without periorbital soft tissue swelling (Figure 7). Inflammatory changes may involve extraconal structures, intraconal structures or both. Imaging shows edema and enhancement, without a rim-enhancing fluid collection to indicate a discrete abscess. It is important to differentiate between orbital and preseptal cellulitis because orbital cellulitis generally requires hospital admission for IV antibiotics and possible surgical intervention.
Subperiosteal Abscess A subperiosteal abscess (SPA) is a collection of purulent material between the bone and periorbita. The most common location is along the medial orbital wall, in association with ethmoid sinusitis. It can also occur in the superior aspect of the orbit, in association with frontal sinusitis, or rarely along the orbital floor, associated with maxillary sinusitis. A trial of IV antibiotics may be sufficient in children if the collection is small and visual function is not impaired. Drainage of the abscess and sinuses is performed in adults, older children, immunocompromised patients, and those who fail to respond to antibiotics. Urgent drainage is indicated when visual or neurologic complications are suspected. An abscess is best demonstrated on post-contrast CT and MR where a rim-enhancing fluid collection is identified (Figure 8). A collection along the medial orbital wall is readily identified on axial images. However, a collection along the roof and floor is best demonstrated in the coronal and sagittal planes. Diffusion-weighted MR demonstrates restricted diffusion. A medial SPA can displace extraocular structures and result in lateral dystopia and/or proptosis. If proptosis is severe, tension develops, and the posterior margin of the globe becomes tethered, which results in stretching of the optic nerve, which may lead to ischemic necrosis of the nerve, which is an ophthalmologic emergency (Figure 9B). Extraocular muscles may be enlarged due to myositis and result in diminished ocular movement.
Orbital Abscess An orbital abscess is a collection of pus that is not subperiosteal in location, less common than SPA, and may be intraconal or extraconal. Extraconal abscess is usually
secondary to orbital cellulitis or rupture of an SPA6. Intraconal abscess is typically due to penetrating trauma or surgical complications25. Clinical symptoms are similar to those of orbital cellulitis. Stretching of the optic nerve with ischemic necrosis, optic neuritis, or compression of the optic nerve at the orbital apex can result in loss of visual acuity and eventual blindness. Mass effect on cranial nerves as they exit the superior orbital fissure may result in ophthalmoplegia and diplopia. Treatment consists of medical therapy and surgical drainage of the orbital abscess and infected sinuses. Imaging shows a rim-enhancing fluid collection with surrounding inflammatory changes. The collection should be clearly separate from osseous structures to diagnose an orbital abscess (Figure 9).
Cavernous Sinus and Ophthalmic Vein Thrombosis: Preseptal soft tissues drain primarily into the systemic venous circulation. Venous drainage of the midface, sinuses, and orbits is via a rich network of valveless veins. These structures drain via the superior and inferior ophthalmic veins into the cavernous sinuses. The infraorbital and deep facial veins drain into the pterygoid venous plexus, which communicates with the cavernous sinuses via emissary veins within the foramen ovale and a tributary of the inferior ophthalmic vein that courses through the inferior orbital fissure (Figure 4)26. Cavernous sinus and ophthalmic vein thrombosis/thrombophlebitis are commonly due to infections in the areas they drain. Patients with cavernous sinus thrombosis are usually very ill and may have multiple cranial nerve palsies, headache, fever and signs of meningitis. Ophthalmologic findings, due to venous congestion, include periorbital edema, proptosis, chemosis and engorgement of retinal veins with papilledema on fundoscopy. Restricted movement or paralysis of extraocular muscles occurs because of involvement of cranial nerves (CN) III, IV, V1 and V2 that course in the lateral wall of the cavernous sinus and cranial nerve VI within the cavernous sinus proper (Figure 10). Cavernous sinus thrombosis due to sinus infection is usually treated with sinus drainage and high-dose intravenous antibiotics. Unlike other forms of cerebral venous and systemic deep vein thrombosis, the use of anticoagulants is controversial because of the risk of intracranial and orbital hemorrhage. On imaging, the normal cavernous sinus should demonstrate lateral margins that are either straight or concave. Convex bulging of the lateral wall is abnormal and should prompt further investigation to exclude pathologies such as, thrombosis, neoplasm, carotid cavernous fistula, aneurysm or tortuous ICA. Non-contrast CT (NCCT) may be normal. Abnormal findings include cavernous sinus and sometimes superior ophthalmic vein enlargement, infiltration of the intraorbital fat, proptosis and enlargement of extraocular muscles. On contrast-enhanced CT (CECT), the lateral dural wall of the cavernous sinus should enhance. After a sufficient delay of at least 45 seconds, venous structures of the cavernous sinus enhance homogeneously
and the cavernous ICA will not be visualized separately27. Thrombus may appear as a localized filling defect or non-enhancement of the entire cavernous sinus. MRI and contrast-enhanced MRV are considered superior to CT venography in evaluating cavernous sinus thrombosis28. MRI demonstrates variable signal in the cavernous sinus, often with high signal on FLAIR images. Filling defects or lack of enhancement may be seen. On routine post-contrast images, the only flow void present in the cavernous sinus is the ICA and should not be confused with thrombus. On both CECT and MRI, the cavernous sinus may be enlarged, with dilatation and thrombosis of the superior ophthalmic vein (Figure 11). Pott’s Puffy Tumor: In addition to orbital and intracranial complications, osteomyelitis may occur, most often associated with frontal sinusitis29. Frontal bone osteomyelitis with an associated subperiosteal/subgaleal abscess involving the overlying scalp is termed the Pott’s Puffy tumor. It can also be seen in the post-traumatic setting. This infection may spread intracranially resulting in meningitis, brain abscess, and extra-axial empyemas. Intracranial spread of infection can occur via three major pathways: 1) along valveless emissary veins that cross the calvarium and allow for bi-directional spread into the scalp or intracranially (Figure 12); 2) along nerves extending through the meninges; 3) through congenital or acquired osseous defects. Clinical presentation includes forehead swelling with pitting edema and tenderness. Headache, fever, and nasal drainage may also be present. Meningeal signs, altered mental status, and focal neurologic findings strongly suggest intracranial involvement. MRI is best for evaluation and should be performed if neurologic complications are clinically suspected. CT is highly sensitive in demonstrating sinusitis and associated subgaleal abscesses in Pott’s Puffy tumor and is often associated with bone destruction involving the inner and outer tables of the frontal sinus. MRI demonstrates marrow edema and enhancement due to osteomyelitis. A subgaleal abscess appears as a rim-enhancing fluid collection, closely adherent to the outer table of the frontal bone, with surrounding inflammatory changes on both CT and MRI, as well as with restricted diffusion on DWI (Figure 13).
Intracranial Complication of Sinusitis Potential intracranial complications include epidural and subdural abscess/empyema, meningitis, cerebritis, brain abscess, and dural sinus thrombosis. Although intracranial complications of sinusitis are rare, they can cause serious neurological deficits and other morbidity and mortality. Thirty to 45% of patients have residual long-term neurologic deficits7,30,31. The true incidence is difficult to determine because most cases of sinusitis are uncomplicated, treated in outpatient settings, and the literature often
contains only case reports and series of complicated cases. Three to 6% of patients hospitalized with sinusitis develop intracranial complications32,33,34,35. Up to 45% of patients exhibit more than one focus of infection: intracranial and/or orbital31,36. Therefore, it is important to maintain a high index of suspicion for intracranial involvement in patients with orbital extension. However, those with intracranial complications tend to have a longer duration of symptoms with more complicated and protracted hospital stays. They typically occur in older patients. The most common symptoms in both adult and pediatric populations are fever and headache30,36. Other symptoms include seizures, altered mental status, focal neurological deficits, meningeal signs and ocular complaints32,33,36,37. However, some patients with intracranial spread may be asymptomatic and detected only on imaging performed to evaluate the sinuses. Extracranial complications, particularly intraorbital, usually dominate the clinical presentation. This results in patients with extracranial complications presenting earlier since intracranial complications often have indolent, nonspecific or clinically silent features.
Extra-axial Collections (Epidural Abscess and Subdural Empyema) Spread of infections from the frontal sinus to the anterior cranial fossa results in the development of epidural abscess (EDA) and subdural empyema (SDE). Older studies report SDE as the most common complication; recent studies show EDA to predominate30,34,37. EDA occurs between the outer layer of the dura and the inner table of the calvarium. Initially, EDA are clinically occult or present with nonspecific symptoms such as headaches. This is likely due to the restricted space in which they develop, which slows progression until they either penetrate the dura resulting in a SDE or become large enough to cause significant mass effect and elevated ICP. SDE, however, can rapidly spread over the convexities and therefore can present more acutely with worrisome neurological findings, including neurological deficits and altered mental status30. EDA seems to be more commonly associated with intraorbital involvement30. Treatment requires surgical intervention. Imaging findings of EDA include a low-density, lenticular-shaped, extra-axial fluid collection on CT with an enhancing rim. An epidural collection does not cross sutures, although they can cross the midline. Adjacent mass effect and parenchymal edema can be present. The appearance on MRI includes T2 hyperintensity with variable T1 signal (depending on the relative proteinaceous/hemorrhagic content) with surrounding rim enhancement (Figure 14). Similar to other abscesses, there is often restricted diffusion on DWI. SDE often appears as a crescent-shaped, hypodense, rim-enhancing collection that can cross sutures, but not the midline. CT is often the first imaging study and may be negative in early cases when collections are small. CECT is often sensitive enough to
visualize SDEs; however, it is not as sensitive as MRI, and may fail to detect smaller collections6,30. Mass effect is often secondary to edema and ischemia, not necessarily from the extra-axial collection36. This can cause effacement of the basilar cisterns and cortical sulci. On MRI, T2WI demonstrate a hyperintense collection with mass effect. The rim is often T1 hyperintense on the non-contrast sequence. Diffusion-weighted imaging may aid in differentiating between SDE and EDA. Tsuchiya et al. noted that, while SDE demonstrated restricted diffusion, EDA had variable signal patterns, often low or mixed, on the diffusion trace images38,39. Reactive subdural effusions are a common complication of meningitis, especially in infants, and can occur in cases of complicated sinusitis. These effusions usually resolve without treatment. Therefore, subdural effusion should be differentiated from SDE. Both are hyperintense on T2 and show enhancement along the cerebral surface of the lesion on post-contrast images; however, SDE will demonstrate restricted diffusion39,40. SDE is a neurosurgical emergency with mortality rates ranging from 10%-70%6. SDE progresses rapidly, spreading over the convexities and often localizing in the supratentorial compartment. If untreated, this will result in increased intracranial pressure, development of focal neurological deficits, seizures, and coma within 1-2 days, thus underscoring the need for prompt diagnosis and aggressive management, including urgent surgical intervention6,36.
Meningitis Meningitis occurs most often in association with extra-axial suppuration rather than in isolation. While many studies report either EDA or SDE as the most common complication of sinusitis, others have found meningitis to be more common41. It is frequently secondary to sphenoid or ethmoid sinusitis. The most common sequelae are seizure and hearing loss. MR is more sensitive than CT for diagnosis. Leptomeningeal enhancement occurs in cisterns and sulci and pachymeningeal enhancement occurs along cerebral convexities and dural reflections (Figures 13, 14 and 15). Associated imaging findings include hydrocephalus and adjacent cerebral edema. Purulent exudate can form in the subarachnoid space, with increased attenuation on CT and incomplete suppression of CSF signal on FLAIR and restricted diffusion on MRI40.
Cerebritis and Cerebral Abscess Spread from the extra-axial space to the parenchyma results in focal cerebritis and abscess formation, which is a rare complication of intracranial spread of sinus disease. The frontal and parietal lobes are most often affected41.
Initially cerebritis may develop with focal brain edema manifesting as low attenuation on noncontrast CT. MRI is more sensitive for detection, particularly in the initial stages with increased signal on T2 and FLAIR sequences. Patchy enhancement on postcontrast sequences may or may not be seen in cerebritis. Frank abscess formation will have the characteristic imaging features of a well-defined, rim-enhancing fluid collection that demonstrates restricted diffusion, with surrounding mass effect and vasogenic edema (Figure 15). Rim enhancement is often thicker along the cortical aspect of the abscess. Treatment should include surgical drainage of the abscess, parenteral antibiotics and definitive management of the sinus disease.
Fungal Sinusitis Fungal sinusitis is classified as non-invasive or invasive. Among noninvasive disease, there are two subtypes: allergic fungal sinusitis and mycetoma. Invasive fungal sinusitis is subdivided into three groups: Acute fulminant, chronic invasive, and granulomatous42. The primary fungal pathogens are Zygomycetes (Mucor spp) and Ascomycetes (Aspergillus spp). A diagnosis of invasive fungal sinusitis requires histopathologic evidence of hyphae penetrating the mucosa, submucosa or bone with invasion of blood vessels and prominent tissue necrosis7,42,43.
Noninvasive Fungal Sinusitis Allergic fungal sinusitis is the most common form of fungal sinusitis19,44. It occurs in patients with a history of atopy (e.g. asthma and allergic rhinitis) and is often found in association with sinonasal polyposis6. It is felt to represent a hypersensitivity reaction to fungal pathogens, rather than an infection. The sinuses contain material referred to as “allergic mucin,” inspissated secretions that contain eosinophils, Charcot-Leyden crystals and eosinophilic degradation products. Mycetomas occur when these secretions become superinfected with fungus and form a ball6,19. Allergic fungal sinusitis is typically bilateral and involves multiple sinuses. Sinuses may be expanded with varying degrees of opacification and central high attenuation on CT corresponding to allergic mucin, desiccated secretions, and fungal concretions (Figure 16)6,45,46. Areas of low density along the margins of the sinus lumen are due to mucosal thickening. Co-existing polyps may be present and result in nodular mucosal thickening with expansion of the sinuses and sinus ostia. Sclerosis of the sinus walls may be seen due to chronic inflammation. Advanced cases of chronic allergic fungal sinusitis may result in marked thinning and erosion of sinus walls with intraorbital and intracranial extension. On MRI, T1 signal is variable and may be high, intermediate or low signal. Metallic ions, including zinc and manganese, can produce high T1 signal. Inflammatory mucosal thickening has high T2 signal. Central markedly diminished signal or signal voids are due to metallic ions, high protein and low water content of inspissated
secretions (Figure 16)6,19. This can mimic an aerated sinus. Polyposis and chronic allergic fungal sinusitis often coexist and there is considerable overlap in the imaging appearances, especially on CT. However, polyposis and inflammatory mucosal thickening demonstrate high T2 signal and enhancement, while fungal elements and desiccated secretions have low T2 signal and little, if any, enhancement. Mycetomas (fungus balls) typically involve one sinus, usually the maxillary sinus, and are hyperdense on CT due to matted hyphae that may contain calcifications (Figure 17). The sinus walls may be thickened due to chronic inflammation or thinned and eroded from expansion or pressure necrosis from the mycetoma. On MRI, the fungal elements in the center of the sinus demonstrate markedly diminished or no signal on T2WI and variable T1 signal (Figure 17). Mycetomas do not enhance; inflammatory changes along the walls of the sinus may enhance and appear hyperintense on T2WI. Treatment of chronic allergic fungal sinusitis is surgical removal of the allergic mucin and restoration of sinus drainage. Topical steroids are used postoperatively to suppress the immune response and prevent recurrence. Since this is a hypersensitivity reaction, antifungal medication is not required. For mycetomas, surgical removal of the fungal material and restoration of sinus drainage are usually curative19,44.
Invasive Fungal Sinusitis Acute (fulminant) invasive sinusitis is the most lethal form of fungal sinusitis with a mortality rate of 50-80%. It typically occurs in diabetics and immunocompromised and severely neutropenic patients. Disease typically progresses rapidly over days to a few weeks with fungal invasion of the mucosa, submucosa, blood vessels and bones of the nasal cavity and sinuses. Skull base invasion, intracranial and orbital extension are common. Angioinvasion may involve the cavernous sinus, ICA, and its branches. Invasive fungal sinusitis initially produces significant unilateral inflammatory changes and mucosal edema in the nasal cavity, though this finding is nonspecific19,47. Disease progresses from the nasal cavity to the sinuses, orbits and intracranially to involve the cavernous sinuses, brain, and meninges (Figure 18). The ethmoid and sphenoid sinuses are more commonly involved19. Sinus mucosal thickening may be subtle or mild. As the disease progresses, sinus opacification increases and bone destruction occurs. Premaxillary or retromaxillary fat inflammation are important indicators of invasive disease and can be seen in acute and chronic forms19 (Figure 19). Invasive disease tends to extend along vasculature. Specifically, sphenoid sinus disease may result in cavernous sinus thrombosis and compromise the ICA and can lead to cerebral infarction with restricted diffusion on DWI (Figure 20). Invasive fungal sinus disease should be considered whenever there is concurrent involvement of the nasal cavity, sinuses, and orbits6, particularly in the immunocompromised.
Chronic invasive sinusitis occurs in immunocompetent or mildly immunocompromised patients with a history of chronic rhinosinusitis. It has a similar pattern of disease to fulminant sinusitis but progresses over a longer time course, typically months. Granulomatous invasive sinusitis occurs primarily in North Africa (in the Sudan) and Southeast Asia. It is rare in the United States. This disease produces noncaseating granulomas with a similar pattern of involvement as chronic invasive sinusitis. Chronic and granulomatous invasive fungal sinusitis may be indistinguishable on imaging and can present with similar findings as advanced fulminant invasive disease. CT may demonstrate high attenuation material within the sinus (much less commonly seen in acute invasive disease) that appears iso to hypointense on T1WI and markedly hypointense on T2WI19,48 (Figure 19). Bony destruction or sclerosis may be present with extension beyond the sinus that can exceed the amount of disease within the sinus48. Sclerosis due to chronic inflammation helps differentiate chronic and granulomatous invasive forms from acute invasive disease19. The mass-like appearance, bone destruction and transpatial involvement of chronic and granulomatous invasive fungal sinusitis may mimic a neoplasm. While it may not always be possible to differentiate the two, the presence of calcifications, markedly diminished T2 signal and lack of enhancement of the non-inflammatory components favor the diagnosis of fungal sinus disease over tumor. For all forms of invasive fungal sinus disease, treatment is aggressive surgical debridement and administration of systemic antifungal medication. Reversal of diabetic ketoacidosis and neutropenia improve mortality19.
Summary Intracranial and orbital complications of sinusitis can have significant morbidity, including vision loss and other serious neurologic impairment and death. Radiologists should have a high index of suspicion when interpreting sinus imaging and closely examine the brain and orbits, particularly in patients with visual or neurologic symptoms. Becoming familiar with common and uncommon complications of sinusitis and patterns of spread of disease will facilitate prompt and accurate diagnosis. In addition, fungal sinusitis can have highly characteristic features and its fulminant invasive forms need to be recognized in immunocompromised patients as disease can progress rapidly and result in fatality. CT is the initial examination of choice and should be supplemented with contrast enhanced MRI to better characterize orbital and intracranial complications seen on CT or if CT is nonrevealing and clinical suspicion remains high.
FIGURE CAPTIONS: Figure 1: Maxillary sinus ostia. Coronal CT demonstrates the maxillary sinus ostia (white arrows), the opening for the drainage pathway of each maxillary sinus.
Figure 2: Periorbita and orbital septum. A) Sagittal illustration shows the location of the periorbita. B) The periorbita continues anteriorly as the orbital septum (arrow) in the upper eyelid, as demonstrated on the sagittal T1WI. Figure 3: Direct spread of infection. Axial CT image demonstrates a defect in the left medial orbital wall (lamina papyracea), a common location for dehiscence. Direct spread of infection occurs through neurovascular foramina or via congenital and acquired defects in bone. Figure 4: Indirect Spread of Infection. Lateral illustration demonstrates the network of communicating veins draining the face, sinuses and orbits. • Superior and inferior ophthalmic veins drain directly into the cavernous sinus (CS). • Infra-orbital vein can drain into the CS via the inferior ophthalmic vein and pterygoid plexus. • The deep facial vein drains into the pterygoid plexus and into the CS. Figure 5. Acute vs. chronic sinusitis. A) Axial T2WI demonstrates right maxillary sinus air fluid level (white arrow), suggestive of acute sinusitis. B) Axial CT demonstrates opacification of left sphenoid sinus with diffuse sclerosis and thickening of its walls (black arrow), indicating chronicity. C) Axial CT demonstrates partial opacification of left maxillary sinus with high density material centrally (white arrow) and wall thickening (black outlined arrow) due to chronic sinusitis. Calcifications can be seen in desiccated secretions from chronic sinusitis and in fungal sinusitis. Figure 6. Preseptal and postseptal cellulitis. Axial noncontrast CT in a patient with preseptal and orbital cellulitis. Soft tissue swelling involving the left eyelid (white arrows) consistent with preseptal cellulitis. Mild infiltration of the left retrobulbar fat is also seen (black outlined arrow) consistent with orbital cellulitis. Figure 7. Orbital cellulitis. Contrast enhanced axial CT scan demonstrates maxillary and ethmoid sinusitis with left orbital cellulitis. There is left preseptal soft tissue swelling (white arrow) and postseptal extension (black arrow) consistent with orbital cellulitis. Figure 8. Subperiosteal abscess. A) Illustration demonstrates the location of a subperiosteal abscess (black arrow) along the medial orbital wall beneath the periorbita (white outlined arrow). B) CECT shows a large peripherally enhancing subperiosteal abscess (asterisk) along the left medial orbital wall and anterior to the maxillary sinus with proptosis. Left maxillary and ethmoid sinus opacification with a dehiscence (white arrow) in the anterior wall of the maxillary sinus. C) Clinical image (same patient) demonstrates downward gaze restriction of the left eye consistent with postseptal involvement. Figure 9. Orbital abscess. Axial (A) and coronal (B) CECT images in a patient with frontal sinusitis and orbital abscess. There is a fusiform extraconal collection (large white arrow) with faint peripheral enhancement in the superior right orbit displacing the
globe inferiorly. The collection is an orbital abscess and not subperiosteal as there is fat plane (small white arrows) separating it from the orbital roof. There is tension on the right globe and optic nerve with tethering at the nerve insertion (white arrowhead). Figure 10. Anatomic basis of cranial neuropathies in CS thrombosis and sphenoid sinusitis. A) Coronal illustration demonstrates the location of the CN III, IV, V1 and V2 in the lateral dural wall of the CS and CN VI coursing within the sinus inferolateral to the cavernous ICA. Gaze palsy is related to involvement of these nerves, which supply the EOM. B) Coronal CT shows the relationship of the optic nerve canal (white arrow) coursing superior to the anterior aspect of the sphenoid sinus (asterisk). Optic neuropathy and afferent pupillary defect are likely secondary to encroachment on or irritation of the optic nerve (CN II) in the optic canal above the sphenoid sinus. Figure 11. Cavernous sinus and superior ophthalmic vein (SOV) thrombosis. A) Axial CE T1WI demonstrates filling defects in the right cavernous sinus (white arrow) consistent with thrombosis in this patient with ethmoid and sphenoid sinusitis (black arrows). B) Axial CECT in the same patient demonstrates the absence of enhancement of the right CS (black arrow) and a thrombosed SOV. Figure 12. Anatomic basis for bidirectional spread of infection via emissary veins. Illustration demonstrates emissary veins traversing the calvarium allowing for spread of infection anteriorly into the overlying subgaleal layer of the scalp or posteriorly into the intracranial compartment. Figure 13. Pott’s puffy tumor. Axial CE T1WI (A) demonstrates a rim enhancing epidural fluid collection (white asterisk) with restricted diffusion on DWI (black arrow, B) consistent with an abscess. There is adjacent dural enhancement in the interhemispheric fissure (outlined white arrows, A) and leptomeningeal enhancement in the sulci (outlined black arrows, B) consistent with meningitis. This process extends anteriorly into the scalp with a subgaleal abscess, also demonstrating peripheral enhancement (white arrow, A) and restricted diffusion (white arrow, B). Figure 14. Intracranial complications of sinusitis: Empyema. Axial CE T1WI demonstrates ethmoid and sphenoid sinusitis (small white arrows), thrombosis of the right superior ophthalmic vein (large white arrow) and cavernous sinuses (not shown) and bilateral extra-axial peripherally enhancing fluid collections (black arrows) consistent with subdural empyemas anterior to the temporal lobes. Figure 15. Intracerebral abscess. Coronal CE T1WI demonstrates a left supraorbital mucopyocele filling and expanding a left supraorbital ethmoid air cell (asterisk) and displacing the left globe (small white arrows). There is an intra-axial rim enhancing lesion in the left frontal lobe consistent with a brain abscess (large white arrow). Linear dural-based enhancement over the superior left frontal lobe is consistent with meningitis (black arrow).
Figure 16. Allergic Fungal Sinusitis (AFS). CT (images A and B) demonstrate complete sinus opacification (with central high and peripheral low attenuation) in the frontal, maxillary and sphenoid sinuses (black arrows) with expansion of the ethmoid air cells (white arrows, B) and widening of the accessory maxillary sinus ostia (white arrow, A). This is the classic appearance of AFS. Sinonasal polyposis often coexists and can have a similar appearance on CT. (C) Axial FLAIR image demonstrates markedly diminished areas of signal (white arrows) with surrounding mucosal thickening in the frontal sinuses. (D) Axial CT scan in the same patient demonstrates corresponding areas of high density material within, and expansion of, the frontal sinuses (black arrows) with marked thinning and dehiscence of the posterior wall (white arrow). Figure 17. Mycetoma. Coronal CT (A) demonstrates opacification of the right ethmoid and maxillary sinuses with a hyperdense, calcified lesion in the region of the medial wall of the right maxillary sinus and ostiomeatal unit (black arrow). The lesion has markedly diminished signal on the coronal T2WI (B, white arrow). Inflammatory mucosal thickening (B, black arrow) and intermediate signal secretions are also noted (B, asterisk). Figure 18. Invasive mucormycosis in a patient with acute myelogenous leukemia, neutropenia and necrotic nasal ulcer. Coronal T2 images demonstrates right sided pansinusitis (black arrows), opacification of the right nasal cavity (white arrows) and inflammatory changes in the right orbital fat (large white arrow, B) and masticator space (circle, B). Figure 19. Chronic invasive fungal sinusitis. (A) Axial CT using soft tissue window demonstrates bilateral maxillary sinus opacification with high density material on the left (black arrow) and marked infiltration of the fat anterior to the sinus (white arrow) in a patient with symptomatology for months. (B) Bone window image demonstrates destruction of the anterior and medial walls of the left maxillary sinus (arrows). Axial T1WI without (C) and with contrast (D) in another patient with chronic symptoms demonstrates effacement of the right pterygopalatine fossa and retromaxillary fat with enhancement (large white arrows). There is involvement of the cavernous sinuses with lack of enhancement and enlargement on the right (small arrows, D). Figure 20. Invasive fungal sinusitis with angioinvasion and cerebral infarction. Coronal CE T1WI (A) demonstrates absent enhancement of the left cavernous sinus (white arrow) consistent with thrombosis and narrowing of the left cavernous ICA. Axial DWI (B) demonstrates multiple left-sided watershed infarcts (white arrows) due to compromise of the left ICA. REFERENCES: 1. Lucas JW, Schiller JS, Benson V. Summary health statistics for U.S. adults: National Health Interview Survey, 2001. Vital health stat 10. 2004. 1-134.
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• • • • • • •
COMPLICATIONS ASSOCIATED WITH INFECTIONS OF SPECIFIC SINUSES FRONTAL AND ETHMOID SINUSITIS SPHENOID SINUSITIS Orbital cellulitis and abscess and • Cavernous sinus thrombosis subperiosteal abscess • Meningitis Meningitis • Temporal lobe and epidural abscess Epidural abscess • Superior orbital fissure syndrome: Subdural empyema proptosis, orbital pain, and Frontal lobe abscess ophthalmoplegia (CN III, IV, VI) + Superior sagittal sinus thrombosis numbness in ophthalmic division of Pott’s Puffy tumor (frontal) trigeminal nerve Direct extension from the maxillary sinus to critical structures is rare.
Table 1. Infection of specific sinuses have a predilection for certain complications
Chandler Classification
Group I: Preseptal Cellulitis
Group II: Orbital Cellulitis
Group III: Subperiosteal Abscess
Group IV: Orbital Abscess
Group V: Cavernous Sinus Thrombosis
Table 2. The Chandler classification system of orbital complications of sinusitis. These classifications do not represent a progression of disease since each category can have various underlying causes.
Clinical Signs of Postseptal Involvement of Orbit Infections
Proptosis Limitation of gaze/extraocular movement Decreased visual acuity Color vision defects Afferent pupillary defect
Table 3. Clinical Signs of Postseptal Involvement of Orbital Infections