Nasal Cavity

The nasal cavity is triangular and is separated in the midline by the nasal septum. The nasal cavity is composed of a cartilaginous portion anteriorly and an osseous portion posteriorly, which is formed by the perpendicular plate of the ethmoid posterosuperiorly and the vomer posteroinferiorly. The opening to each nasal cavity is known as the vestibule, which is bounded medially by the columella and nasal septum and laterally by the nasal alae. The cribriform plate is the roof of the nasal cavity, and the floor is the hard and soft palate. Posteriorly, the nasal cavity communicates with the nasopharynx via the choanae, after rupture of the oronasal membrane during the fetal period. From the lateral wall of the nasal cavity, three pairs of turbinates (superior, middle, and inferior) project into the nasal cavity, each with a corresponding meatus below them. The middle turbinate is attached to the cribriform plate via the vertical lamella and to the lamina papyracea via the basal lamella (Fig. 8-1).

Paranasal Sinuses

The paranasal sinuses form as diverticula from the walls of the nasal cavities and become air-filled extensions in the adjacent bones—maxilla, ethmoid, frontal, and sphenoid. The original openings of the diverticula persist as the ostia of the sinuses that communicate with the nasal cavity (Fig. 8-2, A and B).

The mucosal lining of the nasal cavities is contiguous with the paranasal sinuses and consists of pseudostratified, columnar, ciliated epithelium containing mucinous and serous glands,¹ whereas the nasal septum is lined by squamous mucosa.² In the human embryo, ethmoidal and maxillary sinus budding can be detected at 11 to 12 gestational weeks and at 14 to 15 gestational weeks, respectively.³ In general, only rudimentary maxillary and ethmoid sinuses, which continue to expand until puberty or early adulthood, are present at birth.⁴ The sinuses also are linked to facial growth and dentition and have been studied extensively by different anatomic and imaging methods (Fig. 8-3, A-C).^4–11

Ethmoid Sinuses

At birth the ethmoid sinuses are already developed in number and pneumatized, but they continue to expand, reaching adult proportions at about 12 years of age.¹² The ethmoid sinuses consist of a paired group of a variable number of cells (3 to 18) within the lateral masses of the ethmoid bone, also known as labyrinths. In addition to the lateral masses, the ethmoid bone consists of the cribriform plate superiorly and the perpendicular plate, which is part of the nasal septum (see Fig. 8-3, A). The ethmoid sinus is bordered medially by the nasal cavity and laterally by the lamina papyracea; its roof is formed by the cribriform plate and fovea ethmoidalis (see Fig. 8-1). The anterior and posterior ethmoid air cells are separated by the basal lamella (see Fig. 8-3, C), which is the lateral attachment of the middle turbinate to the lamina papyracea. Drainage of the anterior ethmoid air cells occurs via the ethmoid bulla into the hiatus semilunaris and middle meatus. The posterior ethmoid air cells drain into the superior meatus and then into the sphenoethmoid recess (see Fig. 8-2, A).

The anterior ethmoidal artery arises from the ophthalmic artery in the orbit, pierces the lamina papyracea, and exits via its respective foramina by passing through the ethmoid roof in the superomedial wall of the orbit, 2 to 3 mm behind the anterior wall of the bulla ethmoidalis. Occasionally the anterior ethmoidal artery passes within bony septae of the ethmoid sinuses and is suspended in a mesentery without bony cover (e-Fig. 8-4).¹³

Maxillary Sinuses

The maxillary sinuses are very small and pneumatized at birth, measuring an ellipsoid volume (sinus volume index) of approximately 0.24 ± 0.36 cm³.⁴ During the first years of life, the maxillary sinuses undergo rapid inferolateral expansion, reaching full size between 15 to 18 years of age. The floor of the maxillary sinus usually is seen at the level of the middle meatus during infancy; it reaches the level of the nasal floor by 8 to 9 years of age, and by age 12 years, it is located at the level of the hard palate.⁶ However, variation exists in the final descent of the floor, which lies below the level of the nasal floor in 65% of adults (e-Fig. 8-6, A–D).¹⁶

The maxillary sinus is the largest of the sinuses. Its roof is formed by the orbital floor, which carries the bony canal for the infraorbital nerve; the medial wall is formed by the lateral nasal wall. The posterior wall of the maxillary sinus forms the pterygopalatine fossa (Fig. 8-7, A). The maxillary sinus drains via the maxillary ostium located superomedially into the infundibulum, the hiatus semilunaris, and the middle meatus (Fig. 8-2, A).

Developmental variations of the maxillary sinus include an accessory ostium, isolated unilateral hypoplasia, and prominent septa that appear to compartmentalize the sinus cavity. Occasionally the roots of the maxillary molars impinge on the walls of the sinuses.

Sphenoid Sinus

The sphenoid sinus begins to pneumatize in a ventrodorsal direction from 7 months to 2 years of age. A significant acceleration in sinus expansion occurs between 3 and 8 years of age, with complete pneumatization usually present by age 10 years (e-Fig. 8-8, A–E).⁹ Its border is formed superiorly by the sella turcica, posteriorly by the clivus, anteriorly by the ethmoid sinus, and inferiorly by the nasopharynx (see Fig. 8-2, A and B). This sinus drains anteriorly via the sphenoethmoid recess. Lateral recesses of the sphenoid sinus are formed from pneumatization of the pterygoid process in 44% of people (see Fig. 8-7, A). Benign sphenoid marrow variants, which sometimes are mistaken for lesions, can be seen adjacent to the pneumatized sphenoid sinus (e-Fig. 8-9, A-C).

Important anatomic relationships of the sphenoid sinus include the optic canal and nerve located superolaterally; the foramen rotundum with the maxillary nerve that courses along the inferolateral margin of the sphenoid sinus; the vidian canal, which usually runs along the floor of the sphenoid sinus; and the cavernous portion of the internal carotid artery, which protrudes laterally into the sinus (see Fig. 8-7, B). The sphenoid sinus septum usually is aligned anteriorly with the nasal septum, but the sinus septum can deviate posteriorly, forming unequal sphenoid cavities (see Fig. 8-7, C). Absent pneumatization in a child older than 9 years is usually abnormal and warrants clinical investigation (see Fig. 8-7, D).

Frontal Sinuses

The frontal sinuses are absent at birth and are the last to develop once bone marrow conversion has occurred. The frontal sinus is considered an extension of the anterior ethmoid air cells and pneumatizes between 2 to 8 years, with the most significant growth taking place between ages 1 to 5 years. The frontal sinuses can continue to expand up until the second decade of life.6,11 The frontal sinuses consist of paired, often asymmetric cells. The anterior wall corresponds to the outer cortical table of the frontal bone, and the posterior wall of the sinus separates it from the anterior cranial fossa. Drainage of this sinus occurs via the frontal recess, which is an hourglass-like narrowing between the frontal sinus and the anterior middle meatus (see Fig. 8-2, A). Hypoplasia and aplasia of the frontal sinus can be seen in 4% and 5% of the population, respectively.

Radiography

Although plain radiography is less costly and more widely available than computed tomography (CT), it has significant limitations in evaluating the paranasal sinuses. Specifically, plain radiography often overestimates or underestimates findings, it does not localize pathology well, and it does not provide important anatomic detail.¹⁷ Traditionally, the paranasal sinus series has consisted of four views (Caldwell, Waters, posteroanterior, and lateral) that are technically difficult to perform in children. The Waters view is obtained by angulating the beam in 5-degree increments per year (up to age 6 years) to compensate for the progressive enlargement of the maxillary antra throughout childhood (Fig. 8-10, A and B). Although this approach improves visualization of the maxillary sinuses by projecting them over the petrous pyramids, it also creates double contours that can simulate mucosal thickening. Radiographic density also is critical because overpenetration of the films can completely obscure density differences created by disease, whereas underpenetration can simulate disease. Air fluid levels also can be obscured as a result of beam angulation. Although some have suggested using only the Waters view radiograph, this modality has been shown to have 32% false-negative results and 49.2% false-positive results when compared with CT. Moreover, most of the abnormalities in the ethmoid and sphenoid sinus are not detected in the Waters radiograph.¹⁸ Ethmoid disease on the Caldwell projection can be overdiagnosed or underdiagnosed because of technical and anatomic factors. The lateral view for evaluating the sphenoid sinus is of very little value in children younger than 4 years.^17,19

The American College of Radiology does not recommend the use of plain radiography in diagnosing sinusitis in children. Sinusitis is considered a clinical diagnosis that should not be made on the basis of imaging findings alone.²⁰ Similarly, American Academy of Pediatrics (AAP) guidelines state that plain radiographs are unnecessary for diagnosing sinonasal disease in children younger than 6 years.²¹ Further, plain films do not play a role in evaluating sinonasal masses or complications of sinusitis.

Computed Tomography

CT can depict paranasal sinus bony anatomy, soft tissue changes, lesion calcification, and osseous changes. Coronal CT images best demonstrate the anatomy of the ostiomeatal unit, as well as important anatomic landmarks and variants of the sinuses, effectively providing a road map for functional endoscopic sinus surgery. For these reasons, CT is considered the imaging modality of choice for evaluating inflammatory disease of the paranasal sinuses (i.e., recurrent and chronic sinusitis). CT also plays an important role in detecting orbital and intracranial complications of acute or chronic sinusitis. Along with magnetic resonance imaging (MRI), CT is an excellent tool for evaluating sinonasal masses.

When using nonhelical CT, images of the paranasal sinuses are obtained in a direct coronal plane with the patient in a prone position with the head hyperextended. Multidetector CT with volume isometric imaging allows axial image acquisition perpendicular to the table with the patient in a neutral supine position; images subsequently are reconstructed in coronal and sagittal planes. Slice thickness is usually 2.5 mm, and anatomic coverage extends from the upper teeth to 2 cm above the frontal sinus. If orbital or intracranial complications of sinusitis are suspected clinically, the study should be performed after the intravenous (IV) administration of contrast material, and imaging also should include the brain. Images are reconstructed in both soft tissue and bone algorithms.

In recent years, there has been heightened awareness of and concern about the potentially harmful side effects associated with radiation exposure, particularly in the pediatric population.22,23 For this reason, the practice of the “as low as is reasonably achievable” principle among the radiologic community is critical, with special attention given to CT protocols and parameters.^22,24 In evaluating paranasal sinuses, it is possible to reduce radiation techniques for maxillofacial CT imaging, even to a level comparable to that used for standard radiographic images, without sacrificing diagnostic image quality.²⁵

Magnetic Resonance Imaging

The role of sinus MRI in imaging inflammatory disease is limited, but it is valuable in evaluating complications of sinusitis (e.g., intracranial extension), as well as inflammatory disease associated with sinus or parasinal neoplasm. However, MRI does not depict bony detail and is less sensitive for bony erosions. Other limitations include its availability, higher costs, and the frequent need for sedation in young children.

The normal nasal cycle of vasodilation and mucosal edema followed by vasoconstriction and mucosal shrinkage can produce signal changes that can create significant variability in findings and thus differing interpretations. This cycle varies from 50 minutes to 6 hours, and the signal intensity during the edematous phase is indistinguishable from that of inflammatory change. As with CT and plain radiographs, sinus MRI typically shows a high incidence of findings in asymptomatic persons (13% to 37%) and mucosal thickening of <3 mm that is likely insignificant.² MRI can differentiate mucosal thickening from sinus secretions (Fig. 8-11, A–E).

Along with CT, MRI is very useful in evaluating neoplasms. An estimated 90% to 95% of tumors in the sinuses or nasal cavity exhibit moderately lower signal intensities on T2-weighted images (from hypercellularity) compared with most acute inflammatory diseases (including polyps, mucoceles, and retention cysts), which produce a bright signal on T2-weighted images. However, more mature granulation tissue and fibrosis also have a lower T2 signal, making it difficult to distinguish from tumor. Certain fungal infections, in contrast to other types of acute inflammatory disease, also have a lower T2 signal.

Ostiomeatal Unit

Regarded as an important anatomic region for potential surgical intervention, the ostiomeatal unit is a complex anatomic structure at the crossroads of mucociliary drainage from the frontal, anterior ethmoid, and maxillary sinuses.²⁶ It includes the uncinate process, infundibulum, ethmoid bulla, hiatus semilunaris, and middle meatus (Fig. 8-12, A and B).¹³

The uncinate process arises from the upper medial maxillary wall and defines the wall of the infundibulum.²⁷ The infundibulum is the channel defined laterally by orbit or Haller cells and medially by the uncinate process. The ethmoid bulla is a dominant middle ethmoid air cell that protrudes inferomedially into the infundibulum and hiatus semilunaris. The hiatus semilunaris is a semilunar region between the tip of the uncinate process and ethmoid bulla (see Fig. 8-12, A and B).

Choanal Atresia

Choanal atresia, the most common congenital abnormality of the nasal cavity, is thought to result from failure of rupture of the oronasal membrane during the sixth week of fetal life. It consists of obstruction of the posterior opening of the nasal cavity, which is mixed bony-membranous in approximately 70% of cases and pure bony atresia in 30% of cases. The existence of a purely membranous atresia has been questioned, and evaluation with high-resolution CT often has failed to demonstrate a membranous atresia without a bony component.²⁸ Choanal atresia can be unilateral (in 50% to 60% of cases) or bilateral, and it is more common in girls (the female : male ratio is 2 : 1).

Congenital Nasal Pyriform Aperture Stenosis

Congenital nasal pyriform aperture stenosis is a rare form of nasal obstruction that consists of narrowing of the nasal pyriform aperture as a result of bony overgrowth of the nasal process of the maxilla.³⁰ It should be suspected in any neonate with upper respiratory obstruction and needs to be differentiated from choanal atresia and other congenital nasal masses.

Congenital Nasolacrimal Duct Dacrocystoceles

Congenital nasolacrimal duct dacryocystoceles consist of a cystic dilatation of the nasolacrimal apparatus as a result of proximal and or distal obstruction of the nasolacrimal duct, which is thought to result from failure of duct canalization. Dacryocystoceles can be unilateral or bilateral. Ductal dilatation can occur at any level from the lacrimal sac (a proximal lesion at the medial canthus) to the opening of the duct in the inferior meatus (a distal lesion in the inferior meatus underturbinate), with enlargement of the bony duct.

Sinusitis

Rhinosinusitis is characterized by inflammation of the sinonasal mucosa, usually after an upper respiratory infection (URI). Children contract an average of three to eight viral URIs per year that are generally self-limited, with no antimicrobial therapy required.³⁴ However, acute bacterial sinusitis (ABS) can complicate viral rhinosinusitis in up to 13% of affected children.²¹ Other predisposing conditions for sinusitis are allergic rhinitis, immunoglobulin deficiency, immotile cilia syndrome, cystic fibrosis (CF), and anatomic abnormalities causing obstruction of the drainage pathways. The AAP has defined five categories of bacterial rhinosinusitis: acute, subacute, recurrent acute, ABS superimposed on chronic disease, and chronic sinusitis.²¹

Bacterial sinusitis remains a challenging clinical diagnosis because the signs and symptoms of sinusitis typically seen in adults are noted less frequently in children. Because specific clinical signs in children are generally few, it often is difficult to differentiate ABS from viral rhinosinusitis. Signs and symptoms in children vary and may include cough, purulent nasal discharge, facial pain, fever, headache, and malodorous breath. A frequent cough and the urge to clear the throat usually is due to posterior nasopharyngeal drainage. Nasal congestion is frequent and leads particularly to nocturnal mouth breathing, which results in a sore throat upon awakening in the morning. Constitutional complaints are frequent, including malaise, poor appetite, easy fatigability, and irritability.³⁴

The gold standard for diagnosis of acute or chronic sinusitis remains aspiration from the sinus cavities with the recovery of bacteria in a high density (>10 colony-forming units/mL).²¹ However, this method is impractical, invasive, and time-consuming and is rarely performed. For this reason, the diagnosis of sinusitis usually is based on clinical criteria; it is the duration rather than the severity of symptoms that raises suspicion for ABS. This diagnosis is considered when a URI with purulent discharge lasts for >10 days.

Acute Sinusitis

The AAP defines ABS as sinusitis in which symptoms resolve completely and that lasts <30 days. Common causative microorganisms are Streptococcus pneumoniae, Haemophilus influenzae, and Moraxella catarrhalis.

Chronic Sinusitis

The AAP defines chronic sinusitis as episodes of inflammation of the paranasal sinuses lasting >90 days. Patients have persistent residual respiratory symptoms such as cough, rhinorrhea, and/or nasal obstruction. Children who experience chronic sinusitis usually are older (at least 4 to 7 years of age) and often have a history of recurrent ABS. Other associated factors are recurrent viral URIs, allergic and nonallergic rhinitis, CF, immunodeficiency, ciliary dyskinesia, sinus and facial anatomic abnormalities, and gastroesophageal reflux.³⁵

Clinical findings are similar to those of acute infection but are characterized mostly by a continuous nasal discharge and congestion with a persistent nighttime cough. Other symptoms include chronic headache, chronic halitosis, intermittent fever, sleep deprivation, and general malaise. In persons with chronic sinusitis, Staphylococcus aureus, coagulation negative Staphylococcus, anaerobic organisms, gram-negative bacteria, and fungi are the most commonly encountered colonizing organisms.³⁵

Complications of Rhinosinusitis

Orbital and intracranial complications of rhinosinusitis can result from delayed diagnosis and treatment, antibiotic-resistant or aggressive organisms, or incomplete treatment. Signs and symptoms of orbital complications include periorbital edema, proptosis, chemosis, decreased visual acuity, and/or limited ocular motility. Potential intracranial complications should be suspected when a patient has a history of acute sinusitis combined with severe intractable headache, an altered level of consciousness, focal neurologic deficits, or signs of meningitis.³⁶

Orbital complications usually result from the spread of ethmoid infection that occurs via valveless ethmoid veins that traverse the lamina papyracea. Extension of disease also can arise from the sphenoid, frontal, and maxillary sinuses in order of frequency. Complications include orbital cellulitis with inflammatory edema, preseptal cellulitis, postseptal cellulitis, subperiosteal abscess (Fig. 8-17) (see Chapter 6), orbital abscess (e-Fig. 8-18), optic neuritis, and cavernous sinus thrombosis.

Intracranial complications include epidural empyema, subdural empyema, meningitis, cerebritis, and parenchymal abscess (e-Fig. 8-19, A-G). Subgaleal involvement such as with Pott puffy tumor and osteomyelitis also can occur (Fig. 8-20, A and B). Vascular complications are infrequent and include mycotic aneurysm, stenosis of the cavernous segment of the internal carotid artery (which, in very rare instances, can result in brain infarction³⁷), and venous sinus thrombosis. Superior sagittal thrombosis usually results from frontal sinusitis, whereas sigmoid sinus thrombosis and cavernous sinus thrombosis are associated more often with sphenoid sinusitis (Fig. 8-21, C).

Sinonasal Disease in Persons with Cystic Fibrosis

CF is caused by a genetic defect in the long arm of chromosome 7, which affects the protein that regulates transmembrane passage of chlorine ion and causes dysfunction of multiple organs and systems.⁴⁰ High concentrations of chlorine, mucus thickness, and reduction of mucociliary clearance predisposes to inflammation and chronic infection of the respiratory tract. Nearly 100% of persons with CF present clinically with nasal obstruction and chronic rhinosinusitis (Fig. 8-22, A and B).⁴¹ The most common organisms colonizing the sinonasal mucosa in order of frequency are Pseudomonas aeruginosa, S. aureus, and Streptococcus viridans.⁴²

Allergic Sinusitis

It is estimated that allergic rhinosinusitis affects about 10% of the population. In the United States, the most common form is seasonal pollinosis, resulting from an immunoglobulin E reagin–antibody reaction (type I immunologic disorder), which manifests clinically with sneezing, nasal obstruction, and rhinorrhea. This condition can result in hypertrophic, thickened, and redundant mucosa, known as hypertrophic polypoid mucosa, which is prone to bacterial infection. Allergic sinusitis often coexists with chronic asthma, and 30% of patients will present with polyps (e-Fig. 8-23, A and B). Conversely, up to 80% of patients with polyps have asthma.^47,48 The association of allergic asthma, allergy to aspirin, and aggressive polyposis is known as the Samter triad (e-Fig. 8-23, A and B). Polyps in this condition can be destructive and invade the anterior cranial fossa.²

Fungal Rhinosinusitis Disorders

Fungal infections can cause both acute and chronic rhinosinusitis. These infections have been classified into four clinicopathologic types that can present as either tissue-invasive disorders (acute invasive fulminant disease and chronic invasive infection) or noninvasive disorders (noninvasive mycotic colonization [“fungus ball” or mycetoma] and allergic fungal [mycotic] sinusitis).⁴⁹ All of these entities are rare in children.

Acute invasive fulminant disease occurs in persons who are immunosuppressed and clinically presents as pale mucosa that can progress to gangrene. Spread through neuronal routes can cause vascular invasion with intracranial spread and parenchymal infarcts. Mucormycosis is a disease caused by several types of fungi and can have an acute and fulminant course. In persons with diabetes, mucormycosis can present more as a chronic tissue-invasive infection and frequently causes periorbital invasion (orbital apex syndrome).⁴⁹

A fungal ball or “mycetoma” consists of fungal hyphae compressed into a thick exudate within a sinus lumen.⁴⁹ It is a benign fungal colonization and may occur in patients with previous sinus surgery, oral-sinus fistula, a history of chemotherapy or radiotherapy for cancer, or in those without any known predisposing factor.

Allergic fungal rhinosinusitis should be considered in all adults with chronic sinusitis, but it is rarely seen in young children. Clinical presentation may include a history of allergic sinusitis, chronic rhinosinusitis, nasal polyps, allergic asthma, and immunosuppression, and it can present with proptosis from an inflammatory mass.35,50 The diagnosis is primarily histopathologic. At surgery a characteristic inspissated sinonasal inflammatory exudate called allergic mucin is encountered and must be positive for fungal hyphae on fungal staining or cultures. No evidence for mucosal fungal invasion should be present.⁵⁰

Cysts, Polyps, and Mucoceles

Cysts and polyps are frequent complications of inflammatory rhinosinusitis. A mucous retention cyst results from the obstruction of a submucosal mucinous gland, and the cyst wall is the duct epithelium. These cysts can occur in any sinus but are more frequently found in the inferior aspect of the maxillary sinus. A serous retention cyst results from the accumulation of serous fluid in the submucosal layer of the sinus mucosal lining.² These cysts are not inflammatory lesions and appear as dome-shaped, well-defined, homogeneous, nonenhancing structures on CT; they are hypointense on T1-weighted MR images and hyperintense on T2-weighted images (Fig. 8-24, A). Cysts also can be found incidentally in 10% to 30% of patients.⁵¹

Polyps, in contrast, are a manifestation of an allergic or inflammatory process, or both. When they are associated with an allergy, polyps tend to be multiple. These lesions can become large and cause bony distortion with expansion and erosion. Polyps can be difficult to distinguish from mucous retention cysts in some cases and malignancies in others. Polyps have a high T2-weighted MR signal, in contrast to most neoplasms, which helps in the diagnosis.

An antrochoanal polyp (sinonasal solitary polyp) is a maxillary sinus polyp that fills the sinus, expands the sinus ostium, and prolapses through it into the posterior choana, presenting as a nasal or nasopharyngeal polyp (Fig. 8-24, B and C). Although they are rare, sphenochoanal and ethmochoanal polyps also can occur. In the general population these polyps represent 4% to 6% of all nasal polyps; however, in children the incidence increases to 28% to 33%.⁵² Antrochoanal polyps differ from inflammatory polyps; they tend to be fibrotic with minimal inflammation and are composed of a cystic portion filling the maxillary sinus and a solid dumbbell-shaped portion that emerges into the nasal cavity through the maxillary infundibulum or through an accessory ostium of the maxillary sinus. These polyps are usually unilateral solitary lesions; however, bilateral antrochoanal polyps can be seen in 20% to 25% of cases. The clinical presentation is nasal obstruction and discharge, mouth breathing, snoring, and sleep apnea.

On CT, most antrochoanal polyps have mucoid attenuation. When contrast material is administered, mucosal surface enhancement can occur, but without central enhancement. Antrochoanal polyps can appear denser when inspissated secretions are present. On MRI, antrochoanal polyps usually appear hyperintense on T2-weighted images because of their high water content.

Mucoceles, which are most common in the frontal (60%) and ethmoid (30%) sinuses and result from obstruction or sequestration of a portion of the sinus, are cystic lesions lined with respiratory epithelium and filled with mucoid secretions.⁵³ Mucoceles are rare in the sphenoid⁵⁴ and maxillary sinuses. The association of mucoceles and CF is frequent.⁵⁵ Clinical symptoms result from the mass effect of the lesion and depend on location; these symptoms may include proptosis, headache, cranial nerve impingement, or nasal obstruction (e-Fig. 8-25, A-D).

On CT, mucoceles are low-density, nonenhancing masses that can expand the sinus. Thin rim enhancement can occur; however, if enhancement is thick or nodular, infection should be considered. Calcification in the wall suggests remote infection. The signal varies on MRI, depending on the relative concentrations of water, protein, and mucus.

If the bony wall of the portion of the sinus bordering the brain is disrupted and the rim of the sinus enhances, it is likely that the mucocele is adherent to thickened dura that may lead to complications such as empyema, meningitis, and abscess. A mucocele within the sphenoid sinus before enhancement may mimic the appearance of a pituitary adenoma or chordoma. After administration of IV contrast material, however, these entities should be differentiated easily.

Neoplasms of the Sinonasal Cavity

Benign neoplasms and tumorlike conditions of the sinonasal cavity in children include fibro-osseous lesions and tumors (e.g., fibrous dysplasia and ossifying fibroma), extramedullary hematopoiesis in anemias (e.g., sickle cell anemia and thalassemia), bony tumors (e.g., giant cell tumor and aneurysmal bone cyst) (e-Fig. 8-26), juvenile nasopharyngeal angiofibroma (Fig. 8-27, A-E) and odontogenic cysts or tumors.

Malignant neoplasms of the sinonasal cavity in children include rhabdomyosarcoma (e-Fig. 8-28, A-C), lymphoma/leukemia (e-Fig. 8-29, A and B), esthesioneuroblastoma, nasopharyngeal adenocarcinoma, and metastatic disease (neuroblastoma). These neoplasms will be discussed in greater detail in Chapter 16.

Karmazyn, B, Coley, BD, Robertson, ME, et al. Sinusitis child. American College of Radiology (ACR) appropriatness criteria http://www.acr.org/~/media/485AEEC108E941C6B5551A8D21017EED.pdf, 2012. Available at

Mafee, MF, Tran, BH, Chapa, AR. Imaging of rhinosinusitis and its complications: plain film, CT, and MRI. Clin Rev Allergy Immunol. 2006;30(3):165–186.

Steele, RW. Chronic sinusitis in children. Clin Pediatr (Phila). 2005;44(6):465–471.

Steele, RW. Rhinosinusitis in children. Curr Allergy Asthma Rep. 2006;6(6):508–512.

Ummat, S, Riding, M, Kirkpatrick, D. Development of the ostiomeatal unit in childhood: a radiological study. J Otolaryngol. 1992;21(5):307–314.

1. Antunes, MB, Gudis, DA, Cohen, NA. Epithelium, cilia, and mucus: their importance in chronic rhinosinusitis. Immunol Allergy Clin North Am. 2009;29(4):631–643.

2. Som C, ed. Head and neck imaging, 5th ed, St Louis: Elsevier Mosby, 2011.

3. Wang, R, Jiang, S, Gu, R. The embryonic development of the ostiomeatal complex from 8 to 40 weeks [in Chinese]. Zhonghua Er Bi Yan Hou Ke Za Zhi. 1994;29(3):131–133.

4. Adibelli, ZH, Songu, M, Adibelli, H. Paranasal sinus development in children: a magnetic resonance imaging analysis. Am J Rhinol Allergy. 2011;25(1):30–35.

5. Weiglein, A, Anderhuber, W, Wolf, G. Radiologic anatomy of the paranasal sinuses in the child. Surg Radiol Anat. 1992;14(4):335–339.

6. Shah, RK, Dhingra, JK, Carter, BL, et al. Paranasal sinus development: a radiographic study. Laryngoscope. 2003;113(2):205–209.

7. Medina, J, Hernandez, H, Tom, LW, et al. Development of the paranasal sinuses in children. Am J Rhinol. 1997;11(3):203–209.

8. Nayak, S. Radiologic anatomy of the paranasal air sinuses. Semin Ultrasound CT MR. 1999;20(6):354–378.

9. Szolar, D, Preidler, K, Ranner, G, et al. Magnetic resonance assessment of age-related development of the sphenoid sinus. Br J Radiol. 1994;67(797):431–435.

10. Aoki, S, Dillon, WP, Barkovich, AJ, et al. Marrow conversion before pneumatization of the sphenoid sinus: assessment with MR imaging. Radiology. 1989;172(2):373–375.

11. Barghouth, G, Prior, JO, Lepori, D, et al. Paranasal sinuses in children: size evaluation of maxillary, sphenoid, and frontal sinuses by magnetic resonance imaging and proposal of volume index percentile curves. Eur Radiol. 2002;12(6):1451–1458.

12. Wolf, G, Anderhuber, W, Kuhn, F. Development of the paranasal sinuses in children: implications for paranasal sinus surgery. Ann Otol Rhinol Laryngol. 1993;102(9):705–711.

13. Vaid, S, Vaid, N, Rawat, S, et al. An imaging checklist for pre-FESS CT: framing a surgically relevant report. Clin Radiol. 2011;66(5):459–470.

14. Reiss, M, Reiss, G. Height of right and left ethmoid roofs: aspects of laterality in 644 patients. Int J Otolaryngol. 2011;2011:508907.

15. Lebowitz, RA, Terk, A, Jacobs, JB, et al. Asymmetry of the ethmoid roof: analysis using coronal computed tomography. Laryngoscope. 2001;111(12):2122–2124.

16. Alberti, PW. Applied surgical anatomy of the maxillary sinus. Otolaryngol Clin North Am. 1976;9(1):3–20.

17. McAlister, WH, Lusk, R, Muntz, HR. Comparison of plain radiographs and coronal CT scans in infants and children with recurrent sinusitis. AJR Am J Roentgenol. 1989;153(6):1259–1264.

18. Konen, E, Faibel, M, Kleinbaum, Y, et al. The value of the occipitomental (Waters’) view in diagnosis of sinusitis: a comparative study with computed tomography. Clin Radiol. 2000;55(11):856–860.

19. Triulzi, F, Zirpoli, S. Imaging techniques in the diagnosis and management of rhinosinusitis in children. Pediatr Allergy Immunol. 2007;18(suppl 18):46–49.

20. Karmazyn, B, Coley, BD, Dempsey-Robertson, ME, et al. Sinusitis child. American College of Radiology (ACR) appropriatness criteria http://www.acr.org/~/media/485AEEC108E941C6B5551A8D21017EED.pdf, 2012. [Available at].

21. American Academy of Pediatrics Subcommittee on Management of Sinusitis and Committee on Quality Improvement. Clinical practice guideline: management of sinusitis. Pediatrics. 2001;108(3):798–808.

22. Paterson, A, Frush, DP. Dose reduction in paediatric MDCT: general principles. Clin Radiol. 2007;62(6):507–517.

23. Shah, NB, Platt, SL. ALARA: is there a cause for alarm? Reducing radiation risks from computed tomography scanning in children. Curr Opin Pediatr. 2008;20(3):243–247.

24. Goske, MJ, Applegate, KE, Boylan, J, et al. The ‘Image Gently’ campaign: increasing CT radiation dose awareness through a national education and awareness program. Pediatr Radiol. 2008;38(3):265–269.

25. Mulkens, TH, Broers, C, Fieuws, S, et al. Comparison of effective doses for low-dose MDCT and radiographic examination of sinuses in children. AJR Am J Roentgenol. 2005;184(5):1611–1618.

26. Ummat, S, Riding, M, Kirkpatrick, D. Development of the ostiomeatal unit in childhood: a radiological study. J Otolaryngol. 1992;21(5):307–314.

27. Wake, M, Takeno, S, Hawke, M. The uncinate process: a histological and morphological study. Laryngoscope. 1994;104(3 pt 1):364–369.

28. Brown, OE, Pownell, P, Manning, SC. Choanal atresia: a new anatomic classification and clinical management applications. Laryngoscope. 1996;106(1 pt 1):97–101.

29. Slovis, TL, Renfro, B, Watts, FB, et al. Choanal atresia: precise CT evaluation. Radiology. 1985;155(2):345–348.

30. Brown, OE, Myer, CM, 3rd., Manning, SC. Congenital nasal pyriform aperture stenosis. Laryngoscope. 1989;99(1):86–91.

31. Visvanathan, V, Wynne, DM. Congenital nasal pyriform aperture stenosis: a report of 10 cases and literature review. Int J Pediatr Otorhinolaryngol. 2012;76(1):28–30.

32. Van Den Abbeele, T, Triglia, JM, Francois, M, et al. Congenital nasal pyriform aperture stenosis: diagnosis and management of 20 cases. Ann Otol Rhinol Laryngol. 2001;110(1):70–75.

33. Wong, RK, VanderVeen, DK. Presentation and management of congenital dacryocystocele. Pediatrics. 2008;122(5):e1108–e1112.

34. Steele, RW. Rhinosinusitis in children. Curr Allergy Asthma Rep. 2006;6(6):508–512.

35. Steele, RW. Chronic sinusitis in children. Clin Pediatr (Phila). 2005;44(6):465–471.

36. Hicks, CW, Weber, JG, Reid, JR, et al. Identifying and managing intracranial complications of sinusitis in children: a retrospective series. Pediatr Infect Dis J. 2011;30(3):222–226.

37. Perez Barreto, M, Sahai, S, Ameriso, S, et al. Sinusitis and carotid artery stroke. Ann Otol Rhinol Laryngol. 2000;109(2):227–230.

38. Tsai, BY, Lin, KL, Lin, TY, et al. Pott’s puffy tumor in children. Childs Nerv Syst. 2010;26(1):53–60.

39. Blumfield, E, Misra, M. Pott’s puffy tumor, intracranial, and orbital complications as the initial presentation of sinusitis in healthy adolescents, a case series. Emerg Radiol. 2011;18(3):203–210.

40. Rommens, JM, Iannuzzi, MC, Kerem, B, et al. Identification of the cystic fibrosis gene: chromosome walking and jumping. Science. 1989;245(4922):1059–1065.

41. Sakano, E, Ribeiro, AF, Barth, L, et al. Nasal and paranasal sinus endoscopy, computed tomography and microbiology of upper airways and the correlations with genotype and severity of cystic fibrosis. Int J Pediatr Otorhinolaryngol. 2007;71(1):41–50.

42. Godoy, JM, Godoy, AN, Ribalta, G, et al. Bacterial pattern in chronic sinusitis and cystic fibrosis. Otolaryngol Head Neck Surg. 2011;145(4):673–676.

43. Weber, SA, Ferrari, GF. Incidence and evolution of nasal polyps in children and adolescents with cystic fibrosis. Braz J Otorhinolaryngol. 2008;74(1):16–20.

44. Yung, MW, Gould, J, Upton, GJ. Nasal polyposis in children with cystic fibrosis: a long-term follow-up study. Ann Otol Rhinol Laryngol. 2002;111(12 pt 1):1081–1086.

45. Kovell, LC, Wang, J, Ishman, SL, et al. Cystic fibrosis and sinusitis in children: outcomes and socioeconomic status. Otolaryngol Head Neck Surg. 2011;145(1):146–153.

46. Rickert, S, Banuchi, VE, Germana, JD, et al. Cystic fibrosis and endoscopic sinus surgery: relationship between nasal polyposis and likelihood of revision endoscopic sinus surgery in patients with cystic fibrosis. Arch Otolaryngol Head Neck Surg. 2010;136(10):988–992.

47. Marseglia, GL, Merli, P, Caimmi, D, et al. Nasal disease and asthma. Int J Immunopathol Pharmacol. 2011;24(suppl 4):7–12.

48. Triglia, JM, Nicollas, R. Nasal and sinus polyposis in children. Laryngoscope. 1997;107(7):963–966.

49. deShazo, RD, Chapin, K, Swain, RE. Fungal sinusitis. N Engl J Med. 1997;337(4):254–259.

50. Schubert, MS. Allergic fungal sinusitis: pathophysiology, diagnosis and management. Med Mycol. 2009;47(suppl 1):S324–S330.

51. Kanagalingam, J, Bhatia, K, Georgalas, C, et al. Maxillary mucosal cyst is not a manifestation of rhinosinusitis: results of a prospective three-dimensional CT study of ophthalmic patients. Laryngoscope. 2009;119(1):8–12.

52. Chen, JM, Schloss, MD, Azouz, ME. Antro-choanal polyp: a 10-year retrospective study in the pediatric population with a review of the literature. J Otolaryngol. 1989;18(4):168–172.

53. Lund, VJ, Milroy, CM. Fronto-ethmoidal mucocoeles: a histopathological analysis. J Laryngol Otol. 1991;105(11):921–923.

54. Lui, YW, Dasari, SB, Young, RJ. Sphenoid masses in children: radiologic differential diagnosis with pathologic correlation. AJNR Am J Neuroradiol. 2011;32(4):617–626.

55. Nicollas, R, Facon, F, Sudre-Levillain, I, et al. Pediatric paranasal sinus mucoceles: etiologic factors, management and outcome. Int J Pediatr Otorhinolaryngol. 2006;70(5):905–908.

56. Kim, BH, Seo, HS, Kim, AY, et al. The diagnostic value of the sagittal multiplanar reconstruction CT images for nasal bone fractures. Clin Radiol. 2010;65(4):308–314.

57. Lee, MH, Cha, JG, Hong, HS, et al. Comparison of high-resolution ultrasonography and computed tomography in the diagnosis of nasal fractures. J Ultrasound Med. 2009;28(6):717–723.

58. Hong, HS, Cha, JG, Paik, SH, et al. High-resolution sonography for nasal fracture in children. AJR Am J Roentgenol. 2007;188(1):W86–W92.