The maxillary sinuses are the first of the paranasal sinuses to develop. In the neonate, the maxillary sinuses are quite small and may be partially or completely opacified. The maxillary sinuses grow progressively until the end of puberty. They reach the plane of the hard palate by 9 years of age. Asymmetry of the maxillary sinuses is common. The drainage ostium of the maxillary sinus is located superomedially. It empties into the infundibulum, which is located between the lamina papyracea and the uncinate process. The infundibulum opens into the middle meatus through the hiatus semilunaris. The maxillary sinuses become visible on standard radiographs at approximately 2 to 3 months of age.^1,2

Small anterior ethmoid air cells are present at birth. There is rapid progression in ethmoid sinus development during the first 2 years of life. A second phase of rapid development occurs just before puberty. Pneumatization occurs from an anterior to posterior direction. Complete development occurs by the age of puberty. Each mature ethmoid sinus is bounded superiorly by the floor of the anterior cranial fossa, and laterally by the orbital wall. Aeration of the ethmoid sinuses is first radiographically identified at 3 to 6 months of age. Posterior ethmoid air cell aeration is first visible around the age of 6 or 7 years.

The sphenoid sinuses are tiny marrow-filled cavities at birth. Pneumatization usually begins around 2 years of age, and progresses until puberty. The mature sphenoid sinuses are bounded by the dura and sella superiorly, the cavernous sinuses laterally, posterior ethmoid air cells anteriorly, and the clivus posteriorly. The sphenoid sinuses are visible on radiographs beginning at 1 to 2 years of age.

The frontal sinuses originate as extensions from the anterior ethmoid air cells. Development begins around the age of 2 years, and growth continues until the end of puberty. The frontal sinuses have the greatest degree of developmental variation of any of the paranasal sinuses. Frontal sinus aeration can usually be identified on radiographs beginning at 4 to 8 years of age.

The frontal, anterior ethmoid, and maxillary sinuses drain through the ostiomeatal complex (ostiomeatal unit). There is no clear consensus as to the precise anatomic definition of the ostiomeatal complex. Most authors include the ethmoid infundibulum, middle nasal meatus, ethmoid bulla, nasofrontal recess, and ostia of the anterior ethmoidal, maxillary, and frontal sinuses as components. The hiatus semilunaris as is an opening in the lateral nasal wall adjacent to the uncinate process that allows communication with the middle meatus, which is the space in the nasopharynx inferior to the middle turbinate. The posterior ethmoid air cells and the sphenoid sinus drain into the superior meatus, which is below the superior turbinate. The nasolacrimal duct drains into the inferior meatus.

Developmental variations of the nasopharynx and paranasal sinuses are common. Most are of no clinical significance. Some of these developmental variations, however, impact surgical procedures; therefore, appropriate recognition on preoperative imaging studies is important. A Haller cell is an extramural ethmoidal air cell located along the medial aspect of the roof of the maxillary sinus. Although clinically inconsequential in most patients, a Haller can narrow the ostium and infundibulum. Approximately 20% of children have agger nasi air cells, which are anterior ethmoid air cells that extend anterior to the nasolacrimal duct into the medial aspect of the frontal process of the maxilla or lacrimal bone. Agger nasi air cells can also extend into the uncinate process. Onodi air cells are posterior ethmoid air cells that surround the optic nerve canal and overlap the sphenoid sinus laterally. Concha bullosa refers to pneumatization of the middle turbinate (Figure 28-1). This developmental variation is important as it can result in deviation of the uncinate process or septum. Anomalous, usually incomplete, septa can occur in the maxillary sinuses, most often located anteriorly. Frontal sinus pneumatization sometimes extends into the crista galli, and can extend along the orbital roofs. Likewise, ethmoid air cells can extend into the orbital roof. Sphenoid sinus pneumatization can extend into the greater or lesser wings, as well as the pterygoid plate.³

Septal deviation is a common developmental variation that is often accompanied by deformities of adjacent structures. A substantial minority of individuals with moderate to severe septal deviation have a septal spur that protrudes towards the lateral wall of the nasal cavity, and sometimes contacts the wall. The middle turbinate is often hypoplastic in the presence of septal deviation or a septal spur.

In the normal paranasal sinus, the periosteum is too thin to be visualized on imaging studies, and air within the sinus cavity should directly abut the bony wall of the sinus; when the mucosa is visible, it is thickened. Prominence of the mucosa can occur from physiological engorgement, acute or chronic inflammation, or fibrosis. As a rule, mucosal thickening of up to 3 mm is common in asymptomatic patients. Focal or nodular areas of mucosal thickening, as well as small mucous retention cysts, also are common in patients who have no symptoms of paranasal sinus disease. Prominence of the nasal turbinates on imaging studies is usually a normal finding, particularly when unilateral. Physiological changes in size of the nasal turbinates occur quite rapidly.

Paranasal Sinus Aplasia or Hypoplasia

The most common developmental abnormality of the paranasal sinuses is hypoplasia. The frontal sinuses have the greatest propensity for developmental variation in size. Unilateral hypoplasia that results in asymmetry of the frontal sinuses is common. Bilateral frontal sinus aplasia occurs in approximately 4% of otherwise normal individuals. Aplasia of other paranasal sinuses is quite rare. Likewise, hypoplasia is rare in the ethmoid and sphenoid sinuses, although the sphenoid sinus has great variation between individuals in its extent. Maxillary sinus hypoplasia is relatively common.

Small paranasal sinuses result from 2 basic mechanisms: developmental failure and osseous encroachment. Hypoplasia of a paranasal sinus is usually a sporadic event of little or no clinical significance. A variety of syndromes and developmental bone abnormalities are associated with paranasal sinus hypoplasia; these include Down syndrome, Prader-Willi syndrome, Cockayne syndrome, otopalatodigital syndrome, Binder syndrome, cleidocranial dysplasia, craniometaphyseal dysplasia, mandibulofacial dysostosis, fibrous dysplasia, osteopetrosis, pyknodysostosis, and frontonasal dysplasia. Endocrinopathies such as hypothyroidism can cause hypoplastic sinuses. Expansion of the facial bone marrow spaces due to a hematological condition such as sickle cell disease or thalassemia is another cause. Therapeutic irradiation of the facial bones in the young child frequently interferes with paranasal sinus development. Unilateral maxillary sinus hypoplasia is a component of hemifacial microsomia.

Paranasal sinus hypoplasia and aplasia are usually demonstrated effectively on standard radiographs. Occasionally, it is difficult to differentiate a small sinus from a pathologically opacified sinus. With maxillary sinus hypoplasia, the walls are contracted in all dimensions. Therefore, the orbital floor is depressed on the frontal view and the lateral wall of the nasal cavity deviates laterally. The ipsilateral inferior turbinate may be enlarged in these children. Distinction between opacification and hypoplasia of a frontal sinus may be more difficult. However, the walls of the sinus should remain visible on radiographs despite inflammatory opacification; the lateral view is particularly helpful for determining the dimension of the sinus in correlation with the degree of opacity on the frontal view. CT and MR examinations provide unequivocal documentation of paranasal sinus size and aeration (Figures 28-2 and 28-3).

Enlarged Paranasal Sinus

Abnormal enlargement of 1 or more paranasal sinuses is an occasional finding on imaging studies of children. Three forms are recognized. (1) An enlarged, aerated paranasal sinus that does not expand its normal bony contours is termed a “hypersinus.” (2) A sinus with expanded, but intact, walls of normal thickness is termed “pneumosinus dilatans.” (3) If the walls of an enlarged aerated paranasal sinus are thinned, it is termed a “pneumocele”; this may involve all or part of the sinus. Abnormal paranasal sinus enlargement most commonly affects the frontal sinuses, and can lead to frontal bossing. Conditions that are associated with enlargement of the frontal sinuses include acromegaly, Marfan syndrome, Turner syndrome, Sturge-Weber syndrome, homocystinuria, and Dyke-Davidoff syndrome. Paranasal sinus enlargement, particularly of the frontal and sphenoid sinuses, sometimes occurs in individuals who suffered deficient brain growth during early childhood.

Fibrous Dysplasia

Paranasal sinus involvement can occur in children with fibrous dysplasia. In this condition, normal bone is replaced by fibrous tissue and the bone contour is expanded. Sinonasal involvement occurs by way of bony expansion that narrows the structure or by stenosis of a sinus ostium. CT shows thickening of the diploic space of the involved bone. The cortical margins are expanded and thinned, but otherwise intact. The bone matrix has a dense ground glass appearance, due to a mixture of osseous and fibrous tissue (Figure 28-4).

General Considerations

Viral rhinitis is the most common infectious inflammatory process of the nose and nasopharynx. The infection causes edema of the nasal mucosa. Radiographs show nonspecific thickening of the nasal turbinates and mucosa. The infection can extend to adjacent paranasal sinuses. In addition, edematous occlusion of the draining ostium of a paranasal sinus can lead to a secondary bacterial infection. Primary bacterial or fungal infections can occur in the nasal cavity, usually in conjunction with symptomatic paranasal sinus involvement.⁴

Infectious sinusitis is classified according to the type of organism involved (viral, bacterial, or fungal) and the duration of the disease. Acute sinusitis lasts for days or a few weeks. Subacute sinusitis lasts for weeks to months, and chronic sinusitis lasts for months to years. Acute sinusitis is most often viral and occurs in conjunction with viral rhinitis.

Common clinical manifestations of sinusitis in children include rhinorrhea, nasal obstruction, mouth breathing, snoring, and hyponasal speech. The findings are nonspecific, however, and substantially overlap those of an upper respiratory tract infection. Mouth breathing may also be a sign of adenoid hypertrophy or turbinate hypertrophy. Allergy plays an important role in the pathophysiology of chronic sinusitis in many children. Allergic rhinitis is estimated to affect 10% to 20% of all children, and these patients are at an increased risk for the development of chronic sinusitis.

As with the clinical findings, the diagnostic imaging features of paranasal sinus infection are nonspecific in many patients. Mild paranasal sinus opacification is common in asymptomatic individuals. Mucoperiosteal thickening, mucous retention cysts, and opacification (sometimes complete) of a sinus are frequent findings on neuroimaging examinations of patients who have no symptoms of paranasal sinus disease. Studies of infants and young children in particular have shown a poor correlation between radiographic paranasal sinus opacification and clinical evidence of sinus disease. Therefore, the findings on paranasal sinus diagnostic imaging studies need to be considered in concert with the specific clinical situation. There are instances, however, when the imaging findings are unequivocally abnormal; for example, the presence of an air–fluid level, bone destruction, or an expanded opacified sinus.

Most infections of the paranasal sinuses in children are due to viruses. This typically occurs in conjunction with infection of other components of the upper respiratory tract. Affected children may exhibit fever, nasal congestion, and clear rhinorrhea. Paranasal sinus involvement is sometimes suggested by localized pain. There is inflammatory thickening of the mucosa in the nasal cavity and paranasal sinuses. Radiographs of patients with viral sinusitis may show clear sinuses, mild mucoperiosteal thickening, or (less commonly) a greater degree of paranasal sinus opacification. The findings reflect mucosal edema and increased production of mucus. Fluid levels do not usually occur with uncomplicated viral paranasal sinus infections.

Children with chronic sinusitis may have long-standing complaints of nasal obstruction, rhinorrhea, sore throat, halitosis, and mouth breathing. Intermittent or low-grade fever is common. The progression of acute sinusitis to chronic sinusitis may be facilitated by impaired drainage of the sinus, persistent infection, loss of ciliary function, and anatomic changes in the mucosa. Mechanical factors that can impair paranasal sinus drainage include septal deviation, nasal polyps, adenoid hypertrophy, persistent mucosal edema in the draining ostium, and a nasopharyngeal tumor. Poor drainage of the sinus facilitates growth of bacteria. Multiplication of anaerobic and microaerophilic bacteria often occurs in a poorly aerated sinus. Chronic low-grade infection results in further mucosal abnormalities that contribute to the cycle. Ciliary function is diminished. Eventually, the bony walls of the sinus may be affected.^5,6

Radiographs and imaging studies of patients with chronic sinusitis show thickened hyperplastic mucosa Pseudopolyps are common. Occasionally, dystrophic calcifications are visible within the hyperplastic mucosa. Inflammation of the sinus wall can result in bony sclerosis. Patients with chronic sinusitis are also prone to superimposed acute bacterial infections, resulting in an air–fluid level. CT may show prominent enhancement of the inflamed mucosa.

There are a variety of potential complications of sinusitis, including mucus retention cyst, serous retention cyst, and mucocele. Spread of bacterial or fungal sinus infections can lead to serious complications within the orbit, meninges, or brain.^7–9

Bacterial Sinusitis

The major clinical indicators of acute bacterial sinusitis are fever, purulent nasal discharge, and facial pain. Facial pain and headache in the presence of sinusitis are more common in teenagers than in younger children. Acute sinusitis usually occurs in conjunction with, or as a complication of, an acute upper respiratory tract infection; the presence of sinusitis in these children is sometimes suggested by especially severe or pronged symptoms. The most common bacteria responsible for acute paranasal sinus infection are Streptococcus pneumoniae, Staphylococcus aureus, Haemophilus influenzae, Branhamella catarrhalis, and a variety of anaerobic organisms.^10,11

The mechanism by which an upper respiratory tract viral illness leads to the development of acute bacterial sinusitis likely involves obstruction of the sinus ostium by edematous mucosa. Other obstructive abnormalities can also be complicated by bacterial sinusitis; examples include polyps, foreign bodies, adenoid hyperplasia, tumors, maxillofacial trauma, and nasal septal deviation. Immune compromise or impairment of the mucociliary transport mechanism increases patient susceptibility to acute sinusitis. About one-third of bone marrow transplant recipients develop sinusitis within 2 years of the transplantation; this is a relatively common source of fever in these patients. Dental pathology is an additional predisposing condition.

The diagnostic imaging hallmark of acute bacterial sinusitis is the presence of an air–fluid level in conjunction with mucoperiosteal thickening (Figure 28-5). This can be effectively demonstrated with CT, MR, or upright standard radiographs (Figure 28-6). However, nonspecific mucoperiosteal thickening is the only imaging finding in many patients with bacterial sinusitis. The completely opacified paranasal sinus is also problematic, as this finding can occur with any of the infectious sinusitises, allergy, or chronic sinusitis. However, bacterial sinusitis more often predominantly involves a single sinus, whereas allergic and viral forms of sinusitis tend to be symmetric. Contrast-enhanced CT or MR provides increased specificity relative to standard radiographs by accurately depicting free fluid in conjunction with marked mucoperiosteal thickening (Figure 28-7).

Complications of Bacterial Sinusitis

The most common complication of acute sinusitis is orbital cellulitis (Table 28-1). Most often, this occurs in the form of cellulitis or inflammatory edema of the periorbital soft tissues. Edema of the intraorbital fat and/or inflammatory enlargement of 1 or more extraocular muscles can also occur. An orbital subperiosteal abscess is a more serious complication that results from spread of infection from an adjacent sinus. CT or MR shows a mass projecting from the orbital wall and a thin enhancing margin that represents the displaced periosteal membrane (Figure 28-8). Rupture of a subperiosteal abscess is a rare additional complication that can lead to an intraorbital abscess.^9,12