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Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_4416_Библиотеки_им_академика_М_И_Перельмана

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Section 2 Inammatory Nasal Conditions62
Table 4.2: Complications of acute sinusitis.
CECT/CEMR Findings
Orbital
Cellulitis and periostitis (Fig. 4.3)
Abscess (Fig. 4.4) • Low density collections with rim enhancement
Superior ophthalmic vein thrombosis
Intracranial (Less frequent than orbital complications)
Cavernous Sinus Thrombosis
Extra-axial abscesses • Epidural/ subdural collections
Cerebritis • Edema/ill-dened enhancement of brain parenchyma
Cerebral abscess • Walled off collections with rim enhancement
• Ill-dened soft tissue enhancement
• Contiguous to sinus inammation
• Extra-ocular muscles may be involved
• Critical structure at orbital apex
• Subperiosteal abscesses form along medial wall/roof/oor
• Subdural effusion is the commonest (most common organism: Streptococcus anginosus)
• Enlargement with lateral convexity of unilateral/bilateral cavernous sinuses
• Rim enhancing low density extra-axial collections
• Uncommon, more often in children with frontal sinusitis
• Surrounding edema
• “Pott’s puy tumor”—osteomyelitis of the frontal sinus results in edema (doughy feel) overlying the sinus. Also an accompanying subgaleal abscess contributes to the mass-like appearance.
• Rarely spread of infection from sinuses to cranium may occur through skull base defects (congenital/acquired).
• Also sphenoid sinus is a less frequent site of sinusitis (<3%), it is most common site to result in meningitis.
CHRONIC RHINOSINUSITIS
Imaging Findings
Imaging is the mainstay of diagnosis. Imaging ndings include mucosal thickening, retained secretions and bony changes.
Mucosal thickening
• Normal mucosa is not visualized on CT/MR and hence any vascularized soft tissue seen lining the air lled sinuses is labeled as “thickened”.
• However, some mucosal thickening may be seen in normal individuals (as physiologic), and the criteria vary among dierent sinuses (Figs. 4.5A and B).
2,3
63Chapter 4 Imaging in Rhinosinusitis (Inammatory Diseases)
A
Figs. 4.5A and B: Mucosal thickening. (A) CT: Mucosal thickening of bilateral maxillary
(white arrows) and ethmoid sinuses (asterisks). (B) MRI (T2WI): Right maxillary sinus: Thickened mucosa (white arrow), left maxillary sinus—normal (<3 mm) (black arrow).
A
Figs. 4.6A and B: Opacication of sinuses. Right maxillary sinus: Hypodense secretions
(black arrow). Left: Hyperdense inspissated secretions (white arrow) with decreased size (evolving silent sinus) (arrowhead).
B
B
• Maxillary sinuses: up to 3 mm normal, frontal sinus: any thickening is abnormal, ethmoid sinus: up to 2 mm normal.
Retained secretions
3,4
Accumulation of secretions leads to opacication of sinuses.
Over a period of time, there is resorption of the uid component and increase in the protein content of the secretions. Hence, these become thick and viscous.
On CT (Figs. 4.6A and B), while acute secretions are of water density, these become increasingly more dense, and eventually long inspissated secretions appear hyperdense.
Calcication is infrequent, has a scattered, peripheral distribution, and may give an egg-shell or round appearance. e secretions of calcic density give the appearance of an antrolith (Figs. 4.7A and B)
Section 2 Inammatory Nasal Conditions64
A
Figs. 4.7A and B: Maxillary antrolith in polyposis pattern of CRS. Opacication of left
maxillary and ethmoid sinuses with widening of ostiomeatal unit (arrows). Retained secretions forming maxillary antrolith (arrowhead).
A
Figs. 4.8A and B: MRI appearance of secretions. (A) Axial T1WI; (B) Coronal T2WI
• Right maxillary sinus: – Peripheral secretions (black arrow)-T1 hypointense, T2 hyperintense – Central secretions (white arrow)-T1 hyperintense, T2 hypointense
• Left maxillary sinus: – Mucosal thickening (arrowhead)-T1 hypointense, T2 hyperintense
• Large right ethmoidal mucocoele (asterix) is seen
B
B
Interspersed between the inspissated secretions and the bony sinus wall, the thickened mucosa and submucosal edema appears as a hypodense line.
On MRI (Figs. 4.8A and B), the alterations in the signal intensity of the
secretions on T1 and T2 weighted images depends on the percentage of protein content and the viscosity.2 Dierent protein contents result in
BA
Figs. 4.9A and B: Polypoid mucosal disease with active inammation. (A) Axial T2WI.
Polypoid mucosal disease with submucosal edema in bilateral maxillary sinuses (black arrows). Both appear hyperintense. (B) Coronal postcontrast T1WI. Mucosal enhancement (white arrow) outlining nonenhancing submucosal edema (arrowheads).
dierent signal intensities on T1 and T2W-images with up to 5% protein content appearing hypointense on T1WI and hyperintense on T2WI. Between 5% and 25%, both the T1 and T2 signal is hyperintense whereas between 25% and 30%, the T2 signal becomes hypointense. As the protein content increases to 30–35%, both the T1 and T2 signals become hypointense. High protein content of >35% appears as signal void on T1- and T2WI mimicking an aerated sinus and hence CT correlation is necessary.
On contrast enhanced magnetic resonance (CEMR), if active inammation is present the mucosa enhances as a thin line, and edematous zone seen between this enhancing line and bony wall represents submucosal edema (Figs. 4.9A and B).
In the brotic stage, the thickened mucosa does not enhance.
Bony changes
Over a period of time, chronic rhinosinusitis (CRS) is accompanied by thickening and sclerosis of the sinus walls (Figs. 4.10A and B).
inning or erosion is only seen in mucocele, polyps or fungal forms of the disease.
Staging
ere are various staging systems available but are not commonly used. One of these is the radiological Lund-Mackay system.
e modied Lund-Mackay system (2) includes the following:
• Sinus opacication (0 for normal, 1 for partial and 2 for total); OMC
(0 for no obstruction, 2 for obstructed sinus) and normal variants (0 if absent and 1 for present). ese variants include absent frontal sinus, paradoxic middle turbinate, concha bullosa, Haller cells, Agger nasi cell pneumatization and everted uncinate process.
It is said that these scores correlate with the surgical treatment and its outcome.
65Chapter 4 Imaging in Rhinosinusitis (Inammatory Diseases)
Section 2 Inammatory Nasal Conditions66
BA
Figs. 4.10A and B: Bony changes (sclerosis) in polyposis pattern of chronic
rhinosinusitis (CRS). (A) Opacication of left maxillary and ethmoid sinuses with widening
of osteomeatal unit (arrow). (B) Sclerosis of ethmoid trabeculae (arrowhead).
Patterns of CRS
Based on the distribution of the disease as seen on NCCT, CRS has been divided into ve patterns (Table 4.3; Figs. 4.11 to 4.14)
is classication has management implications in that it covers the choice of surgical technique with patterns III and IV being labeled as complex surgical groups.
5,6
Sinonasal Polyposis
Sinonasal polyposis is a nonobstructive form of CRS diusely involving the sinuses and nasal cavity.
e diuse polyposis characteristically shows central hyperdensity on NCCT (due to inspissated secretions) with background hypodensity, which is due to secretions that are more mucoid.
ere is widening of the ostomeatal units and ethmoid infundibulum with erosion of bony ethmoidal trabeculae and nasal septum. Bulging of the bony ethmoid walls may be seen (Figs. 4.15A and B).
Causes of Obstruction of Drainage Pathways
e common cause of obstruction of drainage pathways includes mucosal inammation (causing thickening), hypertrophied turbinates, adhesions, polyps, tumors and anatomical variants. e anatomical variants and the resultant pattern of CRS are detailed in Table 4.4.
67Chapter 4 Imaging in Rhinosinusitis (Inammatory Diseases)
Simple endoscopic procedure Low
More extensive surgery (vs pattern I) Higher
• Maxillary sinus
• Inferior infundibulum
• Middle meatus and
• Ostiomeatal unit
High
Sphenoethmoid recess • More complex surgery
High
• Higher complication rate
• Surgery in refractory cases
• Extensive difcult surgery
Nonobstructive form • Medical treatment
Table 4.3: Patterns of chronic rhinosinusitis (CRS).
Pattern Sinus/ Sinuses involved Site of obstruction Surgery Recurrence
Unilateral maxillary sinus Ostium of
I: Infundibular pattern
(Figs. 4.11A and B)
• Unilateral
• Maxillary
• Frontal
Pattern (Figs. 4.12A and B)
II: Osteomeatal Unit
• Anterior ethmoidal cells
Unilateral frontal sinus Frontal recess
Subpattern: Frontal
Sphenoid sinus ± Posterior
ethmoid cells
recess pattern
(Figs. 4.13A and B)
III: Sphenoethmoid
recess pattern
(Figs. 4.14A and B)
All sinuses and nasal cavity
Diffuse involvement
IV: Sinonasal polyposis
(Figs. 4.15A and B)
• Not explained by drainage walls
• Often single sinuses
V: Sporadic pattern • Random involvement
Note: In the presence of widening of ostium or bony erosion in the drainage pathway, polyposis or tumor should be suspected and contrast study/sampling is
advised.
Section 2 Inammatory Nasal Conditions68
A
Figs. 4.11A and B: Infundibular pattern (I). (A) Opacied left maxillary sinus (arrowhead);
(B) Obstruction at left infundibulum (arrow).
A
Figs. 4.12A and B: Osteomeatal unit pattern (II). (A) Opacied left anterior ethmoid air
cells and maxillary sinus (arrows); (B) Obstructed osteomeatal unit (arrowhead).
B
B
Chronic Complications/Sequelae
Chronic complications of CRS include retention cysts, polyps, mucocele, silent sinus syndrome and atrophic rhinitis. Retention cysts are detailed in Chapter 5.
Silent sinus syndrome
Synonyms: Imploding antrum syndrome, chronic maxillary sinus
atelectasis
69Chapter 4 Imaging in Rhinosinusitis (Inammatory Diseases)
A
Figs. 4.13A and B: Frontal recess pattern. (A) Opacied left frontal sinus; (B) Occluded left
frontonasal drainage pathway (arrow) compared with normal right side (dotted line).
A
Figs. 4.14A and B: Sphenoethmoidal recess pattern (III). (A) Normal right sphenoethmoidal
recess (dotted line); (B) Soft tissue thickening left sphenoid sinus (arrow) with obliteration of sphenoethmoid recess.
B
B
• Sequelae of chronic occlusion of the maxillary sinus ostium
• Leads to volume loss/shrinkage of the sinus due to negative pressure
• Clinical presentation is of gradual enophthalmos and facial
asymmetry. Patient is often not symptomatic for the sinus symptoms; hence the term “silent”
• Air within the sinus is absorbed and it is lled with thick secretions
(Figs. 4.17A and B)
• Seen in adults, is either the consequence of chronic sinusitis or
occasio nally of trauma of the lateral nasal wall.
Section 2 Inammatory Nasal Conditions70
BA
Figs. 4.15A and B: Sinonasal polyposis pattern (IV). (A) Near complete opacication of
bilateral sinonasal cavities. Deossication of ethmoid trabeculae (arrowheads). (B) Widening of ostiomeatal units (arrows).
Fig. 4.16: Haller cell causing type I pattern. Left Haller cell (arrowhead) causing obstruction
of left infundibulum (arrow) and maxillary sinusitis.
Table 4.4: Anatomical variants causing obstruction of sinus drainage pathways.
Anatomical variants Pattern of CRS
Haller cell (Fig. 4.16) Pattern I
Pneumatized uncinate
Enlarged ethmoidal bulla
Hypoplastic maxillary sinuses
Concha bullosa Pattern II
Paradoxical middle turbinate
Interlamellar cell of Grunwald
Deviated nasal septum
Agger nasi cell Frontal recess pattern
Frontal ethmoidal cells
Interfrontal sinus septal cell (narrow frontal ostium)
BA
Figs. 4.17A and B: Silent sinus syndrome. Small opaque maxillary sinus with infundibular
occlusion (asterisks). Enlargement of orbit with downward displacement of the oor (arrow). Lateral retraction/displacement of uncinate process (arrowhead).
Imaging (Figs. 4.17A and B):
ere is volume loss of sinus with inward bowing of sinus walls
that are also thickened, sinus is opacied with dense secretions.
Downward displacement of the orbital oor is seen with enoph-
thalmos. ere is also increased orbital volume and even
thinning of the orbital oor. ▶ e osteomeatal unit/ostium is blocked. ▶ ere is lateral retraction of the uncinate process which rests
against the inferomedial wall of the orbit. Middle meatus is thus
enlarged. ▶ Increase in retroantral fat pad is seen.
3
Treatment: Surgical with uncinectomy and clearance of the ostium. Additional orbital oor repair may be required.
Dierential diagnosis:
Postoperative changes: following Caldwell-Luc operation. ▶ Hypoplasia: It is an important dierential in the absence of
history of surgery and the dierentiating points are discussed in detail at the end of the chapter.
Atrophic rhinitis
Synonyms: Rhinitis sicca, ozera, open-nose syndrome.
Two forms: Primary or secondary.
• Form of CRS wherein the ciliated columnar epithelium of the sinonasal cavity is replaced by non-ciliated epithelium resulting in “roomy” space.
7
Primary: Decreasing incidence in modern world. May still be seen in developing world in parts of India, China, Middle East and Egypt.
71Chapter 4 Imaging in Rhinosinusitis (Inammatory Diseases)