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Section 6 Systemic Disorders/Surrounding Structures Involving PNS356
Table 25.2: Orbital involvement in facial fractures.
Orbital structure
Type of fractures
Le Fort II • Medial wall
Le Fort III • Medial wall
Naso-orbito-ethmoidal (NOE)
complex fractures
(Figs. 25.10A and B)
Zygomaticomaxillary complex
(ZMC) fractures
Blow out fractures (Figs.
25.11A and B)
involved Special consideration
• Floor
• Lateral wall
• Medial wall • Medial canthus tendon avulsion
• Lateral wall
• Floor
• Floor
• Medial wall
• Nasolacrimal duct (NLD) injury →
Blockage
• Increased orbital volume
(enophthalmos)
• Increased volume
• Extraocular muscle entrapment
A
B
Figs. 25.10A and B: NOE fracture with medial canthal tendon avulsion. (A) Comminuted
naso-orbital-ethmoidal fracture (arrowhead); and (B) Disrupted medial canthal attachment
site (arrow).
A
B
Figs. 25.11A and B: Blow out fracture with entrapment of inferior rectus. (A) Herniation
of intraorbital fat (arrow); and (B) Likely entrapment of inferior rectus muscle (arrowhead).
CONCLUSION
Due to the anatomic proximity lesions originating in the orbit/sinonasal
cavity often involve the other compartment.
REFERENCES
1. Mafee MF, Tran BH, Chapa AR. Imaging of rhinosinusitis and its complications:
plain lm, CT, and MRI. Clin Rev Allergy Immunol. 2006;30(3):165-86.
2. Joshi VM, Sansi R. Imaging in sinonasal inammatory disease. Neuroimaging
Clin N Am. 2015;25(4):549-68.
3. Nguyen VD, Singh AK, Altmeyer WB, et al. Demystifying orbital emergencies: a
pictorial review. Radiographics. 2017;37(3):947-62.
4. Sen S, Chandra A, Mukhopadhyay S, et al. Imaging approach to sinonasal
neoplasms. Neuroimaging Clin N Am. 2015;25(4):577-93.
5. Sen S, Chandra A, Mukhopadhyay S, et al. Sinonasal tumors: computed tomography and MR imaging features. Neuroimaging Clin N Am. 2015;25(4):595-618.
6. Winegar BA, Murillo H, Tantiwongkosi B. Spectrum of critical imaging ndings in
complex facial skeletal trauma. Radiographics. 2013;33(1):3-19.
357Chapter 25 Imaging of Disorders Involving Sinonasal Cavity and Orbit
Section
Clinico-Radiological Approach
26. Approach to Nasal Obstruction
27. Approach to Epistaxis
28. Imaging Approach to Sinus Lesions
7
26
CHAPTER
Approach to Nasal Obstruction
Rakesh Kumar, Ashu Seith Bhalla, Manisha Jana
• Introduction
• Clinical Presentation
– Important Points in History
• Clinical Examination
– Local Examination
▪ Nose
▪ Nasopharynx
• Diagnostic Imaging
• Imaging Findings
– Nasoethmoidal Lesions
– Nasal Cavity/Lateral Wall Lesion
– Nasal Septal Lesions
– External Nose and Vestibular
Lesion
• Management
INTRODUCTION
■ Nasal obstruction is a sensation of blockage or diculty in breathing
out of one or both nostrils. is can be seen with diseases like rhinitis,
sinusitis, septal deviation, and adenoid hypertrophy. ere is also a
physiological nasal cycle—cyclical pattern of turbinate mucosal swelling
alternating between sides at intervals of 2–5 hours.
■ Nasal obstruction may also be divided into mucosal and structural
causes:
• Mucosal causes: e obstruction tends to uctuate. e common causes
are rhinitis, sinusitis, nasal polyp, and soft tissue turbinate hypertrophy.
• Structural causes: It is progressive. e causes are septal deviation
(cartilaginous or bony), concha bullosa (air cell in the middle turbinate),
tumors (benign and malignant), and choanal atresia/stenosis.
■ Etiological classication of the causes of nasal obstruction is listed in
Table 26.1.
CLINICAL PRESENTATION
Important Points in History
■ Unilateral (structural causes) or bilateral (mucosal causes)
■ Trauma: Nasal trauma/surgery
Section 7 Clinico-Radiological Approach362
Table 26.1: Causes of nasal obstruction.
Infective/inammatory • Rhinitis (infective/allergic)
• Fungal infections
• Polyp
• Atypical retention cyst
• Granulomatosis with polyangiitis (GPA)
Neoplastic—Benign • Papilloma
• Pleomorphic adenoma
• Osteoma
• Juvenilenasopharyngealangiobroma(JNA)
• Schwannoma
• Hemangioma
Neoplastic—Malignant • Squamous cell carcinoma
• Adenocarcinoma
• Adenoid cystic carcinoma
• Lymphoma
• Esthesioneuroblastoma
• Malignant melanoma
• Mesenchymal tumors
Neoplastic—Secondary • Metastases
• Lymphoma
Contiguous extension
from surrounding
structures
Congenital • Encephalocele
• Meningioma
• Chordoma
• Lacrimal sac tumors [through nasolacrimal duct (NLD)]
• Sinus tumors
• Hamartoma (glioma)
• Dermoid/epidermoid cysts
• Teratoma
• Hemangioma
■ Diurnal and seasonal variation: Allergies
■ Precipitating factors: Allergic stimuli and airborne exposures
■ Rhinosinusitis: Facial pain/or pressure, congestion, headache, and
purulent nasal discharge
■ Malignancy: Facial deformity, cranial nerve involvement (facial numbness), and epistaxis
■ Drugs:
• Oral contraceptives, antithyroid medication, antihypertensive,
antidepressants, and benzodiazepines
• Local: Prolong use of nasal drops (rhinitis medicamentosa).
■ Part of systemic illness: Wegener’s granulomatosis, cystic brosis, sarcoi-
dosis, and syphilis.
CLINICAL EXAMINATION
Local Examination
Examine neck for cervical lymphadenopathy if nasal malignancy is suspected.
Nose
■ Occluded nasal passage by boggy, red nasal mucosa (allergies, nonallergic
rhinitis, or overuse of nasal decongestants)
■ Septal deviation
■ Glistening, smooth, pale single (AC polyp), or multiple (ethmoidal) nasal
mass at the level of the middle turbinate or midnasal cavity (polyp)
■ Purulent nasal discharge (rhinosinusitis)
■ Ulcerated, friable mucosa bleeds on touch (granulomatous disease or
malignancies).
• Granulomas:
‒ Syphilis: Granular lesion on septum with history and biopsy plus
serology clinches diagnosis.
‒ Lupus vulgaris/tuberculosis: It involves nasal vestibule and slowly
destructive. Granulation tissue/ulceration and mucopurulent
discharge.
‒ Sarcoid: Systemic disease. Lesion involves septum or lateral wall
and secondarily infection causing serosanguineous discharge.
Patient complain of general ill health and disgurement.
‒ Wegener’s granulomatosis: Systemic condition aecting lungs
and kidney. Any unusual appearance in the nose and unexplained
septal perforation need further investigation.
■ Fungi:
• Aspergillosis: Acute form in immune-compromise patients can be very
aggressive and potentially fatal. It can extend from nose to sinuses and
cranial cavity as well as into the soft tissue of face. Chronic form is not
life threatening.
• Mucormycosis: Fulminant infection and rapidly fatal. Nasal blockage
363Chapter 26 Approach to Nasal Obstruction
■ Nose benign tumors/granulomas:
• Papilloma:
‒ Squamous: Wart-like growth arising from vestibular skin if
trauma can bleed.
‒ Inverted: Considered as intermediate tumors. Arises from lateral
nasal wall and involve maxillary and ethmoid sinuses. Tumor is
soft, friable, and bleed with hard nose blowing.
• Angioma:
‒ Fibroangioma of septum: Pedunculated friable red lesion arising
from septum, bleed on touch. Seen in adults.
‒ Angioma of sinuses: Maxillary and ethmoids in early childhood
and presents with frightening epistaxis.
Section 7 Clinico-Radiological Approach364
• Fibroma: Rare soft pedunculated lesions
• Ossifying broma: Frequent in 2nd and 3rd decades. Usually
involve maxillary and ethmoid sinuses. It causes local discomfort
and expansion, present with rm cheek swelling, and unilateral
obstruction.
• Osteomas: Common in 2nd–4th decades and mostly incidental
ndings. 70% are in frontal, 25% in ethmoid, and 5% are in maxillary
and sphenoid sinuses.
• Fibrous dysplasia: Fibro-osseous thickening of facial bones. Present
as swelling around orbit, cheek, or alveolus. Present in 1st and 2nd
decades of life. It can be monostotic or polyostotic.
■ Miscellaneous:
• Rhinosporidiosis: It presents as bleeding polypus. Typical appearance
is strawberry like.
• Rhinolith: Calcareous mass in the nose. Rough hard object in the nose.
Nasopharynx
■ Carcinoma: It mostly arises in lateral wall of nasopharynx (fossa of
Rosenmuller) and present as mucosa covered mass or ulcerative lesion.
ese patients have multiple neck metastases.
■ Angiobroma: Mucosa covered mass in the nasopharynx, nose with
bleeding in a adolescent male is typical feature.
DIAGNOSTIC IMAGING
Only indicated if diagnosis is not clear based upon the history and physical
examination.
■ Computed tomography (CT) scan of the nose and paranasal sinuses is
the primary diagnostic imaging modality.
■ Magnetic resonance imaging: Generally a secondary study and is
indicated for better characterization of nasal tumors.
IMAGING FINDINGS
■ While interpreting imaging ndings as elsewhere clinical details should
be taken into consideration including age, symptom, duration of illness,
and any systemic comorbidities/symptoms.
■ Multiple factors guide the radiological dierential diagnosis such as—
location, bone expansion, bone destruction, soft tissue signal, and calcication. Some of the factors are common to sinus masses and discussed in
Chapter 4. In the nasal cavity the location is an important determinant
and the lesions have been classied accordingly (Table 26.2).
Table 26.2: Lesions according to the region of origin.
Nasoethmoidal • Encephalocele (frontoethmoidal)
• Meningioma
• Esthesioneuroblastoma
• Chordoma
Lateral nasal wall, turbinates, and
nasal cavity
Nasal septum (vide infra) • Granulomatosis with polyangiitis (GPA)
External nose and vestibule • Congenital lesions
From surrounding structures From posterior nasal cavity: Juvenile
• Rhinosinusitis
• Inverted papilloma
• AC polyp
• Melanoma
• Rhinolith
• Rhinoscleroma
• Rhinosporidiosis
• Midline lethal granuloma (now recognized as a
form of NHL)
• Metastasis
• Melanoma
• Basal cell carcinoma, squamous cell
carcinoma, and melanoma
• Cellulitis, vestibulitis, and abscess
• Nasoalveolar cyst
nasopharyngealangiobroma(from
sphenopalatine foramen, pterygopalatine fossa
involved)
365Chapter 26 Approach to Nasal Obstruction
Nasoethmoidal Lesions (Figs. 26.1 to 26.3)
Most of the lesions are described in detail in Chapter 23.
Due to close proximity of the nasal roof and the anterior ethmoid cells
the lesions aecting them are often considered together.
■ Lesions in this region:
• May arise intracranially and extend downward
• May arise from within the sinonasal cavity
• Also there are lesions which may arise on either side of the skull base
(i.e. intracranial or sinonasal), e.g. schwannoma.
■ is is because olfactory nerves pass through the pores of the cribriform
plate to the olfactory bulbs intracranially, and the tumors can arise
anywhere along this path.
■ Osseous lesions (primary or secondary) may arise from the anterior skull
base (ASB) or from the osseous structures within the sinonasal cavity/its
walls.
■ Lesions from the orbit can spread into the ethmoid cells.
■ Some critical points are highlighted and are further covered in detail in
relevant chapters.
Section 7 Clinico-Radiological Approach366
A
C
Figs. 26.1A to D: Esthesioneuroblastoma. (A) Large mass (m) with epicenter at superior
nasal cavity. Hypointense signal on T2WI; (B) Cysts (arrows) in the tumor-CSF interface;
(C) Restricted diffusion in the mass 9 (asterisk); and (D) Intense contrast enhancement.
Intracranial extension of the mass also shows contrast enhancement (arrow).
(CSF: Cerebrospinaluid;T2WI:T2-weightedimage).
B
D
• e close proximity of this region to the ASB result in spread of diseases
intracranially, and similarly to the orbit.
• Disease spread may be direct (with bone erosion), through valveless
diploic veins that traverse the fovea ethmoidalis (roof of ethmoid) or
along olfactory nerves that traverse the cribriform plate (roof of nose).
• Variant anatomy of ASB always to be borne in mind when endoscopic
surgery planned in this region.
• Cerebrospinal uid (CSF) rhinorrhea can occur in fractures aecting
the lesion. Small defects in cribriform plate/lateral lamella can be
normal and are confusing when imaging for site of leak.
• e nasal roof is the part of the nose fullling its “smell function”. Olfac-
tory bulb abnormalities may be seen in those with smell disorders.
• Postnatally the opacication of midline ASB is very variable. Awareness
of normal variants versus abnormal defects of cribriform plate,
crista galli, and foramen cecum is critical when imaging congenital
sinonasal lesions.
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