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Section 2 Inammatory Nasal Conditions132
Late Complications
Recurrence (Table 9.7 and Figs. 9.8A and B)
■ Recurrence of symptoms is a common indication of repeat imaging.
■ is may be due to recurrent or residual disease.
■ Recurrence of the disease can be due to basic nature of the pathology,
e.g. refractory nature of polyps in asthmatics. It is however frequently due
to structural causes.
■ e role of imaging in this scenario is not only to map the extent of disease
but also to identify a structural cause, if any.
Empty Nose Syndrome
■ “Empty nose syndrome” refers to a situation wherein a patient
experiences symptoms of nasal congestion despite the nasal cavity and
sinuses being clear.
■ It is a rare complication that follows extensive reaction especially of the
inferior turbinate.
■ e proposed mechanism is the increase in nasal permeability which
eects the functioning of neurosensitive receptors, as also the function
of humidication of inhaled air.
Rare Complications
■ Gossypiboma: Due to retained gauze. May be seen in sinonasal cavity,
even intracranial. Simulates a mass lesion.
■ CT-MRI low signal intensity of T2-weighted image (T2WI).
Lipogranuloma
■ Periorbital fat containing nodules usually located in eyelids. Imaging
appearance is of ill-dened and irregular nodules showing heterogenous
enhancement.
Table 9.7: Causes of disease recurrence after functional
endoscopic sinus surgery (FESS).
Causes of recurrent disease CT appearance
Postoperative adhesions and mucosal
thickening
Residual cells: Haller/agger nasi/
frontal/anterior ethmoidal
Neo-osteogenesis Amorphous bony attenuation
Recirculation Phenomenon of mucous circulating between
Difculttodifferentiate,adhesionsmayappear
as linear bands
Can enlarge and increasingly ossify over time
the natural ostium and other opening
(accessory ostium) that are not connected
Ring like appearance on computed tomography
(CT)
BA
Figs. 9.8A and B: Post-FESS case with calcied mucoperiosteal thickening and
neo-osteogenesis. Nonvisualized middle turbinates and RT uncinate process. RT
ethmoidectomy had also been done. There are foci of discrete chunky calcication
suggesting calcied mucoperiosteal thickening (arrowheads) in all the visualized sinuses,
obstructing both osteomeatal complexes (OMCs). Arrows show amorphous new bone
formation suggesting neo-osteogenesis.
BIBLIOGRAPHY
1. Figueroa RE. Imaging anatomy in revision sinus surgery. In: Kountakis S, Jacobs
J, Gosepath J. (Eds). Revision Sinus Surgery. Berlin, Heidelberg: Springer; 2008.
2. Ginat DT. Posttreatment imaging of the paranasal sinuses following endoscopic
sinus surgery. Neuroimaging Clin N Am. 2015;25:653-65.
3. Hoang JK, Eastwood JD, Tebbit CL et al. Multiplanar sinus CT: a systematic
approach to imaging before functional endoscopic sinus surgery. AJR Am J
oentgenol. 2010;194:W527-36.
4. Vaid S, Vaid N, Rawat S, et al. An imaging checklist for pre-FESS CT: framing a
surgically relevant report. Clin Radiol. 2011;66:459-70.
133Chapter 9 Pre- and Post-Functional Endoscopic Sinus Surgery Imaging
Section
3
Tumor and Tumor-like Conditions
10. Pathology of Sinonasal Lesions
11. Pathology of Bony/Cartilaginous Sinonasal Tumors
12. Benign Tumors of the Nose and Paranasal Sinuses: Imaging
13. Benign Sinonasal Tumors: Surgical Perspective
14. Malignant Tumors of the Sinonasal Cavities: Imaging
15. Malignant Tumors of Nose and Paranasal Sinuses:
Surgical Perspective
16. Radiation and Chemotherapy in Management of
Malignant Sinonasal Tumors
10
CHAPTER
Pathology of
Sinonasal Lesions
Deepali Jain
• Introduction
• Classication of Sinonasal Lesions
• Non-Neoplastic Lesions
– Infective Rhinosinusitis
– Allergic Sinusitis
– Sinonasal Polyps
– Granulomatosis with Polyangiitis
(GPA) (Earlier called as
Wegener’s Granulo matosis)
• Benign Neoplastic Lesions
– Sinonasal Papillomas
– Salivary Gland Tumors
– Hemangioma
– Nasopharyngeal Angiobromas
• Malignant Neoplastic Lesions
– Carcinomas
– Keratinizing Squamous Cell
Carcinoma and Non-keratinizing
Squamous Cell Carcinoma
▪ Sarcomatoid (Spindle Cell)
Squamous Cell Carcinoma
▪ SMARCB1 (INI1)-decient
Sinonasal Carcinoma
▪ Intestinala and Non-intestinal
Type Adenocarcinomas
• Malignant
– Biphenotypic Sinonasal Sarcoma
– Sinonasal Glomangiopericytoma
• Teratocarcinosarcoma
• Hematolymphoid Tumors
• Olfactory Neuroblastoma
INTRODUCTION
e sinonasal tract may be involved by wide variety of infections,
autoimmune disorders and neoplastic lesions. Among non-neoplastic
lesions, histopathology laboratories commonly receive specimens of
inammatory nasal polyps, allergic, and fungal sinusitis. In neoplastic lesions,
the fourth edition of the World Health Organization (WHO) Classication of
Head and Neck Tumours1 includes few new benign and malignant entities
which include seromucinous hamartoma, NUT (nuclear protein in testis)
carcinoma, biphenotypic sinonasal sarcoma and human papilloma virus
(HPV)-related carcinoma with adenoid cystic features. In this chapter, a brief
overview of commonly encountered sinonasal lesions in routine pathology
practice is given.
Section 3 Tumor and Tumor-like Conditions138
CLASSIFICATION OF SINONASAL LESIONS
■ Non-neoplastic sinonasal lesions have been described in Table 10.1.
Table 10.1: Non-neoplastic sinonasal lesions.
Infective Noninfective
Rhinosinusitis Sinonasal polyps
Rhinoscleroma Nasal glial heterotopia
Rhinosporidiosis Allergic sinusitis
Wegener’s granulomatosis (granulomatosis with polyangiitis)
Respiratory epithelial adenomatoid hamartoma
Myospherulosis
Neoplastic: WHO Classication of Head and Neck Tumors classies nasal
cavity and paranasal sinus tumors into dierent categories according to their
cell lineage and clinical behavior1 (Table 10.2).
Table 10.2: World Health Organization (WHO) classication of sinonasal tumors
Carcinomas • Keratinizing squamous cell carcinomas
Salivary gland tumors Pleomorphic adenoma
Sinonasal papillomas • Inverted papilloma
Benign soft tissue
tumors
Malignant soft tissue
tumors
Hematolymphoid • Extranodal natural killer (NK)/T-cell lymphoma
Neuroectodermal/
melanocytic
*NPA (nasopharyngeal angiobroma) is classied under soft tissue tumors of nasopharynx.
• Non-keratinizing squamous cell carcinomas
• Spindle cell (sarcomatoid) squamous cell carcinoma
• Lymphoepithelial carcinoma
• Sinonasal undifferentiated carcinoma
• NUT (nuclear protein in testis) carcinoma
• Neuroendocrine carcinoma
• Adenocarcinoma
• Oncocytic type
• Exophytic type
• Leiomyoma
• Hemangioma
• Schwannoma
• Neurobroma
• Nasopharyngeal angiobroma*
• Fibrosarcoma
• Undifferentiated pleomorphic sarcoma
• Leiomyosarcoma
• Rhabdomyosarcoma
• Angiosarcoma
• Malignant peripheral nerve sheath tumor
• Biphenotypic sinonasal sarcoma
• Synovial sarcoma
• Borderline/low-grade malignant tumors: Fibromatosis,
solitary brous tumor, sinonasal glomangiopericytoma, and
hemangioendothelioma
• Plasmacytoma
• Ewing sarcoma/primitive neuroectodermal tumor
• Olfactory neuroblastoma
• Mucosal melanoma
NONNEOPLASTIC LESIONS
Inammatory lesions: Subdivided into allergic and infective categories.
Infective: It can be bacterial, viral or fungal.
Infective Rhinosinusitis
■ Infective lesions of nasal cavity and paranasal sinuses is of varying
etiology. Bacterial causes include Streptococcus pneumoniae, Haemo-
philus inuenzae, and Moraxella catarrhalis. Rhinovirus, inuenza, and
parainuenza viruses are most frequent causes of viral sinusitis. During
acute phase of illness biopsy is not required and diagnosis is primarily
made by clinical examination and culture results.
■ Fungal sinusitis can be invasive or allergic. Invasive and allergic types can
be dierentiated by immune status of the patients, causative organisms
and histopathology.
■ Allergic fungal sinusitis (AFS) develops due to allergic reaction to fungal
allergens in immunocompetent hosts.
■ Microscopically, pools of mucin with degenerating eosinophils,
neutrophils and Charcot–Leyden crystals are seen.
■ Fungal hyphae are entangled within mucin, which are highlighted by
special histochemical stains for fungi (Figs. 10.1A and B).
■ Dierential diagnosis is with invasive fungal sinusitis (IFS) where tissue
inltration by fungal hyphae is seen. Most common pathogens of IFS are
Aspergillus and Mucor species.
■ Dierent histochemical stains can be used to diagnose fungal organisms
(Table 10.3).
■ Rhinosporidiosis: Rhinosporidium seeberi is a protozoa which is responsible for the disease. Microscopy: Large cysts with thick walls lled with
numerous endospores (Figs. 10.2A and B).
139Chapter 10 Pathology of Sinonasal Lesions
A B
Figs. 10.1A and B: (A) Zygomycosis: broad aseptate fungal hyphae (arrow); and (B)
Periodic acid-Schiff (PAS) and silver methenamine stains. A is stain. B is sliver methenamine
stain. Arrows for A and B are same.
Section 3 Tumor and Tumor-like Conditions140
Table 10.3: Commonly used histochemical stains for
diagnosis of sinonasal infections.
Periodic
acid-Schiff
(PAS)
Fungal sinusitis
Candida + +
Aspergillus + +
Zygomycosis + +
Cryptococcus + + + +
Rhinosporidium + +
Tuberculosis +
Leprosy +
Vasculitides
GPA (Granulomatosis with
polyangiitis)
Silver
methe-
namine
Alcian
blue
PAS
Muci-
carmine
Ziehl–
Neelsen
Elastic
van Gieson
+
A B
Figs. 10.2A and B: A case of rhinosporidiosis which shows subepithelial large sporangia
(S) (100–500 µ) lled with small 6–8 µ size endospores (arrow).
Allergic Sinusitis
■ Gross pathology: Polypoidal sinus mucosa which may be edematous,
glistening, and shiny.
■ Histopathology: Mucosal edema, thickened basement membrane, squamous metaplasia of the epithelium, and eosinophil rich inammatory
inltrate (Figs. 10.3A and B).
Sinonasal Polyps
Develop due to recurrent chronic sinusitis.
■ Microscopy: Edematous stroma and chronic inammation, variable
brosis usually seen in antrochoanal polyps, and reactive stromal cells
in stroma.
141Chapter 10 Pathology of Sinonasal Lesions
A
Figs. 10.3A and B: Allergic inammatory sinusitis which shows subepithelial dense inam -
mation rich in eosinophils (E).
B
Granulomatosis with Polyangiitis (GPA)
(Earlier called as Wegener’s Granulo matosis)
■ Type of small vessel vasculitides due to cytoplasmic anti neutrophil
cytoplasmic antibody (c-ANCA) directed against enzyme proteinase-3.
■ Kidneys, lungs and sinonasal tract are most commonly involved.
■ Microscopy: Necrotizing granulomatous inammation which includes
biocollagenolytic necrosis and giant cells; evidence of vasculitis is
dicult to nd in extensively involved lesions; elastic stains help in
recognition of destruction of elastin layer of the vessel.
BENIGN NEOPLASTIC LESIONS
Sinonasal Papillomas
■ Inverted type is the most frequent papilloma. Although a benign entity;
malignant transformation is noted in 2–27% cases and recurrences are
common.
On histopathology: Inverted proliferation of epithelium into the stroma
(Figs. 10.4A and B).
■ Oncocytic type: Exophytic and endophytic proliferation of sinonasal
epithelium with oncocytic features. e clinical behavior is same as
inverted type in terms of recurrences and malignant transformation.
Human papilloma virus has not been identied as a causative agent
■ Exophytic type: Associated with HPV in around 60% of cases. Recurrences
are common due to inadequate excision but malignant transformation
rare.
Salivary Gland Tumors
■ Pleomorphic adenoma: Most common benign tumor of salivary glands.
Biphasic tumor of epithelial and mesenchymal cells (Figs. 10.5A and B).
Section 3 Tumor and Tumor-like Conditions142
A
Figs. 10.4A and B: (A) Inverted papilloma: islands of sinonasal epithelium inverted into
the stroma (arrows); (B) Higher magnication of an inverted frond which shows sinonasal
epithelium and cysts (C) lled with inammatory cells.
A
Figs. 10.5A and B: Pleomorphic adenoma: (A) admixture of glands (G) lined by epithelial
and myoepithelial cell layer (arrow); (B) Embedded in cellular stroma (asterisk in A and B).
B
B
■ Adenoid cystic carcinoma: Malignant salivary gland tumor arises from
nose, sinuses, and upper airways, which is arranged in cribriform,
tubular, and solid patterns. Perineural invasion is most frequent
(Figs. 10.6A and B).
Hemangioma
■ Also called as lobular capillary hemangioma/pyogenic granuloma/
capillary hemangioma/cavernous hemangioma.
■ Primarily of two types: (1) Capillary and (2) cavernous.
Nasopharyngeal Angiobromas
■ Arises in the nasopharynx of young men.
■ Beta-catenin mutation is frequent event and present in about 75% of
tumors.
■ Locally aggressive tumors.
■ Microscopically shows vascular and stromal components (Figs. 10.7A
and B).
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