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Файл:Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_4518_Библиотеки_им_академика_М_И_Перельмана
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Fig. 12.26 Nasal polyps: nasal polyp, chronically inamed
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Polyps (Fig.12.26)
• Submucosal edema and outgrowth of lamina propria secondary to accumulation
of uid and proliferation of broblasts—usually allergic etiology
• Stromal edema with basement membrane hyalinization, eosinophilic inammatory inltrate
• Can develop squamous metaplasia due to chronic inammation
• Antrochoanal polyp—variant, unilateral, less edema and eosinophilic inltrate,
minimal hyalinization
• Many inammatory cells: lymphocytes, plasma cells, eosinophils, neutrophils
Mucocele
• Obstruction of sinus outow tract resulting in mucous trapping and expansion of
affected sinus, ethmoid and frontal sinuses most commonly involved
• Microscopic ndings nonspecic—mucin, inammatory mucosa, can periodically demonstrate squamous metaplasia
Allergic Fungal Sinusitis (Fig.12.27)
• Hypersensitivity reaction to fungal antigens, not infectious
• Inspissated mucin:
– Thick, tenacious, brown-green mucus
– “Peanut butter,” “thick rubbery material,” “rubber cement”
– Consists of eosinophils, neutrophils, brin, desquamated epithelial cells, and
Charcot-Leyden crystals (pale rod-like crystals—represent degenerated
eosinophils)
• H&E—pinkish mucin with dark blue areas of striations (“stacked coins,” “tide
lines,” or “ripple formation”—degenerating inammatory cells and debris mixed
with mucin
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Fig. 12.27 Allergic fungal sinusitis: (a) Charcot-Leyden crystals (solid arrows); (b) allergic-type
mucin including tide-lines (open arrow); (c) GMS fungal stain highlights fungal forms (arrows);
(d) nasal polyp tissue with aggregates of histiocytes and eosinophils (arrowhead)
• GMS fungal stain can be done, fungal hyphae may be seen, not required for
diagnosis
• Cultures: Aspergillus, Curvularia, Dreshella, Bipolaris, Exserohilum
Nasal Glial Heterotopia (Fig.12.28)
• Extracranial ectopic glial tissue without a connection to the intracranial space,
can be extranasal (60%), intranasal (30%), or mixed (10%)
• Astrocytes in a glial ber matrix, can contain gemistocytes (swollen, reactive
astrocytes), neurons rare
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Fig. 12.28 Nasal glioma (nasal glial heterotopia): sheets and islands of delicate pink brillary
material (above arrow) positioned between brovascular connective tissue
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Fig. 12.29 Rhinoscleroma: numerous foamy macrophages (Mikulicz cells) intermixed with
chronic inammatory cells
• IHC
– S100+ (neurons, glia, nerve sheath cells)
– GFAP+ (glial brillary acidic protein)
– OLIG2+ (oligodendrocyte transcription factor)
Rhinoscleroma (Fig.12.29)
• Chronic infectious condition caused by Klebsiella rhinoscleromatis (gramnegative coccobacillus)
• Three clinical stages:
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– Rhinitic—exudative, mucopurulent discharge, erythema
– Florid—obstruction, thickened mucosa
– Fibrotic—stenosis, scarring
• Chronic inammation with multiple inammatory cells (lymphocytes, neutrophils, and plasma cells) mixed macrophages
– Mikulicz cells—macrophages with foamy/granular cytoplasm that contain
the causative bacilli
– Russell bodies—immunoglobulin in plasma cells, nonspecic
• Warthin-Starry stain—traditionally used for spirochetes, but can be used to highlight organisms within Mikulicz cells
Rhinosporidiosis (Fig.12.30)
• Chronic zoonotic infection caused by Rhinosporidium seeberi (eukaryote)
• Friable polyps/masses– pseudoepitheliomatous hyperplasia
• Respiratory epithelium and/or submucosa exhibits round structures, often containing spores
– Submucosal cyst/sporangia (10–300 μm) with endospores
– Chronic inammatory response (lymphocytes, plasma cells, eosinophils)
• GMS/PAS can help outline organisms, not required for diagnosis
Granulomatosis with Polyangiitis
• Formerly Wegener’s granulomatosis
• Systemic immune complex small vessel vasculitis, can affect sinuses/lungs/kidneys, present as nonspecic ulcerations in the nasal cavity
• Triad of granulomatous inammation, necrosis, and vasculitis (least common)
Fig. 12.30 Rhinosporidiosis: Dilated thick- or thin-walled structures which may appear empty or
contain numerous endospores (latter has a bag of marbles appearance)
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– Granulomas typically consist of poorly formed multinucleated giant cells
– Geographical necrosis—neutrophilic debris with basophilia (bluish as
opposed to usual pink debris)
– Vasculitis—destruction of blood vessel walls with inammatory cell migration
– c-ANCA+ (cytoplasmic anti-neutrophilic cytoplasmic antibodies)
– PR3+ (proteinase 3)
Benign Sinonasal Neoplasms
Lobular Capillary Hemangioma (Pyogenic Granuloma) (Fig.12.31)
• Benign polypoid vascular tumor
• Usually due to local trauma, hormones, and drugs
• Comprised of proliferation of variable sized vessels surrounded by pericytes
• Arranged in lobules with larger branches centrally, smaller vessels peripherally
• Mitotic gures commonly seen
• Stroma may appear bromyxoid, with inammatory inltrate
Nasopharyngeal Angiobroma (Fig.12.32)
• Formerly juvenile nasopharyngeal angiobroma (JNA)
• Benign, locally aggressive mesenchymal neoplasm
• Male patient, often young age, posterior nasal cavity/nasopharynx
• Composed of variably sized vessels and stellate broblasts in a collagenized stroma
• Vessels can be with or without an intact muscular layer previously embolized
tumors with embolic (foreign material) in vessels
Fig. 12.31 Lobular capillary hemangioma: numerous endothelial-lined vascular channels
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Fig. 12.32 Nasopharyngeal angiobroma: Ectatic vascular channels and broblastic cells embedded in a bland collagenized stroma. Thromboembolic material presents as a result of preoperative
embolization of the neoplasm (arrow)
C. J. Fan et al.
Fig. 12.33 Sinonasal glomangiopericytoma: short fascicles of ovoid-to-spindle cells (white circle) with intervening vascular channels, surfaced by intact respiratory epithelium. Perivascular
hyalinization present (arrows)
• Possible association with familial adenomatous polyposis (Gardner’s syndrome)
Glomangiopericytoma (Fig.12.33)
• Formerly sinonasal-type hemangiopericytoma.
• Local recurrence possible including late local recurrence.
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• Diffusely cellular neoplasm composed of spindled or ovoid neoplastic cells.
• Cells are closely packed and arranged in short fascicles and whorls, with a blue
appearance.
• Large, dilated vessels (“Staghorn” vessels) demonstrate prominent perivascular
hyalinization (pink rind).
• IHC:
– Smooth muscle actin (SMA)+, muscle-specic actin (MSA)+
– ß-catenin+ nuclear staining
– CD31−, STAT6−, cytokeratins−, SOX10−
Sinonasal Papilloma (Formerly Schneiderian Papilloma) (Fig.12.34)
• Sinonasal papilloma, inverted type (47–70%): lateral nasal wall, burrowing pattern
• Formerly inverted Schneiderian papilloma, endophytic papilloma.
• Predominantly endophytic growth; epithelium burrows below submucosa to
form elongated tubular structures.
• Rounded epithelial nests of hyperplastic immature squamous epithelium.
• Admixed respiratory epithelium or ciliated cells.
• A separate subset harbor low-risk HPV.
• Surface keratinization may help identify underlying dysplasia.
• Epithelial dysplasia can be keratinizing and non-keratinizing.
• ~2–4% risk of malignant transformation, usually squamous cell carcinoma.
• Sinonasal papilloma, exophytic type (50%): nasal septum
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– Formerly fungiform papilloma
– Exophytic growth
– Papillary fronds of multilayered non-keratinizing squamous epithelium
– Majority harbor low-risk HPV
– Malignant transformation rare
• Sinonasal papilloma, oncocytic type (~3–15%), lateral wall or maxillary sinus
– Formerly cylindrical cell or columnar cell papilloma
– Mixed exophytic and endophytic growth pattern
– Multilayered epithelium with columnar cells, ample eosinophilic (pink) cyto-
plasm arranged in papillary pattern (papilla, branching), admixed ciliated cells
– Elongated cells with mucus cysts, somewhat cylindrical appearing
Malignant Sinonasal Neoplasms
Sinonasal Squamous Cell Carcinoma (SCC) (Figs.12.35 and 12.36)
• Most common sinonasal malignancy
• Arises from surface squamous epithelium, can be keratinizing or
non-keratinizing
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ab
Fig. 12.34 Sinonasal papilloma. (a) Inverted type: marked hyperplasia of epithelial component.
Epithelium “burrows” or “inverts” into the stromal tissue. (b) Oncocytic type: oncocytic cuboidal
to columnar cells and intraepithelial microcysts with mucin and neutrophils
Non-keratinizing Squamous Cell Carcinoma (NK-SCC) (Fig.12.35)
• Formerly Schneiderian carcinoma, transitional cell carcinoma.
• Sinonasal epithelial surface origin, minimal to no keratinization.
• Etiopathogenesis variable: subset associated with high-risk HPV; subset arise
ex-sinonasal papilloma; emerging data identies recurrent DEK-AFF2 fusions in
a subset.
• Grow as rounded tumor nests into underlying stroma, variable cytologic atypia,
mitoses, peripheral palisading of nests and papillary growth possible, minimal to
no keratinization.
Keratinizing Squamous Cell Carcinoma (K-SCC) (Fig.12.36)
• Sinonasal epithelial surface origin, with overt keratinization
• Conventional-type most common (similar to larynx), with variants uncommon
but possible: carcinoma cuniculatum, verrucous carcinoma, spindle cell carcinoma, etc.
• Grow as rounded tumor nests into underlying stroma, variable cytologic atypia,
mitoses, peripheral palisading of nests and papillary growth possible, minimal to
no keratinization
Nasopharyngeal Carcinoma (NPC) (Fig.12.37)
• Squamous cell carcinoma originating from the nasopharyngeal mucosa
• Three types:
– Keratinizing squamous cell carcinoma (formerly type 1)
Arise de novo or many years after HN radiation treatment
Jagged irregular islands of tumor, surface epithelium typically affected
Overt keratinization: intercellular bridges, keratin pearls
Unlikely to be EBV associated
– Non-keratinizing squamous cell carcinoma (NK-SCC) (formerly type 2)
Most common subtype.
No clinical or prognostic value in separating into NK-SCC (formerly type
2) vs undifferentiated (formerly type 3), though terminology may be used
descriptively in some institutions.
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a
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b
Fig. 12.35 Sinonasal SCC, non-keratinizing: (a) Smooth-edged lobules of tumor with highnuclear cytoplasmic ratio, minimal keratinization inltrating stroma (lower left), p16 immunostain
diffusely positive (lower right), high-risk RNA HPV in situ hybridization positive; (b) non-keratinizing squamous cell carcinoma, DEK-AFF2 fusion tumor. Tumor islands indistinct (white arrows
and contour highlights) due to monotonous tumor nuclei, epithelial discohesion, and dense neutrophilic tumor inltrate (arrowheads)
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Fig. 12.36 Keratinizing sinonasal squamous cell carcinoma. Proliferation of malignant epithelial
cells with squamous differentiation and intercellular bridges. Abuts septal cartilage
C. J. Fan et al.
Fig. 12.37 Nasopharyngeal carcinoma: Non-keratinizing sheets and islands of syncytialappearing tumor cells have vesicular nuclei and large nucleoli admixed with many lymphocytes
and plasma cells
Usually limited morphologic evidence of squamous differentiation.
Broad-based bands or irregular islands permeated by lymphoid inltrates.
Essentially all are EBV associated.
– Basaloid squamous cell carcinoma
Basaloid, high-grade appearance
Nested growth with tumor necrosis
Variable association with EBV
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