Granuloma nose

Granulomatous lesions of nose Dr T. Balasubramanian

Introduction
Presence of granuloma
Macrophages, granulocytes and multinucleated giant cells
Presence of vasculitis
Systemic involvement is common

Types of granulomas
Infective
Inflammatory
Neoplastix

Infective granulomas
Bacterial – Tuberculosis, leprosy, Rhinoscleroma, syphilis and actinomycosis
Fungal – Aspergillus, zygomycosis, Dermatocietes, Blastomycosis, Histoplasmosis, Sporotrichiasis and coccididomycosis
Protozoa – Leishmaniais
Miscellaneous - Rhinosporidiosis

Neoplastic
Non healing granulomas
Midline granulomas
T cell lymphomas

Inflammatory granulomas
Wegner's granulomatosis
Sarcoidosis
Churg-Strauss syndrome
Cholesterol granuloma
Eosinophilic granuloma

Sarcoidosis
Etiology unkonwn
Multisystem disorder
Commonly involved organs include: Lymph nodes, skin, lungs, eye, nose, liver and spleen
Cutaneous lesions are known as lupus pernio
Nasal involvement of sarcoidosis almost always indicate multisystem involvement of the disease

Sarcoidosis (features)
Commonly affects adults
Affected age group 2 nd - 5 th decades
Females outnumber males 2:1

Sarcoidosis (Etiology)
Unknown
Infective agents
Chemicals (Beryllium, Zirconium etc)
Pine pollen
Peanut dust
Immunological

Sarcoidosis (Immunology)
Type IV hypersensitivity reaction reduced in these patients
No depression of CMI
Humoral immunity normal

Sarcoidosis (current hypothesis)

Causes for persistent granuloma (sarcoidosis)
Increased production of calcitriol by monocytes
Continued antigenic stimulation
Failure of supressor mechanism
Abormalities in the regulation of cytokine network

Sarcoidosis (Histology)
Fromation of epitheloid cell tubercles
There is no evidence of caseation
Fibrinoid necrosis may be seen sometimes
Fibrinoid necrosis may be converted to hyaline fibrosis
Tubercles are surrounded by lymphocytes and fibroblasts
These histological features are not diagnostic

Nasal sarcoidosis (clinical features)
Nasal stuffiness & obstruction
Crusting of nasal mucosa is commonly seen
Blood stained nasal discharge
Purulent nasal discharge
Facial pain
Sometimes mucoid discharge
Anosmia (rare) due to mechanical obstruction of the olfactory cleft by crusts

Nasal sarcoid clinical features (contd)
Perforation of anterior portion of nasal septum
Nasal bridge collapse
Nasal bones may be thickened due to osteitis
Secondary infections of sinuses common
Adenoid / tonsillar enlargement
Secretory otitis media

Diagnostic features of nasal sarcoidosis
Clinical acumen
Histology
Imaging
Hematology
Kveim test (cutaneous hypersensitivity test for sarcoidosis) withdrawn now
Angiotensin converting enzyme elevated during acute phase
ESR raised

Sarcoidosis (Radiology)
X-ray nasal bones show rarefaction & osteolytic reaction
Punctate osteolysis of nasal bones may be seen
CT scan of nose and PNS will also reveal soft tissue changes over the nasal bone area
MRI brain is a must to rule of CNS involvement
X-ray chest would show pulmonary infiltrates

CT nasal bone area

X-ray chest in sarcoidosis

Sarcoidosis (treatment)
Spontaneous remission (possible)
Oral steroids
Methotrexate
Hydroxychloroquine

Role of surgery in nasal sarcoidosis
Contraindicated
It could cause extensive nasal deformity
Contraindication is absolute in active nasal sarcoidosis
FESS can be resorted to in order to releive obstruction and to facilitate drainage of the involved paranasal sinuses

Wegner's granulomatosis
Granulomatous inflammation involving nasal mucosa and upper respiratory tract
Necrotizing vasculitis of of small & medium sized blood vessels
Classic triad – airway, lung and renal disease
ANCA test diagnostic (Antineutrophil cytoplasmic antibody test)

Wegner's granuloma (age of presentation)
Seen in the age group 15 – 70)
Younger patients are more prone for multisystem damage
Renal damage is rather common in the young age group

Wegner's granuloma (etiology)
Unknown
Immune response to an unknown stimulus ??
Hypersensitivity reaction ??
Antigen from inhaled bacteria could be the stimulus ?? a reason why it commonly begins as an URI
Vasculitis is caused by deposition of immune complexes

ANCA
Two types of ANCA are present
PANCA (Perinuclear)
CANCA (Cytoplasmic)
Patients with Wegener's have elevated levels of cANCA
These tests are performed using immunoflorescence / radioimmunoassay

Clincial features of Wegners
Involvement of upper and lower respiratory tract
Glomerulonephritis
Nasal block / crusting of nasal mucosa / epistaxis

Sinus imaging in wegners
CT scan shows evidence of mucosal thickening
Bone destruction
New bone formation

Wegner granulomatosis diagnostic criteria
Nasal mucosa /oral mucosal inflammation
Abnormal x ray chest showing the presence of nodules. Cavities andd fixed infiltrates
Microhematuria and urinary sediments
Biopsy from the lesions showing granulomatous inflammation

Treatment
Prednisalone
Azathioprine
Cyclophosphamide (discontinued because of extensive side effects)
Patients on long term steroids should undergo bone densitometry in order to pick up early osteoporotic changes
Mycophenolate mofetil is currently being used instead of azathioprine

Nasal wegeners managment
Saline alkaline douching
Intranasal steroid drops
Glucose glycerine drops
Nasal surgeries like rhinoplasty / augmentation rhinoplasty should be avoided during active stages of the disease

Churg-Strauss syndrome
Characterised by systemic vasculitis and asthma
Granulomas of churg strauss are richly infiltrated by eosinophils
Vasculitis is histologically giant cell necrotizing type
Nasal manifestations include: Mucosal crusting, septal destruction, epistaxis etc

Eosinophilic granuloma
Characterized by clonal proliferation of Langerhan's giant cells associated with a heterogenous inflammatory infiltrates of eosinophils, lymphocytes, plasma cells and neutrophils
Currently this condition is regarded as a neoplastic disorder
It can also be considered as a variant of Histiocytosis X

Eosinophilic granuloma cllinical features
Bones are predominantly affected
Skull is the common site of involvement
Males are affected twice as often as females
Painful swelling involving facial bones associated with cervical adenopathy
Mandibular lesions could cause tooth ache, gum bleeding etc

Eosinophilic granuloma (Histology)
Langerhan's giant cells predominate
These cells are found to be mixed with infiltrates of histiocytes, neutrophils and plama cells
Cytoplasm of Langerhan's giant cells may be eosinophilic with the presence of charcot leyden crystals
Intense osteoclastic activity can be seen in the periphery due to the presence of cytokines and prostaglandins by Langerhan's cells

Eosinophilic granuloma (treatment)
Depends whether it is mono ostototic / polyostotic
Spontaneous regression have also been documented
For managing mono ostotic variety a combination of curettage / excision and radiotherapy have been attempted with varying degrees of success
Combination of etoposide and steroids administered for a period of 12 months is beneficial
Alpha interferon and bone marrow transplant have been found to be useful in polyostotic variety

Giant cell granuloma
Reparative granuloma
Aggregates of giant cells (uninucleate) in a fibrovascular stroma characterizes this condition
Commonly involves the jaw. Cranio facial bones are also commonly involved
Commonly seen in children
Bilateral involvement causes cherubism in children. This is caused by symmetrical involvement of jaws

Imaginng in giant cell granuloma
Expansile lytic lesion with a soap bubble appearance in the middle
Edges are well demarcated

Treatment of giant cell granuloma
Curettage may help
Total excision is advisable when possible
Recurrence rate is very high

Cholesterol granuloma
This is due to granulomatous reaction to the cholesterol crystals precipitated in the tissues
This precipitation is seen in hemorrhage / injuries
Commonly involves maxilla / frontal sinuses
Adjacent normal structures like the orbit may also be displaced
Can be treated by excision

Granulomatous neoplasia
Non healing granuloma
Midline destructive granuloma
T cell / NK cell lymphoma
Stewart granuloma
This lesion classically causes extensive destruction of the middle third of face

Granulomatous neoplasia (features)
Common in males
Common during 5 th - 6 th decades of life
Currently these granulomas are considered to be T cell lymphoma / NK cell lymphoma

Granulomatous neoplasia (stages)
Prodromal
Period of activity
Terminal stage

Prodromal stage
This stage could last for many years
These patients may c/o persistent nasal obstruction with rhinorrhoea
These patients would also be offered surgery for the same

Period of activity
Purulent nasal discharge
Crusting / necrosis / tissue loss
Progressive destruction of nasal framework
Destruction of palate and upper lip
Fever due to secondary infection

Terminal stage
Gross mutilation of face
Exhaution
Distant metastasis would have already occured
Eventual death

Diagnosis
Necrotic areas can be seen in the biopsy
Atypical cellular infiltrates can be seen in the midst of necrotic tissue
Good deep biopsy of the tissue is a must to obtain a representative specimen
Immunohistochemistry using monoclonal antibodies against T cell differentiation antigen can be used

Treatment
Low dose radiation was used previously to manage these cases
Full course of RT is advised these days in order to manage these cases adequately

Nasal tuberculosis
Nasal infections are caused by direct inoculation
Nose picking has been commonly attributed as a cause
Dissemination from cavity in the lung
Hematogenous spread to the nasal cavity mucosa

Nasal tuberculosis (types)
Nodular type
Ulcerative type
Granulomatous type involving the sinuses

Nodular form
Also known as Lupus vulgaris
Usually begins in the vestibule and extends to involve the nasal mucosa
Commonly caused due to direct inoculation
These lesions appear are glistening reddish brown papules / nodules (apple jelly nodules)
These nodules are usually painless
These papules may coalese to form ulcers with pale granular base and undermined edges

Blanching tests
Pressure by using glass slide will cause blanching of surrounding area making these papules more prominent. For mucosal lesions adrenaline / cocaine can be used to cause blanching

Ulcerative type
This type usually involves the cartilagenous portion of nasal septum and inferior turbinate
Mucosal crusting, epistaxis
This lesion can lead to septal perforation and saddle nose deformity
The bony portion of the nasal septum is not involved this differentiates it from syphilis

Sinus granuloma
Isolated involvement of sinus without involvement of nasal cavity
Soft tissue swelling over the involved sinus.
Multiple discharging sinuses from the swelling
Bony destruction of the sinus wall could also be evident in these patients

Diagnosis
Tissue biopsy would show epitheloid cell granulomas
Evidence of caseation +
Presence of AFB is virtually diagnostic if present
PCR has increased the sensitivity

Treatment
Since it is extrapulmonary initially the treatment is started with 4 drug regimen (INH, Rifampicin, ethambutol and pyrazinamide) for 2 months
Two drugs INH and Rifampicin – 4 months

Syphilis
Primay, secondary and tertiary syphilis
Can involve patients of any age group
The organims usually reside and multiply in the perivascular lymphatics of the blood vessel

Primary syphilis
Sore or chancre develops at the site of inoculation
Begins during the third week after inoculation
Regional lymphadenitis is common
These sores are painless nodules
These lesions usually disappears within 3 months
Smears from the lesion usually demonstrate T pallidum

Secondary syphilis
This is the most infectious stage
Simple catarrhal rhinitis is seen
Crusting / fissuring of nasal vestibular skin is seen
Patches could be seen over the nasal mucosa
Best confirmed by serological tests

Tertiary syphilis
This is the commonest lesion involving the nose
Bony portion of the nasal septum is commonly destroyed causing septal perforation
Nocturnal pain is one of the features
Secondary atrophic rhinitis can also be caused
Collapse of nasal bridge

Congenital syphilis
Also known as snuffles
Occurs during the 3 rd week - 3 rd month after birth
Begins as simple catharral rhinitis which later turns purulent
Child has difficulty sucking milk due to excoriation involving the lips

Rhinoscleroma
Caused by Klebsiella rhinoscleromatis
Progressive granulomatous disease involving the nose and later extending to oro and nasopharynx
The causative organisms are usually intracellular and hence are difficult to isolate

Rhinoscleroma (Histology)
Granulomatous tissue infiltrates in the submucosa
Plama cells, lymphocytes and eosinophils are seen in these infiltrates
There are scattered large foam cells known as Miculicz cells. These cells have a central nucleus with vacuolated cytoplasm which contain the bacilli.

Rhinoscleroma (stages)
Atrophic stage
Granulomatous / proliferative stage
Cicatrizing stage

Atrophic stage
This stage resembles atrophic rhinitis
Crusting of nasal mucosa
Epistaxis
Foul smelling discharge

Granulomatous stage
Non ulcerative nodules develop
They are bluish red and rubbery later becomes paler and harder
These nodules dont break down but fibrose
Regional nodal involvment is rare

Cicatrizing stage
Adhesions and stenosis are seen
Distortion of normal nasal anatomy
Spread to nasopharynx
Bone involement could be seen

Leprosy
Chronic granulomatous lesion caused by M leprae
Two types are seen Tuberculoid and lepromatous

Tuberculoid leprosy
Anesthetic cutaneous patches
Nasal mucosa is uninvolved
Vestibular skin is involved
Isolated cranial nerve palsies 5 th and 7 th cranial nerves are commonly involved

Lepromatous leprosy
Nasal mucosal involvement is seen
Nasal mucosal crust formation / epistaxis
Secondary atrophic rhinitis
Destruction of both bony and cartilagenous portions of nasal septum
Collapse of nasal bridge

Thank you

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Granuloma nose

by Balasubramanian Thiagarajan on Jun 11, 2011

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Granuloma nose — Presentation Transcript