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Granuloma nose
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This presentation discusses granulomatous lesions involving the nose
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Granuloma nose
1.
Granulomatous lesions of
nose Dr T. Balasubramanian
2.
3.
Macrophages, granulocytes and
multinucleated giant cells
4.
Presence of vasculitis
5.
Systemic involvement is
common
6.
7.
Inflammatory
8.
Neoplastix
9.
10.
Fungal – Aspergillus,
zygomycosis, Dermatocietes, Blastomycosis, Histoplasmosis, Sporotrichiasis and coccididomycosis
11.
Protozoa – Leishmaniais
12.
Miscellaneous - Rhinosporidiosis
13.
14.
Midline granulomas
15.
T cell lymphomas
16.
17.
Sarcoidosis
18.
Churg-Strauss syndrome
19.
Cholesterol granuloma
20.
Eosinophilic granuloma
21.
22.
Multisystem disorder
23.
Commonly involved organs
include: Lymph nodes, skin, lungs, eye, nose, liver and spleen
24.
Cutaneous lesions are
known as lupus pernio
25.
Nasal involvement of
sarcoidosis almost always indicate multisystem involvement of the disease
26.
27.
Affected age group
2 nd - 5 th decades
28.
Females outnumber males
2:1
29.
30.
Infective agents
31.
Chemicals (Beryllium, Zirconium
etc)
32.
Pine pollen
33.
Peanut dust
34.
Immunological
35.
36.
No depression of
CMI
37.
Humoral immunity normal
38.
Sarcoidosis (current hypothesis)
39.
40.
Continued antigenic stimulation
41.
Failure of supressor
mechanism
42.
Abormalities in the
regulation of cytokine network
43.
44.
There is no
evidence of caseation
45.
Fibrinoid necrosis may
be seen sometimes
46.
Fibrinoid necrosis may
be converted to hyaline fibrosis
47.
Tubercles are surrounded
by lymphocytes and fibroblasts
48.
These histological features
are not diagnostic
49.
50.
Crusting of nasal
mucosa is commonly seen
51.
Blood stained nasal
discharge
52.
Purulent nasal discharge
53.
Facial pain
54.
Sometimes mucoid discharge
55.
Anosmia (rare) due
to mechanical obstruction of the olfactory cleft by crusts
56.
57.
Nasal bridge collapse
58.
Nasal bones may
be thickened due to osteitis
59.
Secondary infections of
sinuses common
60.
Adenoid / tonsillar
enlargement
61.
Secretory otitis media
62.
63.
Histology
64.
Imaging
65.
Hematology
66.
Kveim test (cutaneous
hypersensitivity test for sarcoidosis) withdrawn now
67.
Angiotensin converting enzyme
elevated during acute phase
68.
ESR raised
69.
70.
Punctate osteolysis of
nasal bones may be seen
71.
CT scan of
nose and PNS will also reveal soft tissue changes over the nasal bone area
72.
MRI brain is
a must to rule of CNS involvement
73.
X-ray chest would
show pulmonary infiltrates
74.
CT nasal bone
area
75.
X-ray chest in
sarcoidosis
76.
77.
Oral steroids
78.
Methotrexate
79.
Hydroxychloroquine
80.
81.
It could cause
extensive nasal deformity
82.
Contraindication is absolute
in active nasal sarcoidosis
83.
FESS can be
resorted to in order to releive obstruction and to facilitate drainage of the involved paranasal sinuses
84.
85.
Necrotizing vasculitis of
of small & medium sized blood vessels
86.
Classic triad –
airway, lung and renal disease
87.
ANCA test diagnostic
(Antineutrophil cytoplasmic antibody test)
88.
89.
Younger patients are
more prone for multisystem damage
90.
Renal damage is
rather common in the young age group
91.
92.
Immune response to
an unknown stimulus ??
93.
Hypersensitivity reaction ??
94.
Antigen from inhaled
bacteria could be the stimulus ?? a reason why it commonly begins as an URI
95.
Vasculitis is caused
by deposition of immune complexes
96.
97.
PANCA (Perinuclear)
98.
CANCA (Cytoplasmic)
99.
Patients with Wegener's
have elevated levels of cANCA
100.
These tests are
performed using immunoflorescence / radioimmunoassay
101.
102.
Glomerulonephritis
103.
Nasal block /
crusting of nasal mucosa / epistaxis
104.
105.
Bone destruction
106.
New bone formation
107.
108.
Abnormal x ray
chest showing the presence of nodules. Cavities andd fixed infiltrates
109.
Microhematuria and urinary
sediments
110.
Biopsy from the
lesions showing granulomatous inflammation
111.
112.
Azathioprine
113.
Cyclophosphamide (discontinued because
of extensive side effects)
114.
Patients on long
term steroids should undergo bone densitometry in order to pick up early osteoporotic changes
115.
Mycophenolate mofetil is
currently being used instead of azathioprine
116.
117.
Intranasal steroid drops
118.
Glucose glycerine drops
119.
Nasal surgeries like
rhinoplasty / augmentation rhinoplasty should be avoided during active stages of the disease
120.
121.
Granulomas of churg
strauss are richly infiltrated by eosinophils
122.
Vasculitis is histologically
giant cell necrotizing type
123.
Nasal manifestations include:
Mucosal crusting, septal destruction, epistaxis etc
124.
125.
Currently this condition
is regarded as a neoplastic disorder
126.
It can also
be considered as a variant of Histiocytosis X
127.
128.
Skull is the
common site of involvement
129.
Males are affected
twice as often as females
130.
Painful swelling involving
facial bones associated with cervical adenopathy
131.
Mandibular lesions could
cause tooth ache, gum bleeding etc
132.
133.
These cells are
found to be mixed with infiltrates of histiocytes, neutrophils and plama cells
134.
Cytoplasm of Langerhan's
giant cells may be eosinophilic with the presence of charcot leyden crystals
135.
Intense osteoclastic activity
can be seen in the periphery due to the presence of cytokines and prostaglandins by Langerhan's cells
136.
137.
Spontaneous regression have
also been documented
138.
For managing mono
ostotic variety a combination of curettage / excision and radiotherapy have been attempted with varying degrees of success
139.
Combination of etoposide
and steroids administered for a period of 12 months is beneficial
140.
Alpha interferon and
bone marrow transplant have been found to be useful in polyostotic variety
141.
142.
Aggregates of giant
cells (uninucleate) in a fibrovascular stroma characterizes this condition
143.
Commonly involves the
jaw. Cranio facial bones are also commonly involved
144.
Commonly seen in
children
145.
Bilateral involvement causes
cherubism in children. This is caused by symmetrical involvement of jaws
146.
147.
Edges are well
demarcated
148.
149.
Total excision is
advisable when possible
150.
Recurrence rate is
very high
151.
152.
This precipitation is
seen in hemorrhage / injuries
153.
Commonly involves maxilla
/ frontal sinuses
154.
Adjacent normal structures
like the orbit may also be displaced
155.
Can be treated
by excision
156.
157.
Midline destructive granuloma
158.
T cell /
NK cell lymphoma
159.
Stewart granuloma
160.
This lesion classically
causes extensive destruction of the middle third of face
161.
162.
Common during 5
th - 6 th decades of life
163.
Currently these granulomas
are considered to be T cell lymphoma / NK cell lymphoma
164.
165.
Period of activity
166.
Terminal stage
167.
168.
These patients may
c/o persistent nasal obstruction with rhinorrhoea
169.
These patients would
also be offered surgery for the same
170.
171.
Crusting / necrosis
/ tissue loss
172.
Progressive destruction of
nasal framework
173.
Destruction of palate
and upper lip
174.
Fever due to
secondary infection
175.
176.
Exhaution
177.
Distant metastasis would
have already occured
178.
Eventual death
179.
180.
Atypical cellular infiltrates
can be seen in the midst of necrotic tissue
181.
Good deep biopsy
of the tissue is a must to obtain a representative specimen
182.
Immunohistochemistry using monoclonal
antibodies against T cell differentiation antigen can be used
183.
184.
Full course of
RT is advised these days in order to manage these cases adequately
185.
186.
Nose picking has
been commonly attributed as a cause
187.
Dissemination from cavity
in the lung
188.
Hematogenous spread to
the nasal cavity mucosa
189.
190.
Ulcerative type
191.
Granulomatous type involving
the sinuses
192.
193.
Usually begins in
the vestibule and extends to involve the nasal mucosa
194.
Commonly caused due
to direct inoculation
195.
These lesions appear
are glistening reddish brown papules / nodules (apple jelly nodules)
196.
These nodules are
usually painless
197.
These papules may
coalese to form ulcers with pale granular base and undermined edges
198.
199.
200.
Mucosal crusting, epistaxis
201.
This lesion can
lead to septal perforation and saddle nose deformity
202.
The bony portion
of the nasal septum is not involved this differentiates it from syphilis
203.
204.
Soft tissue swelling
over the involved sinus.
205.
Multiple discharging sinuses
from the swelling
206.
Bony destruction of
the sinus wall could also be evident in these patients
207.
208.
Evidence of caseation
+
209.
Presence of AFB
is virtually diagnostic if present
210.
PCR has increased
the sensitivity
211.
212.
Two drugs INH
and Rifampicin – 4 months
213.
214.
Can involve patients
of any age group
215.
The organims usually
reside and multiply in the perivascular lymphatics of the blood vessel
216.
217.
Begins during the
third week after inoculation
218.
Regional lymphadenitis is
common
219.
These sores are
painless nodules
220.
These lesions usually
disappears within 3 months
221.
Smears from the
lesion usually demonstrate T pallidum
222.
223.
Simple catarrhal rhinitis
is seen
224.
Crusting / fissuring
of nasal vestibular skin is seen
225.
Patches could be
seen over the nasal mucosa
226.
Best confirmed by
serological tests
227.
228.
Bony portion of
the nasal septum is commonly destroyed causing septal perforation
229.
Nocturnal pain is
one of the features
230.
Secondary atrophic rhinitis
can also be caused
231.
Collapse of nasal
bridge
232.
233.
Occurs during the
3 rd week - 3 rd month after birth
234.
Begins as simple
catharral rhinitis which later turns purulent
235.
Child has difficulty
sucking milk due to excoriation involving the lips
236.
237.
Progressive granulomatous disease
involving the nose and later extending to oro and nasopharynx
238.
The causative organisms
are usually intracellular and hence are difficult to isolate
239.
240.
Plama cells, lymphocytes
and eosinophils are seen in these infiltrates
241.
There are scattered
large foam cells known as Miculicz cells. These cells have a central nucleus with vacuolated cytoplasm which contain the bacilli.
242.
243.
Granulomatous / proliferative
stage
244.
Cicatrizing stage
245.
246.
Crusting of nasal
mucosa
247.
Epistaxis
248.
Foul smelling discharge
249.
250.
They are bluish
red and rubbery later becomes paler and harder
251.
These nodules dont
break down but fibrose
252.
Regional nodal involvment
is rare
253.
254.
Distortion of normal
nasal anatomy
255.
Spread to nasopharynx
256.
Bone involement could
be seen
257.
258.
Two types are
seen Tuberculoid and lepromatous
259.
260.
Nasal mucosa is
uninvolved
261.
Vestibular skin is
involved
262.
Isolated cranial nerve
palsies 5 th and 7 th cranial nerves are commonly involved
263.
264.
Nasal mucosal crust
formation / epistaxis
265.
Secondary atrophic rhinitis
266.
Destruction of both
bony and cartilagenous portions of nasal septum
267.
Collapse of nasal
bridge
268.
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