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Granuloma nose
Granuloma nose
Granuloma nose
Granuloma nose
Granuloma nose
Granuloma nose
Granuloma nose
Granuloma nose
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Granuloma nose

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This presentation discusses granulomatous lesions involving the nose

This presentation discusses granulomatous lesions involving the nose

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  • 1. Granulomatous lesions of nose Dr T. Balasubramanian
  • 2. Introduction
    • Presence of granuloma
    • 3. Macrophages, granulocytes and multinucleated giant cells
    • 4. Presence of vasculitis
    • 5. Systemic involvement is common
  • 6. Types of granulomas
    • Infective
    • 7. Inflammatory
    • 8. Neoplastix
  • 9. Infective granulomas
    • Bacterial – Tuberculosis, leprosy, Rhinoscleroma, syphilis and actinomycosis
    • 10. Fungal – Aspergillus, zygomycosis, Dermatocietes, Blastomycosis, Histoplasmosis, Sporotrichiasis and coccididomycosis
    • 11. Protozoa – Leishmaniais
    • 12. Miscellaneous - Rhinosporidiosis
  • 13. Neoplastic
    • Non healing granulomas
    • 14. Midline granulomas
    • 15. T cell lymphomas
  • 16. Inflammatory granulomas
    • Wegner's granulomatosis
    • 17. Sarcoidosis
    • 18. Churg-Strauss syndrome
    • 19. Cholesterol granuloma
    • 20. Eosinophilic granuloma
  • 21. Sarcoidosis
    • Etiology unkonwn
    • 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. Sarcoidosis (features)
    • Commonly affects adults
    • 27. Affected age group 2 nd - 5 th decades
    • 28. Females outnumber males 2:1
  • 29. Sarcoidosis (Etiology)
  • 35. Sarcoidosis (Immunology)
    • Type IV hypersensitivity reaction reduced in these patients
    • 36. No depression of CMI
    • 37. Humoral immunity normal
  • 38. Sarcoidosis (current hypothesis)
  • 39. Causes for persistent granuloma (sarcoidosis)
    • Increased production of calcitriol by monocytes
    • 40. Continued antigenic stimulation
    • 41. Failure of supressor mechanism
    • 42. Abormalities in the regulation of cytokine network
  • 43. Sarcoidosis (Histology)
    • Fromation of epitheloid cell tubercles
    • 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. Nasal sarcoidosis (clinical features)
    • Nasal stuffiness & obstruction
    • 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. Nasal sarcoid clinical features (contd)
    • Perforation of anterior portion of nasal septum
    • 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. Diagnostic features of nasal sarcoidosis
    • Clinical acumen
    • 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. Sarcoidosis (Radiology)
    • X-ray nasal bones show rarefaction & osteolytic reaction
    • 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. Sarcoidosis (treatment)
    • Spontaneous remission (possible)
    • 77. Oral steroids
    • 78. Methotrexate
    • 79. Hydroxychloroquine
  • 80. Role of surgery in nasal sarcoidosis
    • Contraindicated
    • 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. Wegner's granulomatosis
    • Granulomatous inflammation involving nasal mucosa and upper respiratory tract
    • 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. Wegner's granuloma (age of presentation)
    • Seen in the age group 15 – 70)
    • 89. Younger patients are more prone for multisystem damage
    • 90. Renal damage is rather common in the young age group
  • 91. Wegner's granuloma (etiology)
    • Unknown
    • 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. ANCA
    • Two types of ANCA are present
    • 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. Clincial features of Wegners
    • Involvement of upper and lower respiratory tract
    • 102. Glomerulonephritis
    • 103. Nasal block / crusting of nasal mucosa / epistaxis
  • 104. Sinus imaging in wegners
    • CT scan shows evidence of mucosal thickening
    • 105. Bone destruction
    • 106. New bone formation
  • 107. Wegner granulomatosis diagnostic criteria
    • Nasal mucosa /oral mucosal inflammation
    • 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. Treatment
    • Prednisalone
    • 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. Nasal wegeners managment
    • Saline alkaline douching
    • 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. Churg-Strauss syndrome
    • Characterised by systemic vasculitis and asthma
    • 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. Eosinophilic granuloma
    • Characterized by clonal proliferation of Langerhan's giant cells associated with a heterogenous inflammatory infiltrates of eosinophils, lymphocytes, plasma cells and neutrophils
    • 125. Currently this condition is regarded as a neoplastic disorder
    • 126. It can also be considered as a variant of Histiocytosis X
  • 127. Eosinophilic granuloma cllinical features
    • Bones are predominantly affected
    • 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. Eosinophilic granuloma (Histology)
    • Langerhan's giant cells predominate
    • 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. Eosinophilic granuloma (treatment)
    • Depends whether it is mono ostototic / polyostotic
    • 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. Giant cell granuloma
    • Reparative granuloma
    • 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. Imaginng in giant cell granuloma
    • Expansile lytic lesion with a soap bubble appearance in the middle
    • 147. Edges are well demarcated
  • 148. Treatment of giant cell granuloma
    • Curettage may help
    • 149. Total excision is advisable when possible
    • 150. Recurrence rate is very high
  • 151. Cholesterol granuloma
    • This is due to granulomatous reaction to the cholesterol crystals precipitated in the tissues
    • 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. Granulomatous neoplasia
    • Non healing granuloma
    • 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. Granulomatous neoplasia (features)
    • Common in males
    • 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. Granulomatous neoplasia (stages)
  • 167. Prodromal stage
    • This stage could last for many years
    • 168. These patients may c/o persistent nasal obstruction with rhinorrhoea
    • 169. These patients would also be offered surgery for the same
  • 170. Period of activity
    • Purulent nasal discharge
    • 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. Terminal stage
    • Gross mutilation of face
    • 176. Exhaution
    • 177. Distant metastasis would have already occured
    • 178. Eventual death
  • 179. Diagnosis
    • Necrotic areas can be seen in the biopsy
    • 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. Treatment
    • Low dose radiation was used previously to manage these cases
    • 184. Full course of RT is advised these days in order to manage these cases adequately
  • 185. Nasal tuberculosis
    • Nasal infections are caused by direct inoculation
    • 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. Nasal tuberculosis (types)
    • Nodular type
    • 190. Ulcerative type
    • 191. Granulomatous type involving the sinuses
  • 192. Nodular form
    • Also known as Lupus vulgaris
    • 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. 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
  • 199. Ulcerative type
    • This type usually involves the cartilagenous portion of nasal septum and inferior turbinate
    • 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. Sinus granuloma
    • Isolated involvement of sinus without involvement of nasal cavity
    • 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. Diagnosis
    • Tissue biopsy would show epitheloid cell granulomas
    • 208. Evidence of caseation +
    • 209. Presence of AFB is virtually diagnostic if present
    • 210. PCR has increased the sensitivity
  • 211. Treatment
    • Since it is extrapulmonary initially the treatment is started with 4 drug regimen (INH, Rifampicin, ethambutol and pyrazinamide) for 2 months
    • 212. Two drugs INH and Rifampicin – 4 months
  • 213. Syphilis
    • Primay, secondary and tertiary syphilis
    • 214. Can involve patients of any age group
    • 215. The organims usually reside and multiply in the perivascular lymphatics of the blood vessel
  • 216. Primary syphilis
    • Sore or chancre develops at the site of inoculation
    • 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. Secondary syphilis
    • This is the most infectious stage
    • 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. Tertiary syphilis
    • This is the commonest lesion involving the nose
    • 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. Congenital syphilis
    • Also known as snuffles
    • 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. Rhinoscleroma
    • Caused by Klebsiella rhinoscleromatis
    • 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. Rhinoscleroma (Histology)
    • Granulomatous tissue infiltrates in the submucosa
    • 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. Rhinoscleroma (stages)
    • Atrophic stage
    • 243. Granulomatous / proliferative stage
    • 244. Cicatrizing stage
  • 245. Atrophic stage
    • This stage resembles atrophic rhinitis
    • 246. Crusting of nasal mucosa
    • 247. Epistaxis
    • 248. Foul smelling discharge
  • 249. Granulomatous stage
    • Non ulcerative nodules develop
    • 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. Cicatrizing stage
    • Adhesions and stenosis are seen
    • 254. Distortion of normal nasal anatomy
    • 255. Spread to nasopharynx
    • 256. Bone involement could be seen
  • 257. Leprosy
    • Chronic granulomatous lesion caused by M leprae
    • 258. Two types are seen Tuberculoid and lepromatous
  • 259. Tuberculoid leprosy
    • Anesthetic cutaneous patches
    • 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. Lepromatous leprosy
    • Nasal mucosal involvement is seen
    • 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. Thank you

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