This presentation discusses granulomatous lesions involving the nose

1. Granulomatous lesions of nose Dr T. Balasubramanian

3. Macrophages, granulocytes and multinucleated giant cells

4. Presence of vasculitis

5. Systemic involvement is common

7. Inflammatory

8. Neoplastix

10. Fungal – Aspergillus, zygomycosis, Dermatocietes, Blastomycosis, Histoplasmosis, Sporotrichiasis and coccididomycosis

11. Protozoa – Leishmaniais

12. Miscellaneous - Rhinosporidiosis

14. Midline granulomas

15. T cell lymphomas

17. Sarcoidosis

18. Churg-Strauss syndrome

19. Cholesterol granuloma

20. Eosinophilic granuloma

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

27. Affected age group 2 nd - 5 th decades

28. Females outnumber males 2:1

30. Infective agents

31. Chemicals (Beryllium, Zirconium etc)

32. Pine pollen

33. Peanut dust

34. Immunological

36. No depression of CMI

37. Humoral immunity normal

38. Sarcoidosis (current hypothesis)

40. Continued antigenic stimulation

41. Failure of supressor mechanism

42. Abormalities in the regulation of cytokine network

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

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

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

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 Kveim test (cutaneous hypersensitivity test for sarcoidosis) withdrawn now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

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

77. Oral steroids

78. Methotrexate

79. Hydroxychloroquine

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

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)

89. Younger patients are more prone for multisystem damage

90. Renal damage is rather common in the young age group

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

97. PANCA (Perinuclear)

98. CANCA (Cytoplasmic)

99. Patients with Wegener's have elevated levels of cANCA

100. These tests are performed using immunoflorescence / radioimmunoassay

102. Glomerulonephritis

103. Nasal block / crusting of nasal mucosa / epistaxis

105. Bone destruction

106. New bone formation

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

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

117. Intranasal steroid drops

118. Glucose glycerine drops

119. Nasal surgeries like rhinoplasty / augmentation rhinoplasty should be avoided during active stages of the disease

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

125. Currently this condition is regarded as a neoplastic disorder

126. It can also be considered as a variant of Histiocytosis X

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

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

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

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

147. Edges are well demarcated

149. Total excision is advisable when possible

150. Recurrence rate is very high

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

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

162. Common during 5 th - 6 th decades of life

163. Currently these granulomas are considered to be T cell lymphoma / NK cell lymphoma

165. Period of activity

166. Terminal stage

168. These patients may c/o persistent nasal obstruction with rhinorrhoea

169. These patients would also be offered surgery for the same

171. Crusting / necrosis / tissue loss

172. Progressive destruction of nasal framework

173. Destruction of palate and upper lip

174. Fever due to secondary infection

176. Exhaution

177. Distant metastasis would have already occured

178. Eventual death

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

184. Full course of RT is advised these days in order to manage these cases adequately

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

190. Ulcerative type

191. Granulomatous type involving the sinuses

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

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

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

208. Evidence of caseation +

209. Presence of AFB is virtually diagnostic if present

210. PCR has increased the sensitivity

212. Two drugs INH and Rifampicin – 4 months

214. Can involve patients of any age group

215. The organims usually reside and multiply in the perivascular lymphatics of the blood vessel

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

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

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

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

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

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.

243. Granulomatous / proliferative stage

244. Cicatrizing stage

246. Crusting of nasal mucosa

247. Epistaxis

248. Foul smelling discharge

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

254. Distortion of normal nasal anatomy

255. Spread to nasopharynx

256. Bone involement could be seen

258. Two types are seen Tuberculoid and lepromatous

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

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