Granuloma nose

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Granuloma nose

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

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