CASES

1. CASES DR Prashanth G R2 Radiodiagnosis SSG Hospital Baroda 25-01-08

2. Case 1 • A 13yr old patient with a H/O recurrent nasal obstruction & intermittent epistaxis.

5. CT • Mass within the nasopharynx causing splaying of the pterygoid plates thus extending into the pterygopalatine fossa, anterior bowing of the posterior wall of maxillary sinus & extending in the infratemporal fossa & the sphenoid sinus.

6. D/D Nasopharyngeal Angiofibroma Angiomatous polyp Anterocoanal polyp ~posterior choanal tissue ~Widening of pterygopalatine fossa ~Widening of superior orbital fissure ~extends into the anterior inferior cranial fossa ~Enhancing mass ~Angio – major feeding vessels ~MRI – Multiple flow voids ~Origin in Maxillary sinus ~minimally enhancing ~Not extend intracranially ~located in nasal fossa ~not extend into pterygopalatine fossa ~not extend intracranially ~on angio – only a few feeding vessels ~not very well enhancing ~no flow voids on MRI

7. Widening of pterygopalatine fossa • Lymphoma • Lymphoepitheliomas • Schwannomas • Fibrous Histiocytomas • Nasopharyngeal Angiofibroma • But vast majority of antral bowing is caused by Nasopharyngeal angiofibroma .

8. Discussion • Nasopharyngeal angiofibroma is an uncommon highly vascular, non-encapsulated, polypoid tumor which is histologically benign but is locally aggressive. • Occurs almost exclusively in males. • Age :- 10 – 18yrs • C/F :- Nasal obst., epistaxis, deformity, proptosis, nasal discharge, sinusitis.

9. Origin :- Almost all originate in posterior coanal tissue near pterygopalatine fossa & sphenopalalatine foramen & fill up the nasopharynx. • Extension in pterygopalatine fossa is seen in 89% of cases & results in widening of the fossa with anterior bowing of the posterior ipsilateral antral wall. • Sphenoid sinus is involved in 61% of cases through extension through roof of nasopharynx. • Spread occurs to maxillary & ethmoid sinuses. • Intracranial extension is also seen (20%) & it primarily involves the middle cranial fossa. [Biopsy from the lesion should not be attempted in an OPD because of tumor vascularity.]

10. X – Rays :- • Since lesions arise in pterygopalatile fossa there is widening of the fossa & destruction of posterior wall of maxillary sinus. • Anterior bowing of ipsilateral antral wall. • Mass filling the nasal & nasopharyngeal airways. • Opacification of sphenoids. • Widening of superior orbital fissure – If seen suggest intracranial extension.

11. CT – Scan :- • Enhancing mass • Widening of pterygopalatine fossa with filling of posterior nasal cavity & naopharynx. • Extension into superior orbital fissure, cavernous sinus & Meckel’s Cave is common. • Tumor also extends into the anterior inferior cranial fossa, & also erodes the greater wing of sphenoid. • Erosion of skull base. MRI :- • T1 WI :- Intermediate SI • T2 WI :- Multiple flow voids (Tumor Vessels)

12. Importance of imaging :- • Mapping the lesion for the surgeon & documenting intracranial spread. • Angiography :- Demonstrates major feeding vessels – internal maxillary & ascending pharyngeal artery.

13. Case 2 • A 37 year old male presented clinically with - Headache - Ataxia - Vomiting - Vertigo • Blood investigations: raised RBC count.

14. MRI

15. Diagnosis • Cerebellar Hemangioblastoma

16. Discussion • Benign autosomal dominant tumor of vascular origin. • 80% found in cerebellum>spinal cord>medulla>cerebrum. • 10% of posterior cranial fossa tumors. • Most often occurs in ages 30 to 40. • M > F

17. Relationship to von Hippel-Lindau syndrome. • 20% occur in patients with von Hippel-Lindau syndrome (multiple lesions). • Von Hippel-Lindau syndrome consists of • Retinal, spinal, cerebellar and medullary hemangioblastomas • Renal cysts and carcinomas • Pancreatic cysts • Pheochromocytomas • Papillary cystadenoma of the epididymis

18. Clinical findings - Headache - Ataxia - Nausea - Vomiting - Vertigo - Polycythemia caused by increased erythropoietin found in 40%. • Spinal lesions may present with subarachnoid hemorrhage.

19. CT and MRI Findings • Cystic lesion in the cerebellum with an avidly enhancing mural nodule (75%). • Purely solid enhancing lesion (10%). • Enhancing lesion with multiple cystic areas (15%). • Calcification is uncommon.

20. On angiography: • Vascular nodule within an avascular mass. • Serpentine vessels.

21. Differential Diagnosis • Juvenile pilocytic astrocytoma         - But that is typically found in patients 5 to 15 years of age. •  Metastases. • Cystic astrocytoma. - > 5cm - calcifications - no contrast enhancement of mural nodule. - no polycythemia.

22. Juvenile Pilocytic Astrocytoma

23. CASE 4 • 60 Years old male smoker, who was working in the paint industry. • c/o dypnoea, dry cough, left sided vague chest pain. • Pt was subjected to CXR.

25. The provisional radiographic diagnosis was asbestosis: * nodular pleural thickening. * possible left pleural effusion. * reticular opacities in the lungs. • Then the patient was advised a CT scan, to determine the nature of the pleural disease, & the HRCT for parenchymal status.

28. DIAGNOSIS Asbestosis.

29. WHERE DOES THE ASBESTOSE EXPOSURE OCCUR ? • Mining industry. • Thermal insulators. • Brake & clutch wires. • Building industry. • Electric insulators. • Floor tiles • Paints • cement

30. There are two types of asbestos fibers: * chrysolite: commoner type long, serpentine white fibers. * amphibole: short fibers. (a) amosite. (b) crocidolite.

31. WHY IS IT IMPORTANT TO CLASSIFY THE ASBESTOS FIBRES THIS WAY ? • the shorter amphibole fibers are more likely to be inhaled; as well as to be deposited within the distal airways of the lung. • The chrysolite fibers are long; hence fewer fibers are inhaled, and the body eliminates them more easily via the mucociliary elevator or lymphatic vessels. Chrysotile also fragments and is more soluble .

32. HOW TO CONFIRM THAT THE LUNG OR PLEURAL CHANGES ARE DUE TO THE ASBESTOSIS EXPOSURE ? • By the presence of the asbestos bodies in the sputum.

33. RADIOLOGICAL MENIFESTATIONS PULMONARY PARENCHYMAL DISEASE: * Fibrosis. * bronchial carcinoma. * round atelectasis (pseudotumour) EXTRA THORACIC DISEASE: * peritoneal mesothelioma PLEURAL DISEASE: * PLAQUES * THICKENING * MESOTHELIOMA * PLEURAL EFFUSION.

34. PLEURAL DISEASE

35. 1)PLEURAL PLAQUE: • There is a latent period of approximately 10 years between the exposure & the development of the pleural plaque. • Furthermore, the development of calcification within the plaque may take upto 20 years.

36. The lesion is bilateral. • Located in the middle & lower zones; & at the diaphragmatic surface of the pleura. • The lesion has sharp, well defined margins. • They will be best picked up when they are tangential to the x ray beam.

37. This problem is nicely alleviated by CT SCAN, which is: * more sensitive, because it picks up the plaque more easily, without the problem of tangentiality. * more specific, because prominent subpleural fat pad & intercostal muscles can be confused with plaque on an X ray.

38. The classic distribution of pleural plaques seen on chest radiographs is: * the posterolateral chest wall between the seventh and tenth ribs, * lateral chest wall between the sixth and ninth ribs, * the dome of the diaphragm, (pathognomonic) * and the mediastinal pleura.

40. 2) DIFFUSE PLEURAL THICKENING • This is less common, but more significant; because it causes pulmonary restriction. • Unlike the plaque, the margins of the thickening are ill defined, less commonly calcified. • Rather, if calcification is seen within the diffuse pleural thickening, we should first consider organised empyema or organised hemothorax; & not the asbestosis.

41. CT CRITERIA OF A DIFFUSE PLEURAL THICKENING: • continuous sheet of pleural thickening more than 5 cm wide, more than 8 cm in craniocaudal extent, and more than 3 mm thick.

43. 3)MESOTHELIOMA • 90% of the mesotheliomas are due to the asbestos exposure, especially crocidolite. • There may be a latent period of upto 40 years after the exposure. • Constant local pain is a good clinical indicator of the mesothelioma. • It has a poor prognosis, with most patients dying within 1 year of diagnosis

44. There is frequent presence of pleural effusion. HOW TO SAY THAT IT IS A MALIGNANT PLEURAL THICKENING? * Circumferential thickening. * irregular, nodular thickening. * > 1cm thickness. * mediastinal pleural thickening.

45. The tumour leads to ipsilateral lung volume-loss, & crowding of the ribs. • Despite the large tumour, there is no rib destruction. • In advanced stages, the tumour may extend through the diaphragm. • Lymph node spread occurs, as do blood-borne metastases to the lungs, liver, kidneys, and adrenal glands. • Percutaneous biopsy may lead to spread of the tumour, along the biopsy track, through the chest wall.

46. Nodular pleural thickening

47. TUMOUR EXTENDING INTO THE FISSURE.

48. Invasion and encasement of the pericardium

49. Transdiaphragmatic extension and hepatic invasion by a malignant pleural mesothelioma.

50. 4) PLEURAL EFFUSION • Isolated pleural effusion is rare in asbestosis. • When pleural effusion is present, associated with pleural thickening; we are dealing with malignancy of the pleura or lung. • Pleural effusions are typically hemorrhagic exudates of mixed cellularity but do not typically contain asbestos bodies.