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To through a light on the sinonasal tumors.. Classification: Tumors of the nose and Para nasal sinuses are classified into: A-Benign tumors:  Epithelial.

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Presentation on theme: "To through a light on the sinonasal tumors.. Classification: Tumors of the nose and Para nasal sinuses are classified into: A-Benign tumors:  Epithelial."— Presentation transcript:

1 To through a light on the sinonasal tumors.

2 Classification: Tumors of the nose and Para nasal sinuses are classified into: A-Benign tumors:  Epithelial e.g. papilloma, adenoma  Non-epithelial e.g. osteoma, angioma, chondroma, fibroma.

3 B-Malignant tumors:  Epithelial e.g. squamous cell carcinoma, adenocarcinoma, malignant melanoma, adenoid cystic carcinoma.  Non-epithelial e.g. fibrosarcoma, osteosarcoma, angiosarcoma rhabdomyosarcoma, lymphoma

4 A-Benign epithelial tumors:  Papilloma: 1-Papilloma in the nasal vestibule (squamous papilloma): small sessile or pedunculated, single or multiple masses in the nasal vestibule may cause epistaxis and sometimes nasal obstruction. Treatment is by excision and cauterization of the base to prevent recurrence. It may be viral infection like wart.

5 2- Papilloma in the nasal fossae and paranasal sinuses (Inverted papilloma) (Transitional cell papilloma)  It is the most common benign tumor of the nose and paranasal sinuses. Almost exclusively arise from lateral nasal wall and may extends to maxillary and ethmoidal sinuses.

6  Pathologically the tumor covered by transitional epithelium.  Clinically causes unilateral nasal obstruction and epistaxis usually occurs in males over 50 years, examination shows mass in the nasal cavity.  Diagnosed by: 1- Radiology (opacity of the maxillary sinus and could extends to the ethmoid and nasal cavity and thinning of the bone but no frank erosion) 2- Histopathology to exclude malignancy (malignant changes occur in 3%).  Treatment is by adequate local excision (medial maxillectomy by lateral rhinotomy approach)

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9 B-Benign non-epithelial tumors: 1-Osteoma: it is slowly growing tumor. It often occurs in young adult and mostly in the frontal sinuses. Usually they are asymptomatic and found incidentally by routine radiographs. When osteoma become large may cause headache and sometimes cause obstruction of frontonasal duct → mucocoele which may be secondarily infected → pyocoele. Also it may affect ethmoidal sinus causes broad nasal bridge.  Diagnosis: by radiology.  Treatment is by surgical removal if the osteoma is symptomatic (frontal sinus osteoma → osteoplastic flap procedure, ethmoidal osteoma → external ethmoidectomy). If it is symptomless → no treatment is required, just follow up. 2-Angioma (bleeding polyp): It is capillary angioma, most commonly arise from the septum as bleeding polyp causing epistaxis. Treatment is by excision with cauterization of the base to avoid recurrence.

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12  Squamous-cell carcinoma: it is the commonest malignant tumors of the nose and Para nasal sinuses. It is used to be seen in nickel industries workers.  Adenocarcinoma: it arises from gland in the upper respiratory tract mucous membrane. It is used to be seen in hardwood dust workers.  Adenoid cystic carcinoma: it arises from minor salivary glands in the nose & paranasal sinuses, epiglottis and pharynx. It appears as round mass usually on hard palate (most commonly), alveolus and antral floor. They are generally radio resistant.  Malignant melanoma: arises from melanocytes. They appear as dark or pale sessile mass on the nasal septum or lateral nasal wall.

13  Sarcoma e.g. fibrosarcoma, osteosarcoma, rhabdomyosarcoma.  Lymphoma e.g. Burkitt's lymphoma, Stewarts lethal midline granuloma.

14 Sites of malignant tumors:  80% of malignant Sino-nasal tumors are squamous cell carcinoma.  60% of tumors arise in the maxillary sinus.  30% in the nose  10% in the ethmoids.  Tumors of frontal & sphenoid sinuses are rare. *Lymph node metastasis is to retropharyngeal, submandibular and upper deep cervical lymph nodes occurs in 10−15% (the sinus has poor lymphatic drainage).

15 UICC (International Union against Cancer Committee) staging:  Tx: primary tumor cannot be assessed.  T0: no evidence of primary disease.  Tis: carcinoma in situ.

16 Maxillary sinus:  T1: Tumor limited to the antral mucosa with no bone erosion.  T2: Tumor causing bone erosion (except for the posterior wall) including extension into the hard palate and/or middle nasal meatus.  T3: Tumor invades any of the following: bone of posterior wall of maxillary sinus, skin of cheek, floor or medial orbital wall.  T4: Tumor invades orbital contents beyond the floor or medial wall including apex and/or any of the following: cribriform plate, nasopharynx, sphenoid sinus, frontal sinus.

17 Ethmoid sinus:  T1: tumor confined to ethmoid with or without bone erosion.  T2: tumor extends into nasal cavity.  T3: tumor extends to anterior orbit and/or maxillary sinus.  T4: tumor with intracranial extension, orbital extension including apex, involving sphenoid and/or frontal sinus and/or nasal skin.

18 Clinical features of malignant sino-nasal tumours:  Nasal tumors → nasal features e.g. unilateral nasal obstruction, epistaxis, anosmia.  Frontal sinus tumors → orbital features e.g. proptosis, diplopia, and blindness  Sphenoid sinus tumors → neurological features.  Ethmoid sinus tumors → nasal and orbital features

19 Maxillary sinus tumors: 1- Early features: when the tumor is confined in the sinus cavity-features of chronic sinusitis. 2- Late features: when the tumors spread outside the sinus cavity leading to features according to the site of Invasion include:

20  Invasion of anterior sinus wall → cheek swelling, ulceration of cheek skin, involvement of infra orbital nerve causing facial pain and paresthesia.  Invasion of superior wall (orbital floor) → proptosis, epiphora due to damage to nasolacrimal duct, blindness due to invasion of optic nerve, diplopia due to limitation of movement of the eye ball or external ophthalmoplegia due to paralysis of extra ocular muscles.

21  Invasion of medial wall → unilateral nasal obstruction, recurrent epistaxis and anosmia. O/E there is mass inside the nasal cavity.  Invasion of the posterior wall → spread to infratemporal fossa and pterygopalatine fossa → trismus (inability to open the mouth due to invasion of masticatory muscles), facial pain and parasthesia due to involvement of 5 th cranial nerve.

22  Invasion of inferior wall (hard palate) loosening of teeth, ulceration of the palate causing oro-antral fistula and dental pain.  Intracranial spread → headache, vomiting and other neurological features.

23  Lymph node metastasis (10%−15%) → mass in the neck.  Systemic metastasis is occasionally seen.

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25 Investigations:  General blood investigations (CBP, ESR, Renal function test...etc) (as a preoperative measure and to detect distant metastasis)  Plain X-ray of nose & Paranasal sinuses (occipto-mental view). Shows opacification of the sinus and bone erosion.  CT scan & MRI: show the tumor, bone erosion& extension of the tumor.  Biopsy: if the tumor appears inside the nose, we can take incisional biopsy under local anesthesia. If the tumor confined inside the maxillary sinus cavity, we can take biopsy through intra-nasal inferior meatal antrostomy. Cald well is contraindicated in malignancy.

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27 Treatment: Usually the treatment of carcinoma is combined surgery and radiotherapy. There are three main surgical options for carcinoma:  Medial maxillectomy by using lateral rhinotomy approach: used for tumours limited to the lateral nasal wall, nasal cavity and ethmoid.  Total maxillectomy (removal of upper jaw as bony box containing the tumor): used for antral carcinoma.  Craniofacial resection: used when there is involvement of cribriform plate. In general an orbital exenteration is indicated only if tumor breaches periosteum to involve orbital fat.

28 Follow up and after care:  Monthly → for the 1 st postoperative year.  Bimonthly → for the 2 nd postoperative year.  Every 3 months → for the 3 rd postoperative year.  Every 6 months → for the 4 th & 5 th postoperative year.  Annually for a further five years. Prognosis: Poor, overall 5-year survival is 25−30%


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