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Published byDuane Mason Modified over 9 years ago
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Age Poor socio-economic group Virulence of organisms Immune-compromised host Preformed pathways Cholesteatoma
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Direct Bone Erosion Venous Thrombophlebitis Performed pathways
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A) Intratemporal(confines within the temporal bone): Mastoiditis Petrositis Facial paralysis Labyrinthitis
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B)Intracranial: Extradural abscess. Subdural abscess Meninigitis Brain abscess Lateral sinus Thrombophlebitis Otitic Hydrocephalus
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When the infection spreads from mucosal lining to bony wall of mastoid air cells we called it as mastoiditis. Aetiology: It usually accompanies or follows ASOM.The determining factors being high virulence of organisms or lowered resistance of patient.
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Pathology: 1)Production of pus under tension. 2)Hyperaemic decalcification and osteoclastic resorption of bony walls.
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Clinical Features: Symptoms: Pain behind the ear. Fever. Ear discharge
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Signs: Mastoid Tenderness. Ear Discharge Sagging of postero-superior meatal wall Perforation of tympanic membrane Swelling over the mastoid Hearing loss. General findings
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Investigations: Blood counts ESR X-ray mastoid Ear swab
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Treatment: Hospitalisation of patient Antibiotics Myringotomy Cortical Mastoidectomy. It is indicated when there is Sub-periosteal abscess. Sagging of postero-superior meatal wall. Positive resorvoir sign. No response within 48 hrs of adequate medical treatment. Mastoiditis leading to complications
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Spread of infection from middle ear and mastoid to petrous part of temporal bone is called petrositis. Clinical features: Gradenigo’s syndrome : It is the classical presentation, and consist of a triad of a)external rectus palsy b)deep seated ear or retro orbital pain c)persistent ear discharge. Fever, headache, vomiting, neck rigidity,facial paralysis.
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Treatment: Cortical, modified or radical mastoidectomy is often required. Iv antibiotics should precede and follow surgical intervention. Treatment: Cortical, modified or radical mastoidectomy is often required. Iv antibiotics should precede and follow surgical intervention.
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There are three types of labyrinthitis: a)Circumscribed labyrinthitis b)Diffuse serous labyrinthitis c)Diffuse suppurative labyrinthitis
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A)Circumscribed labyrinthitis(Fistula of labyrinth): There is thining or erosion of bony capsule of labyrinth. Aetiology: CSOM with cholesteatoma Neoplasms of middle ear Surgical or accidental trauma to labyrinth
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Clinical features: A part of membranous labyrinth is exposed and becomes sensitive to pressure changes. so complain of: Triensient vertigo often induced by pressure on tragus, cleaning the ear or while performing valsalva manoeuvre. Diagnose by fistula test. Treatment: a)Mastoid exploration. b)Systemic antibiotics.
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It is diffuse intra-labyrinthine inflammation without pus formation and is a reversible condition if treated early. Aetiology: Pre-existing circumscribed labyrinthitis associated with chronic middle ear suppuration or cholesteatoma. In acute infections inflammation spreads through round window.
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Clinical features: In mild cases-vertigo and nausea. In severe cases-vertigo is worse with marked nausea, vomiting and even spontaneous nystagmus. Chochlea is also affected with some degree of SNHL. Total loss of vestibular and cochlear function.
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Treatment: Medical- Bed rest Antibacterial Therapy Labyrinthine sedatives- prochlorperazine(stemetil) Myringotomy if labyrinthitis has followed ASOM and drum is bulging. Surgical: mastoidectomy
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This is diffuse pyogenic infection of labyrinth with permanent loss of vestibular and cochlear functions. Aetiology: It usually follows serous labyrinthitis, pyogenic organisms entering through a fistula.
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Clinical Features: There is severe vertigo, nausea, and vomiting due to acute vestibular failure. Spontaneous nystagmus. Patient looks toxic with total loss of hearing. Treatment:
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Otogenic brain abscess: 50% of brain abscess in adults and 25%in children are otogenic.Cerebral abscess is seen twice as frequently as cerebellar abscess. Routes of infection: They develops as a result of direct extension of middle ear infection through tegmen or by thrombophlebitis.
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Pathology: a)Stage of invasion(initial encephalitis) b)Stage of localisation(latent abscess) c)Stage of enlargement(manifest abscess) d)Stage of termination(rupture of abscess)
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Clinical Features: Brain abscess is often associated with other complications. It can be divided into: a)Those due to raised ICP b)Those due to area of brain affected
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a)Symptoms and sign of raised ICP Headache Nausea and vomiting Level of consciousness Papiloedema Slow pulse and subnormal temp.
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b)Localising Features: Temporal lobe abscess: Nominal Aphasia Homonymous hemianopia Contralateral motor paralysis Epeliptic fits
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Investigations: a)Skull x-rays including mastoids b)CT scan c) LP Treatment: High dose of iv antibiotics. For raised ICP-Dexamethasone 4mg iv 6 hrly Discharge from ear is treated by suction clearance and topical ear drops. Neurosurgical treatment.
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ETIOLOGY: COMPLICATION OF ACUTE COALESCENT MASTOIDITIS,MASKED MASTOIDITIS OR CHRONIC SUPPURATION OF MIDDLE EAR AND CHOLESTEATOMA CLINICAL FEATURE a) HETIC TYPE OF FEVER WITH RIGOR b) HEADACHE c) PROGRESSIVE ANAEMIA &EMACIATION d) PAPILLOEDEMA
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TRETMENT SYSTEMIC ANTIBACTERIAL MASTOIDECTOMY & EXPOSURE OF SINUS LIGATION OF INTERNAL JUGULAR VEIN ANTICOAGULANT THERAPY SUPPORTIVE TRETMENT
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