Complications of suppurative otitis media


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  • Fracture of temporal bone: Bilateral anterior longitudinal temporal bone fractures with ossicular injury. Petrous ICA canal. Longitudinal fracture extending through mastoid air cells into middle ear cavity with hemotympanum. Stapedectomy Stapedectomy is a surgery performed for those with otosclerosis. This procedure results in almost complete restoration of the hearing to the level of the sensorineural hearing or the highest level possible with your inner ear. Stapedectomy is performed for those with otosclerosis . This surgery is performed in an outpatient setting. Surgery is done through the ear canal where the eardrum is reflected forward exposing the middle ear and the bones of hearing. First the fixation of the stapes bone is confirmed. Once confirmed, the stapes bone and the incus bone are separated. A hole is placed in the footplate of the stapes bone using the argon laser and a prosthesis is placed extending from the incus bone into the hole in the stapes bone. This procedure results in almost complete restoration of the hearing to the level of the sensorineural hearing or the highest level possible with your inner ear. Round window fistula. An opening in the round window allows perilymph to leak out into the middle ear. In this artist's depiction, for clarity, bone is not shown between the middle and inner ears. While it is difficult to be sure, it seems likely that in most cases there is only a small oozing of fluid between the perilymphatic space and the air-filled middle ear. Axial CT shows an example of a normal caliber vestibular aqueduct. An enlarged vestibular aqueduct is defined by an anterior-posterior diameter greater than 1.5 mm, at the midpoint between its external aperture and the common crus. Hearing loss usually is bilateral, progressive in nature, and may be associated with vertigo. Some cases may be familial. Large vestibular aqueduct syndrome is seen in Pendred’s syndrome, an autosomal recessive condition characterized by deafness and goiter. In comparison, a narrowed vestibular aqueduct less than 0.5 mm in diameter may be seen with Meniere disease. Operative photograph of the floor of the left middle cranial fossa in a patient with superior canal dehiscence.
  • A cholesteatoma is a benign growth of skin and tissue in the middle ear. Retracted and perforated tympanic membrane. Middle ear space filled with cholesteatoma and middle ear eroded bones. Eustachian tube blocked by inflammatory tissues. Otoscopy showing an ear canal polyp and cholesteatoma. Polyp. Cholesteatoma. Tympanic membrane.
  • Patients with osteitis of the external auditory canal are older, and usually present with a unilateral, dull, chronic pain (probably due to periosteitis), with an associated otorrhea. Furthermore, these patients generally do not have any conductive hearing loss. It appears that this condition is the result of a cutaneous ulceration and inflammation of the overlying epidermis. A large sequestrum of exposed bone can be seen in the inferior canal wall. Cholesteatoma left ear. The disease has eroded the bone above and behind the upper part of the eardrum, the attic. The eardrum is also known as the tympanic membrane. I took this picture in 1988 as part of a research project into the development of cholesteatoma using a Storz Hopkins rod tele-otoscope, Xenon 300W light source, and an Olympus OM-1 SLR camera with Fujichrome 400ASA 35mm slide film. Key: c = cholesteatoma tm = tympanic membrane (eardrum) Erosion by granulation tissue.
  • Mastoiditis with venous sinus thrombosis and venous infarction . This is a 19-year-old man who presented with headache and transient left-sided weakness. T1-weighted midline sagittal MR image shows hyperintense thrombus in the superior sagittal sinus ( arrows ). Magnetic Resonance Imaging 38 years old man with right parietal cortical vein thrombosis. Magnetic resonance imaging of the brain: Sagittal T1 (A) sequence shows a hyperintense signal in the right parietal region, axial gradient echo (B) sequence demonstrates the hemorrhagic component as susceptibility artifact, diffusion weighted (C) imaging shows a bright signal in the right parietal region with a corresponding hyperintense signal on axial T2 weighted (D) imaging. Normal patency of the major cerebral venous sinuses is seen on magnetic resonance venography (E and F).
  • Myringotomy and insertion of a tympanoplasty tube as treatment for otitis media. From Frazier et al., 2000. Incision of the tympanic membrane usually performed to relieve pressure and allow drainage of serous or purulent fluid from the middle ear. Sometimes, as in the case of serous OTITIS MEDIA , a ventilating tube called a GROMMET is inserted to permit continuous ventilation and avoid a chronic middle ear problem with fluid accumulation, pain, and loss of hearing. When a simple myringotomy is done for purposes of draining purulent material resulting from recurrent suppurative otitis media , care should be taken to avoid contamination by the fluid. Eardrops may be prescribed if there is fluid in the ear. The ear should be kept dry for two weeks after the procedure, with no fluid entering the ear until the myringotomy site in the eardrum is healed. CORTICAL MASoIDECroMY. A, the incision behind a child's pinna, showing the approximate position of his antrum. B, the surface of his bone has been cleared. This diagram also shows the surface markings of his mastoid antrum, the area to be cleared, and the danger area where his lateral sinus is closest to the surface, and thus in the greatest danger of being injured. Gouge away from it towards his external auditory meatus. C, the surface of his temporal bone has been chipped away and the more superficial air cells cleared. Note that his cleaned out antrum is the deepest part of the wound. His lateral sinus is more at risk lower down.
  • Extradural abscess in a 74- year-old man 12 years after resection of a meningioma and cranioplasty. (a) Axial T2-weighted MR image shows a high-signal-intensity fluid collection (*) with a location outside the dura mater (arrowhead). (b) Axial T1-weighted gadolinium-enhanced MR image shows peripheral enhancement (arrow) around the fluid collection. (c) Diffusion-weighted MR image ( b = 1000) shows an area of high signal intensity within the fluid collection, a finding indicative of restricted diffusion. Contrast enhancement with gadolinium diethylenetriaminepentaacetic acid (a paramagnetic agent) helps differentiate the abscess, the enhancement ring, and the cerebral edema around the abscess. T1-weighted images enhance the abscess capsule, and T2-weighted images can demonstrate the edema zone around the abscess. Different intracranial lesions secondary to lateral sinus thrombosis. A, Fluid-attenuated inversion recovery imaging: right temporal edema. B, Nonenhanced CT: mixture of hypo- and hyperdensity in the left temporal lobe. C, Coronal T2-weighted imaging: increased T2-weighted MRI signal in the mastoid air spaces homolateral to the lateral sinus hypersignal (thin arrow). D, Fluid-attenuated inversion recovery imaging: left temporal hematoma with mass. Case 1. Initial (A and C) and control (B and D) MR images. Initial MR examination shows increased signal of intensity (arrow) in the left lateral sinus and nearly no flow in the right lateral sinus (hypoplastic sinuses) on T1 weighted transverse image (A). Control MR image shows increased flow in the left lateral sinus, in the right sinus no improvement of blood flow (B). Initial MR venography image showed impaired blood flow in left lateral sinus and limited flow on the right side (C). Control MRI venography slice demonstrates increased flow (arrow) in the left lateral sinus but no change flow in the right lateral sinus (D).
  • Left cervical swelling caused by Bezold's abscess in another patient with similar presentation (arrow) Coalescent mastoiditis with Scalp Abscess. Scalp and upper neck pyogenic abscess on right. Acute otitis media with coalescent mastoiditis on right
  • 1.Asymmetric petrous apex pneumatization. ( A ) Unenhanced T1-weighted MR image shows asymmetry of the petrous apices, with greater signal on the right ( arrow ) that might be mistaken for a mass. ( B ) CT in the same patient shows the high signal to be from marrow fat in a normal petrous apex. The contralateral side contains an air cell. 2. Widening of the diploic space is due to marrow expansion from ineffective and excessive erythropoiesis. Seen in untreated severe congenital hemolytic anaemias (thalassaemia major, sickle cell anaemia), less commonly in patients with severe iron deficiency, cyanotic heart disease, osteopetrosis . The "hair-on-end" appearance is typical. 3. T4N2 poorly differentiated carcinoma with cranial nerve symptoms. On CT (left), sclerotic change was observed at the right side of the skull base (arrows) without apparent bone destruction. On T 1 -weighted MRI after Gd injection (right), low-intensity soft tissue with a Gd enhancement was seen in the clivus, the petrous apex, and the sphenoid wing.
  • Left CN 6 Palsy Patient was asked to look left. Note that left eye will not abduct .
  • A contrast enhanced axial CT scan of the patient showing clouding of the left middle ear cleft with enhancement of the left petrous apex. T1 weighted MRI image with isointense lesion in the right petrous apex (black arrow)
  • A mastoidectomy is the surgical removal of these mastoid air cells; the surgery may extend into the middle ear.
  • Otoscopic view of glomus tumor (arrow). Glomus tumors are a rare cause of conductive hearing loss. These neuroendocrine tumors arise from the adventitia of the jugular bulb or the neural plexus within the middle ear space. Characteristically, patients presenting with glomus tumors are women 40 to 50 years of age who report pulsatile tinnitus and hearing loss. On examination, a pulsating reddish-blue mass may be seen behind an intact tympanic membrane. However, diagnosis of these tumors is difficult, and computed tomography of the temporal bones is required. An anomalous carotid artery or jugular bulb may present in a similar fashion. Latrogenic injury to the labyrinth and facial nerve during mastoid surgery for cholesteatoma. Seearrows
  • Axial MRI sections (T2 weighted) showing (a) intracranial extradural abscess.
  • One of the physically demonstrable symptoms of meningitis is Kernig's sign. Severe stiffness of the hamstrings causes an inability to straighten the leg when the hip is flexed to 90 degree
  • Coronal T1 post-gadolinium MR- right subdural abscess.
  • Craniotomy with Evacuation of Subdural Hematoma: Post-accidnet condition with hematoma. Right subdural hematoma with hemorrhagi contusion. (A)Incision and scalp reflected. A-C shaped incision is made to expose the fronto-temporo-parietal region. (B)Burr hole and craniotomy. Burr holes are made and connected to create a skull flap. The flap is elevated. (C)Bone flap and hematoma evacuation. A large hematoma is encountered and the blood and contusion are evacuated.
  • Brain abscess. Axial T2-weighted MRI in a patient with a right frontal abscess. Note the mass effect and surrounding edema. The wall of the abscess is relatively thin (black arrows).
  • Fifty-six-year-old woman with subacute left proximal lateral sinus thrombosis (duration of symptoms, 5 days). The arteriovenous transit of a contrast bolus is depicted on the dynamic series of combo-4D MRV ( A–E ; coronal MIP reformations of time-resolved contrast-enhanced MRV; temporal interval between images, 1.5 seconds). At early venous phase, faint filling of cortical veins and the superior sagittal sinus is noted ( B ). At subsequent later venous phase, the left proximal transverse sinus does not show increased contrast filling other than very faint peripheral enhancement of its dural wall ( long arrow in C ). At following later venous phases, no increase in contrast filling of this sinus portion is observed ( long arrow in D and E ). On axial static image of combo-4D MRV (contrast-enhanced 3D VIBE sequence), a hypointense filling defect within the proximal left transverse sinus is depicted ( small arrow in F ).
  • Empty delta sign The empty delta sign is a finding that is seen on a contrast enhanced CT (CECT) and was first described in thrombosis of the superior sagittal sinus. The sign consists of a triangular area of enhancement with a relatively low-attenuating center, which is the thrombosed sinus. The likely explanation is enhancement of the rich dural venous collateral circulation surrounding the thrombosed sinus, producing the central region of low attenuation. In early thrombosis the empty delta sign may be absent and you will have to rely on non-visualization of the thrombosed vein on the CECT. The sign may be absent after two months due to recanalization within the thrombus.
  • Complications of suppurative otitis media

    2. 2. INTRODUCTION:• A complication of otitis media is defined as a spread of infection beyond the pneumatized area of the temporal bone and the associated mucosa.• Though there is a general decline in the incidence of complications, they are still frequently seen in our country.
    3. 3. FACTORS INFLUENCING DEVELOPMENT OF COMPLICATION1. Age:  First decade of life.  Elderly when patient’s resistance is low.1. Poor Socio-economic Group:  Over crowding.  Poor health education.  Poor personal hygiene.  Limited access to health care.
    4. 4. 3. Virulence Of Organisms:  Streptococcus pneumoniae type III.  Haemophilus influenzae.  Pseudomonas aeruginosa.  Staphylococcus aureus.3. Immune-Compromised Host:  AIDS.  Uncontrolled diabetes.  Transplant ptients receiving immunosuppressive drugs.  Cancer patients receiving chemotherapy.
    5. 5. 5. Preformed Pathways:  Dehiscence of bony facial canal.  Previous ear surgery.  Fracture of temporal bone.  Stapedectomy.  Perilymph fistula.  Congenitally enlarged aqueduct of vestibule.  Dehiscence in the floor of middle ear.
    6. 6. 6. Cholesteatoma:  Osteitis or granulation tissue in chronic otitis media destroy the bone and help infection penetrate deeper.
    7. 7. PATHWAYS OF SPREAD OF INFECTION1. Direct Bone Erosion:  In acute infections;  Process of hyperaemic decalcification.  In chronic infection;  Osteitis.  Erosion by cholesteatoma.  Erosion by granulation tissue.
    8. 8. 2. Venous Thrombophlebitis:  Infection from the mastoid bone can cause;  Thrombophlebitis of venous sinuses.  Cortical vein thrombosis
    9. 9. 3. Preformed Pathways:  Congenital dehiscences.  e.g. in boby facial canal floor of middle ear over the jugular bulb.  Patent sutures.  e.g. petrosquamous sutures.  Previous skull fractures. The fracture sites heal only by fibrous scar which permits infection.  Surgical defects.  e.g. stapedectomy, fenestration and mastoidectomy with exposure of dura.  Oval and round windows.  Infection from labryinth can travel along internal acoustic meatus, aqueducts of the vastibule and that of the cochlea to the meninges.
    12. 12. MASTOIDITIS The term Mastoiditis is used when infection spreads from the mucosa, lining the mastoid air cells, to involve bony walls of the mastoid air cell system.Types Of Mastoiditis:  Acute Mastoiditis  Masked (Latent) Mastoiditis
    13. 13. ACUTE MASTOIDITIS Inflammation of mucosal lining of antrum and mastoid air cell system.
    14. 14. Aetiology: Acute suppurative otitis media. High virulence of organisms. Lowered resistance of patient.  Due to; • Measles. • Exanthematous Fevers. • Poor nutrition. • Diabetes.Causative Organisms: Beta-Haemolytic Streptococcus (most common).
    15. 15. PATHOLOGY: Two main pathological processes are responsible:  Production of pus under tension. • Extension of inflammatory process to mucoperiosteal lining of air cell system increases the amount of pus produced due to large surface area involve.  Hyperaemic decalcification and osteoclastic resorption of bony walls. • Hyperaemia and engorgement of mucosa causes dissolution of calcium from the bony walls of the mastoid air cells (hyperaemic decalcification). Both these processes combine to cause destruction and coalescence of mastoid air cells, converting them into a single irregular cavity filled with pus ( Empyema of mastoid).
    16. 16. CLINICAL FEATURES:Symptoms: Pain behind the ear. Fever. Ear discharge ( profuse and increase in purulence).
    17. 17. Signs: Mastoid tenderness. Ear discharge (Mucopurulent or purulent discharge) . Sagging of posterosuperior meatal wall. Perforation of tympanic membrane. Swelling over the mastoid. Hearing loss. General findings;  Patient appears ill.  Low grade fever.  In children, high fever with a rise in pulse rate.
    18. 18. INVESTIGATIONS: Blood counts:  Shows polymorphonuclear leucocytosis. ESR:  Usually raised. X-Ray mastoid:  Clouding of air cells due to collection of exudate in them. Ear swab:  For culture and sensitivity.
    19. 19. DIFFERENTIAL DIAGNOSIS: Suppuration of mastoid lymph nodes. Furunculosis of meatus.  It is differentiated from acute mastoiditis by; • Absence of preceding acute otitis media. • Painful movements of pinna. • Swelling of meatus is confined to cartilaginous part only. • Discharge is never mucoid or mucopurulent. • Enlargement of pre or postauricular lymphnodes. • Mild conductive hearing loss. • Normal looking tympanic membrane. • X-Ray mastoid with clear air-cell system. Infected sebaceous cyst.
    20. 20. TREATMENT: MEDICAL:  Hospitalization of the patient.  Antibiotics.  Amoxicillin or Ampicillin.  Chloramphenicol or Metronidazole.
    21. 21.  SURGICAL:  Myringotomy.  Cortical mastoidectomy.  It is indicated when there is; • Subperiosteal abscess. • Sagging of posterosuperior meatal wall. • Positive reservoir sign. • No change or worsen condition of patient . • Complication of mastoiditis.
    22. 22. COMPLICATIONS OF ACUTE MASTOIDITIS Subperiosteal abscess. Labyrinthitis. Facial paralysis. Petrositis. Extradural abscess. Meningitis. Brain abcess. Lateral sinus thrombophlebitis. Otitic hydrocephalous.
    23. 23. ABSCESS IN RELATION TO MASTOID INFECTION Postauricular Abscess:  Commonest abscess.  Forms over mastoid.  Pinna is displaced forwards, outwards and downwards.  In infants and children; forms over the MacEwen’s triangle.
    24. 24.  Zygomatic Abscess:  Occurs due to infection of zygomatic air cells.  Swelling appears infront and above the pinna.  Associated oedema of upper eyelid also present.  Pus collects either superficial or deep to the temporalis muscle. Meatal Abscess(Luc’s Abcess):  Pus breaks through the bony wall between the antrum and external oseous meatus.  Swelling is seen in deep part of bony meatus.  Abscess may burst into the meatus.
    25. 25.  Behind The Mastoid(Citelli’s Abscess):  Abscess is formed behind the mastoid more towards the occipital bone. Parapharyngeal or retropharyngeal abscess:  This results from infection of the peritubal cells due to acute coalescent mastoiditis.
    26. 26.  Bezold Abscess:  Occur following acute coalescent mastoiditis .  Pus breaks through the thin medial side of the tip of the mastoid and presents as a swelling in the upper part of neck.
    27. 27. MASKED (LATENT) MASTOIDITIS It is a condition of slow destruction of mastoid air cells but without the acute signs and symptoms often seen in acute mastoiditis.Aetiology: Inadequate antibiotic therapy. Use of oral penicillin;  given in cases of acute otitis media when acute sypmtoms subsides but smouldering infection continues in the mastoid.
    28. 28. CLINICAL FEATURES: Mild pain behind the ear. Persistent hearing loss. Tympanic membrane appear thick with loss of translucency.INVESTIGATIONS: Audiometry:  Shows conductive hearing loss. X-ray mastoid:  Reveal clouding of air cells with loss of cell outline.TREATMENT: Surgical:  Cortical mastoidectomy.
    29. 29. PETROSITIS Spread of infection from middle ear and mastoid to the petrous part of temporal is called Petrositis.
    30. 30. PATHOLOGY: Petrous bone may be of three types:  Pneumatised with air cells extending to the petrous apex.  Diploic containing only marrow space.  Sclerotic.
    31. 31.  Usually two cell tracts are recognized:  Posterosuperior tract which starts in the mastoid and runs behind or above the bony labyrinth to the petrous apex.  Anteroinferior tract which starts at the hypotympanum near the eustachian tube runs around the cochlea to reach the petrous apex.CLINICAL FEATURES: Gradenigo’s syndrome:  Consist of a triad; • External rectus palsy. • Deep-seated ear or retro-orbital pain. • Persistent ear discharge.
    32. 32.  Other symptoms;  Fever.  Headache.  Vomiting.  Neck rigidity.INVESTIGATIONS: CT Scan of temporal bone:  Show bony details of petrous apex and air cells MRI  Differentiate diploic marrow containing apex from fluid or pus
    33. 33. TREATMENT: Suitable intravenous antibacterial therapy. Surgical:  Cortical, modified radical or radical mastoidectomy.
    34. 34. FACIAL PARALYSIS It can occur as a complication of both acute and chronic otitis media.
    35. 35. AS COMPLICATION OF ACUTE OTITIS MEDIA Dehiscent of bony canal spread the inflammation of middle ear to epi- and peri-neurium, causes facial paralysis, Facial nerve function is fully recovers if acute otitis media is controlled with systemic antibiotics. Myringotomy or cortical mastoidectomy may sometime required.
    36. 36. AS COMPLICATION OF CHRONIC OTITIS MEDIA Facial paralysis results from cholesteatoma or from penetrating granulation tissue. Cholestatoma destroys bony canal and then cause pressure on nerve. Treatment is urgent exploration of the middle ear and mastoid.
    37. 37. LABYRINTHITIS  Labyrinthitis is an inflammation of the inner ear that is often a complication of infection of the middle ear ( otitis media ). It is usually caused by the spread of bacterial or viral infections from the head or respiratory tract into the inner ear.TYPES OF LABYRINTHITIS: There are three types of labyrinthitis:  Circumscribed Labyrinthitis.  Diffuse Serous Labyrinthitis.  Diffuse Suppurative Labyrinthitis.
    38. 38. Circumscribed Labyrinthitis (Fistula of Labyrinth) There is thinning or erosion of bony capsule of labyrinth, usually of the horizontal semicircular canal.Aetiology: Chronic suppurative otitis media with cholesteatome. (most common) Neoplasms of middle ear e.g. carcinoma or glomus tumour. Surgical or accidental trauma to labyrinth.
    39. 39. Clinical Features: Transient vertigo induced by pressure.Diagnosis: It is diagnosed by “Fistula test” which can be performed in two ways;  Pressure on tragus. • Sudden inward pressure applied on tragus. • Air pressure increase and stimulate the labyrinth. • Patient complain of vertigo. • Nystagmus may also be induced.
    40. 40.  Siegle’s speclum. • Positive pressure is applied to ear canal. • Patient complains of vertigo usually with nystagmus. • Quick component of nystagmus would be toward affected ear (ampullopetal displacement of cupula).Treatment: Mastoid exploration is often required in chronic otitis media and lasteatoma. Systemic antibiotic therapy.
    41. 41. Diffuse Serous Labyrinthitis It is diffuse intralabyrinthine inflammation without pus formation and is a reversible condition if treated early.Aetiology: Pre-existing circumscribed labyrinthitis associated with chronic middle suppuration or cholesteatoma. In acute infections of middle ear, cleft inflammation spreads through annular ligament or the round window. It can follow stapedectomy or fenestration operation.
    42. 42. Clinical Features:  Vertigo.  Nausea.  Vomiting.  Spontaneous nystagmus.  Sensorineural hearing loss.  Suppurative labyrinthitis.  Loss of vestibular and cochlear function.
    43. 43. Treatment: Medical:  Bed rest.  Antibacterial therapy.  Labyrinthine sedatives. • Prochloperazine (stemetil). • Dimenhydrinate (Dramamine).  Myringotomy Surgical:  Cortical mastoidectomy.
    44. 44. Diffuse Suppurative Labyrinthitis This is diffuse pyogenic infection of the labyrinth with permanent loss of vestibular and cochlear function.Aetiology: Serous labyrinthitis. Pyogenic organism invading through surgical or pathalogical fistula .Clinical Features: Severe vertigo. Nausea and vomiting Spontaneous nystagmus. Total loss of hearing.Treatment: Same as for serous labyrinthitis.
    46. 46. EXTRADURAL ABSCESS It is a collection of pus between bone and dura. It may occur both in acute and chronic infection of middle ear.
    47. 47. PATHOLOGY: In acute otitis media, bone over the dura is destroyed by hyperaemic decalcification. In chronic otitis media it is destroyed by cholesteatoma. In such cases, the pus come in direct contact of dura. Infection can be spread by venous thrombophlebitis. In this case bone over dura remain intact. Affected dura may be covered with granulations or appear unhealthy and discoloured.
    48. 48. CLINICAL FEATURES: Persistent headache. Severe pain in the ear. General malaise with low grade fever. Pulsatile purulent ear disscharge. Disappearance of headache with free flow of pus from the ear (Spontaneous abscess drainage).
    49. 49. DIAGNOSIS: CT Scan. MRI.
    50. 50. TREATMENT: Cortical or modified radical or radical mastoidectomy. An antibiotic cover.
    51. 51. SUBDURAL ABSCESS This is collection of pus between dura and archnoid.
    52. 52. PATHOLOGY: Infection spreads from the ear by erosion of bone and dura or by thrombophlebitic process in which case intervening bone remains intact. Pus rapidly spreads in subdural space and comes to lie against the convex surface of cerebral hemisphere causing pressure symptoms.
    53. 53. CLINICAL FEATURES: Meningeal irritation.  Headache.  Fever(102 F or more)  Malaise.  Increasing drowsiness.  Neck rigidity.  Positive Kernig’s sign. Cortical venous thrombophlebitis.  Veins over the cerebral hemisphere undergo thrombophlebitis leading to aphasia, hemiplegia, hemianopia. Raised intracranial tension.  Papilloedema.  Ptosis.  Dilated pupil.
    54. 54. DIAGNOSIS: CT Scan. MRI.
    55. 55. TREATMENT: Craniotomy.  To drain subdural empyema. Intravenous antibiotics.  To control the infection.
    56. 56. MENINGITIS It is inflammation of leptomeninges (pia and archnoid) usually with bacterial invasion of CSF in subarachnoid space.
    57. 57. MODE OF INFECTION: In infants and children;  Blood borne infection. In adults;  Follows chronic ear disease.  Spreads by bone erosion or retrograde thrombophlebitis.  It may associated later with; extradural abscess or granulation tissue.
    58. 58. CLINICAL FEATURES: Fever (102-104F) often with rigors and chills. Headache Neck rigidity Photophobia. Mental irritiablity. Nausea. Vomiting (Projectile). Drowsiness may progress to delirium or coma. Cranial nerve palsies and hemiplegia.
    59. 59. ON EXAMINATION: Neck rigidity. Positive Kerning’s Sign. Positive Brudzinki’s sign. Tendon reflexes.  Exaggerated initially.  Later become sluggish. Papilloedema( seen in late stages).
    60. 60. DIAGNOSIS: CT Scan. MRI Lumbar puncture. CSF Examination.  CSF is turbid.  Cell count is raised.
    61. 61. TREATMENT: Medical:  Antimicrobial therapy. Surgical:  Myringotomy.  Cortical mastoidectomy.
    62. 62. OTOGENIC BRAIN ABSCESS In adults;  75 % of brain abscesses.  Follows chronic suppurative otitis media with cholesteatoma. In children;  25% of brain abscesses.  Follows acute otitis media.
    63. 63. ROUTE OF INFECTION: Direct extension of middle ear infection through tegmen or by retrograde thrombophlebitis. Direct extension through the Trautmann’s triangle or by retrograde thrombophlebitis. Often associated with;  Extradural abscess.  Perisinus abscess.  Sigmoid sinus thrombophlebitis or labyrinthitis.
    64. 64. BACTERIOLOGY: Aerobic includes,  Streptococcus pnemoniae.  Streptococcus haemolyticus.  Proteus mirabilis.  Esch coli.  Ps. Aeruginosa. Anaerobic includes,  Peptostreptococcus.  Bacteroides fragilis.  H.influenzae.
    65. 65. PATHOLOGY: Brain abscess develops through four stages;  Stage of invasion(initial encephalitis).  Stage of localisation(latent abscess).  Stage of enlargement(manifest abscess).  Stage of termination (rupture of abscess).
    66. 66.  Stage of invasion (initial encephalitis)  Patient may have headache.  Low-grade fever  Malaise.  Drowsiness.
    67. 67.  Stage of localization (latent abscess) No symptoms. Stage may last for several weeks.
    68. 68.  Stage of enlargement (manifest abscess) Abscess begins to enlarge. A zone of oedema appears around the abscess. Clinical features at this stage are due to: • Raised intracranial tension. • Disturbance of function in the cerebrum or cerebellum, causing focal symptoms and signs.
    69. 69.  Stage of termination(rupture of abscess)• Expanding abscess ruptures into the ventricle or subarachnoid space resulting in fatal meningitis.
    70. 70. CLINICAL FEATURES: Clinical features can be devided into :  Those due to raised intracranial tenssion.  Those due to area of brain affected (localising features).
    71. 71. Symptoms and signs of raisedintracranial tension: Headache.  Often severe and generalised. Nausea. Vomiting.  Projectile in nature. Level of consciousness.  Lethargy Drowsiness Confusion Stupor Coma. Papilloedema.(Appears Late). Slow pulse. Subnormal temperature.
    72. 72. Localising features: Temporal lobe abscess.  Nominal aphasia.  Homonymous hemianopia.  Contralateral motor paralysis.  Epileptic fits.  Pupillary changes and oculomotor palsy. Cerebellar abscess  Headache  Spontaneous nystagmus  Ipsilateral hypotonia and weakness.  Ipsilateral ataxia.  Past pointing and intention tremor.  Dysdiadokokinesia.
    73. 73. INVESTIGATIONS: Skull X-rays.  Midline shift.  If pineal gland is calcified.  Reveals gas in the abscess cavity. CT Scan.  Site and size of an abscess.  Reveals associated complications. X-Ray mastoids or CT scan of temporal bone.  Evaluate associated ear disease. Lumbar puncture.  Rise in pressure of CSF.  Increase protein content .  Normal glucose level.  CSF contains polymorphs or lymphocytes.
    74. 74. TREATMENT: Medical.  Chloramphenicol.  Cephalosporins third generation.  Aminoglycoside antibiotic.  Dexamethasone/ Mannitol (to lower the intracranial tension). Neurosurgical.  Repeated aspiration through a burr hole.  Excision of abscess.  Open incision of the abscess and evacuation of puss. Otologic.  Treatment of associated ear disease.
    75. 75. LATERAL SINUS THROMBOPHLEBITIS (Syn. Sigmoid Sinus Thrombosis) It is an inflammation of inner wall of lateral venous sinus with formation of a thrombus.
    76. 76. AETIOLOGY: Complication of acute coalescent mastoiditis. Complication of masked mastoiditis. Complication of chronic suppuration of middle ear. Cholesteatoma.
    77. 77. PATHOLOGY: The pathological process can be divided into the following stages.  Formation of perisinus abscess.  Endophlebitis and mural thrombus formation.  Obliteration of sinus lumen and intrasinus abscess.  Extension of thrombus.
    78. 78. BACTERIOLOGY: In acute infection;  Hemolytic streptococcus.  Pneumococcus.  Staphylococcus. In chronic infection with cholesteatomas;  B. proteus.  Ps.pyocyaneus.  Esch. Coli.  Staphylococci.
    79. 79. CLINICAL FEATURE: Hectic Picket-fence type of fever with rigors. Headache. Progressive anaemia and emaciation. Tobey-Ayer test.  To record CSF pressure by manometer.  To see the effect of manual compression of one or both jugular vein.
    80. 80.  Papilloedema. Griesinger’s sign.  due to thrombosis of mastoid emissary vein.  Oedema appears over the posterior part of mastoid. Crowe Beck test.  Pressure on jugular vein of healthy side produces engorgement of retinal veins and supraorbital veins.  Engorgement of veins subside on release of pressure. Tenderness along jugular vein.
    81. 81. INVESTIGATIONS: Blood smear.  To rule out malaria. Blood culture.  To find causative organism. CSF examination.  CSF is normal except of rise in pressure.  To exclude meningitis. X-ray mastoids.  Clouding of air cells (acute mastoiditis.  Destruction of bone (Cholesteatoma). Culture and sensitivity of ear swab.
    82. 82.  Imaging studies.  CT Scan • Show sinus thrombosis by typical delta sign.  MRI • Better delineates thrombus.  MR venography. • To assess progression or resolution of thrombus.
    83. 83. TREATMENT: Intravenous antibacterial therapy. Mastoidectomy and exposure of sinus. Ligation of internal jugular vein.  Rarely required.  Indicated when failure of treatment to control embolic phenomenon and rigors or tenderness and swelling along jugular vein is spreading.
    84. 84.  Anticoagulant therapy.  Rarely required.  Used when thrombosis is extending to cavernous sinus. Supportive treatment.  Repeated blood transfusion.
    85. 85. OTITIC HYDROCEPHALUS It is characterised by raised intracranial pressure with normal CSF finding. It is seen in children and adolscents with acute or chronic middle ear infection.
    86. 86. MECHANISM: Lateral sinus thrombosis accompanying middle ear infection causes obstruction to venous return. If thrombosis extends to superior sagittal sinus, it will also impede the function of arachnoid villi to absorb CSF. Both these factors result in raised intracranial tension.
    87. 87. CLINICAL FEATURES Symptoms:  Severe headache.  Nausea.  Vomiting.  Diplopia due to paralysis of Vith cranial nerve.  Blurring of vision due to papilloedema or optic atrophy. Signs:  Papilloedema may be 5-6 diopters.  Nystagmus due to raised intracranial tension.  Lumber puncture. CSF pressure exceeds 300mm of water (normal70-120mm H2O)
    88. 88. TREATMENT: Medical:  Acetazolamide.  Corticosteroids.  Repeated lumber puncture.  Placement of a lumbar drain.  Middle ear infection may require antibiotic.