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COMPLICATIONS
OF OTITIS MEDIA
HISTORICAL NOTES
● Hippocrates (460 B.C)
“Acute pain of the ear with
continued high fever is to be
dreaded for the patient may
become delirious & die”
● Roman physicist celcus (25 AD)
“Inflammation & pains of the ear lead sometimes to insanity &
death”.
● Arabian physician Avicenna (980-1037 AD) stated that the ear
discharge was due to the brain disease.
● Morgagni (1682-1771), noted that the ear infection comes first
before the brain abscess.
● McEwen in 1881 showed great surgical success - 18 patients
recovered out of 19 operated cases of brain abscess.
Factors influencing development of complications
● Infective organism
● Virulence
● Susceptibility to antibiotics
● Adequacy of medication
● Resistance of host
● Type of pneumatization
● History of previous otitis media.
DEFENSE MECHANISM
● Ability of mucous membrane to localise & overcome infection.
● Intact bony walls of tympanic cavity & pneumatic cells.
● Granulation tissue.
PATHWAYS OF SPREAD
OSTEO
THROMBOPHLEBITIS
BONE EROSION
PREFORMED PATHWAYS
OSTEOTHROMBOPHLEBITIS
➢ Infection pass from lining mucosa of the middle ear & mastoid
through intact bone by progressive thrombophlebitis of small
venules.
➢ Occur in acute middle ear infection or acute exacerbations of
chronic infection.
➢ Complication occurs early.
➢ Prodromal period is lacking.
➢ Bony walls of the middle ear & mastoid is intact.
➢ Bone & mucoperiosteum lining of mastoid air cells are inflamed and
bleed easily.
BONE EROSION
➢ Nearly always the manner of spread in COM.
➢ Complication occurs several weeks later.
➢ A prodromal period of partial or intermittent involvement precedes
diffuse involvement.
➢ At operation, dehiscence of the bony barrier is found.
➢ A layer of granulation cover the exposed soft tissue of neighbouring
structure.
➢ Treatment should always include the removal of suppurating, bone
eroding focus.
PREFORMED PATHWAYS
● Normal anatomical pathways.
● Developmental dehiscence.
● Acquired.
COMPLICATIONS
● MENINGITIS
● OTOGENIC BRAIN ABSCESS
● OTOGENIC SUPPURATIVE THROMBOPHLEBITIS
● OTITIC HYDROCEPHALUS
● SUBDURAL EMPYEMA
● EPIDURAL (EXTRADURAL) ABSCESS
MENINGITIS
❖ MC intracranial complication of otitis media.
❖ Spreads directly through necrotic bone of middle ear.
❖ As a complication of suppurative labyrinthitis, through Internal
Acoustic meatus, vestibular & cochlear aqueducts.
contd...
Pia-arachnoid inflamed
Outpouring of fluid in the subarachnoid space
Raised intracranial pressure
White blood cells & multiplying organisms in CSF
Irritation of upper cervical nerve roots
symptoms:
❖ Headache
❖ Fever
❖ Vomiting
❖ Photophobia
❖ irritability
❖ Neck pain
❖ Stiffness
❖ General hyperesthesia
SIGNS:
❖ KERNIG SIGN
❖ BRUDZINSKI SIGN
INVESTIGATIONS
❖ HRCT.
❖ MRI with gadolinium contrast.
❖ Lumbar puncture
➢ Turbid,purulent
➢ Glucose nearly to zero
➢ Protein content
➢ Polymorphs in CSF
➢ Gram staining
➢ Culture & sensitivity.
TREATMENT
❖ HIGH DOSE ANTIBIOTICS
➢ Empirical therapy:
3rd generation cephalosporins + vancomycin.
❖ CORTICOSTEROIDS
➢ A 4 day regime of 0.6 mg/kg/day in four divided doses
started before or with the antibiotics.
SURGERY : surgical exterenation of the diseased mastoid once
patient is stabilised.
OTOGENIC BRAIN ABSCESS
➢ Focal suppurative process within the brain parenchyma
surrounded by a region of encephalitis.
➢ Often the result of venous thrombophlebitis rather than direct
dural extension.
➢ Can occur in temporal lobe or cerebellum.
➢ Polymicrobial culture including anaerobes:
○ Gram +ve-> streptococcus & staphylococcus species
○ Gram -ve -> E coli, proteus, klebsiella & pseudomonas.
○ Anaerobic -> bacteroides.
STAGES
SYMPTOMS
● GENERAL : toxic, drowsy, deep bony pain, triad of headache,
high grade fever, focal neurological deficits,papilloedema.
● TEMPORAL LOBE ABSCESS:
○ seizures.
○ Nominal aphasia.
○ Quadrantic Homonymous hemianopia.
○ Motor paralysis of contralateral side.
● CEREBELLAR ABSCESS:
○ Ataxia.
○ Nystagmus.
○ Dysmetria.
○ Dysdiadochokinesia.
INVESTIGATIONS
CT BRAIN WITH CONTRAST: RING SIGN
-
TREATMENT
➢ MEDICAL
○ High dose IV broad spectrum antibiotics
○ Dexamethasone
○ Anti epileptic- phenytoin.
➢ SURGICAL:
○ Neurosurgical intervention of draining the abscess is quintessential
○ Once the patient is stable , mastoidectomy can be done.
OTOGENIC SUPPURATIVE THROMBOPHLEBITIS
➢ Simultaneous presence of venous thrombosis & suppuration in
the intracranial cavity.
➢ Often associated with perisinus extradural abscess.
➢ Can also occur by osteo thrombophlebitic extension via small
venules.
➢ The infected mural thrombus can extend cranially to sagittal
sinus or cavernous sinus via superior & inferior petrosal sinus.
➢ It can also extend caudally to Internal Jugular vein thereby to
the right atrium.
DURAL VENOUS SINUSES
PATHOGENESIS
Erosion of the bone covering the sigmoid sinus
Immune status of host osteothrombophlebitic extension
Perisinus abscess/inflammation
Inflammation of outer wall (dura) of sinus
Inflammation of intima (inner wall of sinus)
Platelet, RBCs,fibrin,WBCs
Adhere to inflamed area
MURAL THROMBUS
Mural thrombus propagates, obliterating lumen
CLINICAL FEATURES
➢ Picket fence fever, with diurnal temp exceeding 103℉
➢ Headache
➢ Griesinger ’s sign
➢ Papilloedema
➢ Vision loss
➢ Tenderness along the anterior border of sternomastoid muscle
➢ Proptosis & chemosis - CST
➢ Otalgia
➢ Queckenstedt or Tobey-ayer test.
INVESTIGATION
➢ Blood culture
➢ Lumbar puncture test
➢ CECT - DELTA “𝚫” sign in lateral sinus thrombosis
➢ MR angiography.
TREATMENT
➢ High dose antibiotics
➢ Anticoagulation if CST
present.
➢ Surgical exploration &
removal of clot.
➢ Internal jugular vein ligation.
OTITIC HYDROCEPHALUS
➢ Raised intracranial pressure with normal CSF findings.
➢ Benign raised intracranial tension.
➢ Commonly associated with sigmoid sinus thrombosis.
➢ Spontaneous recovery.
MECHANISM
➢ SYMOND: retrograde extension of thrombophlebitis from sigmoid sinus
to superior sagittal sinus
Blockage of arachnoid villi
CSF absorption & secretion
➢ Increase in CSF volume
➢ Secondary to brain edema
➢ Disruption in venous circulation.
CLINICAL FEATURES
➢ Headache
➢ Drowsiness
➢ Vomiting
➢ Blurring of vision
➢ Diplopia
➢ Papilloedema
➢ 6th cranial nerve palsy
➢ Optic atrophy
INVESTIGATIONS
➢ LUMBAR PUNCTURE
○ Elevated CSF pressure with normal biochemistry.
○ Done with caution.
➢ CT SCAN
➢ MRI:
○ Imaging modality of choice.
○ Allows superior evaluation of venous sinuses.
TREATMENT
➢ Eradicate ear disease.
➢ Lowering of CSF pressure:
○ Decompression of sigmoid sinus.
○ CSF drainage procedures.
○ Optic sheath decompression : to prevent optic atrophy.
➢ MEDICAL:
○ Corticosteroids.
○ Mannitol.
○ Acetazolamide.
○ Diuretics.
EPIDURAL (EXTRADURAL) ABSCESS
➢ Occurs after bone demineralisation or bone erosion adjacent to the
middle or posterior fossa sura.
➢ Middle fossa extradural abscess:
○ Lateral: erosion of tegmen tympani, strip a large area of dura
from the inner surface of squamous temporal bone.
○ Medial: infection of petrous apex causes middle fossa
extradural abscess medial to arcuate eminence, irritates
trigeminal nerve & 6th cranial nerve. ( gradenigo syn).
➢ Posterior fossa extradural abscess:
○ In close association with lateral sinus.
○ Spread is laterally limited by internal acoustic meatus.
CLINICAL FEATURES
➢ Usually asymptomatic
➢ Gradenigo syndrome:
○ Otorrhea
○ Retro orbital pain
○ Diplopia
➢ Persistent headache on the side of otitis media.
➢ General malaise with low grade fever.
➢ Disappearance of headache with free flow of pus from the ear (
spontaneous abscess drainage).
➢ DIAGNOSIS:
Contrast enhanced CT or MRI.
➢ TREATMENT:
Antimicrobial therapy.
Surgical exploration.
SUBDURAL EMPYEMA
➢ Collection of pus between dura and arachnoid mater.
➢ Spread of infection through the dura with formation of granulation
tissue in the subdural space.
PATHOLOGY:
OTITIS MEDIA
EROSION OF TEGMEN BRAIN ABSCESS THROMBOPHLEBITIS
EROSION OF DURA BRAIN ABSCESS RUPTURES
INFECTION IN SUBDURAL SPACE
EXPANDING MASS LESION
CLINICAL FEATURES
➢ Meningeal irritation:
○ Fever.
○ Headache.
○ Malaise, drowsiness.
○ Kernig sign
➢ Thrombophlebitis:
○ Aphasia
○ Hemianopia
○ Hemiplegia
○ Jacksonian convulsions
➢ Raised ICP
○ 3rd nerve involvement
○ papilloedema
DIAGNOSIS by CT or MRI
➢ TREATMENT:
○ Surgical drainage of abscess.
○ High dose IV antibiotics.
○ Once stabilised neurologically, then underlying ear disease
managed.
○ Antiepileptic medication
Extracranial (intratemporal) complications
● Mastoiditis
● Petrositis
● Labyrinthitis
● Facial paralysis
Extracranial ( extratemporal) complications
● Subperiosteal abscess
● Bezold’s abscess
● Zygomatic ( Luc’s abscess/Meatal)
● Digastric ( Citelli’s abscess)
ACUTE MASTOIDITIS
● It is the extension of middle ear inflammation into antrum &
mastoid air cells.
● Mastoid antrum & epitympanum communicate freely through
aditus ad antrum.
● Common in children.
● Causative organisms include strep. pneumoniae , strep
pyogenes, staph aureus, Haemophilus influenzae, and
pseudomonas aeruginosa.
Pathogenesis
● Following otitis media - tympanomastoiditis.
● Blockade of aditus - loculation of mucopurulent material within
antrum and air cells.
● Persistent blockade of aditus - retrograde thrombophlebitis -
edema and cellulitis of tissues overlying mastoid.
● If pus not drained - necrosis and demineralisation of bony
trabeculae - ‘coalescent mastoiditis’.
● Where the entire mastoid becomes a single cavity filled with pus.
Clinical features
Symptoms:
● Earache
● Fever
● Ear discharge - profuse and purulent
Signs:
● Mastoid tenderness.
● Sagging of postero-superior meatal wall
● TM perforation
● Swelling, redness, bulging over the mastoid (ironed out mastoid)
● Hearing loss ( conductive)
investigations
● Aural swab for culture & sensitivity
● HRCT temporal bone
TREATMENT
● Hospitalization.
● IV antibiotics.
● Myringotomy.
● Cortical mastoidectomy.
Sequelae of acute coalescent mastoiditis
● Subperiosteal abscess
● Bezold’ abscess
● Citelli’s abscess
● Luc’s abscess
● Petrositis
● Labyrinthitis
● Facial paralysis
● Meningitis
● Brain abscess
● Sigmoid sinus thrombophlebitis.
Sites of pneumatization of mastoid air cell system in
relation to types of mastoid abscess
MASKED MASTOIDITIS
Slow destruction of mastoid air cells.
Acute sign & symptoms of acute mastoiditis are absent.
Inadequate antibiotic therapy - dose, frequency, duration.
Pain, discharge, fever, mastoid swelling - absent.
Mostly progress to complication.
Mastoidectomy - extensive destruction of air cells
Granulation tissue
Dark gelatinous material filling the mastoid.
PETROSITIS
Inflammation of pneumatized spaces of the petrous part of the temporal
bone.
Petrous bone - two groups of air cell tracts- communicate mastoid &
middle ear to the petrous apex.
Postero superior tract: in continuity with mastoid antrum, epitympanum
that clusters around semicircular canals at the base of pyramid.
Antero inferior tract: In continuity with the mesotympanum,
protympanum, and hypotympanum & passes around the cochlea to
petrous apex.
Petrositis may be acute or chronic.
● Acute petrositis
● Middle ear inflammation- antrum and mastoid
air cells - medial progression involving petrous
pyramid.
● If inflammatory products are retained- osteitis
of petrous apex .
● Gradenigo syndrome -
● Ear discharge
● Retro Orbital pain (Trigeminal nerve)
● Diplopia ( lateral rectus palsy -
Abducens nerve)
● Chronic petrositis
● In addition to inflammatory changes - new bone
formation & resorption
Management :
Investigations:
● CT temporal bone.
Treatment :
● Systemic antibiotics.
● Radical mastoidectomy with skeletonization
of semicircular canals to remove disease
from middle ear and petrous apex.
● Approaches to petrous apex
● Eagleton’s approach.
● Thornwalt’s operation.
● Almoor’s approach.
● Ramadier’ s operation.
● Freckner’s operation.
Surgical approaches to petrous apex
FACIAL NERVE PARALYSIS
Complication of both acute and chronic otitis media.
ROUTES OF SPREAD:
● Natural dehiscence - dehiscence of fallopian canal.
● Natural pathways - ex, canal for stapedius, neurovascular bundle.
● Direct extension - ex, osteitis around fallopian canal.
Toxins and ischemia probably have an ancillary role.
TREATMENT:
In AOM- myringotomy & appropriate antibiotic for 10 days.
In COM - CWD mastoidectomy with decompression of the fallopian
canal, antibiotics.
LABYRINTHITIS
Inflammation of inner ear/ labyrinth.
Pathogenesis:
-spread through round window, fistula, preformed pathways.
-inflammatory products pass into perilymph of scala tympani by
diapedesis from adjacent labyrinthine vessels.
- fibrillary precipitate accumulates in perilymphatic and
endolymphatic spaces.
Symptoms & signs
● Vertigo
● Loss of balance
● nausea/ vomiting
● nystagmus
● High frequency SNHL
● Hearing distortion
● diplacusis
Treatment
● Complete bed rest - with restriction of head movement
● Parenteral chlorperazine / cinnarizine
● Dehydration - IV fluids.
● IV antibiotics.
● Acute infection - Myringotomy
● Chronic infection - mastoid exploration
Labyrinthine fistula
Complication of COM
Results from erosion of endochondral bone of bony labyrinth- movement
of perilymph and structures of endolymphatic compartments when
pressure in EAC changes.
Most commonly - dome of lateral SCC.
Cholesteatoma found in all cases.
Incidence of fistula in cholesteatoma is 7-10%
symptoms/signs
● Short periods of imbalance.
● Vertigo
● Tullio’s phenomenon - feeling of imbalance on sudden exposure to
loud noises.
● Fistula sign - positive.
● Investigations
● CT - erosion of lateral SCC
● cholesteatoma
Treatment
Canal wall down mastoidectomy
- All cholesteatoma is removed except for small area around fistula
site. After careful removal of cholesteatoma debri without
disturbing matrix. Matrix is elevated. A small piece of tissue / thin
cap of bone placed over site and secured with fibrin glue / packing
after the cholesteatoma is removed.
- Risk of removing cholesteatoma from fistula is total / partial loss of
hearing.
THANK YOU

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COMPLICATIONS OF OTITIS MEDIA.pptx

  • 2. HISTORICAL NOTES ● Hippocrates (460 B.C) “Acute pain of the ear with continued high fever is to be dreaded for the patient may become delirious & die”
  • 3. ● Roman physicist celcus (25 AD) “Inflammation & pains of the ear lead sometimes to insanity & death”. ● Arabian physician Avicenna (980-1037 AD) stated that the ear discharge was due to the brain disease. ● Morgagni (1682-1771), noted that the ear infection comes first before the brain abscess. ● McEwen in 1881 showed great surgical success - 18 patients recovered out of 19 operated cases of brain abscess.
  • 4. Factors influencing development of complications ● Infective organism ● Virulence ● Susceptibility to antibiotics ● Adequacy of medication ● Resistance of host ● Type of pneumatization ● History of previous otitis media.
  • 5. DEFENSE MECHANISM ● Ability of mucous membrane to localise & overcome infection. ● Intact bony walls of tympanic cavity & pneumatic cells. ● Granulation tissue.
  • 7. OSTEOTHROMBOPHLEBITIS ➢ Infection pass from lining mucosa of the middle ear & mastoid through intact bone by progressive thrombophlebitis of small venules. ➢ Occur in acute middle ear infection or acute exacerbations of chronic infection. ➢ Complication occurs early. ➢ Prodromal period is lacking. ➢ Bony walls of the middle ear & mastoid is intact. ➢ Bone & mucoperiosteum lining of mastoid air cells are inflamed and bleed easily.
  • 8. BONE EROSION ➢ Nearly always the manner of spread in COM. ➢ Complication occurs several weeks later. ➢ A prodromal period of partial or intermittent involvement precedes diffuse involvement. ➢ At operation, dehiscence of the bony barrier is found. ➢ A layer of granulation cover the exposed soft tissue of neighbouring structure. ➢ Treatment should always include the removal of suppurating, bone eroding focus.
  • 9. PREFORMED PATHWAYS ● Normal anatomical pathways. ● Developmental dehiscence. ● Acquired.
  • 10. COMPLICATIONS ● MENINGITIS ● OTOGENIC BRAIN ABSCESS ● OTOGENIC SUPPURATIVE THROMBOPHLEBITIS ● OTITIC HYDROCEPHALUS ● SUBDURAL EMPYEMA ● EPIDURAL (EXTRADURAL) ABSCESS
  • 11.
  • 12. MENINGITIS ❖ MC intracranial complication of otitis media. ❖ Spreads directly through necrotic bone of middle ear. ❖ As a complication of suppurative labyrinthitis, through Internal Acoustic meatus, vestibular & cochlear aqueducts.
  • 13. contd... Pia-arachnoid inflamed Outpouring of fluid in the subarachnoid space Raised intracranial pressure White blood cells & multiplying organisms in CSF Irritation of upper cervical nerve roots
  • 14.
  • 15. symptoms: ❖ Headache ❖ Fever ❖ Vomiting ❖ Photophobia ❖ irritability ❖ Neck pain ❖ Stiffness ❖ General hyperesthesia
  • 16. SIGNS: ❖ KERNIG SIGN ❖ BRUDZINSKI SIGN
  • 17. INVESTIGATIONS ❖ HRCT. ❖ MRI with gadolinium contrast. ❖ Lumbar puncture ➢ Turbid,purulent ➢ Glucose nearly to zero ➢ Protein content ➢ Polymorphs in CSF ➢ Gram staining ➢ Culture & sensitivity.
  • 18. TREATMENT ❖ HIGH DOSE ANTIBIOTICS ➢ Empirical therapy: 3rd generation cephalosporins + vancomycin. ❖ CORTICOSTEROIDS ➢ A 4 day regime of 0.6 mg/kg/day in four divided doses started before or with the antibiotics. SURGERY : surgical exterenation of the diseased mastoid once patient is stabilised.
  • 19. OTOGENIC BRAIN ABSCESS ➢ Focal suppurative process within the brain parenchyma surrounded by a region of encephalitis. ➢ Often the result of venous thrombophlebitis rather than direct dural extension. ➢ Can occur in temporal lobe or cerebellum. ➢ Polymicrobial culture including anaerobes: ○ Gram +ve-> streptococcus & staphylococcus species ○ Gram -ve -> E coli, proteus, klebsiella & pseudomonas. ○ Anaerobic -> bacteroides.
  • 21. SYMPTOMS ● GENERAL : toxic, drowsy, deep bony pain, triad of headache, high grade fever, focal neurological deficits,papilloedema. ● TEMPORAL LOBE ABSCESS: ○ seizures. ○ Nominal aphasia. ○ Quadrantic Homonymous hemianopia. ○ Motor paralysis of contralateral side. ● CEREBELLAR ABSCESS: ○ Ataxia. ○ Nystagmus. ○ Dysmetria. ○ Dysdiadochokinesia.
  • 22. INVESTIGATIONS CT BRAIN WITH CONTRAST: RING SIGN -
  • 23. TREATMENT ➢ MEDICAL ○ High dose IV broad spectrum antibiotics ○ Dexamethasone ○ Anti epileptic- phenytoin. ➢ SURGICAL: ○ Neurosurgical intervention of draining the abscess is quintessential ○ Once the patient is stable , mastoidectomy can be done.
  • 24. OTOGENIC SUPPURATIVE THROMBOPHLEBITIS ➢ Simultaneous presence of venous thrombosis & suppuration in the intracranial cavity. ➢ Often associated with perisinus extradural abscess. ➢ Can also occur by osteo thrombophlebitic extension via small venules. ➢ The infected mural thrombus can extend cranially to sagittal sinus or cavernous sinus via superior & inferior petrosal sinus. ➢ It can also extend caudally to Internal Jugular vein thereby to the right atrium.
  • 26.
  • 27. PATHOGENESIS Erosion of the bone covering the sigmoid sinus Immune status of host osteothrombophlebitic extension Perisinus abscess/inflammation Inflammation of outer wall (dura) of sinus Inflammation of intima (inner wall of sinus) Platelet, RBCs,fibrin,WBCs Adhere to inflamed area MURAL THROMBUS Mural thrombus propagates, obliterating lumen
  • 28. CLINICAL FEATURES ➢ Picket fence fever, with diurnal temp exceeding 103℉ ➢ Headache ➢ Griesinger ’s sign ➢ Papilloedema ➢ Vision loss ➢ Tenderness along the anterior border of sternomastoid muscle ➢ Proptosis & chemosis - CST ➢ Otalgia ➢ Queckenstedt or Tobey-ayer test.
  • 29.
  • 30. INVESTIGATION ➢ Blood culture ➢ Lumbar puncture test ➢ CECT - DELTA “𝚫” sign in lateral sinus thrombosis ➢ MR angiography.
  • 31. TREATMENT ➢ High dose antibiotics ➢ Anticoagulation if CST present. ➢ Surgical exploration & removal of clot. ➢ Internal jugular vein ligation.
  • 32. OTITIC HYDROCEPHALUS ➢ Raised intracranial pressure with normal CSF findings. ➢ Benign raised intracranial tension. ➢ Commonly associated with sigmoid sinus thrombosis. ➢ Spontaneous recovery.
  • 33. MECHANISM ➢ SYMOND: retrograde extension of thrombophlebitis from sigmoid sinus to superior sagittal sinus Blockage of arachnoid villi CSF absorption & secretion ➢ Increase in CSF volume ➢ Secondary to brain edema ➢ Disruption in venous circulation.
  • 34. CLINICAL FEATURES ➢ Headache ➢ Drowsiness ➢ Vomiting ➢ Blurring of vision ➢ Diplopia ➢ Papilloedema ➢ 6th cranial nerve palsy ➢ Optic atrophy
  • 35. INVESTIGATIONS ➢ LUMBAR PUNCTURE ○ Elevated CSF pressure with normal biochemistry. ○ Done with caution. ➢ CT SCAN ➢ MRI: ○ Imaging modality of choice. ○ Allows superior evaluation of venous sinuses.
  • 36. TREATMENT ➢ Eradicate ear disease. ➢ Lowering of CSF pressure: ○ Decompression of sigmoid sinus. ○ CSF drainage procedures. ○ Optic sheath decompression : to prevent optic atrophy. ➢ MEDICAL: ○ Corticosteroids. ○ Mannitol. ○ Acetazolamide. ○ Diuretics.
  • 37. EPIDURAL (EXTRADURAL) ABSCESS ➢ Occurs after bone demineralisation or bone erosion adjacent to the middle or posterior fossa sura. ➢ Middle fossa extradural abscess: ○ Lateral: erosion of tegmen tympani, strip a large area of dura from the inner surface of squamous temporal bone. ○ Medial: infection of petrous apex causes middle fossa extradural abscess medial to arcuate eminence, irritates trigeminal nerve & 6th cranial nerve. ( gradenigo syn). ➢ Posterior fossa extradural abscess: ○ In close association with lateral sinus. ○ Spread is laterally limited by internal acoustic meatus.
  • 38. CLINICAL FEATURES ➢ Usually asymptomatic ➢ Gradenigo syndrome: ○ Otorrhea ○ Retro orbital pain ○ Diplopia ➢ Persistent headache on the side of otitis media. ➢ General malaise with low grade fever. ➢ Disappearance of headache with free flow of pus from the ear ( spontaneous abscess drainage).
  • 39. ➢ DIAGNOSIS: Contrast enhanced CT or MRI. ➢ TREATMENT: Antimicrobial therapy. Surgical exploration.
  • 40. SUBDURAL EMPYEMA ➢ Collection of pus between dura and arachnoid mater. ➢ Spread of infection through the dura with formation of granulation tissue in the subdural space.
  • 41. PATHOLOGY: OTITIS MEDIA EROSION OF TEGMEN BRAIN ABSCESS THROMBOPHLEBITIS EROSION OF DURA BRAIN ABSCESS RUPTURES INFECTION IN SUBDURAL SPACE EXPANDING MASS LESION
  • 42. CLINICAL FEATURES ➢ Meningeal irritation: ○ Fever. ○ Headache. ○ Malaise, drowsiness. ○ Kernig sign ➢ Thrombophlebitis: ○ Aphasia ○ Hemianopia ○ Hemiplegia ○ Jacksonian convulsions ➢ Raised ICP ○ 3rd nerve involvement ○ papilloedema
  • 43. DIAGNOSIS by CT or MRI ➢ TREATMENT: ○ Surgical drainage of abscess. ○ High dose IV antibiotics. ○ Once stabilised neurologically, then underlying ear disease managed. ○ Antiepileptic medication
  • 44. Extracranial (intratemporal) complications ● Mastoiditis ● Petrositis ● Labyrinthitis ● Facial paralysis
  • 45. Extracranial ( extratemporal) complications ● Subperiosteal abscess ● Bezold’s abscess ● Zygomatic ( Luc’s abscess/Meatal) ● Digastric ( Citelli’s abscess)
  • 46. ACUTE MASTOIDITIS ● It is the extension of middle ear inflammation into antrum & mastoid air cells. ● Mastoid antrum & epitympanum communicate freely through aditus ad antrum. ● Common in children. ● Causative organisms include strep. pneumoniae , strep pyogenes, staph aureus, Haemophilus influenzae, and pseudomonas aeruginosa.
  • 47. Pathogenesis ● Following otitis media - tympanomastoiditis. ● Blockade of aditus - loculation of mucopurulent material within antrum and air cells. ● Persistent blockade of aditus - retrograde thrombophlebitis - edema and cellulitis of tissues overlying mastoid. ● If pus not drained - necrosis and demineralisation of bony trabeculae - ‘coalescent mastoiditis’. ● Where the entire mastoid becomes a single cavity filled with pus.
  • 48. Clinical features Symptoms: ● Earache ● Fever ● Ear discharge - profuse and purulent Signs: ● Mastoid tenderness. ● Sagging of postero-superior meatal wall ● TM perforation ● Swelling, redness, bulging over the mastoid (ironed out mastoid) ● Hearing loss ( conductive)
  • 49. investigations ● Aural swab for culture & sensitivity ● HRCT temporal bone
  • 50. TREATMENT ● Hospitalization. ● IV antibiotics. ● Myringotomy. ● Cortical mastoidectomy.
  • 51. Sequelae of acute coalescent mastoiditis ● Subperiosteal abscess ● Bezold’ abscess ● Citelli’s abscess ● Luc’s abscess ● Petrositis ● Labyrinthitis ● Facial paralysis ● Meningitis ● Brain abscess ● Sigmoid sinus thrombophlebitis.
  • 52. Sites of pneumatization of mastoid air cell system in relation to types of mastoid abscess
  • 53. MASKED MASTOIDITIS Slow destruction of mastoid air cells. Acute sign & symptoms of acute mastoiditis are absent. Inadequate antibiotic therapy - dose, frequency, duration. Pain, discharge, fever, mastoid swelling - absent. Mostly progress to complication. Mastoidectomy - extensive destruction of air cells Granulation tissue Dark gelatinous material filling the mastoid.
  • 54. PETROSITIS Inflammation of pneumatized spaces of the petrous part of the temporal bone. Petrous bone - two groups of air cell tracts- communicate mastoid & middle ear to the petrous apex. Postero superior tract: in continuity with mastoid antrum, epitympanum that clusters around semicircular canals at the base of pyramid. Antero inferior tract: In continuity with the mesotympanum, protympanum, and hypotympanum & passes around the cochlea to petrous apex. Petrositis may be acute or chronic.
  • 55. ● Acute petrositis ● Middle ear inflammation- antrum and mastoid air cells - medial progression involving petrous pyramid. ● If inflammatory products are retained- osteitis of petrous apex . ● Gradenigo syndrome - ● Ear discharge ● Retro Orbital pain (Trigeminal nerve) ● Diplopia ( lateral rectus palsy - Abducens nerve) ● Chronic petrositis ● In addition to inflammatory changes - new bone formation & resorption
  • 56. Management : Investigations: ● CT temporal bone. Treatment : ● Systemic antibiotics. ● Radical mastoidectomy with skeletonization of semicircular canals to remove disease from middle ear and petrous apex. ● Approaches to petrous apex ● Eagleton’s approach. ● Thornwalt’s operation. ● Almoor’s approach. ● Ramadier’ s operation. ● Freckner’s operation.
  • 57. Surgical approaches to petrous apex
  • 58. FACIAL NERVE PARALYSIS Complication of both acute and chronic otitis media. ROUTES OF SPREAD: ● Natural dehiscence - dehiscence of fallopian canal. ● Natural pathways - ex, canal for stapedius, neurovascular bundle. ● Direct extension - ex, osteitis around fallopian canal. Toxins and ischemia probably have an ancillary role. TREATMENT: In AOM- myringotomy & appropriate antibiotic for 10 days. In COM - CWD mastoidectomy with decompression of the fallopian canal, antibiotics.
  • 59. LABYRINTHITIS Inflammation of inner ear/ labyrinth. Pathogenesis: -spread through round window, fistula, preformed pathways. -inflammatory products pass into perilymph of scala tympani by diapedesis from adjacent labyrinthine vessels. - fibrillary precipitate accumulates in perilymphatic and endolymphatic spaces.
  • 60. Symptoms & signs ● Vertigo ● Loss of balance ● nausea/ vomiting ● nystagmus ● High frequency SNHL ● Hearing distortion ● diplacusis
  • 61. Treatment ● Complete bed rest - with restriction of head movement ● Parenteral chlorperazine / cinnarizine ● Dehydration - IV fluids. ● IV antibiotics. ● Acute infection - Myringotomy ● Chronic infection - mastoid exploration
  • 62. Labyrinthine fistula Complication of COM Results from erosion of endochondral bone of bony labyrinth- movement of perilymph and structures of endolymphatic compartments when pressure in EAC changes. Most commonly - dome of lateral SCC. Cholesteatoma found in all cases. Incidence of fistula in cholesteatoma is 7-10%
  • 63. symptoms/signs ● Short periods of imbalance. ● Vertigo ● Tullio’s phenomenon - feeling of imbalance on sudden exposure to loud noises. ● Fistula sign - positive. ● Investigations ● CT - erosion of lateral SCC ● cholesteatoma
  • 64. Treatment Canal wall down mastoidectomy - All cholesteatoma is removed except for small area around fistula site. After careful removal of cholesteatoma debri without disturbing matrix. Matrix is elevated. A small piece of tissue / thin cap of bone placed over site and secured with fibrin glue / packing after the cholesteatoma is removed. - Risk of removing cholesteatoma from fistula is total / partial loss of hearing.