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Subtitle
Complications Of CSOM
Define complication with reference to CSOM
Enumerate the complications of CSOM
Identify a case of CSOM with complications
based on clinical features
Evaluation & management of CSOM with
complications
OBJECTIVES
Spread of infection beyond the confines of the
mucosal spaces of middle ear cleft
Definition
Complications of csom
 Meningitis
 Sigmoid sinus thrombosis
 Brain abscess
 Extradural abscess
 Subdural abscess
 Otitic hydrocephalus
Intra cranial complications
Mastoiditis
Petrositis
Labyrinthitis
Facial paralysis
Extracranial ( Intratemporal ) complications
Sub periosteal abscess
Bezold’s abscess
Zygomatic ( Luc’s abscess/ Meatal )
Digastric ( Cittelli’s abscess)
Extracranial ( Extratemporal ) complications
Attico antral disease ( cholesteatoma )
Highly virulent organism
Poor host immune response
Presence of preformed pathways for spread
Extremes of age
poor socioeconomic status
Predisposing factors
 Bone erosion
 Suppurative retrograde thrombophlebitis
 Preformed pathways
Routes of spread
 In ASOM-Hyperemic decalcification
 In CSOM-Cholesteatoma or granulation tissue.
Direct bone erosion
Suppurative retrograde thrombophlebitis
 Congenital dehiscence: Dehiscence in facial canal and over the
jugular bulb
 Patent sutures: Petro squamous suture
 Temporal bone fractures: The fibrous scar permits infection
 Surgical defects: Stapedectomy, fenestration and exposure of dura
 Perilymphatic fistula: Congenital or acquired
 Normal anatomical openings: Infection of labyrinth and from labyrinth
Preformed pathways
 Ear pain
 Fever
 Severe headache
 Projectile vomiting
 Neck stiffness
 Photophobia
 Irritability / altered consciousness.
Features of impending complications
 when infection spreads from the mucosa lining the mastoid air cells
to involve bony walls of the mastoid air cell system
Mastoiditis
Acute coalescent mastoiditis
Clinical Features of acute mastoiditis
Symptoms
 Earache
 Fever
 Ear discharge-profuse & purulent
Signs
 Mastoid tenderness
 Sagging of postero-superior meatal wall
 Eardrum perforation
 Swelling, redness and bulging over the mastoid ( ironed out mastoid )
 Hearing loss (conductive)
The persistence of otorrhea beyond 3 weeks in a case of AOM indicates
mastoiditis
 HRCT Temporal Bone Aural swab for culture &
sensitivity
Investigations
 Hospitalization
 I.V antibiotics
 Myringotomy
 Cortical mastoidectomy
TREATMENT
 Subperiosteal abscess
 Bezold’s abscess
 Cittelli's abscess
 Luc’s abscess
 Petrositis
 Labyrinthitis
 Facial paralysis
Sequelae of acute coalescent mastoiditis
Luc’s
abscess
Luc’s
abscess
Subperiosteal
abscess
Subperiosteal
abscess
Bezold’s abscessBezold’s abscess
Bezold’s abscess
slow destruction of mastoid air cells
acute sign and symptoms of acute mastoiditis are absent
Inadequate antibiotic therapy - Dose, frequency ,duration
pain, discharge, fever , mastoid swelling - Absent
mastoidectomy -extensive destruction of the air cells with
granulation tissue and dark gelatinous material filling the mastoid
Masked mastoiditis
 Petrous bone - pneumatized in about 30% individuals
 Two groups of air cells’ tracts -communicate mastoid and
middle ear to the petrous apex
 Postero superior tract: From the attic and antrum the tract
passes around semicircular canals to petrous apex
 Antero inferior tract: From the hypotympanum the tract
passes around the ET and cochlea to the petrous apex
 Infection may pass through these cell tracts and reach petrous
apex
Petrositis
Cranial nerve VI palsy
Deep seated ear or retro-orbital pain
Persistent ear discharge
Persistent ear discharge in cases of cortical or modified
radical mastoidectomy may be due to Petrositis.
Gradenigo’s syndrome or triad
Management
HRCT
I.V antibiotics
Surgical exploration
complication of both acute and chronic otitis media
Due to dehiscent facial canal-ASOM
Destruction of facial canal- CSOM-AAD
Treatment- in ASOM- myringotomy
- in CSOM- Cortical Mastoidectomy
Facial nerve paralysis
 Acute inflammation of the labyrinth
 Diffusion of toxins via the round window from the middle ear –
Serous Labyrinthitis
 Labyrinthine fistula caused by hyperemic decalcification-
Circumscribed Labyrinthitis
 Pyogenic infection of the labyrinth- suppurative Labyrinthitis
 Retrospective diagnosis –with treatment improves in serous
labyrinthitis
LABYRINTHITIS
 inflammation of leptomeninges (pia-arachnoid)and CSF of
subarachnoid space
 most common intracranial complication
 One third cases of meningitis are otogenic in origin
Otogenic meningitis
 Circumscribed meningitis: no bacteria in CSF.
 Generalized meningitis: bacteria are present in CSF
 Retrograde thrombophlebitis, bone erosion, preformed
pathways.
 Through oval and round windows.
 Via perineural spaces to int. auditory canal or via endolymphatic
ducts.
 Fracture, Dural tear, CSF leak
Serous stage: characterized by outpouring of fluid and
increased CSF pressure.
Cellular stage: characterized by increase number of
cells especially lymphocytes.
Bacterial stage: bacteria and polymorph nuclear
leucocytes are present in large numbers
stages of generalized meningitis
Rise in temperature (102–104°F) often with chills and rigors
Headache
Neck rigidity
Photophobia and mental irritability
Nausea and vomiting (sometimes projectile)
Cranial nerve palsies and hemiplegia
Symptoms
 neck rigidity
 positive Kernig’s sign
 positive Brudzinski’s sign
 tendon reflexes are exaggerated initially but later become
sluggish or absent
 papilloedema (usually seen in late stages).
Signs
HRCT Temporal bone
MRI
Funduscopic
Lumbar puncture is diagnostic:
CSF is cloudy and
CSF pressure is increased.
Contains bacteria and many polymorphs.
Protein concentration is raised but
Glucose and chlorides are decreased.
Investigations
Thrombophlebitis of the lateral venous sinus
usually develops secondary to direct extension from a
perisinus abscess due to an advanced otitis media
Acute otitis media: Hemolytic streptococcus,
Pneumococci
Cholesteatoma: Bacillus proteus, Pseudomonas
pyocynea, Escherichia coli and Staphylococci
Lateral sinus thrombosis
Pathogenesis
Intracranial Complications: Lateral Sinus
Thrombosis-clinical
Signs of blood invasion:
- Fever (spiking) with rigors and chills or persistent
fever(septicemia)
Positive Greisinger’s sign which is edema and
tenderness over the area of the mastoid emissary vein.
Signs of increased intracranial pressure:
Headache, vomiting, and papilledema.
When the clot extends to the jugular vein, the vein
might be felt in the neck as a tender cord.
Intracranial Complications:
Lateral Sinus Thrombosis-
diagnosis
 CT scan with contrast, “delta” sign
 MRI, Angiography, Venography
 Angiography, venography
 Blood cultures is positive
during the febrile phase.
MR venography showing obstructed
sigmoid sinus on the right side and good
venous filling on the left
clinical features
Signs of blood invasion:
- Fever (spiking) with rigors and chills or persistent
fever(septicemia)
– Positive Greisinger’s sign which is edema and tenderness
over the area of the mastoid emissary vein.
Signs of increased intracranial pressure:
Headache, vomiting, and papilledema.
When the clot extends to the jugular vein, the vein might be
felt in the neck as a tender cord.
Treatment
Medical:
• High dose IV antibiotics and supportive treatment
• Anticoagulants
Surgical:
• Mastoidectomy with exposure of the affected sinus and
the intra-sinus abscess is drained.
 Localized suppuration in the brain substance
 Most lethal complication of suppurative otitis media
Otogenic brain abscess
Pathogenesis
Intracranial Complications: Brain
Abscess-treatment
Medical:
• Broad-spectrum antibiotics.
• Measures to decrease intracranial pressure.
Surgical:
• Neurosurgical drainage or excision of the
abscess .
• Mastoidectomy operation after subsidence of
the acute stage.
 Increased intracranial pressure with normal CSF
 Severe headache
 Diplopia due to paralysis of VIth cranial nerve
 Blurring of vision due to papilledema
Otitic hydrocephalus
Otitic hydrocephalus
 HRCT Temporal bone
 Lumbar puncture-elevated CSF pressure
 Treatment - acetazolamide
corticosteroids
 Lumbo peritoneal shunt
 Treatment of the underlying cause
Evaluation & management
 Collection of pus against the Dura of the middle or
posterior cranial fossa
EXTRADURAL ABSCESS
Extradural abscess – clinical & treatment
Clinical Picture
– Persistent headache on the side of otitis media
– Pulsating discharge
– Fever
– May be asymptomatic (discovered during surgery)
Diagnosis:
– CT scans reveal the abscess as well as the middle
ear pathology.
- MRI reveals associated dural inflammation.
Treatment:
– Mastoidectomy and drainage of the abscess.
subdural empyema
 Lumbar puncture contra indicated
 HRCT temporal bone and brain
 Craniotomy and evacuation of pus
Management

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Complications of csom dr.sithanandha kumar,29.02.2016

  • 2. Define complication with reference to CSOM Enumerate the complications of CSOM Identify a case of CSOM with complications based on clinical features Evaluation & management of CSOM with complications OBJECTIVES
  • 3. Spread of infection beyond the confines of the mucosal spaces of middle ear cleft Definition
  • 5.  Meningitis  Sigmoid sinus thrombosis  Brain abscess  Extradural abscess  Subdural abscess  Otitic hydrocephalus Intra cranial complications
  • 7. Sub periosteal abscess Bezold’s abscess Zygomatic ( Luc’s abscess/ Meatal ) Digastric ( Cittelli’s abscess) Extracranial ( Extratemporal ) complications
  • 8. Attico antral disease ( cholesteatoma ) Highly virulent organism Poor host immune response Presence of preformed pathways for spread Extremes of age poor socioeconomic status Predisposing factors
  • 9.  Bone erosion  Suppurative retrograde thrombophlebitis  Preformed pathways Routes of spread
  • 10.  In ASOM-Hyperemic decalcification  In CSOM-Cholesteatoma or granulation tissue. Direct bone erosion
  • 12.  Congenital dehiscence: Dehiscence in facial canal and over the jugular bulb  Patent sutures: Petro squamous suture  Temporal bone fractures: The fibrous scar permits infection  Surgical defects: Stapedectomy, fenestration and exposure of dura  Perilymphatic fistula: Congenital or acquired  Normal anatomical openings: Infection of labyrinth and from labyrinth Preformed pathways
  • 13.  Ear pain  Fever  Severe headache  Projectile vomiting  Neck stiffness  Photophobia  Irritability / altered consciousness. Features of impending complications
  • 14.  when infection spreads from the mucosa lining the mastoid air cells to involve bony walls of the mastoid air cell system Mastoiditis
  • 16. Clinical Features of acute mastoiditis Symptoms  Earache  Fever  Ear discharge-profuse & purulent Signs  Mastoid tenderness  Sagging of postero-superior meatal wall  Eardrum perforation  Swelling, redness and bulging over the mastoid ( ironed out mastoid )  Hearing loss (conductive) The persistence of otorrhea beyond 3 weeks in a case of AOM indicates mastoiditis
  • 17.  HRCT Temporal Bone Aural swab for culture & sensitivity Investigations
  • 18.
  • 19.  Hospitalization  I.V antibiotics  Myringotomy  Cortical mastoidectomy TREATMENT
  • 20.  Subperiosteal abscess  Bezold’s abscess  Cittelli's abscess  Luc’s abscess  Petrositis  Labyrinthitis  Facial paralysis Sequelae of acute coalescent mastoiditis Luc’s abscess Luc’s abscess Subperiosteal abscess Subperiosteal abscess Bezold’s abscessBezold’s abscess
  • 21.
  • 23. slow destruction of mastoid air cells acute sign and symptoms of acute mastoiditis are absent Inadequate antibiotic therapy - Dose, frequency ,duration pain, discharge, fever , mastoid swelling - Absent mastoidectomy -extensive destruction of the air cells with granulation tissue and dark gelatinous material filling the mastoid Masked mastoiditis
  • 24.  Petrous bone - pneumatized in about 30% individuals  Two groups of air cells’ tracts -communicate mastoid and middle ear to the petrous apex  Postero superior tract: From the attic and antrum the tract passes around semicircular canals to petrous apex  Antero inferior tract: From the hypotympanum the tract passes around the ET and cochlea to the petrous apex  Infection may pass through these cell tracts and reach petrous apex Petrositis
  • 25. Cranial nerve VI palsy Deep seated ear or retro-orbital pain Persistent ear discharge Persistent ear discharge in cases of cortical or modified radical mastoidectomy may be due to Petrositis. Gradenigo’s syndrome or triad
  • 27. complication of both acute and chronic otitis media Due to dehiscent facial canal-ASOM Destruction of facial canal- CSOM-AAD Treatment- in ASOM- myringotomy - in CSOM- Cortical Mastoidectomy Facial nerve paralysis
  • 28.  Acute inflammation of the labyrinth  Diffusion of toxins via the round window from the middle ear – Serous Labyrinthitis  Labyrinthine fistula caused by hyperemic decalcification- Circumscribed Labyrinthitis  Pyogenic infection of the labyrinth- suppurative Labyrinthitis  Retrospective diagnosis –with treatment improves in serous labyrinthitis LABYRINTHITIS
  • 29.  inflammation of leptomeninges (pia-arachnoid)and CSF of subarachnoid space  most common intracranial complication  One third cases of meningitis are otogenic in origin Otogenic meningitis
  • 30.  Circumscribed meningitis: no bacteria in CSF.  Generalized meningitis: bacteria are present in CSF  Retrograde thrombophlebitis, bone erosion, preformed pathways.  Through oval and round windows.  Via perineural spaces to int. auditory canal or via endolymphatic ducts.  Fracture, Dural tear, CSF leak
  • 31. Serous stage: characterized by outpouring of fluid and increased CSF pressure. Cellular stage: characterized by increase number of cells especially lymphocytes. Bacterial stage: bacteria and polymorph nuclear leucocytes are present in large numbers stages of generalized meningitis
  • 32. Rise in temperature (102–104°F) often with chills and rigors Headache Neck rigidity Photophobia and mental irritability Nausea and vomiting (sometimes projectile) Cranial nerve palsies and hemiplegia Symptoms
  • 33.  neck rigidity  positive Kernig’s sign  positive Brudzinski’s sign  tendon reflexes are exaggerated initially but later become sluggish or absent  papilloedema (usually seen in late stages). Signs
  • 34.
  • 35. HRCT Temporal bone MRI Funduscopic Lumbar puncture is diagnostic: CSF is cloudy and CSF pressure is increased. Contains bacteria and many polymorphs. Protein concentration is raised but Glucose and chlorides are decreased. Investigations
  • 36.
  • 37. Thrombophlebitis of the lateral venous sinus usually develops secondary to direct extension from a perisinus abscess due to an advanced otitis media Acute otitis media: Hemolytic streptococcus, Pneumococci Cholesteatoma: Bacillus proteus, Pseudomonas pyocynea, Escherichia coli and Staphylococci Lateral sinus thrombosis
  • 39.
  • 40. Intracranial Complications: Lateral Sinus Thrombosis-clinical Signs of blood invasion: - Fever (spiking) with rigors and chills or persistent fever(septicemia) Positive Greisinger’s sign which is edema and tenderness over the area of the mastoid emissary vein. Signs of increased intracranial pressure: Headache, vomiting, and papilledema. When the clot extends to the jugular vein, the vein might be felt in the neck as a tender cord.
  • 41. Intracranial Complications: Lateral Sinus Thrombosis- diagnosis  CT scan with contrast, “delta” sign  MRI, Angiography, Venography  Angiography, venography  Blood cultures is positive during the febrile phase. MR venography showing obstructed sigmoid sinus on the right side and good venous filling on the left
  • 42. clinical features Signs of blood invasion: - Fever (spiking) with rigors and chills or persistent fever(septicemia) – Positive Greisinger’s sign which is edema and tenderness over the area of the mastoid emissary vein. Signs of increased intracranial pressure: Headache, vomiting, and papilledema. When the clot extends to the jugular vein, the vein might be felt in the neck as a tender cord.
  • 43. Treatment Medical: • High dose IV antibiotics and supportive treatment • Anticoagulants Surgical: • Mastoidectomy with exposure of the affected sinus and the intra-sinus abscess is drained.
  • 44.  Localized suppuration in the brain substance  Most lethal complication of suppurative otitis media Otogenic brain abscess
  • 46.
  • 47.
  • 48. Intracranial Complications: Brain Abscess-treatment Medical: • Broad-spectrum antibiotics. • Measures to decrease intracranial pressure. Surgical: • Neurosurgical drainage or excision of the abscess . • Mastoidectomy operation after subsidence of the acute stage.
  • 49.  Increased intracranial pressure with normal CSF  Severe headache  Diplopia due to paralysis of VIth cranial nerve  Blurring of vision due to papilledema Otitic hydrocephalus
  • 51.  HRCT Temporal bone  Lumbar puncture-elevated CSF pressure  Treatment - acetazolamide corticosteroids  Lumbo peritoneal shunt  Treatment of the underlying cause Evaluation & management
  • 52.  Collection of pus against the Dura of the middle or posterior cranial fossa EXTRADURAL ABSCESS
  • 53. Extradural abscess – clinical & treatment Clinical Picture – Persistent headache on the side of otitis media – Pulsating discharge – Fever – May be asymptomatic (discovered during surgery) Diagnosis: – CT scans reveal the abscess as well as the middle ear pathology. - MRI reveals associated dural inflammation. Treatment: – Mastoidectomy and drainage of the abscess.
  • 55.  Lumbar puncture contra indicated  HRCT temporal bone and brain  Craniotomy and evacuation of pus Management