COMPLICATIONS OF EAR INFECTION

1. COMPLICATIONS OF COM
Dr. AJAY MANICKAM
JUNIOR RESIDENT, DEPT OF ENT
RG KAR MEDICAL COLLEGE

2. INTRODUCTION
 Infection spreads beyond muco-periosteal lining of
middle ear cleft to involve bone & neighboring
structures like facial nerve, inner ear, dural venous
sinuses, meninges, brain tissue & extra-temporal
soft tissue
 Mortality due to intracranial complication is still high

3. Complications
ExtracranialIntracranial
• Meningitis
• Extradural abscess
• Subdural empyema
• Lateral sinus thrombophlebitis
• Brain abscess
• Otitic hydrocephalus
• CSF otorrhoea
Extratemporal
• Subperiosteal abscesses
Intratemporal
• Mastoiditis
• Labyrinth involvement
• Petrous apicitis
• Facial nerve paralysis
• Sensorineural hearing loss

4. Routes of access
• Bony defects
anatomical dehiscences (jugular bulb, dural plate, Fallopian
canal)
erosion (cholesteatoma, granulation tissue)
trauma (accidental, dural plate breach during mastoidectomy)
• Normal anatomical pathways
oval window
round window
aqueducts
• Haematogenous
infected thrombus
venous spread (sinus, emissary veins, systemic )
• Periarteriolar spread (of Virchow-Robin)
seeding in the white matter of brain

5. SPREAD OF INFECTION

6. FACTORS
Pathogen Factors Patient Factors
 High virulence bacteria  Young age
Antimicrobial resistance  Poor immune status
 Chronic disease (DM,
TB)
 Poor socio-economic
status
 Lack of health awareness

7. EXTRADURAL
ABSCESS

8. EXTRA DURAL ABSCESS
 2nd Most common otogenic
intracranial complication
 Acute infection by
demineralization and
chronic by erosion

9. MIDDLE CRANIAL FOSSA
• Tegmen tympani (lateral to the arcuate eminence)
• Petrous apicitis (medial to the arcuate eminence)
POSTERIOR CRANIAL FOSSA
• Sinus plate (perisinus abscess, lateral sinus
thrombophlebitis)
• Trautmann’s triangle
ANTERIOR CRANIAL FOSSA
• Pott’s puffy tumour

10. • 2nd most common intracranial complication
• Coalescence, cholesteatoma, granulation
• Non-specific symptoms (unilateral headache, fever,
otorrhoea)
• Often diagnosed peroperatively (silent abscess)
• MRI (Gadolinium-enhanced) > CT scan
• Systemic antibiotics + surgery (mastiodectomy +
removal of necrosed bone and non-adherant
granulation tissue over dura)

11. SUBDURAL
EMPYEMA

12. SUBDURAL EMPYEMA
 Least common complication
 Non hemolytic streptococci
 Inflammatory reaction underneath
dura- granulation- fibrosis-necrosis
of bone
 Seropurulent – purulent collection
• Subdural space, along tentorium
cerebelli and interhemispheric
spaces

13. CLINICAL FEATURES
 Dramatic presentation , rapid detioration
 Severe headache, fever, drowsiness, follwed by
focal neurological symptoms
 Much more rapid than brain abscess
 Jacksonian fits
 Hemianopia ,hemianaesthesia , aphasia
 Mortality 15%

14. • along the falx
• loculated
• hypodense
• ring enhancement
• contrast imaging
• mass effect
• blunted sulci
Gd-DTPA enhanced T1 weighted MRI
CECT

15. DIAGNOSIS AND MANAGEMENT
 CT scan
 CSF culture sterile
 With neurosurgeons
 Systemic antibiotics + removal of subdural fluid
(burr hole) + ear infections acute by myringotomy
and cortical mastiodectomy
 Now craniotomy abscess excision
 Radical mastoidectomy after patient is stable

16. MENINGITIS

17. MENINGITIS
 Most common intracranial complication
 In children following acute and adults following
chronic infection
 Mortality 5-30 %
 Otogenic meningitis is most serious than
meningococcal meningitis
 Hemophilus influenzae , streptococcus pneumonia
type iii – acute
 Chronic – proteus and pseudomonas
 Anaerobic – bacteroid

18.  Routes of entry into the meninges –
haematogenous (MC)
direct extension by bone erosion (cholesteatoma, encephalocoel)
preformed channels (Hyrtl’s fissures)
labyrinth, aqueduct (suppurative labyrinthitis, Mondini
malformation)
 Suspicious signs –
persistent/intermittent fever lethargy
nausea and vomiting persistent headache
irritability
 Ominous signs –
visual changes ataxia
new onset seizures altered sensorium
nuchal rigidity
 Associted intracranial complications in 50% of
cases
Meningitis

19. DIAGNOSIS AND TREATMENT
CSF study by LP (cytology, chemistry, smear, culture)
Broad spectrum IV antibiotics, steroids (to prevent
subsequent
hearingloss)
Myringotomy
Mastoidectomy (cholesteatoma, coalescent mastoiditis,
extension
through bone erosion, failure of maximal
medical
therapy)

20. LATERAL SINUS
THROMBOPHLEBITIS

21. LATERAL SINUS THROMBOPHLEBITIS
Lateral sinus = Sigmoid sinus + Transverse sinus
sinus plate  peri-sinus abscess  inflammation of
Erosion of sigmoid outer wall  endophlebitis  mural
thrombus  occlusion of sinus lumen  intra-sinus
abscess  propagating infected thrombus

22. PATHOGENESIS

23. Lateral sinus
thrombophlebitis
Sagittal sinus
(papilloedema,
visual loss)
Petrosal and cavernous
sinus
(proptosis, chemosis)
Mastoid emissary vein
(Griesinger’s sign)
Internal jugular
vein
Subclavian vein
Systemic spread
(bacteraemia,
septicaemia, septic
embolisation)
Torcula

24. LATERAL SINUS THROMBOPHLEBITIS
Proximal: 1. To superior sagittal sinus via torcula
Herophili  hydrocephalus
2. To cavernous sinus  proptosis
3. To mastoid emissary vein  Griesinger’s sign
Distal: To internal jugular vein & subclavian vein 
pulmonary thrombo-embolism & septicaemia

25. CLINICAL FEATURES
 Remittent high fever with rigors (picket fence)
 Pitting edema over retro-mastoid area & occipital
bone due to mastoid emissary vein thrombosis
(Griesinger’s sign)
 Tenderness along Internal Jugular Vein
 Headache
 Anaemia

26. SYMPTOMS & SIGNS
 High fever, swinging type
 Chills precedes fever
 Temperature subsides with sweating
 Each fever spike due to release of fresh septic
embolus

27. INVESTIGATIONS
 Queckenstedt or Tobey-Ayer test: compression of
I.J.V.  rapid rise of C.S.F. pressure (50 – 100 mm
water  rapid fall on release of compression. In
L.S.T. no rise / rise by only 10 – 20 mm water.
 Low sensitivity and specificity

28. INVESTIGATIONS
Lumbar puncture: to rule out
meningitis
CT brain with contrast: Delta sign
or Empty triangle sign
MRI brain with contrast
MR angiography
Blood culture
Culture & sensitivity of ear
discharge

29. • Intravenous antibiotics
• Surgery
• Anticoagulants
• Ligation of internal jugular vein
Treatment

30. Algorithm for Surgery
Mastoidectomy Inspection of the sinus wall
NORMAL
(compressible, healthy-looking)
DISEASED
(inflammed, immobile, pale, opaque)
Wide bore needle aspiration
Free flow blood No blood, pus
Conservative Thrombectomy, drainage
(healthy thrombus, free flow blood)
Dry tap

31. OTOGENIC BRAIN ABSCESS

32. OTOGENIC BRAIN ABSCESS
50-75 % adult brain abscess & 25% in child = otogenic
Temporal abscess : Cerebellar abscess = 2:1
Route of infection:
1. Direct spread:
 via Tegmen plate: Temporal abscess
 via Trautmann’s triangle: Cerebellar abscess
2. Retrograde thrombophlebitis and 3. virchow robin space

33. TRAUTMANN’S TRIANGLE
Superiorly: superior
petrosal sinus
Posteriorly: sigmoid sinus
Anteriorly: solid angle
(semi-circular canals)
Pathway to posterior
cranial fossa from mastoid
cavity

34. 4 STAGES (NEELY, MAWSON)
1. Invasion or Encephalitis (1-10
days)
2. Localization or Latent Abscess
(10-14 days)
3. Expansion or Manifest
Abscess (> 14 days): leads to
raised intracranial tension & focal
signs
4. Termination or Abscess
rupture: leads to fatal meningitis

35. RAISED ICT
Seen more in cerebellar abscess
 Severe persistent headache, worse in morning
 Projectile vomiting
 Blurring of vision & Papilloedema
 Lethargy  drowsiness  confusion  coma
 Bradycardia
 Subnormal temperature

36. DIFFERENT FINDINGS
Temporal Lobe Cerebellum
 Nominal aphasia  I/L nystagmus
 homonymous  I/L weakness
hemianopia (C/L)  I/L hypotonia
 Epileptic seizures  I/L ataxia
 Pupillary dilatation  Intention tremor
 Hallucination (smell & taste)  Past-pointing
 C/L hemiplegia  Dysdiadochokinesia

37. INVESTIGATIONS
CT scan of brain & temporal bone with
contrast
 Site, size & staging of abscess
 Observe progression of brain abscess
 Associated intra-cranial complications
MRI brain
 D/D: pus, abscess capsule, edema &
normal brain
 Spread to ventricles & subarachnoid
space
Avoid lumbar puncture to prevent
coning

38. DIFFERENTIAL DIAGNOSIS
 Meningitis- high fever, neck stiffness , CSF findings
 Subdural abscess – the progression
 Lateral sinus thrombosis – precursor of cerebellar
abscess
 Otitic hydrocephalous absence of focal neurological
sign , CT scan findings and CSF features

39. MANAGEMENT
• High dose broad spectrum I.V. antibiotics: Ceftriaxone
+ Metronidazole + Gentamicin
• I.V. Dexamethasone 4mg Q6H: es oedema
• I.V. 20% Mannitol (0.5 gm/kg): es I.C.T.
• Anti-epileptics: Phenytoin sodium
• Antibiotic ear drops & aural toilet

40. SURGICAL MANAGEMENT
•Repeated burr hole aspirations – safer for ill patients
• Excision of brain abscess with capsule: best Tx – extensive
damage to cerebral tissue , residual neurological deficit
• Open incision & evacuation of pus
• Radical mastoidectomy after pt becomes stable

41. OTITIC
HYDROCEPHALUS

42. • syn. Benign intracranial hypertension
• Symptomatic ↑ in ICT (>240 mm H2o in LP), papilloedema,
normal CSF studies, in absence of brain abscess or
meningitis
• A misnomer
• Lateral sinus thrombophlebitis → torcula →
sagittal sinus thrombosis → inhibition of CSF
resorption through arachnoid villi → ↑ICT [Symonds]
Otitic hydrocephalus

43. OTITIC HYDROCEPHALUS
Clinical Features: 1. Severe headache, vomiting
2. Blurred vision, papilloedema, optic atrophy
3. Abducens palsy & diplopia due to raised
intra-cranial tension (Falselocalizing sign)
• Conservative (acetazolamide, fluid restriction, diuretics,mannitol,
serial LP, ± systemic anticoagulants in case of
sagittal sinus thrombosis)
• Mastoidectomy ± thrombectomy (in COM with
cholesteatoma)

44. MANAGEMENT
Investigations:
1. Lumbar puncture: ed CSF pressure (> 300 mm
H2O). Biochemistry & bacteriology normal
2. CT scan brain: normal ventricles
Treatment: 1. Tx of L.S.T.: I.V. antibiotics & MRM
2. se CSF pressure (prevents optic atrophy) by:
 I.V. Dexamethasone 4mg Q6H
 I.V. 20% Mannitol 0.5 gm/kg ,acetazolamide , diuretics
 Repeated lumbar puncture / lumbar drain
 Ventriculo-peritoneal shunt

45. CSF OTORRHOEA

46. • More common with COM
• Cholesteatoma → tegmen dehiscence → middle or
posterior cranial fossa dural tear → CSF
leak/encephalocoel
• Iatrogenic
• Presentations
clear, colourless, watery fluid
from mastoid cavity or external auditory canal
through nose, in intact TM
middle ear/myringotomy fluid rich in glucose
• Proper exposure → temporalis muscle/fascia graft
with gelfoam compression
• Sinodural angle tear most difficult to control
• Repair via intracranial route (extradural/intradural)

47. BRAIN FUNGUS
 Prolapse of brain into middle ear cavity / mastoid
cavity due to erosion of dural plate.
 Common in pre-antibiotic era. Rarely seen now in
resistant infections.
 Diagnosis: C.T. scan temporal bone.
 Treatment: Removal of necrotic tissue, replacement
of healthy prolapsed brain into cranial cavity &
repair of bone defect.

48. SUBPERIOSTEAL
ABSCESS

49. • Extension of mastoid infection through the cortex and air cells into the
subperiosteal region
• Types –
Mastoid abscess (subperiosteal abscess “proper”) [MC]
von Bezold’s abscess
Luc’s (meatal) abscess
Zygomatic abscess
Citelli’s abscess
Para-/retropharyngeal abscess
• Haematogenous spread (perforators, especially in children)
• Differential diagnosis –
Mastoiditis without abscess
Suppurative lymphadenopathy
Superficial abscess
Infected sebaceous cyst

50. PATHOGENESIS
Production of pus under tension
 hyperaemic decalcification
+ osteoclastic resorption of bone
 sub-periosteal abscess
 penetration of periosteum + skin
 fistula formation

51. SUBPERIOSTEAL FISTULA

52. Subperiosteal abscess
(lateral wall)
Bezold’s abscess (tip cells)
Zygomatic abscess (zygomatic cells)
Luc’s (meatal) abscess
Parapharyngeal/retropharyngeal
abscess (peritubal cells)

53. POSTAURICULAR ABSCESS
Commonest. Present behind the ear.
Pinna pushed forward & downward

54. BEZOLD & CITELLI’S ABSCESS
Bezold: neck swelling
over sternocleido-
mastoid muscle
Citelli: neck swelling
over posterior belly
of digastric muscle

55. D/D OF BEZOLD’S ABSCESS
1. Suppurative lymphadenopathy of upper deep
cervical lymph node
2. Para-pharyngeal abscess
3. Parotid tail abscess
4. Infected branchial cyst
5. Internal jugular vein thrombosis

56. LUC’S ABSCESS
Luc: swelling in external auditory canal
Zygomatic: swelling antero-superior to pinna +
upper eyelid oedema
Parapharyngeal & Retropharyngeal: due to spread
of pus along Eustachian tube

57. CLINICAL FEATURES & TREATMENT
• Late feature of neglected COM
• CT scan (extent of the lesion, intracranial and
 intratemporal complications)
• Subperiosteal abscess + cholesteatoma

 Drainage + cortical mastoidectomy + IV antibiotics
• Subperiosteal abscess – cholesteatoma

 Drainage + cortical mastoidectomy + IV antibiotics
 Drainage + myringotomy + IV antibiotics
 Aspiration + myringotomy + IV antibiotics

58. MASTOIDITIS

59. • Mastoiditis = mucositis of mastoid cavity and air
cells + effusion
part of the spectrum of uncomplicated otitis media
per se, not a complication
• Acute (clinical) mastoiditis
red, oedematous soft tissue over mastoid antrum
painful/tender
pinna directed laterally, downward and forward
loss of post-auricular crease
otorrhoea
localised reactive lymphadenopathy
pain the only presentation in adults (thicker cortex)

60. PATHOGENESIS
Aditus Blockage
 Failure of drainage
 Stasis of secretions
 Hyperemic decalcification
 Resorption of bony septa of air
cells
 Coalescence of small air cells to
form cavity
 Empyema of mastoid cavity

61.  Disease of childhood (>2 years, peak at 6 years)
 Mostly a sequelae of ASOM (Pneumococcus,
Haemophilus)
 25% of coalescent mastoiditis seen in
sclerotic temporal bone with COM and
cholesteatoma

62. Fate of an inflammed mastoid cavity
Acute mastoiditis
Spontaneous resolution, perforation of tympanic
membrane
Persists
Blockage of aditus by granulation/cholesteatoma
Mastoid empyema
Acute
coalescent mastoiditis
Acidosis
Osteoclast activity
Pressure of pent-up pus
DEMINERALISATION
Subperiosteal abscess Petrositis
Intratemporal & intracranial
complications

63. SYMPTOMS & SIGNS
 Otorrhoea > 3 weeks, pain behind the ear & fever
 Mastoid reservoir sign: pus fills up on mopping
 Sagging of postero-superior canal wall due to peri-
osteitis of bony wall b/w antrum & posterior E.A.C.
 Ironed out appearance of skin over mastoid due to
thickened periosteum
 Mastoid tenderness present
 Blood counts , ESR raised , Mastoid cavity in X-ray &
CT scan , ear swab culture & sensitivity

64. MASTOID RESERVOIR SIGN

65. POSTERIOR SAGGING OF POSTERIOR CANAL
WALL

66. MASTOIDITIS

67. COALESCENCE OF CELLS

68. Mastoiditis Furunculosis
H/o otitis media + -
Deafness + -
Position of pinna Down + outward
+ forward
Forward
Ear discharge Muco-purulent Serous / purulent
Sagging of EAC wall + -
TM congestion + -
Tenderness Mastoid Tragal
Post-aural lymph node - +
X-ray Mastoid Coalescence of
cells + cavity
Normal

69. MANAGEMENT
 Urgent hospital admission
 Broad spectrum I.V. antibiotics
 Cortical mastoidectomy
 No response to medical treatment in 48 hrs ,
sagging of post meatal wall
 Development of new complication
 Presence of sub-periosteal abscess
 Myringotomy to drain out painful pus
 Incision drainage of sub-periosteal abscess

70.  Masked mastoiditis
Natural progress of acute mastoiditis halted by antibiotics
Middle ear apparently free from infection
Persistence of symptoms of mastoiditis
TM fails to return to normalcy
Blockage of aditus by granulation/cholesteatoma

71. PETROSITIS

72. Pneumatisation of the petrous pyramid
30% (anterior petrous apex), 10% (posterior petrous apex)
after 3 years of age
continuous with the middle ear cleft
POSTEROSUPERIOR/INFRALABYRINTHINE CHAIN
(attic, antrum → semicircular canal → apex)
ANTEROINFERIOR/PERITUBAL CHAIN
(hypotympanum, PT tube → cochlea → apex)

73. ACUTE PETROSITIS
• Gradenigo’s syndrome
deep-seated retro-orbital/aural pain (50%)
diplopia (lateral rectus palsy) (25%)
otorrhoea
TYPICAL GRADENIGO’S SYNDROME IS RARE
NOT PATHOGNOMONIC OF APICITIS
SIMILAR PRESENTATIONS WITH EXTRADURAL ABSCESS AT THE APEX
• Cochleo-vestibular symptoms, facial weakness,
constitutional symptoms

74. PETROSITIS
• Pneumatisation of petrous apex not
a prerequisite
ALTERNATIVE ROUTES OF SPREAD
Thrombophlebitis
Osteitis
• Long standing persistent otorrhoea
(discharging petrous
tract), with indolent symptoms

75. • Long term, high dose systemic antibiotics
• Myringotomy (± grommet), corticosteroids (neuropathy)
• Surgery –
petrous abscess, necrosis, failure of medical traetment
• Simple mastoidectomy
• Surgery in a hearing ear –
approaches following the infected air-cells
• Surgery in a non-hearing ear –
translabyrinthine & transcochlear approaches

77. INVOLVEMENT OF
THE LABYRINTH
(Otitis interna)

78. • Most common complication of COM with
cholesteatoma
• Arch of the horizontal semicircular canal most
commonly affected (~90%) [nearest to the antrum
• Breach of the otic capsule
Resorptive osteitis (inflammatory mediators in COM with
cholesteatoma/granulation tissue)
Pressure necrosis (cholesteatoma mass)
• Cholesteatoma and/or granulation

79. • Presentations of labyrinthine fistula
sensorineural hearing loss
subjective episodic vertigo
positive fistula test
Tullio phenomenon
• Preoperative CT scan (30° tilted)
(57-60% sensitivity, even with 1mm cuts)
• Intraoperative diagnosis
• The presence of labyrinthine fistula to be assumed
to
be present in every case of COM with
cholesteatoma

80. Fistula test in relation to labyrinthine fistula
• Tragal pressure, Politzer bag with ear canal
adapter,
pneumatic speculum
• Conjugate ocular movements with vertigo
• Not sensitive; its absence does not rule out a
labyrinthine fistula
• False positive fistula sign (Hennebert’s sign)
intact tympanic membrane
no fistula
characteristic, though not diagnostic, of labyrinthine syphilis
• False negetive fistula sign
inadequate sealing
cholesteatoma blocking the fistula
wax in the external canal
dead labyrinth

81. Treatment of labyrinthine fistula
• Tympanomastoidectomy (CWD) + addressing the fistula
• Removal of cholesteatoma, exteriorising the fistula covered by
matrix (single sitting in open cavity/staged in closed cavity) –
prevents aggravation of SNHL by minimising tissue handling
removal of cholesteatoma itself releives pressure
keeping matrix safe until no granulation tissue lies
underneath
• Complete removal of cholesteatoma including matrix (single or
staged/2nd look sitting), repair of fistula (fascia, bone pâté)
prevention of bone erosion and infection
prevention of SNHL in the long term

82. SEROUS LABYRINTHITIS
• Translocation of toxins and inflammatory mediators
Associated perilabyrinthine infection, especially fistula
• Meningogenic (Pneumococcal mengitis → aqueducts)
Tympanogenic (round window, internal auditory canal)
• Clinical diagnosis : Sudden onset vertigo in a patient with AOM
• IV antibiotics + myringotomy ± mastoidectomy (in progressive cases)
• Hearing loss, vertigo and imbalance are reversible

83. SUPPURATIVE LABYRINTHITIS
Comparatively less common (<1%)
• Invasion of bacteria into the labyrinth
• Tympanogenic (round window, fistula)
• Haematogenic (venous channels)
• Endolymphatic hydrops (resistence of Reissner’s membrane to
bacterial invasion )
• Meningitis, intracranial (cerebellar) abscess
• Clinical diagnosis (aided by CT scan)
sudden onset severe rotatory vertigo with vomiting
profound unilateral deafness
disorder of balance
spontaneous horizontal nystagmus
• Tissue destruction and loss of functions are permanent
• IV antibiotics + myringotomy + corticosteroids + labyrinthine
sedatives + mastoidectomy ± drainage/labyrinthectomy

84. FACIAL NERVE
PARALYSIS

85. • Otitis media → 3-5% of incidences of facial palsy
• More common in children, after ASOM
• Acute onset (<1 week) in AOM, chronic protracted
course in COM
• Cholesteatoma, granulation tissue, suppurative
labyrinthitis (sequestra), petrous osteomyelitis
• Congenital petrous cholesteatoma (progressive palsy with
longstanding severe deafness, without otorrhoea)
• Facial nerve exposed by cholesteatoma mostly
escapes
palsy (epineurium replaced by matrix)

86. Causes of Facial nerve palsy
AOM
• Neurotoxic effect (inflammatory mediators, bacterial toxins
through natural dehiscences and vascular channels)
• Mass effect on the bare nerve
COM
Osteitis, erosion, direct pressure Oedema, neuropraxia,
neuronotmesis
• Cholesteatoma > granulation tissue
• Acquired Fallopian canal dehiscence
• Tubercular otitis media

87. • Clinical diagnosis
• Role of CT scan
not a routine procedure
investigation of choice
<2mm cuts, with proper exposure of tympanic cavity & facial
canal
• IV antibiotics + myringotomy ± grommet [AOM]
• Surgical exploration [COM]
CWD modified radical mastoidectomy
Removal of cholesteatoma and granulation tissue
Facial nerve decompression by removing matrix from epineurium
Nerve repair, if needed
The management

88. Thank
you