COMPLICATIONS OF COM

Dr. AJAY MANICKAM

JUNIOR RESIDENT, DEPT OF ENT
RG KAR MEDICAL COLLEGE
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

 Complications

Intracranial Extracranial
• Meningitis Extratemporal
• Extradural abscess
• Subdural empyema • Subperiosteal abscesses
• Lateral sinus thrombophlebitis
• Brain abscess Intratemporal
• Otitic hydrocephalus
• CSF otorrhoea • Mastoiditis
• Labyrinth involvement
• Petrous apicitis
• Facial nerve paralysis
• Sensorineural hearing loss
 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
SPREAD OF INFECTION
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
EXTRADURAL
ABSCESS
EXTRA DURAL ABSCESS

 2nd Most common otogenic

intracranial complication
 Acute infection by
demineralization and
chronic by erosion
 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
• 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)
SUBDURAL
EMPYEMA
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
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%
CECT

• along the falx

• loculated
• hypodense

Gd-DTPA enhanced T1 weighted MRI

• ring enhancement
• contrast imaging
• mass effect
• blunted sulci
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

MENINGITIS
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
 Meningitis

 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
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)
 LATERAL SINUS
THROMBOPHLEBITIS
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

PATHOGENESIS
 Petrosal and cavernous
Sagittal sinus sinus Torcula
(papilloedema, (proptosis, chemosis)
visual loss)
Mastoid emissary vei
(Griesinger’s sign)

Lateral sinus
thrombophlebitis

Internal jugular Systemic spread

vein
Subclavian vein (bacteraemia,
septicaemia, septic
embolisation)
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

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

• Intravenous antibiotics

• Surgery

• Anticoagulants

• Ligation of internal jugular vein

 Algorithm for Surgery

Mastoidectomy Inspection of the sinus wall

NORMAL DISEASED
(compressible, healthy-looking) (inflammed, immobile, pale, opaque)

Wide bore needle aspiration

Free flow blood Dry tap No blood, pus

Conservative Thrombectomy, drainage

(healthy thrombus, free flow blood)
OTOGENIC BRAIN ABSCESS
OTOGENIC BRAIN ABSCESS

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

TRAUTMANN’S TRIANGLE
Superiorly: superior

petrosal sinus
Posteriorly: sigmoid sinus
Anteriorly: solid angle
(semi-circular canals)
Pathway to posterior
cranial fossa from mastoid
cavity
4 STAGES (NEELY, MAWSON)
1. Invasion or Encephalitis (1-10
days)

2. Localization or Latent Abscess

(10-14 days)

[Link] or Manifest
Abscess (> 14 days): leads to
raised intracranial tension & focal
signs

[Link] or Abscess
rupture: leads to fatal meningitis
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
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
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
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
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

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

 OTITIC
HYDROCEPHALUS
 Otitic hydrocephalus

• 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
Clinical Features: 1. Severe headache, vomiting
2. Blurred vision, papilloedema, optic atrophy
[Link] 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)
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
CSF OTORRHOEA
• 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)
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.
SUBPERIOSTEAL
ABSCESS
• 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
PATHOGENESIS

Production of pus under tension

 hyperaemic decalcification

+ osteoclastic resorption of bone

 sub-periosteal abscess

 penetration of periosteum + skin

 fistula formation
SUBPERIOSTEAL FISTULA
 Zygomatic abscess (zygomatic cells)

Luc’s (meatal) abscess

Parapharyngeal/retropharyngeal Subperiosteal abscess

abscess (peritubal cells) (lateral wall)

Bezold’s abscess (tip cells)

POSTAURICULAR ABSCESS

Commonest. Present behind the ear.

Pinna pushed forward & downward
BEZOLD & CITELLI’S ABSCESS

Bezold: neck swelling

over sternocleido-

mastoid muscle

Citelli: neck swelling

over posterior belly

of digastric muscle
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

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

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
MASTOIDITIS
• 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)
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

 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
 Fate of an inflammed mastoid cavity

Spontaneous resolution, perforation of tympani c

membrane
Acute mastoiditis
Persists

Blockage of aditus by granulation/cholesteatoma

Acidosis
Osteoclast activity
Pressure of pent-up pus Acute
Mastoid empyema
coalescent mastoiditis
DEMINERALISATION

Intratemporal & intracranial

Subperiosteal abscess Petrositis
complications
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
MASTOID RESERVOIR SIGN
POSTERIOR SAGGING OF POSTERIOR CANAL
WALL
MASTOIDITIS
COALESCENCE OF CELLS
 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 Normal
cells + cavity
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
 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
PETROSITIS
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)
 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
PETROSITIS
• Pneumatisation of petrous apex not
a prerequisite

ALTERNATIVE ROUTES OF SPREAD

Thrombophlebitis
Osteitis

• Long standing persistent otorrhoea

(discharging petrous
tract), with indolent symptoms
• 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
 INVOLVEMENT OF

THE LABYRINTH
(Otitis interna)
• 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

• 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
 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
 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
 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 withAOM

• IV antibiotics + myringotomy ± mastoidectomy (in progressive cases)

• Hearing loss, vertigo and imbalance are reversible

 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
FACIAL NERVE
PARALYSIS
• 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)
 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
 The management

• 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
Thank
you