COMPLICATIONS OF COMDr. AJAY MANICKAMJUNIOR RESIDENT, DEPT OF ENTRG 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

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

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

FACTORSPathogen 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%

• along the falx• loculated• hypodense

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

Gd-DTPA enhanced T1 weighted MRI

CECT

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

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

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

Lateral sinus thrombophlebitis

Sagittal sinus(papilloedema, visual loss)

Petrosal and cavernous sinus

(proptosis, chemosis)Mastoid emissary

vein(Griesinger’s sign)

Internal jugular vein Subclavian

veinSystemic spread

(bacteraemia, septicaemia, septic

embolisation)

Torcula

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

INVESTIGATIONSLumbar 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

• Intravenous antibiotics

• Surgery

• Anticoagulants

• Ligation of internal jugular vein

Treatment

Algorithm for SurgeryMastoidectomy 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

OTOGENIC BRAIN ABSCESS

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

TRAUTMANN’S TRIANGLESuperiorly: superior

petrosal sinusPosteriorly: sigmoid sinusAnteriorly: 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)

3. Expansion or Manifest

Abscess (> 14 days): leads to

raised intracranial tension & focal

signs

4. Termination 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 FINDINGSTemporal 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

INVESTIGATIONSCT 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

spaceAvoid 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 HYDROCEPHA

LUS

• 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

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)

MANAGEMENTInvestigations:1. Lumbar puncture: ed CSF pressure (> 300 mm

H2O). Biochemistry & bacteriology normal2. CT scan brain: normal ventriclesTreatment: 1. Tx of L.S.T.: I.V. antibiotics & MRM2. 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

Subperiosteal abscess (lateral wall)

Bezold’s abscess (tip cells)

Zygomatic abscess (zygomatic cells)

Luc’s (meatal) abscess

Parapharyngeal/retropharyngeal abscess

(peritubal 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)

PATHOGENESISAditus 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

Acute mastoiditis

Spontaneous resolution, perforation of tympanic membrane

Persists

Blockage of aditus by granulation/cholesteatoma

Mastoid empyema Acute coalescent mastoiditis

AcidosisOsteoclast activity

Pressure of pent-up pus

DEMINERALISATION

Subperiosteal abscess Petrositis Intratemporal & intracranial 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 FurunculosisH/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

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 with AOM

• 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

COMOsteitis, erosion, direct pressure Oedema,

neuropraxia, neuronotmesis

• Cholesteatoma > granulation tissue• Acquired Fallopian canal dehiscence• Tubercular otitis media

• 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

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