INTRACRANIAL

COMPLICATIONS

OF

OTITIS MEDIA

INTRODUCTION

ASOM MIDDLE EAR INTRACRANIAL

SPACE

CSOM INTRATEMPORAL

CLASSIFICATION

INTRATEMPORAL INTRACRANIAL

1.Mastoiditis 1.Extradural abscess

2.Petrtositis 2.Subdural abscess

3.Facial paralysis 3.Otogenic Meningitis

4.Labrynthitis 4.Brain abscess

5.Subperiosteal abscess 5.Lateral sinus thrombophlebitis

6.Postauricular fistula 6.Otitc hydrocephalus

7.Labrynthine fistula 7.Pnemocoele

8.Cerebrospinal fluid otorrhea

Factors affecting indicators of impending intra cranial complications

1.Age 1.otorrhea- creamier,thicker

2.Poor socio-economic group 2.pain-deep nboring

3.Virulence of organisms 3.headache,toxemia,altered sensorioum,

4.Immunocompromised host photophbia

5.Preformed pathways 4.neck stiffness,malaise

6.Cholesteotoma

Routes of spread of infection from the middle ear space

Mode of spread of infection

1.Bone erosion

Acute infection Hyperaemic decalcification

Chronic infection osteitis(cholesteotoma,granulation)

2.Thrombophlebitis

Extracranial Mastoid Emissary Intracranial

Venous system Veins Venous system

Sigmoid

sinus

Superior and Inferior

Petrosal sinus

Thrombophlebitis

Venous Arterial

Cerebellar abscess Temporal abscess,septicemia

3.Pervascural(intra brain spread) described by Atkinson

Via Periarterial spaces of spares cortical vasculature

Robin Virchow frequent in white matter

4.Preformed pathways

Congenital dehiscences

Patent sutures

Previous skull fractures

Surgical defects

Oval and Round window

Spread of infection through different walls of middle wall

Extradural abscess

Subdural abscess

Meningitis

Brain abscess

Lateral sinus thrombophlebitis

Otitc hydrocephalus

Pnemocoele

Acute mastoidis

Facial nerve palsy labrynthitis

Lateral sinus thrombophlebitis

Thrombosis of jugular bulb

MIDDLE EAR

Extradural abscess

Collection of pus between bone and dura

Occur in acute and chronic infection of middle ear.

Common sites

1.around lateral sinus

2.opposite middle cranial fossa

Tegmen

Extradural

Dura

PATHOLOGY

Acute bone over dura destroyed hyperaemic decalcification

Chronic bone over dura destroyed cholesteotoma

If by venous thrombophlebitis bone over dura intact

Abscess well encapsulated

Middle fossa abscess precipitates GRADENIGO,,s syndrome.

Spread from petrous apex

Result in irritation of Trigeminal ganglion and 6th cranial nerve

Otorrhoea ,facial pain and diplopia

Posterior fossa abscess associated with lateral sinus thrombophlebitis and medially limited by internal auditory meatus.

Clinical Features TREATMENT

Depends on site.duration and rate of development 1.Antibiotics

Most of time incidental finding 2.Surgical -Cortical or Radical or

However suspected when Modified radical mastoidectomy

1.Persistent severe headache 3.Neurosurgical –evacuated by 2.severe pain ear removing overlying bone till 3.general malaise with low grade fever. Limits of healty dura reached.

4.Pulsatile purulent discharge.

5.Disappearance of headache with free flow of pus.

SUBDURAL ABSCESS

Collection of pus between dura and arachnoid

PATHOLOGY

Infection spread from ear by erosion of bone and dura or by thrombophlebitis

Rate of spread of abscess determines clinical and pathological pattern

Dura resistant to infection, granulation tissue formed on inner surface to localize inflammatory reaction and eventually converted to fibrous tissue and necrosis of dura lead to subdural compartment.

Pus spreads over surface of cerebral hemisphere and along falx cerebri

Limitation of spread provided by obliteration of space by granulation tissue

CLINICAL FEATURES

Prime is rapidity of neurological deterioration.

Signs and symptoms due to

1.Meningeal irritation- Headache

Fever

Malaise

Increasing drowsiness

Neck rigidity

Positive kernig’ssign

2.Cortical venous- aphasia

thrombophlebitis hemiplegia

hemianopia

jacksonian epileptic fits

3.Raised intracranial papilloedema

tension ptosis

dilated pupil (3rdnerve)

other cranial nerve

Diagnosis is difficult

By rapid deterioration

Enhanced CT scan (although changes subtle)

MRI

Fundoscopy for papilloedema

TREATMENT

1.Antibiotics

2.Series of burr holes or craniotomy is done to drain empyema followed by iv antibiotics followed by modified mastoidectomy.

3.long term anticonvulsant

Otogenic brain abscess

Circumscribed collection of inflammatory product.

50% in adult &25% in children otogenic

In Adult by CSOM(cholesteotomma)

In children by ASOM

Cerebral more common than cerebellar.

Route of in infection

Cererbral abscess by Direct extension(tegmen)

Retrograde thrombophlebitis

Often with extradural

Cerebellar abscess by Direct extension (trautman triangle)

Retrograde thrombophlebitis

Often with extradural ,perisinus,sigmoid sinus thrombophlebitis or labrynthitis

Bacteriology

Both aerobic and anaerobic

Anaerobic common are bacteriodes fragilis & Peptococcus.

Pathophysiology

STAGE No.OF DAYS CHANGES CLINICAL FEATURESEarly Cerebritis(invasion)

1 to 3 days Perivascular infla. ResponseCauses focal necrosis & liquefaction with

Usually unnoticedHeadache mild fever malaise

surrounding edema drowsinessLate Cerebritis(quiescent)(localization)

4 to 10 days Formation of capsule of inflatory tissue &fibrosis

No symptoms

Enlargement(manifest abscess)

10 to 13 days Abcess enlarge Aggravation of symptoms Cl. Features due toRaised ICTDisturbed func. Of cerebrum or cerebellum(focal symptoms &signs)

Termination (rupture)

14 days Cerebral into lateral ventricle or white matter Cerebellar into fourth ventricle

Severity increases

Clinical Features

A.Due to raised ICT

Headache

Nausea &projectile vomiting

Lethargy,drowsy,stupor,coma

Papilloedema

Slow pulse

Fever low grade &later hypothermia

B.Localising features

Temporal abscess

Nominal aphasia

Homonymous hemianopia

Contalateral motor paralysis

Epileptic fits

Papillary changes and occullomotor palsy

Extensor plantar reflex

Hallucinatin of smell & taste

Cerebellar abscess

Headache suboccipital radiated to neck

Spontaneous nystagmus

Ipsilateral hypotopnia & weakness

Ipsilateral ataxia

Past pointing & intention tremor

Dysdiadokokinesia

Diagram of tentorial herniation due to supratentorial hydrocephalus accompanying

A temporal lobe abscess . the uncus has been displaced through the tentorium and is compressing the midbrain

Investigation

Skull Xrays

Xray mastyoid

CT scan showing cerebellar abscess

CT scan showing temporal abscess

CT scan

CSF analysis(if no papilloedema)

MRI

Treatment

Medical : antibiotics parenterally

Dexamethason or mannitol

Neurosurgical: repeated aspiration

Excision

Common sites of burr holes used in the management of otogeic brain abscess

Otologic: discharge clean with suction

Ear drops

Mastoidectomy(abscess controlled)

Meningits

Inflammation of leptomeninges(pia & arachnoid)

Most common complication

Spread via- Bone erosion

Retrograde thrombophlebitis

Preformed pathways

Via labyrinth or perineural spaces to IAC

#, dural tear & CSF leak

Eiology H.influenza and S.pnemoniae

Anaerobes rare

Pathophysiology – Pia arachnoid inflamed

Outpouring of fluid into subarachnoid space

Increased CSF pressure

CSF clear turbid purulent

WBCs +organisms

Types- a.Generalised

b.localised

Clinical features

Symptoms & signs due to presence of infection

Raised ICT

Meningeal & cerebral irritation

Symptoms Signs

Fever with chills & rigors neck rigidity

Headache kernigs sign

Photophobia & mental irritability brudzinski sign

Nausea &vomiting(sometimes projectile) tendon reflex

Drowsiness,delirium,coma initial exaggerated

Cranial palsy & hemiplegia later sluggish

Investigation

Fundus examination

Csf analysis

CT scan

MRI

PCR bacterial DNA

Treatment

a.medical- 2nd/3rd gen cephalosporins corticosteroids

LP (reduced ICP)

b.surgical- myringotomy & grommet

mastoidectomy

MENINGITS

AOM COM

IV antibiotics Perforation cholesteotoma

Resolution AOM+

IV antibiotics Surgery

Audiometry CTscan

CTscan

Mastoid Resolution Partial

resolution

Observation

Elective urgent

Clear Opaque mastoid mastoid

Exploration exploration

Grommet Cortical Mas.

Antibiotics Antibiotics

Lateral Sinus Thrombophlebitis

Also called sigmoid sinus thrombophlebitis

Inflammation of lateral or sigmoid sinus with formation of thrombosis inside lumen of sinus

Commonest organisms

Streptococcus

Pnemmococcus type 3

Pathophysiology

AOM COM

Erosion of bone covering sigmoid sinus

immune

status Perisinus abscess/Inflammation

Inflammation of outer wall (dura) of sinus

Platlets,rbcs Inflammation of inner wall (intima) of sinus

Fibrin,wbcs osteothrombophlebitic

Mural thrombus extension via small

venules

Propagates obliterating empties virulent

Lumen organisms into

Sigmoid sinus

Septicemia

Clinical features

Symptoms

.Hectic Picket fence type fever with rigors:

Headache: early stage mild due to perisinus abscess

late stage severe due to venous obstruction

Projectile vomiting & neck rigidity

Ear discharge

Deafness

Opthalmoplegia

Blindness

Signs

Tenderness over mastoid

Progessive anemia and emaciation.

Griesinger,s sign: due to thrombosis of mastoid emissary vein

oedema appears over the posterior part of mastoid

Papilloedema: fundus shows blurring of disc margins ,retinal hemorrhages or dilated vein.

Tobey-Ayer test:(Quenckenstedt test)

compression of each external jugular vein rise of 50 to 100 mm Hg

difference bet two sides <50 mm Hg

thrombosed side no increase in pressure

normal side rapid increase in CSF pressure

false positive if normal sinus very small/absent

false negative if collateral draining venous sinus

Crowe – Beck test :pressure on jugular vein of healthy side produces engorgement of retinal vein (seen by opthalmoscope) & supraorbital veins.

Engorgement subside on release opf pressure.

Tenderness on along jugular vein:may associated enlarged & inflammed jugular chain lymphnodes & torticolis

Investigations:

Blood smear to r/o malaria

Blood culture : causative organism

Csf examination :normal except rise in pressure

Xray mastoid: clouding of air cells-acute mastoiditis

\ destruction of bone –cholesteotoma

Imaging studies

CECT : sinus thrombosis by Delta sign

Triangular area with rim enhancement& central low density area is seen in posterior cranial fossa on axial cuts

MRI : better delineates thrombus

Venography ot asses progression or resolution of thrombuis

Gadolinium enhanced MRI

Digital subtraction angiography

Complications

Tender cord like septic embolisation

Internal jugular lungs & joints

vein

Sagital sinus

Sigmoid sinus

Papilloedema

Neck stiffness Cavernous sinus mastoid emissary vein

thrombosis

Proptosis

Chemosis tenderness & edema

Ptosis over mastoid

Opthalmoplegia GRIESINGERS SIGN

Lateral Sinus thrombophlebitis

Child with cavernous thrombophlebitis complicating lateral sinus thrombophlebitis

Treatment

Medical

High dose IV antibiotics

Anticoagulants

Surgical

Cause AOM cortical mastoidectomy

COM open cavity mastoidectomy

Expose sinus

Palpate soft & pliable left alone

Rubbery,clot,firm

Sinus aspirated

Blood clot confirmed

Wrong diagnosis prior IJV ligation

Complete clot evacuation

IJV ligation

If continued sepsis

Septic embolisation

Anticoagulant therapy

Supportive treatment

Repated blood transfusion

Otitic Hydrocephaslus

Benign Intracranial Hypertension

Increased ICT

Normal CSF

Ventricles normal

No abscess

Pathophysiology

Disruption in venous circulation

Increased CSF vol

Brain edema

Retrograde extension of thrombophlebitis from sigmoid sinus

To superior sagittal sinus

Blockage of arachnoid villi

CSF decreased absorption

Increased secretion

Raised CSF pressure

Clinical features

Headache severe presenting feature

Drowsiness, blurring of vision ,vomiting, diplopia(6thnerve palsy)

Papilloedema, optic atrophy, 6th nerve4 palsy

Investigation

Increased CSF pressure but CSF analysis normal

CT scan normal ventricular size

MRI

Treatment

Aim to decreased ICT to prevent optic atrophy & blindness

Medical Surgical

Steroids decompression of sigmoid sinus

Mannitol CSF drainage shunts

Diuretics optic nerve decompression

Acetazolamide

Eradicate disease

Antibiotic therapy

Mastoid exp[loration to deal sinus thrombosis

Pneumocoele

Rare entity

For air to retained in intracranial tissue planes, a valvular communication must exist

Such communication follow skull fracture or surgical injury

Most commonly percolates into subarachnoid space and traumatized area

Eventually may communicate with ventriles

Present with headache

Diagnosis by skull Xray show loculated air within cranial cavity

Treatment

Mastoid explored and vslvular track plugged by muscle

Pneumocoele gradually absorbs and patient recoverd

CEREBROSPINAL FLUID OTORRHEA

Causes:

Chronic ear disease congenital malformation

Post surgical perilymph fistula

# temporal barotrauma

Irradiation

Clinical features; Clear colourless watery fluid

Aural fullness

Rhinorrhea

Diagnosis :

Glucose

Beta two transferrin assay

Hankerchief does not become hard

Treatment

Medical bed rest

300 head high

Surgical

Aim – isolate CSF from middle ear/Eustachian tube

Size of defect

Status of hearing

Minute large >2cms

Anacusic ear grafting grafting craniotomy repair

+suturing from above

E.tube obliteration

Perilymph Fistula

Patching of windows by perichodrium.

REFERENCES: 4TH SCOTT BROWN

7TH SCOTT BROWN

LUDMANN WRIGHT

SCHAMBURGH

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