SEMINAR MADE BY Dr NIKESH M GOSRANI,MS ENT &HNF ,IGGMCH

1. INTRACRANIAL
COMPLICATIONS
OF
OTITIS MEDIA

2. 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

3. 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

4. Routes of spread of infection from the middle ear space

5. 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

6. 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 MIDDLE EAR labrynthitis
Lateral sinus thrombophlebitis
Thrombosis of jugular bulb

7. Extradural abscess
Collection of pus between bone and dura
Occur in acute and chronic infection of middle ear.
Tegmen
Extradural
Dura

8. Common sites
1.around lateral sinus
2.opposite middle cranial fossa
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.

9. 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.

10. 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

11. 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

12. STAGE No.OF DAYS CHANGES CLINICAL FEATURES
Early Cerebritis 1 to 3 days Perivascular infla. Usually unnoticed
(invasion) Response Headache
Causes focal necrosis mild fever
& liquefaction with malaise
surrounding edema drowsiness
Late Cerebritis 4 to 10 days Formation of capsule No symptoms
(quiescent) of inflatory tissue
(localization) &fibrosis
Enlargement 10 to 13 days Abcess enlarge Aggravation of
(manifest abscess) symptoms
Cl. Features due to
Raised ICT
Disturbed func. Of
cerebrum or
cerebellum(focal
symptoms &signs)
Termination 14 days Cerebral into lateral Severity increases
(rupture) ventricle or white
matter
Cerebellar into
fourth ventricle
Clinical Features

13. 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

14. 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

15. Investigation
Skull Xrays
Xray mastyoid
CT scan showing cerebellar abscess
CT scan showing temporal abscess

16. 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)

17. 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

18. 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)

19. 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

20. 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

21. Clinical features
Symptoms
.
Hectic Picket fence type fever with rigors:

22. 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.

23. 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

24. Gadolinium enhanced MRI
Digital subtraction angiography
Complications
Tender cord like septic embolisation
Internal jugular lungs & joints
vein
Sagital sinus Lateral Sinus thrombophlebitis
Sigmoid sinus
Papilloedema
Neck stiffness Cavernous sinus mastoid emissary vein
thrombosis
Proptosis
Chemosis tenderness & edema
Ptosis over mastoid
Opthalmoplegia GRIESINGERS SIGN

25. Child with cavernous thrombophlebitis complicating lateral sinus thrombophlebitis
Treatment
Medical
High dose IV antibiotics
Anticoagulants
Surgical
Cause AOM cortical mastoidectomy
COM open cavity mastoidectomy

26. 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

27. 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

28. 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

29. 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.

30. REFERENCES: 4TH SCOTT BROWN
7TH SCOTT BROWN
LUDMANN WRIGHT
SCHAMBURGH
THANK YOU