Intracranial

Complications of Otitis
Media
Prepared for: Prof. Shakova E.G.
Prepared by: Ahmed Kamarulzaman

Volgograd 2010
Factors Influencing Complications
1. Age (newborn & elderly)
2. Poor socio-economic group (poor health
education, poor personal hygiene, limited
healthcare)
3. Virulence of organisms (resistant organisms)
4. Immune-compromised host (AIDS, diabetes,
immunosuppressive drug user)
5. Preformed pathways
6. Cholesteatoma (destroy bones)
 Pathways of Infection Spread
1. Direct bone erosion.
◦ In acute infections, it is the process of hyperaemic
decalcification. In chronic infection, it may be osteitis,
erosion by cholesteatoma or granulation tissue.
2. Venous thrombophlebitis.
◦ Veins of Haversian canals are connected with dural veins
which in turn connect with dural venous sinuses and
superficial veins of brain.
◦ Thus, infection from the mastoid bone can cause
thrombophlebitis of venous sinuses and even cortical vein
thrombosis.
◦ This mode of spread is common in acute infections.
3. Preformed pathways.
◦ Congenital dehiscences, e.g. in bony facial canal, floor of middle ear
over the jugular bulb.
◦ Patent sutures, e.g. petrosquamous suture.
◦ Previous skull fractures. The fracture sites heal only by fibrous scar
which permits infection.
◦ Surgical defects, e.g. stapedectomy, fenestration and mastoidectomy
with exposure of dura.
◦ Oval and round windows.
◦ Infection from labyrinth can travel along internal acoustic meatus,
aqueducts of the vestibule and that of the cochlea to the meninges.

4. General circulation (hematogenous metastases)

5. Osteomyelitis
Intracranial Complications
Extradural abscess
Subdural abscess
Meningitis
Otogenic brain abscess
Lateral sinus thrombophlebitis
Otitic hydrocephalus
 Extradural Abscess
Puscollection between bone and dura
Occurs in chronic & acute otitis media
AOM  hyperaemic decalcification
COM  cholesteatoma
Both bone destruction  abscess
May lie in:
◦ Post cranial fossa
◦ Perisinus abscess
• Affected dura mater covered with
granulations/unhealthy appearance/discoloured
Clinical pictures
Most of time: asymptomatic & silent
Persistent headache on side of OM
Severe pain in ear
Malaise with low-grade fever
Pulsatile purulent ear discharge
Disappearance with free flow of pus from
ear(spontaneously)
(+) signs of contrast-enhanced CT or MRI
At right temporal bone area
Treatment
Cortical/modified radical/radical
mastoidectomy
◦ Remove overlying bone till limits of healthy
dura reached
Abx
◦ Minimum 5 days & patient closely observed
for other complications
Subdural Abscess
Thrombophlebitic process  erosion of
bone intact  spread of pus in subdural
space  accumulation of pus in various
places
Clinical Pictures
Meningeal irritation 
◦ Headache, fever, malaise, ↑ drowsiness, neck
rigidity, (+) Kernig’s sign
Cortical venous thrombophlebitis 
◦ Aphasia, hemiplegia, hemianopia, Jacksonian
type of epilepsy
↑ intracranial tension
◦ Papilloedema, ptosis, dilated pupil
In left temporal / parietal area In left parietal area
Treatment
Craniotomy (drain subdural empyema)
Intravenous Abx (control infection)
Treat cause of ear disease
Meningitis
Inflammation of pia mater & arachnoid
mater
Usually present with bacterial invasion of
CSF in subarachnoid space
In infants & children, spread by blood
In adults, spread by none
erosion/retrograde thrombophlebitis
Clinical Pictures
Symptoms due to :
◦ Presence of infection
◦ ↑ intracranial tension
◦ Meningeal & cerebral irritation
◦ ↑ temperature (with chills and rigors)
◦ Headache
◦ Neck rigidity
◦ Photophobia & mental irritability
◦ Nausea & vomiting
◦ Drowsiness
◦ Cranial nerve palsies & hemiplegia
Examination:
◦ Neck rigidity
◦ (+) Kernig’s sign (extension leg, thigh flexed
on abdomen  pain)
◦ (+) Brudzinski’s sign (flexion neck  flexion
hip & knee)
◦ Tendon reflex exaggerted, then become absent
◦ Papilloedema (in late stage)
Diagnosis
◦ CT/MRI with contrast
◦ Lumbar puncture & CSF examination
 Turbid
 Cell count ↑
 ↑ protein level
 Decreased sugar & chlorides
 Culture reveal causative organisms
Treatment
Antimicrobial therapy
◦ Corticosteroid + Abx (helps reduce
neurological / audiological complication)
Myringotomy/cortical mastoidectomy
(AOM)
Radical/modified radical mastoidectomy
(COM with cholesteatoma)
Otogenic Sinus Thrombosis
◦ Mastoiditis  destruction of bone  rupture
into perisinus space  abscess of perisinus 
periphlebitis  sinus phlebitis
Symptoms:
◦ Parasinus abscess
◦ Periphlebitis
◦ Septicemia
 Chills
 Spiking temperature
 ↑pulse rate
 Headache
 Vomit
 Somnolence
 Neck stiffness
 Dyspnoea (due to lung metastases)
Diagnosis:
◦ Skull x-ray
◦ CT scan
◦ Mastoid x-ray
◦ Lumbar puncture
 ↑ pressure
 ↑protein
 Normal glucose
 WBC < meningitis
Thrombus in lateral sinus
postcontrast enhancement of the sinus wall on the left side
venogram that shows nonfilling of the lateral sinus on the left side
Treatment
Immediate surgical excision of 1°
inflammation foci in mastoid & sigmoid
sinus
Radical mastoidectomy
Thrombectomy
Internal jugular vein ligated
Otitic Hydrocephalus
↑ intracranial pressure + normal CSF
findings
Mid ear infection  lat sinus thrombosis
 venous return obstruction
If thrombosis go to sup saggital sinus 
impedes f(x) of arachnoid villi (absorb
CSF)
Clinical Pictures
Symptoms:
◦ Severe headcahe (maybe accompanied by nausea &
vomiting)
◦ Diplopia (bcoz paralysis of 6th cranial nerve)
◦ Blurring of vision (bcoz papilloedema / optic
atrophy)
Signs:
◦ Papilloedema 5-6 diopters (also with exudates &
hemorrhages)
◦ Nystagmus
◦ Lumbar puncture (CSF pressure >300mm)
Treatment
Aim: decrease CSF & prevent optic
atrophy & blindness
Acetazolamide + corticosteroids +
repeated lumbar puncture/lumbar drain
Abx therapy (in middle ear infection)
Mastoid exploration (in sinus thrombosis)