The complications of otitis media

Complications within the cranium

Complications within the

temporal bone

Extradural complications

Extradural abscessMeningitissigmoid sinus thrombosis

Intradural complications:

.Subdural absceSS .Brain abscess

.Otitic hydrocephalus

.mastoiditis .Labyrinthitis

.Petrositis .Facial palsy

Diagramatic representation of intracranial complications of otitis media

Route of spread of infection from the ear:

1. Extension through bone

2. Spread through venous channels

3. Spread through normal anatomical pathways

4.Spread may occur through non anatomical bony defects

5.Spread may occur through surgical defects

Factors that determine the spread of infection:

Patient's general condition and immunologic status .

The virulence of the infecting organism. Adequacy / Inadequacy of treatment of the

middle ear condition. Pneumatization of mastiod air cells.

Intra cranial complication A)Extra dural complication: 1)Extra dural abscess:

Def: it’s accumulation of pus against dura matter ,It’s the commonest of all intracranial complications.

A)Extra dural complication:

1)Extra dural abscessPathogenesis -This is commonly preceded by loss of bone, either through demineralisation in acute infection or erosion by cholesteatoma in chronic disease.A) If cholesteatoma is non infected expose dura without inflammation.B) If cholesteatoma is infected form granulation tissue over dura

A)Extra dural complication:

1)Extra dural abscess

Clinical features:

1- Headache on the side of otitis media.

2-pulsating discharge.

3-fever.

A)Extra dural complication

1)Extra dural abscess

Management:

a)Diagnosis:

CT SCAN

b)Treatment:

mastoidectomy and drainge of abcess.

A)Extra dural complications

2)Meningitis :

Pathology:

Csf characteristic:

1- contains WBCs.

2-Contains rapidly

multiplying bacteria.

3-Decreases glucose level .

A)Extra dural complication

2)Meningitis :

Clinical features

-General symptoms

-Signs due to meningeal irritation:

1- Neck stiffness

A)Extra dural complication

2)Meningitis :

2- poitive kernigs sign

2)Meningitis :3-Brudzinski's sign

A)Extra dural complication2)Meningitis :

Management:

a)Diagnosis:

lumbar puncture

b)Treatment:

systemic antibiotics, Penicillin, Streptomycin , Chloramphenicol, Ceftrioxine

A)Extra dural complication3)Lateral sinus thrombosis:Pathogenesis:

A)Extra dural complication3)Lateral sinus thrombosis:Clinical features:Signs of blood invasionPositive greissinger’s sign Raised intracranial pressure:Papilloedema and visual loss.Hydrocephalus Tenderness and oedema along the course of

the vein in the neck

A)Extra dural complication

3)Lateral sinus thrombosis:

Investigations:

1)-A lumbar puncture

2)Queckenstedt test( Tobey - Ayer test)

A)Extra dural complication

3)Lateral sinus thrombosis:

Management:

a)Diagnosis:

CSF show:

1) increased white cells and reduced glucose levels.

2) Increase bacteria content.

A)Extra dural complication

b)Treatment:

Medical:

systemic antibiotics

- Streptomycin.

-Chloramphenicol

Surgical:

modified radical mastoidectomy

B)Intra dural complication:

1)Brain abcessStages of formation :

1-stage of cerebral

oedema.

2-stage of Liquefaction

necrosis.

3-Stage of rupture.

4-Stage of chronic

abcess.

B)Intra dural complication:1)Brain abcess

Clinical features:

1-Stage of invasion:-

headache, fever, malaise and vomiting.

2-latent stage:-

asymptomatic.

3-stage of expansion:

signs of increased intracranial pressure:

B)Intra dural complication:1)Brain abcess

1)Cerebral 2)Cerebellar abscess

localizing signs

- nominal aphasia- Visual field defects

-Hemiplegia or hemiparesis.- weakness and muscle incoordination - Ataxia

Intention tremorsSpontaneous nystagmus.Dysdiadokinesis 4-Last stage: Unless brain abcess treated : it ends by

death due to -coning of brain steam. -rupture of abcess.

B)Intra dural complication:1)Brain abcess

Management:a)Investigations:CT scan and MRI scansLumbar punctureB)TREATMENT:large doses of antibiotics. -Measures to decrease intracranial pressures.Incision and drainge.-mastoidectomy

B)Intra dural complication:2)Otitic hydrocephalus:

Def: It is a syndrome of raised intracranial pressure during or following middle ear infection.

Pathogenesis:

Obstruction of the lateral sinus affects cerebral venous outflow, or the extension of the thrombus into the superior sagittal sinus impedes CSF resorption by pacch ionian bodies.

B)Intra dural complication:2)Otitic hydrocephalus:

Clinical features: symptoms :1. headache2. drowsiness3. blurred vision4. nausea5. vomiting6. diplopia

Signs:1)papillodema2)Lateral

rectus palsy.

Management:

a)Diagnosis:

CT scan is diagnostic.

b)Treatment:

1) Reduce CSF pressure

2)Treat the ear infection

B)Intra dural complication:2)Otitic hydrocephalus:

Intratemporal complications1)Acute mastioditis

Def: acute infection of the mastoid antrum and air cells with destruction of the intercellular bony septa.

Pathology:

Outer table mastoid abcess Mastiod tip bezold's abcess. Roor of zygoma zygomatic

abcess. Lateral sinus lateral sinus

thrombosis. Petrous apex ptreositis.

Intratemporal complications1)Acute mastioditis

Clinical picture:Symptoms :1-fever2- otalgia3- mucopurulent discharge Signs: 1-Profuse mucopurulent discharge 2-Tenderness and redness over the mastoid.3-Oedema of the posterior superior wall of external auditory canal.

Intratemporal complications1)Acute mastioditis

Mangement:

a)Investigation:

X-ray will showhaziness in mastioditis.

abcess cavity in mastoid abcess.

Intratemporal complications1)Acute mastioditis

b)Treatment:

-Medical treatment :

1-Cleaning ear discharge

2-Antibiotic.

3-Antipyritic

-Surgical treatment:Cortical mastiodictomyInsertion of tympanostomy tube to drain pus.

Intratemporal complications1)Acute mastioditis

Intratemporal complications2)Petrositis:

Def: It's inflammation of the petrous air cells with destruction of the intercellular bony septae.

Pathology:

Accumulation of pus under pressure in the petrous air cells will lead to pressure necrosis of the inter cellular bony septa.

Clinical picture:

It's characterized by triad (gradenigo's sign):

1- Otorrhea

2-Retrobulber pain

3- Diplopia

Treatment:

Mastoidectomy

Intratemporal complications2)Petrositis:

Intratemporal complications3)Labyrinthitis:

Def: is an inflammation of the membranous labyrinth which may be:1)Toxic2)Bacterial

Intratemporal complications3)Labyrinthitis:

Pathology:1)Serous stage2)Suppurative stage: It's irreversible

stage.3)fibrous stage4)Osseous stage

Intratemporal complications3)Labyrinthitis:clinical picture

(1)-serous stage:

(2)-Suppurtive stage: the same manifestation but become more severer.

(3)-Fibrous stage

(4)Osseous stage: there's difficulty in cochlear implantation

Treatment:

1-Antibiotic

2-Surgical :

-Myringotomy in AOM.

-Mastiodictomy in COM.

3-Drainge of labyrinth

Intratemporal complications3)Labyrinthitis:

Intratemporal complications4) Facial palsy:

It occur due to facial canal dehiscent leading to lower motor neuron facial.

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It is formed by two roots

Nervus intermedius

Nervus intermedius

Motor Motor

1. Sensory afferents

2. Preganglionic parasympathetic

It emerges from the brainstem between the pons and the medulla.

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Divided into 6 segments

Divided into 6 segments

Facial nerve

Horizontal segment Mastoid segment

facial nerve in meddle ear

♦It extends from the geniculate ganglion to the horizontal semicircular canal and is 8-11 mm in length.

Tympanic or horizontal segment

♥The nerve passes behind the cochlear form process and the

tensor tympani. ♥The nerve lies against the medial wall of the vacuum tympani, above and posterior to the oval window.

♦ The wall can be very thin or dehiscent in this area, and the middle ear mucosa may lay in direct contact with the facial nerve sheath. ♦The fallopian canal has been reported to be dehiscent in the area of the oval window in 25-55% of postmortem specimens. Always anticipate finding a dehiscent or prolapsed facial nerve in its tympanic segment, especially in patients with congenital ear deformities.

♦The most important landmarks for identifying the facial nerve in the mastoid are the horizontal semicircular canal, the fossa incudis, and the digastric ridge.

N.B N.B

♦The second genu marks the beginning of the mastoid segment. The nerve continues vertically down the anterior wall of the mastoid process to the stylomastoid foramen.

♦The mastoid segment is the longest part of the intratemporal course of the facial nerve, approximately 10-14 mm long.

Mastoid segment.

The 3 branches that exit from the mastoid segment of the facial nerve ar

• (1) the nerve to the stapedius

muscle. (2) the chorda tympani nerve(3 )the nerve from the auricular branch of the vagus .

•auricular branch of the vagus nerve arises from the jugular foramen and joins the facial nerve just distal to the point at which the nerve to the stapedius muscle arises. Pain fibers to the posterior auditory canal may be carried with this nerve .

N.BN.B

•Structure of facial nerve•The axons are surrounded by myelin,

produced by the Schwann cells surrounding the axons.

•Three membranes comprise the nerve sheath.

•a-The epineurium is the outer covering. •b-The perineurium is the next more

inner layer. •C- endoneurium surrounds the

individual nerve fibers.

• It is a weakness or paralysis of the nerve that control facial expression on one side of the face .

• Facial paralysis is most often caused by a virus infection of the facial nerve. However, other conditions such as tumors, other infections,

• trauma, among others. • The condition is more • frequent in diabetics• and pregnant women. 

N.B N.B

Causes of facial nerve lesion

Supranuclear and

nuclear lesion Infranuclear

lesions

Causes of Infranuclear

lesions…….???

1-Trauma:-• physical, especially fracturesof the

temporal bone, may also cause acute facial nerve paralysis.Transverse fractures-;

♦ present the highest likelihood of facial paralysis (40-50%) .

♦Patients may also present with hemotympanum , sensory deafness, and vertigo – the latter two symptoms due to damage to vestibulocochlear nerve and the inner ear.

•Longitudinal fracture •present a lower likelihood of

paralysis (20%). •♥Patients may present with •hematorrhea , tympanic

membrane tear, fracture of external auditory canal, and conductive hearing lossDiagnosis-:

Computed tomography (CT) nerve conduction studies (ENoG)

• Management:-• ♦If nerve conduction studies show a large

(>90%) change in nerve conduction, the nerve should be decompressed.

• ♦The facial paralysis can follow immediately the trauma due to direct damage to the facial nerve, in such cases a surgical treatment may be attempted.

• ♦In other cases the facial paralysis can occur a long time after the trauma due to oedema and inflammation.

• 2-Herpes zoster oticus:• -(Ramsay Hunt syndrome (RHS)

type 2) • It is a disorder that is caused by the

reactivation of pre-existing • Herpes zoster virus in • a nerve cell bundle in the head• (the geniculate ganglion).

• Symptoms and signs:-• ♦ acute facial nerve paralysis, (pain in the

ear, • taste loss in the front two-thirds of the

tongue, dry mouth and eyes), • ♦eruption of a erythematous vesicular rash

in the ear canal, the tongue, and/or hard palate.

• ♦ It may also affect vestibulocochlear nerve and patients may also suffer from tinnitus, hearing loss, and vertigo.

• Prognosis:-• ♦complete recovery can be achieved in 75%

of patients if treatment with prednisone and acyclovir is started within the first 3 days of onset of facial paralysis.

♦ Chances of complete recovery decrease as treatment is delayed, may lead to complete loss of response to facial nerve stimulation.

• Treatment apparently has no effect on the recovery of hearing loss.

• Diazepam is sometimes used to treat the vertigo. N.B N.B

3-Acute and chronic otitis media:-

• Facial palsy can present as complication of acute suppurative otitis media, otitis media with effusion, chronic otitis media, and mastoiditis.

♥ infection involving the fallopian canal can lead to inflammation and neural edema.

N.B

♥Immediate treatment should be directed toward eradicating the infection.

♥myringotomy is performed promptly to drain the middle ear space.

♥ antibiotic therapy against the offending organism.

♦ The incidence of facial palsy in acute otitis media is approximately 1:20,000 cases.

☻Most cases are seen in children due to the greater incidence of acute otitis media in them.

♦The prognosis is excellent. Recovery of facial function begins rapidly in conjunction with resolution of infection.

♥Operative management is limited to myrigotomy and tube.

• ☺ Facial palsy in association with chronic otitis media or cholesteatoma carries amore ominous prognosis.

• ☺The development of paralysis is often more insidious.

• ☺ Aural toilet and antibiotic • are initiated promptly. • If the tympanic • membrane is intact, • myringotomy • is performed.

• 4- Neurosarcoidosis:-• - sometimes bilateral, itself a rare condition.

• 5-Tumors:-• A tumor compressing the facial nerve

anywhere along its complex pathway can result in facial paralysis. Common culprits are facial neuromas , congenital cholesteatomas, hemangiomas, acoustic neuromas,

• parotid gland neoplasms,• or metastases • of other tumors

• Diagnosis:-•1-Computed tomography (CT) or

magnetic resonance (MR) .•2-Physical:- ♥Head and neck examination

•Tests for facial innervation include the following:

☻Forehead wrinkling (frontalis muscle) ☻ Eye closure (orbicularis oculi muscle) ☻ Wide smile ☻Whistling

☻Blowing

• Clinical diagnosis is based on 3 steps, identification of the affected site, underlying etiology (trauma, infectious, neoplastic),

•and finally, clinical staging • (eg, with use of the House-

Brackmann scale).

N.B N.B

Grade Description Characteristics

I Normal Normal facial function in all areas

II Mild dysfunction Slight weakness noticeable on close inspection; may have very slight synkinesis

III Moderate dysfunction

Obvious, but not disfiguring, difference between 2 sides; noticeable, but not severe, synkinesis, contracture, or hemifacial spasm; complete eye closure with effort

IV Moderately severe dysfunction

Obvious weakness or disfiguring asymmetry; normal symmetry and tone at rest; incomplete eye closure

V Severe dysfunction

Only barely perceptible motion; asymmetry at rest

VI Total paralysis No movement

House-Brackmann Classification of Facial Function

Treatment:-• ♦Treatment of the facial paralysis depends on

the cause of the facial paralysis. • ♦In cases of infections, antibiotics are

prescribed and surgery may be necessary. • ♦In other cases, steroid medication

(prednisone) is prescribed in combination with an anti-viral medication.

• In cases of tumor or paralysis resulting from resection of tumors of head and neck, the treatment usually consists of one or more of various facial reanimation procedures.

• ♥A critical element of the treatment of facial paralysis is the care of the eye.

facial nerve repair

Primary facial nerve repair

Cable nerve grafting

Nerve substitution

techniques

♦Hypoglossal-facial anastomosis

♦Cross-face grafting