COMPLICATIONS OF SUPPURATIVE OTITIS MEDIA

Factors influencing development of complications

Age Poor socio-economic group Virulence of organisms Immune-compromised host Preformed pathways Cholesteatoma

Pathways of spread of Infection

Direct Bone Erosion

Venous Thrombophlebitis

Performed pathways

Classification

A) Intratemporal(confines within the temporal bone):

Mastoiditis Petrositis Facial paralysis Labyrinthitis

B)Intracranial: Extradural abscess. Subdural abscess Meninigitis Brain abscess Lateral sinus Thrombophlebitis Otitic Hydrocephalus

1)Acute mastoiditis

When the infection spreads from mucosal lining to bony wall of mastoid air cells we called it as mastoiditis.

Aetiology: It usually accompanies or follows ASOM.The

determining factors being high virulence of organisms or lowered resistance of patient.

Pathology:

1)Production of pus under tension.

2)Hyperaemic decalcification and osteoclastic resorption of bony walls.

Clinical Features: Symptoms:

Pain behind the ear. Fever. Ear discharge

Signs: Mastoid Tenderness. Ear Discharge Sagging of postero-superior meatal wall Perforation of tympanic membrane Swelling over the mastoid Hearing loss. General findings

Investigations:

Blood counts ESR X-ray mastoid Ear swab

Treatment: Hospitalisation of patient Antibiotics Myringotomy Cortical Mastoidectomy. It is indicated when there is Sub-periosteal abscess. Sagging of postero-superior meatal wall. Positive resorvoir sign. No response within 48 hrs of adequate

medical treatment. Mastoiditis leading to complications

2)Petrositis

Spread of infection from middle ear and mastoid to petrous part of temporal bone is called petrositis.

Clinical features: Gradenigo’s syndrome : It is the classical

presentation , and consist of a triad of a)external rectus palsy b)deep seated ear or retro orbital pain c)persistent ear discharge.

Fever , headache , vomiting , neck rigidity,facial paralysis.

Treatment: Cortical , modified or radical

mastoidectomy is often required. Iv antibiotics should precede and follow

surgical intervention.

3)Labyrinthitis:

There are three types of labyrinthitis:a)Circumscribed labyrinthitisb)Diffuse serous labyrinthitisc)Diffuse suppurative labyrinthitis

A)Circumscribed labyrinthitis(Fistula of labyrinth): There is thining or erosion of bony capsule of labyrinth.

Aetiology: CSOM with cholesteatoma Neoplasms of middle ear Surgical or accidental trauma to labyrinth

Clinical features:A part of membranous labyrinth is exposed

and becomes sensitive to pressure changes . so complain of:

Triensient vertigo often induced by pressure on tragus, cleaning the ear or while performing valsalva manoeuvre.

Diagnose by fistula test.Treatment:a)Mastoid exploration.b)Systemic antibiotics.

B)Diffuse serous labyrinthitis

It is diffuse intra-labyrinthine inflammation without pus formation and is a reversible condition if treated early.

Aetiology: Pre-existing circumscribed labyrinthitis

associated with chronic middle ear suppuration or cholesteatoma.

In acute infections inflammation spreads through round window.

Clinical features:In mild cases-vertigo and nausea.

In severe cases-vertigo is worse with marked nausea , vomiting and even spontaneous nystagmus.

Chochlea is also affected with some degree of SNHL.

Total loss of vestibular and cochlear function.

Treatment:Medical- Bed rest Antibacterial Therapy Labyrinthine sedatives-

prochlorperazine(stemetil) Myringotomy if labyrinthitis has followed

ASOM and drum is bulging.

Surgical: mastoidectomy

Diffuse suppurative labyrinthitis:This is diffuse pyogenic infection of

labyrinth with permanent loss of vestibular and cochlear functions.

Aetiology:It usually follows serous labyrinthitis,

pyogenic organisms entering through a fistula.

Clinical Features: There is severe vertigo, nausea,

and vomiting due to acute vestibular failure.

Spontaneous nystagmus. Patient looks toxic with total loss of

hearing.

Treatment:

B)Intracranial complications :

Otogenic brain abscess:50% of brain abscess in adults and 25%in

children are otogenic .Cerebral abscess is seen twice as frequently as cerebellar abscess.

Routes of infection: They develops as a result of direct extension of middle ear infection through tegmen or by thrombophlebitis.

Pathology:

a)Stage of invasion(initial encephalitis)

b)Stage of localisation(latent abscess)

c)Stage of enlargement(manifest abscess)

d)Stage of termination(rupture of abscess)

Clinical Features:Brain abscess is often associated with other

complications.

It can be divided into:

a)Those due to raised ICPb)Those due to area of brain affected

a)Symptoms and sign of raised ICP

Headache Nausea and vomiting Level of consciousness Papiloedema Slow pulse and subnormal temp.

b)Localising Features:

Temporal lobe abscess:

Nominal Aphasia Homonymous hemianopia Contralateral motor paralysis Epeliptic fits

Investigations:a)Skull x-rays including mastoidsb)CT scanc) LP

Treatment: High dose of iv antibiotics. For raised ICP-Dexamethasone 4mg iv 6

hrly Discharge from ear is treated by suction

clearance and topical ear drops. Neurosurgical treatment.

LATERAL SINUS THROMBOPHELEBITIS

ETIOLOGY: COMPLICATION OF ACUTE COALESCENT

MASTOIDITIS,MASKED MASTOIDITIS OR CHRONIC SUPPURATION OF MIDDLE EAR AND CHOLESTEATOMA

CLINICAL FEATUREa) HETIC TYPE OF FEVER WITH RIGORb) HEADACHEc) PROGRESSIVE ANAEMIA &EMACIATIONd) PAPILLOEDEMA

TRETMENT SYSTEMIC ANTIBACTERIAL MASTOIDECTOMY & EXPOSURE OF SINUS LIGATION OF INTERNAL JUGULAR VEIN ANTICOAGULANT THERAPY SUPPORTIVE TRETMENT