complication of otitis media

Complications of Suppurative Otitis Media

Classification:
A-Extra-cranial include:
Mastoiditis: acute, chronic; and masked mastoiditis
Lower motor neuron facial nerve palsy.
Labrynthitis.
Tympanosclerosis.
Chronic adhesive otitis media.
Ossicular discontinuity from ossicular erosion → Conductive deafness.
Otitis externa due to pus discharge from middle ear to external auditory canal otitis externa.
Squamous cell carcinoma of middle ear.

B-Intracranial :

Lateral sinus thrombophlehitis.
Meningitis.
Extra-dural, Subdural, brain (cerebellar or temporal lobe) abscess.
Otitic hydrocephalus.


Routes of spread of infection:
1-Direct spread through bone erosion.
2-Venous spread: by the spread of infected clot within small veins through bone and dura to venous sinuses (venous thrombophlebitis). 3-Spread through normal anatomical pathways:
A-Through oval and rounded windows to inner ear, then the infection spread from inner ear to inside cranial cavity through vestibular and cochlear aqueducts.
B-Through dehiscent suture line and congenital dehiscences.
4-Spread through non-anatomical bony defects:
A-Fracture line,
B-Neoplastic erosion.
5-Spread into brain tissues through periarteriolar spaces of Virchow Robin.

Acute Mastoiditis:

It occurs as a complication of acute otitis media due, to spread of infection from mastoid antrum to mastoid air-cells. Spread of infection from the middle ear to mastoid antrum and mastoid air cells result in pus formation inside the antrum and air cells with bone destruction, then pus come to lie under the periosteum after erosion of the lateral bony wall of mastoid, then it may discharge through the skin covering the mastoid process or it may spread from the mastoid tip along the digastric muscle or the sheath of sternomastoid muscle (called Bezold's abscess), or it may spread to posterior cranial fossa causing intracranial complications.

Clinical features:

It is more common in children, there is fever, pain tenderness over the Mastoid , displacement of pinna forward and downward due to soft tissue edema, fluctuant swelling over the mastoid (when there is subperiosteal abscess); & abnormal tympanic membrane (redness and perforation with discharge) present in 1/3 of patients.

Investigations:

Blood investigations: increased ESR and polymorphonuclear leucocytosis.
Mastoid X-ray → cloudy mastoid air cells, radiolucency is seen when there is abscess.
Pus for culture and sensitivity.


Treatment:
Intravenous antibiotics effective against the causative microorganism (the causative microorganisms are the same as those found in acute suppurative otitis media).
Analgesia.
Cortical mastiodectomy is indicated when there is failure if medical treatment for 24−48 hrs, or when there is subperiosteal abscess.

Masked Mastoiditis:

It usually results from under treatment of underlying acute otitis media; clinically the features are less severe than in acute mastoiditis. The patient presented with persistent fever, mild pain; and deafness after history of acute otitis media. Also there tenderness over the mastoid.
The tympanic membrane is red and there may be discharge due to tympanic membrane perforation.
Mastoid X-ray shows cloudy air cells.

The treatment is by:

1-Admission to hospital.
2-Intravenous antibiotics.
3-Analgesia.
4-Cortical Mastoidectomy is indicated when there is failure of medical treatment.

Lower motor neuron facial nerve palsy

1-Facial nerve palsy occurs in about 10% of acute otitis media when there is congenital dehiscence of horizontal part of facial nerve canal (facial canal on the medial wall of tympanic cavity).
It is neuropraxia and full recovery is expected after treatment of the infection, or a treatment is by systemic antibiotics, occasionally myringotamy or cortical mastoidectomy could be needed.

2-Facial nerve palsy in CSOM is due to erosion by cholesteatoma or granulation tissue or pressure by cholesteatoma. Treatment is by urgent mastoidectomy and decompression of facial nerve by removal of bone from either side of facial nerve to give space for edema of the nerve.


Labrynthitis:
It is defined as an inflammation of labyrinth (inner ear infection), it occurs in ASOM CSOM due to spread of infection through oval or round window to inner ear. The infection involve both perilymphatic and endolymphatic spaces leading initially to serous exudates (serous labrynthitis) then there will be pus (suppurative labrynthitis).

Clinical features:

Severe rotatory vertigo with nausea and vomiting.
Deafness (sensori-neural deafness).
Nystagmus: initially there is irritative nystagmus towards the diseased ear, and then the nystagmus will be paralytic nystagmus towards the healthy ear.
The patient lies immobile with the affected side uppermost to decrease nystagmus.

Investigations:

Ear swab for C/S when there is discharge.
PTA: shows sensori-neural deafness (should be done at bedside).
Caloric test: shows canal paresis (should not be done in the acute phase but done later on because it can exacerbate vertigo).

Treatment:

Bed rest and avoidance of head movement.
Labyrinthine sedative like cinnarizine or prochlorperazine to control vertigo, nausea; and vomiting.
Antibiotics .
I.V. fluid when there is vomiting.
Treatment of underlying ASOM by antibiotics, occasionally myringo-tomy or cortical mastoidectomy and treatment of underlying CSOM by radical or modified radical mastoidectomy, mastoidectomy is delayed until the symptoms of acute labrynthitis have subsided.


Sequele:
Meningitis due to spread if infection through vestibular cochlear aqueduct to meninges.
Unbalance when the patient tries to walk in the dark.
Total and permanent sensori-neural deafness.

Tympanosclerosis:

Definition:
It is abnormal condition of middle ear characterized by calcareous deposits in the tympanic membrane, tympanic cavity and occasionally the mastoid.

Etiology:

Trauma e.g. myringotomy.
Recurrent acute otitis media.
CSOM.
Secretory otitis media.

Pathology:

Inflammatory stage → formation of exudates and granulation tissue.
Reparative stage → collagen synthesis by fibroblast and hyalinization.
Stage of calcification and occasionally ossification.

Clinical features:

There is white chalk like plaques in the tympanic membrane.
Conductive deafness only occurs when these plaques are large, otherwise there is no deafness.
Investigations:
PTA shows conductive deafness (only when the plaques are large).
Tympanometry → shallow graph (type As).


Treatment:
No treatment in asymptomatic patients.
Hearing aids when there is disabling deafness.

Chronic adhesive otitis media:

Definition: formation of adhesions in the middle ear.
Etiology:
Suppurative otitis media.
Secretary otitis media.
Tympanic membrane may show areas of atrophy, thickening and often with white chalk plaques and it is adherent to medial wall of middle ear, so that the tympanic membrane is immobile when examined by for example Siegel's Speculum.

Investigations:

PTA shows conductive deafness.
Tympanometry show immobile tympanic membrane (flat tympanogram).
Treatment: hearing aids are the best.

Lateral sinus thrombophlebitis:

The sigmoid sinus lies just postero-medial to mastoid antrum. The lateral sinus comprising the sigmoid and transverse sinuses. The condition may occur in ASOM CSOM.

Pathogenesis:

The process usually preceded by the development of extra-dural perisinus abscess → inflammation of the wall of the sinus → thrombus formation → occlusion of the sinus lumen by the thrombus → infection of the thrombus → softening of the thrombus → septic embolization may spread to the lung, subcutaneous tissue, bones and joints


Clinical features:
Clinical presentation more likely to be seen today includes; fever without violent swinging, rigor or: sweating, aural pain and tenderness over the mastoid process, papillodema and drowsiness, some rare features (tenderness over the course of internal jugular vein, pitting edema over the occipital region behind the Mastoid due to obstruction of large mastoid emissary vein called Griesinger's sign).

Investigations:

CBP shows anemia, leucocytosis and increased ESR:
Blood culture.
Lumbar puncture may show increased CSF pressure (it should only be done after exclusion of brain: abscess and other intracranial complications that may precipitate coning).
Tobey-Ayer test: consist of compression. of internal jugular vein of normal side which causes increased in CSF pressure by 50−100 mm Hg , the manometer connected to lumbar puncture needle, while compression of internal jugular vein on the affected side cause little increase or no rise in CSF pressure.
Angiography shows the site of obstruction.
CT scan or MRI shows increased density and intensity respectively of the clot. Usage of contrast, material that show enhancement of the wall of the sinus but not of the clot called delta sign.

Treatment:

I.V. antibiotics (ampicillin, gentamycin, metronidazole).
Exposure of the sinus with incision and removal of the clot.
Treatment of middle ear disease: cortical mastoidectomy in ASOM; Radical or modified radical mastoidectomy in CSOM.
Prognosis: mortality rate is about 50%.

Otitic Hydrocephalus:

Etiology:
The etiology is unknown, but it may be due to lateral sinus thrombosis which impairs cerebral venous outflow, also extension of the thrombus to superior sagittal sinus impairs absorption of CSF by arachnoid villi, this will lead to increase intracranial pressure.
Also, it may be due to abnormalities of the venous sinuses in the skull.


Clinical features:
Headache and drowsiness.
Nausea and vomiting.
Blurred vision and diplopia.
O/E there is papillodema and lateral rectus palsy due to VI cranial nerve stretching (a false localizing sign in raised intracranial pressure).
Differential diagnosis:
Any cause of increased intracranial pressure e.g. brain abscess.

Investigations:

CT scan: to exclude brain abscess, it shows normal ventricles.
Lumbar puncture: shows markedly increased intracranial pressure.
Treatment:
Reduction of intracranial pressure by steroids, diuretics, mannitol, repeated lumbar puncture, occasionally ventriculo-peritoneal shunt in needed.
Treatment of middle ear disease; ASOM by antibiotics, sometimes myringotomy or cortical mastoidectomy; CSOM by radical or modified radical mastoidectomy.

Prognosis :Persistent raised intracranial pressure and persistent papilloedema may cause permanent visual impairment.

General Principles of Treatment of Intracranial Complications of Suppurative Otitis Media

Systemic antibiotic therapy:
Antibiotics must be chosen on an empirical basis, i.e. the most likely causative organisms, and then we change the antibiotic according to the results of culture & sensitivity.
The antibiotics must be able to cross the blood brain barrier, given in large doses in combination & IV. When the intracranial complications occur as a result of ASOM, we have to use antibiotics effective against the most likely causative organisms; so we use empirically ampiclox (effective against G+ve bacteria like Hemophilus influenzae and Staphylococcus aureus) and gentamicin, azlocillin or ticracillin (which are effective against G−ve bacteria like Pseudomonas and Proteus) and metronidazole (which is effective against anaerobes like Bacteroid fragilis).


Treatment of neurosurgical complications e.g. brain abscess, meningitis.
Treatment of ear diseases:
a-ASOM → by antibiotics, occasionally by myringotomy, or cortical mastoidectomy.
b-CSOM → by radical or modified radical mastoidectomy.
The treatment of ear disease is postponed until the neurosurgical complications do not respond to treatment, and then the ear disease should be treated earlier.