Otogenic Infective

Complications
 Labyrinthitis

Symptoms
Dizziness, nausea, vomiting,
whistling. noises in the ears, and
deafness develop within a brief
period. The patient has no fever and
no pain.
Pathogenesis
Toxins diffuse through the
labyrinthine windows in acute otitis
media, and the infection extends
along the vessels.
Pathogenesis

In chronic otitis media, with

cholesteatoma a fistula forms into the
labyrinth, and the infection extends
directly into the perilymphatic space.
After a transverse fracture of the
temporal bone or operative trauma,
there is direct damage to the
membranous labyrinth with secondary
infection.
Pathogenesis

Pathogenesis and
pathways of Spread
Of Otogenic
Complications.
intratemporal
complications:
1a Otogenic facial
paralysis
1b labyrinthitis;
1c petrositis
1d sinus
thrombosis.
Pathogenesis
Extratemporal
complicatioons
2 external rupture of
mastoiditis to form a
subperiosteal
abscess.

Pathogenesis
 Intracranial
Pathogenesis
complications:
3a extension into the
middle cranial fossa to
cause meningitis or
temporal lobe abscess;
3b extension to the
posterior cranial fossa
to cause meningitis or
cerebellar abscess.
Extension of otitis media
into the posterior cranial
fossa and development
of a cerebellar abscess
Pathogenesis

1, presinus abscess,
2, postsinus
abscess,
3, middle ear
cavity.
4, sigmoid sinus.
Diagnosis

• The patient has the cochlear

and vestibular symptoms of a
rapidly progressive inner ear
failure.
Differental diagnosis

• Menieres disease
• sudden deafness
• acute
vestibulopathy.
Treatment
Intravenous antibiotics are administered in
high doses by continuous infusion. The
middle ear should be drained, and a
mastoidectomy may need to be carried out. A
mastoidectomy is carried out for
cholesteatoma. Surgery is only undertaken
after fractures if there is a simultaneous CSF
otorrhea, facial nerve paralysis, or meningitis.
Labyrinthectomy must be carried out for
purulent labyrinthitis with meningitis.
Course and prognosis

Because of the varying pathologic

anatomy, several different clinical
forms of labyrinthitis are possible
Course and prognosis
serous in posttraumatic or viral cases,
purulent due to bacterial invasion of the
perilymphatic space, circumscribed due to a
labyrinthine fistula in cholesteatoma, and
generalized with involvement of the entire
labyrinth due to extension of infection or
generalized infection. In the latter form the course
is fulminant with irreversible total loss of function,
Possible extension of the infection to the meninges.
Epidural Empyema

Symptoms
Dull pulsating pain in the head, otorrhea,
and subfebrile temperature occur.
There is no completely characteristic
pattern of symptoms.
Pathogenesis

Acute or chronic infection extends

from the mastoid process into the
epidural space due to destruction of
the inner table by infection.
The infection may also spread by
preformed pathways along the
perforating vessels in the bone which
remains intact.
Diagnosis

This disease is characterized by a

paucity of symptoms. It is usually an
incidental finding at mastoidectomy,
but may be demonstrated by
neruoradiologic techniques including
angiography and computed
tomography.
Treatment

Immediate mastoidectomy with wide

exposure of the dura, drainage, and
antibiotics are indicated.
Course and prognosis

The prognosis is good if the disease is

recognized early. Otherwise there is
the danger of development of
pachymeningitis with extension to
the leptomeninges.
Subdural empyemata are rare and
only occur during the course of a
diffuse meningitis.
Otogenic Meningitis
Symptoms

These include headaches, stiffness of the

neck, scaphoid abdomen, increasing loss
of consciousness, photophobia,
restlessness, tonicclonic convulsions, and
facial paralysis. Otorrhea, otalgia, and
even deafness may be absent or occult.
Typically there is bounding pulse, irregular
breathing, and a fever of 39 °C to 40 °C.
The patient may have an oculomotor or
abducens paralysis and abnormal optic
fundi.
Pathogenesis

• The cause is spread of an acute or chronic bacterial

infection, usually due to pneumococci, into the
subarachnoid space
• By direct continuity due to inflammatory destruction
of the bony walls
• Along preformed pathways via the perforating
vessels and nerves in the bone, e,g, via the
caroticotympanic nerves.
• By a thrombophlebtis extending along the diploic
veins
• Via the labyrinth and as a result of spread into the
internal auditory meatus (this is rare)
 Diagnosis
In addition to the typical clinical symptoms of
acute meningitis, including abnormalities of the
cerebrospinal fluid (CSF), there are signs of an
acute, subacute, or chronic middle ear
inflammation of varying degrees of severity. If the
hearing is more or less normal, and the otoscopic
findings are equivocal, the signs of the
inflammation of the pneumatic system on
radiographs of the temporal bone
(in Schueller’s view, Stenver’s view, or
tomography) can be decisive in making the
diagnosis and the decision to operate.
Diagnosis

The CSF shows pleocytosis, a marked

increase of protein, and a reduced
sugar and chloride content. The
pressure is greater than 200 mm Hg.
In the acute phase, bacteria, usually
pneumococci, can be found in the
fluid.
Differential diagnosis

includes viral or epidemic

meningococcal meningitis and
tuberculous meningitis (low sugar
level).
Treatment

Antibiotics are given intravenously in

high dosages determined by sensitivity
tests, e.g, penicillin 40 to 60 million U
in 24 h for a pneumococcal infection.
Repeated lumbar or suboccipital
punctures are done.
 •
TreatmentThe blood-brain barrier for antibiotics varies
greatly depending on the severity of the
meningitis. Some of the antibiotic is inactivated by
binding to the CSF protein. Cephalosporin penetrates
poorly into the CSF, the broad-spectrum penicillins,
chloramphenicol, and gentamicin penetrate beter, but
there is a risk of pancytopenia with chloramphenicol
and of ototoxicity with gentamicin. Intrathecal
antibiotics are only used in exceptional cases.
Immediate drainage of the middle ear cavity by
mastoidectomy or radical mastoidectomy is required,
weith wide exposure of the dura.
Course and prognosis

• The disease ends fatally if it is untreated

or not treated correctly. The prospects of
recovery are about 90%provided that the
otitis media is recognized early as the
cause of the meningitis and provided that
energetic treatment is begun.
• Note: Any unexplained attack of
meningitis must be suspected as having a
nasal or aural cause.
Course and prognosis

In doubtful cases with obscure

otoscopic and radiographic findings,
the risk of an exploratory operation is
less than that of an expectant policy
if the middle ear space is infected.
Intensive treatment by antibiotics
doed not cause resolution so long as
the primary focus of infection has not
been eliminated by surgery.
Otogenic Sinus
Thrombosis
Symptoms

A perisinus abscess, periphlebitis,

and incipient sinus thrombosis cause
the same diagnostic difficultiues as
an epidural empyema. The release of
emboli of infective thrombi alone
causes the characterstic signs of
septicemia.
SymptomsThese include:
• Chills
• A spiking temperature chart, with several
peaks on the same day
• Increased pulse rate
• Headaches
• Vomiting
• Somnolence
• Neck stiffness (accompanying meningitis)
• Dyspnea due to septic lung metastases or
pneumonia
• Jaundice due to septic metastases in the liver
or to nonspecific reactive hepatitis
Pathogenesis

• Infection due to mastoiditis or cholesteatoma

destroys bone in continuity so that it can rupture
into the perisinus space. A perisinus abscess
forms with periphlebitis of the sigmoid sinus
followed by sinus phlebitis. The thrombus is
initially mural but later it occludes the lumen and
extends superiorly to involve the transverse and
sagittal sinuses and the mastoid emissary vein
and inferiorly toward the internal jugular vein.
Pathogenesis

• The thrombus undergoes

thrombolysis due to bacterial
infiltration, and septic metastases
are set up by blood-borne infected
emboli.
Diagnosis
• The following symptoms during acute
otitis media or chronic otitis media with
cholesteatoma suggest sinus thrombosis:
• High fever above 40 °C
• Spiking temperature with chills
• Swelling and sensitivity to pressure over
the mastoid emissary foramen at the
posterior border of the mastoid process
(Griesinger’s sign)
Diagnosis

• Induration and tenderness of the

internal jugular vein and of the
anterior border of the
sternocleidomastoid muscle
• Petechiae in septic coagulopathy
• Splenomegaly
Laboratory investigations

• Blood culture is strongly positive.

Urine testing shows hematuria due to
septic interstitial focal nephritis,
albuminuria,
and cylinduria.
Radiography

Schueller’s view shows osteolytic foci

in the mastoid. CT shows bone
destruction in the area of the sinus.
Angiography shows narrowing or
occlusion of the sigmoid sinus in the
venous phase of carotid
angiography.
Differential diagnosis

includes
• military tuberculosis, typhus,
malaria, brucellosis, viralpneumonia,
and cystopyelitis.
Treatment
• Immediate surgical excision of the primary
inflammatory focus in the mastoid and
sigmoid sinus by cortical or radical
mastoidectomy for cholesteatoma is
performed. The sigmoid sinus must be
exposed widely, the sinus wall is slit, and
thrombectomy is carried out. The internal
jugular vein is ligated and divided with a
margin of healthy tissue. Parenteral
antiobiotics are given in high dosages for a
long period, if possible determined by the
results of culture and sensitivity tests.
Course and prognosis

The disease is fatal if it is not treated

correctly, or if the basic cause and its
secondary consequences are not
recognized promptly. Eighty percent
of patients are cured with adequate
treatment begun early.
Note: Every unexplained septicemia
requires investigation not only of the
tonsils but also of the ear sincethe
otitis media which is primarily
responsible may be unrecognized
and only manifests itself by
septicemia.
Otitic Hydrocephalus
This disease is caused by an
intracranial pressure due to
obstruction to drainage of CSF
caused by a sterile otogenic sinus
thrombosis.
Symptoms

• Failing vision
• Vomiting
• Double vision
• Jacksonian epilepsy
• Pareses and disorders of sensation
Pathogenesis
A relatively symptomless chronic
mastoiditis follows an acute otitis media,
leading to sterile erosion of perisinous
bone and sigmoid sinus phlebitis with
formation of a mural thrombus which
extends to the confluence of the sinuses
and the superior sagittal sinus. This
causes occlusion of Pacchioni’s
granulations which interferes with
resorption of CSF, lending to increased
CSF pressue.
Diagnosis
• Abducens paralysis without Gradenigo’s
Syndrome
• Increased CSF pressure without pleocytosis
• Free CSF circulation without obstruction to
the CSF
• Congested optic fundi with failing vision
• Normal air encephalogram since the
ventricular system is not expanded
• Opacity and osteolytic perisinous lesions on
mastoid radiograms
• A history of acute otitis media 3 to 5 weeks
previously
Differential Disgnosis

• Petrositis with arachnoiditis in the

cerebellopontine angle
• Carotid aneurysm at the petrous
apex
Treatment

• Treatment includes a
mastoidectomy, exposure of the
sinus, thrombectomy, and
neurosurgical decompression to
allow drainage of the CSF.
Course and prognosis

These are good if the disease is

recognized and treated early.
Otherwise, the disease progresses to
blindness and the development of
Jacksonian epilepsy.
Otogenic Brain
Abscess
Today this is a relatively unusual
disease, but it was formerly one of
the most serious late complications
of chronic inflammatory middle ear
cholesteatoma.
 Symptoms
Table Symptoms of Otogenic Brain Abscess
1.Intitial stage Meningismus, nausea, headache, psychological , changes , The CSF shows pleocytosis and
fever increase of pressure and protein

2.Latent stage Epileptiform, attacks, neurologic signs Abnormal colloid curve

3.Manifest stage Papilledema, psychological changes, focal signs of aphasia, Vomiting and bradycardia
alexia, agraphia, hemiplegia, epileptic attacks, and ataxia in
cerebellar abscess.
Symptoms due to spread to neighboring organs include
cranial nerve paralyses, visual field defects, disorders of the
oculomotor system and of posture.

4,Terminal stage Stupor, coma, conjugated deviation to the side of the lesion,
bradycardia, and Cheyne-Dtokes respiration
Pathogenesis
The disease may spread as follows:
By direct continuity by one of the following
pathways
• (1) through the tegmen tympani to form a
temporal lobe abscess;
• (2)through the sigmoid sinus to the posterior
cranial fossa to form a cerebellar abscess;
• (3)from the labyrinth to the saccus
endolymphaticus to form a cerebellar abscess.
Pathogenesis

Along preformed pathways via

vessels
(the diploc veins, advancing septic
thromboangiitis of the cerebral veins)
or via the internal auditory meatus in
labyrinthitis.
temporal lobe abscess
Symptoms

• Speech disturbances revealed by a history of

aphasia, and difficulty in undersatanding
words. (This disorder of speech is exclusively
sensory and is never motor.)
• Central hearing disorders which are mostly
discrete
• Acoustic hallucinations
• Disorders of smell which are usually discrete
• Visual disturbances such as quadrantic
hemianopsia and gaze paresis
• Cranial neuropathies of the IIIrd to VIIth
cranial nerves
• Crossed lesions of the pyramidal tracts
Differential diagnosis

One must consider intracerebral

tumor.
cerebellar abscess
Symptoms

These include disorders of the

oculomotor and postural system, a
coarse spontaneous nystagmus to the
side of the lesion, vestibular provocation
nystagmus with irregular positional
nystagmus, gaze-directional nystagmus
due to secondary damage to the pons,
and gaze-paretic nystagmus to the side
of the lesion.
Further symptoms

include ataxia, intention tremor,

dysmetria, adiadochokinesia,
hypotonia, and symptoms due to
dpread to neighboring organs such
as paralysis of the IIIrd, Vth VIth VIIth
,IXth, and Xth cranial nerves.
Differential diagnosis

Labyrinthitis, acute vestibulopathy,

multiple sclerosis, cerebellar tumor,
and cerebellopontine angle
syndrome must be considered.
Investigations
In addition to otologic examination, include
• Neurootologic investigation: ERA, ENG, and
electrodiagnostic methods for the facial nerve
• Neuroophthalmologic investigation of the optic
fundi, visual field, and the ocular motor nerves
• Neurologic and neuroradiologic investigation
including computerized axial tomography (CT)
SCAN, MRI, EEC, brain scan, and possibly
angiography, echoencephalography, and
investigations of the CSF
Treatment
• The primary focus is removed by
mastoidectomy or radical mastoidectomy
by an otologist before a neurosurgical
procedure to remove the abscess.
• Primary removal of the brain abscess is
performed by a neurosurgeon. Treatment
by aspiration has now been abandoned
apart from a few exceptional
circumstances because it is more logical
to eliminate the focus of infection radically
by surgery along the pathway of infection.
Treatment

• Appropriate, intense antibiotic therapy

is administered.
• Course and prognosis. Despite intensive
surgical treatment, the mortality is still
20% to 30%.The defect often heals, but
there may be neurologic deficits after
neurosurgical excision of the abscess.
Petrositis
Previously, this was the most
important site of origin of an
otogenic intracranial complication,
Nowadays, it is usually controlled by
antibiotics and has therefore become
rare.
Pathogenesis
Good pneumatization of the entire
petrous pyramid is a prerequisite for
the development of petrositis. As a
result of extension of inflammation
from the middle ear to the
paralabyrinthine cells, purulent
liquefaction is set up in the cells triad
is due to the close relationship of the
pyramidal apex to the trigeminal
nerve and the abducens nerve.
Symptoms
Include otorrhea, ipsilateral irritation of the
trigeminal nerve, and abducens paralysis. The
facial, vagusm, and glossopharyngeal nerves
are also often paralyzed. Furthermore, the
patient may have signs of labyrinthitis due to
extension of the inflammatory process. With
the advent of antibiotics, the symptoms of the
primary otitis media may be hidden due to
antibiotic treatment. Predisposing factors
include advanced age and diabetes.
Diagnosis

The main symptoms are

• Trigeminal neuralgia
• Abducens paralysis with double vision
• Dizziness and deafness
• Deep throbbing headache
• Abnormal radiographs in Schueller’s and
Stenver’s view and CT
Differential diagnosis

• This includes brain abscess and sinus

phlebitis.
Treatment

Massive and prolonged parenteral

antibiotics are administered and
mastoidectomy, and translabyrinthine
clearance and drainage of the apical
cells, with preservation of the facial
nerve, are performed.
Prognosis

If the disease is recognized early and

treated effectively, the prognosis is
relatively good. However, the prognosis
is poor in patients of advanced age and
with diabetes (development of a
circumscript meningitis at the base of
the brain, with consecutive multifocal
microinfarctions of the pons).