COMPLICATION OF CSOM

Dr.R.Madana Gopal
Asst. professor
Dept. Of E.N.T.
Govt. General Hospital
Madras Medical College
 History
• Recognized since the age of Hippocrates in 460 BC “Acute
pain of the ear with continued High fever is to be dreaded
for the patient may become delirious and die”
• Celsus 25 AD “Inflammmation and pain of the ear leads to
insanity and death”
• Avicenna first described brain abscess in detail described
• Lepert – L.S of trombosis in detail
• Balance – ear increased
– brain decreased
• 20% of csom complication
• 1/3 Multiple Complication
• Pre Antibiotic Era Death was 1:40
• All L.S.T. was fatal in PRE
ANTIBIOTIC PERIOD
 COMPLICATION DUE TO
---AOM
---CSOM
INTRACRANIAL EXTRACRANIAL
• Extradural abscess • Facial Paralysis
• Intradural abscess
• Labyrinthits
• Sigmoid Sinus
Thrombosis • Extradural
• Meningitis abscess
• Brain abscess • Petrositis
• Otitic
Hydrocephalus
 ROUTES OF SPREAD
• Extension by Thrombophlebitis
• Extension by bone erosion(most
frequent)
• Extension by preformed pathway
a. Anatomical-round and oval window
b. Non anatomical –trauma
c. Surgical defect-stapedectomy
d. Along periarteriolar spaces of
Virchow Robin
 FACTOR INFLUENCING THE
DEVOLOPMENT OF
1. PatientCOMPLICATION
Attributes :
Age, immune status, intercurrent
chronic disease
(DM,Leukemia).
2. Bacterial Attributes
Virulence, susceptibility
3. Efficacy of treatment of
underlying middle ear disease
 GENERAL PRINCIPLES
• Complications should be regarded as a
group, since there are multiple in
about 1/3 of instances.
• Danger symptoms/signs
Headache, malaise, fewer,drowsiness
• Principles of Treatment
1. Systemic antibiotic therapy.
2. Local neurosurgical attention to the
complication(s) identified.
3. Treatment of the ear lesion.
1. SYSTEMATIC ANTIBIOTICS

• Multiple organisms – Multidrug therapy

• Acute infection – str.pneumoniae & H.infl
• Chronic infection – gram ‘–ve’ & anearobes
• H.influenza – chloramphenicol, rifampicin
• Gram ‘–ve’ amino glycosides
• Anaerobes – metronidazole
• Combination like gentamycin /
chloramphenicol + ampi + metrogyl
2. TREATMENT OF EAR

• Timing.

• Intracranial complications
controlled
before operating the ear.

• Exception – Deteriorating state.

 EXTRADURAL ABSCESS
• Between the dura and bone
• Granulation tissue limits the disease
• Petrous bone – Gradenigo’s synd
facial pain
diplopia
aural discharge
 EXTRADURAL ABSCESS

• Clinical features
- Incidental finding
- Chronic ear discharge + headache +
malaise
• Diagnosis – CT
• Management
- Pus evacuated, bone removed,
granulation tissue left
- Antibiotics, treat other complication
SUBDURAL ABSCESS (EMPYEMA)

• Spread of infection through dura to

subdural space
• Non hemolytic streptococci –
microaerophilic or anaerobic str.
Milleri
• H.Influenza
SUBDURAL ABSCESS (EMPYEMA)

CLINICAL FEATURES:
Severe headache, fever,
drowsiness

fits
• Focal neurological
symptoms paralytic
-- hemiplegia
-- hemianopia
-- aphasia
SUBDURAL ABSCESS (EMPYEMA)

• DIAGNOSIS :
meningism accompany headache
DD-meningitis ,brain abscess
CT
• MANAGEMENT :
Massive doses of systemic antibiotics
Burr hole/craniotomy and Abscess excision
Middle fosa extradural abscess
LATEREL SINUS Thrombosis
• Sigmoid and transverse sinus
• Preceded by extradural perisinus
abscess
• Venous thrombophelitis –Brain
abscess
• Proetus mirabilis,Staph,Pnuemo,
Bacteroids oralis, E.coli
CLINICAL FEATURES
• PRE ANTIBIOTIC ERA :
1. Picket –fence fever (40 c)
rigors ,sweating,shivering
2.Headache and neck pain
3.Progressive anemia and
emaciation
4.ICP-Hydrocephalus,pappilodema
5.Cavernous sinus-Chemosis and
proptosis of eye
6.Embolic propagation to lungs ,
large joints,subcutaneous tissue.

•
 LATEREL SINUS Thrombosis
• Present DAY
1. Otalgic, neck pain,mastoid
tenderness
2. Stiffness along SCM muscle
3. Pappiloedema 50%
4. Drowsiness,lethargy, and coma
5.Griesinger’s sign and
Odema over the post aspect of
mastoid
LATEREL SINUS Thrombosis

• Investigations
1. Blood – anemia,WBC,^ESR
2. Blood culture
3. lumber puncture
4. Quenckenstedt or Tobey-
Ayer
test
Quenckenstedt or Tobey-
Ayer test
1. Compression of each ext jug v.–50-
100mm Hg
2. Difference bet 2 sides < 50 mm Hg
3. Thrombosed side – no ^ CSF Press
4. Normal side – Rapid increase
5. False +ve – normal sinus very
small/absent
6. False –ve – collateral draining dural v.
sinuses
 LATEREL SINUS Thrombosis
INVESTIGATION:
• CT Scan
Conray enhancement – enhancement
of walls but not the contents of sinus-
empty triangle or Delta triangle
• Angiography
Digital subtraction venography
• MRI
Empty triangle or Delta sign
 LATEREL SINUS Thrombosis
TREATMENT:
 MEDICAL
• Systemic antibiotic
 SURGICAL
• Exception of gen. Principles – operation
should be taken up early
• Mastoid exposed within the first 2 days
• LS Thrombosis follg AOM Cortical
CSOM MRM
TEMPERATURE CHART
PULSE CHART
 MENINGITIS
• Commonest intracranial complication
• Patho
By direct spread
Thro suppurative labyrinthitis
Rupture of abscess into subarachnoid
ORGANISMS:
H.influenza, Str.Pnuemo type III
G-ve – proteus, pseudomonas
Anaerobes - bacteroides
MENINGITIS - CLINICAL FEATURES

• Head ache and neck stiffness – most constant

• Malaise and pyrexia 39-40 C
• Positive Kernig’s sign
• Positive Brudzinski’s sign
• Positive Babinski’s sign
• Mental hyperactivity, restlessness child
• Anxiety, drowsiness adult
• Photophobia – constant characteristic symptom
• Vomiting
• Cranial n. palsies
• Cheyne stokes respiration
• Delirium, stupor, coma, death
• Focal neurological sign – subdural or
cerebral abscess
• Epileptic fits don’t occur
MENINGITIS – DIAGNOSIS
LUMBAR PUNCTURE

MENINGITIS NORMAL
Appearance Cloudy Clear
ICP Increased 100-150mm
Hg
Cell count 100-10000
Prot 2 - 3 g/l 150 - 400 mg/l

Chloride 80 mmol/l 120 mmol/l

Glucose Reduced 1.7 – 3 mmol/l
 MENINGITIS - DIAGNOSIS

• CT SCAN
associated abscess
• MRI
typical signal changes in
meningitis
• PCR
bacterial DNA
 MENINGITIS - TREATMENT
• SURGICAL
Timing
Deterioration or failure of response over
48 hrs implies loculated infection in the
mastoid, needing surgical drainage
• MEDICAL
LP (reduced ICP)
Large doses of systemic antibiotics –
mainstay of treatment
Reduction of neurological sequelae
JEFFERSON’S BRAIN CANNUALE WITH STILETTES
 BRAIN ABSCESS
• Temporal lobe : cerebellum – 2:1
• Children – 25% of brain abscess otogenic
• Adults – 50%
• Route – direct extension common
cerebellar abscess ----- lateral sinus
thrombosis
----- suppurative
labyrinthitis
• 3 Stages : Initial encephalitis
Localisation(latent/quiescent stage)
Enlarging abscess (manifest stage)
 BRAIN ABSCESS
• Abscess in posterior fossa, cerebellum cause
^ICP earlier.
• Temporal lobe ----- pear shaped.
• Cerebellum ----- ovoid/irregular.
• Mortality rate ------ 60-70% in the past
14% nowadays
• Bacteriology :
complex mixture
anaerobic streptococci common
 BRAIN ABSCESS – CLINICAL
FEATURES
• Early stage- headache,fever,malise,vomiting,
drowsiness
• AOM : drowsiness
• CSOM : head ache
• Latent period 10 days to several weeks
• ^ICP
• Cerebral abscess in dominant hemisphere –
Nominal aphasia, quadrantic homonymous
hemianopia (upper part)
• Motor paralysis
• Cerebellar abscess : Ataxia, dysdiadochokinesia,
etc
 BRAIN ABSCESS -
INVESTIGATIONS
• CT Scan
Position, size
Other complications
Observing the progress of an abscess
• MRI
Distinguish bet pus, abscess capsule,
edema and normal brain
Spread of ventricles
BRAIN ABSCESS - TREATMENT
• Neurologically controlled and antibiotics
• Radical mastoidectomy after 10-14 days
• 20% mannitol 0.5 g/kg iv, Dexamethasone 4
mg iv q6h
• Antibiotics for 3-4 weeks
• Surgical
 Drain the abscess thro repeated burr holes
 Abscess excision
• antiepileptic
 OTITIC HYDROCEPHALUS
• Misnomer – benign Intracranial Hypertension
• Psuedotumour cerebri
• Patho : Unknown etiology – lateral
sinus thrombosis
• Clinical features
 Head ache, drowsiness, blurred vision, nausea,
vomiting, diplopia, papilloedema
• Differential diagnosis
 Other cause of ^ICP
 Brain abscess
• Treatment
 Steriods, diuretics, mannitol, repeated LP?
 Theco peritoneal shunting
COMPLICATION OF INFECTIONS OF MIDDLE
EAR
 CHILD WITH CAVERNOUS THROMBOPHLEBITIS
COMPLICATING LATERAL SINUS THROMBOPHLEBITIS
SEQUENCE OF PARALYSIS CAUSED BY AN ABSCESS IN THE
TEMPOROSPHENOIDAL LOBE
COMMON SITES OF BURR-HOLE USED IN MANAGEMENT OF
OTOGENIC BRAIN ABSCESS
RELATIONS OF POSTERIOR SURFACE OF THE TEMPORAL
BONE TO THE CEREBELLUM
TENTOIRAL HERNIATION DUE TO A SUPRATENTOIRAL
HYDROCEPHALUS
 FACIAL PARALYSIS
AOM
 <10% of pts
 Congenital dehiscence of the horizontal portion
 Infection --- infl. Of epi and perineurial spaces
 Neuropraxis
 Full recovery
 Appropriate systemic antibiotics
 Myringotomy (occasionaly)
 Cortical mastoidectomy (rarely)
 Operative decompression is unnecessary
 FACIAL PARALYSIS
CSOM
• Bony covering eroded by cholesteatoma or granulation tissue
• Pressure by a cholesteatoma sac
• Tympanic
• Diagnosis
 Slow onset, associated ear discharge
 EOT
 CT Scan
• Treatment
 Urgent operative exploration
 Cholesteatoma removed from surface of nerve
 Granulation tissue left untouched
 Healthy bone removed – decompression
 Full recovery in 70% of pts
LABYRINTHINE COMPLICATIONS
• Vestibular and cochlear
• Pathology
AOM
Round window
If infl changes induces in labyrinth
transgresses - serious labyrinthitis
If intralabyrinthine suppuration destroys
cochelar and vestibular fns. --- suppurative
labyrinthitis
CSOM
Cholesteatoma --- fistula
10% of all cases of CSOM - fistula
 SUPPURATIVE LABYRINTHITIS
• Clinical features
 Violent vertigo and vomiting
 SN loss
 Nystagmus
 Loss of cochelar fn is evidence of transition to
irreversible suppurative state – dead labyrinthitis
• Diagnosis
 EOT
 DD – VZ virus, cerebellar abscess
 CT Scan
 SUPPURATIVE LABYRINTHITIS
• Sequelae --- meningitis
• Management
Complete bed rest
Parental prochlorperazine /
cinnarizine, Parental antibiotics
Exploration of mastoid
Not necessary to drain a dead
labyrinth
Vestibular head exercises
 LABYRINTHINE FISTULA
• Most common –dome of lat semicircular
canal silent, brief episodes of vertigo
• CT Scan with 30 tilted axial scan
• Cold air caloric test
• Fistula sign:
On increasing pressure conjugate
deviation of eyes away from the examined
ear, on releasing, eyes return to midline
Vertigo
LSCC (ant to ampulla) – towards the
diseased side
 Vestibule – horizontal rotatory towards
the diseased
SSCC – rotatory towards normal
PSCC - vertical deviation
• False +ve
- Menniere’s disease
- Cong syphilis
• False –ve-
- Dead labyrinth
- Cholesteatoma protecting the fistula
- Inadequate sealing of speculum
 LABYRINTHINE FISTULA
TREATMENT
• Matrix peeled from other sides first
• Slight change in colour
• Compartmentalization
• Leave the matrix
.State of the other ear, second
exploration
• Remove the matrix
.Open cavity
 PETROSITIS
• Pneumatised petrous apex
• Pneumatised space:
- PERILABRINTHINE REGION :
Supralabyrinthine
Infralabyrinthine
- PETROUS APEX REGION :
Peritubal area
Apical area
• Gradenigo’s syndrome
 PETROSITIS
• Eagletons’ operation :
- superior approach – removal of
tegmen
• Thornwaldt’s operation :
- superior approach – along
supralabyrinthine tract
• Almoor’s operation :
- inferior approach – space bounded by
cochlea, carotid artery and tegnem
• Lempert – Ramadier’s operation :
- anterior to Almoor’s – peritubal cells
• Freckner’s operation :
- through arch of SSCC
INFLAMATION OF THE LABYRINTH
RELATIONS OF PETROUS APEX
LUMBAR PUNCTURE
HORIZONTAL SECTION THROUGH
FOURTHLUMBAR VERTEBRA
LEFT CEREBRAL HEMISPHERE SHOWS A RAGGED
ABSCESS CAVITY
MULTIPLE CEREBRAL ABSCESSES WHICH ROSE
FROM A LATERAL SINUS THROMBOPHLEBITIS