Transcript Complications COM

Complications of Cholesteatoma
Dr. Supreet Singh Nayyar, AFMC
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Overview
 Cholesteatoma –A Historical perspective
 Cholesteatoma
 Origin of cholesteatoma
 Pathophysiology of cholesteatoma
 Intracranial complications of cholesteatoma
 Conclusion
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Bewildering History
 1683- Durverney , first described abscess of bone originating
form external auditory canal ,described it as .scales
 1892-Cruveilhier described it as avascular tumor arising
from subarachnoid space
 1838- Muller coined the term cholesteatoma as he
demostrated presence of chloestrin and fat in the
lesion.(despite this misnomer its still used today.)
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History contd..
 1855 –Virchow classified cholesteatoma among squamous
cell carcinoma and atheromas, postulated that cholesteatoma
arise from mesenchymal cells
 1873-Von Troeltch was first to consider the epidermal
origin of the disease, epidermal debri originating in EAC
lead to pressure on TM –pressure induced necrosis of bone
 1889- Gruber , Wendt & Rokitanski considered that middle
ear mucosa undergoes metaplasia in response to chronic
inflammation
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 Haberman & Bezold (1889)-proved that cholesteatoma arises
from from skin of EAC under influence of chronic middle ear
inflammation
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Cholesteatoma
Cholesteatoma is a three dimensional epidermal and
connective tissue structure, usually in the form of a sac
and frequently conforming to the architecture of the
various spaces of the middle ear, attic, and mastoid.
This structure has the capacity for progressive and
independent growth at the expense of underlying bone,
displacing or replacing the middle ear mucosa, and has
a tendency to recur after removal
- Abramson
(Cholesteatoma – First International Conference, Birmingham, 1977
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Epithelial invagination
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Structure of cholesteatoma
Perimatrix
Matrix
Keratin (dry
or active
bacterial
infection
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Pathophysiology of cholesteatoma
 Pressure induced bone resorption
 Enzymatic disollution of bone by cytokine mediated
inflammation
-Enzyme – matrix metalloproteinases (MMP)
- MMP 2,MMP9
cytokines IL-1a .IL-1b,TNF a, TGF a, EGF.
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Pathology of complications of
cholesteatoma
Direct
erosion of
the bone
Most common
pathway by which
disease extends
beyond middle
ear cleft
Round window
,oval window
Natural
communications
Progressive
thrombophlebitis of small
venules
Along periarteriolar
spaces of VirchowRobin
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Routes of
spread of
the disease
Vascular
channels
Abnormal
preformed
pathways
Congenital:
-aberrant
arachnoid
granulations
-Meningo
encephaloceles
Acquired
-temporal
bone #
involving otic
capsule
-Surgically
created defects
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Relative incidence of Complications in
mucosal and squamosal COM*
Extra cranial complications %
Intracranial complications %
Postauricular abscess
Meningitis
12
Brain abscess
52
20
Facial palsy
1
1
75
6
Bezolds abscess
2
Subdural abscess
Petrous apicitis
0.2
Extra Dural abscess
10
Lateral sinus thrombosis
20
* Scott- Brown’s Otolaryngology ,Head and Neck Surgery
www.nayyarENT.com : seventh edition. pg 3435
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Intracranial complications
 Meningitis
Temporal lobe abscess
 Brain abscess
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Cerebellar abscess
Lateral sinus thrombophlebitis
Extradural abscess
Subdural abscess
Otitic hydrocephalus
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Although it is thought that majority of
intracranial complications are due to squamous
disease as compared to mucosal disease it is
not the case.
Squamous(%)
Mucosal(%)
Intracranial
59
41
Extra cranial
41
59
overall
58
42
*Scott- Browns : Otolaryngology, Head & Neck
Surgery ; Seventh edition pg3436
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Extradural abscess
 Anatomically Dura is a very tough structure
 when the disease reaches Dura Pachymeningitis results
 Dura lightly attached
Lateral to arcuate Eminence
- large abscess
Medial to its attachment
- small abscess
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 Large abscesses compress squamous part of temporal bone
causing ostietic erosion and comes out as sub periosteal
abscess – Potts puffy tumour
Extra Dural abscess more common in posterior cranial fossa
compared to middle fossa
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Clinical features
 Extradural abscess has no specific features
 Headache
 Deep seated boring pain
 Malaise
 Tenderness on tapping temporal region
 Communication with EAC pus discharge –relief following
discharge
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Investigations
 Routine hematological profile
 Pus culture
 CT scan
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Treatment
 Broad spectrum Antibiotics
 Surgical evacuation of pus by removing underlying osteitic
bone
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Posterior cranial fossa
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Perisinus abscess
Lateral Sinus
Thrombophlebitis
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Lateral sinus Thrombophlebitis
 50% of all the cases have concomitant
Conditions like cerebellar abscess or meningitis
Peri sinus abscess
Acute mastoiditis
Lateral sinus
thrombosis
Internal jugular
vein(common)
Cavernous sinus (rare)
Superior petrosal
sinus(rare)
Pyaemia
Pyaemic abscess
lung
Subdural abscess
Brain abscess
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Clinical Features
 Classical presentation “Picket fence fever”
 Fever- sweating- symptom free period- again fever
 Chills
 Rigors (temp reaching up to 40 degree Celsius)
 Vomiting
 Dehydration
 Tenderness along IJV
 *However in present day and age classical presentation is seldom
seen due to advent of broad spectrum antibiotics
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contd…
 Greisengers sign: pitting edema in post aural region due to
thrombosis of mastoid emissary vein
 Rise in CSF pressure as demonstrated by
 Queckenstedts test
 Tobey Ayer test.
 Lillie Crowe test
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Investigations
 Complete blood count
 Falling Hb values
 Polymorphonuclear leucocytosis
 HRCT temporal
bone
 CECT – filling defect
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Management
 Medical
 a)
IV Antibiotics
 b) Anticoagulants not recommended routinely
 coagulation favorable to prevent bacterimia
 thrombosis generally not too much extensive as
anticipated
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 Surgical
 Undertaken early to expose and treat infected lesion
Timing of Mastoidectomy depends on the response to medical treatment
Internal jugular vein ligation-Doubtful
- thrombosis already spread beyond elective site
- vein difficult to expose amidst inflamed surrounding tissues
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Brain abscess
 Commonest intra cranial complication
 Cerebellar abscess
 Temporal lobe abscess
 Cerebellar abscess is nearly always otogenic
 Majority of brain abscess are associated with chronic otitis
media although acute otitis media also accounts for
significant number
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Temporal lobe abscess
Extra Dural abscess
Localized
encephalitis
Septic thrombosis of
pial veins (ASOM)
Sub cortical
white matter
Perivascular
Liquifactive
necrosis
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Cerebellar abscess
 Mastoiditis
Peri sinus abscess
Cerebellar Abscess
labyrinthitis
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Clinical features
 Increased intracranial tension
 Focal signs
 Systemic disturbances
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 Increased intracranial tension
Vomiting
Drowsiness
Confusion
lethargy
Papillodema - long standing abscess
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 Focal signs
Temporal lobe –visual field defect
(homonymous hemianopia)
-Aphasia (nominal aphasia)
if dominant hemisphere is
involved
- Seizures
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 Focal signs –
Cerebellar abscess – Truncal and limb
ataxia
- Cerebellar signs
-Rhombergs test positive
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Systemic features
 Fever.
- In cases of Temporal lobe abscess the temperature may
remain sub normal
- High fever incase abscess raptures into ventricular system
 Loss of appetite
 malaise
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 CT Scan
 MRI
 EEG
 Arteriography
 Pus culture and sensitivity from offending ear
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Treatment
 Emergency in case pt deteriorating fast due to raised ICT- inj
hydrocortisone 2-4 gms
- 20% Mannitol
 Antibiotics- essential to cross BBB
 Definitive – Neurosurgical
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CWD
mastoidectomy
(COM)/cortical
mastoidectomy
(AOM)
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D/D
 Circumscribed serous meningitis may mimic clinical and
radiological features of Cerebellar Abscess
 Formed due to localized meningitis and cyst formation cyst
in subarachnoid region
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Meningitis
 Infection reaching pia arachnoid
by routes already described , commonly
 Serous meningitis
 Purulent meningitis
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Clinical features
 Headache
 Neck Stiffness
 Fever –initial rigors ,fever settles down to continuous fever
of 38- 38.5 degree Celsius
 Positive Kernigs sign
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Investigations
 Hematological investigations
 CSF examination
 MRI / CECT
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Treatment
 Parentral antibiotic therapy- penicillin still drug of choice, 2-
4 megaunits 6 hourly
 Intrathecal penicillin10,000 units
 if initial CSF tap is turbid
 When pt is stabilized can be taken up for Tympano-Mastoid
exploration.
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Subdural abscess
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Collection of pus between Dura & Arachnoid
Manifests as leptomeningitis, effusion or abscess
Rate of spread determines the clinical & pathological pattern.
Associated with other complications
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Clinical presentation
Clinical features
 Headache, fever, drowsiness
 Focal neurological symptoms
a) irritative epilepsy
b) hemi paresis
 Papilloedema and
cranial nerve palsies
are uncommon
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 Investigations : CT scan
MRI
 Management.
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Evacuation of abscess by burr hole / craniotomy
IV Antibiotics
Treatment of ear
Antiepileptic medication after recovery
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Otitic hydrocephalus
 Benign intra cranial hypertension
 Frequently affects children and adolescents
 Obscure etiology; possibly sequale to bilateral lateral sinus
thrombosis
 C/F – Intermittant headache
Uni/bilateral papillodema
CT scan to rule out other more serious complication
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Treatment
 Repeated Lumbar puncture at 48 hr intervals
 Medical –diuretics / Acetazolamide
 Long standing cases – surgical ventriculoperitonial
shunt/subtemporal decompression
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Conclusion
 Intracranial complications of COM have drastically reduced however
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mortality from complication remains significantly high even today
(8%).
The incidence of complications are nearly as common in mucosal
disease as in squamous disease.
MRI remains gold standard for most of the intracranial complications
Broad spectrum antibiotic cover is to be started immediately as soon
as diagnosis is established followed by specific antibiotic cover
according to the culture and sensitivity
Minimum Ear surgery for a complicated COM AAD remains CWD
mastoidectomy
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References
 Scott- Browns ;Otolaryngology , Head & Neck Surgery; Seventh
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Edition
Scott –Browns ;Diseases of Ear Nose and throat; Fourth Edition
Mawson’s; Diseases of the Ear ; Fifth Edition
Logan Turners Diseases of the Nose Throat & Ear ;Tenth Edition
Otolaryngologic Clinics of North America Volume 39, Issue
6,(December 2006)
Various internet searches using Google ,Google images
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