Complication Of Csom1

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 • Intradural abscess • Sigmoid Sinus Thrombosis • Meningitis • Brain abscess • Otitic Hydrocephalus

• Facial Paralysis • Labyrinthits • Extradural abscess • Petrositis

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 TobeyAyer test

Quenckenstedt or TobeyAyer test 1. Compression of each ext jug v.–50100mm 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 sinusempty 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 Cortical • LS Thrombosis follg AOM

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 Appearance ICP

MENINGITIS Cloudy Increased

NORMAL Clear 100-150mm Hg

Cell count Prot

100-10000 2 - 3 g/l

150 - 400 mg/l

Chloride Glucose

80 mmol/l Reduced

120 mmol/l 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 : Initial encephalitis • 3 Stages 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