INTRACRANIAL COMPL.- CSOM

• EXTRADURAL ABSCESS• SUBDURAL ABSCESS• MENINGITIS• OTOGENIC BRAIN ABSCESS• LATERAL SINUS THROMBOPHLEBITIS• OTITIC HYDROCEPHALUS

EXTRADURAL ABSCESS

PATHOLOGY• Coll. of pus b/w bone & dura-middle or post. Cranial

fossa• Affected dura- covered i granulation & discoloured.• a/c- bone over dura-destroyed by hyperaemic

decalcification.• c/c-destroyed by cholesteatoma• Spread

– destruc. Of bone– venous thrombophlebitis- bone over dura remains

intact

• C/Fmostly asymp.- discovered CM or MRMpresence suspected when

persistent headache on side of otitis mediasevere ear achepulsatile purulent ear d/sdisapp. Of headache- i flow of pus from eargeneral malaise i low grade fever

• DIAGNOSISContrast enhanced CT or MRI

• Rxabscesss- evacuated by removing overlying bone till healthy dura are reached.Causative d/s- CM broad spectrum antibiotics

SUBDURAL ABSCESS• PATHOLOGY

Spread- erosion of bone & duraor thrombophlebitic process- bone intact.

pus lie against surface of cerebral hemisphere causing pr. Symp and pus get loculated.

•

C/FMENINGEAL IRRITATION

fever(102F or more)Headachemalaise, drowsinessneck rigidity+ve kernig’s sign

THROMBOPHLEBITIS-CORTICAL VEINS OF CEREBRUM

aphasia, hemianopia, hemiplegiajacksonian type of epileptic fits

RAISED ICT III nerve- Papilloedema, ptosis, dilated pupil

• DIAGNOSISCT scan or MRI

• RxSeries of burr hole ORCraniotomyBSAonce infection subsides- CM

LP- cause herniation of cerebellar tonsils.

MENINGITIS

• Inflm. Of Leptomeninges.(piamater and arachnoid )+ bact. Invasion of CSF in subarachnoid space.

• Most common intracranial complication• 2nd most compl. Of OM.• Infants & children- a/c- blood borne

adults-c/c - bone erosion or thrombophlebitis- asso Extradural abs. or granulation tissue

 

C/fInfectionRaised ICTmeningeal or cerebral irritation.

• Fever 102-104F+ chills & rigor• Headache• Neck rigidity• Photophobia & mental irritability• N, V(projectile)• Drowsiness• CN palsies & hemiplegia

EXMN

Tendon reflexes -exaggerated during initial stage, later – sluggish or absent

Papilloedema – late stages

Diagnosis:examination of CSF-culture and antibiotic sesitivity

lumbar puncture• Turbid• increased cell count-polymorphs.• Protein level- increased• reduced glucose levels (1.7-3 mmol/l )• Chloride content - fall from 120 mmol/l to 80mmol/l.

CT or MRI

Rx• Med

-systemic antibiotics-BSACorticosteroids

• Surgical– a/c- CM– c/c- MRM or RM

OTOGENIC BRAIN ABSCESS• always develop in the temporal lobe or the cerebellum of the same

side of the infected ear. Temporal lobe abscess is twice as common as cerebellar abscess.

• In children -25% of brain abscesses are otogenic – a/c• In adults -50% of brain abscess are otogenic- c/c

TEMPORAL LOBE ABSCESS CEREBELLAR ABSCESS

Spread direct extension -eroded tegmen plate. Retrograde thrombophlebitis

direct extension -Trautmann's triangle.Retrograde thrombophlebitis

Asso- EDA EDA, perisinus abs, SST or labtrinythitis

• PATHOLOGY

• C/FRAISED ICT TEMPORAL LOBE ABSCESS CEREBELLAR ABSCESS

HEADACHE- generalised, worse in mrng.

N,V(proj.)

DROWSINESS, CONFUSION, STUPOR, COMA

PAPPILLOEDEMA- late, early in cerebellar abscess

Slow pulse

Subnl temp

NOMINAL APHASIA- pt fails to tell name but can demonstrate their use

HOMONYMOUS HEMIANOPIA- visual field oppo to side of lesion is lostDue to pr on optic radiations.

CONTRALATERAL MOTOR PARALYSISUpward-face, arm leg

EPILEPTIC FITSUncinate gyrus-taste hallucination, mvmt lips & tongue, generalised fits

PUPILLARY CHANGES & OCCULOMOTOR PALSY-transtentorial herniation

HEADACHE-subocci. Asso i neck rigidity

SPONT. NYSTAGMUS- irreg, side of lesion

IPSILAT. HYPOTONIA & WEAKNESS

IPSILAT. ATAXIA

PAST-POINTING & INTENTION TREMOR- finger nose test

DYSDIADOKOKINESIA- rapid pronation & supination of forearm show slow irreg mvmt on affected side.

• INVESTIGATIONSKULL X- RAY To see midline shift,

if pineal gland is calcified, gas in abscess cavity

X-RAY MASTOID Evaluating asso ear d/s

CT SCAN & MRI To find the site & size of abscess cavityAsso compl- EDA,SST,

LP danger because of the risk of coning.CSF- rise in pr, turbid raised WBC- polymorphs 0r lymphocytes raised protein level nl glucose level

TREATMENT:MEDICAL High dose iv antibiotics- Chloramphenicol+3rd gen

Cephalosporin bacteroides- Metronidazole pseudomonas , proteus- aminoglycoside- gentamicinRaised ICT- Dexamethasone- 4mg iv 6th hrly or mannitol 20% - 0.5 g/kg body wt.Ear discharge- suction clearence & topical ear drops

NEUROSURGICAL -drained by placement of burr holes, -excision of the necrotic tissue along with the capsule.--Open incision of abscess and pus evacuation

-If abscess is treated by aspiration- repeat CT or MRI to see if it diminish in size. Penicillin is instilled into abscess after aspiration

OTOLOGIC a/c- may resolve i antibioticsC/c- RM

LATERAL SINUS THROMBOPHLEBITIS

FORMATION OF PERISINUS ABSCESSENDOPHLEBITIS AND MURAL THROMBUS FORMATIONOBLITERATION OF SINUS LUMEN AND INTRASINUS ABSCESSEXTENSION OF THROMBUS- prox- sup sagittal sinus dist- mastoid emissary vein, to jugular bulb or jugular vein

C/FHECTIC PICKET- FENCE TYPE OF FEVER I RIGOR Irregular fever-1 or > peaks/day, in b/w bouts

of fever- sense of well being. profuse sweating follows fall of temp. Due to septicaemia-release of septic emboli

HEADACHE Early- perisinus abscessLate- raised ICT

ANAEMIA progressive

GRIESINGER’S SIGN Edema over post part of mastoid Due to thrombosis of mastoid emissary veins

PAPILLOEDEMA Seen when rt sinus is thrombosed or when clot extends to sup sagittal sinus

TOBEY- AYER TEST

CROWE- BECK TEST Pr on jugular vein of healthy side produce engorgement of retinal veins & supraorbital veins

TENDERNESS ALONG JUGULAR VEIN Asso i enlarge & inflmm of jugular LN & torticollis

INVESTIGATIONBLOOD SMEAR To rule out malaria

BLOOD CULTURE To find causative organismBlood-taken at the time of chills

CSF EXMN Normal except for rise in pr,To exclude meningitis

X-RAY MASTOID Asso ear d/s

CONTRAST ENHANCED CT SCAN Sinus thrombosis by typical delta sign or empty triangle sign- rim show enhancement on post cranial fossa central low density area on axial cut

MRI CONTRAST ENHANCED- Delta signMR venography- progression or resolution of thrombus

CULTURE & ANTIBIOTIC SENSITIVITY Ear swab

TREATMENTIV ANTIBIOTICS BSA- continued at least for a week after operation

MASTOIDECTOMY & EXPOSURE OF SINUS

CM-a/c or MRM-c/cSinus bony plate is removed to expose dura- perisinus abscess is drainedIntrasinus abscess of infected clots- dura is incised & infected clot & abscess drained

IJV- LIGATION When above 2 therapy fail- to control embolic phenomena & rigors OR tenderness & swelling- JV spreading

ANTICOAGULANT THERAPY If thrombus extend to cavernous sinus

SUPPORTIVE TREATMENT Anaemia- repeated blood transfusion

OTITIC HYDROCEPHALUS• It is a syndrome of raised intracranial pressure during or following

middle ear infection. • also known as Pseudotumorcerebri.• Pathogenesis:

– lateral sinus thrombosis -affects cerebral venous outflow, – or the extension of the thrombus into the superior sagittal sinus impedes CSF

resorption by arachnoid villi

C/FSYMPTOMS

headache Severe

diplopia Paralysis of VI CN

blurred vision Papilloedema or optic atrophy

SIGNS

papilloedema.

Nystagmus Due to raised ICT

LP Pr- >300mm of water (70-120mm water)All other normal

TREATMENT• ACETAZOLAMIDE• CORTICOSTERIODS• REPEATED LP OR PLACEMENT OF LUMBAR DRAIN• LUMPOPERITONEAL SHUNT • ASSO EAR INFECTION

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