Factors affecting indicators of impending intra cranial complications1.Age 1.otorrhea- creamier,thicker2.Poor socio-economic group 2.pain-deep nboring3.Virulence of organisms 3.headache,toxemia,altered sensorioum,4.Immunocompromised host photophbia5.Preformed pathways 4.neck stiffness,malaise6.Cholesteotoma
Routes of spread of infection from the middle ear space
Mode of spread of infection1.Bone erosion Acute infection Hyperaemic decalcification Chronic infection osteitis(cholesteotoma,granulation)2.Thrombophlebitis Extracranial Mastoid Emissary Intracranial Venous system Veins Venous system Sigmoid sinus Superior and Inferior Petrosal sinus Thrombophlebitis Venous ArterialCerebellar abscess Temporal abscess,septicemia3.Pervascural(intra brain spread) described by Atkinson Via Periarterial spaces of spares cortical vasculature Robin Virchow frequent in white matter4.Preformed pathways Congenital dehiscences Patent sutures Previous skull fractures Surgical defects
Oval and Round windowSpread of infection through different walls of middle wall Extradural abscess Subdural abscess Meningitis Brain abscess Lateral sinus thrombophlebitis Otitc hydrocephalus PnemocoeleAcute mastoidisFacial nerve palsy MIDDLE EAR labrynthitisLateral sinus thrombophlebitis Thrombosis of jugular bulb
Extradural abscessCollection of pus between bone and duraOccur in acute and chronic infection of middle ear. Tegmen Extradural Dura
Common sites1.around lateral sinus2.opposite middle cranial fossaPATHOLOGY Acute bone over dura destroyed hyperaemic decalcification Chronic bone over dura destroyed cholesteotomaIf by venous thrombophlebitis bone over dura intactAbscess well encapsulatedMiddle fossa abscess precipitates GRADENIGO,,s syndrome. Spread from petrous apex Result in irritation of Trigeminal ganglion and 6th cranial nerve Otorrhoea ,facial pain and diplopiaPosterior fossa abscess associated with lateral sinus thrombophlebitis and medially limitedby internal auditory meatus.
Clinical Features TREATMENTDepends on site.duration and rate of development 1.AntibioticsMost of time incidental finding 2.Surgical -Cortical or Radical orHowever suspected when Modified radical mastoidectomy1.Persistent severe headache 3.Neurosurgical –evacuated by2.severe pain ear removing overlying bone till3.general malaise with low grade fever. Limits of healty dura reached.4.Pulsatile purulent discharge.5.Disappearance of headache with free flow of pus. SUBDURAL ABSCESSCollection of pus between dura and arachnoidPATHOLOGYInfection spread from ear by erosion of bone and dura or by thrombophlebitisRate of spread of abscess determines clinical and pathological patternDura resistant to infection, granulation tissue formed on inner surface to localizeinflammatory reaction and eventually converted to fibrous tissue and necrosis of dura leadto subdural compartment.Pus spreads over surface of cerebral hemisphere and along falx cerebriLimitation of spread provided by obliteration of space by granulation tissueCLINICAL FEATURESPrime is rapidity of neurological deterioration.
Signs and symptoms due to1.Meningeal irritation- Headache Fever Malaise Increasing drowsiness Neck rigidity Positive kernig’ssign2.Cortical venous- aphasiathrombophlebitis hemiplegia hemianopia jacksonian epileptic fits3.Raised intracranial papilloedematension ptosis dilated pupil (3rdnerve) other cranial nerveDiagnosis is difficult By rapid deterioration Enhanced CT scan (although changes subtle) MRI Fundoscopy for papilloedemaTREATMENT1.Antibiotics2.Series of burr holes or craniotomy is done to drain empyema followed by iv antibioticsfollowed by modified mastoidectomy.3.long term anticonvulsant Otogenic brain abscess
Circumscribed collection of inflammatory product.50% in adult &25% in children otogenicIn Adult by CSOM(cholesteotomma)In children by ASOMCerebral more common than cerebellar.Route of in infection Cererbral abscess by Direct extension(tegmen) Retrograde thrombophlebitis Often with extradural Cerebellar abscess by Direct extension (trautman triangle) Retrograde thrombophlebitis Often with extradural ,perisinus,sigmoid sinus thrombophlebitis or labrynthitisBacteriologyBoth aerobic and anaerobic Anaerobic common are bacteriodes fragilis & Peptococcus.Pathophysiology
STAGE No.OF DAYS CHANGES CLINICAL FEATURESEarly Cerebritis 1 to 3 days Perivascular infla. Usually unnoticed(invasion) Response Headache Causes focal necrosis mild fever & liquefaction with malaise surrounding edema drowsinessLate Cerebritis 4 to 10 days Formation of capsule No symptoms(quiescent) of inflatory tissue(localization) &fibrosisEnlargement 10 to 13 days Abcess enlarge Aggravation of(manifest abscess) symptoms Cl. Features due to Raised ICT Disturbed func. Of cerebrum or cerebellum(focal symptoms &signs)Termination 14 days Cerebral into lateral Severity increases(rupture) ventricle or white matter Cerebellar into fourth ventricleClinical Features
A.Due to raised ICT Headache Nausea &projectile vomiting Lethargy,drowsy,stupor,coma Papilloedema Slow pulse Fever low grade &later hypothermiaB.Localising features Temporal abscess Nominal aphasia Homonymous hemianopia Contalateral motor paralysis Epileptic fits Papillary changes and occullomotor palsy Extensor plantar reflex Hallucinatin of smell & taste Cerebellar abscess Headache suboccipital radiated to neck Spontaneous nystagmus Ipsilateral hypotopnia & weakness Ipsilateral ataxia Past pointing & intention tremor Dysdiadokokinesia
Diagram of tentorial herniation due to supratentorial hydrocephalus accompanyingA temporal lobe abscess . the uncus has been displaced through the tentorium and iscompressing the midbrain
CT scan CSF analysis(if no papilloedema) MRITreatment Medical : antibiotics parenterally Dexamethason or mannitol Neurosurgical: repeated aspiration ExcisionCommon sites of burr holes used in the management of otogeic brain abscessOtologic: discharge clean with suction Ear drops Mastoidectomy(abscess controlled)
MeningitsInflammation of leptomeninges(pia & arachnoid)Most common complicationSpread via- Bone erosion Retrograde thrombophlebitis Preformed pathways Via labyrinth or perineural spaces to IAC #, dural tear & CSF leakEiology H.influenza and S.pnemoniae Anaerobes rarePathophysiology – Pia arachnoid inflamed Outpouring of fluid into subarachnoid space Increased CSF pressureCSF clear turbid purulent WBCs +organismsTypes- a.Generalised b.localisedClinical featuresSymptoms & signs due to presence of infection Raised ICT Meningeal & cerebral irritation
Lateral Sinus ThrombophlebitisAlso called sigmoid sinus thrombophlebitisInflammation of lateral or sigmoid sinus with formation of thrombosis inside lumen of sinusCommonest organisms Streptococcus Pnemmococcus type 3Pathophysiology AOM COM Erosion of bone covering sigmoid sinusimmunestatus Perisinus abscess/Inflammation Inflammation of outer wall (dura) of sinusPlatlets,rbcs Inflammation of inner wall (intima) of sinusFibrin,wbcs osteothrombophlebitic Mural thrombus extension via small venules Propagates obliterating empties virulent Lumen organisms into Sigmoid sinus Septicemia
Clinical features Symptoms . Hectic Picket fence type fever with rigors:
Headache: early stage mild due to perisinus abscess late stage severe due to venous obstruction Projectile vomiting & neck rigidity Ear discharge Deafness Opthalmoplegia BlindnessSigns Tenderness over mastoid Progessive anemia and emaciation. Griesinger,s sign: due to thrombosis of mastoid emissary vein oedema appears over the posterior part of mastoid Papilloedema: fundus shows blurring of disc margins ,retinal hemorrhages or dilated vein.
Tobey-Ayer test:(Quenckenstedt test) compression of each external jugular vein rise of 50 to 100 mm Hg difference bet two sides <50 mm Hg thrombosed side no increase in pressure normal side rapid increase in CSF pressure false positive if normal sinus very small/absent false negative if collateral draining venous sinus Crowe – Beck test : pressure on jugular vein of healthy side produces engorgement of retinal vein (seen by opthalmoscope) & supraorbital veins. Engorgement subside on release opf pressure. Tenderness on along jugular vein: may associated enlarged & inflammed jugular chain lymphnodes & torticolisInvestigations: Blood smear to r/o malaria Blood culture : causative organism Csf examination :normal except rise in pressure Xray mastoid: clouding of air cells-acute mastoiditis destruction of bone –cholesteotomaImaging studies CECT : sinus thrombosis by Delta sign Triangular area with rim enhancement& central low density area is seen in posterior cranial fossa on axial cuts MRI : better delineates thrombus Venography ot asses progression or resolution of thrombuis
Child with cavernous thrombophlebitis complicating lateral sinus thrombophlebitisTreatment Medical High dose IV antibiotics Anticoagulants Surgical Cause AOM cortical mastoidectomy COM open cavity mastoidectomy
Otitic HydrocephaslusBenign Intracranial HypertensionIncreased ICTNormal CSFVentricles normalNo abscessPathophysiology Disruption in venous circulation Increased CSF vol Brain edema Retrograde extension of thrombophlebitis from sigmoid sinus To superior sagittal sinus Blockage of arachnoid villi CSF decreased absorption Increased secretion Raised CSF pressureClinical featuresHeadache severe presenting featureDrowsiness, blurring of vision ,vomiting, diplopia(6thnerve palsy)Papilloedema, optic atrophy, 6th nerve4 palsyInvestigation Increased CSF pressure but CSF analysis normal CT scan normal ventricular size
MRITreatment Aim to decreased ICT to prevent optic atrophy & blindness Medical Surgical Steroids decompression of sigmoid sinus Mannitol CSF drainage shunts Diuretics optic nerve decompression Acetazolamide Eradicate disease Antibiotic therapy Mastoid exp[loration to deal sinus thrombosis PneumocoeleRare entityFor air to retained in intracranial tissue planes, a valvular communication must existSuch communication follow skull fracture or surgical injuryMost commonly percolates into subarachnoid space and traumatized areaEventually may communicate with ventrilesPresent with headacheDiagnosis by skull Xray show loculated air within cranial cavityTreatment Mastoid explored and vslvular track plugged by muscle Pneumocoele gradually absorbs and patient recoverd
CEREBROSPINAL FLUID OTORRHEACauses: Chronic ear disease congenital malformation Post surgical perilymph fistula # temporal barotrauma IrradiationClinical features; Clear colourless watery fluid Aural fullness RhinorrheaDiagnosis : Glucose Beta two transferrin assay Hankerchief does not become hardTreatment Medical bed rest 300 head high Surgical Aim – isolate CSF from middle ear/Eustachian tube Size of defect Status of hearing Minute large >2cms Anacusic ear grafting grafting craniotomy repair +suturing from above E.tube obliterationPerilymph Fistula Patching of windows by perichodrium.
REFERENCES: 4TH SCOTT BROWN 7TH SCOTT BROWN LUDMANN WRIGHT SCHAMBURGH THANK YOU