COMPLICATIONS OF COM Dr. AJAY MANICKAM JUNIOR RESIDENT, DEPT OF ENT RG KAR MEDICAL COLLEGE
Introduction Infection spreads beyond muco-periosteal lining of middle ear cleft to involve bone & neighboring structures like facial nerve, inner ear, dural venous sinuses, meninges , brain tissue & extra-temporal soft tissue Mortality due to intracranial complication is still high
Routes of access Bony defects anatomical dehiscences (jugular bulb, dural plate, Fallopian canal) erosion ( cholesteatoma , granulation tissue) trauma (accidental, dural plate breach during mastoidectomy ) Normal anatomical pathways oval window round window aqueducts Haematogenous infected thrombus venous spread (sinus, emissary veins, systemic ) Periarteriolar spread (of Virchow-Robin) seeding in the white matter of brain
Spread of Infection
FACTORS Pathogen Factors Patient Factors High virulence bacteria Young age Antimicrobial resistance Poor immune status Chronic disease (DM, TB) Poor socio-economic status Lack of health awareness
EXTRADURAL ABSCESS
Extra Dural abscess 2 nd Most common otogenic intracranial complication Acute infection by demineralization and chronic by erosion
MIDDLE CRANIAL FOSSA Tegmen tympani (lateral to the arcuate eminence) Petrous apicitis (medial to the arcuate eminence ) POSTERIOR CRANIAL FOSSA Sinus plate ( perisinus abscess, lateral sinus thrombophlebitis ) Trautmann’s triangle ANTERIOR CRANIAL FOSSA Pott’s puffy tumour
2 nd most common intracranial complication Coalescence, cholesteatoma , granulation Non-specific symptoms (unilateral headache, fever, otorrhoea ) Often diagnosed peroperatively (silent abscess) MRI (Gadolinium-enhanced) > CT scan Systemic antibiotics + surgery ( mastiodectomy + removal of necrosed bone and non- adherant granulation tissue over dura )
SUBDURAL EMPYEMA
Subdural Empyema Least common complication Non hemolytic streptococci Inflammatory reaction underneath dura - granulation- fibrosis-necrosis of bone Seropurulent – purulent collection Subdural space, along tentorium cerebelli and interhemispheric spaces
CLINICAL FEATURES Dramatic presentation , rapid detioration Severe headache, fever, drowsiness, follwed by focal neurological symptoms Much more rapid than brain abscess Jacksonian fits Hemianopia , hemianaesthesia , aphasia Mortality 15%
along the falx loculated hypodense ring enhancement contrast imaging mass effect blunted sulci Gd-DTPA enhanced T1 weighted MRI CECT
Diagnosis and management CT scan CSF culture sterile With neurosurgeons Systemic antibiotics + removal of subdural fluid (burr hole) + ear infections acute by myringotomy and cortical mastiodectomy Now craniotomy abscess excision Radical mastoidectomy after patient is stable
MENINGITIS
Meningitis Most common intracranial complication In children following acute and adults following chronic infection Mortality 5-30 % Otogenic meningitis is most serious than meningococcal meningitis Hemophilus influenzae , streptococcus pneumonia type iii – acute Chronic – proteus and pseudomonas Anaerobic – bacteroid
Routes of entry into the meninges – haematogenous (MC) direct extension by bone erosion ( cholesteatoma , encephalocoel ) preformed channels ( Hyrtl’s fissures) labyrinth, aqueduct ( suppurative labyrinthitis , Mondini malformation) Suspicious signs – persistent/intermittent fever lethargy nausea and vomiting persistent headache irritability Ominous signs – visual changes ataxia new onset seizures altered sensorium nuchal rigidity Associted intracranial complications in 50% of cases Meningitis
Diagnosis and treatment CSF study by LP (cytology, chemistry, smear, culture) Broad spectrum IV antibiotics, steroids (to prevent subsequent hearingloss ) Myringotomy Mastoidectomy ( cholesteatoma , coalescent mastoiditis , extension through bone erosion, failure of maximal medical therapy)
Lateral sinus thrombophlebitis Proximal: 1. To superior sagittal sinus via torcula Herophili hydrocephalus 2. To cavernous sinus proptosis 3. To mastoid emissary vein Griesinger’s sign Distal: To internal jugular vein & subclavian vein pulmonary thrombo -embolism & septicaemia
CLINICAL FEATURES Remittent high fever with rigors (picket fence) Pitting edema over retro-mastoid area & occipital bone due to mastoid emissary vein thrombosis ( Griesinger’s sign) Tenderness along Internal Jugular Vein Headache Anaemia
Symptoms & signs High fever, swinging type Chills precedes fever Temperature subsides with sweating Each fever spike due to release of fresh septic embolus
Investigations Queckenstedt or Tobey-Ayer test: compression of I.J.V. rapid rise of C.S.F. pressure (50 – 100 mm water rapid fall on release of compression. In L.S.T. no rise / rise by only 10 – 20 mm water. Low sensitivity and specificity
investigations Lumbar puncture: to rule out meningitis CT brain with contrast: Delta sign or Empty triangle sign MRI brain with contrast MR angiography Blood culture Culture & sensitivity of ear discharge
Intravenous antibiotics Surgery Anticoagulants Ligation of internal jugular vein Treatment
Algorithm for Surgery Mastoidectomy Inspection of the sinus wall NORMAL (compressible, healthy-looking) DISEASED (inflammed, immobile, pale, opaque) Wide bore needle aspiration Free flow blood No blood, pus Conservative Thrombectomy, drainage (healthy thrombus, free flow blood) Dry tap
Otogenic brain abscess
OTOGENIC BRAIN ABSCESS 50-75 % adult brain abscess & 25% in child = otogenic Temporal abscess : Cerebellar abscess = 2:1 Route of infection: 1. Direct spread: via Tegmen plate: Temporal abscess via Trautmann’s triangle: Cerebellar abscess 2. Retrograde thrombophlebitis and 3. virchow robin space
Trautmann’s triangle Superiorly: superior petrosal sinus Posteriorly : sigmoid sinus Anteriorly : solid angle (semi-circular canals) Pathway to posterior cranial fossa from mastoid cavity
4 stages (Neely, Mawson ) 1. Invasion or Encephalitis (1-10 days) 2. Localization or Latent Abscess (10-14 days) 3. Expansion or Manifest Abscess (> 14 days): leads to raised intracranial tension & focal signs 4. Termination or Abscess rupture: leads to fatal meningitis
RAISED ICT Seen more in cerebellar abscess Severe persistent headache, worse in morning Projectile vomiting Blurring of vision & Papilloedema Lethargy drowsiness confusion coma Bradycardia Subnormal temperature
Surgical management Repeated burr hole aspirations – safer for ill patients Excision of brain abscess with capsule: best Tx – extensive damage to cerebral tissue , residual neurological deficit Open incision & evacuation of pus Radical mastoidectomy after pt becomes stable
OTITIC HYDROCEPHALUS
syn . Benign intracranial hypertension Symptomatic ↑ in ICT (>240 mm H 2 o in LP) , papilloedema , normal CSF studies, in absence of brain abscess or meningitis A misnomer Lateral sinus thrombophlebitis → torcula → sagittal sinus thrombosis → inhibition of CSF resorption through arachnoid villi → ↑ ICT [Symonds] Otitic hydrocephalus
Otitic hydrocephalus Clinical Features: 1. Severe headache, vomiting 2. Blurred vision, papilloedema , optic atrophy 3. Abducens palsy & diplopia due to raised intra-cranial tension ( Falselocalizing sign) Conservative (acetazolamide, fluid restriction, diuretics,mannitol , serial LP, ± systemic anticoagulants in case of sagittal sinus thrombosis) Mastoidectomy ± thrombectomy (in COM with cholesteatoma )
More common with COM Cholesteatoma → tegmen dehiscence → middle or posterior cranial fossa dural tear → CSF leak/ encephalocoel Iatrogenic Presentations clear, colourless , watery fluid from mastoid cavity or external auditory canal through nose, in intact TM middle ear/ myringotomy fluid rich in glucose Proper exposure → temporalis muscle/fascia graft with gelfoam compression Sinodural angle tear most difficult to control Repair via intracranial route ( extradural / intradural )
BRAIN FUNGUS Prolapse of brain into middle ear cavity / mastoid cavity due to erosion of dural plate. Common in pre-antibiotic era. Rarely seen now in resistant infections. Diagnosis: C.T. scan temporal bone. Treatment: Removal of necrotic tissue, replacement of healthy prolapsed brain into cranial cavity & repair of bone defect.
SUBPERIOSTEAL ABSCESS
Extension of mastoid infection through the cortex and air cells into the subperiosteal region Types – Mastoid abscess ( subperiosteal abscess “proper”) [MC] von Bezold’s abscess Luc’s ( meatal ) abscess Zygomatic abscess Citelli’s abscess Para-/retropharyngeal abscess Haematogenous spread (perforators, especially in children) Differential diagnosis – Mastoiditis without abscess Suppurative lymphadenopathy Superficial abscess Infected sebaceous cyst
pathogenesis Production of pus under tension hyperaemic decalcification + osteoclastic resorption of bone sub- periosteal abscess penetration of periosteum + skin fistula formation
Postauricular abscess Commonest. Present behind the ear. Pinna pushed forward & downward
Bezold & citelli’s abscess Bezold : neck swelling over sternocleido - mastoid muscle Citelli : neck swelling over posterior belly of digastric muscle
D/D OF BEZOLD’S ABSCESS Suppurative lymphadenopathy of upper deep cervical lymph node Para-pharyngeal abscess Parotid tail abscess Infected branchial cyst Internal jugular vein thrombosis
Luc’s abscess Luc: swelling in external auditory canal Zygomatic : swelling antero -superior to pinna + upper eyelid oedema Parapharyngeal & Retropharyngeal: due to spread of pus along Eustachian tube
Clinical features & treatment Late feature of neglected COM CT scan (extent of the lesion, intracranial and intratemporal complications) Subperiosteal abscess + cholesteatoma Drainage + cortical mastoidectomy + IV antibiotics Subperiosteal abscess – cholesteatoma Drainage + cortical mastoidectomy + IV antibiotics Drainage + myringotomy + IV antibiotics Aspiration + myringotomy + IV antibiotics
MASTOIDITIS
Mastoiditis = mucositis of mastoid cavity and air cells + effusion part of the spectrum of uncomplicated otitis media per se , not a complication Acute (clinical) mastoiditis red, oedematous soft tissue over mastoid antrum painful/tender pinna directed laterally, downward and forward loss of post-auricular crease otorrhoea localised reactive lymphadenopathy pain the only presentation in adults (thicker cortex)
pathogenesis Aditus Blockage Failure of drainage Stasis of secretions Hyperemic decalcification Resorption of bony septa of air cells Coalescence of small air cells to form cavity Empyema of mastoid cavity
Disease of childhood (>2 years, peak at 6 years) Mostly a sequelae of ASOM ( Pneumococcus , Haemophilus ) 25% of coalescent mastoiditis seen in sclerotic temporal bone with COM and cholesteatoma
Fate of an inflammed mastoid cavity Acute mastoiditis Spontaneous resolution, perforation of tympanic membrane Persists Blockage of aditus by granulation/ cholesteatoma Mastoid empyema Acute coalescent mastoiditis Acidosis Osteoclast activity Pressure of pent-up pus DEMINERALISATION Subperiosteal abscess Petrositis Intratemporal & intracranial complications
Symptoms & signs Otorrhoea > 3 weeks, pain behind the ear & fever Mastoid reservoir sign: pus fills up on mopping Sagging of postero -superior canal wall due to peri-osteitis of bony wall b/w antrum & posterior E.A.C. Ironed out appearance of skin over mastoid due to thickened periosteum Mastoid tenderness present Blood counts , ESR raised , Mastoid cavity in X-ray & CT scan , ear swab culture & sensitivity
Mastoid reservoir sign
Posterior sagging of posterior canal wall
mastoiditis
Coalescence of cells
Mastoiditis Furunculosis H/o otitis media + - Deafness + - Position of pinna Down + outward + forward Forward Ear discharge Muco -purulent Serous / purulent Sagging of EAC wall + - TM congestion + - Tenderness Mastoid Tragal Post-aural lymph node - + X-ray Mastoid Coalescence of cells + cavity Normal
management Urgent hospital admission Broad spectrum I.V. antibiotics Cortical mastoidectomy No response to medical treatment in 48 hrs , sagging of post meatal wall Development of new complication Presence of sub- periosteal abscess Myringotomy to drain out painful pus Incision drainage of sub- periosteal abscess
Masked mastoiditis Natural progress of acute mastoiditis halted by antibiotics Middle ear apparently free from infection Persistence of symptoms of mastoiditis TM fails to return to normalcy Blockage of aditus by granulation/ cholesteatoma
PETROSITIS
Pneumatisation of the petrous pyramid 30% (anterior petrous apex), 10% (posterior petrous apex) after 3 years of age continuous with the middle ear cleft POSTEROSUPERIOR/INFRALABYRINTHINE CHAIN (attic, antrum → semicircular canal → apex) ANTEROINFERIOR/PERITUBAL CHAIN ( hypotympanum , PT tube → cochlea → apex)
ACUTE PETROSITIS Gradenigo’s syndrome deep-seated retro-orbital/aural pain (50%) diplopia (lateral rectus palsy) (25%) otorrhoea TYPICAL GRADENIGO’S SYNDROME IS RARE NOT PATHOGNOMONIC OF APICITIS SIMILAR PRESENTATIONS WITH EXTRADURAL ABSCESS AT THE APEX Cochleo -vestibular symptoms, facial weakness, constitutional symptoms
Petrositis Pneumatisation of petrous apex not a prerequisite ALTERNATIVE ROUTES OF SPREAD Thrombophlebitis Osteitis Long standing persistent otorrhoea (discharging petrous tract) , with indolent symptoms
Long term, high dose systemic antibiotics Myringotomy (± grommet), corticosteroids (neuropathy) Surgery – petrous abscess, necrosis, failure of medical traetment Simple mastoidectomy Surgery in a hearing ear – approaches following the infected air-cells Surgery in a non-hearing ear – translabyrinthine & transcochlear approaches
INVOLVEMENT OF THE LABYRINTH (Otitis interna)
Most common complication of COM with cholesteatoma Arch of the horizontal semicircular canal most commonly affected (~90%) [nearest to the antrum Breach of the otic capsule Resorptive osteitis (inflammatory mediators in COM with cholesteatoma /granulation tissue) Pressure necrosis ( cholesteatoma mass) Cholesteatoma and/or granulation
Presentations of labyrinthine fistula sensorineural hearing loss subjective episodic vertigo positive fistula test Tullio phenomenon Preoperative CT scan (30° tilted) (57-60% sensitivity, even with 1mm cuts) Intraoperative diagnosis The presence of labyrinthine fistula to be assumed to be present in every case of COM with cholesteatoma
Fistula test in relation to labyrinthine fistula Tragal pressure, Politzer bag with ear canal adapter, pneumatic speculum Conjugate ocular movements with vertigo Not sensitive; its absence does not rule out a labyrinthine fistula False positive fistula sign ( Hennebert’s sign) intact tympanic membrane no fistula characteristic, though not diagnostic, of labyrinthine syphilis False negetive fistula sign inadequate sealing cholesteatoma blocking the fistula wax in the external canal dead labyrinth
Treatment of labyrinthine fistula Tympanomastoidectomy (CWD) + addressing the fistula Removal of cholesteatoma , exteriorising the fistula covered by matrix (single sitting in open cavity/staged in closed cavity) – prevents aggravation of SNHL by minimising tissue handling removal of cholesteatoma itself releives pressure keeping matrix safe until no granulation tissue lies underneath Complete removal of cholesteatoma including matrix (single or staged/2 nd look sitting) , repair of fistula (fascia, bone pâté) prevention of bone erosion and infection prevention of SNHL in the long term
SEROUS LABYRINTHITIS Translocation of toxins and inflammatory mediators Associated perilabyrinthine infection, especially fistula Meningogenic (Pneumococcal mengitis → aqueducts) Tympanogenic (round window, internal auditory canal) Clinical diagnosis : Sudden onset vertigo in a patient with AOM IV antibiotics + myringotomy ± mastoidectomy (in progressive cases) Hearing loss, vertigo and imbalance are reversible
SUPPURATIVE LABYRINTHITIS Comparatively less common (<1%) Invasion of bacteria into the labyrinth Tympanogenic (round window, fistula) Haematogenic (venous channels) Endolymphatic hydrops ( resistence of Reissner’s membrane to bacterial invasion ) Meningitis, intracranial ( cerebellar ) abscess Clinical diagnosis (aided by CT scan) sudden onset severe rotatory vertigo with vomiting profound unilateral deafness disorder of balance spontaneous horizontal nystagmus Tissue destruction and loss of functions are permanent IV antibiotics + myringotomy + corticosteroids + labyrinthine sedatives + mastoidectomy ± drainage/ labyrinthectomy
FACIAL NERVE PARALYSIS
Otitis media → 3-5% of incidences of facial palsy More common in children, after ASOM Acute onset (<1 week) in AOM, chronic protracted course in COM Cholesteatoma , granulation tissue, suppurative labyrinthitis ( sequestra ) , petrous osteomyelitis Congenital petrous cholesteatoma (progressive palsy with longstanding severe deafness, without otorrhoea ) Facial nerve exposed by cholesteatoma mostly escapes palsy ( epineurium replaced by matrix)
Causes of Facial nerve palsy AOM Neurotoxic effect (inflammatory mediators, bacterial toxins through natural dehiscences and vascular channels) Mass effect on the bare nerve COM Osteitis, erosion, direct pressure Oedema , neuropraxia , neuronotmesis Cholesteatoma > granulation tissue Acquired Fallopian canal dehiscence Tubercular otitis media
Clinical diagnosis Role of CT scan not a routine procedure investigation of choice <2mm cuts, with proper exposure of tympanic cavity & facial canal IV antibiotics + myringotomy ± grommet [AOM ] Surgical exploration [COM] CWD modified radical mastoidectomy Removal of cholesteatoma and granulation tissue Facial nerve decompression by removing matrix from epineurium Nerve repair, if needed The management