MASTOIDITIS
FOR THE PROCESS TO LEAD TO COMPLICATION INFECTION SPREADS FROM PNEUMATIZED AREAS OF TEMPORAL BONE——GRANULATION TISSUE MUST OBSTRUCT AREA SUCH THAT PURULENCE CAN NOT DRAIN AND THE AREA IS UNABLE TO BE AERATED—-PROFBABLY A CONTINUOUM FROM MUCOSAL “CONCOMITANT” MASTOIDITIS WHICH CAN EITHER LEAD TO CHRONIC GRANULOMATOUS MASTOIDITIS OR COALESCENT OR CHRONIC OSTEOLYTIC MASTOIDITIS “OSTEITIS MASTOIDEA”
USUAL PATHOGENS FOR BOTH ADULTS AND CHILDREN—-PNEUMOCOCCUS—–H. INF—-MCAT—ALSO KLEBSIELLA AND Sa
NEONATES >2 WEEKS=G-ENTERICS >2WEEKS=Sa
CLINICAL INDICATORS OF IMPENDING COMPLICATIONS:
1. INFECTION PERSISTS > 2 WEEKS OR RECURS WITHIN 2-3 WEEKS
2. ACUTE EXACERBATION OF CHRONIC INFECTION–FEVER
3. FETID DISCHARGE
4. ETIOLOGIC PATHOGEN : TYPE B H. FLU, ANAEROBE, OR MULTIPLE PATHOGENS
OBVIOUS SIGN OF COMPLICATIONS
1. PINNA DISPLACEMENT INFERIOR/LATERAL SECONDARY TO SUBPERIOSTEAL ABSCESS—LOSS OF POST AURICULAR CREASE—RETROAURICULAR ERYTHEMA AND EDEMA
2. RETRO-ORBITAL PAIN/HEADACHE
3. CRANIAL NERVE DEFICITS/MAJOR NEUROLOGICAL DEFICITS (88% ASSOC WITH CHOLESTEATOMA)
4. PAPILLEDEMA
5. MENINGISMUS—TORTICOLLIS (MAY BE ASSOC WITH VENOUS THROMBOSIS)
6. LETHARGY
7. SEIZURES
CLINICAL COURSE -IN CHILDREN ACUTE INFECTIONS CAN LEAD TO COMPLICATIONS SUCH AS MENINGITIS, FACIAL PARALYSIS, LABYRINTHITIS, OR SUBDURAL ABSCESS
–ALL COMPLICATIONS MORE COMMONLY OCCUR SECONDARY TO SUBACUTE OR CHRONIC INFECTIONS
ROUTES OF SPREAD
-DIRECT EXTENSION ASSOCIATED WITH CHOLESTEATOMA OR VIA PREFORMED PATHWAYS (SANTORINI)
-DIPLOIC VEINS SPREAD CAN LEAD TO THROMBOPHLEBITIS
-HEMATOGENOUS SPREAD CAN LEAD TO MENINGITIS
COMPLICATIONS ** IN GENERAL ALL COMPLICATIONS ARE MANAGED INITIALLY BY BROAD SPECTRUM ANTIBIOTICS AND TREATMENT WHICH CAN LATER BE DIRECTED BY C+S AND SURGICAL INTERVENTION AS INDICATED FOR THE PRIMARY DISEASE OR COMPLICATION**
EXTRACRANIAL
ACUTE MASTOIDITIS -USUALLY PRESENTS AS PERSISTENT PAIN 2 WEEKS AFTER TX OF AOM OR NO RESPONSE TO 3-5 DAYS OF ABX TX
IS THE MOST COMMON COMPLICATION OF AOM
USUALLY IN CHILDREN WITH LARGE WELL PNEUMATIZED MASTOIDS WITH THIN BONEY TRABECULAE
-MOST HAVE EDEMA/ERYTHEMA/TENDERNESS OF THE POST-AURICULAR AREA–LOSS OF THE POST AURICULAR SULCUS (CREASE)–INCREASED PROJECTION OF THE PINNA AND SAGGING OF THE POSTERIOR/SUPERIOR EAC (OSTEITIS)
-MUST HAVE RADIOGRAPHIC EVIDENCE OF BONY DESTRUCTION—LOSS OF SEPTATIONS
PERIOSTITIS——OSTEITIS——-COALESCENT MASTOIDITIS= A RADIOGRAPHIC DIAGNOSIS!
-APPROXIMATELY ½ WILL HAVE AN ASSOCIATED SUBPERIOSTEAL ABSCESS
Rx: (WIDE FIELD?—PROBABLY LEAVE A PET) MYRINGOTOMY FOR DRAINAGE / DROPS AND IV ABX FOR 3 WEEKS INITIALLY (Cx AND S)—-PROBABLY DO A SIMPLE CORTICAL MASTOIDECTOMY AND LEAVE A PENROSE—BE SURE TO CLEAR THE ADITUS!
-MUST FOLLOW CLOSELY BECAUSE ME DZ CAN CLEAR BUT MASTOID DZ PERSISTS “MASKED MASTOIDITIS”—-CLOSED ADITUS—TERM USED TO DESCRIBE A PAUSITY OF OTOSCOPIC FINDINGS
-MAY EVENTUALLY REQUIRE ME EXPLORATION FOR REMOVAL OF GRANULATION TISSUE AND MODIFIED RADICAL MASTOIDECTOMY—WHEN IS CONTROVERSIAL—AVG IN LIT IS 5-10 DAYS
EMPIRICALLY ROCEPHIN AND FLAGYL
CHRONIC MASTOIDITIS -SIMILAR TO ABOVE BUT LONGER COURSE OF DISEASE
-USUALLY HAVE FETID DISCHARGE PERSISTS AFTER 2 WEEK COURSE OF ABX
Rx: IV ABX (EMPIRICALLY NAFCILLIN, FORTAZ, AND FLAGYL) AND MODIFIED RADICAL MASTOIDECTOMY
PETROSITIS -RARE
–GRADENIGO SYNDROME 1. AOM/COM/OTORRHEA, 2. RETROORBITAL PAIN (MECKELS CAVE PAIN), 3. ABDUCENS PARALYSIS (DORELLOS CANAL)——TRAINSIENT FACIAL PARALYSIS, MILD RECURRENT VERTIGO, FEVER, MENINGEAL SIGNS
-CAN OCCUR IN NON-PNEUMATIZED BONE–USUALLY IN PNEUMATIZED BONE
Dx: TN99——DOCUMENT RESOLUTION WITH GALLIUM SCAN
Rx: -IV ABX AND RADICAL MASTOIDECTOMY AND +/- PETROSECTOMY
LABYRINTHITIS—USUALLY VIRAL AND UNRELATED TO AOM/COM
-THE MOST COMMON INTRATEMPORAL COMPLICATION OF OM
-PRESENTS WITH SIMULTANEOUS HEARING LOSS AND VERTIGO
-3 VARIANTS
1.PERILABYRINTHITIS—- PERILYMPH FISTULA – RARE UNLESS ASSOCIATED WITH A CHOLESTEATOMA ERODING LATERAL SCC–75%—GET CT SCAN—-CONTROVERSY IN SURGERY ABOUT WHAT TO DO WITH THE MATRIX AND CHOLESTEATOME—CERTAIN LEAVE THE MATRIX DOWN IF PLF > 2MM AND ALWAYS DO A CANAL WALL DOWN IN THIS SITUATION AND IN AN ONLY HEARING EAR TO ALLOW FOR CLEANING AND DIRECT EXAMINATION IN THE CLINIC
2. SEROUS LABYRINTHITIS—-”WOUNDED LABYRINTH”- -RELATED TO TOXINS OR METABOLIC PRODUCTS OF INFECTION; SOME RECOVERY
3. SUPPURATIVE LABYRINTHITIS—-”DEAD EAR”– INITIAL LABYRINTHIAN CRISIS WITH IRRITIVE NYSTAGMUS TOWARD THE LESION AND THEN LATER AWAY FROM THE DEAD EAR—-PURULENCE AND BACTERIA PRESENT; PROFOUND, PERMANENT LOSSES, POTENTIALLY FATAL
Rx: -AOM – IV ABX AND MYRINGOTOMY
-SUBACUTE/COM – IV ABX AND MEE WITH POSSIBLE MASTOIDECTOMY; CONTROVERSY EXISTS OVER THE FACTORS WHICH DETERMINE THE PRESENCE OF A SUPPURATIVE CASE AND THE NEED FOR LABYRINTHECTOMY AS WELL AS FOR THE BEST MANAGEMENT OF A FISTULA
FACIAL PARALYSIS
-AOM – MAY BE TEMPORARY SECONDARY TO COMPRESSION, EDEMA, OR TOXINS
-SUBACUTE/COM – MAY BE MORE DESTRUCTIVE PERMANENT PROCESS WITH CHOLESTEATOMA COMMONLY PRESENT(80%) -MRI WILL HELP LOCALIZE BUT USUALLY AFFECTED IN TYMPANIC SEGMENT
Rx: -AOM – IV ABX AND MYRINGOTOMY
-SUBACUTE/COM – IV ABX, MEE, MASTOIDECTOMY, REMOVAL OF FALLOPIAN CANAL LEAVING NERVE SHEATH INTACT UNLESS EXTENSIVELY INVOLVED WITH GRANULATION TISSUE OR CHOLESTEATOMA
SUBPERIOSTEAL ABSCESS—-POST AURICULAR THROUGH SUPRAMEATAL (MACEWEN’S) TRIANGLE
ZYGOMATIC ABSCESS, MASTOID TIP–BEZOLD’S ABSCESS—VIA THE INCISURA MASTOIDEA (DIGASTRIC RIDGE) –ORIGINALLY DESCRIBED BY FREIDRICH BEZOLD A GERMANT OTOLOGIST IN 1881—DESCRIBED PURULENCE OUT THE DIGASTRIC GROOV—FILLING THE RETROMAXILLARY FOSSA AND EXTENDING ALONG THE COURSE OF THE OCCIPITAL ARTERY, PERITUBAL AND PARAPHARYNGEAL REGIONS POSSIBLE
Rx: I&D (CORTICAL MASTOIDECTOMY)—PACK WITH DSG CHANGES. PET, IV ABX
INTRACRANIAL COMPLICATIONS—-START WITH NEUROSURG CONSULT
EXTRA(EPI)DURAL ABSCESS
-USUALLY OCCULT AND FOUND SECONDARY TO EVALUATION/PROCEDURE GRANULATION FOR ANOTHER COMPLICATION
RELIEF OF HA BY PROFUSE OTTORHEA
Rx: -IV ABX AND WIDELY OPEN AREA WITH REMOVAL AS MUCH GRANULATION TISSUE AS POSSIBLE; ADEQUATE AERATION IS KEY—-CAN USUALLY DRAIN THROUGH A MASTOIDECTOMY—DO A PET AND IV ABX
SUBDURAL ABSCESS—–RARE—-USUALLY FROM THROMBOPHLEBITIS–PURULENT STAGE OF PACHYMENINGITIS INTERNA—SEVERE HA, SOMNELENCE, POSSIBLE COMA, FOCAL (JACKSONIAN) SIEZURES, MENINGISMUS (BRUDZINSKI’S & KERNIG’S), NEURO SIGNS—-APHASIA, HEMIPARESIS, HEMIANOPIA
SIGMOID SINUS THROMBOPHLEBITIS
-USUALLY ASSOCIATED WITH GRANULATION TISSUE OR CHOLESTEATOMA ON ADJACENT BONE (A PERISINUS ABSCESS)
-MAY BE ASYMPTOMATIC TO SEVERELY TOXIC WITH SEPTIC EMBOLI, TORTICOLLIS— BRUDZINSKI’S & KERNIG’S, OTITIC HYDROCEPHALUS, VERNET’S JUGULAR FORAMEN SYNDROME—DUE TO INFLAMED NODES OF KRAUSE; USUALLY HAVE SPIKING (PICKET-FENCE) FEVERS (TACHY-SWEATING/CHILLS)
–GRIESINGER’S SIGN -PAIN AND BOGGY SWELLING OF MASTOID TIP REGION ASSOCIATED WITH EXTENSION OF THROMBOPHELBITIS INTO MASTOID EMISSARY VEIN
–QUICKENSTEDT’S TEST / TOBEY-AYER TEST—–DO AN LP AND MEASURE ICP WHILE OCCLUDING IJV
–LILLIE CROWE TEST—-RETINAL VEIN DILITATION WITH IJV COMPRESSION
Dx: MRA
Rx: -IV ABX, PET
-WIDE EXPOSURE VIA MODIFIED RADICAL MASTOIDECTOMY AND REMOVE GRANULATION TISSUE
-NEEDLE ASPIRATE SINUS TO RULE OUT PRESENCE OF PURULENCE
-IF SEPTIC EMBOLI OR PERSISTENT BACTEREMIA MAY (? EVACUATE THROMBUS AFTER) IJ LIGATION
-? ANTICOAGULATION
-TREAT OTITIC HYDROCEPHALUS AS BELOW
OTITIC HYDROCEPHALUS
-ALSO CAN BE CALLED PSEUDOTUMOR CEREBREI (LIKE BIH)
A COMPLICATION OF ACUTE OR CHRONIC SUPPURATIVE OM—-PATHOPHYS IS QUESTIONABLE
-WILL HAVE INCREASED ICP WITHOUT OTHER INTRACRANIAL DZ—NO ENLARGEMENT OF VENTRICLES
-PRESENTS WITH HEADACHE AND LETHARGY
OFTEN AN IPSI LR PAULSEY & PAPILLEDEMA—-SPINAL FLUID PRESSURE IS GREATER THAN 300 MM H2O
PRIMARY DANGER IS VISUAL LOSS!
-NEED TO LOOK FOR SIGMOID SINUS THROMBOSIS (DUPLEX)
-CAN LEAD TO BLINDNESS OR BRAIN HERNIATION
Rx: -MEDICALLY LOWER ICP WITH LASIX, MANNITOL, STEROIDS, AND MAY HYPERVENTILATE
-IV ABX—-SERIAL LP’S?
-MAY NEED PERMANENT SHUNT
-MODIFIED RADICAL MASTOIDECTOMY EXPOSING ALL DISEASES DURA AND ASPIRATING TO RULE OUT SIGMOID SINUS THROMBOSIS
BRAIN ABSCESS
-MOST COMMON FATAL INTRACRANIAL COMPLICATION OF OM
USUALLY DEVELOPS IN ASSOCIATION WITH THROMBOPHELBITIS
MAY BE ASYMPTOMATIC TO CATASTROPHIC NEUROLOGICAL DEFICITS
USUALLY INVOLVE THE TEMPORAL LOBE OR CEREBELLUM
-30-35% WILL HAVE SEIZURES OR OTHER NEUROLOGICAL DEFICITS
-STEPS OF DEVELOPMENT
1. INVASIVE STAGE—-INITIALLY ENCEPHALITIS – FEVER, HA, LETHARGY, MALAISE
2. QUIESCENT STAGE—-ORGANIZATION/LOCALIZATION – MAY TAKE WEEKS AND NOT HAVE ANY SIGN. SYMPTOMS
3. EXPANDING STAGE—– ENLARGEMENT – SYMPTOMS PROGRESS—35% SIEZURES
4. RUPTURE – RAPID PROGRESSION AND DEATH
Rx: -MAJORITY (65%) WILL HAVE INCREASE ICP AND NEED TX TO LOWER ICP
-IV ABX MAY BE USED ALONE IF NO SIGNIFICANT SYMPTOMS
-IF SYMPTOMATIC ALSO NEED TO DRAIN
-MOST REQUIRE MODIFIED RADICAL MASTOIDECTOMY TO TREAT EAR DZ
MENINGITIS
-MOST COMMON INTRACRANIAL COMPLICATION OF OM
-PRESENT WITH FEVER, HEADACHE, AND MENINGISMUS, PHOTOPHOBIA, AND MENTAL STATUS CHANGES
-MOSTLY AFFECTS CHILDREN
-USUALLY HEMATOGENOUS SPREAD OF TYPE B H. FLU
-IF OCCURS WITHIN HOURS OF ONSET OF AOM SUSPECT MONDINI
-IF RELATED TO SUBACUTE/COM MAY HAVE DIRECT EXTENSION
Rx: -AOM – IV ABX AND MYRINGOTOMY
– 1/3 WILL HAVE SIGN. NEUROLOGICAL DEFICITS SUCH AS DEAFNESS OR RETARDATION WHICH MAY BE PREVENTED BY STEROIDS—–BEWARE OF LABYRINTHITIS OSSIFICANS WHICH MAY PRECLUDE COCHLEAR LIMPLANTATION
-SUBACUTE/COM – IV ABX AND MODIFIED RADICAL MASTOIDECTOMY WITH REMOVAL OF DISEASED DURA
PATHOGENS
-ACUTE -STREP PNEMONIAE, H FLU
-SUBACUTE/CHRONIC—-AEROBES -PSEUDOMONAS, STAPH—ANAEROBES (IN 50%) -BACTEROIDES, PEPTOCOCCUS
INITIAL ABX—AOM – CEFTRIAXONE +/- FLAGYL IF MASTOIDITIS -SUBACUTE/COM – NAFCILLIN, CEFTAZIDIME, FLAGYL
INADEQUATE ANTIBIOTIC COVERAGE OR DRAINAGE OF EXTRATEMPORAL COMPLICATIONS USUALLY INVOLVED IF INTRACRANIAL COMPLICATIONS DEVELOP
COMPLICATIONS OF SURGERY
-EXCESSIVE BLOOD LOSS – RELATED TO GRANULATION TISSUE
BRAIN HERNIATION – CAN RESULT FROM DISEASE OR AS RESULT OF TREATMENT
– CT FINDING OF HIGH RISK PATIENTS
1. MIDLINE SHIFT 2. OBLITERATION OF VENTRICLES 3. OBLITERATION OF CISTERNS
– CAN RESULT IN CARDIOPULMONARY ARREST, CERVICAL CORD COMPRESSION, OR INFARCTION
– MUST SUPPORT VITAL FUNCTIONS AND REDUCE ICP
-PULMONARY EMBOLI – ? IF ANTICOAGULATION SECONDARY TO RISK OF INTRACRANIAL BLEED
-AIR EMBOLI – HYPERBARIC O2 TREATMENT—-GET MACHINE MURMUR—–LAY L LAT DECUB AND SLIGHTLY TRENDELENBURG