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2. COMPLICATIONS OF TEMPORAL BONE INFECTIONS Chapter 134 Lee A. Harker Clough Shelton

3. GENERAL CONSIDERATIONS > in children/ in the first two decades of life. postauricular abscess, <6 years. in Turkey, 58%,<20 years. males \females=2 More that who: are poor and live in overcrowded surroundings, have poor personal hygiene, poor health, decreased resistance to infection, inadequate health education, and limited access to medical care large series of patients with complications of otitis media have not been reported in patients with HIV infection or AIDS or in those receiving immunosuppressive therapy after organ transplantation, even though such individuals do have suppurative ear disease.

4. Acute Otitis Media most common bacterial infection of childhood Predisposing factors:1- young age 2- male sex, 3-receiving bottle feedings, 3-exposed to a day care environment, crowded living conditions,4- or smoking within the home. Medical conditions such as cleft palate, Down syndrome, and mucous membrane abnormalities such as cystic fibrosis, ciliary dyskinesia, and immunodeficiency states also predispose persons to otitis media. Tympanocentesis ----for culture &----------------reduce the bacterial population. After treatment,-----  document that the AOM has completely resolved----  by tympanometry and otoscopy. If the complication was intracranial, ------  (CT) scan or a (MRI) should be obtained

5. Chronic Otitis Media COM =infectious process persists for longer than the 1 to 3w usually necessary for resolving AOM If infection does not resolve--  mucosal edema and exudation,mucous glands proliferate. --  antrum block between the middle ear and the epitympanum and in the aditus between the epitympanum and mastoid the normal pathways for aeration and decrease both oxygenation and vascularity. bacteriology of COM: cultures of 30 cholesteatomas isolated at least one anaerobic :in 67%, at least one aerobic 70%, and both aerobes and anaerobes in 50%. In 57% multiple /in 30% five or more bacteria COM in patients with VT  different bacterial.treatment with antibiotic drops OR oral antibiotics,^ fungal overgrowth &&resistant organisms developing. The resistant bacteria most often found are Pseudomonas aeruginosa, Achromobacter xylosoxidans, and even methicillin- resistant Staphylococcus aureus.

6. PATHOPHYSIOLOGY complication from AOM  result from bacteremia ( hematogenous:like meningitis. Or by access to adjacent or distant structures. develop facial paralysis  if congenital dehiscence of the bony fallopian canal above the stapes If  pathways leading to the meninges or the labyrinth,  at risk to develop meningitis, subdural effusion, or suppurative labyrinthitis( Developmental labyrinthine abnormalities like enlarged vestibular aqueducts or the Mondini ) In older children and adults, :pathways left from previous surgery or temporal bone fractures.

7. PATHOPHYSIOLOGY In AOM  complications develop by hematogenous dissemination or by direct extension of infection along preformed pathways. AOM: medical treatment, and mastoidectomy is not necessary. In COM and mastoiditis, complications are always associated with : 1-bone destruction, 2-granulation tissue formation, 3-or the presence of cholesteatoma

8. DIAGNOSIS HX (when free, last examine the involved ear, past history and treatment of the patient's otitis, symptom of AOM: pain, fever, and fussiness not otorrhea symptom of COM: painless purulent drainage The cessation of drainage with the onset of pain suggests the presence of aditus or epitympanic block with increased pressure within the mastoid. imbalance or vertigo  possibility of imminent labyrinthitis. by chronology of this alteration of sensorium  differentiate among brain abscess, meningitis, and subdural empyema. A brain abscess takes weeks to develop, several days for meningitis subdural empyema to become fulminant and progress to coma.

9. Physical Examination The vital signs, especially T&temperature curve A complete neurologic examination (mental assessment, gait and perform the Romberg and sharpened Romberg tests. motor and sensory function,complete cranial nerve evaluation, nystagmus, nuchal rigidity,Kernig's and Brudzinski's tests, optic discs ) The otologic examination (pinna, The external auditory cana and tympanic membrane By using a microscope and fine suction, Pneumatic otoscopy for conjugate deviation of the eyes -  presence of a labyrinthine fistula ) The TM :can normal or near normal even complication With TX in ME&Mastoid : middle ear may revert to normal  while the mastoid may not.( Especially in aditus block). with any infectious condition that could be caused by acute or chronic otitis, CT to R/O COM as the cause, even TM be normal

10. PARACLINIC LAB (CBC,Hb--  for GA) Imaging (CT scan : status of the middle ear and the mastoid air cell system, bony details of the middle ear, epitympanic, and mastoid structures, erosion of the bony plates covering the sigmoid sinus, cerebellum, or tegmen of the middle ear and mastoid, establish the specific primary otologic diagnosis (e.g., AOM, COM, cholesteatoma) assessing the results of therapy and provide a baseline posttreatment study MRI is a far more sensitive imaging technique than CT scanning for diagnosing intracranial complications T2W-->intraparenchymal edema from subtle brain infection much earlier than can a CT scan CT&MRI: complimentary

11. TREATMENT AOM: antibiotic therapy+tympanocentesis or myringotomy. NO surgery complications resulte from COM and mastoiditis, broad-spectrum antibiotics (against anaerobic And aerobic )+ mastoidectomy in intracranial complications, the neurosurgeon operates first, immediately followed by the otologist Postoperative follow-up :. Even when the patient responded perfectly, follow-up CT scan to objectively confirm the status of the mastoid  because there is a risk of recurrence or emergence of new intracranial complications In lateral sinus thrombosis, epidural abscess, subdural empyema, or brain abscess, follow-up evaluation with enhanced MRI 2 to 4 weeks after treatment

12. Extracranial (Intratemporal) Complications 1-Acute Mastoiditis 2-Coalescent Mastoiditis 3-Chronic Mastoiditis 4-Masked Mastoiditis 5-Postauricular Abscess 6-Bezold Abscess 7-Temporal Root Abscess 8-Petrous Apicitis 9-Labyrinthine Fistula 10-Facial Nerve Paralysis 11-Acute Suppurative Labyrinthitis 12-Encephalocele and CSF Leakage

13. Acute Mastoiditis when AOM fails to resolve signs of AOM and local inflammatory findings over the mastoid proc 28% < 1 year, 38% 1 - 4 years, 21% 4 -8,M:16m TM perforation: in <1/4; TM bulging or erythematous in two-thirds 22% : complications on admission, the most common of which was subperiosteal abscess average duration from the onset of disease (AOM) until admission for acute mastoiditis was 9 days. Only 1/3 :asymptomatic interval between their AOM symptoms and the mastoiditis.

14. Coalescent Mastoiditis AOM and mastoiditis that persist unabated for 2 to 4 weeks, coalescent mastoiditis develops. disease of the young, especially of boys.<4y Bacterial virulence and decreased host resistance are important in its etiology, but mastoid development also plays a role changes in the bone and mucoperiosteum of the mastoid air cell system.(decalcifies the bony partitions, causing the small air cells to coalesce into a larger cavity. intense inflammation and infection  phlebitis and periphlebitis  Extend to adjacent meninges, sigmoid sinus, cerebellum, and the temporal The most common pathway for infection to extend beyond the mastoid is through the lateral cortex behind the ear.

15. Coalescent Mastoiditis SYM:purulent otorrhea, fever, toxicity, and ear pain.same AOM but more tox&T hX :chronology :purulent drainage or significant otalgia persists >2W SIGN:mastoid tenderness, erythema, and sagging of the posterior superior EAC IMAG:CT/intracranial complication :MRI Tx:can be either medical or surgical ( without surgery AB  3-6W  (SUR+-?  high risk)= complete mastoidectomy with VT end of medTX,  IMAG (for doc)

17. Chronic Mastoiditis 1)with a longstanding TM perforation, 2)with cholesteatoma,3) or as a complication from an infection after placement of a middle ear VT central perforation  infected  mastoid(chronically drain). Even though uninfected cholesteatoma for long periods of time,  it tends to suppurate, form granulation tissue, and erode bone. purulent drainage> 8 W,  the likelihood of a complete resolution with antibiotics Chronic mastoiditis requires surgical intervention to heal, and an infected cholesteatoma requires surgical ablation, regardless of duration

18. Masked Mastoiditis granulation tissue formation and bone erosion can occur without otorrhea received numerous courses of antibiotics normal or near normal TM Age:M:13Y chronic but not severe auricular and postauricular pain, tenderness to mastoid CT : localized opacification Tx:surgical (regardless of the appearance of the TM)

19. Postauricular Abscess most common complication of mastoiditis accompanying acute or coalescent mastoiditis in young children mastoid near the spine of Henle exist in newborns as a series of open channels between the interior of the mastoid and the cortex direct extension subsequent to bone destruction process in that upper portion and the tissue edema and the abscess drive the auricle downward and laterally TX:excision and drainage + mastoidectomy

21. Bezold Abscess perforation in the bony plate  Pus burrows downward in the neck beneath the sternomastoid, or may be confined between layers of the deep cervical fascia >in older children in( pneumatization has extended into the mastoid tip) Dx:deep, tender, upper cervical masses  miss Tx:1 -excision of the mastoid pathology 2-drainage of the abscess, 3-removal of granulation tissue

23. Temporal Root Abscess infection of soft tissues sup. and ant. auricle can  abscess  involves the cells of the zygomatic root of the mastoid (temporal root of the zygoma ) 1)direct extension via bone erosion through the epitympanic temporal root cells 2)or phlebitis and periphlebitis. The clinical picture is very confusing because abscesses in that location are rare. CT :to R/o mastoiditis as the source. TX:SURGERY

24. Petrous Apicitis. Pneumatization in only 30% of PETROS.Rare/ pathology :mirror of coalescent mastoiditis, or granulation tissue with chronic mastoiditis. Cholesteatoma Rarely, Dx:CT(bone)&MRI(BM) SYM  1- retroorbital pain (irritation of the Vganglion in Meckel's cave), 2- paralysis of the VI ( passes through Dorello's canal ) 3-or dysfunction CNs VII and VIII (Gradenigo's syndrome ):retroorbital pain, sixth nerve paralysis, and otorrhea TX:prolonged AB+-Surgery(if obvious necrotic bone )

26. Labyrinthine Fistula erosive loss of the endochondral bone overlying the semicircular canals without loss of perilymph( without loss of perilymph) majority :involve only the lateral semicircular canal./secondary to cholesteatoma, in 7% of the cholesteatomas The mechanisms:demineralization of the dense endochondral bone(at surgery as a "blue line" parallel to the underlying semicircular canal) coexisting complications:. 1- facial nerve dysfunction in 60%/ 2-dehiscences of the tegmen occurred in 39%

27. Labyrinthine Fistula Symptoms : vestibular. imbalance, dysequilibrium, or vertigo but have normal equilibrium most of the time momentary imbalance by pushing on their external ear canal& (Tullio's phenomenon). Sign :fistula test =positive pressure  conjugate deviation of the eyes away from the side of compression(only 55% to 70% of patients) Tx:surgical for underlying cholesteatoma:mastoidectomy /in a canal-wall-up technique is made on the basis of the surgeon's ability+ Repair:1)microsuction elevates the cholesteatoma  2) the endosteum is torn  3)a small piece of tissue or a shaped cap of bone is placed over the site and secured in place with fibrin glue or packing large fistulas, :canal-wall-down procedure and leave the fistula covered by matrix, which later forms the mastoid cavity lining.

28. Fistula of the right lateral semicircular canal (arrow) seen on axial temporal bone CT.

29. Facial Nerve Paralysis result from AOM, COM without cholesteatoma, or cholesteatoma. edema  pressure and inflammation  avascular necrosis & suppurative neuritis  destroys the neural elements. AOM:In young children, incomplete :only in infants with congenital dehiscence of the fallopian canal,<3w Facial nerve paralysis :by cholesteatoma  involve the nerve in the middle COM without cholesteatoma:horizontal portion of the facial nerve near the stapes TX:IN AOM:AB+-myringotomy IN COM: surgical decompression of the facial nerve

30. »Coronal CT scan showing epitympanic mass (arrowheads) involving facial nerve geniculate ganglion area (arrow) causing facial paralysis in a case of chronic otitis media.

31. Acute Suppurative Labyrinthitis Bacterial invasion of the labyrinth  total loss of both auditory and vestibular function ETIOLOGY:1)congenital labyrinthine deformities such as Mondini deformity and enlarged vestibular aqueducts2) through a cholesteatomatous lateral semicircular canal fistula is another DX:Clinical: tinnitus and vertigo, pallor, diaphoresis, nausea, and vomiting. The vestibular symptoms :max for 8 to 12 h, even if s totally immobile and IV AB Brisk labyrinthine nystagmus directed toward the opposite ear next 2or3W CNS adaptation  normal or near normal balance No specific diagnostic studies are necessary when the typical clinical picture develops IV AB for 10D to  prevent propagation to the meninges(NO REVERS CLIN.COURSE labyrinthectomy is not necessary in labyrinthitis secondary to AOM.

32. Encephalocele and CSF Leakage CSF leakage due to :defects in the tegmen tympani or, less commonly, the tegmen mastoideum./80% > 45 y Etiology:1)cholesteatoma and granulation tissue(80%): erode bony plates between mastoid and temporal lobe, the cerebellum, and the dura 2)truma or previuse surgery Symp:1) hearing loss  ( reduced ossicular motion from the middle ear fluid or the encephalocele )2) signs and symptoms of meningitis, TX:surgical repair. Depend to size The middle fossa approach provides excellent exposure of the tegmen defect and access to repair the dural defect temporalis fascia graft  dura.& calvarial bone graft taken from the inner table of the craniotomy flap-  The bony defect

33. Intracranial Complications Meningitis immunizations H. influenzae  meningitis dramatically decreased/<2y/AOM:hematogen RF:1) longitudinal temporal bone fractures. 2)Congenital defects of the tegmen 3)unrecognized injury to the dura of the posterior or middle cranial fossae during mastoid surgery.4) Patients with syndromic or nonsyndromic congenital stapes fixation, Mondini dysplasia, and enlarged vestibular aqueducts Sym:1)generalized severe headache. /2)tends to lie quietly, /3)photophobia 4) general hyperesthesia,5) vomits. Chang level of consciousness from normal, to coma 6)Fever Sign:Nuchal rigidity 2) pain with attempted flexion of the neck 3)abnormal abdominal reflexes. 4) Brudzinski's sign, 5) Kernig's sign,

34. Meningitis Paraclinic:meningitis is suspected  CT scan  R/O abscess&safe LP CSF from the LP :for pressure, cells, bacteria, glucose, protein, chloride, and other factors TX:IN AOM:AB+Myringotomy (no surgery) from COM and mastoiditis: AB+mastoidectomy In profound ipsilateral SNHL  route of infection : the labyrinth.  If the sensorineural function in the affected ear remains at the patient's premeningitis baseline, the route was extralabyrinthine enhanced MRI should be obtained to rule out the presence of any additional intracranial complications mastoidectomy should be performed as soon as the patient is stable

35. Brain Abscess 3th etiology after CHD&truma Abscesses from AOM and COM were almost always found on the same side as the otitis / in the temporal lobe and cerebellum. 3/4 secondary to cholesteatoma, 50% occurred in the second decade of life, 2/3M arrival of bacteria into the cortex  migration of polymorphs into local capillaries  focal cerebritis( managed by IV AB)  hemorrhagic, and necrotic, and the abscess is formed. SYM:sepsis, cerebellar abscess : coarse horizontal nystagmus, dysmetria, dysdiadokokinesia, or action tremor. Temporal lobe abscess : homonymous visual field defects, contralateral hemiparesis DX:MRI TX:broad-spectrum IV AB( directed at aerobic and anaerobic ). patient's condition is stable, neurosurgical drainage or abscess excision is performed within the first 24 hours of admission and is followed immediately by mastoidectomy,

36. Subdural Empyema fulminating purulent infection that develops between the dura and the pia arachnoid otologic etiology is uncommon 2/3 M, in the second decade of life. infection enters the subdural space, pus forms rapidly.  thrombophlebitis of cortical veins  raised ICP, focal signs, and seizures SYM:severe headache?( earliest & persistent)  T rises dramatically /General malaise, chills, and nuchal rigidity. Change level of consciousness  focal signs left-sided collections  aphasia & contralateral hemiparesis Sign:Paralysis of conjugate gaze, Jacksonian seizures papilledema In posterior fossa collections, localizing signs are often absent, but marked neck stiffness and papilledema are always present DX:contrast CT(In early NL  MRI) TX:Emergency neurosurgical drainage & AB therapy

37. Epidural Abscess cholesteatoma, G.T  bone erosion  inflammatory response  abscess between the temporal bone and the underlying dura mater  pachymeningitis sym:deep mastoid pain, but some without sym.  only at surgery DX:CT –contrast/MRI TX:Surgery(I&D)+Mastoidectomy exenterate the air cells, proceeding from lateral to medial and from regions of less disease to those with more disease. posterior aspect of the bony EAC; the tip cells should be removed. This will maximize exposure and hemostasis dura is thickened by the infection, blunt flat instruments such as a Freer elevator or large curettes can safely scrape the granulation tissue from the abscess cavity and identify the most centripetal extent of the abscess. using diamond burrs, rongeurs, or curettes until healthy dura without granulation tissue is evident on all margins of the abscess

38. Lateral Sinus Thrombosis cholesteatoma, GT  bone erosion  perisinus abscess  pressure on the dural outer wall of the sinus  necrosis  mural thrombus  infected, enlarges  thrombus extend in a retrograde direction to the transverse sinus &the torcular Herophili, and even to the superior sagittal sinus  IVG(to neck)&cavernous. Infection of.  septicemia and the possibility of metastatic abscesses (most commonly to the lungs. most common in adults or older children with cholesteatoma Mix complication (meningitis, epidural abscess, subdural empyema, cerebritis, or cerebellar abscess)  obscure the clinical picture signs and symptoms: septicemia or blockage of blood flow through the sinus\The picket-fence fever pattern /neck pain &stiffness  pain and tenderness along the anterior border of the SCM\tenderness of the mastoid tip sudden intracranial hypertension resulting from  decreased venous drainage Most prominent is the occurrence or sudden worsening of a severe headache.

39. Lateral Sinus Thrombosis DX:imaging:both CT(contrast)&MRI delta sign seen on the CT scan(enhancement of the wall of the sigmoid sinus ) TX:all mastoidectomy+management of the infected clot and sinus wall (time:controversy)if abscess:I&D befor mastoidectomy / in+meningitis if stable Management of the clot : anticoagulation(not routin BUT IN extension of the clot to the transverse sinus or cavernous sinus )+ligation of the jugular vein in the neck(if extension to neck)+ and opening the sinus and evacuating the infected clot +neurosurgical decompression and steroids Intravenous thrombolytics are not routinely used in the presence of the infected vessel wall. The sinus: only after the mastoidectomy a reported from mastoidectomy without opening and evacuating the lateral sinus clot. All patients survived, but long hospitalization

40. Otitic Hydrocephalus Block venous drainage after sudden interruption of a portion of the venous drainage system near one ear  acute hydrocephalus  ICP rises  brain edema a diffuse severe headache  with (or occasionally without) medical management, the continuous headache gradually ameliorates and dissipates over 3 to 7 days If no adequate collateral  dulling of the sensorium or decreased visual acuity from retinal vein occlusion appear  coma and death DX:CT scanning MANAG: immediate neurologic and neurosurgical consultation