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Acute Mastoiditis

Mastoiditis
Anatomy and pathophysiology The pathophysiology of acute and chronic suppurative otitis media and the progression to mastoiditis10,82,103,105 is only briefly reviewed here. The temporal bone is intimately associated with the middle ear space by its connection through the narrow aditus ad antrum !igure 155"5#. $n most cases of uncomplicated otitis media or otitis media with effusion, evidence of inflammation into the mastoid is often shown radiographically by fluid collection or mucosal thic%ening within the mastoid air cells. $n a histologic study of 222 temporal bones with evidence of otitis media, &'( also had fluid or pathologic tissue in the mastoid.&' )s described, secretory cells of the middle ear are not found in the mastoid cavity. Thus, fluid in the mastoid cavity results from otitis media, and its presence does not indicate an acute or chronic mastoiditis.

The natural progression of acute otitis media to coalescent or surgical mastoiditis follows a well" described se*uence of stages.+,,105 -epending on the virulence of the infecting organism, the health of the host, and the timing of medical or surgical intervention, the disease process can be reversed at any stage. .ecause of the continuity of the middle ear space with the mastoid cavity, all patients with otitis media e/hibit some degree of mastoid inflammation. )n acute coalescent mastoiditis, however, is distinguished by the inflammatory erosion of the bony septations, which divide the mastoid cavity into a honeycomb arrangement of air cells !igure 155"'#. Thus, the mastoid cavity becomes a cistern of purulent material and ongoing infection. !irst, hyperemia and edema of the mucoperiosteal lining of the pneumati0ed mastoid air cells obstruct the narrow additus and disrupt aeration. Thic%ened mucous membrane and impaired ciliary function prevent normal drainage of the middle ear through the eustachian tube.&, The early e/udate is serous but becomes purulent as inflammatory cells accumulate. 1ontinued inflammation, hyperemia, and accumulation of purulent debris cause venous stasis, local acidosis, and dissolution of calcium from the bony septae. 2steoclastic activity in the inflamed periosteum softens and removes the decalcifying bony partitions, causing the small air cells to coalesce into a larger cavity. 3istologic e/amination shows that areas of coalescent bone erosion are combined with ad4acent areas of beginning healing by bone deposition.105 Thus, the tendency toward spontaneous

resolution is particularly stri%ing in the stage of coalescent mastoiditis. )s the acute inflammation subsides, the healing processes replace the mucoperiosteum with maturing granulation tissue. !ibrosing osteitis appears in areas of bone destruction. 5ith healing, the osteoplastic activity results in the production of dense, compact bone. 1hronic mastoiditis results in a sclerotic, poorly aerated mastoid cavity !igure 155",#. 6everal cases proceed from the acute stage to the subacute stage, in which active progression has been arrested, to the chronic stage. $n a few cases, one or multiple reversions to the stage of acute mastoiditis occur so that the disease should be considered.+, Incidence $n the pre"antibiotic era, acute coalescent mastoiditis was a complication of acute otitis media in 25( to 50( of cases.'+ .y the 1&+0s, the use of sulfonamides significantly reduced the number of deaths from potentially lethal complication and reduced the mortality rate to 3(, although the reported incidence of acute mastoiditis had not changed.11,,& $ntroduction of penicillins and broader spectrum antibiotics altered the natural course of otitis media. $n 1&+', 3ouse+' showed that the use of sulfonamides alone decreased the incidence of mastoidectomy by two thirds.+' The reported rate of a surgical mastoiditis developing from acute otitis media was 0.3( to '( in the 1&50s+,,1 and 0.02( to 0.00+( in the 1&80s.,3,80 !our studies, however, reported an increase in the incidence of acute mastoiditis.2',+5,51,8& ) study of children with acute mastoiditis noted that the incidence 7 8 0.05# in the number of children managed significantly increased from 1&,5 to 1&,& 1.+ patients per year# to 1&8, to 1&&2 +.2 patients per year#.+5 The authors identified several predisposing factors for the development of acute mastoiditis, including withholding antimicrobials for the management of acute otitis media, using suboptimal drugs for therapy penicillin and erythromycin#, and managing for insufficient duration. ) study of 2, cases of mastoiditis between 1&85 and 1&88 reported a threefold increase in the incidence of acute mastoiditis compared with that in the preceeding 15 years.2' 9ore than half of the patients had no history of infection before the episode of acute mastoiditis. 3alf of the patients had been ade*uately managed with antibiotics. The authors could not determine the reason for the increase in the number of cases of acute mastoiditis. Microbiology The bacteriology of acute mastoiditis is slightly different than that of acute otitis media. 9ost studies report pneumococci and group ) streptococci as the most fre*uently isolated pathogens in mastoiditis,2',32,+1,'5,,+ whereas the more resistant 3. influen0ae, the second most common pathogen

in acute otitis media, is rarely found . .acteriologic e/aminations were performed on surgical aspirates from 2& children who underwent mastoidectomy between 1&,0 and 1&8&. 6lightly different results were observed between the children who were managed with antibiotics before admission n : 15# and those who were not n : 1+#. $n patients not given antibiotics, pneumococci or b"hemolytic streptococci were isolated in ,1(. ;o isolates of 3. influen0ae or 9. catarrhalis were found. $n patients managed with antibiotics, no isolates of b"hemolytic streptococci were found< the organisms were pneumococci and 3. influen0ae. )lso, no organisms were isolated in +&( of the cultures.80 $n a study of 28 mastoid cavity operative specimens, cultures of only 20 yielded 22 organisms. 6. pneumoniae n : 13, '5(# was the most common isolate, followed by 6treptococcus pyogenes n : +, 20(#, 6. aureus n : 2, 10(#, coagulase" negative staphylococcus n : 2, 10(#, and =. coli n : 1, 5(#. Two of three isolates of 6. pyogenes were from patients managed with penicillin.+5 >insberg and others32 reported that although 3. influen0ae is one of the more common isolates from acute otitis media, it has a predilection for mucous membranes and is less li%ely to invade bone, possibly e/plaining the infre*uency of isolates from mastoidectomy cultures.32 Acute coalescent mastoiditis 1lassically, acute coalescent mastoiditis forms appro/imately 2 wee%s after the onset of otorrhea.10' The symptoms are very similar to those of acute suppurative otitis media, but they do not warrant surgery when they occur early in a middle ear infection. 3owever, if they persist or recur after several wee%s from the onset of acute otitis media, particularly in a patient managed with appropriate antibiotic therapy, an evolving coalescent mastoiditis should be considered.33 The time at which symptoms and signs appear is more important than their severity in evaluating the need for a mastoidectomy in acute suppurative otitis media. 6ymptoms of acute coalescent mastoiditis include otorrhea for more than 2 wee%s, persistent fevers, persistent or recurrent pain behind the ear, erythema, edema, tenderness over the mastoid process, and sagging of the posterosuperior meatal wall resulting from thic%ening of the periosteum of the osseous meatus ad4acent to the antrum .o/ 155"2#. The tenderness over the mastoid is the most consistent physical sign of coalescent mastoiditis. The tenderness is greatest where the trapped pus is nearest to the periosteum< in adults, this is over the tip of the mastoid process, but in children with incomplete pneumati0ation, the tenderness is more often over the fossa mastoidea near the antrum.33 This shallow depression is appro/imately 1 cm posterior to the spine of 3enle, where the corte/ is perforated by numerous

blood vessels. ?adiologically, the clouding of the mastoid seen with acute otitis media evolves into a loss of distinct bony partitions as decalcification and osteoclastic bone removal occur. .efore routine computed tomography 1T# of the mastoid, serial mastoid films were compared to show the progressive bone changes of coalescence. )lthough any of these symptoms may present in varying degrees of severity, the presence of one or a few symptoms may alert the physician to coalescent mastoiditis. ?arely, the otorrhea may cease, yet a walled"off abscess may remain within the mastoid cavity to cause persistent symptoms and radiographic changes. This arises with petrous ape/ e/tension or in acute otitis media inade*uately managed by antibiotics. Masked mastoiditis )lthough the incidence of surgical mastoiditis appears to be decreasing, several authors continue to stress the need for a high inde/ of suspicion of acute mastoiditis in children with otitis media that could be mas%ed by antibiotic therapy.12,++,8',12',12, =ven with the advent of antimicrobial therapy for the management of acute otitis media, otitis media should still be considered a potentially dangerous disease because the clinical course is less predictable than in the past. ?eview of the literature reveals that 3'( to ,2( of patients with acute mastoiditis developed the disease despite prior antibiotic management.++,'0,80,8, )cute mastoiditis has fre*uently been reported in patients with a well"aerated tympanic cavity and normal appearing tympanic membrane. 9any authors in the last 2 decades have called this mas%ed mastoiditis and attribute it to inade*uate antibiotic management of acute otitis media.+3,&2 The clinical course is more insidious than that of classical coalescent mastoiditis. $n a recent review, ,2( of 18 patients with acute mastoiditis had no history of ear disease, and ',( had middle ear symptoms for less than , days before developing a clinically significant mastoiditis.'0 $n another study, 28( of 5, children managed for acute mastoiditis had a history of acute otitis media, and only '0( had an episode of acute otitis media in the + wee%s before the development of acute mastoiditis. $n addition, +0( had a normal appearing tympanic membrane when they presented with acute mastoiditis.+5 )ntibiotic management for acute otitis media cannot be considered as an absolute safeguard against acute mastoiditis or against otogenic intracranial or intratemporal complications. Management

9anagement of acute mastoiditis remains controversial. $n the pre"antibiotic era, acute mastoiditis was referred to as surgical mastoiditis to differentiate it from chronic mastoiditis. The generally accepted indications for mastoidectomy were otorrhea for more than 2 wee%s, anterior displacement of the auricle, sagging of the posterior superior canal wall, mastoid tenderness, and edema over the mastoid process. Today, many cases of acute mastoiditis will resolve with antibiotic management alone. 3ence the controversy@ when should a mastoidectomy be performed for management of acute mastoiditis i.e., mastoid inflammation with evidence of coalescence but without cholesteatoma#A 1urrently, there are two approaches to the management of acute mastoiditis. $n 1&80, 6hambaugh and >lasscoc%105 advocated that the timing of the symptoms, rather than the presence of the symptoms, is more important in determining the indication for mastoidectomy. 6ymptoms of acute mastoiditis were otorrhea for more than 2 wee%s, mastoid tenderness, sagging of the posterior superior meatal wall resulting from periosteal thic%ening ad4acent to the antrum, persistent low"grade fever, and radiologic evidence of erosion of the bony septations within the mastoid cavity. )lthough 6hambaugh and >lasscoc%105 ac%nowledge that many cases of acute mastoiditis will resolve with antibiotic therapy alone, they assert that the ris% of intracranial e/tension by bone erosion before spontaneous healing is such that surgical evacuation of the abscess cavity is indicated. 3ouse and 1rabtree+, advocated a more conservative approach to management of acute mastoiditis, asserting that the physician could initially manage the patient with medical or surgical therapy. The indications for surgery were a draining ear for more than 2 wee%s despite antibiotic therapy, continued signs or symptoms of mastoiditis pain, edema over the mastoid tip or the posterosuperior canal wall#, radiographic loss of bony partitions, and signs or symptoms of threatened or definite complication. $n addition, 3ouse and 1rabtree+, assert that if the patient shows signs of improvement on antibiotics, surgery is not indicated.' Three studies of acute mastoiditis grouped patients into medical or surgical therapy based on the presence or absence of a subperiosteal abscess.+1,88,8& 7atients with an abscess underwent mastoidectomy. 7atients with mastoiditis but no postauricular abscess were managed with myringotomy if the ear was not draining#, decongestants, parenteral antibiotics, and close observation. $n the first study, 5,( 31 patients# responded to conservative management.+1 $n the second, 50( 1, patients# responded to medical therapy< two patients failed to improve and re*uired mastoidectomy.8& $n the third study, '8( +, patients# responded to conservative management< mastoidectomy was performed in si/ patients who failed to respond@ four patients developed a subperiosteal abscess while on parenteral antibiotics, one developed sepsis and a 0ygomatic

subperiosteal abscess, and one developed signs of meningeal irritation.88

Subperiosteal Abscess
Mastoid subperiosteal abscess Clinical presentation The mastoid, or postauricular, abscess is the most common subperiosteal abscess. $t forms as a result of hematogenous spread of infection through the minute vascular channels in the suprameatal 9acewenBs# triangle. 5hen the infection erodes the outer corte/ of the mastoid tip, a subperiosteal abscess results. The auricle is displaced anteriorly and inferiorly, the postauricular crease is obliterated, and the s%in over the mastoid process is fluctuant and erythematous. The abscess may spontaneously rupture to drain through the s%in !igure 155"8#. 2torrhea may or may not be present. The patient may be to/ic and febrile with systemic signs of acute illness, or the fever may be prolonged and low grade with occasional temperature spi%es. 1T shows erosion of the bony corte/ of the mastoid with a subperiosteal fluid collection !igure 155"&#. Management The postauricular abscess is managed with myringotomy, postauricular incision and drainage of the abscess, and complete mastoidectomy preferably performed under a single general anesthetic in the operating room. $n myringotomy, fluid is aspirated and sent for culture, and a tympanostomy tube is placed to re"establish middle ear aeration and facilitate drainage. The postauricular abscess is opened with a postauricular incision !igure 155"10#. The incision is carried through the subcutaneous tissues and into the periosteum, which has been separated from the underlying bone by the purulence. 2nce the periosteum has been divided, pus drains through the incision and should be cultured for aerobic and anaerobic bacteria. $f the patient has a well"pneumati0ed mastoid cavity, an intact canal wall mastoidectomy is performed. 6ome surgeons assert that, because the mastoid is poorly pneumati0ed in the child, a postauricular incision is all that is necessary if the patient is younger than 3 or + years. 6ome believe, however, that performing a cortical mastoidectomy is preferred at the time the postauricular abscess is drained to prevent e/posure to a second general anesthetic should mastoidectomy be re*uired. The wound is then thoroughly irrigated with antibiotic saline solution, and a small rubber 7enrose drain is introduced into the abscess cavity and sutured to the s%in. The s%in is closed loosely with widely spaced interrupted nylon sutures to allow fluid to drain from the cavity. The drain is left in place until drainage has nearly stopped or for appro/imately +8 hours. 1ulture"directed antibiotics should be started when sensitivity results are available.

7ostoperatively, intravenous antibiotics are continued until the cellulitis resolves. The patient can be maintained on culture"directed oral antibiotics for 2 wee%s postoperatively. Zygomatic subperiosteal abscess ) 0ygomatic subperiosteal abscess is formed when infection in the 0ygomatic air cells erodes through the cortical bone at the 0ygoma. $t presents as a swelling above and in front of the ear and may be confused with a parotid abscess !igure 155" 11 ), .#. The periosteum under the temporalis muscle is elevated, and the upper half of the auricle is displaced from the s%ull by the abscess !igure 155"12 ), .#. )n unusual variation of the 0ygomatic subperiosteal abscess resulting from perforation of the outer corte/ at the root of the 0ygoma into the mandibular fossa has been reported.101 ) tender, fluctuant abscess appears 4ust in front of the tragus, with a displacement of the mandible toward the normal side so that the teeth no longer meet in occlusion.33 9anagement consists of mastoidectomy with e/enteration of the 0ygomatic air cells and drainage of the facial abscess through the postauricular incision. 7urulence from the abscess should be cultured for aerobic and anaerobic organisms. ) small passive drain is left in the s%in incision for appro/imately +8 hours or until drainage subsides. 7ostoperatively, intravenous antibiotics are continued until the facial cellulitis resolves. The patient can be maintained on culture"directed oral antibiotics for 2 wee%s postoperatively. Bezolds abscess 7erforation on the medial aspect of the mastoid tip into the digastric groove incisura mastoidea# produces a deep abscess of the nec% %nown as .e0oldBs abscess !igure 155"13 ), .#. This unusual complication presents as a fluctuant nec% mass in a patient with acute or chronic otitis media !igure 155"1+#. 9anagement is similar to that of a 0ygomatic subperiosteal abscess. ) mastoidectomy should be performed. The nec% should be e/plored for drainage of the cervical abscess. 7urulence from the abscess should be cultured for aerobic and anaerobic organisms. ) small passive drain is left in the s%in incision for appro/imately +8 hours or until drainage subsides. 7ostoperatively, intravenous antibiotics are continued until the cervical cellulitis resolves. The patient can be maintained on culture"directed oral antibiotics for 2 wee%s postoperatively.

7etrous apicitis
Etiology

7etrositis is an e/tension of the inflammation of the middle ear or mastoid cavity into the pneumati0ed cells of the petrous ape/. This can occur by direct e/tension through the pneumati0ed air cell tracts of the petrous pyramid or by thrombophlebitis through the small vascular channels of the temporal bone. )ppro/imately 30( of temporal bones have a pneumati0ed petrous ape/,10+ but the e/tent of pneumati0ation of the petrous bone is not a factor in the development of petrositis.2 .ecause the pneumati0ed petrous pyramid is a direct e/tension of the mastoid cavity, the stages of petrositis parallel those of mastoiditis. 3owever, when the marrow"containing portion of the petrous pyramid becomes infected, osteomyelitis results. The clinical picture is essentially the same. .ecause the petrous pyramid does not have an established drainage system as does the mastoid cavity, spontaneous drainage of an abscess cannot occur and purulence in the petrous ape/ has a greater tendency toward intracranial e/tension . Two groups of air cells e/tend into the petrous pyramid@ perilabyrinthine and apical2 !igure 155"1'#. These are separated by a vertical plane passing through the a/is of the modiolus of the cochlea. The perilabyrinthine region lies posterior to this plane and is further subdivided into supralabyrinthine and infralabyrinthine areas. The supralabyrinthine area consists of air cells ad4acent to the superior semicircular canal above the internal auditory meatus, between the endolymphatic sac and the dura of the posterior cranial fossa, and through the arc of the superior semicircular canal subarcuate cell tract#. The infralabyrinthine area consists of air cells medial to the hypotympanum and below the labyrinth and a retrofacial air cell tract originating from the air cells near the eustachian tube. The apical area lies anterior to the plane through the a/is of the modiolus and is further divided into the hypotympanic tract medial to the ascending carotid artery, the peritubal tract around the eustachian tube, and a perilabyrinthine tract e/tending from the supralabyrinthine or the infralabyrinthine areas.1 This latter group of air cells is present in appro/imately 15( of temporal bones. Clinical presentation >radenigo22 first described the triad of symptoms that accompany petrous apicitis in 1&0,. 1lassically, these are retro"orbital pain from cranial nerve C irritation#, otorrhea, and cranial nerve C$ paralysis. 3owever, additional symptoms may include fever, sensorineural hearing loss, transient facial paresis, mild recurrent vertigo, and meningismus. The patient may complain of diplopia and otalgia but neglect to mention DDpain behind the eye.BB Esually, this symptom is elicited by direct *uestioning. Management 6urgical eradication of all diseased tissue in the petrous ape/ is the management of choice.

Enli%e acute coalescent mastoiditis, petrositis should not be conservatively managed with intravenous antibiotics and observation because of the tendency towards intracranial e/tension. 6urgery aims to provide ade*uate drainage from the suppurative focus in the petrous ape/. The easiest and safest surgical approach is systematic e/ploration of all cell tracts that e/tend into the petrous pyramid !igure 155"1,#. 1omplete mastoidectomy is performed. The semicircular canals are s%eletoni0ed. The perilabyrinthine and apical groups of air cells are systematically e/plored, and granulation tissue or purulence is removed until dense, compact bone is encountered. 1are should be ta%en to thoroughly e/plore all suspicious air cell tracts, including those that traverse through the center of the superior semicircular canal !igure 155"18 ), .#. >enerally, granulation tissue can be followed in an air cell tract into the abscess. ) currette is useful to remove air cells and granulation tissue around hard labyrinthine bone, thus avoiding fenestration of the labyrinth with a drill.

Labyrinthitis
Fabyrinthinitis is an uncommon complication of acute otitis media and mastoiditis. 6chu%necht&8 defined the types of labyrinthitis resulting from acute or chronic suppurative middle ear disease according to the substance or tissue that enters the perilymphatic space. They are suppurative labyrinthitis, serous labyrinthitis, chronic labyrinthitis, and labyrinthine ossificans. -ifferentiation of serous labyrinthitis, suppurative labyrinthitis, and labyrinthine fistula can be difficult preoperatively< in many cases, ade*uate therapy can only be instituted after surgical e/ploration and definitive diagnosis. 6uppurative labyrinthitis results from bacterial invasion of the inner ear from contiguous areas of the temporal bone or meninges. 6erous labyrinthitis is an irritation of the labyrinth caused by otitic or meningitic infection without bacterial invasion of the inner ear. 1hronic labyrinthitis results from a fistula of one of the semicircular canals. Fabyrinthitis ossificans is otitic or meningitic sclerosis of the labyrinth in the healed inactive state after labyrinthitis. $t is a se*uela of an acute process. Serous labyrinthitis Etiology 6erous or to/ic# labyrinthitis results from irritation of the labyrinth by the by"products of infection and inflammation. To/ins are thought to enter the inner ear via the oval and round windows or through a fistula in the bony labyrinth. 6erous labyrinthitis may be a complication of acute or chronic otitis media< meningitis, in which case the condition may be mas%ed by the more severe meningeal symptoms< or syphilitic or tuberculous otitis media. $t is the mechanism of the deafness of congenital syphilis.

Clinical presentation The patient presents with vertigo, which may be transient and recurrent over months or years< sensorineural hearing loss may fluctuate and is less severe than that seen in purulent labyrinthitis. ;ystagmus, past pointing, and falling may be present. ?etention of labyrinthine function can be shown by caloric responses and hearing tests. $n the acute phase, it may not be distinguishable from purulent labyrinthitis, e/cept for retention of some audiovestibular function. The signs and symptoms are less dramatic than those of purulent labyrinthitis, and the pathologic conse*uences in the inner ear are less destructive. =very patient with a serous labyrinthitis should be observed closely for development of suppurative labyrinthitis, which presents as abrupt worsening of the vestibular symptoms and sudden loss of all hearing. Management 9anagement is directed toward the infectious source. $f the labyrinthitis results from acute otitis media, myringotomy and antibiotic therapy are sufficient. $f coalescent mastoiditis or chronic otitis media with possible cholesteatoma is present, a labyrinthine fistula should be suspected and mastoidectomy should be performed. Suppurati e labyrinthitis Etiology 6uppurative labyrinthitis can develop as a complication of acute and chronic otitis media from migration of the bacteria through the preformed pathways of the oval window, round window, and pree/isting fractures of the temporal bone and from direct invasion by erosion of the labyrinthine bone by cholesteatoma. .acteria may traverse the cochlear a*ueduct in bacterial meningitis.50 .acterial invasion of the inner ear produces irreversible damage to the neuroepithelium, atrophy of the stria vascularis, collapse of ?eissnerBs membrane, and endolymphatic hydrops. $f the patient survives without surgery, healing occurs with fibrosis and obliterative osteitis of the labyrinth and cochlea. ;o audiovestibular function is retained. Clinical presentation The sudden onset of severe vertigo with profound sensorineural hearing loss during an episode of acute otitis media indicates destruction of the labyrinth. ;ystagmus, past pointing, and falling toward the opposite side occur. )t first, the nystagmus is toward the

involved ear, but after several days, the fast component is toward the opposite side. Cegetative symptoms such as nausea and vomiting are severe. !ever may not be present. There may be a prodromal period of serous labyrinthitis< prostration, complete loss of hearing, and severe worsening of vertigo indicate progression to suppurative labyrinthitis.The labyrinth, cochlea, and cranial nerve C$$$ may enhance on magnetic resonance imaging 9?$# . The symptoms are most severe during the acute bacterial invasion of the labyrinth. The vertigo and nystagmus result from sudden loss of the healthy tonic neural impulses from the involved labyrinth, without any change in the input from the healthy side. ?ecovery from a unilateral peripheral vestibular lesion is attributed to the brainBs ability to compensate for the sensory mismatch by adapting to the asymmetric sensory input. This occurs gradually as the cerebellum and brainstem integrate the conflicting information and adapt over time to a stable lesion. The severity of the symptoms gradually lessens over the ne/t few days, but central compensation occurs over several wee%s with complete resolution of nystagmus and vertigo. 2ften, the onset of purulent labyrinthitis is followed in hours or days by facial paralysis, meningitis, or both. $n the pre"antibiotic era, 50( of cerebellar abscesses secondary to chronic otitis media were labyrinthogenic.10& )lthough this is very unusual today, a high inde/ of suspicion of a cerebellar abscess in a patient with suppurative labyrinthitis should be maintained because of the e/isting connections between the labyrinth and the posterior cranial fossa. Management The most important aspect of management of otogenic suppurative labyrinthitis is close and continuous observation of the patient for symptoms and signs of intracranial e/tension. .road"spectrum antibiotics are instituted, more to prevent intracranial e/tension than to manage labyrinthitis.10+ 6ome assert that management of purulent labyrinthitis in the absence of meningitis re*uires prompt labyrinthectomy to prevent the development of meningitis.10& $f suppurative labyrinthitis is a complication of meningitis, surgery is not indicated. Labyrinthine !istula Etiology !istuli0ation of the labyrinth occurs most commonly as a result of erosion of the bony covering of the lateral semicircular canal by cholesteatoma. ?arely, a spontaneous labyrinthine fistula may be caused by syphilitic osteitis, tubercular otitis media, chronic perilabyrinthine osteomyelitis, or a middle ear neoplasm e.g., carcinoma, glomus 4ugulare tumor#. 3owever,

because development of labyrinthine fistula is so characteristic of cholesteatoma, it should be suspected even in the case of a dry, stable perforation that has been inactive for years.10+ The incidence of labyrinthine fistulas from chronic otitis media has been reported in the modern literature as 3.'( to 12.&(.,2,&5,108 Clinical presentation The patient will have active or inactive chronic otitis media for many years. The mainstay of the diagnosis, the fistula test, is performed by application of positive and negative pressure to the middle ear with a pneumatic otoscope. ) positive fistula test produces nystagmus with the fast component toward the tested ear with application of positive pressure, and away from the tested ear with application of negative pressure. The nystagmus results from motion of the soft tissue over the fistula< positive pressure causes ampullofugal movement of endolymph away from the ampulla#, and negative pressure causes ampullopetal movement of the endolymph toward the ampulla#. 5ith a fistula of the lateral semicircular canal more common#, the nystagmus is always hori0ontal. 5ith a fistula of the superior or posterior canal, the nystagmus is vertical. 5ith a large anterior fistula that e/poses the ampullae of the lateral and superior canals, the nystagmus is rotary. ) temporal bone 1T will show bony dehiscence of the hori0ontal semicircular canal or soft tissue abutting the canal !igure 155"20 ), .#. Management 9anagement is mastoidectomy with eradication of cholesteatoma< there are several options regarding the management of the fistula. 1are should be ta%en when a fistula of the labyrinth is suspected because inadvertent removal of cholesteatoma matri/ from an unidentified fistula has disasterous results< the incidence of severe or total sensorineural hearing loss has been reported as 5'( when the cholesteatoma matri/ was removed from e/tensive fistulas. There are some general principles regarding the management of a labyrinthine fistula. 5hen a cholesteatoma has been found, the sac should be opened and the contents evacuated. The medial wall of the matri/ should be palpated to detect any bony erosion. 2nce a fistula is identified, matri/ should be left over the site to protect the labyrinth even if eventual removal is planned# while the remainder of the ear is cleared of disease. This protects the labyrinth from irrigation solution and bony debris. 2nce a fistula has been identified in a noninfected ear, the options are removal of cholesteatoma with immediate repair of the fistula or removal of cholesteatoma leaving a small amount of matri/ over the fistula and repairing this as a staged procedure ' months later. ?epair of the fistula at the initial operation should be underta%en at the end of the procedure, after removal of

cholesteatoma and completion of the mastoidectomy. ?epair should be staged in an infected ear. 5hen the fistula is e/posed, it should be *uic%ly covered with a tissue seal fascia, vein, or perichondrium#. 9ost authors advocate leaving the matri/ intact over e/tensive fistulas involving more than one canal, the vestibule, or the cochlea.121

"acial ner e paralysis


Etiology !acial paralysis secondary to otitis media has been reported to account for '( to 8( of peripheral facial paralysis, which is behind that of idiopathic disease, trauma, tumors, and herpes 0oster oticus.1,,2, !acial paralysis may be a complication of acute or chronic otitis media. $t occurs more commonly in children with otitis media than in adults.2, $n the young child, facial paralysis may be the first symptom of acute otitis media.3 The pathogenesis can be suspected based on the timing of the paralysis with respect to the onset of the ear disease. 5hen the paralysis occurs within 2 wee%s of acute otitis media, it is most li%ely caused by edema of the nerve, which can become inflamed as a result of e/posure of a dehiscent segment to the active infection. $n postmortem e/amination of 535 temporal bones, the facial nerve was found to be dehiscent in 55( &1( in the tympanic segment, &( in the mastoid segment#. 2f dehiscences in the tympanic segment, 83( were located ad4acent to the oval window involving the lateral, inferior, and medial portion of the canal, with the facial nerve protruding from its canal in 2'(., -iet0el cited by Gettel#5' reported that 5,( of 211 temporal bones had a dehiscent segment of the facial nerve. The mechanism of paralysis is presumably acute neuritis with hyperemia and cellular infiltration, leading to inflammatory edema of the nerve and compression within its bony canal. 6ubse*uent ischemia leads to neurapra/ia of the nerve.3 2thers have postulated that the route of inflammation may be the physiologic canaliculi between the middle ear and the fallopian canal such as those for the stapedial and chorda tympani nerves#. 5hen facial paralysis occurs later than 2 wee%s after the onset of otitis media, it should be assumed to be the result of erosion of the bony fallopian canal with e/posure of the nerve to the active infection !igure 155"21#. 7rogressive facial paralysis in the presence of stable conductive hearing loss without a history of chronic otitis media suggests the presence of congenital cholesteatoma.10+ !acial paralysis associated with chronic otitis media is usually caused by neural compression from the mass effect of cholesteatoma. Fabyrinthine fistula may co"e/ist in these cases. Management 9anagement of facial paralysis from acute otitis media is myringotomy and antibiotics< more aggressive management is indicated

only if the infection fails to resolve or if electroneurography indicates neural degeneration.2, 1omplete recovery after resolution of the acute infection is typical. 9astoidectomy is indicated 1# if the paralysis occurs more than 2 wee%s after the onset of otitis media, 2# if the patient has a history of chronic otitis media, 3# if the paralysis fails to resolve after ade*uate management of the acute otitis media, or +# if electroneurography indicates degeneration of more than &0( of the motor nerve fibers within ' days of onset of the paralysis.2, The goal of surgery in this setting is twofold@ eradication of disease and e/ploration of the fallopian canal for invasive granulation tissue. ) complete canal wall"up mastoidectomy is performed. The bone of the fallopian canal is thinned to allow observation of the nerve without uncovering it< unnecessary opening of the canal in the presence of active infection should be avoided, if possible. $n addition, it is best not to open the facial nerve sheath in the presence of acute infection. 3owever, if there is evidence of granulation tissue e/tending from a dehiscent segment into the bony canal, the canal should be opened pro/imally and distally for the length of the e/tent of the granulation. =/traneural sheath granulations may be removed, but no granulations should be removed from within the sheath< this tissue tends to infiltrate between fibers, and attempts to remove it may result in permanent in4ury to the nerve. !or patients with chronic otitis media and cholesteatoma, urgent surgery is indicated to remove the cholesteatoma mass, which will result in decompression of the facial nerve at the site of involvement. ;o other facial nerve decompression is needed and the nerve sheath should not be opened.

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