What is the microbiology of acute otitis media for different age groups? Recommended therapy?

Number Complications of Otitis Media 3.7.1 Matt What is the microbiology of acute otitis media for different age groups? Recommended therapy? 3.7.2 Matt What are the routes of spread of infection from the middle ear? What is the relevant anatomy of intracranial venous drainage? 3.7.3 SW Discuss the incidence, anatomy, and pathophysiology of acute mastoiditis. What are the signs and symptoms of acute mastoiditis? Treatment? What is "masked mastoiditis"? What is the 3.7.4 SW role of conservative management (I&D, PE tube, IV abx)versus cortical mastoidectomy? 3.7.5 SW Discuss the differences in presentation and management of subperiosteal, Bezold's, and Luc's abscesses. A 7 year old patient presents with right otorrhea, and double vision. A MRI is obtained. What is the diagnosis? Describe the normal relevant anatomy and the pathophysiology of this condition. What are the management options for this patient? 3.7.6 AL Gradenigo s syndrome: In 1907, Gradenigo described his classic triad of abducens nerve paralysis, severe pain in the distribution of the trigeminal nerve, and acute suppurative otitis media. The symptoms were attributed to suppurative disease of the petrous apex. The petrous apicitis is detectable on CT scan of the temporal bones. This complication is often found with synchronous intracranial complications. Small series of patients show complete resolution of the petrous apicitis with complete mastoidectomy, PE tube, and IV antibiotics. (15) The definition of acute mastoiditis is characterised by infectious, inflammatory extension towards mastoid air cells, with accumulation of purulent fluid, osteitis and destruction of bone trabeculae forming a common cavity. Extension may occur into six anatomical areas. Medial extension will cause distribution towards the labyrinth or the petrous apex causing labyrinthitis, peripheral facial paralysis or petrositis. Subperiosteal and Bezold abscesses are secondary to subperiosteal extension of infection from mastoiditis. Petrositis and Gradenigo s syndrome are caused by the extension of the infectious process into the cells of the petrous portion of the temporal bone. Gradenigo s triad consists of otitis media, paralysis of the sixth cranial nerve and neuralgia of the fifth cranial nerve. Neuralgia of the fifth cranial nerve is characterised by intense hemifacial and retro-orbital pain. These can be complicated by intracranial extension.5 Abscesses may result directly from perivascular extension of middle ear infection or may follow the development of an adjacent infection, such as lateral sinus thrombophlebitis, petrositis or meningitis, as described by Trimis et al.6 A Cochrane Review of 20107 states antibiotics are not indicated in uncomplicated AOM. There is insufficient evidence demonstrating a reduction in complications such as mastoiditis. The clinician must therefore avoid routine use of antibiotic therapy for simple otitis media, and then recognise complications, in order to start appropriate therapy. Petrositis has traditionally been treated with aggressive surgical methods. The four cases described by Goldstein et al.3 all underwent mastoidectomy. Recent reports have documented good results with more conservative therapy with high-dose broad-spectrum antibiotics that have intracranial penetration and VT insertion. Aggressive surgical intervention is recommended for patients who failed to respond to conservative therapy including VT insertion.8 The severity of disease in children with intracranial complications of AOM shows the importance of early recognition of inflammatory processes in the bones surrounding the middle ear. Although all presented studies regarding acute mastoiditis

3.7.7 AL use different inclusion criteria, none have included preauricular or facial swelling and/or tenderness. Petrositis usually presents with symptoms such as Gradenigo s syndrome, which were not found in this case. The clinical features in this case demonstrate the heterogeneity of complications in children with acute mastoiditis. Discuss serous vs. suppurative labyrinthitis: etiology, presentation and management. Bacterial labyrinthitis may occur by either direct bacterial invasion (suppurative labyrinthitis) or through the passage of bacterial toxins and other inflammatory mediators into the inner ear (serous labyrinthitis). Meningitis typically affects both ears, whereas otogenic infections typically cause unilateral symptoms. Profound hearing loss, severe vertigo, ataxia, and nausea and vomiting are common symptoms of bacterial labyrinthitis. Bacterial infections of the middle ear or mastoid most commonly spread to the labyrinth through a dehiscent horizontal semicircular canal. Usually, the dehiscence is the result of erosion by a cholesteatoma. This complication is potentially lifethreatening; infection in the inner ear can spread to the subarachnoid space causing meningitis. Early mastoidectomy is indicated in these cases to fully decompress and drain the purulent infection. As with other complications of otitis media, culture-directed antibiotics are an integral part of the treatment regimen. The sensorineural hearing loss is usually irreversible. Labyrinthitis ossificans often follows suppurative labyrinthitis; therefore, decisions regarding cochlear implantation must be made early. Serial MRIs have been have been advocated to monitor for this complication, since CT may not be sensitive enough for early detection. Serous labyrinthitis occurs when bacterial toxins and host inflammatory mediators, such as cytokines, enzymes, and complement, cross the round window membrane, causing inflammation of the labyrinth in the absence of direct bacterial contamination. Penetration of the inflammatory agents into the endolymph at the basilar turn of the cochlea results in a mild-to-moderate high-frequency SNHL. Audiologic testing reveals a mixed hearing loss when a middle ear effusion is present. Vestibular symptoms may occur but are less common. Treatment is aimed at eliminating the underlying infection and clearing the middle ear space of effusion. A small series of patients was examined as part a larger study. 3 of 3 pediatric patients with isolated serous labyrinthitis had resolution of hearing loss with myringotomy, PE tube, and IV antibiotics. (15) Labyrinthitis Labyrinthitis characteristically is viral -induced endolabyrinthitis and is not potentially fatal. However, labyrinthitis secondary to middle ear infection can be fatal if suppurative labyrinthitis and, subsequently, meningitis occur. Therefore, each call from the emergency department to see a patient in whom severe vertigo and hearing loss occur simultaneously requires the clinician to determine whether the middle ear is normal. Experimental and human experience with acute and chronic otitis media reveals serous labyrinthitis and endolymphatic hydrops are fairly frequent complications of suppurative middle ear disease. However, suppurative labyrinthitis is extremely rare and potentially fatal. These conditions may occur together or separately. Cholesteatomas may erode the otic capsule, creating perilymph fistulae that may cause mechanical cochlear effects, serous labyrinthitis, and a preformed pathway for acute infection to enter the labyrinth; therefore, vertigo in the presence of a cholesteatoma must be evaluated immediately and very carefully. Until recently, diagnosis of labyrinthitis was made on clinical grounds. Serous labyrinthitis, in which toxic or metabolic products of bacteria or the host inflammatory response enter the inner ear through the round window membrane or cholesteatomainduced fistula, results in sensorineural loss and vertigo with nystagmus. However, the degree of loss is not total, and some recovery is possible. Conversely, suppurative labyrinthitis from the entrance of bacteria into the labyrinth through the same route creates similar symptoms but profound losses that never resolve and result in extensive inner ear and spiral ganglia cell loss. Hegarty et al. (10) have found evidence of labyrinthine disease by contrast -enhanced MRI; this technique may prove to be helpful in the future to confirm the presumptive diagnosis of labyrinthitis. Acute Suppurative Labyrinthitis

3.7.8 AL Bacterial invasion of the labyrinth is always promptly followed by total loss of auditory and vestibular function (Figs. 140-26 through 140-29). Usually, AOM extends into the labyrinth through a weakened or dehiscent oval window membrane, as occurs in congenital labyrinthine deformities such as Mondini s deformity and enlarged vestibular aqueducts, and in individuals who have undergone stapes surgery. Although it is not proven, suppurative labyrinthitis may be a common mechanism for unilateral anacusis in children with Mondini s deformity. These children are at additional risk. The foramina of the internal auditory canal opening into the medial aspects of the labyrinth may also be weak or dehiscent, and those foramina and the cochlear aqueduct can permit bacterial infection to progress from the labyrinth to the meninges or vice versa. It is unknown how frequently suppurative labyrinthitis causes meningitis, or how often meningitis subsequently causes bacterial labyrinthitis, but both probably occur, especially in the special population of children with congenital labyrinthine abnormalities. Direct bacterial invasion of the labyrinth through a cholesteatomatous lateral semicircular canal fistula is another cause for acute suppurative labyrinthitis. In this situation, infected granulation tissue beneath the cholesteatoma matrix lies directly on the endosteal membrane and its underlying perilymph. The bacteria causing the labyrinthitis are those of the underlying AOM or the cholesteatoma. The diagnosis of acute suppurative labyrinthitis is clinical. Tinnitus and dizziness rapidly progress to whirling vertigo, pallor, diaphoresis, nausea, and vomiting. Brisk labyrinthine nystagmus directed toward the opposite ear accompanies the vertigo. After the first several hours, the spontaneous vertigo and nystagmus gradually begin to abate. Symptomatic improvement continues during the next few days. Over the next 2 to 3 weeks, central nervous system compensation occurs, and normal or near-normal balance is restored. Tinnitus often abates, but all hearing is lost. No specific diagnostic studies are necessary when the typical clinical picture develops in a patient with AOM or COM and a predisposing condition. Although there is no possibility of reversing the clinical course, appropriate antibiotic treatment for 10 days is recommended to eradicate the labyrinthine infection and to prevent propagation to the meninges. Other therapeutic measures are dictated by the underlying otitis, but labyrinthectomy is unnecessary in labyrinthitis secondary to AOM. Describe the management of VII paralysis with AOM and COM. How is pathogenesis associated with timing? Facial Nerve Paralysis Facial nerve paralysis associated with acute otitis media is a rare, but disturbing complication. The incidence is estimated at 0.005%. Despite the striking presentation of this complication, the prognosis is excellent. A recent review of 11 patients over 26 years reported a full recovery to House-Brackman I or II. All of these patients received a myringotomy with tube placement, along with IV antibiotics; Only 1 patient underwent mastoidectomy. Interestingly, 5 of 7 positive cultures grew Staphylococcus aureus, suggesting that the bacteriology of otitis media with associated facial paralysis may be different. (14) Another study reviewed 10 children who presented with facial paralysis after the onset of acute otitis media. 8 patients with incomplete paralysis had full return of function after myringotomy and intravenous antibiotics. The 2 patients with complete paralysis required mastoidectomy to control otorrhea and fever after initial myringotomy and antibiotics. Both patients had a prolonged recovery, but eventually recovered to House- Brackman I or II. (13) A larger study of 22 patients showed complete resolution of paralysis in 21. (15)These studies support the conservative management of this complication. Corticosteroids should be considered, though there is no good evidence for their effectiveness. Mastoidectomy should be performed only when it is necessary to treat otitis media. Surgical facial nerve decompression is not indicated in these cases. The major diagnostic challenge in facial paralysis from the suppurative ear disease is to identify the possibility of a nerve-destructive lesion versus neuropraxia from toxicity or slight compression and edema. Facial paralysis from acute suppurative otitis media may not be destructive. However, facial paralysis in the presence of a subacute infection, acute coalescent mastoiditis, masked mastoiditis, petrositis, or chronic suppurative otitis media, with or without cholesteatoma, may well be destructive, particularly in the

tympanic segment. P.2047 The typical topognostic techniques for site -of-lesion identification are useful to confirm the intratemporal site of lesion. Degree-of-lesion techniques, such as the nerve excitability test, the maximum nerve excitability test, electroneurography, and electromyography, are extremely important, although imperfect, tools to identify a nervedestructive lesion. MRI with gadolinium is useful in identifying neoplastic and inflammatory lesions of the facial nerve but as yet cannot determine the degree of lesion. The most useful tool of all is a detailed careful history of the patient's current illness and past medical history of ear disease with a specific attempt to define the exact pathophysiology that may be involved with each case. It is probably prudent to err on the side of assuming a nerve-destructive lesion when in doubt and plan to explore the nerve. Cholesteatoma is by far the most common cause of facial paralysis. The lesion characteristically is most common in the tympanic and upper mastoid segments; however, the labyrinthine segment also may be involved in deep petrous cholesteatomas. Degeneration and inflammation are variably present in the localized area of the facial nerve and may be partially or more rarely completely destructive of the facial nerve. Granulation tissue that invades the epineurium is more dangerous than cholesteatoma matrix; granulation tissue may infiltrate between nerve fibers and, if surgically pursued, may result in transection of the nerve. Facial Nerve Paralysis Facial nerve paralysis can result from AOM, COM without cholesteatoma, or cholesteatoma. Bacteria reach the nerve because of congenital dehiscences of the bony fallopian canal or via erosion with granulation tissue or cholesteatoma. Facial nerve function is lost with inflammatory pressure or suppurative neurapraxia. If the edema persists, axonotmesis can ensue. In young children, facial paralysis that is caused by AOM is frequently incomplete and probably occurs only in infants with congenital dehiscence of the fallopian canal in the middle ear adjacent to the stapes. Facial weakness in these cases rarely lasts longer than 3 weeks even when complete paralysis is present. Facial nerve paralysis caused by COM without cholesteatoma also usually affects the horizontal portion of the facial nerve near the stapes.19 In these cases, the clinical course of the paralysis is more likely to be prolonged, with a gradual progression from slight weakness to full paralysis; sometimes the progression to complete paralysis is rapid (Figs. 140-24 and 140-25). Facial nerve paralysis caused by cholesteatoma can produce extensive erosion of the horizontal segment of the fallopian canal especially common in large, uninfected, primary acquired cholesteatomas. An erosive cholesteatoma can expose the facial nerve anywhere in the temporal bone and cause paralysis. In these cases, the onset of the paralysis is usually gradual, and sometimes the progression is so slow that patients do not seek medical attention for months. When the onset of facial paralysis is this slow, the paralysis is more likely to persist after surgical treatment. When facial paralysis is caused by AOM, appropriate antibiotic therapy for AOM may be adequate treatment, although myringotomy with evacuation of the purulent material and reduction of the numbers of bacteria is recommended. When facial nerve paralysis follows chronic suppurative otitis media (with or without cholesteatoma), the surgeon should remove the infection surrounding the nerve as part of the mastoidectomy. The surgeon gradually approaches the granulation tissue or cholesteatoma overlying the nerve from the proximal and distal portions of the nerve, which are uninvolved by the chronic infection. Diamond burs should be used to remove carefully the bone of the fallopian canal on both sides of the diseased portion. The surgeon uses a flat blunt instrument to dissect the chronic inflammatory tissue from the nerve while elevating the diseased tissue with a small suction tip. It may be necessary to use sharp dissection to separate the inflammatory tissue from the epineurium. The outcome for surgical decompression of the facial nerve caused by chronic suppurative otitis media primarily depends on whether the nerve has undergone complete degeneration before surgery. 3.7.09 Review the signs and symptoms of impending intracranial complications. Compare and contrast the

CB 3.7.10 CB 3.7.11 CB 3.7.12 3.7.13 3.7.14 presentation of the different intracranial complications. How do you work these patients up? What is the treatment of lateral sinus thrombosis? What is the role of anticoagulation? What is the etiology and management of brain abscess, epidural abscess, subdural empyema? 5 days after I & D of a right mastoid subperiosteal abscess your patient develops nausea, vomiting and double vision. Exam reveals an afebrile patient with bilateral 6th cranial nerve palsies. How would you work this patient up? What is the treatment for this condition? A 2 year old presents to the emergency room with lethargy, fever, stiff neck, and otalgia. Examination reveals a purulent middle ear effusion and pain with thick flexion and knee extension. Flexion of the patient's neck results in elevation of their legs? What is your differential diagnosis? How would you work this patient up? What treatment would you initiate? What are the indications for a canal wall down mastoidectomy in the setting of complications of otitis media?