Title: Complications of Otitis Media
Source: Department of Otolaryngology, UTMB, Grand Rounds
Date: May 20, 1998
Resident Physician: Karen L. Stierman, M.D.
Faculty Physician: Jeffrey T. Vrabec, M.D.
Series Editor: Francis B. Quinn, Jr., M.D.

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"This material was prepared by resident physicians in partial fulfillment of educational requirements established for the Postgraduate Training Program of the UTMB Department of Otolaryngology/Head and Neck Surgery and was not intended for clinical use in its present form. It was prepared for the purpose of stimulating group discussion in a conference setting. No warranties, either express or implied, are made with respect to its accuracy, completeness, or timeliness. The material does not necessarily reflect the current or past opinions of members of the UTMB faculty and should not be used for purposes of diagnosis or treatment without consulting appropriate literature sources and informed professional opinion."

Introduction

A complication of otitis media is defined as a spread of infection beyond the pneumatized area of the temporal bone and the associated mucosa. Complications can be classified as intratemporal or intracranial. Intratemporal complications include mastoiditis, petrositis, labyrinthitis, and facial nerve paralysis. Intracranial complications include extradural abscess, brain abscess, subdural abscess, sigmoid sinus thrombophlebitis, otic hydrocephalus, and meningitis. Since the introduction of antibiotics, intracranial complications in otitis media are less common, however the occurrence should not be underestimated due to the morbidity and mortality associated with such occurrences.

Pathology

The pathophysiology of complications of otitis media remains somewhat of a mystery. Due to the rarity of complications, not many systematic studies have been performed. From studies performed thus far, five factors have been associated with the spread of infection. These include the type and invasiveness of the organism, the antimicrobial therapy, the host resistance, anatomic barriers, and the available drainage sites. The production of granulation tissue that becomes obstructive to the drainage and aeration of the bone plays an important role. In one study of the intracranial complications occurring in thirteen years at one hospital, out of 321 patients, 87(27%) had complications. Intratemporal and intracranial complications co-existed in almost 50% of these patients. Any patient with an extracranial complication from otitis media should have a neurological exam to rule out additional complications intracranially. Most of the patients developing complications were in their twenties or early teens in this particular study.

Most complications result from subacute or chronic infection. An exception to this statement is the association of acute otitis media with meningitis in young children. Impending signs of complications include persistence of infection for greater than 2 weeks, recurrence of symptoms within 2 weeks, acute exacerbation of a chronic infection, fetid discharge during treatment, and infection with Haemophilus influenza, type B or anaerobes. On physical exam, the physician should be suspicious of a complication if there is fever associated with a chronic perforation, a pinna that is displaced inferolaterally and/or edema of the posterosuperior canal wall skin, retro-orbital pain on side of the infected ear(petrositis), vertigo and nystagmus in a patient with an infected ear(labryrinthitis), facial paralysis on the side of an infected ear, headache or lethargy, papilledema, meningismus, or focal neurological signs or seizures.

Infections with Streptococcus pneumoniae,nontypable Haemophilus influenza, and Moraxella catarrhalis are the most common causes or acute suppurative otitis media. Haemophilus influenza type B is a major etiological agent in cases of otitis media associated meningitis. Mastoiditis associated with suppurative otitis media is usually associated with Bacteroides. Anaerobic organisms have been shown to play a role by creating good environments for other more invasive organisms and by inactivating antibiotics.

There are four main mechanisms of extension. These include: preformed pathways, bony erosion, thrombophlebitis, and hematogenous seeding. Most complications of otitis media are associated with chronic or subacute disease. An exception to this statement is the case of meningitis in infants and young children following acute otitis media resulting from preformed pathways and hematogenous seeding. Usually, mastoiditis is the initial complication resulting from bony erosion. Petrositis is typically seen in the presence of mastoiditis. Facial paralysis and fistula of the labyrinth usually occur in the presence of cholesteatomas again as a result of bony erosion. In chronic infections that reach the dura near the sigmoid sinus, thrombosis of the sinus may occur. If this happens, intracranial hypertension, known as otitic hydocephalus, can occur. In addition, retrograde thrombophebitis can result in a brain abscess.

Specific conditions and treatment

Intratemporal complications

The physician must maintain a high index of suspicion in diagnosing complications of otitis media. Treatment of intratemporal complications frequently involves intravenous antibiotics and myringotomy in those cases with an intact tympanic membrane. The decision whether to insert a ventilation tube depends on the findings at the time of myringotomy. Pus in the middle ear is an indication to insert a tube. The process of edema, osteitis, demineralization, and breakdown of bone can result in many intratemporal complications. Once granulation tissue and osteitis occur, the local tissue concentration of antibiotics remains low, and surgical treatment is usually necessary.

Mastoiditis, per se, actually occurs with most infections of the middle ear. It is not considered a complication until bone destruction occurs. Pinnae displacement inferolaterally and edema of the posterior superior canal wall is very suggestive of mastoiditis. However, if these clinical signs are not present, it does not rule out the possibility of mastoiditis. One should suspect masked mastoiditis if there is persistent pain for 2 weeks after antibiotic treatment in an ear without adequate aeration or if there is radiographic evidence of coalescence. Mastoiditis can be present in association with a subperiosteal abscess. Rarely, the abscess can extend into the neck through the medial tip cells as in a Bezold’s abscess. Mastoiditis is a clinical diagnosis where the patient is usually febrile with boring pain and retroauricular swelling. If mastoiditis is suspected, myringotomy for culture and sensitivity should be considered and CT imaging of the mastoid should be obtained. It usually requires antibiotic therapy for 2-3 weeks. If otorrhea remains after 2 weeks of appropriate antibiotic therapy, the diagnosis of chronic mastoiditis and the need for surgical intervention should be considered. Controversy exists as to whether all cases of mastoiditis require surgical intervention.

Petrositis is a rare diagnosis. The symptoms are the same as for mastoiditis with the addition of retroorbital pain and/or abducens paralysis. Gradenigo’s triad or syndrome is the finding of CN VI paralysis, pain in the distribution of CN V, and aural drainage - all on the same side. This is due to a petrous apex abscess. Petrositis differs from mastoiditis in three ways: 1) the anatomy of the petrous region tends to obstruct drainage; 2) the proximity of air cells to bone marrow in the petrous apex predisposes to osteomyelitis; 3) there is greater propensity for intracranial extension due to proximity and propensity for obstruction. Radical mastoidectomy extending toward the petrous apex by following the pneumatized tracts is usually sufficient to resolve the infection.

Labrynthitis denotes inflammation of the epithelial contents of the otic capsule. Labrynthitis is usually viral induced and not fatal. However, if the labrynthitis is suppurative and due to middle ear bacterial infection, meningitis can follow. Viral infections characteristically involve the endolymphatic system, whereas bacterial infection initially affect the perilymphatic spaces. The symptoms are usually severe vertigo, nystagmus and hearing loss. A call to see a patient with peripheral vertigo, nystagmus, and a sudden sensorineural hearing loss is a true emergency until it is established that the middle ear is normal. A contrast enhanced MRI can be obtained to image the labyrinthine system. Treatment is based on clearing the middle ear infection with antibiotics and myringotomy.

Facial palsy can present as a complication of acute suppurative otitis media, otitis media with effusion, chronic otitis media, and mastoiditis, and is possibly a result of the inflammatory response within the fallopian canal to the infection. Facial nerve paralysis associated with otitis media most commonly affects the tympanic and upper mastoid segments. The possibility of reactivation of latent viral infection near the geniculate ganglion also exists. In the case of acute otitis media with facial nerve paralysis, the lesion is often not destructive. However, in subacute or chronic otitis media, the lesion is more often destructive and associated with a cholesteatoma. In one study by Kangsanarak, et al, eighty percent of patients with complications from chronic otitis media were associated with cholesteatoma. Cholesteatoma is most commonly associated with infection with Psuedomonas aeruginosa, Bacteroides spp and anaerobic Streptococcus.. Treatment involves a mastoidectomy with antibiotic treatment. CT of the temporal bone and nerve tests such as the NET, maximum NET, ENOG, and EMG are useful in outlining the lesion and for prognosis. Treatment of facial nerve paralysis is usually aimed at resolving the middle ear infection. However, in the case of a complete paralysis in the presence of chronic otitis media, facial nerve decompression may be necessary to debride the infection from the nerve.

 Intracranial complications

Since the introduction of antibiotic therapy, the percentage of deaths attributed to intracranial complications from otitic disease has decreased. However, the clinician must maintain a high index of suspicion because of the mortality associated with the complications. Early diagnosis is the key. The most common early symptoms of intracranial complications in one study were increased otorrhea, fever, headache, and cholesteatoma or granulation tissue which was visible. Symptoms which occur later are altered mental status, cranial nerve palsies, cerebellar findings, and nuchal rigidity. In the preantibiotic era, standard treatment for any intracranial complication was radical mastoidectomy, even in the ear without cholesteatoma. Today however, therapy is targeted at the specific condition suspected. Meningitis is the most common intracranial complication followed by brain abscess and then sigmoid sinus thrombosis. One study showed the predominant organisms involved with intracranial complications to be P. mirabilis, P. aeurginosa, and Staphlococcus.

Meningitis is usually associated with headache, fever, nuchal rigidity, and abnormal reflexes(Kernig’s or Brudzinski’s sign). The majority of cases are in children and occur by hematogenous dissemination of infection with invasive organisms such as H. influenzae type B. However, one study looked at the temporal bones of children who died of meningitis following otitis media compared with controls of children who just had otitis media and found that the round window, cochlear aqueduct and the modiolus showed chronic inflammation. This suggests that these structures may serve at ports for infection in children. Children with middle ear malformations are at a particularly higher risk for meningitis due to unusual connections between the CSF system and the middle ear space. Meningitis can also occur(although more rarely) in adults following otologic surgery, after chronic otitis media, and after a cholesteatoma forms. Diagnosis can be made by analysis of the CSF from a lumbar puncture. A CT scan should be done prior to the puncture to rule out increased intracranial pressure or other pathology. Treatment of meningitis from acute otitis media requires intravenous antibiotics and myringotomy . Classically, ampicillin plus chloramphenicol has been the antibiotic of choice. However, more recently cephalosporins have become the drug of choice. Patients infected with aggressive organisms with menigitis from acute otitis media may suffer neurological sequela such as mental retardation or deafness, despite antibiotic treatment. This is suspected to be due to damage by inflammatory mediators. Steroids have been shown to decrease these sequela and not interfere with antibiotic treatment. Treatment of meningitis from an otitic source is initially antibiotics and myringotomy. In cases of subacute or chronic infection debridement of the mastoid may be necessary.

Extradural granulation tissue, epidural, perisinus, or subdural abscess are difficult diagnoses. Clinically focal neurological deficits, seizures, and a rapid loss of consciousness can occur. However, this is not always the case and headache, otalgia with malaise may be the only suspicious symptoms. The occurrence of these are usually associated with a cholesteatoma which erodes through structures. MRI or CT can be used to image the lesion. Subdural abscesses are more commonly associated with sinusitis rather than otitis media, but they can occur with otitis. Surgical debridement is necessary and enough infected bone must be removed until healthy dura becomes apparent. A neurosurgical consultation should be obtained. Some granulation tissue attached to dura may need to be left to avoid tearing the dura and spreading the infection to the subdural space. If subdural abscess is found, burr holes should be placed.

Clinically with a brain abscess, the patient may lose consciousness, have a focal neurological deficit, or have signs of increased intracranial pressure. The abscess usually has four stages. The first stage is invasive where the patient has low grade fever, malaise, and fatigue. The second stage is the localization phase where the abscess is clinically quiet. This stage can last up to a couple of weeks. The third stage is the enlargement stage where an actual abscess forms. The termination, or fourth stage is when the abscess ruptures or causes the ventricle to rupture which usually results in a fatal outcome. CT or MRI can be used to image the abscess. However, repeat scans may be necessary to image the abscess depending on the stage it is in. Streptococcus faecalis, Proteus spp, and Bacteroides fragilis are most frequently found in brain abscesses. However, in a study of brain abscesses in 21 patients in a Greek hospital, the most common pathogens isolated were Gram negative anaerobes such as Bacteroides and Fusobacterlum and aerobic Streptococcus which suggests that the causative organisms may depend on the environment you are in. Management of a brain abscess requires surgical intervention of the infection in the ear as well as the brain. A neurosurgical consultation should be obtained. Antibiotics given intravenously are recommended before and after surgery. One article suggested penicillin, an aminoglycoside, and Flagyl for 2 weeks post-operatively.

Sigmoid sinus thrombophlebitis may be completely asymptomatic or can be associated with signs of toxemia, torticollis and septic embolization. If the thrombus propagates far enough, it can be associated with intracranial hypertension or otic hydrocephalus. Clinically, the patient will present with a picket fence fever pattern, headache, lethargy, papilledema and an ear infection. Septic thrombus can propagate to involve the cavernous sinus. If there is involvement of the cavernous sinus, signs include bilateral orbital involvement, sever chemosis and opthalmoplegia, retinal engorgement, and high fever. MRI with gadolinium is the imaging technique of choice for sigmoid sinus thrombophlebitis. MRI with MRA(magnetic resonance angiography) is also an ideal diagnostic tool. Conventional angiography requires vessel puncture, use of IV contrast agents, and uses ionizing radiation. Therefore, angiography is less desirable. The treatment is to surgically expose the diseased dura and remove the excess granulation tissue. If otic hydrocephalus is present, one must treat or monitor the intracranial hypertension. If a septic emboli is present , it may require sigmoid sinus decompression or ligation of the internal jugular vein to avoid further embolization of the tissue. Alternative forms of treatment include anticoagulation therapy and IV antibiotics. However, anticoagulation is not usually recommended as it can be associated with spreading septic emoboli or hemorrhage.

Otitis media can also be associated with otitic hydrocephalus or benign intracranial hypertension(BIH). The pathology is unknown except when associated with sigmoid sinus thrombosis. Symptoms include headache, lethargy, blurred vision, nausea and vomiting, and diploplia as a result of sixth nerve palsy. The most impressive clinical sign is bilateral papilledema. CSF analysis is usually normal except for increase pressure intracranially. BIH usually resolves spontaneously in several months. Surgical intervention consisting of a lumbar-peritoneal shunt is reserved for cases in which there is evidence of decreased vision due to papilledema or disabling tinnitus persisting for greater than one year that has failed medical management.

Complications of surgical intervention

Excessive blood loss can be an unexpected complication from mastoidectomy in children. Brain herniation after lumbar puncture in the presence of increased intracranial pressure should be avoided by ordering a CT scan prior to the puncture. As in all cases of mastoidectomy, there are many adjacent structures of importance such as the facial nerve to avoid injury to.

Summary

Complications of otitis media are much more rare today due to the presence of prompt antibiotic treatment of otitis media. However, the morbidity and mortality rates remain high, especially in the case of intracranial involvement. In addition, the emergence of resistant organisms may play a role in increasing rates of complications in the future. The signs and symptoms can be so subtle that they may make the diagnosis difficult. Therefore, the clinician treating otitis media must always have a high index of suspicion in order not to miss a critical diagnosis.

 

Bibliography

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