TITLE: Complications of Acute <=
span
class=3DSpellE>Otitis Media
SOURCE: Grand Rounds Presentation, UTMB, Dept. of Otolaryngology
DATE: October 26, 2009
RESIDENT PHYSICIAN:
FACULTY PHYSICIAN: Harold Pine, MD
SERIES EDITORS: Francis B. Quinn, Jr., MD
ARCHIVIST: Melinda Stoner Qui=
nn, MS(ICS)
&q=
uot;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 purp=
ose
of stimulating group discussion in a conference setting. No warranties,
either express or implied, are made with respect to its accuracy, completen=
ess,
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."
History
Hippocrates noted in 160 BC that “acute pa= in in the ear with continued high fever is to be dreaded for the patient may beco= me delirious and die.” Prior to the antibiotic era, ¼ to ½= of the patients with acute otitis media presented with mastoiditis, subperiost= eal abscess, and sigmoid sinus thrombophlebitis. 2-6% of all patients developed an intracranial suppurative complication, with a fatal outcome in ¾ of them. (3) Intracranial and extracranial extensi= on of middle ear infection continues to serious medical problem especially in children. The incidence of mastoiditis and intracranial suppurative intracranial complications in pediatric age group has consistently increased over the past 2 decades. Abuse or inadequacy of antibiotic treatment have b= een attributed a role in selecting resistant bacterial strains. (3) Another explanation is that antibiotic therapy masks the sign and symptoms of mastoiditis, providing time for the process to extend to the mucoperiosteum and erode the bony septae. (5)
Pathophysiology
The tendency of middle ear infections to spread = beyond the confines of the middle ear and its adjacent spaces is influenced by a number of factors, including the virulence of the infecting organism and its sensitivity to antibiotics, host resistance, the adequacy of antibiotic therapy, the anatomic pathways and barriers to spread, and the drainage of = the pneumatic spaces, both natural and surgical. One should also consider the immune status of the host: Immunocompromised individuals are at increased risk of developing not only otitis media but a= lso complications of otitis media. Moreover, the organisms causing the infection are more likely to be atypical pathogens. One should consider infants to be= in this group of patients, since their immune systems are not fully mature.
Diagnosis
Initial diagnostic workup of complicated acute o= titis media is usually triggered by a history and physical that is incongruent wi= th with a standard middle ear infection. A complete head= and neck exam should be performed with attention to the ot= oscopic exam and the cranial nerve exam. For patients with high suspicion of meningitis, a Kernig’s and Brudzinski’s sign should be checked.= A fundoscopic exam may reveal signs of intracranial pressure. The workup usua= lly includes a CT of the temporal bones with contrast. In patients that are suspected of having a sinus thrombosis, magnetic resonance venography may b= e performed. A complete blood count with differential and an erythrocyte sedimentation ra= te are often performed. Audiogram should be performed when feasible to evaluate for sensorineural hearing loss associated with labyrinthitis.
Intratemporal complicati= ons
Mastoiditis
Mastoiditis is the m=
ost
common intratemporal complication of acute otitis media. Work from
Mastoiditis should be initially treated at least= with IV antibiotics. Culture and gram-stain directed therapy is optimal. The most common pathogen recovered from culture is Streptococcus pneumoniae. = Streptococcus pyogenes, Staphylococcus aureus, and coagulase-negative Staph= ylococcus species are also common. There is also a higher incidence of Pseudom= onas aeruginosa as compared to cases of uncomplicated acute otitis media. The AAOHNS guide to antimicrobial therapy recommends vancomycin plus ceftriaxone as empiric therapy.
The use of interventions bey= ond antibiotic therapy have been debated in the literature. The dilemmas that the otologist faces when dealing with mastoiditis are: the indications= for a surgical treatment, the timing of surgery (immediate versus delayed), and= the choice of surgical procedure. Whether a myringotomy, a myringotomy with PE tube, or a mastoidectomy is performed, the goals of surgery are to drain the infection and to obtain pus for culture.
A review of 45 patients showed that in 32 cases = of uncomplicated mastoiditis, there were no treatment failures among 20 patients treated wit= h IV antibiotics alone. However when these patients were compared to the 12 pati= ents that had PE tubes with or without mastoidectomy, they had slightly longer h= ospital stays with a longer time to symptomatic resolution. (3) It should be noted = that the patients selected for medical therapy may have had less severe disease = at presentation. Another review of 44 patients showed that among the 38 patien= ts with uncomplicated mastoiditis, only 1 did not improve with myringot= omy, tube, and IV antibiotics. This patient underwent mastoidectomy after he did= not clinically improve within 96 hours of initial surgery. (5) Still another retrospective review of 58 cases examined conservative versus aggressive therapy. 17 patients received IV antibiotics alone with a 100% c= ure rate. A second group of 28 patients, presumably with more severe disease underwent myringotomy and/ or tubes in addition to antibiotics. There were 4 treatment failures in this group. Of these, 3 had a subperiosteal abscess a= nd 1 had a cholesteatoma. (9) None of these treatment failures had preoperative = CT scan. It is possible that imaging would have detected these additional complications and triggered more aggressive therapy, preventing treatment failure.
Facial Nerve Paralysis
Facial nerve paralysis associated with acute oti= tis 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 St= aphylococcus 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 paral= ysis required mastoidectomy to control otorrhea and fever after initial myringot= omy and antibiotics. Both patients had a prolonged recovery, but eventually rec= overed to House-Brackman I or II. (13) A larger study of 22 patients showed comple= te resolution of paralysis in 21. (15)These studies support the conservative management of this complication. Corticosteroids should be considered, thou= gh 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.
Labyrithitis
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 l= oss, 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 life-threatening; 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 infecti= on. As with other complications of otitis media, culture-directed antibiotics a= re 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. Ser= ous 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-frequen= cy 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 pa= rt 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)
Gradenigo’s syndrom= e:
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 compl= ete resolution of the petrous apicitis with complete mastoidectomy, PE tube, an= d IV antibiotics. (15)
Subperiostea= l abscess.
Drainage of subperiosteal abscess. They found a 93% success rate in the 43 patients reported. = (10) It should be noted that close follow up is needed for patients if this treatment regimen is used. Recurrences do occur even in cases that undergo aggressive therapy with mastoidectomy. (11) A low threshold for repeat imag= ing should be kept, especially for infants and other immunosuppressed patients.= However, this regimen avoids the morbidity and potential complications of mastoidect= omy in young patients. (7)
Bezold abscess
In 1881, Bezold described a complication of mastoiditis presenting as a laterocervical abscess. Bezold’s abscess = is caused when a suppurative process erodes the mastoid cortex along the digas= tric ridge and spreads between the digastric and sternocleidomastoid muscles. Th= is is a serious complication because of its ability to spread downwards along great vessels and reach the mediastinum. This complication is exceedingly r= are in children, probably because of the absence of extensive pneumatization of= the mastoid in younger patients. These abscesses may be difficult to detect clinically. Diagnosis can be hindered by infrequency of presentation and inconsistency of signs and symptoms. The common clinical signs and symptoms= are pyrexia (74%), otalgia (52%), neck swelling (48%), otorrhea (41%), restrict= ion of neck motion (41%), neck pain (41%), and facial nerve paralysis (15%).(12) There is a paucity of published data on the management of Bezold’s ab= scess. At minimum, these patients should undergo initial myringotomy with tube pla= cement, and culture directed antibiotics. Early aggressive surgical management in t= he form of mastoidectomy and incision and drainage of the neck abscess should = be considered because of the potential of this infection to spread throughout = the neck.
Intracranial Complications
Meningitis is the most common intracranial complication of otitis media. The earliest symptoms are headache, fever, vomiting, photophobia, irritability, and restlessness. Infants may have seizures. As the infection progresses, the headache increases, and vomiting becomes more pronounced. Neck stiffness, with resistanc= e to flexing the neck so that the chin does not touch the chest, may start with minimal discomfort and progress. Brudzinski’s sign, the inabil= ity to flex the leg without moving the opposite leg (or flexion of the neck resulting in flexion of the hip and knee), is a sign of meningitis. Similar= ly, Kernig’s sign, an inability to extend the leg when lying supine with = the thigh flexed toward the abdomen, is suggestive of meningitis. When meningit= is is suspected, a lumbar puncture is performed to obtain CSF for bacteriologic analysis. In meningitis, the CSF is cloudy or yellow (xanthochromic); also,= an elevated white blood cell count, low glucose, and high protein are expected= . Treatment for meningitis resulting from acute otitis media should be directed at H. influenzae type B with second- or third-generation cephalosporins. One should be aware that rapid bacteriolysis releases large amounts of inflamma= tory fragments that can have severe neurologic and auditory sequelae (sensorineu= ral hearing loss). Glucocorticoids, such as dexamethasone, have been shown to decrease these sequelae). Serial audiograms are recommended as hearing loss= can occur as a late complication. In addition, the aforementioned labyrinthitis ossificans = can occur with meningitis, preventing future cochlear implantation. Consequentl= y, serial MRIs should be performed in children with profound hearing loss as a= sequla of meningitis to detect this development early= .
Brain abscess
Brain abscess is a particularly morbid complicat= ion of otitis media. The mortality associated with brain abscess of otogenic origi= n in the antibiotic era is about 25%. Multiple organisms are usually present in brain abscesses. Polymicrobial cultures with a high incidence of anaerobes = are reported in various studies. Streptococcus and staphylococcus are common gr= am positive organisms that are isolated from brain abscesses. Escherichia coli a= nd Proteus, Klebsiella, and Pseudomonas species are typical gram-negative isolates. It is interesting to note that H. influenzae is rarely fou= nd in otogenic brain abscesses. Otogenic brain abscesses are often the result = of venous thrombophlebitis rather than direct dural extension. Brain abscess formation is indicated by high fever, headache, and neurologic deficit. Currently, the management of brain abscesses is a controversial. The patient must be hospitalized and treated with appropriate, high-dose antibiotics immediately. The management of the brain abscess takes precedence over that= of the primary infective source because the patient is seriously ill and the neurosurgical procedure may be the life-saving procedure. The patient shoul= d be first stabilized neurologically; only then should the ear causing the infec= tion be operated on.
Extradural abscess
Infection can also accumulate in the epidural (extradural) space= , a potential space between the dura mater and the = bone of the intracranial cavity. Large accumulations of pus are rare. Granulation along the dura mater is seen more commonly than an actual epidural abscess. Epidural collections that are accessible from the mastoid cavity should be drained at the time of surgery.
Sigmoid sinus thrombophlebitis
Sigmoid sinus and lateral sinus thrombosis is a = rare, but feared complication of otitis media. The thrombosis typically begins in= the sigmoid sinus and propagates to the lateral sinus and occasionally to the internal jugular vein. In rare cases, emboli may shower to distant locations and cause significant morbidity and mortality. Patients present with the typical symptoms of mastoiditis, along with worsening headache. Picket fence fevers and signs of sepsis are occasionally present. More than half of pati= ents may present with associated cranial nerve findings. These cranial nerve findings are often seen with accompanying elevated intracranial pressure on lumbar puncture. (16) Imaging should be performed in patients suspected of having this condition. Though CT will delineate bony abnormalities and prov= ide a road map for surgery, MRI/ MRV is slightly more sensitive at detecting thromboses. The two imaging modalities should both be performed to maximize diagnostic accuracy. On contrasted CT scan, a filling defect may be seen in= the affected sinus. In 1/3 of these, contrast may accumulate in the collateral veins surrounding the non-enhancing thrombus to yield a pathognomonic “empty delta sign.” The proper treatment of this condition has = only been studied in small case series. Accepted standard practices include myringotomy with tube, IV antibiotics, and mastoidectomy. The plate overlyi= ng the sigmoid sinus is opened and the sinus aspirated. If there is return of blood, the sinus is not opened. If there is no blood return, the sinus is opened, and the clot removed. Postoperative anticoagulation remains controversial. Some authors cite the low incidence of septic emboli as a re= ason to withhold anticoagulation. (17) Others believe anticoagulation should be = used for patients who already have had evidence of embolic events or for those w= ho have thrombus extension past the sigmoid sinus.
Otitic hydrocephalus
Otitic hydrocephalus involves increased intracranial pressure without effect or signs of hydrocephalus. Furthermore, there is no evidence of ventricular dilatation = and focal neurologic signs are absent. Headache, drowsiness, vomiting, blurring= of vision, and diplopia are typical symptoms. Papilledema and sixth cranial ne= rve palsy are usually evident. Optic atrophy can eventually develop. A normal C= SF cytology and biochemistry along with an opening pressure greater than 24 mm= H2O are necessary to make the diagnosis, and to exclude meningitis. Otitic hydrocephalus is very commonly associated with sigmoid sinus thrombophlebit= is; however, not all patients with sigmoid sinus thrombophlebitis develop otitic hydrocephalus. Treatment should include proper therapy for associated sinus thromboses. Medical therapy includes corticosteroids, = mannitol, diuretics, and acetazolamide.
Conclusion
Based on the information gathered in this text, =
one can
construct a practicle algorithm to treat compli=
cated otitis media. If a patient has simple coalescent mastoiditis or meningitis, a myr=
ingotomy
with tube and culture-directed antibiotics should be attempted first. If th=
ere
is no improvement after 72 hours, mastoidectomy
should be performed. This approach can also be used when children have a
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