2 Otology
4. Tympanomastoidectomy with canal wall down: this technique is em- ployed in managing COM with extensive cholesteatoma, and rarely in
2.2.3 Complications of Acute and Chronic Otitis Media
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Key Features
● Antibiotics have produced an overall decline in the frequency of complications of otitis media.
● Complications of acute and chronic otitis media may be both intracranial and extracranial.
● The most common extracranial complication is postauricular ab- scess; the most common intracranial complication is meningitis.
Acute otitis media is one of the most common diagnoses in patients pre- senting to physicians. Approximately 85% of all children will have at least one episode. A fraction of patients go on to suffer complications due to progression of infectious and inflammatory processes. More than 60% of patients who suffer complications do so within the first two decades of life.
Complications are subdivided by site (extratemporal, intratemporal, and intracranial).
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Extratemporal Complications
Subperiosteal AbscessMastoiditis either directly erodes the bone of the lateral wall of the mastoid or traverses mastoid emissary veins into the subperiosteal space adjacent to the mastoid.
Signs and Symptoms
Fever, malaise, and pain are associated with a subperiosteal abscess.
Physical Exam
On the physical exam the patient may present with otalgia, otorrhea, an anteriorly and laterally displaced auricle, and fluctuant, erythematous, postauricular fluid collection.
Imaging
CT is the preferred imaging mode.
Treatment Options
The recommended treatment typically includes myringotomy with or with- out tube, incision and drainage of the abscess, and IV antibiotics. Cortical mastoidectomy is frequently recommended, particularly in the presence of cholesteatoma.
Bezold Abscess
Mastoiditis leads to erosion of the mastoid tip bone deep to the digastric ridge. Purulent material is directed into the neck, deep to the sternocleido- mastoid muscle (SCM).
Signs and Symptoms
Fever, malaise, and neck pain are associated with a Bezold abscess.
Physical Exam
The patient may present with otalgia, otorrhea, and a tender upper cervi- cal mass.
Imaging
Contrast-enhanced CT will confirm the presence of a rim-enhancing cervi- cal abscess in combination with mastoiditis.
Treatment Options
Recommended treatment includes IV antibiotics, myringotomy with or without tube, cortical mastoidectomy, and incision and drainage of the neck abscess.
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Intratemporal Complications
Labyrinthine FistulaA labyrinthine fistula is caused by an erosion of otic capsule bone and exposure of the membranous labyrinth. The incidence is 7% of patients with cholesteatoma. 90% of fistulas occur in the horizontal semicircular canal.
Signs and Symptoms
A significant number of patients will be asymptomatic, and fistulas will only be discovered within the course of mastoidectomy. 62% of patients com- plain of periodic vertigo or imbalance. Patients may experience the Tullio phenomenon (vertigo induced by loud sounds). SNHL may also be present, but is neither sensitive nor specific.
Physical Exam
Fistula testing (nystagmus with pneumatoscopy) is positive in ⬃50% of patients.
Imaging
Thin-cut temporal bone CT is preferred; however, small fistulas may still be missed.
Treatment Options
Treatment is controversial, as violation of the labyrinth may result in a dead ear. Many authors recommend canal wall down mastoidectomy, leaving
cholesteatoma matrix overlying the fistula to form the lining of the exteriorized mastoid cavity. In cases of small fistulas that have not violated the membranous labyrinth, some authors advocate complete matrix removal and semicircular canal resurfacing with bone pate, fascia, or a similar sealant. Others recom- mend leaving the matrix in place, leaving the canal wall up, and coming back to remove the matrix and resurface the labyrinth at a second stage.
Coalescent Mastoiditis
Suppurative progression of untreated or incompletely treated acute OM results in erosion of the mastoid cavity trabecular bone. Time course of progression is typically 2 to 4 weeks.
Signs and Symptoms
Symptoms include fever, malaise, and otalgia.
Physical Exam
On the physical examination, purulent otorrhea or a bulging TM, postau- ricular erythema, tenderness, and edema displacing the auricle anteriorly and inferiorly are found.
Imaging
A CT scan confirms mastoid and middle ear opacification with erosion of trabecular mastoid cavity bone. Frequently, erosion occurs primarily adja- cent to the sigmoid sinus.
Treatment Options
Recommended treatment includes myringotomy with or without tube, IV antibiotics, and cortical mastoidectomy. Others advocate myringotomy alone and IV antibiotics for 3 to 6 weeks with serial CT confirmation of resolution of mastoid and middle ear opacification.
Petrous Apicitis
Petrous apicitis is a rare complication resulting from the spread of infec- tion into air cells within a pneumatized petrous apex (the prevalence of pneumatization is 30%).
Signs and Symptoms
The classic triad of deep retroorbital pain, purulent otorrhea, and ipsilateral abducens palsy (Gradenigo syndrome) is seen. CN VII and VIII dysfunction also may occur.
Imaging
A CT scan will show opacification of a pneumatized petrous apex.
Other Tests
MRI and lumbar puncture (LP) are helpful to assess concurrent intracranial processes.
Treatment Options
First-line therapy is long-term IV antibiotics secondary to the difficulty of surgical access to the petrous apex. Abscess, necrotic bone, or failed medical therapy requires surgical drainage. Hearing status determines the choice of approach. Hearing preservation may be attempted by infraco- chlear, infralabyrinthine, retrolabyrinthine, subarcuate, and middle fossa approaches. Translabyrinthine or transcochlear approaches may be used for nonhearing ears.
Facial Paralysis
Facial paralysis results from inflammation of dehiscent segments of the facial nerve secondary to infection.
Imaging
CT scanning for AOM-associated incomplete paralysis may not be neces- sary, but may help in operative planning in the setting of cholesteatoma or complete paralysis.
Pathology
In the setting of children with AOM, a congenitally dehiscent tympanic segment of the facial nerve is suspected. The paralysis is usually incom- plete and resolves within 3 weeks. In the face of COM and cholesteatoma, dehiscence is typically due to fallopian canal erosion secondary to disease.
Onset may be slow and progressive. The prognosis is poorer and recovery slower.
Treatment Options
Paralysis due to AOM is treated with IV antibiotics and myringotomy.
Cholesteatoma-associated paralysis requires mastoidectomy, nerve decom- pression proximal and distal to the diseased segment, and débridement of inflammatory tissue.
Acute Suppurative Labyrinthitis
Acute suppurative labyrinthitis results from direct bacterial invasion of the labyrinth, resulting in total auditory and vestibular loss. Acute suppurative labyrinthitis may lead to meningitis and vice versa.
Signs and Symptoms
Acute-onset total sensorineural deafness and severe vertigo are signs of acute suppurative labyrinthitis.
Pathology
Predisposing factors include congenital inner ear malformations and otic capsule erosion secondary to cholesteatoma.
Treatment Options
Labyrinthine functional loss is unavoidable, but patients should be treated with antibiotics to prevent the progression to meningitis. Vertigo is treated symptomatically and typically improves as patients compensate.
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Intracranial Complications
MeningitisMeningitis is the most common intracranial complication of OM.
Signs and Symptoms
Fever, headache, nausea, vomiting, photophobia, and nuchal rigidity are symptoms of meningitis. Seizures, ataxia, and other focal neurologic signs are ominous findings.
Imaging
CT or MRI is essential to rule out other intracranial processes and establish the safety of LP.
Other Testing
LP is diagnostic (suggestive CSF findings: increased pressure, increased protein, decreased glucose, inflammatory cells or bacteria present).
Pathology
The potential routes of bacterial spread from the ear to the CSF include hematogenous seeding, bony erosion with direct spread, and bony channels (suppurative labyrinthitis, Hyrtl’s fissures, congenital defects, and traumatic defects).
Treatment Options
Because meningitis is the most common complication seen with OM, de- tailed antibiotic guidelines are listed in Table 2.5. First-line therapy is IV antibiotics, myringotomy, and steroids (decreases hearing and neurologic sequelae). In the presence of cholesteatoma, coalescent mastoiditis, or failure of medical therapy, mastoidectomy is indicated.
Brain Abscess
The most frequently lethal intracranial complication of OM is a brain abscess.
Signs and Symptoms
The clinical course is multistage, starting with fever, malaise, nausea, vomit- ing, headache, mental status changes, and seizures. This may be followed by a quiescent phase with moderate clinical improvement. The third stage, thought to represent abscess growth and ultimate rupture, is a rapid and fulminant return of symptoms with sudden clinical decline.
Imaging
CT and/or MRI may aid surgical planning.
Pathology
Infection spreads secondary to thrombophlebitis of venous channels leading from the mastoid to brain parenchyma. The temporal lobe and cerebellum are the most common sites of abscess.
Treatment Options
Treatment is with IV antibiotics and urgent surgical drainage when the patient is medically stable. IV steroids may reduce brain edema. Anticon- vulsants are given if needed. Surgery consists of craniotomy with drainage of the abscess. Mastoidectomy is typically recommended at the same time but may be delayed if the patient is medically unstable.
Table 2.5 Intravenous Antibiotic Treatment for Meningitis*†
Neonate (1 month)
• Ampicillin gentamicin; or ampicillin third generation cephalosporin Newborn (1–3 months)
• First choice: Ampicillin (cefotaxime or ceftriaxone) dexamethasone (0.15 mg/kg every 6 h 4 d)
• Alternative: Chloramphenicol gentamicin Infant or Child (3 months)
• First choice: (Cefotaxime or ceftriaxone) dexamethasone
• Alternative: Ampicillin Older Child or Adult
• (Cefotaxime 2 g IV every 6 h or ceftriaxone 2 g IV every 12 h) ampicillin 2 g IV every 4 h dexamethasone 0.4 mg/kg every 12 h 2 d vancomy- cin (child 15 to 22.5 mg/kg IV every 6 h; adult 1 g IV every 12 h)
• If Pseudomonas suspected: Cefepime 2 g IV every 8 h instead of cefotaxime or ceftriaxone
• For a penicillin-allergic patient in whom cephalosporin cannot be used:
Vancomycin 15–22.5 mg/kg IV every 12 h trimethoprim/sulfamethox- azole 15 to 20 mg/kg/day IV divided every 6 h
or
• Vancomycin 15 to 22.5 mg/kg IV every 12 h chloramphenicol 1 g IV every 6 h rifampin 600 mg once daily
*Other regimens may be indicated for certain situations, such as an alcoholic patient, a patient with a cerebrospinal fluid leak or a debilitating condition such as acquired immunodeficiency syndrome, or a postneurosurgical patient.
†Length of treatment is generally at least 14 days.
Data from Johns Hopkins Online Antibiotic Guide, http://hopkins-abxguide.org; and Greenberg MS.
Handbook of Neurosurgery. 7th ed. Stuttgart/New York: Thieme, 2010.
Lateral Sinus Thrombosis
Bone overlying the sigmoid is eroded by infection, and perisinus inflamma- tion leads to vessel wall necrosis and mural thrombus formation. Thrombus may propagate proximally to the confluence of sinuses and superior sagittal sinus, resulting in life-threatening hydrocephalus. Clot may also propagate distally into the internal jugular vein, leading to possible pulmonary em- bolus. Additionally, the infected thrombus may shower leading to septice- mia or deeper intracranial infections.
Signs
Tobey-Ayer or Queckenstedt’s test (lack of CSF pressure elevation with occlusion of the internal jugular vein ipsilateral to the thrombosis) is sug- gestive of the diagnosis.
Symptoms
Headache, malaise, and “picket-fence” pattern of diurnal spiking fevers. Neck pain may imply distal clot propagation, while obtundation and papilledema may imply resulting hydrocephalus.
Imaging
Contrasted CT may show “delta sign” resulting from sinus wall enhance- ment with a central filling defect. MRI with magnetic resonance venography (MRV) is very sensitive.
Treatment Options
IV antibiotics and mastoidectomy are the treatment options. Treatment of the dural sinus is controversial. Most authors advocate full exposure of the sigmoid with removal of granulation tissue. Some advocate opening the sinus and removing infected clot. IJ ligation may be performed in the face of significant distal propagation and resulting cervical infection. Anticoagulation is typically reserved for involvement of the cavernous sinus or distal clot propagation.
Epidural Abscess
Granulation tissue and abscess form between the bone of the skull base and overlying dura.
Signs and Symptoms
There are no specific symptoms. Most patients experience deep mastoid pain. Epi- dural abscess may be encountered incidentally at the time of mastoidectomy.
Imaging
MRI or CT is typically diagnostic.
Treatment Options
IV antibiotics and mastoidectomy with removal of granulation tissue and wide débridement of overlying bone until normal dura is found.
Subdural Empyema
A subdural empyema is a rapidly progressive, fulminant bacterial infection between the dura and arachnoid layers. Infection spreads rapidly, resulting in significant brain edema, herniation, and death.
Epidemiology
A subdural empyema most often results from sources other than OM/mas- toiditis.
Signs and Symptoms
Early symptoms are similar to meningitis, with progression to decreased mental status, seizures, and focal neurologic signs.
Imaging
CT or MRI is diagnostic.
Other Tests
LP is contraindicated, as edema puts patients at high risk of herniation.
Treatment Options
Treatment is with an IV antibiotic and urgent neurosurgical drainage.
If the patient is stable, mastoidectomy may be performed following craniotomy.
Otitic Hydrocephalus
Otitic hydrocephalus is a condition of increased intracranial pressure as- sociated with temporal bone infection.
Signs and Symptoms
The symptoms include headache, nausea, vomiting, visual changes, diplo- pia, and lethargy.
Physical Exam
Papilledema or abducens palsy may be observed.
Imaging
MRI or MRV will detect dural thrombosis, rule out other causes, and con- firm the safety of LP. Unlike typical hydrocephalus, the ventricles are not dilated.
Pathology
The condition is thought secondary to lateral sinus thrombosis with proximal clot propagation, resulting in blockage of CSF flow through the arachnoid villi of the superior sagittal sinus.
Treatment Options
Treatment of coincident lateral sinus thrombosis is as above. The otitic hydrocephalus is treated medically with acetazolamide, fluid restriction, steroids. If medical management fails, lumbar drainage or long-term ven- triculoperitoneal shunting may be considered.
Further Reading
Greenberg MS. Handbook of Neurosurgery. 7th ed. Stuttgart/New York: Thieme; 2010 Harker LA, Shelton C. Complications of temporal bone infections. In: Cummings CW,
ed. Cummings Otolaryngology Head and Neck Surgery. 4th ed. Philadelphia, PA:
Elsevier Mosby; 2005:3013–3039
Lin JW, Prasad M, Selesnick SH. Complications of Otitis Media. In: Hughes GB, Pensak ML, eds. Clinical Otology. 3rd ed. Stuttgart/New York: Thieme; 2007:250–257 Neely JG. Facial nerve and intracranial complications of otitis media. In: Jackler
RK, Brackmann DE eds. Neurotology. 2nd ed. Philadelphia, PA: Elsevier Mosby;
2005:912–925
Smith JA, Danner CJ. Complications of chronic otitis media and cholesteatoma. Otolar- yngol Clin North Am 2006;39(6):1237–1255