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Author: PP Devan, MBBS, MS, Chief of ENT, A J Institute of Medical Sciences, India

Coauthor(s): John D Donaldson, MD, FRCS(C), FAAP, FACS, Chairman, Board of Directors, Lee Memorial Health System; Vice-President, Florida Pediatric Society

Editors: John C Li, MD, Private Practice in Otology and Neurotology; Medical Director, Balance Center; Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine; Gerard J Gianoli, MD, Clinical Associate Professor, Department of Otolaryngology-Head and Neck Surgery, Tulane University School of Medicine; Vice President, The Ear and Balance Institute; Chief Executive Officer, Ponchartrain Surgery Center; Christopher L Slack, MD, Otolaryngology-Facial Plastic Surgery, Private Practice, Associated Coastal ENT; Medical Director, Treasure Coast Sleep Disorders; Arlen D Meyers, MD, MBA, Professor, Department of Otolaryngology-Head and Neck Surgery, University of Colorado School of Medicine

Author and Editor Disclosure

Synonyms and related keywords: mastoiditis, acute surgical mastoiditis, ASM, chronic middle ear inflammatory disease, chronic suppurative otitis media, acute otitis media, AOM, acute mastoiditis, earache, ear ache, ear pain, ear infection, hearing loss, cholesteatoma, middle ear disease, coalescent mastoiditis, mastoid, mastoidectomy, tympanocentesis, mastoid disease

A purist's definition of mastoiditis includes all inflammatory processes of the mastoid air cells of the temporal bone. As the mastoid is contiguous to and an extension of the middle ear cleft, virtually every child or adult with acute otitis media (AOM) or chronic middle ear inflammatory disease has mastoiditis. In most cases, the symptomatology of the middle ear predominates (eg, fever, pain, conductive hearing loss), and the disease within the mastoid is not considered a separate entity.

In some patients, the infection spreads beyond the mucosa of the middle ear cleft, and they develop osteitis within the mastoid air-cell system or periosteitis of the mastoid process, either directly by bone erosion through the cortex or indirectly via the emissary vein of the mastoid. These patients have acute surgical mastoiditis (ASM), an intratemporal complication of otitis media. Chronic mastoiditis is most commonly associated with chronic suppurative otitis media and particularly with cholesteatoma formation.

History of the Procedure

In the preantimicrobial era, mastoidectomy was performed in as many as 20% of patients with AOM. By 1948, this figure had dropped to less than 3%, and it is presently thought to be performed in fewer than 5 cases per 100,000 persons with AOM.

Problem

Mastoiditis (see Physical) is considered a complication of otitis media. Complications of mastoiditis are further extensions of the infectious process within or beyond the mastoid itself. The following are common complications:

  • Posterior extension to the sigmoid sinus (causing thrombosis)
  • Posterior extension to the occipital bone to create an osteomyelitis of calvaria or a Citelli abscess
  • Superior extension to posterior cranial fossa, subdural space, and meninges
  • Anterior extension to the zygomatic root
  • Lateral extension to form a subperiosteal abscess
  • Inferior extension to form a Bezold abscess
  • Medial extension to the petrous apex
  • Intratemporal involvement of facial nerve and/or labyrinth

Frequency

Frequency is unknown. Prevalence is most likely to rise with the emergence of multidrug-resistant streptococcal pneumonia (MDRSP), but it should decline with the availability and administration of the conjugated pneumococcal vaccine recently released for clinical use.

For all forms of mastoiditis, frequency parallels that of otitis media and varies with race. In some populations, such as the Inuit, descendants of an Indian tribe living in Alaska and the northwest United States, almost everyone has middle ear disease; the mastoiditis forms exhibited by these populations are invariably chronic.

No sex predilection exists.

Acute mastoiditis is a disease of the very young. Most patients present when younger than 2 years, with a median age of 12 months. However, it can occur in persons of any age.

The mean interval from onset of illness to mastoiditis is usually 4.5 days.

Etiology

ASM occurs as a result of chronic otitis media.

  • Etiologic agents are discussed under Microbial factors. Invasive strains of the bacteria associated with AOM are most commonly recovered from ASM.
  • Gram-negative organisms and Staphylococcus aureus are recovered more frequently from patients with chronic mastoiditis.
  • Decreased or immature host resistance factors appear to cause predisposition to ASM.

Of late, ear cultures have most often grown Streptococcus pneumoniae and Pseudomonas aeruginosa.

A high white blood cell count on admission may serve as a predictive factor for complicated cases.

Half of children admitted with acute mastoiditis have no previous history of recurrent AOM. In those children, S pneumoniae was the leading pathogen, while P aeruginosa was more prevalent in children with recurrent AOM.

Pathophysiology

As with most infectious processes, consider host and microbial factors when evaluating surgical mastoiditis. Host factors include mucosal immunology, temporal bone anatomy, and systemic immunity. Microbial factors include protective coating, antimicrobial resistance, and ability to penetrate local tissue or vessels (ie, invasive strains).

Host factors

Most children presenting with ASM are younger than 2 years and have little history of otitis media. This is an age at which the immune system is relatively immature, particularly with regard to its ability to respond to challenges from polysaccharide antigens.

Host anatomical factors may have a role. The mastoid develops from a narrow outpouching of the posterior epitympanum (ie, the aditus ad antrum). Pneumatization occurs shortly after birth, once the middle ear becomes aerated, and this process is complete by age 10 years. Mastoid air cells are created by invasion of epithelia-lined sacs between spicules of new bone and by degeneration and redifferentiation of existing bone marrow spaces. Other areas of the temporal bone pneumatize similarly, including the petrous apex and the zygomatic root. The antrum, as with the mastoid air cells, is lined with respiratory epithelium that swells when infection is present. Blockage of the antrum by inflamed mucosa entraps infection within the air cells by inhibiting drainage and precluding reaeration from the middle ear side.

Persistent acute infection within the mastoid cavity may lead to a rarifying osteitis, which destroys the bony trabeculae that form the mastoid cells, hence the term coalescent mastoiditis. Essentially, coalescent mastoiditis is an empyema of the temporal bone that, unless its progress is arrested, drains either through the natural antrum to give spontaneous resolution or creates further complication by draining unnaturally to the mastoid surface, petrous apex, or intracranial spaces. Other temporal bone or nearby structures, such as the facial nerve, labyrinth, or venous sinuses, may become involved.

Microbial factors

As AOM is the antecedent disease, the most common etiologic agent causing surgical mastoiditis is S pneumoniae followed by Haemophilus influenzae and group A Streptococcus pyogenes (GAS). Each of these bacteria has invasive forms and is recovered most often from children presenting with ASM. More than half of the S pneumoniae recovered are of serotype 19, followed by serotypes 23 and 3. The literature and the authors' experience indicate that a high frequency of MDRSP is now associated with ASM, and this may alter selection of antimicrobials (40-50% penicillin-resistant, approximately 25% ceftriaxone-resistant). Treatment of AOM with antimicrobials in the previous month increases the frequency of MDRSP. Cultures from chronic draining otitis media with mastoiditis can also yield coagulase-positive staphylococci and/or pseudomonal species. Microbiologic diagnosis is important to guide specific therapy.

Clinical

Terminology

  • Otitis media: This term refers to an inflammation of the mucosal lining of the middle ear, which, in fact, is a mucoperiosteum.
  • Osteitis: During otitis media, if the underlying bone becomes involved as a secondary development, this involvement is known as osteitis or, rarely, osteomyelitis.
  • Mucositis: Inflammation confined to the middle ear cleft is known as tympanitis. When this mucositis spreads to the retrotympanic spaces, it is called mastoiditis. In clinical practice, mastoiditis is used to refer to a complication of otitis media with erosion of the pneumatized bone.
  • Mastoidectomy: This term refers to complete and meticulous opening of the mastoid cells, either endaurally or by using a transcortical approach.

History

Persistent otorrhea beyond 3 weeks is the most consistent sign that a process involving the mastoid has evolved.

The patient’s fever may be high and unrelenting in acute mastoiditis, but this may be related to the associated AOM. Persistence of fever, particularly when the patient is receiving adequate and appropriate antimicrobial agents, is common in ASM.

Pain is localized deep in or behind the ear and is typically worse at night. Persistence of pain is a warning sign of mastoid disease. This may be difficult to evaluate in very young patients.

Hearing loss is common with all processes that involve the middle ear cleft. Most patients (>80%) have no history of recurrent otitis media.

Physical

Mastoiditis progresses in the following 5 stages and may be arrested at any point:

  1. Hyperemia of the mucosal lining of the mastoid air cells
  2. Transudation and exudation of fluid and/or pus within the cells
  3. Necrosis of bone by loss of vascularity of the septa
  4. Cell wall loss with coalescence into abscess cavities
  5. Extension of inflammatory process to contiguous areas

Tenderness and inflammation over the mastoid process is the most consistent sign of ASM. Periosteal thickening requires comparison to the other side, and some lateral displacement of the auricle may be present. Subperiosteal abscess displaces the auricle laterally and obliterates the postauricular skin crease. If the crease remains, the process is lateral to the periosteum.

Acute mastoiditis is a serious bacterial infection of the temporal bone and is the most common complication of otitis media. Frequent symptoms include mastoid area erythema, proptosis of the auricle, and fever.

Although the diagnosis of acute mastoiditis can often be made on clinical basis alone, CT scanning should be performed for confirmation of the diagnosis, evaluation of potential complications, and surgical planning. Half of the children admitted with acute mastoiditis had no previous history of recurrent AOM. In those children, S pneumoniae was the leading pathogen, while P aeruginosa was more prevalent in children with recurrent AOM.

Otitis media is revealed on otoscopy, often with one of the following additional features:

  • Sagging of the posterosuperior canal wall (possibly a sign of ASM)
  • Nipplelike protrusion of the central tympanic membrane, usually oozing pus
  • Findings consistent with a complication of extension beyond the mastoid process and its covering periosteum or another intratemporal complication such as facial palsy

In adults, the most common symptoms of mastoiditis are otalgia, otorrhea, and hearing loss, and the physical signs of mastoiditis (ie, swelling, erythema, tenderness of the retroauricular region) are usually present. Localization and enlargement of the pathological process within the middle ear spaces can be determined based on CT scan findings.

Differentials

Wegener Granulomatosis

Histiocytoses

Sarcoidosis

External otitis

Mastoid trauma

Suppuration of postauricular lymph node

Furuncle of meatus of the ear

Suppuration of the postauricular (mastoid) lymph node (This node collects drainage from the scalp and becomes inflamed with infections involving this region.)

Catscratch disease and atypical mycobacteria tend to have poor response to antimicrobials and a high frequency of nodal abscess formation. Differentiation from ASM is relatively easy with preservation of the skin crease and presence of a normal middle ear.

Lateral sinus thrombosis (LST) is now known to cause mastoid air sinus abnormalities; this is due to venous congestion as a consequence of LST. 



Indications for the simple mastoid operation include cases of acute suppurative otitis media that fail to respond to appropriate antibiotic therapy and progress to coalescent mastoiditis.

Mastoid conditions and management

  • Acute mastoiditis without osteitis or periosteitis (the condition normally associated with AOM)
    • This is the only mastoid condition treated purely with medical management.
    • Standard antibiotic therapy is administered for AOM, and resolution is anticipated within 2 weeks.
    • If complications occur (pain and fever persist beyond 48 h or tenderness increases), obtain cultures via the middle ear, commence new antimicrobial therapy, and obtain imaging of the mastoid.
    • Consider mastoidectomy if symptoms persist or if the new antibiotics fail.
  • Acute mastoiditis with osteitis
    • This is a surgically treated disease, although coverage with appropriate antibiotics is mandatory. Mastoidectomy with insertion of a tympanostomy tube is necessary to remove areas of coalescence within the temporal bone.
    • Antibiotic selection should provide good intracranial penetration and MDRSP coverage. With the high frequency of invasive resistant strains in mastoiditis, initial therapy of intravenous vancomycin and ceftriaxone is most appropriate until results of the culture and sensitivity (C&S) studies are available.
    • Postoperatively, antibiotic/steroid drops are used to keep the tube patent and to reduce middle ear swelling.
    • Patients with spread of empyema beyond the mastoid require drainage of the abscess and mastoidectomy.
    • Intracranial spread requires a combined neurosurgical and otolaryngological approach.
  • Acute mastoiditis with periosteitis
    • Postauricular swelling and erythema without subperiosteal abscess or mastoid osteitis can be treated more conservatively using parenteral antibiotics, high-dose steroids, and tympanostomy tube insertion.
    • Vancomycin and ceftriaxone are recommended until cultures become available.
    • If substantial resolution of pain, fever, and erythema does not occur within 36-48 hours after institution of therapy, mastoidectomy is warranted.



See Intraoperative details.



When considering surgery, the risks of exposure to general anesthesia must be weighed against the risk of complications and progression of the infection. Contraindication to surgery include a low hemoglobin concentration and general systemic illness that must be controlled (eg, diabetes, hypertension, poor cardiac condition, bleeding disorders with prolonged bleeding and clotting time).



Lab Studies

  • Microbiology: Material for culture and sensitivity should be obtained from the ear (via tympanocentesis or myringotomy), blood, any abscess, and mastoid tissue (if it becomes available).
  • A CBC count and sedimentation rate are obtained for baseline studies used to evaluate efficacy of therapy.
  • Obtain and evaluate spinal fluid if any suggestion exists of intracranial extension of the process.

Imaging Studies

  • CT scanning of the temporal bone is the standard for evaluation of mastoiditis. The following findings are used to differentiate AOM/acute mastoiditis without osteitis, ASM, and chronic mastoiditis:  
    • Opacification of the mastoid air cells and middle ear by inflammatory swelling of mucosa and by collection of fluid
    • Loss of sharpness or visibility of mastoid cell walls due to demineralization, atrophy, or necrosis of bony septa
    • Haziness or distortion of the mastoid outline, possibly with visible defects of the tegmen or mastoid cortex
    • Enhancement of areas of abscess formation
    • Elevation of periosteum of mastoid process or posterior cranial fossa
    • Osteoblastic activity in chronic mastoiditis
  • MRI is not typically the radiographic study of choice; however, it is helpful in showing inflammatory processes and differentiating certain tumors. Do not use MRI as a method of evaluating the mastoid, although it is the standard for evaluation of contiguous soft tissue, particularly the intracranial structures. However, MRI is the preferred imaging modality for the potential complications of ASM (ie, abscess formation, sinus thrombosis).
  • Plain radiography: In areas of the world where CT scanning is not immediately available, plain radiographs of the mastoids demonstrate clouding of the air cells with bone destruction in ASM. In the vast majority of cases, radiographs suffice to establish the diagnosis but lack the sensitivity to differentiate the stages of the disease and fail to show the petrous apex in any great detail.

Other Tests

  • In the light of the prevailing medicolegal climate, an audiometric evaluation must be obtained. Audiometry is seldom appropriate or useful for children with ASM, but it must be performed after convalescence from the acute phase and with children who have chronic mastoiditis. In the at-risk population (children <2 y), thresholds for air and bone conduction under headphones are only rarely obtained.

Diagnostic Procedures

  • Tympanocentesis/myringotomy
    • A culture from the middle ear fluid should be obtained prior to beginning antimicrobial therapy. While it is ideal to use an operating microscope and specifically designed suction traps, an otoscope, spinal needle, and syringe can also be used in obtaining specimens from the middle ear.
    • Sterilize the canal with an antiseptic, and, with the child restrained, aspirate from the anterior half of the tympanic membrane.
  • Lumbar puncture: Perform a spinal tap if intracranial spread of infection is suspected.



Medical Therapy

Antibiotics are the principal medications used in ASM. Culture results and the sensitivity of the organism ultimately govern selection of medications. Until microbiology information is available, the following principles guide the selection: (1) the antimicrobial must be appropriate to cover the invasive strains of bacteria most common for AOM, (2) the selected antibiotic should cross the blood-brain barrier, and (3) the selected therapeutic spectrum should include consideration of those MDRSP prevalent in the individual community. Specific microbiologic diagnoses should be treated with appropriate antibiotics.

If open mastoid surgery is not undertaken, use of single, high-dose intravenous steroids is warranted to decrease mucosal swelling and to promote natural drainage through the aditus ad antrum into the middle ear.

Other medications used include analgesics, antipyretics, and topical antibiotic/steroid combinations. After placement of a tympanostomy tube with or without mastoidectomy, a pH-balanced solution or suspension of an antibiotic and steroid is useful to decrease mucosal swelling and to deliver topical antibiotics to the middle ear and mastoid. Continue the drops until otorrhea ceases and the view through the tube shows healing mucosa without swelling or obstruction. Multiple combinations are available, the best being those thin enough to rub through the tube into the middle ear.

Drug Category: Antibiotics-Therapy must cover all likely pathogens in the context of this clinical setting.

Drug name – Vancomycin (Lyphocin, Vancocin): As an increasing proportion of invasive strains of S pneumoniae are of the MDRSP types, beginning therapy with this medication is thought appropriate. After surgery or after C&S studies confirm sensitivity to other medications, the patient may be prescribed other medications that do not require the same degree of monitoring. For patients demonstrating sensitivity to vancomycin, high-dose ceftriaxone or cefotaxime or possibly rifampin may be used to fulfill criteria noted above and to have efficacy in the management of MDRSP.
Preferred method of administration is the individual analytic method. Adjust initial doses to provide peak levels 25-40 mcg/mL and trough levels <10 mcg/mL. Half-life is 4-8 h.

Adult Dose – 40 mg/kg/d IV divided q6-12h

Pediatric Dose – Empiric method: 40-60 mg/kg/d IV divided q6-8h; not to exceed 2 g/d

Contraindications – Documented hypersensitivity

Interactions – Erythema, histaminelike flushing, and anaphylactic reactions may occur when administered with anesthetic agents; when taken concurrently with aminoglycosides, risk of nephrotoxicity may increase above that with aminoglycoside monotherapy; effects in neuromuscular blockade may be enhanced when coadministered with nondepolarizing muscle relaxants

Pregnancy – Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions - Caution in renal failure, neutropenia; red man syndrome is caused by too rapid IV infusion (dose given over a few min) but rarely happens when dose given IV over 2 h administration or as PO or IP administration; red man syndrome is not an allergic reaction; ototoxic, possibly nephrotoxic (monitor levels if possible); severe hypotension may occur with rapid administration; wheezing, pruritus, and cardiac arrest are infrequent occurrences



Drug name
– Ceftriaxone (Rocephin): Third-generation cephalosporin with broad-spectrum, gram-negative activity.
Arrests bacterial growth by binding to 1 or more penicillin-binding proteins.

Adult Dose – 1-2 g/dose IV q12-24h

Pediatric Dose – Meningitis dose: 100-160 mg/kg/d IV q1-2d, then 60-100 mg/kg/d IV divided q12-24h

Contraindications – Documented hypersensitivity

Interactions – Probenecid may increase ceftriaxone levels; coadministration with ethacrynic acid, furosemide, and aminoglycosides may increase nephrotoxicity

Pregnancy – Fetal risk not confirmed in studies in humans but has been shown in some studies in animals

Precautions - Adjust dose in severe renal insufficiency (high doses may cause CNS toxicity); superinfections and promotion of nonsusceptible organisms may occur with prolonged use or repeated therapy; half-life 6-9 h; toxicity, allergy (rash, pruritus, fever, chills), local irritation, nausea, diarrhea, pseudomembranous colitis, thrombocytosis, leukopenia, eosinophilia, elevated BUN level; caution in breastfeeding women and persons with allergy to penicillin



Drug name
– Rifampin (Rifadin, Rimactane): Inhibits RNA synthesis in bacteria by binding to beta subunit of DNA-dependent RNA polymerase, which in turn blocks RNA transcription.

Adult Dose – 20 mg/kg/d PO/IV divided q12h; not to exceed 600 mg/dose; well absorbed from GI tract

Pediatric Dose – Administer as in adults

Contraindications – Documented hypersensitivity

Interactions – Induces microsomal enzymes, which may decrease effects of acetaminophen, oral anticoagulants, barbiturates, benzodiazepines, beta-blockers, chloramphenicol, oral contraceptives, corticosteroids, mexiletine, cyclosporine, digitoxin, disopyramide, estrogens, hydantoins, methadone, clofibrate, quinidine, dapsone, tazobactam, sulfonylureas, theophyllines, tocainide, and digoxin
Blood pressure may increase with coadministration of enalapril; coadministration with isoniazid may result in higher rate of hepatotoxicity than with either agent alone (discontinue 1 or both agents if alterations in LFTs occur)

Pregnancy – Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions - Obtain CBCs and baseline clinical chemistries prior to and throughout therapy; in liver disease, weigh benefits against risk of further liver damage; interruption of therapy and high-dose intermittent therapy are associated with thrombocytopenia that is reversible if therapy is discontinued as soon as purpura occurs
If treatment is continued or resumed after appearance of purpura, cerebral hemorrhage or death may occur; eliminated in biliary system (40-45%) and renal system (30-40%); discolors urine, saliva, sweat, tears, and stains some contact lenses; half-life is 1.5-3 h; toxicity, GI irritation, allergy, neurological headache, confusion, ataxia, blood dyscrasias, hepatic dysfunction, fatigue, and fever may occur



Drug name
– Cefotaxime (Claforan): Third-generation cephalosporin, crosses blood-brain barrier and may be effective against MDRSP. Arrests bacterial cell wall synthesis, which in turn inhibits bacterial growth.

Adult Dose – 1-2 g IV q4-6h; not to exceed 12 g/d

Pediatric Dose – 150-200 mg/kg/d IV divided q4-8h; not to exceed 12 g/d

Contraindications – Documented hypersensitivity

Interactions – Probenecid may increase levels; coadministration with furosemide and aminoglycosides may increase nephrotoxicity

Pregnancy – Fetal risk not confirmed in studies in humans but has been shown in some studies in animals

Precautions - Obtain CBCs and baseline clinical chemistries prior to and throughout therapy; in liver disease, weigh benefits against risk of further liver damage; interruption of therapy and high-dose intermittent therapy are associated with thrombocytopenia that is reversible if therapy is discontinued as soon as purpura occurs
If treatment is continued or resumed after appearance of purpura, cerebral hemorrhage or death may occur; eliminated in biliary system (40-45%) and renal system (30-40%); discolors urine, saliva, sweat, tears, and stains some contact lenses; half-life is 1.5-3 h; toxicity, GI irritation, allergy, neurological headache, confusion, ataxia, blood dyscrasias, hepatic dysfunction, fatigue, and fever may occur

Consultations

Early consultation with an otolaryngologist is appropriate and necessary if the pediatrician is not comfortable performing tympanocentesis. If cultures indicate the presence of resistant or unusual microbes, consultation with appropriate infectious-disease specialists may be required. Consultation with a neurosurgeon is appropriate if evidence of intracranial extension with abscess formation exists.

Transfer

If transfer is required, it invariably relates to the availability of subspecialists, most notably pediatric otolaryngologists or otologists, pediatric neurosurgeons, or pediatric critical care specialists. Available radiographs should be copied and should accompany the patient, along with any available laboratory data. Instruct patients to take nothing by mouth until the receiving subspecialists evaluate their conditions.

Surgical therapy

Surgical therapy confined to the ear includes myringotomy/tympanocentesis, tympanostomy tube placement, and mastoidectomy.

Myringotomy/tympanocentesis

This is primarily used to obtain specimens and to relieve discomfort from AOM. These openings usually heal within a few days.

Tympanostomy tube placement

A tympanostomy tube allows for drainage of entrapped pus and aeration of the middle ear and mastoid. It may sometimes allow topical antimicrobials to enter the middle ear space. Because it is used as a drain, a tympanostomy tube is usually placed during mastoidectomy.

A tube maintains the opening in the tympanic membrane and provides access to the middle ear and mastoid for antibiotic/steroid drops and for drainage without concern for patency of the eustachian tube.

Mastoidectomy

This procedure involves opening the mastoid air cells by making a postauricular incision and entering the mastoid by removing the mastoid cortex using a drill. Any subperiosteal abscess is opened during this time. Upon entering the mastoid, the surgeon most often encounters granulation tissue and swollen polypoid mucosa that block the aditus ad antrum. Most of the diseased air cells are opened, and access to the middle ear is gained by removing the blockage at the antrum. After irrigating the ear, a drain is inserted through the wound, where it is left for at least 2 days.

Preoperative details

Warn patients and their families of possible cosmetic deformity following mastoid surgery.

Preoperative preparation entails shaving the area behind the involved side (in the postaural area) a width of 3 fingers to avoid wound contamination.

Intraoperative details

A postaural incision is placed a few millimeters from the postaural sulcus. In infants, the incision is placed higher and more horizontally because the mastoid process is not developed and the facial nerve is more superficial.

The incision is deepened through the periosteum to the bone. At this stage, a subperiosteal abscess will discharge pus. Care must be taken in the upper half of the incision. The lower border of the temporalis muscle should be identified and conserved. If incising it to obtain adequate exposure is necessary, the vessels running at its lower border are first ligated or diathermized. The periosteum is lifted from the underlying bone with periosteal elevators to expose the spine of Henle, the Macewen triangle, and the posterior bony margin of the meatus. In older children and adults, the tendon of the sternomastoid muscle has a wide attachment to the superficial aspect of the mastoid process; the fibers are scraped off with a periosteal elevator.

The periosteum is elevated forward as far as the lateral end of the posterior bony meatal wall, backward for a few millimeters, and upward (simultaneously pushing up the temporalis muscle) to the level of the upper attachment of the pinna. A Mollison self-retaining hemostatic mastoid retractor is inserted to hold the soft tissues away from the underlying exposed bone.

The surgeon should use known visible landmarks to find the deeper landmarks. Drilling is commenced posterior to the posterior canal wall in a vertical direction. A triangular-shaped excavation is created with the superior limit bounded by the extension of the linea temporalis (which becomes the floor of the middle fossa as one drills deeper), the posterior margin bounded by the sigmoid sinus, and the anterior margin bounded by the thinned wall of the posterior external ear canal.

The mastoid cortex is now removed over the Macewen triangle (which is a rough guide to the position of the underlying mastoid antrum), using a drill fitted with a large cutting burr (5-6 mm). In adults, the antrum is encountered at a depth of 15-17 mm. If there is a deviation in the direction of drilling, the approach to the antrum can be seriously misaligned.

An ideal method to gauge the antrum is to insert an angled cell seeker beyond the posterosuperior bony meatal wall (which will be the site of the antrum) and then to drill toward it.

The antrum is usually apparent when opened by the drill. It can be confirmed by gentle anterior probing with a Dundas-Grant probe, which will slip into the aditus. Exercise care to avoid dislodging the short process of the incus. Simultaneously, the size of the aditus should be judged. If it is very small, it may be enlarged slightly with a fine bone curette to ensure adequate drainage of the middle ear.

The antral exposure is enlarged, opening adjacent cells until the lateral semicircular canal (the important landmark at this stage) can be identified. The position of middle and posterior fossa dura and the sigmoid sinus plate must be judged from the lateral oblique radiograph of the mastoid. Next, all cells in all directions are opened by drilling gently through their separating trabecula. Clearing all cells from the sinodural angle is particularly important. The smooth plate of bone covering the middle fossa dura above and lateral sinus posteriorly is recognized easily.

If the region is filled with necrotic mucosa, it may be safer to scoop out the material with a curette, always sweeping from the vertical position of the facial nerve as it descends just below the back of the lateral semicircular canal. Cells along the vertical portion of the facial nerve are best removed under microscope visualization with a diamond burr.

In a well-pneumatized skull, cells may extend anteriorly into the root of the zygoma and posteriorly into the occipital bone. These must also be followed as far as practicable. Consequent to mastoid clearance, a cavity is created with the antrum at the deepest point. The cavity is bounded above by the bony tegmen separating the region from the dura of the middle cranial fossa, behind by the bony plate over the sigmoid sinus, and in front by the posterior meatal wall and the aditus ad antrum.

In front of the bulge of the sigmoid sinus plate, cell removal uncovers the bone of the Trautman triangular space, protecting the dura of the posterior canal fossa and leading to the solid angle where the dense bone of the otic capsule protects the posterior semicircular canal. Anteriorly and much more superficially, cells should be opened as far as they extend into the root of the zygoma. Inferiorly, cell pursuit leads to the bone covering the digastric muscle as it passes forward, deep to the inferior part of the facial nerve at the stylomastoid foramen.

When cortical mastoidectomy is performed for proved suppurative mastoiditis, the bone over the sigmoid sinus should be sufficiently removed to allow insertion of a fine needle into that vessel to confirm that no thrombophlebitis exists within.

Closure of the wound is with interrupted sutures, and most otologists leave a soft drain in the lower part of the cavity for 1-2 days. A firm pressure dressing controls the bleeding.

Postoperative details

Monitor the patient's temperature; it usually falls dramatically within the first 24 hours, after which the patient can be allowed up. If all diseased cells are cleared, the discharge completely ceases, and the ear dries and heals in the ensuing few days (usually in about a week), the patient can then return to normal activities.

The firm pressure dressing is removed on the sixth postoperative day, when stitches are removed.

Follow-up

  • After obtaining cultures (either by tympanocentesis or during tympanostomy tube placement with or without mastoidectomy), continue initial antibiotic selection until cultures are reported. If the patient becomes afebrile and if swelling decreases at 48-72 hours, oral medication may be selected based on culture reports.
  • Children who have had a mastoidectomy are released from the hospital after the discharge from the surgically implanted drain abates. The drain is normally removed 48-72 hours postoperatively.
  • Antibiotic/steroid drops are continued until the otorrhea ceases and the tympanostomy tube is noted to be open with healing or healed mucosa behind.



Complications associated with mastoiditis

Meningitis and facial nerve paralysis are possible. Despite use of antibiotics, acute mastoiditis still remains a threat for patients with AOM, especially for children younger than 5 years. Great care is required on the part of clinicians to make an early diagnosis in order to promote adequate treatment and to prevent complications.

Approximately 7% of patients may develop intracranial complications related to acute mastoiditis. These complications can include sigmoid sinus thrombosis, epidural abscess, and meningitis. Persistent otalgia or otorrhea with associated neurologic symptoms in a patient taking oral antibiotics are ominous signs that suggest a complication.

Otogenic meningitis is the most common intracranial complication of neglected otitis media. In the western world, such complications seldom occur in children and adolescents and are extremely rare in adults. The current use of antibiotics and of more sophisticated surgery has greatly diminished the incidence of otogenic meningitis; however, this has resulted in physicians having less experience with diagnosis and treatment of this complication. Emergency surgical treatment is mandatory.

In a study done by Luntz et al, of 223 consecutive cases of acute mastoiditis, sixteen patients presented with complications (cerebellar abscess, perisinus empyema, subdural abscess or empyema, extradural abscess, cavernous sinus thrombosis, lateral sinus thrombosis, bacterial meningitis, labyrinthitis, petrositis, or facial nerve palsy).1

A study by Niv et al concluded that (1) A significant increase in the incidence of AM in infants was recorded over the last decade, although a specific reason for this trend remains uncertain; (2) most of the cases of AM followed the infant's initial AOM episode, and most of the infants had not received prior antibiotic therapy; (3) the clinical signs and symptoms of AM were more severe in infants than in older patients; (4) Although S pneumonia was the most common pathogen isolated in middle ear fluid cultures, the involvement of S pyogenes in AM was higher than that reported in AOM.2

Bezold abscesses are very rare complications and are usually found only in adults with a well-pneumatized mastoid tip.

Complications associated with mastoidectomy

  • Injury to the facial nerve
  • Dislocation of the incus
  • Penetration of the middle or posterior fossa
  • Rupture of the sigmoid sinus
  • Labyrinthine transgression and destruction
  • Persistent deafness
    • This may be due to incus dislocation or removal. The ear dries, and the tympanic membrane heals; however, conductive deafness persists. Impedance audiometry indicates disruption of the ossicular chain. Anterior tympanotomy and reconstruction of the ossicular chain may be performed.
    • Persistent deafness may also be caused by persistent infection due to residual cells. Infection should resolve with proper medical treatment and good drainage. If infection persists, reopening of the mastoid and exenteration of the remaining cells is required.
  • Complete facial nerve paralysis
    • If present immediately postoperatively, the facial nerve has been damaged intraoperatively.
    • The mastoid must be reopened, and the vertical part of the nerve must be explored and, if necessary, grafted.
  • Meatal stenosis
    • This may ensue if the bony meatal wall has been taken down and if the skin has been dissected off the bony wall.
    • Meatal stenosis requires excision of the stenosed area and firm packing of the canal until reepithelization occurs.

Additional intracranial complications are possible following mastoidectomy.

Although mastoidectomy is a common surgical procedure in otology, postoperative complications of various degrees of severity may occur. Complications reported include brain abscess one week after mastoidectomy in a child and, in another child, seizures 5 days after the initial mastoidectomy and a subdural empyema that was drained during the revision surgery. Large bone defects with exposed middle cranial fossa dura were found during revision surgery in both patients, and Proteus vulgaris and methicillin-resistant S aureus were isolated from the mastoid and abscess cavities in these children.

A small epidural collection was diagnosed 2 days after initial mastoid surgery and was managed with intravenous antibiotics only.

In another reported case, sigmoid sinus thrombosis developed the day after mastoidectomy was performed for nonresponsive acute mastoiditis. This child received both intravenous antibiotics and anticoagulants. Timely revision surgery, combinations of third- or fourth-generation cephalosporins with vancomycin or metronidazole, and the addition of anticoagulants in cases of sinus thrombosis can lead to full recovery.

Medicolegal pitfalls

Medicolegal pitfalls relate almost entirely either to delay of diagnosis or to iatrogenic injury during therapy. A high index of suspicion, judicious use of diagnostic modalities, and close follow-up care are recommended to make a diagnosis in a timely manner. Although facial nerve monitoring is a useful adjunct, nothing substitutes for experience and attention to detail when preserving the facial nerve. Experienced otologists are unlikely to injure the ossicular chain during mastoid surgery.

Care must be taken to avoid damage to the ossicular chain. Persistent conductive hearing loss caused by tympanosclerotic plaques formed from residual bone dust can be avoided with copious irrigation at the end of the surgery.



  • Expect patients with ASM to recover completely provided that the facial nerve, vestibule, and intracranial structures are not involved.
  • Cosmetic deformity of the operated ear can usually be prevented with judicious placement of the incision and the development of flaps to pull the ears posteriorly when replaced.
  • Conductive hearing loss should resolve provided that the ossicular chain remains intact. Conduct testing after otorrhea has ended and the ear has healed.



Incidence of mastoiditis and, thus, mastoidectomy should decline further with the availability and administration of the conjugated pneumococcal vaccine.

In a study by Oestreicher-Kedem et al, the mean interval from onset of illness to mastoiditis was found to be 4.5 days.3 Ear cultures most often grew S pneumoniae and P aeruginosa (23.7% each). Complications occurred in 15.8% of cases. The only factor differentiating children with and without complications was the white blood cell count (high in children with complications). These findings indicate that acute mastoiditis is not only a complication of prolonged infection of the middle ear but also may present as an acute infection of the mastoid bone that can progress within 48 hours. The complication rate remains high, and antibiotic treatment at the onset of symptoms does not prevent complications. A high white blood cell count on admission may serve as a predictive factor for complicated cases.

A study done by Roddy et al shows that in the post pneumococcal vaccine era, ceftriaxone nonsusceptibility was seen in 30% of post-PCV S pneumoniae isolates compared with 7% of pre-PCV isolates.4 We can conclude that empiric antimicrobial therapy with ceftriaxone alone is insufficient in the post-PCV era.



Media file 1:  Extent of cortical mastoidectomy in a well-pneumatized mastoid.
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Media file 2:  Cortical mastoidectomy in a densely sclerosed mastoid.
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Media file 3:  Preoperative preparation of the patient. (Images 3-15 are surgical series.)
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Media file 4:  Draping the surgical area. (Images 3-15 are surgical series.)
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Media file 5:  Injection of the area with 2% Xylocaine and 1:100,000 adrenaline to reduce bleeding. (Images 3-15 are surgical series.)
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Media file 6:  Marking the incision site. (Images 3-15 are surgical series.)
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Media file 7:  Placement of the incision, a few mm behind the postauricular sulcus. (Images 3-15 are surgical series.)
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Media file 8:  Deepening the incision down to the bone. (Images 3-15 are surgical series.)
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Media file 9:  Elevation of the periosteum to expose the mastoid cortex to the mastoid tip. (Images 3-15 are surgical series.)
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Media file 10:  Mastoid drilling in progress with simultaneous saline irrigation. (Images 3-15 are surgical series.)
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Media file 11:  Creation of the initial groove and the vertical line. (Images 3-15 are surgical series.)
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Media file 12:  Exposure of the antrum and exenteration of the mastoid air cells. (Images 3-15 are surgical series.)
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Media file 13:  Curetting the aditus to enlarge it. (Images 3-15 are surgical series.)
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Media file 14:  Further exposure. (Images 3-15 are surgical series.)
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Media file 15:  Healed postaural scar. (Images 3-15 are surgical series.)
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Middle Ear, Mastoiditis excerpt

Article Last Updated: Mar 19, 2008