Mastoiditis

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Mehrian Jafarizade, M.D [2]

Mastoiditis is the infection of mastoid air cells in the process of temporal bone. It is mostly a complication of ear diseases such as acute otitis media and chronic otitis media, and it tends to occur in children. However after development of antibiotics, acute otitis media complications have decreased significantly.

Mastoiditis was first described by Hippocrates in the 5th century B.C.E. The first recorded surgical incision for treatment of medial ear infection was in the 16th century C.E., performed by French physician Ambroise Pare. Initial therapies for middle ear diseases were surgical, particularly mastoidectomy, which was first performed by French physician Jean-Louis Petit in the 17th century C.E. German physicians Hermann Schwartze, Anton von Troltsch, and Adam Politzer published the first journal dedicated to ear pathology and treatment in 1865. Antibiotic therapy for mastoiditis treatment emerged with the invention of mass production of penicillin in 1940 by Alexander Fleming, Howard Florey, and Ernst Chain. The pneumococcal conjugate vaccine (PCV) emerged in 2000, greatly reducing the incidence of otitis media and mastoiditis by vaccinating individuals against the causative pathogens.

Mastoiditis may be classified into acute, subacute, and chronic forms, depending on the timing of presentation and duration.

Mastoiditis is the infection in the cavities of mastoid process of temporal bone that occurs after otitis media. At birth, the mastoid consists of a single cavity, which is connected to the middle ear by a canal. As the child grows, the mastoid bone becomes pneumatized, resulting in a series of connected cavities, lined by a mucosa diverted from respiratory epithelium. There is a relationship between the middle ear, the eustachian tube, and the mastoid. This connection has a fundamental role in the pathogenesis of mastoiditis. In the setting of acute otitis media, the mucosa that lines the middle ear and mastoid air cells become inflamed. In most cases of acute otitis media, inflammation resolves, but it sometimes persists, leading to bacterial and fluid accumulation within the mastoid air cells. Gradually, as a result of pressure rising in the mastoid, air cell septae may be destroyed and mastoiditis could proceed to osteomyelitis. The mastoid is near vital organs in the head and neck and mastoid infection may cause serious complications. There is evidence of genetic predisposition to recurrent otitis media and therefore mastoiditis. The following genes have been identified as having potential pathogenic qualities for otitis media: CAPN14, GALNT14, BPIFA3, BPIFA1, BMP5, GALNT13, NELL1, and TGFB3.

Mastoiditis results from middle ear infection. The most common bacteria that cause acute mastoiditis are Streptococcus pneumoniae, Streptococcus pyogenes, and Staphylococcus aureus. Staphylococci, Pseudomonas species, and polymicrobials are predominantly seen in non-acute mastoiditis. Pseudomonas aeruginosa may be found in children with acute mastoiditis as a consequence of recurrent acute otitis media and antibiotic use.

Mastoiditis must be differentiated from other diseases that cause postauricular inflammation or swelling such as lymphadenopathy, periauricular cellulitis, auricle perichondritis, mumps, and mastoid tumors. These diseases may be distinguished from mastoiditis via clinical findings and laboratory testing.

Mastoiditis incidence is 1.2–6.1 per 100,000 inhabitants in developed countries. Serious progressions appear more frequently in young children. After using pneumococcal vaccination, the rate of acute otitis media and mastoiditis decreased dramatically. However, there is a concern about rising incidence, which is connected to inadequate antibiotic dosing in otitis media, choice of antibiotics, and increasing resistance of bacteria. Acute mastoiditis is most common among children under two years of age.^[1] Men and women are affected equally by mastoiditis. Otitis media and therefore mastoiditis are more prevalent in developing countries, specifically Sub-Saharan West Africa, Southeast Asia, and Oceania. Risk factors that may contribute to higher incidence in developing countries include exposure to HIV, malnutrition, a large proportion of children under 5 years in the population, and higher chance of water contamination.

The risk factors for mastoiditis are related to acute otitis media risk factors. Risk factors are allergy, upper respiratory tract infection, snoring, previous history of acute otitis media, passive smoking, mother smoking during pregnancy, and low social status. Exposure of infants to day-care centers is a controversial risk factor.

There is insufficient evidence to recommend routine screening for mastoiditis.

If left untreated, mastoiditis will result in severe complications such as intracranial extension and permanent neurological deficits or death. The consequences of mastoiditis have been reduced after introduction of antimicrobial agents and adequate therapy of acute otitis media. However, if mastoiditis is not eradicated completely, it may give rise to severe complications. These complications are extracranial, such as osteomyelitis, labyrinthitis, facial nerve palsy, Bezold’s abscess, hearing loss, subperiosteal abscess, or intracranial, such as epidural and subdural abscess, meningitis, temporal bone or brain abscess and venous sinus thrombosis. The prognosis of mastoiditis is good with treatment. Excellent outcomes can be expected for those who are managed without delay.

History and symptoms of mastoiditis range from asymptomatic disease to symptomatic and progressive mastoiditis with serious life-threatening complications. History should be taken considering onset, duration, and progression of symptoms, allergies, previous history of acute otitis media, upper respiratory tract infection, associated symptoms (otalgia, fever, confusion), medications including antibiotic usage in acute otitis media, snoring, attendance to day care, history of trauma, co-morbid conditions like diabetes, immunodeficiency, and smoking. Common symptoms of mastoiditis are: ear pain, fever, feeling of “fullness” in the ear, recent episode of acute otitis media, discharge from the affected ear, partial hearing loss, irritability (in infants), headache, and lethargy/malaise. Neurological symptoms from chronic mastoiditis and otitis media with effusion include poor attention span, delayed speech development, clumsiness, and poor balance. Less common symptoms are gastrointestinal symptoms such as vomiting and diarrhea, meningismus, and torticollis

Mastoiditis physical examination includes posterior auricular signs such as postauricular swelling, erythema, tenderness, protrusion of pinna, and sagging external ear canal. Otoscopic examination of the middle ear shows erythema, bulging, cloudy appearance, and immobility of the tympanic membrane. Partial hearing loss from fluid buildup is indicative of otitis media, revealed by tympanometry. Acute mastoiditis patients are usually ill-appearing and usually present with low-grade fever, while complicated mastoiditis patients may present with severely ill appearance.

There are no diagnostic blood laboratory findings associated with mastoiditis. Some patients with mastoiditis may have elevated ESR, CRP, and white blood cells with a left shift. These laboratory findings are nonspecific and not helpful in making the diagnosis. It is very important to obtain clinical specimens for microbiology. Microbial results are crucial in the proper antimicrobial choice for treatment. There are multiple types of bacteria that may cause mastoiditis like Streptococcus species and Staphylococcus aureus, and there are rising concerns about antibiotic resistance in some microorganisms. The obtained fluid or pus should be sent for Gram stain, aerobic and anaerobic culture, and antimicrobial susceptibility testing. Specimens for mastoiditis treatment could be obtained via multiple sites such as middle ear via tympanocentesis or myringotomy, percutaneous aspiration from subperiosteal abscess, cerebrospinal fluid, or blood cultures.

There are no diagnostic X-ray findings associated with mastoiditis.

High Resolution CT scans of the temporal bone in mastoiditis patients are the preferred diagnostic tool and may reveal mastoiditis and its complications. CT findings in acute mastoiditis are: partial-to-complete opacification of mastoid air cells, erosion of mastoid air cell bony septum, mastoid cortex destruction and irregularity, periosteal thickening, periosteal disruption, and subperiosteal abscess. CT findings in subacute and chronic mastoiditis are: markers for inflammation, sclerosis, or opacification of mastoid process, tympanic membrane changes including thickening, retraction, tympanic membrane perforation, or calcification, ossicle erosion or other possible causes for hearing loss, determination of cholesteatoma, intratemporal complications such as petrositis, labyrinthitis, subperiosteal abscess, or labyrinthine fistula, intracranial complications such as brain abscess and meningitis, presence of fibrous tissue, tympanosclerosis, formation of new bone matter, ossicle erosion, and displacement and extension of cholesteatoma to sinuses.

Both CT and MRI are used in the evaluation of mastoiditis and its complications. MRI in mastoiditis plays a role in the detection of cholesteatoma, also when intracranial and some intratemporal complications are suspected. Specifically, MRI has shown superiority in assessing the severity of intracranial involvement and abscess border visualization.

There are no ultrasound findings associated with mastoiditis.

There are no other diagnostic findings for mastoiditis.

Other mastoiditis imaging findings include otoscopic images of the tympanic membrane displaying middle ear effusion and infection. Also, tympanograms may be used for measuring pressure from fluid buildup in the middle ear.

Medical treatment for acute and subacute mastoiditis without intracranial complications consists of intravenous antibiotics and myringotomy. Antibiotics for acute mastoiditis must cover the most common bacterial pathogens: Streptococcus pneumoniae, Streptococcus pyogenes, and Staphylococcus aureus (including methicillin-resistant S. aureus). If there is a history of recurrent acute otitis media or recent antibiotic usage, the intravenous antibiotic also should cover Pseudomonas aeruginosa. Bacteria commonly covered include Streptococcus pneumonia, Group A streptococcus, and Staphylococcus aureus. The empiric antibiotics are ampicillin-sulbactam or ampicillin; add vancomycin for severe infection with adjacent complications or suspicion of MRSA. For chronic mastoiditis, bacteria commonly covered are Pseudomonas aeruginosa, Staphylococcus aureus and anaerobes. Antibiotics include piperacillin-tazobactam or piperacillin, and ofloxacin otic solution; add vancomycin for severe infection with adjacent complications or suspicion of MRSA.

Different surgical procedures may be performed to treat mastoiditis. Myringotomy is surgical perforation of the tympanic membrane. It should be considered the primary treatment in all cases of infectious mastoiditis following otitis media, particularly when there is an unperforated tympanic membrane or inadequate drainage. Tympanocentesis should be performed in all mastoiditis patients to obtain middle ear fluid for culture and susceptibility testing. Myringotomy accompanied by the additional insertion of a tympanostomy tube is indicated in some cases, such as Eustachian tube dysfunction, suppurative complications requiring additional drainage, and when tympanic membrane must be repaired from Eustachian tube dysfunction. Definitive surgery is mastoidectomy, which is the surgical removal of the mastoid cortical bone and underlying air cells. Indications for mastoidectomy may include subperiosteal abscess such as postauricular fluctuance or mass, chronic suppurative otitis media or cholesteatoma, progression of postauricular swelling or fluctuance, fever, and other clinical findings or continuous drainage despite parenteral antimicrobial therapy and myringotomy.

Preventing mastoiditis primarily involves preventing development of otitis media and nasopharyngitis. This is achieved by administration of the pneumococcal and influenza vaccines, frequently washing hands, and avoiding fluid transmission and respiratory droplets from nasopharyngitis patients. Preventing exposure to air pollution, as potential middle ear irritants such as secondhand smoke helps prevent otitis media, is also helpful in preventing mastoiditis. For infants, preventative measures include avoiding pacifiers, avoiding daycare enrollment, and breastfeeding until at least 6 months of age. A prophylactic regimen of antibiotics can prevent otitis media in at-risk infants and children.

For mastoiditis following chronic or recurrent otitis media, preventing recurrence of the disease involves surgery, assuming the manifestation is not self-limited. Myringotomy with tympanostomy tube and mastoidectomy is the most common surgical preventative measure.

Template:WH Template:WS

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Mehrian Jafarizade, M.D [2]

Mastoiditis and middle ear diseases have evidently been present in the human race for centuries. Mastoiditis was first described by Hippocrates in the 5th century B.C. The first recorded surgical incision for the treatment of middle ear infection was performed in the 16th century by French physician Ambroise Pare. Initial therapies for middle ear diseases were surgical; mastoidectomy was first performed by French physician Jean-Louis Petit in the 17th century. German physicians Hermann Schwartze, Anton von Troltsch, and Adam Politzer published the first journal dedicated to ear pathology and treatment in 1865. Antibiotic therapy for the treatment of mastoiditis emerged with the mass production of penicillin in 1940 by Alexander Fleming, Howard Florey, and Ernst Chain. The pneumococcal conjugate vaccine (PCV), which emerged in 2000, greatly reduced the incidence of otitis media and mastoiditis by providing individuals with protection against the causative pathogens.

• Roman physicians Hippocrates (450 BC) and Celsus (25 AD) described intracranial complications of otitis media, including mastoiditis.
• Morgagni and Lebert (1856) and Macewan (1881) later explained the study of the pathophysiology and management of intracranial complications of otitis media, including mastoiditis.^[1]

• The first recorded surgical incision for the treatment of middle ear infection was performed in the 16th century by French physician Ambroise Pare.
• Initial therapies for middle ear infections and mastoiditis were surgical; mastoidectomy was first performed by French physician Jean-Louis Petit in the 17th century.
  • The procedure was first used for the purpose of draining pus from an abscess.
• German physicians Hermann Schwartze, Anton von Troltsch, and Adam Politzer advanced the discourse of clinical study of otitis media by publishing the first journal dedicated to ear pathology and treatment in 1865.^[2]
• Adam Politzer founded the first otology clinic in 1873 in Austria, beginning the codification and standardization of the treatment of such ear diseases as otitis media and mastoiditis.
• The use of antibiotics for the treatment of mastoiditis emerged with the mass production of penicillin in 1940 by Alexander Fleming, Howard Florey, and Ernst Chain.^[3]
  • This was the first instance of the modern use of antibiotic therapy, as opposed to surgery, for the treatment of middle ear diseases.
• The pneumococcal conjugate vaccine (PCV), which emerged in 2000, greatly reduced the incidence of otitis media by providing individuals with protection against the causative pathogens.^[4]

Template:WH Template:WS

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Mehrian Jafarizade, M.D [2]

Mastoiditis may be classified into acute, subacute, and chronic forms, depending on the timing of presentation and the duration of the disease.

Mastoiditis may be classified into acute, subacute, and chronic forms based on disease duration:^[1][2]

• Acute: Mastoid air cells infection lasts less than 1 month.

• Subacute: Indolent infection (>1 month)

• Chronic: Mastoid air cells infection lasts for months to years.

Template:WH Template:WS

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Mehrian Jafarizade, M.D [2]

Mastoiditis refers to an infection that occurs in the cavities of the mastoid process of temporal bone after otitis media. At birth, the mastoid consists of a single cavity, which is connected to the middle ear by a canal. As the child grows, the mastoid bone becomes pneumatized, resulting in a series of connected cavities lined by a mucosa derived from respiratory epithelium. The connection between the middle ear, the eustachian tube, and the mastoid has a fundamental role in the pathogenesis of mastoiditis. In the setting of acute otitis media, the mucosa that lines the middle ear and mastoid air cells become inflamed. In a majority of cases of acute otitis media, inflammation resolves; when it persists, it leads to bacterial and fluid accumulation within the mastoid air cells. Gradually, as a result of pressure rising in the mastoid, air cell septae may be destroyed and mastoiditis could proceed to periostitis, cavity abscess, and osteomyelitis. The mastoid is near vital organs in the head and neck and mastoid infection may cause serious complications. There is evidence of a genetic predisposition to recurrent otitis media, and therefore mastoiditis, with statistically significant evidence that it has high heritability. The following genes have been identified as having potential pathogenic qualities for otitis media: CAPN14, GALNT14, BPIFA3, BPIFA1, BMP5, GALNT13, NELL1, and TGFB3.

Mastoiditis is the infection in the cavities of mastoid process of temporal bone that occurs after otitis media. At birth, the mastoid consists of a single cavity, which is connected to the middle ear by a canal. As the child grows, the mastoid bone becomes pneumatized, resulting in a series of connected cavities lined by a mucosa derived from respiratory epithelium. There is a relationship between the middle ear, eustachian tube, and the mastoid. This connection has a fundamental role in the pathogenesis of mastoiditis. In the setting of acute otitis media, the mucosa that lines the middle ear and mastoid air cells become inflamed. In the majority of cases of acute otitis media, the inflammation resolves, but it sometimes persists, leading to bacterial and fluid accumulation within the mastoid air cells. Gradually, as a result of pressure rising in the mastoid, air cell septae may be destroyed and mastoiditis could proceed to periostitis, cavity abscess, and osteomyelitis.

• The mastoid is near important structures like the facial nerve, sternocleidomastoid muscle, jugular vein, internal carotid artery, sigmoid sinus, brain, and meninges; as a result of this proximity, spreading infection to these places may cause complications.^[1][2]

Mastoiditis results from the extension of adjacent infection in the middle ear.

• There is evidence of a genetic predisposition to recurrent otitis media, and thereby mastoiditis, with statistically significant evidence that it has high heritability.^[3]
  • Hereditary factors comprise 45-75% of risk factors for recurrent otitis media, as revealed by heritability studies involving twins and triplets.^[4]
• The following genes have been identified as having potential pathogenic qualities for recurrent otitis media and mastoiditis:^[4][2]
  • 2p23.1
    • CAPN14
    • GALNT14
  • 20q11.21
    • BPIFA3
    • BPIFA1
  • Those that interact with the TGFβ pathway:
    • BMP5
    • GALNT13
    • NELL1
    • TGFB3
• Up-regulation of the genes correlated to recurrent otitis media pathogenesis contributes to individual susceptibility to mastoiditis.

• Mastoiditis is often associated with other upper respiratory conditions caused by nasopharyngeal pathogens, including:^[5][2]
  • Common cold
  • Strep throat
  • Sinusitis
• Allergy-related conditions, such as allergic rhinitis, are also associated with mastoiditis.

Gross pathological findings of mastoiditis may include:^[6]

• Clouded appearance of tympanic membrane
• Presence of exudate
• Obliteration of external ear canal
• Pus

Microscopic pathological findings in mastoiditis may include the following:^[6]

• Neutrophilic exudate seen in mastoid cavities

• Prominent dilated blood vessels
• Edema and focal inflammation

Template:WH Template:WS

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Mehrian Jafarizade, M.D [2]

Mastoiditis results from middle ear infection. The most common bacteria that cause acute mastoiditis are Streptococcus pneumoniae, Streptococcus pyogenes, and Staphylococcus aureus.^[1] Staphylococci, Pseudomonas species, and polymicrobials are predominantly seen in non-acute mastoiditis. Pseudomonas aeruginosa may be found in children with acute mastoiditis as a consequence of recurrent acute otitis media and antibiotic use.^[2]

Life-threatening causes include conditions which may result in death or permanent disability within 24 hours if left untreated. There are no life-threatening causes of mastoiditis, though complications resulting from untreated mastoiditis are common.

Mastoiditis is caused by untreated acute otitis media (middle ear infection). Accordingly, the bacterial pathogens that cause mastoiditis are similar to the pathogens that cause infectious otitis media. The most common causes are:^[3][4][5]

• Streptococcus pneumonia
• Streptococcus pyogenes
• Staphylococcus aureus (including methicillin-resistant S. aureus)

• Pseudomonas aeruginosa

• Haemophilus influenzae is rare in mastoiditis during childhood despite being the second most frequent cause of acute otitis media.^[6]
• Cochlear implant infections^[7]

• Langerhans Cell Histiocytosis^[8]
• Cholesteatoma

Cardiovascular	No underlying causes
Chemical/Poisoning	No underlying causes
Dental	No underlying causes
Dermatologic	No underlying causes
Drug Side Effect	No underlying causes
Ear Nose Throat	Cholesteatoma, cochlear implant infections
Endocrine	No underlying causes
Environmental	No underlying causes
Gastroenterologic	No underlying causes
Genetic	Neutrophil-specific granule deficiency, Nijmegen breakage syndrome
Hematologic	Histiocytosis X
Iatrogenic	Cochlear implant infections
Infectious Disease	Anaerobic bacteria, Bacteroides, Blastomycosis, Enterobacteriaceae, Fusobacterium, Haemophilus influenzae, Moraxella catarrhalis, MRSA, Mycobacterium bovis, Mycobacterium tuberculosis, Pasteurella multocida, Peptostreptococcus, Porphyromonas, Prevotella, Pseudomonas aeruginosa, Staphylococcus aureus, Stenotrophomonas maltophilia, Streptococcus Group A, Streptococcus pneumoniae, Streptococcus pyogenes
Musculoskeletal/Orthopedic	No underlying causes
Neurologic	No underlying causes
Nutritional/Metabolic	No underlying causes
Obstetric/Gynecologic	No underlying causes
Oncologic	Histiocytosis X
Ophthalmologic	No underlying causes
Overdose/Toxicity	No underlying causes
Psychiatric	No underlying causes
Pulmonary	Mycobacterium tuberculosis
Renal/Electrolyte	No underlying causes
Rheumatology/Immunology/Allergy	Histiocytosis X
Sexual	No underlying causes
Trauma	No underlying causes
Urologic	No underlying causes
Miscellaneous	No underlying causes

Template:WH Template:WS

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Mehrian Jafarizade, M.D [2]

Mastoiditis must be differentiated from other diseases that cause postauricular inflammation or swelling such as lymphadenopathy, periauricular cellulitis, auricle perichondritis, mumps, and mastoid tumors. These diseases may be distinguished from mastoiditis via clinical findings and laboratory testing.

Mastoiditis must be differentiated from other diseases that cause postauricular inflammation or swelling.^[1][2][3]

Disease	Clinical findings		Laboratory findings
	History and symptoms	Physical examinations
Mastoiditis	History of otitis media Posterior ear pain	Local erythema and tenderness and edema on the mastoid bone Outward and upward displaced auricle Abnormal tympanic membrane	Leukocytosis High erythrocyte sedimentation rate may be present
Enlarged lymph node	Well defined and mobile mass No inflammatory signs	No effect on auricle and tympanic membrane	Leukocytosis may be present High erythrocyte sedimentation rate may be presented or may be normal
Periauricular cellulitis	History of a minor bite or minor trauma commonly exists Pain and redness in the site	Tympanic membrane is normal.	Leukocytosis may be present High erythrocyte sedimentation rate may be present
Perichondritis of the auricle	Swelling and erythema of the pinna	The postauricular crease is preserved The tympanic membrane appears normal.	Leukocytosis may be present High erythrocyte sedimentation rate may be present
Mumps	Parotid glands swelling Inflammation and pain present	Tympanic membrane is normal	Mild leukocytosis may be present
Mastoid tumors	Painless mass No inflammation	Tympanic membrane is normal	Normal white blood cell count Normal erythrocyte sedimentation rate

Template:WH Template:WS

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Mehrian Jafarizade, M.D [2]

Mastoiditis incidence is 1.2–6.1 per 100,000 inhabitants in developed countries. Serious progressions appear more frequently in young children. After using pneumococcal vaccination, the rate of acute otitis media and mastoiditis decreased dramatically. However, there is a concern about rising incidence, which is connected to inadequate antibiotic dosing in otitis media, choice of antibiotics, and increasing resistance of bacteria. Acute mastoiditis is most common among children under two years of age.^[1] Men and women are affected equally by mastoiditis. Otitis media and therefore mastoiditis are more prevalent in developing countries, specifically Sub-Saharan West Africa, Southeast Asia, and Oceania. Risk factors that may contribute to higher incidence in developing countries include exposure to HIV, malnutrition, a large proportion of children under 5 years in the population, and higher chance of water contamination.

Mastoiditis incidence is 1.2–6.1 per 100,000 inhabitants in developed countries.^[2][3] Rapid disease progression appears to be more frequent in young children. After using pneumococcal vaccination, the rate of acute otitis media and mastoiditis decreased dramatically. However, there is a concern about rising incidence, which is connected to inadequate antibiotic dosing in otitis media, choice of antibiotics, and increasing resistance of bacteria.^[4]

• Acute mastoiditis is most common in children under two years of age. ^[5]

• The most common ages affected are 6–13 months because, during these ages, ear infections are common.^[5]

• Males and women are affected equally by mastoiditis.

• There is no racial predilection for mastoiditis.

Otitis media and therefore mastoiditis is most prevalent in developing countries, specifically Sub-Saharan West Africa, Southeast Asia, and Oceania.^[6]

• The incidence of otitis media in the above countries is between two and eight times higher than the rest of the world.

The following risk factors are more prevalent in developing countries, correlated to the increase in otitis media incidence:^[7]

• Exposure to HIV
• Malnutrition
• Large proportion of children under 5 years old in population
• Higher chance of water contamination

Template:WH Template:WS

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Mehrian Jafarizade, M.D [2]

Risk factors for mastoiditis are related to acute otitis media risk factors. These include: allergy, upper respiratory tract infection, snoring, previous history of acute otitis media, passive smoker, smoking during pregnancy, and low social status. Exposure of infants to day-care centers is a controversial risk factor. ^[1]

Risk factors for mastoiditis are related to acute otitis media risk factors.

• Allergy
• Upper respiratory tract infection
• Snoring
• Previous history of acute otitis media
• Passive smoker
• Smoking during pregnancy
• Low social status^[1]

• Infancy
• Elderly
• Diabetic
• Immunosuppressed and debilitated patients^[2]

A controversial risk factor is the exposure of infants to day-care centers. Day care attendance may cause an increased incidence of upper respiratory infections and acute otitis media and therefore, mastoiditis. Countries with variations in the age of starting a day-care have shown differences in incidence peaks of acute otitis media.^[3][4]

Template:WH Template:WS

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Mehrian Jafarizade, M.D [2]

If left untreated, mastoiditis will result in severe complications such as intracranial extension and permanent neurological deficits or death. The consequences of mastoiditis have been reduced since the introduction of antimicrobial agents and adequate therapy of acute otitis media. However, if mastoiditis is not eradicated completely, it may give rise to severe complications. These complications can be extracranial, such as osteomyelitis, labyrinthitis, facial nerve palsy, Bezold’s abscess, hearing loss, subperiosteal abscess, or intracranial, such as epidural and subdural abscess, meningitis, temporal bone or brain abscess and venous sinus thrombosis. The prognosis of mastoiditis is good with treatment. Excellent outcomes can be expected for those who are managed without delay.

If left untreated, mastoiditis will result in severe complications such as intracranial extension and permanent neurological deficits or death.^[1][2]

The consequences of mastoiditis have been reduced after introduction of antimicrobial agents and adequate therapy of acute otitis media. However, mastoiditis has not been eradicated completely and may give rise to severe complications. The incidence of mastoiditis complications ranges from 4% to 16.6% according to multiple studies.^[3][4][5][6]

Mastoiditis complications may be classified into extracranial and intracranial as in the table below:^[3][7][8][9]

Location	Disease	Manifestations
Extracranial complications	Osteomyelitis	Mastoid infection may spread to other parts of the skull which leads to osteomyelitis. Petrositis is petrous bone osteomyelitis, which could be a part of Gradenigo’s syndrome (retro-orbital pain, otorrhea, abducens nerve palsy, and acute or chronic otitis media).
	Labyrinthitis	Inflammation or infection of the bony part of labyrinth could cause labyrinthitis. Sensorineural hearing loss, tinnitus, vomiting, vertigo, and spontaneous nystagmus may be the presenting symptoms.
	Facial nerve palsy	May occur when the facial nerve passes throw the canal in the petrous part of temporal bone.
	Bezold’s abscess	This abscess is a neck abscess under the digastric and sternocleidomastoid muscles. Clinical features of Bezold’s abscess include swelling and tenderness below the mastoid process and below the sternocleidomastoid muscle.[10]
	Hearing loss	Acute mastoiditis can cause hearing loss because of middle ear effusion or external auditory canal obstruction. This condition can be transient and resolves with appropriate treatment. However, in some situations, hearing loss may be permanent, such as middle ear ossicles damage or cochlea damage due to suppurative labyrinthitis.
	Subperiosteal abscess	Fluctuation, erythema, and a tender mass overlying the mastoid bone are clinical clues to diagnosis of this complication.
Intracranial complications	Epidural and subdural abscess	Fever, otalgia, cephalgia are general clinical features. An altered mental status along with an otitis media may also be a sign of intracranial complication.
	Meningitis
	Temporal bone or brain abscess
	Venous sinus thrombosis

The prognosis of mastoiditis is good with treatment. Excellent outcomes may be expected for those who are managed without delay and patients recover without complications.^[11]

Template:WH Template:WS