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NAME OF DISEASE: Otitis media
ETIOLOGICAL AGENTS:
MOST COMMON | RELATIVELY COMMON | UNUSUAL BUT IMPORTANT |
Streptococcus pneumoniae | Staphylococcus aureus | Pseudomonas sp. |
Haemophilus influenzae | Streptococcus pyogenes | Proteus sp. |
OVERVIEW:
Inflammatory disease of the mucosal lining of the middle ear with exudation is one of the most common infections besetting children. It is also one of the most frequently misdiagnosed and maltreated diseases. The acute form is almost invariably consequent to upper respiratory tract infection. Thus, although acute suppurative otitis media is a bacterial process, viral respiratory infection is important as an antecedent event. Aspiration of middle ear fluid in the syndrome of acute otitis media yields a bacteriologically sterile fluid in about 25% of cases.
In acute suppurative otitis media, Streptococcus pneumoniae causes more than half the cases at all ages. Haemophilus influenzae is mainly a pathogen of infancy, accounting for about one-third of the cases.
Before antibacterial antimicrobics were available,
Streptococcus
pyogenes was common, but it now is found in no more than 10-15% of
cases. These three bacterial agents account for more than 90% of acute
suppurative otitis media except in the newborn infant in whom coliform
bacteria or staphylococci are often pathogens.
PATHOGENESIS AND PATHOLOGY:
The eustachian tube is the principal portal for the entry of bacterial into the middle ear. Partial obstruction facilitates the ingress of nasopharyngeal bacteria into the middle ear or, in the case of complete obstruction, leads to negative pressure in the middle ear cavity and serous effusion.
Anatomy, immunologic virginity, bottle propping and microbiologic inexperience conspire against the infant to produce a far greater frequency of otitis media in this age group than in older children and adults. The eustachian tube of the child, as compare to the adult:
1. Is more horizontal
2. Contains less cartilage
3. Contains less stiff cartilage
4. Has more patency
5. Is more subject to intrinsic obstruction
These factors predispose the child to otitis media. Because he is exposed to a succession of infectious agents to which he has no immunity, mucosal swelling and adenoidal hypertrophy provide an ideal setting for pathogenic bacteria resident in the nasopharynx to establish themselves in the middle ear. Allergens may initiate the same process in allergic persons. Because almost all upper respiratory tract infections are caused by viruses, the usual sequence is viral infection, followed in 5-10 days by the onset of bacterial middle ear infection. Otitis media occasionally complicates streptococcal sore throat, but this is unusual.
The acute inflammatory response to the initiating
viral infection or allergic reaction changes the thin, cuboidal lining
of the middle ear cavity into a structure that is two to three times its
normal thickness. The neutrophils of the acute inflammatory response migrate
into the cavity to render purulent the initially serous fluid. As swelling
involves the orifice of the eustachian tube, the lumen becomes occluded
and exudate accumulates. As pressure increases, not only does the tympanic
membrane bulge outward, but also pus may be forced into pneumatized portions
of the petrous bone. Relief of the pressure is critical to resolution of
the process and may occur through rupture of the eardrum.
CLINICAL SYMPTOMS:
The onset of suppurative otitis media is typically abrupt, producing pain in the ears, a feeling of fullness, and fever. The peripheral blood shows a moderate leukocytosis. There is no regional lymphadenopathy. There generally are no other symptoms except those of the viral respiratory infection or the allergic reaction that precedes the middle ear infection. However, in infancy, the major manifestations may be fever, ear pain, irritability, vomiting and loose stools. Unilateral otitis is twice as common as bilateral ear disease in infants.
In pneumococcal or streptococcal otitis media, inspection
reveals a fiery red tympanic membrane with bulging and loss of all normal
landmarks. Spontaneous perforation may occur in the first 24-48 hours,
resulting in alleviation of pain. The findings are generally less dramatic
when H. influenzae is the etiologic agent. There is less redness
and less tension on the tympanic membrane, and spontaneous perforation
is uncommon. When there is a question about the presence of fluid in the
middle ear, pneumatic otoscopy can be useful to demonstrate the degree
of movement of the tympanic membrane in response to external pressure.
DIAGNOSIS:
In the presence of ear pain, fever, vomiting and
diarrhea, middle ear effusion is definitive of acute otitis media. Check
for normalcy of the tympanic membrane:
1. Neutral position
2. Flexible
3. Transparent
4. Ground glass appearance
These will change in otitis media. If the tympanic
membrane is intact and myringotomy is decided on, the canal and surface
of the tympanic membrane should be cleaned with 70% ethanol or iodine before
the incision is made. Smears and cultures should be made from the pus on
the myringotomy knife blade. Needle aspiration is preferred over myringotomy
in most circumstances. It is less traumatic and a better specimen for culture
is obtained. Pus should be inoculated in culture media appropriate to the
isolation of the pathogens common to otitis media. However, middle ear
effusion is not normally cultured.
TREATMENT:
1. Relieve pressure by myringotomy (rupture of the tympanic membrane) or needle aspiration.
2. Follow the management
scheme below:
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You have diagnosed acute otitis media in your patient who attends day care, and you are considering antibiotic therapy |
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•Patient younger
than 2 y?
•Complications such as perforated tympanic membrane? •Underlying anatomic middle ear deformity? AND •Recurrent episodes? |
NO-----------> |
Consider delaying antibiotic Rx; recommend symptomatic Rx with a decongestant and analgesic (acetaminophen or ibuprofen) and careful observation for 2 d | ||||
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>3 previous episodes?
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NO-----------> | If appropriate,
prescribe
amoxicillin, 20-40 mg/kg/d for 5-10 d |
<---NO | Symptoms improve?
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Consider whether
•A resistant strain has developed (contact hospital for information on local resistance patterns and rates) •A drug other than amoxicillin may be needed •Referral to an otolaryngologist is warranted |
Amoxicillin fails
OR
Amoxicillin inappropriate? l
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NO---> | No further Rx indicated. Consider pneumococcal polysaccharide vaccination for children 2 y and older at risk for invasive pneumococcal disease | |||
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NO
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Switch
to an alternative:
trimethoprim/sulfamethoxazole, amoxicillin/clavulanate, or cefuroxime axetil |
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Failure to respond after 1 or 2 courses? | ||||
YES
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Drugs and vaccines mentioned |
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Acetaminophen
Ibuprofen (Children's Advil, PediaProfen)
Amoxicillin (Amoxil, Trimox, Pneumococcal polysaccharide Wymox, etc.) vaccine, polyvalent Amoxicillin/clavulanate (Pneumovax 23, Pnu-Imune 23) (Augmentin) Trimethoprim/sulfamethoxazole Cefuroxime axetil (Ceftin) (Bactrim, Cotrim, Septra, etc.) |
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NAME OF DISEASE: Otitis externa
ETIOLOGICAL AGENT: Pseudomonas aeruginosa
DIAGNOSIS:
There are two forms of this disease, benign and malignant. The benign form is a superficial infection of the external auditory canal that is frequently initiated by moisture. The patient complains of pain, itching and a sensation of fullness in the ear. Exudate, erythema and edema may be seen in the canal. Although the tympanic membrane may be involved, it moves well with the pneumatic otoscope in contrast to the immobility seen in otitis media.
Malignant otitis externa is seen in elderly diabetics
and has a 20% fatality rate. The infection rapidly spreads to the adjacent
soft tissues and bone structures. The seventh cranial nerve becomes infected
at its exit from the stylomastoid foramen. Later cranial nerves X, XI and
XII become involved. Occasionally there is osteomyelitis of the long canal.
TREATMENT:
The benign form can be treated topically with antibiotic drops (polymyxin or neomycin). The malignant form is treated in an in-patient setting with parental administration of ticarcillin, piperacillin, tobramycin or ceftazidime.
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