Tuesday, 12 February 2013

Acute Otitis Media






Please note that the following is a general guideline only. For a full assessment, exclusion of any other underlying cause for your symptoms and an individualised treatment approach, you will need to be seen by a qualified specialist.


Definitions

-AOM is defined acute inflammation of the middle ear 
-OME is defined as middle ear effusion without signs or symptoms of an acute infection
-Recurrent AOM is defined as 4 or more episodes in one year or three or more episodes in one 6 month period

Epidemiology
sex: M>F (some studies show no difference)age: 6-11 months  declines around 18-20 months
Incidence: 70% experience one or more attacks before 2 years of age
 Race: higher incidence in indeginous (95% of Aboriginal children by 2 months) 
Familial-higher predisposition if in siblings or parental history
peaks in winter months which corresponds to the peak in respiratory infect


Aetiology

Bacterial (50-70%)
Streptococcus p, HI, Moraxella Catarrhalis,  Group A streptococcus    >    S. aureus, E. coli,      Klebsiella, Pseudomonas aeruginosa
       
Resistance- 100% M. catarrhalis B-lactamase producers 

Pneumococcal vaccinated with severe OM have 2x more gram negatives
                          50% S. pneumoniae decrease in penicillin binding proteins


Virus (20%- causative or co pathogenic)
Peak incidence 2-4 days after URTI, most develop with in 2 weeks of URTITypes same as URTI -RSV / rhinovirus/  influenza virus/  adenovirus, enterovirus / parainfleunza virus



Pathophysiology- Viral

1 URTI → oedema and narrowing of the  ET → increase in negative ME pressure and decreased clearance → influx of bacteria when open → inflammatory response elicited in the ME → mucosal oedema, capillary engorgement and infiltration of neutrophils

2 URTI- directly inflaming the middle ear. Result is usually serous OME, secondary bacterial infection may occur




Pathophysiology Bacterial

Acute suppurative otitis media typically progresses in four stages: hyperemia, exudation, suppuration, coalescence and resolution
1 Hyperemia
Initial infection by bacteria results in simple hyperemia, causing otalgia
The otologic examination demonstrates injection of the vessels of the tympanic membrane
Drum is edematous, although landmarks can still be distinguished


2   Exudation 
After 12 to 24 hours tympanomastoid compartment becomes filled with exudate under pressure. 
Manifestations -increased otalgia and fever, conductive hearing loss.
Otoscopy, the tympanic membrane is red, thickened, and bulging.
Drum may appear pale instead of red
may have mastoid tenderness



Bulging TM, loss of landmarks


3 coalescence   


When the infection is severe and persists beyond 2 weeks

Pus is under pressure


Destroy septa of the mastoid bone - coalescence of the mastoid

Symptomatology, in comparison to the stage of exudation, is deceptively mild. 
It is the timing of the symptomatology rather than its severity that is critical to the correct diagnosis
4 Suppuration
may drain naturally via a perforated tympanic membrane

4 Complicated AOM
Develops Mastoiditis with subperiosteal abscess formation
Abscess can extend to the neck along the facial planes or intra cranial
Other complications include sigmoid sinus thrombosis/ labyrinthitis/ facial nerve palsy




Note the subperiosteal abscess, pain is over the high mastoid-the antrum





Symptoms & Signs


Clinical Presentation

Initially acute ear ache / hearing loss/  fever
Temporal course of bacterial infection is as above
Drum may perforate and discharge
Mastoiditis take up to two weeks to develop
Tenderness in mastoiditis occurs over the antrum (high-up posterior) NOT over the tip (more likely a lymph node)




Examination

Tympanic membrane- hyperemia ---Budging--- perforation 
Suspect mastoiditis if post auricular swelling due to subperiosteal abscess


Investigations
     Imaging (CT +/- MRI) only if signs of complication (intratemporal and extratemporal)
     tympanocentesis and myringotomy: if non resolving/ mastoiditis



Note the destruction of septa on the left side leading to coalescence
    




                            

Treatment

1 Observation
     if uncomplicated
     reassess at 48-72 hours
      analgesia

2 Antimicrobials
Benefit
  decrease treatment failure and rate of effusion
   short term benefit → more rapid resolution of symptoms AOM
   late benefit → more rapid resolution of MEE
   antibiotics reduce risk of bacteraemia and may prevent focal infections i.e. mastoiditis

When to prescribe
    younger children < 2y more risk of complications → prescribe from onset
    Others if no improvement in 3-4 days

Type of antibiotics
amoxicillin for uncomplicated AOM-if not working day 3 change


3 Surgical Treatment

A Myringotomy (if pus under pressure) and not settling
 Therapeutic and obtains fluid for culture
low risk but TM heals within 3 days → insufficient time for mucosal recovery → high likelihood of recurrent OME

B  Grommets-Indications
for recurrent AOM > 3 in 3 months or > 4 in 1 yr
failure of medical therapy and significant symptoms
suppurative complications (Mastoiditis/ facial nerve palsy- initial treatment along with IV abs)
immunocompromised patients after failure of medical therapy with 48-72 hours


C  Adenoidectomy
recommended removal (irrespective of size) during placement of second set of tympanostomy tubes
addition of tonsillectomy as little, if any, benefit and is not recommended
D Mastoidectomy
Suppurative complications/ not responded to grommet and IV ABS




4 Prevention



Antimicrobial prophylaxis: reduces 1 episode of AOM per 9 month treatment of antibiotics per child




Allergy control: may help if a specific allergen can be identified

Vaccination-Prevenar: pneumococcal vaccine
        use of the hepavalent (7 strains) conjugate pneumococcal vaccine-decrease in invasive  pneumococcal infection 
        Only 6-7% decrease in episodes of AOM
        reduced efficacy, as other pathogens causing AOM
        reduces the URTI that predisposes to AOM

influenza vaccine 
      some studies -32% decrease in AOM others have shown only placebo
Changing environmental contributors: feeding methods, day care, passive smoke exposure and allergen exposure

Natural History and Prognosis

60-70% resolve MEE by 30 days follow up
up to 90% in 3 months
younger children less likely to resolve a MEE and more likely to have an effusion that persists for > 12 weeks






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