Acute Otitis Media

Lecture 4 Acute Otitis Media
The term Acute Otitis Media implies a viral or bacterial infection of the mucosal lining of theMiddle ear and mastoid air cell system
AOM is one of the commonest illness in childhood, defined as inflammation of the middle ear cleft of rapid onset and infective origin 25% of child prescriptions in USA
The adult cases constitutes 16% of all cases seen,making it a not infrequent event in healthy adult
AOM is of four subgroups:
1 Sporadic
Episodes occurs as frequent isolated events,typically occurring with URTI
2 Resistant AOM
Persistence of signs and symptoms of middle ear infection beyond 3-5 days of AB treatment
3 Persistent AOM
Persistent or recurrence of symptoms and signs of AOM within six days of finishing a course of AB
4 Recurrence AOM
Either three or more episodes of AOM occurring within a six months period,or at
least four to six episodes within a 12 month period
Diagnosis
Diagnosis by symptomatology alone is inaccurate because of young age of most patients,and nonspecific nature of the symptoms.
One-third of children may have no ear related symptoms ,two- thirds may be apyrexial

Symptoms:
1 Rapid onset otalgia
2 Hearing loss
3 Otorrhea
4 Fever
5 Excessive crying
6 Irritability,restlessness
7 Coryzal symptoms
8 Rhinitis
9 Cough
10 Vomiting
11 Poor feeding
12 ear pulling,rubbing of the ear
13 Clumsiness
Signs
The child may appear unwell ,and may rub his or her ear ,the diagnosis is often confirmed by otoscopic assessment of TM colour,position and mobility .
The TM usually opaque,most commenly yellow or yellowish pink, being red in only 18-19%.
The position of TM reliably predect OME only when it is bulging hypomobility demonstrated by pneumatic otoscopy
Mucopurulent otorrhea may be seen
While in adult the normal pearl grey and transparent with clear light reflex exclude AOM ,the inject TM indicate early otitis media
But this may also caused by crying or by a common cold .A clear difference between both ears support the diagnosis of AOM , an intensely red TM confirm the diagnosis as well buldging
Of TM indicates the presence of liquid in the middle ear under pressure ,perforation of TM with otorrhrea (with acute clinical symptoms)also confirm the diagnosis of AOM adult with AOM consults their physician within 48 hrs which is more sooner on average than children
Challenges in otoscopic examination
?poorly functioning otoscope
??Moving child s head
???Narrow ear canal
????Natural redness of TM in a screaming child
?????Wax
??????Untrained eye
Investigations
1 tympanometry to establish the presence of middle ear effusion
2 Tympanocentesis and culture of middle ear effusion
3 Bacterial swab of persistent otorrhea
4 Nasopharyngeal swab for bacterial culture
5 tests for iron deficiency anaemia and white blood cell disorders
6 Immunoglobulin assay IgA,IgG,IgM
Differential diagnosis
1 pain may be referred from tonsillitis,teething,TM joint disorder
2 Red TM in screaming child
3 Acute mastoiditis
4 OME
5 Trauma
6 OE
7 Ramsey Hunt syndrome
8 Bullous maryngitis
9 Rarely,AOM may be the first indication of serous underlying disease,such as leukeaemia and wegener s granulomatosis

Microbiology
Viruses
Respiratory syncytial virus RSV
Influenza A virus
Parainfluenza viruses
Human rhinivirus
Adenovirus

Bacteria While in adult
Haemophilus influenza 16-37% same in adult 26%
Moraxella catarrhalis 11-23% streptococcal pneumonia 21 21%
St. coccus pyogene Moraxilla catarhalis 3%
Staphylococcus aureus streptococcus areus 3%
Pneumococci

Routes of spread of infection
1 Eustachian tube
Is the main route by which the organisms reach the middle ear,shorter,straighter,and more patulous is more prone to develop infection in middle ear like in native Americans more than white 2 TM perforations
Pathogen entry through TM perforation or ventilation tube (grommet)
Most commonly with water exposure
3 Haematogenic
Viral identification in the blood and middle ear was described
Risk factors
1 Genetic factors
There is familial tendency to develop OM and there is gene association ,certain HLA human leukocyte antigen classes have been associated with increase risk OM
2 Immune factors
Low level IgG2 subclass have been reported in several studies to be more common in otitis prone child, Cytokines like interleukins affect host defence and cause persistent infection
3Environmental factors
Seasonal URTI in winter,poor socioeconomic status,poor housing,overcrowding,and bottle feeding as breast feeding for three months is protective against AOM
4 Systemic disease and syndromes
Iron deficiency anemia
Turner s syndrome
Down syndrome
Cleft palate
Management
Most children with AOM will get better quickly without treatment and,2\3 recover within 24 hour
Conservative treatment:
Most children will benefit from simple analgesias and anti-pyrexials like paracetamol,ibuprofen
Antibiotics:
If not prescribed initially ,should be given if t he child failed to improve after Watchful Waiting for 2-3 days, also given to child with irregular illness course,and given also to high risk child.
Five days treatment was enough in uncomplicated cases, in low risk child, without recurrence or TM perforation
Amoxicilline remains the first choice higher than previously recommended dose 80mg\kg\day
Antihistamines and decongestants:
There use could not be supported,but combining the two show slightly reduce persistence AOM
Surgery:
Maryngotomy was practiced in pre-antibiotic era,many studies show that AB plus maryngotomy had no advantages over AB alone


Complications

Extracranial
1Tympanic membrane
TM perforation is associated with purulent or bloody otorrhea and immediate relief of pain typically occur in posterior half of pars tensa and may predispose to further retraction pockets,the outcome of perforation is one of these four
1 Healing of perforation in most cases
2 Resolve infection but perforation persists
3 Persist perforation and otorrhea manifested as CSOM usually after 3 months
2 Acute mastoiditis Mastoiditis was common in pre AB era
Usually preceded by 10-14 days of middle ear symptoms and it is a disease of childhood

Microbiology is little bit differ from AOM
St pneumonia
St pyogenes
Pseudomonas aeruginosa
Staph aurius
H influenza is less common
Presented in four stages
Stage 1
During episodes of AOM infection may naturally extend to mastoid cavity and be visualized radiologically this is not considered as complication and not associated with typical sign of mastoiditis
Stage 2
Periosteitis infection may spread to periosteum via emissary veins
Stage 3
Osteitis when the infection has begun to destroy the bone of mastoid air cell and subperiosteal abscess may develop
Stage 4
Subacute or masked mastoiditis in incompletely treated AOM after 10-14 days of infection ,sign may be absent but otalgia and fever persist this can also progress to serious complications
Symptoms
Otalgia
Irritability
Pyrexia less common in thoe treated with AB
Otorrhea
On examination
Red or bulging TM,normal TM not exclude the diagnosis
Retroauricular swelling
Retroauricular erythema
Tenderness is typically on (MacEwen s triangle) on palpation through the conchal bowl
Pinna protrution
Investigations
Full blood count
C-reactive protein
Blood culture
CT scan of mastoid may show evidence of osteitis,abscess or intracranial complications
Differential diagnosis
AOM
OE
Furunculosis
Reactive lymphadenopathy
Management
Maryngotomy with or without ventilation tube
High dose IV AB
Drain of abscess with or without cortical mastoidectomy

3 Petrositis
Extension of infection to petrous apex, the classical features of Grandenigo s traid are not always present (VI nerve palsy+sever pain in trigeminal nerve distribution+middle ear infection)
4 Facial nerve palsy
5 Labyrinthitis
Bacterial toxins may enter the round window due to change of it s permeability during acute infection
Sever vertigo,nausea,vomiting,nystagmus,permanent
Intrcranial complications
Meningitis
Extradural abscess
Suubdural empyema
Sigmoid sinus thrombosis
Focal otitic encephalitis (cerebritis)
Brain abscess
Otitic hydrocephalus

Lecture 5 chronic suppurative otitis media