OTITIS_EXTERNA;

External otitis is a condition that occurs when the ear

canal becomes irritated. The ear canal is the part of the
ear that leads from the outer ear to the ear drum (figure
1). External otitis can develop as a result of an infection,
allergy, or skin problem.
Otitis externa (OE) is an inflammation or infection of the external auditory canal (EAC), the auricle, or
both.[1, 2, 3] This condition can be found in all age groups.[4]See the image below.

Acute otitis externa. Ear canal is red and

edematous, and discharge is present.

Classification
OE may be classified as follows:
Acute diffuse OE - Most common form of OE, typically seen
in swimmers

Acute localized OE (furunculosis) - Associated with

infection of a hair follicle

Chronic OE - Same as acute diffuse OE but is of longer

duration (>6 weeks)

Eczematous (eczematoid) OE - Encompasses various

dermatologic conditions (eg, atopic dermatitis, psoriasis,
systemic lupus erythematosus, and eczema) that may
infect the EAC and cause OE

Necrotizing (malignant) OE - Infection that extends into

the deeper tissues adjacent to the EAC; occurs primarily in
immunocompromised adults (eg, diabetics, patients with
AIDS

Otomycosis - Infection of the ear canal from a fungal

species (eg, Candida,Aspergillus)

Signs and symptoms

The key physical finding of OE is pain upon palpation of
the tragus (anterior to ear canal) or application of traction
to the pinna (the hallmark of OE). Patients may also have
the following signs and symptoms:
Otalgia - Ranges from mild to severe, typically progressing
over 1-2 days
Hearing loss
Ear fullness or pressure
Erythema, edema, and narrowing of the EAC
Tinnitus
Fever (occasionally)
Itching (especially in fungal OE or chronic OE)
Severe deep pain - Immunocompromised patients may
have necrotizing (malignant) OE
Discharge - Initially, clear; quickly becomes purulent and
foul-smelling

Cellulitis of the face or neck or lymphadenopathy of the

ipsilateral neck (occasionally)
Bilateral symptoms (rare)
History of exposure to or activities in water (frequently)
(eg, swimming, surfing, kayaking)
History of preceding ear trauma (usually) (eg, forceful ear
cleaning, use of cotton swabs, or water in the ear canal)
See Clinical Presentation for more detail.
Diagnosis
The patients history and physical examination, including
otoscopy, usually provide sufficient information for the
clinician to make the diagnosis of OE. Note that a patient
who is diabetic or immunocompromised with severe pain
in the ear should have necrotizing OE excluded by an
otolaryngologist.
Laboratory testing
Typically, laboratory studies are not needed, but they may
be helpful if the patient is immunocompromised, if the
usual treatment measures are ineffective, or if a fungal
cause is suspected. Tests may include the following:
Gram stain and culture of any discharge from the auditory
canal

Blood glucose level

Urine dipstick
Imaging studies
Imaging studies are not required for most cases of OE.
However, radiologic investigation may be helpful if an
invasive infection such as necrotizing (malignant) OE is
suspected or if the diagnosis of mastoiditis is being
considered.
Imaging modalities may include the following:
High-resolution computed tomography (CT) - Preferred;
better depicts bony erosion [5]
of the EAC
Assess patients with diffuse acute OE for factors that may
modify therapeutic management (eg, non-intact tympanic
membrane, immune-compromised state)
Radionucleotide bone scanning
Gallium scanning
Magnetic resonance imaging (MRI) - Not used as often as
the other modalities; may be considered secondarily or if
soft-tissue extension is the predominant concern [6].

Management; Assess patients with diffuse acute OE for

factors that may modify therapeutic management (eg,
non-intact tympanic membrane, immune-compromised
state)

Most persons with OE are treated empirically. Primary

treatment involves the following:
Pain management.
Removal of debris from the EAC.
Administration of topical medications to control edema
and infection.
Avoidance of contributing factors.
AAO-HNSF diagnosis and management guidelines for
acute otitis externa
In 2014, the American Academy of and Neck
OtolaryngologyHead Surgery Foundation (AAO-HNSF)
released updated clinical practice guidelines for the
diagnosis and treatment of acute OE. The
recommendations included the following[12] :

Differentiate diffuse acute OE from other possible causes of otalgia, otorrhea,

and inflammation Assess for pain in patients with acute OE; base the
analgesia recommendation on the patients pain severity

Administer topical medications as initial therapy for diffuse, uncomplicated

acute OE

Do not administer systemic antimicrobial agents as initial therapy for diffuse,

uncomplicated acute OE; reserve such treatment for cases in which there is
extension outside of the EAC or there are specific host factors that require
systemic agents

Instruct patients on how to administer topical drops; perform an aural toilet,

place a wick, or both, when the ear canal is obstructed

Use a non-ototoxic topical agent in patients with a known

or suspected perforation of the tympanic membrane (eg,
tympanostomy tube)
Confirm the diagnosis of acute OE and reassess the
differential diagnosis within 48-72 hours in cases
refractory to the initial therapy
Risk factors for OE include the following:
Previous episodes of OE
Swimming, diving, or participating in aquatic activities
Use of earplugs or probing of the EAC (possibly secondary
to trauma to the EAC)
Hot, humid weather
Use of a hearing aid
Coexistence of eczema, allergic rhinitis, or asthma
Comorbidities such as diabetes mellitus, AIDS, leukopenia,
or malnutrition

United States and international statistics

OE is found in all regions of the United States, occurring in 4 of every 1000 people
annually.[8, 10] The infection is believed to be more prevalent in hot and humid
conditions such as prevail during the summer months, presumably because
participation in aquatic activities is higher.[4, 8] Acute, chronic, and eczematous OE
are also common. Necrotizing OE is rare.
The international frequencies of OE have not been fully determined; however, the
incidence is increased in tropical countries. [9]
Age-, sex-, and race-related demographics
Although the infection can affect all age groups, OE appears to be most prevalent in
the older pediatric and young adult population, with a peak incidence in children
aged 7-12 years.[13] A single epidemiologic study from the United Kingdom found a
similar 12-month prevalence for individuals aged 5-64 years and a slight increase in
prevalence for those older than 65 years.[4] This was postulated to occur secondary
to an increase in comorbidities, as well as an increase in the use of hearing aids,
which may cause trauma to the EAC.
OE affects both sexes equally. No racial predilection has been established, though
people in some racial groups have small ear canals, which may predispose them to
obstruction and infection.

Etiology
OE is most often caused by a bacterial pathogen; other varieties include fungal OE
(otomycosis) and eczematoid (psoriatic) OE.[13] In one study, 91% of cases of OE
were caused by bacteria.[7] Others have found that as many as 40% of cases of OE
have no primary identifiable microorganism as a causative agent. The most
common causative bacteria are Pseudomonas species (38% of all cases),
[13]
Staphylococcus species, and anaerobes and gram-negative organisms.
Fungal OE may result from overtreatment with topical antibiotics or may arise de
novo from moisture trapped in the EAC. It is caused by Aspergillus 80-90% of the
time; Candida and other organisms have also been isolated. This condition is
characterized by long, white, filamentous hyphae growing from the skin surface.
Besides otorrhea, erythema and edema of the EAC are common. In severe cases,
soft tissue stenosis may be present. Extension of the infection may manifest as
cellulitic skin changes involving the concha of the auricle and the tragus.

Pathophysiology
OE is a superficial infection of the skin in the EAC. The processes involved in the development of OE can be
divided into the following four categories:

Obstruction (eg, cerumen buildup, surfers exostosis, or a narrow or tortuous canal), resulting in water
retention
Absence of cerumen, which may occur as a result of repeated water exposure or overcleaning the ear
canal
Trauma
Alteration of the pH of the ear canal

Eczematoid (psoriatic) OE is associated with the following conditions:

Eczema

Seborrhea

Neurodermatitis

Contact dermatitis from earrings or hearing aid use

Purulent otitis media with perforation of the tympanic membrane and

drainage; this may mimic OE to an extent, but it is usually painless and does
not cause any swelling of the ear canal

Sensitivity to topical medications

Chronic OE is a fairly common condition that is sometimes the result of incomplete

treatment of acute OE.[14] More often, however, chronic OE is caused by
overmanipulation of the ear canal as a consequence of cleaning and scratching.
Such overmanipulation results in a low-grade inflammatory response that causes
further itching of the skin. Eventually, the skin thickens, and canal stenosis may
occur.
Necrotizing OE occurs in patients who are immunocompromised and represents a
true osteomyelitis of the temporal bone

. Elements of the diagnosis of diffuse acute otitis externa.

1. Rapid onset (generally within 48 hours) in the past 3 weeks, AND
2. Symptoms of ear canal inflammation, which include: otalgia (often severe),
itching, or fullness, WITH OR WITHOUT hearing loss or jaw pain,
3. Signs of ear canal inflammation, which include: tenderness of the tragus, pinna,
or both OR diffuse ear canal edema, erythema, or both WITH OR WITHOUT otorrhea,

regional lymphadenitis, tympanic membrane erythema, or cellulitis of the pinna and

adjacent skin.
a Pain in the ear canal and temporomandibular joint region intensified by jaw
motion.

Most patients will experience considerable improvement in symptoms after one day
of treatment. If there is no improvement within 48 to 72 hours, physicians should
reevaluate .

TREATMENT of OTITISEXTERNA.
IN ALL CASES: Treating focal sepsis (adeno-tonsillitis.URI.rhinosinusitis)---mainly in
pediatrics..
.

Remove foreign body from ear ,if present.

Treatment of pain and fever with Analgesics.
EAR IRRIGATION IS CONTRAINDICATED, if the tympanic membrane is ruptured or if it
cannot be fully visualised. EAR DROPS ARE NOT INDICATED.
INDICATIONS FOR ANTIBIOTIC THERAPY:

Infants <2yrs and in children whose assessment suggests severe infection

(vomiting,fever>39C,severe pain).
is no improvement or worsening of symptoms after 48 to 72 hrs.
If the child cannot be re-examined: Antibiotics are prescribed.
Children at risk of unfavourable out come(Malnutrition,immunodefieciency, ear malformation).
FOR other children:
If the child can be re examined within 48 to 72 hrs;it is preferable to delay Antibiotic
prescription.Spontaneous resolution is probable and a short symptomatic treatment of fever

AMOXYCILLIN

is the first line treatment:

AMOXYCILLIN PO:
CHILdren: 80mg to 100mg/kg/day in 3 divided doses for 5 days.
ADULTS: 1500mg/day in 3 divided doses for 5 days.
AMOXICYLLIN/CLAUVULINIC ACID is used as second line treatment, in the case
of treatment failure.
AMOXICYLLIN/CLAUVULINIC ACID(CO-AMOXYCLAV) po for 5 days.
The dose is expressed in AMOXYCILIN:
CHILDREN LESS THAN 40 KG:45 TO 50MG/KG/DAY IN 2 DIVIDED DOSES(IF
USING RATIO8:1 OR 7:1) OR IN 3 DIVEDE DOSES (IF USING RATIO 4:.1).NOTE:
the dose of clavulanic acid should not exceed 12.5mg /kg/day or 375 mg/day.
CHIDREN >=40KG AND ADULTS ; 1500 TO 2000MG/DAY D3PENDING ON THE
FORMULATION AVAILABLE:
RATIO 8:1 :2000MG/DAY=2TABS OF 500/62.5MG 2 TIMES PER DAY
RATIO7:1:1750MG/DAY=1 TAB OF 875/125MG 2 TIMES PER DAY
Ratio 4:1:1500mg/day=1 tablet of 500/125mg 3 times per day.
Note: the dose of clavulanic acid should not exceed 375mg per day.
Persistence of ear drainage alone,without fever and pain,in a child who has
otherwise improved (reduction in systemic symptoms and local
inflammation)does not warrant a change in antibiotic therapy
Clean ear canal by gentle dry moping until no more drainage is obtained .
Azithromycin or erythromycin should be reserved for very rare pencillin
allergic patients as treatment failure is frequent(resistants to macrolides)
Azithromycin PO
Children over 6 months /10mg/kg once daily for three days.
Erythromycin PO

30 to 50mg/kg /day in 2 to 3 divided doses for 10 days.

Parcetomol for pain in pediatrics:
>1 month to 12 years: 10 to 15 mg/kg/dose every 4 to 6 hours as needed (Maximum: 5
doses in 24 hours)
>=12 years: 20 to 30 mg kg//dose 4 to 6 hours.
Usual Adult Paracetamol Dose for Fever:
General Dosing Guidelines: 325 to 650 mg every 4 to 6 hours or 1000 mg every 6 to 8 hours orally or
rectally.
Paracetamol 500mg tablets: Two 500 mg tablets orally every 4 to 6 hours
Usual Adult Paracetamol Dose for Pain:
General Dosing Guidelines: 325 to 650 mg every 4 to 6 hours or 1000 mg every 6 to 8 hours orally or
rectally.
Paracetamol 500mg tablets: Two 500 mg tablets orally every 4 to 6 hours.
:AVOID PARACETAMOL IN LIVER PROBLEMS AND IN RENAL FAILURE PATIENTS.S
AVOID OVER DOSING AS IT MAY CAUSE LIVER DAMAGE & IN INFANTs<2yrs.

http://www.drugs.com/paracetamol.html

outer ear canal. It is more common in the tropical countries. The

infection may be OTOMYCOSIS: Otomycosis is a fungal ear infection,
[1]
a superficial mycotic infection of the either subacute or acute and
is characterized by malodorous

discharge, inflammation, pruritus, scaling, and severe

discomfort
The mycosis results in inflammation, superficial epithelial exfoliation,
masses of debris containing hyphae, suppuration, and pain.[2]
Aspergillus and Candida spp are the most frequently isolated fungi in patients with otomycosis.
The diagnosis of otitis externa relies on the patient's history, otoscopic examination under
microscopic control, and imaging studies
Topical antifungals, such as clotrimazole, miconazole, bifonazole, ciclopiroxolamine, and
tolnaftate, are potentially safe choices for the treatment of otomycosis, especially in patients
with a perforated eardrum.
The oral triazole drugs, itraconazole, voriconazole, and posaconazole are effective against
Candida and Aspergillus, with good penetration of bone and the central nervous system. These
drugs are essential in the treatment of patients with malignant fungal otitis externa complicated
by mastoiditis and meningitis.

The most characteristic finding on ear examination is the presence of greyish white thick
debris known as "wet blotting paper". Most fungal ear infections are caused
byAspergillus niger and Candida albicans, but exceptions exist.[3][4]

http://www.ncbi.nlm.nih.gov/pubmed/20347664#
Pharmacotherapy

Topical medications (eg, acetic acid in aluminum acetate, hydrocortisone and

acetic acid otic solution, alcohol vinegar otic mix)

Analgesic agents (eg, acetaminophen, acetaminophen and codeine)

Antibiotics (eg, hydrocortisone/neomycin/polymyxin B, otic ofloxacin, otic

ciprofloxacin, otic finafloxacin, gentamicin 0.3%/prednisolone 1% ophthalmic,
dexamethasone/tobramycin, otic ciprofloxacin and dexamethasone, otic
ciprofloxacin and hydrocortisone suspension)
Oral antibiotics (eg, ciprofloxacin)
Antifungal agents (eg, otic clotrimazole 1% solution, nystatin powder)

Surgery

Surgical debridement of the ear canal - Usually reserved for necrotizing OE or for complications of OE (eg,
external canal stenosis); often necessary in more severe cases of OE or in cases where a significant amount
of discharge is present in the ear; mainstay of treatment for fungal infection.

REFER FOR ANTIBIOTIC THERAPY FROM CHAPTER OTITIS EXTERNA.

REFER HOW AND WHEN TO GIVE EAR DROPS FROM PREVIOUS CHAPTER.
http://emedicine.medscape.com/article/994550-overview