CASE REPORT Diffuse Otitis Externa

CASE REPORT Diffuse Otitis Externa

Presented by: Emanuel Felicia Hilma Kholida

10/296267/KU/13589 10/304831/KU/14175

Sanindita Kusumatusti

10/296547/KU/13633

Lee Jay Mie

10/304715/KU/14134

Noor Aqilah Saadon

10/304644/KU/14063

Ranjidam Ramasamy 09/290420/KU/13572 William Sumoro

MA

Moderator: dr. Rangga Putra

Department of Otorhinolaryngology Head and Neck Surgery Faculty of Medicine Gadjah Mada University Dr. Sardjito General Hospital Yogyakarta 2015

I.

INTRODUCTION 1

Otitis externa is an inflammatory and infectious process of the external auditory canal. The appearanceofthe canal varies according to the time course ofinfection: acute, subacute, orchronic.OE usually represents an acute bacterial infection of the skin of the ear canal (most commonly attributable to Pseudomonas aeruginosa orStaphylococcus aureus) but can also be caused by other bacteria, viruses, or a fungal infection. 1 Data from ambulatory care centers and emergency departments indicate that in 2007 in US there were about 2.4 million visits for AOE or Acute Otitis Externa (8.1 visits per 1000 population), affecting 1 in 123 persons in the United States. Just less than half of all visits were for children 5 to 14 years of age. AOE has a lifetime incidence of 10%.

2

The condition is

known to affect people of all age groups but was found to peak in the 7- to 12-year-old age group and to decline in incidence among subjects >50 years of age.

3

One review article estimated that AOE affects 4 in 1000 people

annually in the US. 4A 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. 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.In the same study, the incidence of otitis externa increased towards the end of the summer, especially in the youngest age group (5-19 years old). It is common in warmer temperatures and high-humidity conditions and after swimming.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. 5 There are continued variations in management of acute otitis externa. Because otalgia (70%) is usually the main complaint, there is a need to assess patients with AOE for pain and recommend analgesic treatment based on severity of pain.The use of topical treatments alone, as distinct from systemic ones, are effective for uncomplicated AOE. Clinicians should not prescribe systemic antimicrobials as initial therapy fo diffuse, uncomplicated AOE unless there is extension outside ear canal or the presence of specific host factors that would indicate a need for systemic 2

therapy. Despite the well-demonstrated safety and efficacy of topical preparations for treating AOE, about 20% to 40% of subjects with AOE receive oral antibiotics, often in addition to topical antibiotics. 2

II. OVERVIEW A. ANATOMY of EXTERNAL EAR The external ear is composed of auricle or pinna and meatus acusticus externus (ear canal), which collects sound and conducts sound from the sound sources to the tympanic membrane.

6

Figure 1. Ear Overview.Coronal section through right ear, anterior view 6

1. Auricle (Pinna) Pinna is formed by irregular shaped plate of elastic cartilage that covered by thin skin. There are several elevations and depressed structures. The elevation margin of pinna is helix and below this structure is antihelix. The tongue-like projection is tragus (anterior) and antitragus (posterior). And the deepest depression of pinna is concha auricle, which connects with the ostium of ear canal (ostium canalis auditoris). The lobule is inferior part of 3

the pinna, which formed by fibrous tissue, that component makes the ear is easily pierced for taking blood sample and inserting earing.

6

Figure 2. External ear6

Vascularisation of the anterior ear is supplied by superficial temporal artery, which is the branch of external carotid artery. And for the posterior part of pinna is supplied by posterior auricle artery. The main sensory nerve of the auricle are the great auricular nerve, which is the branch of glossopharyngeal

nerve

and

auriculotemporal

nerve,

a

branch

of

mandibular nerve. The great auricular nerve will innervates the back part of the ear, helix, antihelix, and lobule. And the remainder parts (anterior part and the opening) is innervated by auriculotemporal nerve. 6 For the lymphatic drainage of pinna is as follows, the lateral surface of superior half of the aurice drains to the superficial parotid lymph nodes, the remainder of the superior part drains to the mastoid lymph nodes and deep cervical lymph nodes. the lobule and inferior part drains into superficial cervical lymph nodes.6

4

Figure 3. Lymphatic drainage of head6 2. Ear canal ( External Acoustic Meatus) Ear canal leads inwards through the tympanic part of the temporal bone from the auricle to the tympanic membrane. The length of this canal is about 23cm in adults. The lateral third of ear canal is formed by cartilage tissue and is lined with thin skin which is continuous with auricular skin (posterolaterally. And the medial two third is bony component (temporal bone), which is covered by skin that continuous with external layer of the lateral surface of tympanic membrane.6 Histologically, the external auditory meatus is lined by keratinized stratified squamous epithelium that is continuous with the epidermis of the auricle. The epithelium is firmly anchored to the surrounding perichondrium or periosteum by dense collagenous connective tissue. Numerous small hairs are present in the epithelium of the outer part of the meatus and are associated with large sebaceous glands in the underlying connective tissue. A special form of simple coiled tubular apocrine sweat gland, the ceruminous gland, occurs in the skin that lines the meatus. The ducts may open directly on the surface or, together with adjacent sebaceous glands, into hair follicles. Their secretory product is cerumen, a waxy material that prevents drying of the skin that lines the external auditory meatus. Hairs and glands occur primarily along the roof of the inner (bony) part of the external auditory meatus.7 The lymphatic drainage of the canal is an important channel for the spread of infection. Anteriorly and superiorly, the canal drains to the 5

preauricular lymphatics in the parotid gland (superficial parotid nodes) and the superior deep cervical nodes. The inferior portion of the canal drains into the infra-auricular nodes near the angle of the mandible. Posteriorly, the lymphatic drain into the postauricular (mastoid) nodes and the superior deep cervical nodes. Ear canal receive their blood supply from the superficial temporal and posterior auricular branches of the external carotid artery. Venous drainage from meatus is via the superficial temporal and posterior auricular veins. From superficial temporal vein joins into the retromandibular vein, which usually divides and joins both jugular veins, and from posterior auricular veins drains into external jugular vein but may also drain to the sigmoid sinus through the mastoid emissary vein. Sensory innervations of ear canal is supplied from cutaneous and cranial nerves, with contributions the anterior wall is from the auriculotemporal branches of the trigeminal nerves, the roof of canal by facial (VII), the floor by glossopharyngeal (IX), and the posterior wall is from vagus (X) nerves.6,8

B. OTITIS EXTERNA 1. Definition Otitis externa is an inflammation or infection of the external auditory canal (EAC), the auricle, or both. This condition can be found in all age groups, prevalence between man and woman is 1:1. Otitis externa can be caused by bacteria, viral, and fungi. Infection signs that could be seen are pain at the outer ear, redness on skin and variation of discharge. The prevalence of external otitis was similar between sexes, no specific age nor race of predilection. The external otitis could be classified as below 9 : 1. Furuncul ar otitis externa

Acute Otitis Externa





It affect the outer third ear canal, there were abundant hair follicle, sebaceous and cerumen glands. In term, infection take place at the pilosebaceous gland whicch turn to furuncle Alternate name is circumscribe(localized) otitis externa

6

2. Diffuse otitis externa





Chronic Otitis Externa

Eczematoid Otitis Externa

Malignant/Necrotic ans Otitis Externa Maligna/Nekrosis

Diffuse otitis externa which persist more than 6 months

Some dermatologic condition such as atopic eczema, psoriasis, SLE may cause the infection





Otomycosis

Affecting the inner 2/3 of outer ear canal. The skin is redden and the boder is diffused Prevalence is higher than Furuncular otitis externa

Diffuse infection which progressively involved subcutaneous tissue, cartilage, bone and peripheral tissue Imunocompromized/diabetes melitus patients are more prone

Fungal Infection could happen in moist ear canal. Such fungal as Pityrosporum, Aspergillus, Candida

Figure 5. Classification of Otitis Externa9

2. Etiology The most commont agent that may cause infection of otitis externa is bacterial

infection.

Such

bacteria

are

Staphyilococcus

aureus,

Staphylococcus albus, E. Colli, Pseudomonas Aeruginosa, and other gram negatives. Other non-infectious cause may have a hand. Some known factor are base shiifted PH, that could weaken the protection against infection, warm and moist ear canal will provide best suit environment for bacteria

7

and fungi to grow. Also minor trauma while clean the canal and swimming.10,11

3. Pathophysiology The ear canal has its auto cleaning mechanism, by movement of the hair of the epithel towards the outside of the canal. The movement will bring the dead epithelial cells.10 Clean the ear canal with cotton bud however will intervene this mechanism, by using cotton bud will push the dead cells toward the inner side of ear canal. The dead epithelial cells and cerumen will left over at the inner canal. Those remnants will absorb water; from shower or swimming. The absorbed water will make the skin wetter and moister, thus the infection of bacteria and/or fungal happen in the canal.

is more likely to be

11

Because of the inflammation, the tissue will swell (edema) and the visualization of tympanic membrane is difficult. Exudate will produced. In some severe infection, infection could progress beyond skin causing cellulitis in head/neck tissue.11 4. Staging for otitis externa The clinical course of external otitis may be divided into the following stages: preinflammatory; acute inflammatory, which can be mild, moderate, or severe; and chronic inflammatory. Typically, the preinflammatory stage begins when the stratum corneum becomes edematous due to the removal of the protective lipid layer and acid mantle from the canal, resulting in plugging of the apopilosebaceous unit. As obstruction continues, a sense of fullness and itching begins. 8 The disruption of the epithelial layer allows invasion of bacteria that either reside in the canal or are introduced on foreign objects inserted into the canal, such as a cotton swab or a dirty fingernail. This produces the acute inflammatory stage, which is accompanied by pain and tenderness of the auricle. In the earliest stage, the skin of the EAC shows mild erythema and minimal edema. A small amount of clear or slightly cloudy secretion may be seen in the canal.

As pain and itching increase, the patient

progresses to the moderate stage, in which the canal shows more edema and a thicker more profuse exudates.8 8

Further progression of the inflammation in the absence of treatment produces the severe inflammatory stage, characterized by increased pain and obliteration of the lumen of the canal. A profuse, purulent exudate and edema of the canal skin may obscure the TM. In addition, small white papules are often visible on the surface of the canal skin. P. aeruginosa or another gram-negative bacillus can almost always be cultured at this stage. In the severe stage, the physician often sees evidence of extension of infection beyond the canal to involve the adjacent soft tissues and cervical lymph nodes. 8 In the chronic inflammatory stage, the patient experiences less pain but more profound itching. The skin of the external canal is thickened, and superficial flaking may be seen. The auricle and concha often show secondary changes such as eczematization, lichenification, and superficial ulceration. This condition is likened to eczema and may range from mild drying and thickening of the canal to complete obliteration of the external canal by chronically infected, hypertrophic skin. 8 5. Clinical Manifestation Patient with otitis externa usually complained about otalgia that 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 which at first it was clear and then 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 frequent activities in water (eg, swimming, surfing, kayaking), history of preceding ear trauma (eg, forceful ear cleaning, use of cotton swabs, or water in the ear canal), pressure pain on tragus.7In severe condition, patient may complains pain while chewing or open mouth.

10,12

C. Predisposing Factors Anything that disrupts the epithelium of the ear canal canpermit invasion by bacteria that cause diffuse AOE. Commonpredisposing factors for AOE are humidity or prolongedexposure to water, dermatologic conditions (eczema, seborrhea, psoriasis), anatomic abnormalities (narrow 9

canal,

exostoses),

trauma

or

external

devices

(wax

removal,

insertingearplugs, using hearing aids), and otorrhea caused by middleear disease. AOE may also occur secondary to ear canalobstruction by impacted cerumen, a foreign object, a dermoidcyst, a sebaceous cyst, or a furuncle. 2 D. DIAGNOSIS A detailed recent and long term history are essential. A protracted, relapsing course suggests an eczematous base, fungal infection, or an occupational or “endogenous” disposition.14 An accurate, careful history taking and thoroughly physical examination can diagnose the acute otitis externa (AOE). Typically, patients present with 1.otalgia (70%), 2.itching (60%) or 3.fullness (22%), 4. with or without hearing loss (32%) or 5. ear canal pain when chewing. Many patients with AOE have discharge from their ear canal. A distinguishing sign of OAE from acute otitis media (AOM) with ottorhea is the finding of tenderness of the tragus when pushed and of the pinna when pulled in AOE. These signs are often intense and disproportionate to what might be expected based on visual inspection.15 Elements of the diagnosis of diffuse acute otitis externa, 1) Rapid onset (generally within 48 hours) in the past three weeks, AND 2) Symptoms of ear canal inflammation, including, otalgia (often severe), itching or fullness, WITH or WITHOUT hearing loss or jaw pain (pain in the ear canal and temporomandibular joint region intensified by jaw motion), AND 3) Signs of ear canal inflammation, including, tenderness of the tragus, pinna, or both, OR diffuse ear canal edema, erythema, or both WITH or WITHOUT ottorhea,

regional

lymphadenitis,

tympanic

membrane

erythema,

or

cellulitis of the pinna and adjacent skin. 2 Otoscopy may show a swollen, red, moist, macerated ear canal with a fetid, sticky discharge, or it may show a dry and perhaps scaly canal whose skin may be thin and “atrophic” or sticky and puffy. Stenosis of the ear canal is a common finding. Generally the tympanic membrane is intact in episodic otitis externa. Diffuse external otitis may develop as a sequel to acute

or

chronic

suppurative

otitis

media;

corresponding

tympanic

membrane changes are evident on otoscopy. Slight redness of the tympanic membrane does not necessarily signify middle ear involvement. 14 10

AOE can mimic the appearance of AOM because of erythema that involve the tympanic membrane. Distinguishing AOE from AOM is important because the latter may require systemic antimicrobials. Pneumatic otoscopy will demonstrate good tympanic membrane mobility with AOE but will show absent or limited mobility with AOM and associated middle-ear effusion. Similarly, tympanometry will show a normal peaked curve (type A) with AOE, but a flat tracing (type B) with AOM. The validity of acoustic reflectometry with AOE is unknown.2 Bacteriologic and mycologic smears from the external auditory canal can also be used in diagnosing acute otitis externa. A prolonged, recurrent, refractory course warrants dermatologic consultation to evaluate for eczema and/or examination to exclude diabetes and other predisposing factors.14 E. MANAGEMENT The four fundamental principles in the treatment of external otitis in all stages are frequent and thorough cleaning, judicious use of appropriate antibiotics, treatment of associated inflammation and pain, and recommendations regarding the prevention of future infections. In any stageof infection, thorough cleaning is a priority. Meticulous debridement of exfoliated debris, purulence, and cerumen will do as much ifnot more than simply placing thepatienton eardrops.8 Aural toilet can be done by dry mopping, suction clearance, irrigating the canal with warm, sterile normal saline or hydrogen peroxide, removal of obstructing cerumen or foreign object. After thorough toilet, a gauze wick soaked in antibiotic preparation is inserted into ear canal. Wick is changed daily for 2-3 days.2 Topical antibiotic preparations are recommended as initial therapy for diffuse, uncomplicated AOE. Antibiotic, which may be an aminoglycoside, polymyxin B, a quinolone, or a combination of these agents. A twice-daily (bid) dose regimen is adequate. Recent studies suggest that 7 days of therapy can be implemented, at least for quinolone antibiotics. Broad spectrum systemic antibiotics are used when there is cellulitis and acute tender lymphadenitis or in immunocopromised patients.

2

11

Other topical treatment includes acetic acid, boric acid, aluminum acetate, silver nitrate, and an endogenous antiseptic N-chlorotaurine. The rationale for the use of acetic acid is to return the pH to an acidic and make it more antimicrobial environment.Local steroid drops help to relieve edema and erythema, and prevent itching.2 The use of analgesics in acute otitis externa is to provide an adequate pain relief. Pain caused by AOE can be intense and severe, because the highly sensitive periosteum of the underlying bone is in close proximity to ear canal skin, especially in the deeper portion of the canal, Mild to moderate pain usually responds to acetaminophen or nonsteroidal antiinflammatory drugs given alone or in fixed combination with an opioid (eg, acetaminophen with codeine, oxycodone, or hydrocodone; ibuprofen with oxycodone). Opiods such as fentanyl citrate, morphine sulphate, and hydromorphone hydrochloride, are indicated for procedure-related pain and moderate to severe around-the-clock pain.2 Patient should be educated to resist manipulation to minimize ear trauma, minimize the introduction of water or moisture into the ear, insertion of hearing aids or ear phones should be limited until pain and discharge have subsided .2

12

Figure 6. Flow chart for managing acute otitis externa2 F.Complications Although complications associated with otitis externa are uncommon, there is a small risk of further problems developing. Some of the complications of otitis externa are such as malignant / necrotizing otitis externa,

perichondritis,

chondritis,

abscess,

cellulitis/

erysipelas

,

13

mastoiditis, bony erosion of the base of the skull (skull base osteomyelitis), central nervous infection, and lymphadenitis.

2,8

G. Prevention Strategies to prevent AOE are aimed at limiting water accumulation and moisture retention in the external auditorycanal and maintaining a healthy skin barrier. No randomizedtrials have compared the efficacy of different strategies to prevent AOE. Available reports include case series and expert opinion, which emphasize preventing moisture and waterretention in the external auditory canal. Recommendations to prevent AOE include removing obstructing cerumen; using acidifying ear drops shortly before swimming, after swimming, at bedtime, or all three; drying the ear canal with hairdryer; using ear plugs while swimming; and avoiding traumato the external auditory canal.2 But in using acidifying ear drops is still controversion. It

may can

make a changing in ear canal environment and it require clearly explanation to the patient about the function of that ear drops. The best prevention is maintaining the moisture of ear canal. Minimizing the usage of hearing aid and manipulation of ear canal.

14

III. CASE REPORT A. Identitiy • Name : Mrs. YS • Age : 28 years old • Sex : Female • Address : Prambanan • M. R. : 10337XX B.

Anamnesis

Main complaint

: Pain on the left ear

History of present illness : Patient came to the ENT Polyclinic, with left ear pain, since 4 days ago. Together with pain, there were also itchiness and sensation of aural fullness, on the left ear. There were no blood nor fluid coming out from the ear. Patient admitted to using cotton bud frequently to relieve the itching sensation. Patient denied the entrance of water or any other foreign objects into the ear. Other complaints such as reduced hearing ability, tinnitus, dizziness, cold, fl u, sore throat or fever were also denied. There were also no complaints on the right ear. Patient had no complaints on nose, mouth and throat. History of past illness : Patient never had similar complaint in the ear previously. There is no history of asthma, allergy,gastritis, hypertension, diabetes mellitus, and surgery. Patient have not consulted a doctor nor taken any medication for the current complaint. History of family illness : There is no history of similar complaints, asthma, allergy, hypertension, and diabetes mellitus. Anamnesis Summary • Pain in the left ear. • Itchiness on left ear. • Sensation of aural fullness in the left ear.

C.

Physical Examination

General status : Good, compos mentis, vital sign: BP 90/60 mmHg, pulse: 78x/minute, RR : 20x/minute, T : 36,7 oC, VAS : 6 15

ENT status Ear Outer ear

Ear canal

Tympanic

Right ear no lesion, no

Left ear Hyperemic

hyperemic, no

(-),edema(-), pain on

mass, no edema

tragus palpation and

no discharge, no

retraction(+) hyperemic(+),edema

hyperemic, no

(+)

mass, no edema Intact, cone of light

membrane

(+)

Unable to asses

Nose and Paranasal Sinuses Right Inspectio n Palpation Anterior rhinosco py Posterior rhinosco py

Left

Within normal limit

Within normal limit

no tenderness no tenderness discharge (-), edematous conchae(-),septal deviation (-) , mass (-)

discharge (-), edematous conchae(-),septal deviation (-) , mass (-)

Mouth and Throat Lips

Within normal limit

Gum & teeth

Within normal limit

Tongue

Within normal limit

Palate

Within normal limit

Uvula Tonsil

Within normal limit T1-T1, hyperemic

Posterior

(-),

widenedcrypt (-) Within normal limit

oropharynx 16

Indirect

Within normal limit

laryngoscopy D. Diagnosis Diffuse Acute Otitis Externa of the left ear E.

Management & Treatment R. ear drop Otilon fl I S. 3 dd 3 gtt AS R. Tab. Diclofenac Potassium mg 50 No. XVIII S. 2 dd Tab I p.c Education 

The patient should meet the doctor for follow-up to know the



progress of the disease. Take care of the ear hygiene, keep the ear dry and prevent the



entrance of water or any foreign objects into the ear. Prevent frequent cleaning and scratching with cotton buds. E.

Planning

Patient is advised to follow up after 5 days to evaluate the condition of the ear. F.Follow Up On the follow up visit, pain on the left ear and edema of the left ear canal was resolved and no longer erythematous.

G.

Prognosis

Dubia ad bonam H.

Problem

Treatment

17

III. Discussion

Acute otitis externa is diagnosed clinically based on 1) a rapid onset (generally within 48 hours) in the past 3 weeks with 2) signs and 3) symptoms of ear canal inflammation 2 The clinical course of external otitis may

be

divided

into

the

following

stages:

preinflammatory;

acute

inflammatory, which can be mild, moderate, or severe; and chronic inflammatory15 The main findings of our patient through history taking were four days of ear pain, itchiness, and aural fullness in the left ear; in physical examination, there was tenderness and pain of the tragus on palpation and when retracted; while in otoscopic examination, we found that the ear canal of the left ear was erythematous with edema. Tympanic membrane of the left ear was unable to asses. Our patient is hence diagnosed with diffuse acute otitis externa of the left ear (mild acute inflammtory stage). The four fundamental principles in the treatment of otitis externa in all stages are 1) frequent and thorough cleaning, 2) judicious use of appropriate antibiotics, 3) treatment of associated inflammation and pain, and 4) recommendations regarding the prevention of future infections. In any

stageof

infection,

thorough

cleaning

is

a

priority.

Meticulous

debridement of exfoliated debris, purulence, and cerumen will do as much if not more than simply placing thepatient on ear drops. 15 In the preinflammatory stage, a complete cleaning may be all that is required. In the absence of purulence, a brief course of an acidifying drop such as aluminium sulfate-calcium sulfate (Domeboro) is efficacious in discouraging bacterial or fungal growth.15 Treatment of the acute inflammatory stage varies with the extent of disease. In the mildest form, cleaning as above is indicated. An antibiotic otic drop is recommended to cover what is probably a Pseudomonas infection. At this stage, edema of the EAC should not be severe, and the patient should be able to instill drops into the ear by tilting the head to the side or by lying down with the involved ear upright.15 In the moderate stage of inflammation, edema of the canal may interfere with the instillation of drops. When there is marked canal edema, a wick of compressed cellulose or ribbon gauze may be placed in the canal and instill drop on it to facilitate antimicrobial or antibiotic administration. 18

Wick placement permits antibiotic drops to reach portions of the external auditory canal that are inaccessible because of canal swelling. Often the canal may accommodate two or even three wick. As the wick expands, it presses the soft tissues and periosteum toward the nondistracted position; this alone may relieve pain. As the canal responds to treatment and patency returns to the ear canal, the wick often falls out.15 All instrumentation of the ear is best done under the microscope. The wick is removed by the physician at the time of re-examination. If the edema has not been significantly reduced, repacking is indicated. Antibiotic drops should be continued for at least 2 to 3 days after the cessation of pain, itching, and drainage so that complete eradication of infection may be ensured. Also in this stage, an oral analgesic is often prescribed because pain can be pronounced. If the infection has not spread beyond the boundaries of the external canal, the use of oral antibiotics will be of little if any value.15 In the severe stage, infection usually extends beyond the limits of the canal. In addition to the cleaning, packing, and use of antibiotic drops as discussed previously, attends to any soft tissue involvement by using an oral antibiotic with broad-spectrum coverage. Successive generations of the cephalosporins widen gram-negative coverage at the expense of grampositive coverage. In addition to anti-Pseudomonas ear drops, common choices of oral antibiotics are one of the antipseudomonal fluoroquinolones such as ciprofloxacin or levofloxacin, antistaphylococcal penicillins, or cephalosporins.

The

fluoroquinolone

antibiotics

are

effective

against

Pseudomonas species. In children under 12 years old, one should check with the pediatrician prior to starting oral fluoroquinolones. Warm soaks (normal saline or a mild aluminum sulfate- calcium acetate solution) are also useful in the treatment of the crusting and edema involving the auricle and surrounding skin. Culture of the canal for aerobic bacteria and/ or fungi is indicated only for the severe stage or for patients who have previously been treated without resolution. Treatment is generally continued for 10 to 14 days if there is a good response. In rare patients who do not respond to this regimen, hospitalization and vigorous daily local care, repeat culturing, and intravenous antibiotics are indicated.15 The chronic stage of external otitis is manifested by marked thickening of the skin of the EAC due to long-standing infection. Examination 19

reveals flakes of dry scaly skin in the canal. Although removal of debris isrecommended, this may be difficult due to the narrowing of the lumen of the canal. Repeated cleaning and instillation of antibiotics and steroids are indicated. Triamcinolone acetonide 0.25% cream or ointment (Kenalog), fluocinolone 0.01% oil (DermOtic), or dexamethasone sodium phosphate 0.1% ophthalmic drops (Decadron, Pred Forte 1%) may be used.15 In all cases of acute or chronic external otitis, instruct the patient to avoid future infections by not instrumenting the ear. Foreign objects such as Q-tips often excoriate the canal skin and push debris further into the canal rather than remove it. Swimmers should be taught to towel dry the concha and lateral canal, to shake water out of the canal, or to instill an acidifying drop after swimming, Also, patients who have repeated infections despite adhering to these measures are best advised to use an acidifying drop composed of equal measures of vinegar and water, or ethyl alcohol and water, when exposed to high humidity. One should suspect otomycosis if all other reasonable measures have failed and should treat with drying agents, especially powders. Custom-made ear molds are useful for these patients. A final office visit is important to ensure that the infection has completely resolved and the canal is back to its normal state.15 In our case, Otilon ear drop (3 drops each time, 3 times per day) was prescribed as topical therapy for left ear and an oral analgesic, diclofenac potassium (1 tablet each time, 2 times per day) was given to ease the pain of the patient. Our patient was advised to come back for the next visit after 5 days to evaluate the condition of the ear. Also, the patient was advised to take care of her ear hygiene, keep the ear dry and prevent the entrance of water or any foreign objects into the ear and avoid cleaning or scratching the ear with cotton buds. Topical preparations are recommended as initial therapy for diffuse, uncomplicated AOE because of safety, efficacy over placebo in randomized trials, and excellent clinical and bacteriologic outcomes in comparative studies. There are no data on the efficacy of systemic therapy with the use of appropriate antibacterials and stratified by severity of the infection. Moreover, orally administered antibiotics have significant adverse effects that

include

rashes,

vomiting,

diarrhea,

allergic

reactions,

altered

nasopharyngeal flora, and development of bacterial resistance. 2 20

An advantage of topical therapy is the very high concentration of antimicrobial that can be delivered to infected tissue, often 100 to 1000 times higher than can be achieved with systemic therapy. For example a 0.3% solution of antibiotic (a typical concentration in commercial otic drops) has a concentration of 3000 mcg/mL. Any organisms known to cause AOE, even those considered “resistant,” will be unlikely to survive contact with this antibiotic concentration. Because there are between 10 to 20 drops/ mL, depending on the nature of the liquid (solution vs suspension, viscosity, etc), each dose of 3 to 5 drops contains about 0.5 to 1.5 mg of antibiotic. Topical therapy avoids prolonged exposure of bacteria to subtherapeutic concentrations of antibiotic, and may therefore be less likely than systemic therapy to result in selective pressure for resistant organisms. The avoidance of antibiotic exposure of host bacteria resident outside the ear canal, as occurs with systemic therapy, provides a further advantage to the reduction of the selection of resistant microorganisms. Restrictive use of oral antibiotics for AOE is important because of the increased resistance among common AOE pathogens, especially S. Aureus and P. Aeruginosa2

21

IV. Conclusion A 28 year old female patient diagnosed with diffuse acute otitis externa of the left ear. The patient was treated with Otilon ear drop and an oral analgesic for 5 days and was advised to take care of her ear hygiene, keep the ear dry and prevent the entrance of water or any foreign objects into the ear and avoid cleaning or scratching the ear with cotton buds. On the follow up visit, pain on the left ear and edema of the left ear canal was resolved and no longer erythematous.

22

REFERENCES

1.

Clark WB, Brook I, Bianki D, Thompson DH. Microbiology of otitis externa. Otolaryngol Head Neck Surg. 1997 Jan. 116(1):23-5.

2.

Rosenfeld RM, Schwartz SR, Cannon CR, et al. American Academy of Otolaryngology-Head

and

Neck

Surgery

Foundation.

Clinical

practice

guideline: acute otitis externa. Otolaryngol Head Neck Surg. 2006;150(suppl 1):S1-S24. 3.

Roland

PS,

Stroman

DW.

Microbiology

of

acute

otitis

externa.

Laryngoscope. 2002;112:1166-1177. 4.

Osguthorpe JD, Nielsen DR. Otitis externa: review and clinical update. Am Fam Physician. 2006;74:1510-1516.

5.

Rowlands S, Devalia H, Smith C, et al. Otitis externa in UK general practice: a survey using the UK General Practice Research Database. Br J Gen Pract. 2001;51:533-538.

6.

Moore, et al. Moore clinically oriented anatomy. 7 th ed.Baltimore, Lippincott Williams & Wilkins.2014

7.

Krause, WJ. Krause’s Essential Human Hystology for Medical Student. 3rd edition. 2005

8.

Johnson Jonas T., Rosen Clark A., Bailey’s Head &Neck Surgery Otolarynology. 5th edition. Baltimore, Lippincott Williams & Wilkins, 2014; Vol 2:2335-2340

9.

Waitzman AA, MD. Otitis Externa. Canadian Society of OtolaryngologyHead & Neck Surgery, American Academy of Otolaryngology-Head and Neck Surgery,American Medical Association, Michigan State Medical Society, 2014 Dec 29 1;58(4):446-452

10.

Bluestone R. CD, Et all. Pediatric Otolaryngology, 2nd ed., Philadelphia ;

WB. Saunders Company, 1990: 312 – 4 23

11.

Sander M, MD. Otitis Externa: A Practical Guide to Treatment and

Prevention. Medical College of Wisconsin, Milwaukee, Wisconsin. Am Fam Physician. 2001 Mar 1;63(5):927-937. 12.

Lee KJ. Essential Orolaryngology. Head and Neck Surgery 8 th edition

McGraw-Hill. New York 2003. 841-44 13.

Austin

DF.

Anatomy

of

the

ear.

In:

Ballenger

JJ.16

Editors.

Otolaryngology head and neck surgery 15 th Ed. Baltimore, Philadelphia, WB Saunders Co. 2003 14.

Naumann HH, Martin F., Shcerer H., Schorn K. 1993. Differential

Diagnosis

of

Otorhinolaryngology;

Symptoms,

Syndromes

Interdisciplinary Issues. Thieme Medical Publisher, Inc. 15. Hui CP, Canadian Paediatric Society, Infectious

Diseases

and and

Immunization Committee. Acute otitis externa. Paediatrics & Child Health. 2013;18(2):96-98.

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