The Nose Knows - ENT for the Family Physician
Jennifer Caudle, DO
ACOFP FULL DISCLOSURE FOR CME ACTIVITIES Please check where applicable and sign below. Provide additional pages as necessary.
Name of CME Activity: ACOFP Intensive Update and Board Review in Osteopathic Family Medicine
Dates and Location of CME Activity: August 21-24, 2014, InterContinental Chicago O'Hare, Rosemont, IL
Topic(s): The Nose Knows - ENT for the Family Physician Saturday, 8/23/14 1:45-2:15pm
Name of Faculty/Moderator: Jennifer Caudle, DO
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Signature: Jennifer Caudle, DO Date: 6/1/14
Jennifer Caudle, DO
Please fax this form to ACOFP at 866-328-1835 or email to [email protected] as soon as possible
Deadline: Saturday, May 31, 2014
8/6/2014
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EAR NOSE & THROAT DR. JENNIFER CAUDLE
ASST PROFESSOR, DEPT OF FAMILY MEDICINE
3RD YEAR FM CLERKSHIP DIRECTOR
ROWAN UNIVERSITY SCHOOL OF OSTEOPATHIC
MEDICINE
ACOFP Family Medicine Board Review
August 23, 2014
Otolaryngology Topics
Dizziness
Hearing Loss
Rhinosinusitis
Otitis Externa
Hoarseness & SCC of Larynx
Dizziness
Dizziness: A Diagnostic Approach ROBERT E. POST, MD, LORI M. DICKERSON, PharmD, Medical University of South Carolina,
Charleston, South Carolina. Am Fam Physician. 2010 Aug 15;82(4):361-368.
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Dizziness
Disturbance of the sensory modalities which allow perception of body's motion and position in space
vision
vestibular input
joint position
touch
hearing
CC in ~ 3% of primary care visits for patients 25 years and older
The final cause of dizziness is not identified in up to one in five patients.
Categories of Dizziness
1. Vertigo - Central Origin (Brainstem, Cerebellum, etc)
- Peripheral Origin
A. Benign paroxysmal positional vertigo (BPPV)
B. Meniere disease
C. Vestibular neuritis
D. Labyrinthitis
E. Migrainous vertigo / vestibular migraine
2. Presyncope
3. Lightheadedness
4. Disequilibrium
Symptoms
Vertigo
Perceived sense of motion, spinning sensation (45 - 54%)
Pre-syncope
Feeling of losing consciousness or blacking out (~14%)
Lightheadedness
Vague symptoms, feeling disconnected with the environment (~10%)
Disequilibrium
Feeling off-balance or wobbly (~16%)
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1. Vertigo
Perceived sense of motion, possibly spinning
sensation
1. Central Origin 2. Peripheral Origin (MCC of vertigo)
Peripheral Vestibular Disorders
Peripheral vestibular disorders are the MCC of
Vertigo:
A. Benign paroxysmal positional vertigo (BPPV)
B. Meniere disease
C. Vestibular neuritis
D. Labyrinthitis
E. Migrainous vertigo / Vestibular migraine
Peripheral Vestibular Causes of Vertigo
A. Benign Positional Paroxysmal Vertigo
MCC of peripheral vestibular vertigo
Pathophysiology
Crystalline debris forms/moves in semicircular canals which
causes labyrinthine irritation vertigo & nystagmus. Head
movement often cause symptoms.
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Benign Positional Paroxysmal Vertigo
Symptoms/Diagnosis
Brief episodes of vertigo (2-10 seconds)
Nystagmus and vertigo often caused by turning the head
Dix-Hallpike Maneuver
Reproduces vertigo, resulting in nystagmus
Diagnostic if (+) but does not rule it out if (-). Sensitivity =
50–88% for BPPV.
Has a PPV of 83% and a negative predictive value of 52%
for the diagnosis of BPPV
BPPV Diagnosis: Dix-Hallpike
Maneuver
The patient is seated, the physician (A) turns the patient's head 45 degrees to one side, then (B) rapidly lays the patient into a supine position with the head hanging about 20 degrees over the end of the table, observing the patient's eyes for approximately 30 seconds. The maneuver is repeated for the opposite side. Nystagmus is diagnostic of vestibular debris in the ear facing down, closest to the exam table. A video demonstration of this maneuver is available at http://www.youtube.com/watch?v=vRpwf2mI3SU.
Dizziness: A Diagnostic Approach ROBERT E. POST, MD, LORI M. DICKERSON, PharmD, Medical University of South Carolina, Charleston,
South Carolina. Am Fam Physician. 2010 Aug 15;82(4):361-368.
Benign Positional Paroxysmal Vertigo
Treatment Epley, modified Epley and Semont maneuvers (slide at end of lecture)
Canolith repositioning maneuvers. Goal is to reposition the
crystals into the vestibule.
80% success rate in relieving symptoms
Often resolves with time whether or not exercises are done
Vestibular Rehabilitation
Should not be routinely treated w vestibular suppressants, i.e
antihistamines or benzodiazepines
Potential side effects including drowsiness, cognitive side effects,
etc., & may interfere with CNS compensation for vestibular injury
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Treatment: Epley maneuver
Dizziness: A Diagnostic Approach ROBERT E. POST, MD, LORI M.
DICKERSON, PharmD, Medical University of South Carolina, Charleston,
South Carolina. Am Fam Physician. 2010 Aug 15;82(4):361-368.
Peripheral Vestibular Causes of Vertigo
B. Meniere's disease
Pathophysiology (‘endolymphatic hydrops’)
Buildup of fluid in endolymphatic system, caused by excess
fluid production or decreased fluid resorption. This results in
dilation of the endolymphatic system.
Symptoms/Diagnosis
Recurrent episodes of vertigo that last hours (not mins or
days)
Sensorineural low-frequency hearing loss
Tinnitus
Aural fullness in affected ear
Meniere's disease
Treatment No cure, aim for symptom reduction
Salt restriction
Diuretic therapy, HCTZ
If acutely sensitive to ETOH, Caffeine or both, avoid these
Anti-emetics
Benzodiazepines
Surgical decompression of endolymphatic system for refractory patients
EPLEY MANEUVER & STEROIDS= NOT HELPFUL
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Peripheral Vestibular Causes of Vertigo
C. Vestibular Neuronitis
Pathophysiology Inflammation of the vestibular nerve with total sparing of the
cochlear area.
Symptoms/Diagnosis Often associated with viral infection
Severe prolonged vertigo (days) with ataxia, nausea and vomiting.
NO hearing loss, no tinnitus, no aural pain
Symptoms often initially severe and gradually decrease over 1-2 weeks.
Reduced/absent caloric response, at least initially
Vestibular Neuronitis
Treatment
Rest
Reassurance and anti-emetics
Vestibular suppressants (diazepam, meclizine)
Vestibular Rehab, Surgery (possibly for refractory cases)
Peripheral Vestibular Causes of Vertigo
D. Labyrinthitis
Pathophysiology
Inflammation of the labyrinthine organs.
Symptoms
Often associated w/ otitis media or URI (viral or
bacterial infection).
Severe vertigo, can last > days
Tinnitus
Sensorineural hearing loss
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Labyrinthitis
Diagnostic Clue
Labyrinthitis and vestibular neuronitis can occur after URI
or viral/bacterial infection, but labyrinthitis has tinnitus
and hearing loss (vestibular neuritis has neither)
Treatment
Rest, anti-emetics, antibiotics (if bacterial etiology)
Distinguishing Vertigo
VERTIGO With
Hearing
Loss
Without
Hearing
Loss
Tinnitus Without
Tinnitus
Episodic
Vertigo
Persistent
Vertigo
Associated
With URI
Meniere's
Disease
X X X
BPPV X X X
Vestibular
Neuritis
X
X
X
X
Labyrinthitis X X X X
E. Migrainous Vertigo/
Vestibular migraine
Symptoms Episodic vertigo with a current migraine or history of
migraine and one of the following during at least two
episodes of vertigo:
migraine headache
photophobia
phonophobia
aura
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2. Presyncope
Feeling of losing consciousness or blacking out
Cardiovascular causes include: Arrhythmias
Myocardial infarction
Carotid artery stenosis
Ortho-static hypotension.
Symptoms caused by postural changes suggest orthostatic hypotension.
Many cardiovascular medications increase the risk of orthostatic hypotension in older persons, including reserpine (at doses > 0.25 mg), doxazosin, and clonidine.
3. Lightheadedness
Vague symptoms, feeling disconnected with the environment
Psychiatric causes of lightheadedness are common Anxiety
Depression
Depression and alcohol intoxication have also been found to overlap with dizziness.
Hyperventilation syndrome causes lightheadedness. Patients may sigh repeatedly, have chest pain, paraesthesias, bloating, and epigastric pain.
4. Disequilibrium
Sense of feeling off-balance
Potential causes include:
Stroke
Poor vision
Parkinson disease
Peripheral neuropathy
Musculoskeletal disorders
Meds: Benzodiazepines and tricyclic antidepressants increase the risk of ataxia and falls in older persons.
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Dizziness: A Diagnostic Approach ROBERT E. POST, MD, LORI M. DICKERSON, PharmD, Medical University of South Carolina, Charleston, South Carolina. Am Fam Physician. 2010 Aug
15;82(4):361-368.
Hearing Loss
Hearing loss
Normal conversations use frequencies of 500 to
3,000 Hz at 45 - 60 dB.
After 60 years of age, hearing declines by about
1 dB annually.
Men usually experience greater hearing loss
and earlier onset compared with women.
Hearing Loss
Sensorineural Conductive
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Sensorineural vs Conductive
Hearing Loss
Sensorineural hearing loss
Problem converting mechanical vibrations to electrical potential in the cochlea and/or in auditory nerve transmission to the brain. Usually caused by permanent damage in the organ of Corti.
Conductive hearing loss
Usually caused by problems in the external or middle ear that interfere with transmitting sound and its conversion to mechanical vibrations.
Sensorineural Hearing Loss
>90% of older persons with hearing loss have age-related sensorineural hearing loss
Presbycusis= hearing loss related to aging.
Symptoms
Gradual, high-frequency, symmetric loss of hearing, worse in noisy environments.
Pathophysiology
Degenerative changes in the hair cells, auditory neurons and cochlear nuclei. (noise trauma; meds; autoimmune d/o; mechanical trauma; Meniere disease; infection)
Treatment Hearing Aid
Conductive Hearing loss
Symptoms Gradual hearing loss (otosclerosis), laterality (obstruction),
rapid onset (TM perforation).
Pathophysiology Pathologic- damage to TM or ossicular chain in middle ear
Cerumen; foreign body; perforated tympanic membrane; tympanosclerosis; Otitis media with effusion; otosclerosis; cholesteatoma.
Otosclerosis= spongy bone replaces normal bone in otic capsule causing ankylosis/fixation of stapes
Treatment Tx underlying cause
Surgical
Hearing aid (otosclerosis)
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Sensorineural hearing loss
Sudden Sensorineural Hearing Loss (SSNHL)
Otologic emergency, requiring prompt evaluation
Etiologies include vascular, thromboembolic, viral,
autoimmune and ototoxicity
Without treatment: 1/3 lose hearing, 1/3 have
partial improvement in hearing and 1/3 regain
hearing
Steroids
Diagnosing Hearing Loss
Weber Test
Tuning fork on the skull in midline (both cochlae stimulated)
Normal exam= sound heard midline or equally in both ears.
If conductive hearing loss in 1 ear, the sound will be loudest in that same ear (will lateralize)
When unilateral sensorineural hearing loss is present, tone is heard in unaffected / opposite ear
Rinne Test
Tuning fork is placed at mastoid bone, when can no longer hear sound, the tuning fork is placed in front of ear.
Compares air conduction (AC) with bone conduction (BC)
Normally AC > BC- which means that sound in front of pinna is normally perceived twice as long as sound placed on mastoid process (AC>BC)
Conductive Hearing loss= AC < BC (negative Rinne) or BC= AC
Sensorineural hearing loss= duration of both AC and BC are reduced, but 2:1 ratio remains the same (Pos Rinne)- AC > BC
Rhinosinusitis
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Rhinosinusitis
Pathophysiology
Inflammation of the mucosa of 1 or more of the paranasal
sinuses, usually occurs with rhinitis
Causes include mucosal edema, impaired local immmunity
and ciliary dysfunction which impaired sinus drainage
and mucous stasis. Bacterial infection.
Rhinosinusitis
The American Academy of Otolaryngology–Head and Neck
Surgery defines subtypes of rhinosinusitis based on symptom
duration:
Acute, sub-acute, recurrent acute, and chronic
Acute rhinosinusitis is further categorized as bacterial or viral.
Rhinosinusitis Duration of Symptoms
Acute Up to 4 weeks
Subacute At least 4 weeks, but less than
12weeks
Recurrent Acute 4 or more episodes/year with
remission btw episodes (each lasting 7
days at least)
Chronic 12 weeks or longer (variable)
Acute Rhinosinusitis in Adults. ANN M. ARING, MD, and MIRIAM M. CHAN, PharmD, Riverside Methodist Hospital, Columbus, Ohio. Am Fam
Physician. 2011 May 1;83(9):1057-1063.
Acute Rhinosinusitis
Making the Dx of Rhinosinusitis
Major vs Minor criteria Major- facial pain and pressure, nasal congestion and obstruction, nasal
discharge, discolored posterior discharge, anosmia or hyposmia, fever and purulence on intranasal exam
Minor- headache, otalgia or ear pressure, halitosis, dental pain, cough, fever (irritability in children).
Dx probable if 2 or more major factors or 1 major and 2 or more
minor factors are present
Dx suggestive if 1 major factor or 2 minor factors are present
IDSA: these diagnostic criteria do not adequately distinguish
bacterial from viral infection.
According to the 1996 Task Force on Rhinosinusitis, by Amer Acad of Otolaryngology- Head and Neck Surgery, via Rakel
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Acute Rhinosinusitis
Risk Factors
Rhinitis
Anatomic abnormalities (septal deviation, choanal atresia,
foreign body, etc)
Nasal polyps
Immunodeficiency
Kartagener’s syndrome (primary ciliary dysfunction)
Smoking, nasal decongestant abuse or cocaine abuse
(ciliary dysfunction)
GERD
Acute Rhinosinusitis
Etiology
Viral MCC of rhinosinusitis; prevalence 90-98%
MC viruses are rhinovirus, adenovirus, influenza virus, and parainfluenza virus.
In most patients improves in 7-10 days w/o treatment.
Mild symptoms < 7 days duration can be managed with supportive care: Analgesics, Saline nasal irrigation, Intranasal corticosteroids.
Symptom persistence increases likelihood of bacterial infection
Acute Rhinosinusitis
Etiology, cont’d
Bacterial Prevalence is 2-10%
MCC causes are 1) Pneumococcus spp., 2) Haemophilus influenzae, 3) Moraxella catarrhalis (beta-lactamase production is common), Staph (esp in chronic).
Allergic, Fungal, etc
June 2013, AAP released new guidelines for Sinusitis in children
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Acute Rhinosinusitis
Complications
Periorbital cellulitis
Orbital abscess
Cavernous sinus thrombosis
Meningitis
Intracranial abscess
Osteomyelitis
Mucocele
Making the Diagnosis of
Acute Bacterial Rhinosinusitis
IDSA Guidelines 2012
Symptoms lasting ≥ 10 days without evidence of clinical
improvement (strong, low moderate)
Onset with severe symptoms/signs of high fever [102F] and purulent nasal discharge or facial pain lasting for at least 3–4 consecutive days at the beginning of illness (strong, low-moderate)
‘‘Doublesickening.’’ Worsening symptoms or signs [new onset of fever, headache, or increase in nasal discharge] following a typical viral upper respiratory infection that has lasted 5–6 days and was initially improving (strong, low-moderate).
Oral Antibiotics for ABRS
(IDSA 2012 Guidelines)
Initial Empiric Tx = Amoxicillin/Clavulanate (changed from amox alone)
Amoxicillin/Clavulanate 500 mg/125 mg q8 or 875
mg/125 mg q12
Recommended length of tx = 10 days. (3-5 day tx may
be effective/have fewer adverse effects.)
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Can “High Dose Amox” be used for
Initial Empiric Therapy?
Yes! Amoxicillin/Clavunate 2 g po bid or 90 mg/kg/day po bid CAN be used as initial empiric therapy in the following situations:
Adults with ABRS from areas with high endemic rates (≥10%) of invasive penicillin-nonsusceptible S. pneumoniae,
Severe infection (eg, evidence of systemic toxicity with fever of 39C [102F] or higher, and threat of suppurative complications)
Daycare attendance
Age <2 or >65 years
Recent hospitalization
Antibiotic use within the past month
Immunocompromised
Alternatives to Amox/Clavulanate as
Empiric Therapy:
Alternatives to Amoxicillin/Clavulanate for initial empiric therapy include (PCN allergy, etc) :
Doxycycline 100 bid or 200 qdaily: Highly active against respiratory pathogens and with excellent pharmacokinetic/dynamic properties
[Fluoroquinolones (2nd line)]
The following are NO LONGER recommended as alternatives to amoxicillin/clavulanate according to IDSA: 2nd / 3rd generation cephalosporins (as monotherapy) due to variable rates of
resistance
Trimethoprim/sulfamethoxazole- high rates of resistance against S.pneumoniae and H. Influenza
Macrolides: Azithromycin, Clarithromycin- due to high rates of resistance among S. pneumoniae (strong, moderate)
Oral Antibiotics for ABRS
For moderate disease, recent antibiotic
use, or failed initial therapy, the following ARE recommended:
Amoxicillin/clavulanate XR 2,000 mg/125 mg bid for
10 days
Levofloxacin 500 mg qdaily for 10 to 14 days or 750 mg qdaily for 5 days
Moxifloxacin 400 mg per day for 10 days
IDSA.
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Chronic Sinusitis
Pearls:
Imaging is not recommended for uncomplicated
sinusitis (grade b/c).
CT is the most sensitive test for detecting
maxillary sinusitis
Otitis Externa
Otitis Externa
Inflammation/infection of the external auditory canal and/or auricle
Pathophysiology
Glands in ear canal produce cerumen that provides protection via a antimicrobial lysozyme. Cerumen has a pH level of 6.9, which discourages microbial growth.
Risk factors for otitis externa include:
Absence of cerumen (excessive cleaning)
Thickened cerumen fosters retention of H20 and debris
Water (macerates skin of canal and raises pH)
Trauma (cotton swab or foreign body)
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Symptoms
Otalgia
Itching
Fullness
With or without hearing loss or jaw pain
Tenderness of the tragus or pinna
Diffuse ear edema or erythema or both
With or without otorrhea
Regional lymphadenitis
Tympanic membrane erythema
Cellulitis of the pinna
Otitis Externa
Causes:
Pseudomonas aeruginosa (50%)
Staph aureus (23%)
Anaerobes and gram-negative organisms (12.5%)
Fungi; Aspergillus and Candida species (12.5%).
Others = furunculosis, seb derm, psoriasis, contact dermatitis
Necrotizing "malignant" otitis externa
infection that extends into deep tissues adjacent to the auditory
canal.
may cause cellulitis and osteomyelitis
RF= immunocompromised, diabetes mellitus
rarely described in children.
Otitis Externa
Topical Antibiotic Treatments
Neomycin, polymyxin B, hydrocortisone. Neomycin sensitizing in 5 to 18 percent of patients; ototoxic potential
Fluoroquinolone, with or without steroid. Minimally irritating and infrequently sensitizing; only agent approved if tympanic membrane is perforated
Aminoglycoside- Usually ophthalmic preparation (e.g., gentamicin, tobramycin) but also for bacterial acute OE; minimally irritating; ototoxic potential
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Otitis Externa
Other Topical Preparations
Steroid. For underlying dermatitis (e.g., atopic, psoriasis) if it is the cause of chronic OE; cutaneous atrophy with prolonged use
2.0% acetic acid (Vosol), with or without steroid. OE of bacterial or fungal origin in immunocompetent patients;
2.75% boric acid or 90% to 95% isopropyl alcohol. OE of bacterial or fungal origin in immunocompetent patients, but mainly applied as prophylaxis after swimming.
Tolnaftate (Tinactin) or clotrimazole (Lotrimin). OE of fungal origin solution easier than cream; minimally irritating
Hoarseness
Hoarseness
Any patient with hoarseness lasting longer than two weeks in the absence of an apparent benign cause requires a thorough evaluation of the larynx by direct or indirect laryngoscopy.
Causes of Chronic Hoarseness
Malignancy
GERD
Polyps
Nodules
Functional voice disorders
Neurological disorders
Causes of Acute Hoarseness
Vocal abuse
Laryngitis
Smoking
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Hoarseness
Important points
Cough- could indicate inflammation of vocal cords or Cancer of larynx or lung
Dysphagia/odynophagia= disorders of pharynx and esophagus
Hemoptysis with hoarseness should be considered malignancy until proven otherwise
Take note of smoking history
Visualization of the larynx by direct or indirect laryngoscopy is absolutely necessary for all patients with hoarseness that does not resolve on its own or with medical therapy.
Referral to ENT
SCC of the larynx
Hoarseness can be a very early symptom of
SCC of larynx and should never be simply
attributed to “laryngitis” without proper
evaluation
Detection of cancer requires visualization of
the larynx
Indirect or direct laryngoscopy usually shows
Well-circumscribed exophytic lesion in endolarynx
most frequently on one of the true vocal cords
SCC of the larynx
Squamous cell carcinoma of the larynx is the
most common malignancy of the larynx
Peak age= 60-65 y/o, Men > women
Malignancies of larynx are MC in smokers
and ETOH abusers
When both factors are present, the risk of cancer
becomes 50% greater than additive risk of each
Only 2-5% of laryngeal cancer patients have no
history of smoking
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Additional Slides
Vertigo:
Peripheral vs. Central
Peripheral vestibular disorder
Originates from vestibular nerve and inner ear
Vertigo often episodic
Not associated with neurology symptoms or LOC
Nystagmus is usually horizontal and rotational
Central vestibular disorder
Originates from cerebellum, brainstem, thalamus, cortex
Vertigo often constant
MAY be associated with neurological symptoms or LOC
Nystagmus is purely horizontal, vertical or rotational
BPPV treatment:
Description of the Epley Maneuver
Epley maneuver (canalith repositioning). (A) The patient sits with head rotated 45 degrees to the right.
(B) Physician lays the patient into supine position with head hanging over the end of the table.
(C) The head is then rotated 90 degrees to the left
(D) Head and body are rotated together an additional 90 degrees until the patient is 135 degrees from the initial supine position.
(E) Patient is brought to a sitting position while the head remains tilted. Finally, the head is brought forward and downward to an angle of 20 degrees. The physician should pause at each position until nystagmus resolves, and repeat the series until no nystagmus is present.
A video demonstration of this maneuver is available at: http://www.youtube.com/watch?v=ZqokxZRbJfw&NR=1
Dizziness: A Diagnostic Approach ROBERT E. POST, MD, LORI M. DICKERSON, PharmD, Medical University of South Carolina, Charleston,
South Carolina. Am Fam Physician. 2010 Aug 15;82(4):361-368.
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Prevention Tips for Otitis Externa
Prevention
Who needs prevention? Immunocompromised; systemic dermatologic condition, contact sensitivities to an ototopical agent, excessive perspiration excessively; when water sports activities are common
Can use acidifying or alcohol drops during the at-risk period (e.g., swim season, scuba diving trip)
Use of a hair dryer with or without a head tilt to aid fluid clearance
Avoid of cotton swabs.
Use of hypoallergenic ear canal molds with or without tight swim caps to reduce infections is controversial.
Bibliography
Treatment of Vertigo. RANDY SWARTZ, M.D., University of California, San Diego, School of Medicine, La Jolla. PAXTON LONGWELL, M.D., California; Corpus Christi, Texas. Am Fam Physician. 2005 Mar 15;71(6):1115-1122.
Dizziness: A Diagnostic Approach. ROBERT E. POST, MD, LORI M. DICKERSON, PharmD, Medical University of South Carolina, Charleston, South Carolina. Am Fam Physician. 2010 Aug 15;82(4):361-368.
Initial Evaluation of Vertigo. RONALD H. LABUGUEN, M.D., University of Southern California, Los Angeles, California. Am Fam Physician. 2006 Jan 15;73(2):244-251..
Hearing Loss in Older Adults. ANNE D. WALLING, MB, ChB, and GRETCHEN M. DICKSON, MD, MBA. University of Kansas School of Medicine—Wichita, Wichita, Kansas. Am Fam Physician. 2012 Jun 15;85(12):1150-1156.
Acute Rhinosinusitis in Adults. ANN M. ARING, MD, and MIRIAM M. CHAN, PharmD, Riverside Methodist Hospital, Columbus, Ohio. Am Fam Physician. 2011 May 1;83(9):1057-1063
Otitis Externa: Review and Clinical UpdateJ. DAVID OSGUTHORPE, M.D., Medical University of South Carolina, Charleston, South Carolina. DAVID R. NIELSEN, M.D., American Academy of Otolaryngology–Head and Neck Surgery, Alexandria, Virginia. Am Fam Physician. 2006 Nov 1;74(9):1510-1516.
Otitis Externa. Medscape. Joseph P Garry, MD, FACSM, FAAFP Associate Professor, Sports Medicine Faculty, Department of Family and Community Medicine, University of Minnesota Medical School
Hoarseness in Adults. RAYMOND H. FEIERABEND, MD, and SHAHRAM N. MALIK, MD, Department of Family Medicine, East Tennessee State University, Bristol, Tennessee. Am Fam Physician. 2009 Aug 15;80(4):363-370.
Textbook for Family Medicine, 8th edition. Robert E. Rakel and David P. Rakel. Elselvier Saunders, 2011
Vestibular neuritis. JOSEPH B. NADOL, JR., MD, OTOLARYNGOL HEAD NECK SURG 1995; I 12:162-72.
IDSA Guidelines: IDSA Clinical Practice Guideline for Acute Bacterial Rhinosinusitis in Children and Adults. 2012
Dynamed
Essential Evidence Plus
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