11-19-14%20ENT%20in%20primary%20care%20

Report
ENT IN PRIMARY CARE
Ted A. Bonebrake, M.D.
ENT IN PRIMARY CARE
• Ears
• Throat
• Otitis media
• Strep pharyngitis
• Hearing loss
• Tonsillitis
• Otitis externa
• Vertigo
• Nose
• Sinusitis
• Allergic rhinitis
• Epistaxis
• Epiglottitis
• Croup
OTITIS MEDIA
• Otitis media (OM) may be defined as inflammation of the middle
ear due to any cause.
• It is the second most common disease diagnosed in young
children.
• There are two common variants:
• (1) acute otitis media (AOM) and
• (2) otitis media with effusion (OME).
OTITIS MEDIA IS AN ANATOMICAL PROBLEM
OTITIS MEDIA -- DIAGNOSIS
• Children with acute otitis media frequently present with sudden
onset of fever, ear pain, and fussiness.
• On exam, the eardrum is bulging, yellow or white in color with
dilated vessels. There is decreased movement of the eardrum
on pneumatic otoscopy (insufflation of air into the ear canal).
• Common bacteria that cause acute OM in children are
Streptococcus pneumoniae, Haemophilus influenzae, and
Moraxella catarrhalis.
• In healthy children older than two years of age who present with
less severe symptoms, observation for 48 hours may be
considered.
OTITIS MEDIA – OTOSCOPIC EXAM
Otitis media with purulent
material seen behind the
tympanic membrane
Normal tympanic membrane
OTITIS MEDIA – OTOSCOPIC EXAM
Otitis media with effusion
AOM with bulging tympanic
membrane
OTITIS MEDIA – OTOSCOPIC EXAM
AOM with perforation draining
Myringitis during AOM
OTITIS MEDIA -- TREATMENT
• If the decision is made to treat with antibiotics:
• Amoxicillin 80-90 mg/kg/day – 1st line antibiotic therapy.
• Azithromycin or clindamycin can be used to treat patients
who have a penicillin allergy.
• There is a high incidence of resistant organisms in AOM.
• 2nd line therapy includes high-dose amoxicillin/clavulanate,
and 2nd or 3rd generation cephalosporins.
• Alternative: IM Rocephin 50 mg/kg up to 1 g single dose.
OTITIS MEDIA -- EPIDEMIOLOGY
• Beneficial factors
• Breastfeeding
• Immunizations
• Predisposing factors
• Exposure to tobacco smoke
• Daycare attendance
• Younger siblings in the home
OTITIS MEDIA – MYRINGOTOMY TUBES
• Indications
• Recurrent AOM (3-4 episodes in 6 months)
• Middle ear effusion lasting 3 months or more
• Speech or learning delays, possibly due to OME
• Benefits
• Corrects middle ear drainage problems due to horizontal ET
• AOM can be treated with topical antibiotics
OTITIS MEDIA -- COMPLICATIONS
• Complications of acute otitis media were common in the preantibiotic era.
• Perforation of TM
• Tympanosclerosis – May lead to conductive hearing loss.
• Mastoiditis -- Patients with acute mastoiditis present with fever, ear pain,
and a protruding auricle.
• Meningitis
• With increasing antibiotic resistance, especially Streptococcus
pneumoniae, these complications may again become more
common.
HEARING LOSS
• Conductive hearing loss
• Cerumen impactions
• Swelling of the external auditory canal
• Tympanic membrane perforation
• Middle ear fluid
• Ossicular chain abnormalities
• Sensorineural hearing loss
• Injury to hair cells in the cochlea or neural elements innervating the hair cells.
• Due to: persistent noise exposure, age-related (presbycusis), genetic factors,
and infectious or postinflammatory processes.
• Acoustic neuroma
HEARING LOSS – TUNING FORK TESTING
• Tuning fork should be 512 Hz (preferred) to 1024 Hz
• Weber
•
Tuning Fork placed at midline forehead
• If Sound lateralizes to one ear, this indicates
1.Ipsilateral Conductive Hearing Loss OR
2.Contralateral Sensorineural Hearing Loss
• Rinne
•
Bone Conduction: Vibrating Tuning Fork held on Mastoid; patient covers opposite ear with hand
and signals when sound ceases
•
Air Conduction: Move the vibrating tuning fork over the ear canal; patient indicates when the
sound ceases
• Normal: Air Conduction is better than Bone Conduction
• Air conduction usually persists twice as long as bone; Referred to as "positive test"
• Abnormal: Bone conduction better than air conduction
• Suggests Conductive Hearing Loss; Referred to as "negative test"
HEARING LOSS -- AUDIOMETRY
Hearing threshold levels are determined between 250 and
8000 Hertz (Hz) for pure tones and measured in decibels (dB). The
0-dB level is “normalized” to young, healthy adults and doesn’t
mean there is absence of detectable sound. Some patients hear 0
dB, but reaching the threshold of hearing usually requires louder
test signals. The higher the threshold is, the poorer the patient’s
hearing. Thresholds higher than 25 dB are considered abnormal.
During the audiogram, independent thresholds are
determined for each ear for both air conduction (conductive
hearing) and bone conduction (sensorineural hearing).
HEARING LOSS -- AUDIOMETRY
A conductive hearing loss in the left ear due to otitis media with effusion. Note that bone
conduction thresholds are normal in both ears, but air conduction on the left is 30 dB poorer
than that measured on the right.
HEARING LOSS -- AUDIOMETRY
This audiogram suggests noise exposure that may be encountered occasionally in younger
individuals who have been exposed to hazardous or “toxic” noise. Note the high-frequency dip, with
a maximum loss at 4000 Hz.
HEARING LOSS -- AUDIOMETRY
Audiogram of a patient with presbycusis. Note that low-tone thresholds are relatively normal,
with a drop in thresholds at higher frequencies. This is a consequence of the normal aging
process and may vary widely from patient to patient.
HEARING LOSS -- TYMPANOGRAM
• Tympanometry is commonly used to evaluate the tympanic
membrane (TM) and middle ear status.
• This test assesses the mobility of the TM and its response to
pressure changes in the external auditory canal.
Three tympanograms demonstrating
change in compliance of the middle ear
(vertical axis) with changes in ear canal
pressure.
Type A is normal, with the greatest
compliance at the point where the pressure
in the ear canal is equal to that of
atmospheric pressure (peak is at 0).
Type B demonstrates very poor
compliance at any frequency, suggestive of
a tympanic membrane (TM) immobilized by
fluid in the middle ear or a TM perforation
(no peak).
Type C represents a tympanogram in
which the compliance of the membrane is
greatest at a point where the pressure in
the canal is 200 mm of water below that of
atmospheric pressure (peak shifted to the
left). This suggests inefficient eustachian
tube function with persistent negative
pressure in the middle ear.
OTITIS EXTERNA
• Otitis externa (OE) is an inflammation or infection of the external
auditory canal (EAC), the auricle, or both
• This condition can be found in all age groups.
OTITIS EXTERNA -- CONSIDERATIONS
• Necrotizing (malignant) OE: Infection that extends into the deeper
tissues adjacent to the EAC; occurs primarily in immunocompromised
adults (eg, diabetics, patients with acquired immunodeficiency
syndrome [AIDS])
• Although malignant tumors of the ear canal are rare, they do occur
and sometimes are misdiagnosed as OE. If the condition does not
respond to treatment as expected, an otolaryngologist should evaluate
the patient.
• Skull base osteomyelitis occurs most often in patients who are
diabetic or immunocompromised. The usual bacterial pathogen is
Pseudomonas aeruginosa. The diagnosis is strongly suggested by a
history of diabetes mellitus, severe otalgia, cranial neuropathies, and
characteristic EAC findings.
OTITIS EXTERNA -- CONSIDERATIONS
• Ramsay Hunt syndrome, more accurately known as herpes
zoster oticus, is caused by varicella-zoster virus (VZV) infection.
It is characterized by facial nerve paralysis and sensorineural
hearing loss, with bullous myringitis and a vesicular eruption of
the concha of the pinna and the external auditory canal (EAC).
Painful OE may be present as well. Treatment includes use of
an antiviral agent (eg, valacyclovir) and systemic steroids.
• A furuncle is usually caused by staphylococcal infection of a hair
follicle. This infection occurs in the lateral cartilaginous hairbearing portion of the EAC.
OTITIS EXTERNA -- TREATMENT
• Commonly used topical eardrops are acetic acid drops (which
decrease pH), antibacterial drops, and antifungal preparations.
• Oral or parenteral antibiotics may be needed for severe cases.
• Otic antibiotic and steroid combinations are very effective.
Examples include Cipro HC Otic and Cortisporin Otic.
• Auralgan (benzocaine + antipyrine) is an effective analgesic.
• Swimmers can use Swim-Ear (OTC) for prevention.
• The agents commonly prescribed produce cure rates between
87% and 97%
DIZZINESS
• Patients frequently present with a complaint of “dizziness,”
including symptoms such as disequilibrium, syncope,
lightheadedness, ataxia, and vertigo.
• True vertigo (an illusion of motion) is primarily associated with
the balance organs of the inner ear. These are referred to as
peripheral vestibular disorders.
• Evaluations can be done by many physical therapy
departments.
DIZZINESS – VESTIBULAR TESTING
• Vestibular testing can be performed to help determine whether
the problem exists within the vestibular (balance) portion of the
inner ear.
• Audiogram
• Electronystagmography (ENG)
• Rotational chair test
• Posturography
• Electrocochleography (ECOG)
DIZZINESS – VESTIBULAR TESTING
•
There are four main parts to ENG testing
• Calibration test, which measures rapid eye movements
• Tracking test, which evaluates the ability of the eyes to track a moving target
• Positional test, which measures responses due to head movements
• Caloric test, which measures responses to warm and cold water introduced to the
ear canal.
• ENG is the “gold standard” for detecting unilateral peripheral vestibular disorders.
•
Rotatory chair testing is the “gold standard” for diagnosing bilateral vestibular weakness.
The patient is slowly spun in a rotating chair and dizzinessis is measured with optokinetic
testing and a fixation test.
•
Moving platform posturography is a method of quantifying balance, but should not be
used alone to diagnose vestibular disorders. It is most useful in quantifying balance
improvement (or worsening) following treatment for a particular problem, and can help
identify the functional dizzy patient.
•
ECOG is not really a test of the vestibular system, but is a useful test of hearing in the
evaluation of Ménière’s disease. The test is a variant of brainstem audio-evoked response
and, if possible, should be performed during active Ménière’s attacks.
BENIGN PAROXYSMAL POSITIONAL VERTIGO
(BPPV)
• One of the most common causes of vertigo is benign paroxysmal
positional vertigo (BPPV).
• BPPV is caused by sediment, such as calcium carbonate crystals, that
have become free floating within the inner ear.
• Turning the head quickly or into a certain position, causes this freefloating material to move the endolymph in the inner ear, stimulating
the vestibular division of the eighth cranial nerve.
• Vertigo lasts less than 60 sec., and passes when the material settles.
• Patients can usually describe the precise motion that causes vertigo.
• Rolling over in bed that initiates an episode is a fairly specific
symptom.
BENIGN PAROXYSMAL POSITIONAL VERTIGO
(BPPV)
• BPPV can usually be successfully treated with a canolith
reposition maneuver (Epley or Semont maneuver) in the office
setting.
• Dislodged otoliths repositioned into the vestibule is about 80
percent effective in eliminating symptoms of BPPV.
• Symptoms may recur, requiring retreatment.
• Retreatment is equally effective in relieving symptoms.
• Medical therapy with vestibular suppressants is ineffective
because the episodes of vertigo are so fleeting, and should be
discouraged.
BPPV -- TREATMENT
Bedside maneuver for the treatment of a patient with
benign paroxysmal positional vertigo (BPPV) affecting
the right posterior semicircular canal. The presumed
position of the debris within the labyrinth during the
maneuver is shown in panels A–D. The maneuver is a
three-step procedure. The Dix-Hallpike test is
performed with the patient’s head rotated 45º toward
the right ear, and the neck slightly extended with the
chin pointed slightly upward. This position results in
the patient’s head hanging to the right (panel A).
Once the vertigo and the nystagmus provoked by the
Dix-Hallpike test cease, the patient’s head is rotated
about the rostral-caudal body axis until the left ear is
down (panel B). Then the head and body are further
rotated until the head is face down (panel C). The
vertex of the head is kept tilted downward throughout
the rotation. The maneuver usually provokes brief
vertigo. The patient should be kept in the final,
facedown position for about 10–15 seconds.
With the head kept turned toward the left shoulder,
the patient is rought into the seated position (panel
D). Once the patient is upright, the head is tilted so
that the chin is pointed slightly downward.
LABRYNTHITIS
• Another common cause of vertigo is vestibular neuronitis or
labyrinthitis.
• It is thought to be caused by inflammation, secondary to a viral
infection, of the vestibular portion of the eighth cranial nerve or
of the inner ear balance organs (vestibular labyrinth).
• It is frequently associated with recent URI.
• The patient will usually awaken with room-spinning vertigo that
will gradually become less intense over 24–48 hours.
• The patient’s hearing is generally unchanged, and nausea with
or without emesis is common.
LABRYNTHITIS -- TREATMENT
• Treatment is symptomatic
• Vestibular suppressant medications (meclizine)
• Antiemetics
• Short, tapering course of oral steroids
• It may take several weeks for symptoms to completely resolve
• Residual vestibulopathy that persists for months or even years
is not uncommon, and is best managed with vestibular
rehabilitation.
MÉNIÈRE’S DISEASE
• Ménière’s disease is usually diagnosed by history.
• Patients develop intense, episodic vertigo, usually lasting from
30 minutes to four hours, and associated with fluctuating
hearing loss, roaring tinnitus, and the sensation of aural
fullness.
• Even after the episode is over, some hearing loss often remains.
• Although the cause of Ménière’s disease has not been
determined, the symptoms are thought to be due to a distention
of the endolymphatic space within the balance organs of the
inner ear.
MÉNIÈRE’S DISEASE -- TREATMENT
• The disease can be difficult to treat because its course is very
unpredictable. Patients can suffer from frequent attacks and then
abruptly stop having symptoms, only to resume attacks years later.
• Treatment focuses on decreasing the endolymphatic fluid pressure
within the inner ear.
• Salt restriction and thiazide diuretics are frequently used as first-line
agents.
• Additional intervention and referral to ENT may be neccessary.
• Vestibular ablation by instillation of ototoxic medication (i.e.,
gentamicin) into the middle ear for absorption through the round
window membrane has been used. Surgical options also exist.
ACUTE SINUSITIS
• Prolonged mucosal edema, from sinus obstruction and retention of
secretions, may lead to acute bacterial rhinosinusitis.
• Patients may exhibit several of the major symptoms:
•
Facial pressure/pain
•
Facial congestion/fullness
•
Purulent nasal discharge
•
Nasal obstruction
• And one or more of the minor symptoms:
• Headache
• Toothache
• Fever
• Halitosis
• Fatigue
• Ear fullness/pressure
• Cough
ACUTE SINUSITIS
• Radiographic studies (plain films or CT scans) do not
differentiate acute bacterial rhinosinusitis from a viral upper
respiratory infection (URI). More than 80% of patients with a
viral URI also have an abnormal sinus CT scan.
• Time will assist with diagnosis.
• It usually takes 7–10 days for a viral infection to resolve.
• Symptoms lasting beyond 7–10 days, or worsening after 5 days,
suggest bacterial infection.
• Organisms responsible include Streptococcus pneumoniae,
Haemophilus influenzae, and Moraxella catarrhalis.
ACUTE SINUSITIS -- TREATMENT
• The treatment of choice for acute rhinosinusitis has been
amoxicillin or trimethoprim/sulfamethoxazole.
• Resistance to amoxicillin has prompted amoxicillin/clavulanate
or a 2nd generation cephalosporin, macrolide, or quinolone as
first-line.
• More recently, the appearance of penicillin resistance in S.
pneumoniae infection (which has a different resistance
mechanism than beta-lactamase) has resulted in the
recommendation that higher doses of amoxicillin be used
routinely.
• Drugs that do not adequately cover H. influenzae are
inappropriate treatment for either otitis media or rhinosinusitis.
ACUTE SINUSITIS -- TREATMENT
• Adjunctive measures may include topical decongestants
(oxymetazoline) for three days, mucolytics (guaifenisen), and
oral decongestants.
• Severe or recurrent cases may require systemic steroids.
• Antihistamines and topical steroids are not usually indicated,
unless allergy is also a major concern.
• Patients with sinusitis should be referred to an otolaryngologist
if they have three to four infections per year, an infection that
does not respond to two three-week courses of antibiotics, nasal
polyps on exam, or any complications of sinusitis.
ALLERGIC RHINITIS
• Over 20 million Americans suffer from inhalant allergies.
• Symptoms are nasal congestion, clear rhinorrhea, itchy watery
eyes, and sometimes ear or palatal itching, post-nasal drip, and
throat irritation.
• Fatigue is common, caused by sleep disturbance from nasal
obstruction, perhaps with other immune contributors.
• Symptoms may occur only in certain seasons or locations.
• If one parent has inhalant allergies, a child has about a 30
percent chance of developing allergies. If both parents have
allergies, this increases to about 60 percent.
ALLERGIC RHINITIS
• The percentage of the population with allergy problems has
been increasing in developed countries.
• One possible explanation for this is that the infectious diseases
more common in less developed countries help tilt an
individual’s immune system more toward the T-helper 1 (Th1)
system, minimizing the chance of developing theTh2-mediated
atopic reaction, and the resulting allergic symptoms.
ALLERGIC RHINITIS
There are three mainstays of treating inhalant allergies:
• Pharmacotherapy
• Avoidance of the provoking allergen
• Immunotherapy
ALLERGIC RHINITIS -- TREATMENT
• Pharmacotherapy helpful for allergic symptoms includes:
• Antihistamines (oral or nasal topical)
• Nasal steroid sprays
• Decongestants
• Topical nasal cromolyn
• Oral antileukotrienes
• Allergy pharmacotherapy is often started empirically, before
allergy testing. If symptoms respond well, the medication can be
continued as needed, and allergy testing may not be necessary.
ALLERGIC RHINITIS -- TREATMENT
Allergen avoidance requires determining what allergens are specific
triggers for an individual, either by skin testing or in-vitro testing for
elevated levels of IgE. In-vitro testing is preferred for patients who:
• Are pregnant
• Have poorly controlled asthma
• Take a beta blocker medication
• Take a tricyclic antidepressant
• Take a monoamine oxydase inhibitor
• Have a history of severe anaphylaxis
Antihistamine medications (oral or nasal) must be discontinued three to
five days before testing to avoid false negative results.
EPISTAXIS
• Epistaxis has been reported to occur in up to 60 percent of the
general population
• The condition has a bimodal distribution, with incidence peaks
at ages younger than 10 years and older than 50 years
• Certain high-risk groups, such as the elderly, require rapid
intervention to stem bleeding and prevent further complications
EPISTAXIS -- ANATOMY
The vascular supply of the nose originates from the ethmoid branches of the internal carotid
arteries and the facial and internal maxillary divisions of the external carotid arteries
Although nasal circulation is complex (Figure 1), epistaxis usually is described as either anterior
or posterior bleeding. This simple distinction provides a useful basis for management.
EPISTAXIS -- ANATOMY
• Most cases of epistaxis occur in the anterior part of the nose, with the
bleeding usually arising from the rich arterial anastomoses of the nasal
septum (Kiesselbach’s plexus).
• Posterior epistaxis generally arises from the posterior nasal cavity via
branches of the sphenopalatine arteries.
• In most cases, anterior bleeding is clinically obvious.
• Posterior bleeding may be asymptomatic or may present insidiously as
nausea, hematemesis, anemia, hemoptysis, or melena.
• Infrequently, larger vessels are involved in posterior epistaxis and can result
in sudden, massive bleeding.
EPISTAXIS -- ETIOLOGY
LOCAL CAUSES
•
Chronic sinusitis
•
Epistaxis digitorum (nose picking)
•
Foreign bodies
•
Intranasal neoplasm or polyps
•
SYSTEMIC CAUSES
•
Hemophilia
•
Hypertension
•
Leukemia
Irritants (e.g., cigarette smoke)
•
Liver disease (e.g., cirrhosis)
•
Medications (e.g., topical
corticosteroids)
•
•
Rhinitis
Medications (e.g., aspirin,
anticoagulants, nonsteroidal antiinflammatory drugs)
•
Septal deviation or perforation
•
Platelet dysfunction
•
Trauma
•
Thrombocytopenia
•
Vascular malformation or telangiectasia
EPISTAXIS -- MANAGEMENT
• Initial management includes compression of the nostrils (application of direct
pressure to the septal area) and plugging of the affected nostril with gauze or
cotton that has been soaked in a topical decongestant.
• Direct pressure should be applied continuously for at least five minutes, and
for up to 20 minutes.
• Tilting the head forward prevents blood from pooling in the posterior pharynx,
thereby avoiding nausea and airway obstruction.
• Hemodynamic stability and airway patency should be confirmed. Fluid
resuscitation should be initiated if volume depletion is suspected.
EPISTAXIS -- MANAGEMENT
Typical contents of an epistaxis tray. Top row: nasal decongestant sprays and local anesthetic, silver
nitrate cautery sticks, bayonet forceps, nasal speculum, Frazier suction tip, posterior double balloon
system and syringe for balloon inflation. Bottom row: Packing materials, including nonadherent
gauze impregnated with petroleum jelly and 3 percent bismuth tribromophenate (Xeroform),
Merocel, Gelfoam, and suction cautery.
EPISTAXIS -- MANAGEMENT
•
Every attempt should be made to locate the source of bleeding that does not
respond to simple compression and nasal plugging
•
Diffuse oozing, multiple bleeding sites, or recurrent bleeding may indicate a systemic
process such as hypertension, anticoagulation, or coagulopathy. In such cases, a
hematologic evaluation should be performed
•
Tests include CBC, PT/INR, PTT and, if indicated, blood typing and crossmatching
•
Although most patients with epistaxis can be treated as outpatients, hospital
admission and close observation should be considered for elderly patients and
patients with posterior bleeding or coagulopathy. Admission also may be prudent for
patients with complicating comorbid conditions such as coronary artery disease,
severe hypertension, or significant anemia
EPISTAXIS -- MANAGEMENT
ANTERIOR BLEEDS
•
Topical oxymetazoline (Afrin) spray alone often stops the hemorrhage.
•
LET solution (lidocaine 4%, epinephrine 0.1%, and tetracaine 0.4%) applied to a
cotton ball or gauze and allowed to remain in the nares for 10-15 minutes is very
useful in providing vasoconstriction and analgesia.
•
For bleeding that is likely to require more aggressive treatment, a local anesthetic,
such as a 4 percent cocaine solution or tetracaine or lidocaine (Xylocaine) solution,
should be used.
•
Adequate anesthesia should be obtained before treatment proceeds.
•
Intravenous access should be obtained in difficult cases, especially when anxiolytic
medications are to be used.
EPISTAXIS -- MANAGEMENT
ANTERIOR BLEEDS
•
Cotton pledgets soaked in vasoconstrictor and anesthetic should be placed in the
anterior nasal cavity, and direct pressure should be applied at both sides of the nose
for at least five minutes.
•
If this measure is unsuccessful, chemical cautery can be attempted using a silver
nitrate stick applied directly to the bleeding site for approximately 30 seconds .
•
Other treatment options include hemostatic packing with absorbable gelatin foam
(Gelfoam) or oxidized cellulose (Surgicel). Use of desmopressin spray (DDAVP) may
be considered in a patient with a known bleeding disorder.
•
Larger vessels generally respond more readily to electrocautery.
•
Note that use of electrocautery on both sides of the septum may increase the risk of
septal perforation.
EPISTAXIS -- MANAGEMENT
If local treatments fail to stop anterior bleeding, the anterior nasal cavity should be packed,
from posterior to anterior, with ribbon gauze impregnated with petroleum jelly or polymyxin Bbacitracin zinc-neomycin (Neosporin) ointment. Nonadherent gauze impregnated with
petroleum jelly and 3 percent bismuth tribromophenate (Xeroform) also works well for this
purpose.5,9 Bayonet forceps and a nasal speculum are used to approximate the accordionfolded layers of the gauze, which should extend as far back into the nose as possible.
Alternatively, a preformed nasal tampon (Merocel or Doyle sponge) may be used
EPISTAXIS -- MANAGEMENT
POSTERIOR BLEEDS
•
Posterior bleeding is much less common than anterior bleeding and usually is treated
by an otolaryngologist.
•
Various balloon systems are effective for managing posterior bleeding and are less
complicated than the packing procedure.
•
The double-balloon device is passed into the affected nostril under topical
anesthesia until it reaches the nasopharynx. The posterior balloon then is inflated
with 7 to 10 mL of saline, and the catheter is withdrawn carefully so that the balloon
seats in the posterior nasal cavity to tamponade the bleeding source. Next, the
anterior balloon is inflated with roughly 15 to 30 mL of saline in the anterior nasal
cavity to prevent retrograde travel of the posterior balloon and subsequent airway
obstruction.
•
If a specialized balloon device is not available, a Foley catheter (10 to 14 French)
with a 30-mL balloon may be used.
STREP PHARYNGITIS
•
Sore throat is one of the most
common reasons for visits to family
physicians.
•
Most patients with sore throat have
an infectious cause (pharyngitis), but
less than 20 percent have a clear
indication for antibiotic therapy.
•
Because of recent improvements in
rapid streptococcal antigen tests,
throat culture can be reserved for
patients whose symptoms do not
improve over time or who do not
respond to antibiotics .
STREP PHARYGITIS
•
Pharyngitis is diagnosed in 11 million patients in U.S. emergency departments and
ambulatory settings annually.
•
Most episodes are viral.
•
Group A beta-hemolytic streptococcus (GABHS), the most common bacterial
etiology, accounts for 15 to 30 percent of cases of acute pharyngitis in children and 5
to 20 percent in adults.
•
One in four children with acute sore throat has serologically confirmed GABHS
pharyngitis.
•
Late winter and early spring are peak GABHS seasons.
•
The infection is transmitted via respiratory secretions, and the incubation period is 24
to 72 hours.
STREP PHARYNGITIS -- CENTOR CRITERIA
There are four criteria, with one point added for each positive criterion:
• History of fever
• Tonsillar exudates
• Tender anterior cervical adenopathy
• Absence of cough
The Modified Centor Criteria add the patient's age to the criteria:
• Age 2-15 add 1 point
• Age >44 subtract 1 point
STREP PHARYNGITIS -- CENTOR CRITERIA
Guidelines for management:
• -1, 0 or 1 points - No antibiotic or throat culture necessary (Risk of strep.
infection <10%)
• 2 or 3 points - Should receive a throat culture and treat with an antibiotic if
culture is positive (Risk of strep. infection 32% if 3 criteria, 15% if 2)
• 4 or 5 points - Treat empirically with an antibiotic (Risk of strep. infection
56%)
The presence of all four variables indicates a 40 - 60% positive predictive value for a
culture of the throat to test positive for Group A Streptococcus bacteria. The absence of
all four variables indicates a negative predictive value of greater than 80%.
STREP PHARYNGITIS -- DIAGNOSIS
• With correct sampling and plating techniques, a single-swab throat culture is
90 – 95% sensitive
• Rapid antigen detection testing (RADT) allows for earlier treatment, symptom
improvement, and reduced disease spread.
• RADT specificity ranges from 90 – 99%.
• Sensitivity depends on the commercial RADT kit used and was
approximately 70% with older latex agglutination assays. Newer ELISA,
optical immunoassays, and DNA probes are 90 - 99% sensitive.
• The American Academy of Pediatrics (AAP) recommends that negative
RADT results in children be confirmed using throat culture unless physicians
can guarantee that RADT sensitivity is similar to that of throat culture in their
practice
STREP PHARYNGITIS -- TREATMENT
•
GABHS pharyngitis is self-limited and resolves within a few days, even without
treatment.
•
Arguments for antibiotic treatment include acute symptom relief, prevention of
complications, and reduced communicability.
•
Antibiotics shorten symptom duration by about 16 hours; the number needed to treat
(NNT) for symptom relief at 72 hours is four in those with positive throat swabs.
•
In addition, rates of suppurative peritonsillar and retropharyngeal abscesses are
reduced (approximately one in 1,000 cases).
STREP PHARYNGITIS -- TREATMENT
• Antibiotics also reduce the
incidence of acute rheumatic
fever
• It is estimated that 3,000 to 4,000
patients must be given antibiotics
to prevent one case of acute
rheumatic fever in developed
nations.
• Children with GABHS pharyngitis
may return to school after 24
hours of antibiotic therapy.
STREP PHARYNGITIS -- TREATMENT
Based on cost, narrow spectrum of activity, safety, and effectiveness, penicillin is
recommended by the American Academy of Family Physicians (AAFP), the AAP, the American
Heart Association, the Infectious Diseases Society of America (IDSA), and the World Health
Organization for the treatment of streptococcal pharyngitis.
DOSING
Children
Adults & Adolescents
PenVeeK
250 mg TID x 10 days
500 mg BID x 10 days
Amoxicillin
10 mg/kg TID x 10 d
Penicillin G benzathine
600,000 units IM
(Bicillin L-A)
(< 27 kg)
Erythromycin ethylsuccinate 20 mg/kg BID x 10 d
500 mg BID x 10 days
1.2 million units IM
800 mg BID x 10 days
STREP PHARYNGITIS -- TREATMENT
Other alternatives for PCN allergic patients
Cephalexin
20 mg/kg/dose twice daily (max = 500 mg/dose)
10 days
Cefadroxil
30 mg/kg once daily (max = 1 g)
10 days
Clindamycin
7 mg/kg/dose 3 times daily (max = 300 mg/dose)
10 days
Azithromycin
12 mg/kg once daily (max = 500 mg)
Clarithromycin
7.5 mg/kg/dose twice daily (max = 250 mg/dose)
5 days
10 days
RECURRENT TONSILLITIS
• Some children have several bouts of tonsillitis per year that require
evaluation by a physician.
• In treating recurrent tonsillitis, you should obtain culture documentation of
Group A, ß hemolytic strep, and if possible, obtain documentation of
infections treated at other locations.
• The Clinical Practice Guideline: Tonsillectomy in Children recommends that
tonsillectomy is indicated when children present with
• Seven or more infections in one year
• Five per year for two years
• Or three per year for three years
• If the recommended number of infections has not been documented, then
watchful waiting is suggested.
CHRONIC TONSILLITIS
• Chronic low-grade infection of the tonsils can occur in older children,
adolescents, and adults.
• These patients often have large crypts, or spaces within the tonsils that
collect food and debris, that are difficult to treat with antibiotics.
• The lymph nodes in the neck are usually inflamed from constant tonsillar
infection.
• Sometimes, the retained food and debris lead to chronic halitosis (bad
breath).
• The typical history from these patients is that their sore throat gets better on
antibiotics, but then comes back as soon as they stop taking their
medication.
TONSILLAR HYPERTROPHY
OBSTRUCTIVE SLEEP DISORDERS
• Enlarged tonsils and adenoids are often the source of airway obstruction in
children, and they result in sleep-disordered breathing.
• Daytime lethargy, obstructive symptoms, growth retardation, behavioral
problems, including poor school performance and hyperactivity, and
nocturnal enuresis are often associated with the obstructive sleep disorder.
• In severe—although rare—cases, pulmonary or cardiac disease can result.
• Diagnosis is usually straightforward, based on history and physical
examination.
• In some instances, a formal sleep study may be required.
• If the diagnosis of obstruction is substantiated, tonsillectomy and
adenoidectomy is often curative, although in some populations persistent or
recurrent symptoms may occur.
EPIGLOTTITIS
• Acute epiglottitis is an infection of the supraglottic (above the vocal cords)
structures that causes swelling of the portion of the larynx above the vocal
cords.
• The swelling can become so severe that it blocks the airway.
• It is fulminant and usually caused by Haemophilus influenzae type B
organisms.
• This fatal disease was common 20 years ago, but the incidence has
decreased dramatically with widespread use of the H. influenzae (HiB)
vaccine.
• The typical affected child is three to six years old and septic.
EPIGLOTTITIS
• Often, the child was breathing
normally just hours earlier.
• The cardinal signs of acute
epiglottitis are stridor, leaning
forward in a tripod posture, and
drooling because it hurts to
swallow.
• If you suspect acute epiglottitis,
immediately call an
otolaryngologist, anesthetist, and
pediatrician.
• A lateral soft-tissue view of neck
will show a “thumb sign”
CROUP
• Although both are forms of acute upper-airway obstruction in children, croup
should be distinguished from acute epiglottitis because the management is
different.
• Croup is the common name for laryngotracheobronchitis, a viral infection of
the upper airway causing swelling in the subglottic (below the vocal cords)
area and stridor.
• It usually occurs in children three–six months to three years old who have
had a prodromal URI, usually for about a week.
CROUP -- DIAGNOSIS
•
Patients are not septic, but may have a low-grade fever.
•
The stridor is high pitched, biphasic (with both inspiration and expiration), and
associated with a “barking” cough—often sounding like a seal.
•
It does not hurt to swallow, so the patient is not drooling and the epiglottis is not
swollen, so the patient is not always leaning forward.
•
The classic radiographic finding is the “steeple sign,” showing subglottic narrowing on
a chest or neck x-ray.
CROUP -- TREATMENT
CROUP -- TREATMENT
• The treatment for croup is humidity, oxygen, and, if necessary,
racemic epinephrine treatments or steroids, or both.
• Antibiotic therapy may be used if bacterial superinfection is
suspected.
• If croup is severe, the child should be admitted to the hospital
for observation.
• Intubation is rarely required.

similar documents