ENT IN PRIMARY CARE Ted A. Bonebrake, M.D. ENT IN PRIMARY CARE Ears Throat Otitis media Strep pharyngitis Hearing loss Tonsillitis
Otitis externa Epiglottitis Vertigo Croup Nose Sinusitis Allergic rhinitis Epistaxis 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 doesnt 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 patients 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 Mnires disease. The test is a variant of brainstem audio-evoked response and, if possible, should be performed during active Mnires 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 AD. The maneuver is a three-step procedure. The Dix-Hallpike test is performed with the patients head rotated 45 toward the right ear, and the neck slightly extended with the chin pointed slightly upward. This position results in the patients head hanging to the right (panel A). Once the vertigo and the nystagmus provoked by the DixHallpike test cease, the patients 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 1015 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 2448 hours.
The patients 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. MNIRES DISEASE Mnires 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 Mnires 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. MNIRES 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 710 days for a viral infection to resolve. Symptoms lasting beyond 710 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 firstline. 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 individuals 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 (Kiesselbachs 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 SYSTEMIC CAUSES Chronic sinusitis Hemophilia Epistaxis digitorum (nose picking)
Hypertension Foreign bodies Leukemia Intranasal neoplasm or polyps
Liver disease (e.g., cirrhosis) Irritants (e.g., cigarette smoke) 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 500 mg BID x 10 days Penicillin G benzathine 600,000 units IM 1.2 million units IM (Bicillin L-A) (< 27 kg) Erythromycin ethylsuccinate 20 mg/kg BID x 10 d 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) Cefadroxil
30 mg/kg once daily (max = 1 g) 10 days Clindamycin 7 mg/kg/dose 3 times daily (max = 300 mg/dose) Azithromycin 12 mg/kg once daily (max = 500 mg) Clarithromycin 10 days 10 days 5 days 7.5 mg/kg/dose twice daily (max = 250 mg/dose) 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, 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 severealthough rarecases, 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 threesix 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 coughoften 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.