Epiglottitis

Epiglottitis (or “supraglottitis”) is a condition that requires prompt attention by the physician. Epiglottitis results from bacterial (and rarely viral) infection of the supraglottic structures, that is, the epiglottis and arytenoid cartilages. A high level of suspicion is necessary to make a diagnosis and avoid significant morbidity. Rapid decompensation and complete loss of the airway are the sequelae of most concern. The physician should always be suspicious when a patient presents with fever, sore throat, and difficulty swallowing, and when the severity of oropharyngeal physical findings is not in proportion to the symptoms. Croup, tonsillitis, peritonsillar abscess, and other neck infection may be incorrectly diagnosed in these patients. Epiglottitis occurs mainly in children age 2 to 7 years, although infants, older children, and adults can be affected. Mortality rates of 6% to 7% have been reported in adults.

Signs and symptoms of epiglottitis include rapidly developing sore throat, high fever, restlessness, and lethargy. A “supraglottic,” muffled voice is common. Many patients have difficulty with their saliva and drool. Classically, these patients are in a sitting position leaning forward, because this position tends to alleviate obstructive symptoms from the supraglottic swelling. They may show signs of “air hunger” or may have stridor.

Differential diagnosis includes tonsillitis, peritonsillar abscess, retropharyngeal abscess, airway foreign body, and croup. Physical examination with laryngoscopy is extremely useful in differentiating these diagnoses. Endoscopy should not be performed if there is concern of impending airway obstruction. Endoscopy will typically show erythema and edema of the epiglottis and arytenoid cartilages. Other findings include laryngeal tenderness on neck palpation, although palpation should be avoided when the diagnosis is being considered.

Any time the diagnosis of epiglottitis is in question, otorhinolaryngologic (ear-nose-throat, ENT) and infectious disease consultations are warranted. Placement of a tongue depressor has been known to precipitate acute airway obstruction and should be avoided entirely if epiglottitis is strongly suspected. Differentiation from croup can be difficult because there is considerable overlap of symptoms (Table 19-1) (Berry and Yemen, 1994). A lateral extended neck radiograph can help in the diagnosis. X-ray evidence includes the classic “thumbprint” sign. If epiglottitis is suspected or lateral neck radiography is confirmatory, the patient should be taken to the operating room (OR) for orotracheal intubation in the presence of an anesthesiologist and an otorhinolaryngologist. In any case of airway obstruction, cricothyrotomy or tracheotomy can be lifesaving, because orotracheal intubation can be difficult and sometimes impossible. Some patients, usually adults, may be treated expectantly with intravenous (IV) medications and intensive care unit (ICU) observation as long as personnel are available for control of the airway if necessary. If airway stability is questionable, observation is not recommended.

Table 19-1 Distinguishing Features of Epiglottitis and Croup

After control of the airway is achieved, cultures of the epiglottis should be obtained and directed antibiotics instituted. Haemophilus influenzae type b (Hib) is common and can be beta-lactamase producing. Other, less common organisms include beta-hemolytic streptococci, Streptococcus pneumoniae, and Staphylococcus aureus. Antibiotics should be administered parenterally; effective antibiotics include cefotaxime, ceftriaxone, ampicillin plus sulbactam, or ampicillin plus chloramphenicol. Steroids can be useful for edema and inflammation, but their effectiveness has not been proved in controlled studies.

The incidence of epiglottitis in children is decreasing since the introduction of the Hib vaccine in the late 1980s. However, the incidence has remained stable or slightly increased in adults.

Peritonsillar Abscess

A peritonsillar abscess is the accumulation of pus in the peritonsillar space that surrounds the tonsil. The same organisms responsible for common tonsillar infections— Streptococcus and Staphylococcus species and anaerobes—are also found in peritonsillar abscesses.

The typical signs and symptoms of peritonsillar abscess include fever, sore throat for 3 to 5 days, dysphagia, odynophagia, and a muffled, “hot potato” voice. Trismus is extremely common. Examination confirms asymmetric tonsils and peritonsillar edema and erythema. The soft palate and uvula are swollen and displaced away from the side of the abscess. It is often difficult to distinguish between abscess and peritonsillar cellulitis. If possible, it is helpful to palpate because fluctuance indicates a loculation of pus. Diagnosis is often made by clinical impression, but computed tomography (CT) can be confirmatory and useful when the diagnosis is uncertain (Fig. 19-1).

Figure 19-1 Large left peritonsillar abscess (arrow) that required surgical drainage.

If untreated, a peritonsillar abscess may spontaneously drain, progress to involve the deep neck, or even lead to airway obstruction. The most important part of the treatment is drainage of the abscess cavity by needle aspiration, incision and drainage, or tonsillectomy. Cultures of the aspirate can be obtained, and broad-spectrum antibiotics should be started. Appropriate antibiotics include ampicillin-sulbactam (Unasyn) or clindamycin (Cleocin). Many patients present with dehydration, and parenteral fluids should be given if necessary. Analgesics should be prescribed as needed. One or two doses of IV corticosteroids may be given to decrease inflammation and pain.

Children presenting with peritonsillar abscess should be admitted to the hospital. Treatment with IV hydration and parenteral antibiotics is appropriate initially. Patients with peritonsillar cellulitis/phlegmon or early abscess often demonstrate a rapid response to treatment, whereas those with a well-formed peritonsillar abscess do not improve. Drainage is necessary in nonresponders. Abscesses in cooperative adults can be drained under local anesthesia in the emergency department (ED) or office and treated in an outpatient setting. Children usually require general anesthesia for drainage, and a tonsillectomy may also be performed. An elective tonsillectomy is often recommended for any patient with a peritonsillar abscess to prevent recurrence, especially with a history of recurrent tonsillitis, although few, if any, controlled studies support this recommendation.

Sudden Sensorineural Hearing Loss

Although most types of hearing loss are nonurgent problems, sudden sensorineural hearing loss (SSNHL) deserves special note because it is considered “otologic emergency.” Any patient complaining of sudden hearing loss requires prompt evaluation. An obvious cause such as cerumen impaction or middle ear fluid can be treated appropriately and routinely. If a cause is not identified, sudden sensorineural hearing loss should be suspected and prompt ENT referral arranged. SSNHL is thought to be secondary to vascular, thromboembolic, viral, or autoimmune causes. It may also be the result of ototoxicity. Without treatment, hearing returns in one third of patients, partial hearing returns in one third, and there is no improvement in the remaining third. Early intervention with oral corticosteroids (and possibly antivirals, directed at the herpesvirus [Awad et al., 2008]) appears to improve outcomes, although few controlled studies have been done. The Cochrane Collaboration believes that there is a lack of good-quality evidence to support the use of steroids and that more research is needed (Wei et al., 2006). Finally, for patients who do not respond to systemic steroids, controlled studies do support the use intratympanic infusion of corticosteroids, demonstrating improved outcomes (Xenellis et al., 2006). Intratympanic steroids are also appealing for patients with contraindications to oral steroids (e.g., “brittle diabetics”)

Foreign Bodies

Swallowing or aspiration of objects is most common in children but also occurs in the adult population. These objects can become lodged anywhere in the upper aerodigestive tract.

Esophagus

The most common location for esophageal foreign bodies is at the level of the cricopharyngeal muscle. Other regions include the anatomic narrowings of the esophagus, such as the gastroesophageal junction, and the area of indentation of the esophagus by the left main stem bronchus and the arch of the aorta. Coins are by far the most common objects found in the esophagus in children. Chicken or fish bones are more common in adults.

The diagnosis of an esophageal foreign body is primarily based on the medical history and physical examination, with the aid of radiologic studies. Parents might witness ingestion of the foreign body and subsequent coughing, gagging, refusal to eat, or drooling. Often, however, the incident goes unwitnessed, and reliance on other diagnostic techniques is necessary.

Plain radiographs (including lateral films) are often diagnostic in pediatric patients because most esophageal foreign objects are radiopaque (Fig. 19-2). Other radiologic findings that can suggest a foreign body include increased soft tissue density in the prevertebral space, mediastinal widening, air-fluid levels in the esophagus, and paraesophageal air. Disk batteries require a high index of suspicion because they can cause significant tissue injury and lead to esophageal perforation if they are not removed emergently. They have a classic appearance when viewed laterally, approximating a dime resting on a nickel (similar to the appearance of Fig. 19-2).

Figure 19-2 Lateral neck x-ray film of a child presenting with gagging and drooling, showing two coins (arrow) in the esophagus near the cricopharyngeal junction.

If there is sufficient evidence of an esophageal foreign body, ENT consultation is indicated for rigid esophagoscopy and removal. When radiolucent objects have been ingested, contrast esophagography might be indicated, although esophagograms can give a false-negative result and can also complicate visualization during rigid esophagoscopy.

Airway

As with esophageal foreign bodies, airway foreign bodies are much more common in infants and young children. Many deaths from foreign-body aspiration occur in the home before medical intervention can be administered. The most frequently aspirated foreign bodies are foods, with nuts leading the list. Foreign bodies aspirated into the airway are usually found lodged in the bronchial tree but can also be found in the larynx or trachea. If the event is witnessed and results in complete airway obstruction, a Heimlich maneuver should be administered; however, the event is often not witnessed. Symptoms can include hoarseness, persistent cough, wheezing, or stridor if the foreign body is lodged in the trachea or larynx. Because the potential for morbidity and mortality is substantial, this condition requires urgent diagnosis and timely intervention to prevent catastrophe.

Any time a small child presents with wheezing or noisy breathing without a previous history of reactive airway disease, an airway foreign body should be included in the differential diagnosis. Typically, patients and parents recount a transient episode of coughing during eating that then subsided; the patient might even be symptom free for a time, then later have symptoms such as coughing or wheezing.

The most important diagnostic step for identifying a foreign body is a high index of suspicion. Careful auscultation of the lung fields is essential because subtle asymmetric differences may be found. Because most airway foreign bodies are radiolucent, chest radiographs can be normal, but abnormalities such as hyperinflation, atelectasis, or pneumonia can be present (Fig. 19-3). If plain radiographs are equivocal or normal and the patient is in stable condition, airway fluoroscopy can be helpful.

Figure 19-3 Inspiratory (A) and expiratory (B) radiographs of 8-year-old boy with left airway foreign body (peanut). No foreign object is visible on plain films, but the expiratory film shows overinflation of the left lung with mediastinal shift to the contralateral side.

Consultation with a physician experienced in foreign body removal is required. Definitive treatment of airway foreign bodies is direct laryngoscopy and rigid bronchoscopy to indentify and remove the object.

Epistaxis

Although epistaxis is usually nothing more than a minor annoyance, some episodes are severe enough to require urgent medical attention and intervention. In rare cases, epistaxis can also be a life-threatening emergency.

Predisposing factors for epistaxis include trauma (facial trauma or self-inflicted digital trauma), dry weather, hypertension, bleeding dyscrasias (factor deficiencies, hereditary hemorrhagic telangiectasia, lymphoproliferative disorders), anticoagulation therapy (acetylsalicylic acid, heparin, warfarin), and intranasal tumors. Special consideration should be given to adolescent boys with recurrent epistaxis and nasal obstruction, because these symptoms might be the result of a juvenile nasopharyngeal angiofibroma. These are benign but locally aggressive tumors. All these potential risk factors should be considered because they must be addressed to treat the patient appropriately.

Epistaxis is classified according to its location. Bleeding from the anterior nasal cavity is most common and usually originates from a rich plexus of vessels at the anterior septum called Kiesselbach’s plexus (Fig. 19-4). Bleeding from this location, although troublesome, is less likely to be severe and is usually easier to control than posterior epistaxis. Posterior epistaxis originates from the posterior two thirds of the nasal cavity and can be quite severe and much more difficult to control.

Figure 19-4 Kiesselbach’s plexus. 1 and 2, Anterior and posterior ethmoid arteries; 3, septal branch of the sphenopalatine; 4, greater palatine; 5, branch from superior labial; 6, Kiesselbach’s plexus.

(From Colman BH, Hall IS (eds): Hall and Colman’s Diseases of the Ear, Nose and Throat, 15th ed. Philadelphia, Churchill Livingstone, 2000, p 82.)

Initial management of epistaxis includes assessment and stabilization of vital signs. Rarely, severe bleeding can lead to airway compromise or hemodynamic compromise, or both, especially in patients with underlying cardiopulmonary dysfunction. The airway should be assessed and stabilized, urgently if necessary. Hypertension, if severe, should be controlled, with care taken to avoid subsequent hypotension. Hematologic studies, including complete blood count (CBC), prothrombin time, and partial thromboplastin time, should be ordered. Intravenous access should be established, allowing administration of fluids as well as IV medications, if necessary during treatment.

Physical Examination

See the discussion online at www.expertconsult.com.

Otalgia

While the vast majority of patients with otalgia have an otologic cause, the clinician must recognize that otalgia may be referred. Sensory innervation of the ear includes cranial nerves V, VII, IX, and X, and therefore disorders of structures with similar innervation can cause otalgia. It is imperative that the physician not simply attribute otalgia to an ear infection unless the physical examination supports this diagnosis. Otalgia can result from dysfunction of the nose, sinuses, oral cavity, pharynx, larynx, dentition, temporomandibular joints, and salivary glands. These structures must be thoroughly assessed, especially if the examination of the ear appears normal. This is especially true in smokers, whose initial symptom of laryngopharyngeal carcinoma may be otalgia. Otolaryngologic referral for laryngoscopy may be indicated with suspected referred otalgia. (See eBox 19-1 and eBox 19-2 online at www.expertconsult.com for differential diagnosis of otalgia.)

Tumors of the Ear

Tumors of the ear are rare. Classification is based on their location (external ear, middle ear, inner ear). A tumor of the external or middle ear is often easily diagnosed by visualizing a lesion on otoscopy. In some cases, symptoms may mimic infection (pain, otorrhea). Tumors of the inner ear can manifest with symptoms of hearing loss, tinnitus, disequilibrium, or facial weakness. (eBox 19-3 online lists tumors of the ear by location.)

Vertigo

Key Points

The sense of balance or equilibrium occurs when there is normal and harmonious function of several systems and organs in the body. These include the musculoskeletal system, the cardiovascular system, the central nervous system, the eyes, and the ears. Abnormal function of any of these can result in the sensation of dizziness or disequilibrium. The term vertigo is reserved to describe a perceived sensation of motion, usually spinning, of the person relative to the environment, or vice versa. Causes of disequilibrium can be categorized into one of three groups: peripheral (inner ear or labyrinthine), central nervous system (CNS), or systemic (e.g., cardiovascular, metabolic). Although not pathognomonic of a labyrinthine disorder, true vertigo most often indicates aberrant function of the inner ear.

Because patients use “dizzy” to describe many sensations, the actual sensation is best clarified by a detailed history (Box 19-1). The major studies on the causes of persistent dizziness, from Drachman and Hart (1972) to Davis (1994), all describe four diagnostic categories: lightheadedness, presyncope, disequilibrium, and vertigo. The investigators all conclude that the most common cause of persistent dizziness is a peripheral vestibular disorder (38%-56% of cases) followed closely by a psychogenic disorder (6%-33%). In about 25% of patients, the complaint is the result of the combined effects of multiple sensory deficits, medications, or orthostasis, leading to complaints of presyncope, lightheadedness, or disequilibrium. Finally, central vestibular etiologies are unusual and represent less than 10% of all causes.

A thorough medical history allows the physician to distinguish between true vertigo (a sensation of spinning) and other sensations, such as presyncope, lightheadedness, and unsteadiness. The physical examination and laboratory evaluation are guided by the accuracy of the history. A sensation of vertigo originates from within the vestibular system but can be either peripheral (vestibular nerve and inner ear) or central (cerebellum, brainstem, thalamus, and cortex).

Questions regarding hearing and neurologic deficits can help elicit which part of the vestibular system is involved (Wiet et al., 1999) (see eTable 19-1 online). Peripheral vertigo tends to be episodic, whereas central vertigo is constant. Neurologic symptoms or loss of consciousness do not occur with peripheral vertigo but are possible with central vertigo. Nystagmus, which is labeled by the direction of the fast component, can be present in both types of vertigo and can be horizontal or rotary; vertical nystagmus occurs only in central vertigo.

The physical examination should include assessment of orthostatic blood pressure changes, a complete ocular examination, tuning fork tests (Weber’s and Rinne’s), pneumatic otoscopy (elicits vertigo in patients with perilymphatic fistula), balance tests (Romberg’s), gait (including tandem walking), and cranial nerve evaluation. The Dix-Hallpike maneuver (see eFig. 19-3 online) is especially helpful in diagnosing benign paroxysmal positional vertigo (BPPV). Head movement always worsens the feeling of true vertigo. If it does not, the dizziness can be attributed to a cause other than vestibular dysfunction.

Laboratory testing can include an audiogram if no specific cause of vertigo can be found after the medical history and physical examination. Electronystagmography (ENG) is an objective study of the vestibular system and can help localize a vestibular lesion. Electrodes placed about the eye sense the movements of nystagmus as either spontaneous or initiated by maneuvers such as caloric testing, positioning, optokinetics, and pendulum tracing. A brain MRI scan is indicated in patients with unilateral otologic symptoms and in those unresponsive to treatment. Blood tests, when necessary, can include CBC, rapid plasma reagin (RPR), vitamin B₁₂ level, folate level, drug screens, and heavy metal testing when indicated.

Tinnitus

Tinnitus is a term used to describe an internal noise perceived by the patient. It is usually, but not always, indicative of an otologic problem. Tinnitus is most often subjective, that is, heard only by the patient. However, it can be objective and heard by the patient and the examiner. In most cases, tinnitus is secondary to bilateral sensorineural hearing loss and requires no further evaluation. In rare cases, tinnitus can be a symptom of a vascular abnormality (aneurysm or arteriovenous malformation), hypermetabolic state, or intracranial mass that, if not evaluated, could result in delayed treatment. Middle ear and rarely external ear pathology can also cause tinnitus, as can numerous medications (Box 19-2). The patient’s medications should be reviewed.

Evaluation of tinnitus begins with a complete medical history, including duration of symptoms, possible inciting event (e.g., acoustic trauma), and accompanying symptoms (e.g., vertigo, hearing loss, headache, vision changes). Specific questions regarding the tinnitus are critical: Is it unilateral or bilateral? What is the quality of the tinnitus (pitch, volume)? Does it sound like a heartbeat or rushing blood? Does it change? A complete ENT evaluation should be performed, and audiometry is mandatory.

In general, if the tinnitus is bilateral, not particularly intrusive, not pulsatile, and associated with symmetric hearing loss, it is likely secondary to the hearing loss itself. The hearing loss requires further evaluation with magnetic resonance imaging (MRI) with contrast if it is asymmetric.

In cases of pulsatile tinnitus with normal otoscopy, magnetic resonance angiography (MRA) is performed to evaluate for vascular abnormalities. If otoscopy identifies a retrotympanic mass, a temporal bone CT is obtained to evaluate for a vascular mass or abnormality. Blood tests can be performed to rule out anemia or hyperthyroidism, which can result in a hypermetabolic state and cause tinnitus secondary to increased blood flow near the cochlea. Auscultation of the neck, periauricular area, and chest may identify a bruit or murmur, indicating a need for a carotid duplex ultrasound study or echocardiogram, respectively. Most cases of arterial pulsatile tinnitus are secondary to atherosclerotic carotid artery disease. Venous pulsatile tinnitus often improves with digital pressure over the internal jugular vein. Etiologies include idiopathic venous hum, a high-riding jugular bulb, or benign intracranial hypertension.

Effective treatment of tinnitus is difficult and usually requires various approaches. Finding and eliminating potential causes (especially pharmaceutical) is imperative. Patients should be counseled to avoid caffeine and nicotine. No single medicine has been proved effective in treating tinnitus. Antidepressants have shown promise, especially if depression coexists. Intravenous lidocaine eliminates tinnitus in some patients but is not practical and has obvious potential side effects. Various homeopathic treatments and nutritional supplements are effective in some cases, but most have not been evaluated in controlled studies. Hearing aids are beneficial in masking the tinnitus if hearing loss exists. Tinnitus maskers can be purchased that essentially drown out the tinnitus with various distracting noises. Biofeedback and a technique called tinnitus retraining therapy are helpful for some patients. These techniques can be learned through various publications or at a tinnitus treatment center. All patients with obtrusive tinnitus are encouraged to join the American Tinnitus Association, the largest tinnitus support group and an excellent source of reliable information.

Disorders of the External Ear

Auricular Hematoma

Blunt auricular trauma, most commonly in wrestlers and boxers, may shear the perichondrium from the underlying cartilage, leading to a hematoma. The presence of a fluctuant swelling with loss of normal auricular landmarks helps to distinguish a hematoma from ecchymosis. If left untreated, an auricular hematoma may cause fibrosis and neocartilage formation, leading to a deformity of the auricle termed cauliflower ear. Therefore, treatment in a timely manner is recommended.

Although a Cochrane review could not define the best treatment for an acute auricular hematoma, a frequently successful treatment involves incision and drainage with dental rolls sutured to the anterior and posterior auricle (Fig. 19-5). Needle aspiration alone will often lead to recurrences. The bolster is usually left in place for 4 to 7 days, with the patient permitted to return to wrestling or boxing with headgear. Prophylactic antistaphylococcal antibiotics are given. For a long-standing hematoma or a cauliflower ear, debridement of fibrosis and cartilage is necessary (Jones and Mahendran, 2008).

Figure 19-5 Photograph of 16-year-old boy who sustained auricular hematoma in wrestling match. He underwent incision and drainage with placement of dental rolls.

KEY TREATMENT

Successful treatment of auricular hematoma is incision and drainage with dental rolls sutured to the anterior and posterior auricle (SOR: B) (Jones and Mahendran, 2008).

Disorders of the Middle Ear

Key Points

Otitis Media

Acute Otitis Media

The most common infection for which children are seen in a physician’s office is acute otitis media (AOM). The annual cost of AOM in the United States is an estimated $5 billion (Bondy et al., 2000). By age 7 years, 93% of children have had at least one episode of AOM, and 75% have had recurrent infections. AOM can occur at any age, but the highest incidence is between 6 and 24 months in the United States.

The primary cause of bacterial colonization of the middle ear is eustachian tube dysfunction. Abnormal tubal compliance in addition to delayed innervation of the tensor veli palatini muscle leads to collapse of the eustachian tube. Aerobic and anaerobic organisms, as well as viruses, can contribute to middle ear infection (Heikkinen et al., 1999). The three most common bacteria involved in AOM are S. pneumoniae (25%-40% of cases), H. influenzae (10%-30%), and Moraxella catarrhalis (2%-15%) (Klein, 2004). Risk factors most often associated with AOM are child care outside the home and parental smoking. Box 19-3 lists the common risk factors for AOM. A viral upper respiratory infection usually precedes an episode of AOM.

Three criteria are necessary to confirm the diagnosis of AOM: acute onset, presence of middle ear effusion, and signs or symptoms of middle ear inflammation (American Academy of Pediatrics [AAP], 2004; Level of evidence [Grade] B). Middle ear effusion can be diagnosed by direct visualization of air-fluid levels behind the tympanic membrane, a bulging drum, lack of movement on pneumatic otoscopy, or a flat tympanogram readout that indicates no tympanic membrane movement and therefore the presence of middle ear effusion. Redness of the tympanic membrane, pain, and fever are the most common signs and symptoms of middle ear inflammation (see eBox 19-4 online). Erythema of the tympanic membrane without middle ear effusion is myringitis or tympanitis and is a separate diagnosis from AOM. Ear pain in the presence of a normal-appearing, flaccid tympanic membrane indicates causes other than AOM (Box 19-4).

Box 19-4 Causes of Otalgia Other than Acute Otitis Media

Abscessed teeth

Cervical arthritis

Dental malocclusion

Nasopharyngeal carcinoma

Sinus infection

Sore throat

Temporomandibular joint disorders

The standard of care for the treatment of AOM in children older than 2 years is not to treat with antibiotics at the first visit, but to treat the pain and either observe the patient or prescribe an antimicrobial agent depending on certain criteria. The decision either to begin antibiotics or to observe the patient without them is based on the certainty of diagnosis, severity of symptoms, and age of the patient (AAP, 2004). (Table 19-2).

Table 19-2 Treatment of Acute Otitis Media

Features	Treatment
Low-Risk Patients
Older than 6 years, no antimicrobial therapy within past 3 months, no otorrhea, not in daycare, and temperature <38° C (<100.5° F)	Amoxicillin: 40-50 mg/kg/day in divided doses for 5 days
High-Risk Patients
Younger than 2 years, in daycare, treated with antimicrobials within past 3 months, otorrhea, or temperature >38° C (>100.5° F)	Amoxicillin: 80-90 mg/kg/day in divided doses for 10 days
Treatment Failure
Signs and symptoms persisting after 3 days	Amoxicillin–clavulanic acid (Augmentin): 80-90 mg/kg/day for 10 days Cefuroxime axetil (Ceftin): 20-30 mg/kg/day bid for 10 days Ceftriaxone (Rocephin): 50 mg/kg intramuscularly for 1 dose
Penicillin-Allergic Patient
Any	Cefuroxime axetil: <2 years, 125 mg bid; ≥2 years, 250 mg bid TMP-SMX (Bactrim, Septra): 8 mg/kg TMP, 40 mg/kg SMX, per 24 hours in 2 doses Cefprozil (Cefzil): 30 mg/kg/day in 2 doses Cefaclor (Ceclor): 40 mg/kg/day in 3 doses Cefixime (Suprax): 8 mg/kg/day as a single dose

TMP-SMX, Trimethoprim-sulfamethoxazole; bid, twice daily.

When all three criteria for the diagnosis of AOM are met (acute onset, middle ear effusion, and inflammation), the diagnosis is certain, and antibiotic therapy is indicated for any child 2 years old or younger (AAP, 2004; Grade A). For children older than 2 years, observation is an option if the illness is not severe and the parents can be relied on to report the patient’s status and can obtain medication if necessary. Severe illness is defined as moderate to severe otalgia and fever higher than 39° C. (102.2° F.) When two or fewer diagnostic criteria are present, diagnosis is considered uncertain, and observation is allowed for children 6 months and older with nonsevere illness.

Resistance of Streptococcus pneumoniae to penicillin is an increasing problem and ranges from 15% to 50% depending on the area. The mechanism of resistance is based on an alteration of penicillin-binding proteins rather than the production of beta-lactamase, as occurs with H. influenzae and M. catarrhalis. Resistance rates are higher in children than in adults, especially if the children are in daycare or have received antimicrobial therapy in the previous 3 months (Dowell and Schwartz, 1997).

The dose to treat AOM is 80 to 90 mg/kg/day in two divided doses (AAP, 2004). This allows the drug to overcome resistance in the causative organism (Dowell et al., 1999). For patients with a penicillin allergy, alternative medications include cefdinir, cefpodoxime, or cefuroxime. A meta-analysis found that first-generation cephalosporins have cross-allergy with penicillin, although the cross-allergy with second- and third-generation cephalosporins is negligible (Pichichero and Casey, 2007). Macrolides are not recommended for AOM in children because H. influenzae is the dominant organism causing AOM in this age group. Middle ear fluid becomes sterile 3 to 6 days after starting treatment (Carlin et al., 1991), so duration of therapy for uncomplicated AOM is 5 to 7 days, except for the child with an episode of AOM in the past 30 days, for whom a 10-day course of therapy is recommended (Pichichero and Brixner, 2006).

If the initial antibiotic fails to resolve symptoms in 72 hours (pain, fever, redness and bulging of the tympanic membrane, otorrhea), high-dose amoxicillin–clavulanic acid is recommended. Alternatives in penicillin-allergic patients include the antibiotics cited earlier. Patients who do not respond to amoxicillin–clavulanic acid therapy should be treated with intramuscular ceftriaxone for 3 days. This antibiotic in a single dose can also be used initially if the child is vomiting or unable to keep down oral medication. Doses of antimicrobials are given in Table 19-2.

Influenza vaccine has been shown to decrease the number of cases of AOM in immunized patients compared to controls and is recommended for all children age 6 to 24 months.

KEY TREATMENT

Antibiotics are most beneficial in children younger than 2 years with bilateral acute otitis media (AOM) and/or otorrhea (SOR: A).

For most other children with mild disease, close observation and follow-up is an option (SOR: A) (Vouloumanou et al., 2009).

Administration of the seven-valent pneumococcal vaccine (PCV7) in infancy reduces the risk for AOM by 6% to 7%. Administering PCV7 to older children with a history of AOM appears to have no benefit in preventing further episodes (SOR: A) (Jansen et al., 2009).

Second- and third-generation cephalosporins may be used to treat AOM in penicillin-allergic patients (SOR: A) (Pichichero and Casey, 2007).

Uncomplicated AOM may be treated for 5 to 7 days (Pichichero and Brixner, 2006). SOR: A

Otitis Media with Effusion

Otitis media with effusion (OME) is defined as persistent middle ear fluid without pain, fever, or redness of the tympanic membrane. It is often the result of AOM but can occur de novo. About 90% of children have OME before they reach school age. About 80% to 90% of cases resolve within 3 months and 95% within 1 year. Table 19-3 provides the Agency for Health Care Policy and Research (AHCPR) guidelines for treatment of OME.

Table 19-3 AHCPR Guidelines for Treatment of OME

Duration of OME

Treatment

6 weeks

Observation or antimicrobial therapy Only gold members can continue reading. Log In or Register to continue Share this: Click to share on Twitter (Opens in new window) Click to share on Facebook (Opens in new window) Related Related posts: The Family Physician Herbs and Other Dietary Supplements Sports Medicine Care of the Newborn Urinary Tract Disorders Gastroenterology Stay updated, free articles. Join our Telegram channel Join Tags: Textbook of Family Medicine Oct 3, 2016 | Posted by admin in MANUAL THERAPIST | Comments Off on Otorhinolaryngology Full access? Get Clinical Tree Get Clinical Tree app for offline access Get Clinical Tree app for offline access