This chapter reviews infectious and noninfectious conditions that can obstruct the upper airway. These disorders must be recognized quickly because early airway management may be lifesaving. Neck trauma is discussed in the chapter 260, “Trauma to the Neck,” and angioedema is discussed in the chapter 14, “Anaphylaxis, Allergies, and Angioedema.”

PHARYNGITIS/TONSILLITIS

Viruses account for the majority of cases of pharyngitis or tonsillitis. Acute viral pharyngitis is most commonly caused by rhinovirus but can be caused by multiple other viral agents (Table 246-1).¹

VIRAL PHARYNGITIS

Viral pharyngitis generally displays a vesicular or petechial pattern on the soft palate and tonsils and is associated with rhinorrhea. However, in patients with nonstreptococcal pharyngitis (mostly viral), 16% have tonsillar exudate, 55% have cervical adenopathy, and 64% lack cough.² Most cases of viral pharyngitis require no specific diagnostic testing. There are three notable exceptions where testing may be indicated: suspected influenza, infectious mononucleosis, and acute retroviral syndrome. See Centers for Disease Control and Prevention influenza Web site for testing and treatment recommendations (http://www.cdc.gov/flu/). Infectious mononucleosis, influenza herpesvirus, and cytomegalovirus infections are discussed in the chapter 153, “Serious Viral Infections.” The acute retroviral syndrome of early human immunodeficiency virus infection can also mimic mononucleosis. Symptoms of pharyngitis develop 2 to 4 weeks after exposure and resolve within 2 weeks. See the chapter 154, “Human Immunodeficiency Virus Infection” for recommendations on testing and treatment. Non–human immunodeficiency virus, noninfluenza viral pharyngitis should be treated symptomatically with oral hydration, antipyretics, analgesics, and rest. Patients unable to tolerate oral fluids or who become dehydrated should be given IV fluids.

BACTERIAL PHARYNGITIS

Group A β-Hemolytic Streptococcus

Group A β-hemolytic Streptococcus (GABHS) pharyngitis, Lancefield group A species of Streptococcus pyogenes, is responsible for 5% to 15% of pharyngitis in adults.^1,2 After an incubation period of 2 to 5 days, patients develop the sudden onset of sore throat, painful swallowing, chills, and fever. Headache, nausea, and vomiting are common. Signs and symptoms of GABHS pharyngitis include marked erythema of the tonsils and tonsillar pillars (found in 62% of cases); tonsillar exudate (32%); and enlarged, tender cervical lymph nodes (76%).² A 2012 epidemiologic study found that only 6% of GABHS cases had fever and 28% had cough.² Patients may have uvular edema, myalgias, and malaise but are less likely to have rhinorrhea or conjunctivitis compared to viral pharyngitis.

Uvula edema, sometimes referred to as Quincke’s edema, can be associated with upper airway infections such as GABHS pharyngitis, peritonsillar abscess, or epiglottitis. It can also be idiopathic. If it is an isolated finding and symptoms are uncomfortable to the patient, dexamethasone, 4 milligrams IV or PO, can be given as a single dose in the ED.

The original Centor criteria listed four clinical indicators of GABHS pharyngitis: (1) tonsillar exudates, (2) tender anterior cervical adenopathy, (3) absence of cough, and (4) history of fever.² The Centers for Disease Control and Prevention reversed its prior recommendation for empiric treatment based on clinical findings in 2012 in concert with the Infectious Diseases Society of America.³ The Centers for Disease Control and Prevention and Infectious Diseases Society of America recommend using two or more Centor criteria as a threshold for selecting patients for rapid strep testing and treating only those with positive tests.^3,4 Guidelines do not recommend throat cultures in adult patients with one or fewer Centor criteria or routine throat culture for those with negative rapid strep tests, unless considering other bacterial pathogens.³

Untreated, GABHS infection lasts 7 to 10 days. Antibiotic therapy of GABHS hastens resolution by 1 to 2 days if initiated within 2 to 3 days of symptom onset and prevents suppurative complications and rheumatic fever, although not glomerulonephritis.³ GABHS has never been resistant to penicillin, so penicillin remains the recommended first-line drug for GABHS.^5,6 Adults should receive a single IM dose of 1.2 million units of benzathine penicillin G, 500 milligrams of penicillin VK PO two times daily for 10 days, or amoxicillin 500 milligrams PO two times daily or 1000 milligrams one time daily. A first-generation cephalosporin antibiotic or clindamycin may be used for penicillin-allergic patients.⁵ A single dose of PO or IM dexamethasone in immunocompetent adults with moderate to severe pharyngitis can achieve an earlier onset of pain relief and a shorter duration of pain.⁷

Other Causes of Bacterial Pharyngitis

Several other bacteria can cause pharyngitis, although these infections are less common (Table 246-1). S. dysgalactiae subspecies equisimilis, previously known as β-hemolytic groups C and G streptococci, are important pathogens causing pharyngitis, skin infections, and more serious infections such as meningitis or toxic shock syndrome in the elderly or immunocompromised.⁸ S. dysgalactiae subspecies equisimilis frequently colonizes the upper respiratory tract (60% who are culture positive are asymptomatic),⁸ so distinguishing acute infection from a carrier state may be difficult;⁹ treatment is recommend for patients with acute symptoms.⁸ S. dysgalactiae subspecies equisimilis pharyngitis is almost uniformly susceptible to penicillin.⁸ Clindamycin and fluoroquinolones are alternatives.⁸

Fusobacterium necrophorum, a gram-negative anaerobe,¹⁰ is the causative agent in Lemierre’s syndrome, a complication of pharyngitis causing suppurative thrombophlebitis of the internal jugular vein, with or without bacteremia and septic emboli. Suspect F. necrophorum in adolescents or young adults with worsening symptoms and neck swelling.¹¹ Treatment is with penicillin, clindamycin, or third-generation cephalosporins; F. necrophorum resistance to macrolides is high.¹¹

Gonococcal pharyngitis is usually associated with genital infection and is treated by the same antibiotics. Diphtheria is caused by Corynebacterium diphtheriae and is rare in well-immunized populations. It is characterized by a slow onset of mild to moderate pharyngeal discomfort and low-grade fever. On physical examination, a gray membrane is seen adherent to the tonsillar or pharyngeal surface and may extend to the uvula, soft palate, pharynx, and larynx. Treatment is with diphtheria antitoxin and metronidazole to prevent transmission to others.

PERITONSILLAR ABSCESS

A peritonsillar abscess is a collection of purulent material between the tonsillar capsule, the superior constrictor, and palatopharyngeus muscles. Risk factors include periodontal disease, smoking, chronic tonsillitis, multiple trials of antibiotics, and previous peritonsillar abscess.¹² Peritonsillar abscess develops primarily in adolescents and young adults without seasonal variation as previously thought.^12,13 Although peritonsillar abscesses are typically polymicrobial infections, in patients 15 to 24 years of age, Fusobacterium necrophorum has been the most common organism in many communities.^13,14

CLINICAL FEATURES AND DIAGNOSIS

Patients with peritonsillar abscess (adolescents and adults) appear ill and present with sore throat (99%), fever (54%), malaise, odynophagia, dysphagia, and/or otalgia.¹⁵ Physical signs include inferior and medial displacement of the infected tonsil(s) (46%), contralateral deflection of the swollen uvula (43%), tender cervical lymphadenopathy (41%), trismus (32%), muffled voice (“hot potato voice”), palatal edema, and dehydration¹⁵ (Figure 246-1). The differential diagnosis of a peritonsillar abscess includes peritonsillar cellulitis, mononucleosis, lymphoma, herpes simplex tonsillitis, retropharyngeal abscess, neoplasm, and internal carotid artery aneurysm. In peritonsillar cellulitis, erythema and edema of the tonsillar pillar and soft palate are evident, but pus has not yet formed. Diagnosis of a peritonsillar abscess is often made by history and physical examination alone. When the diagnosis is in question, intraoral US has a sensitivity of 89% to 95% with a specificity of 79% to 100% for peritonsillar abscess.¹⁶ CT scan with contrast is indicated if there is concern for spread beyond the peritonsillar space or lateral neck space complications.¹⁶

TREATMENT

Treatment options include drainage of the abscess by needle aspiration, incision and drainage, or, rarely, immediate tonsillectomy. Choice of treatment depends on clinical symptoms, degree of patient cooperation, history of previous tonsil disease, and healthcare personnel experience. There is no difference in outcome when comparing needle aspiration with incision and drainage.¹⁶ Abscess tonsillectomy (“quinsy tonsillectomy”) should only be considered when patients have strong indication for tonsillectomy, such as sleep apnea, recurrent tonsillitis, or recurrent peritonsillar abscess.¹⁶ Needle aspiration is minimally invasive, less painful than incision and drainage, and may be performed by general or specialized medical personnel. Approximately 90% of patients will be treated effectively after a single needle aspiration.¹⁶

Needle aspiration should be performed by an individual trained in the technique. First, apply lidocaine spray or gel or benzocaine-tetracaine spray to the overlying mucosa. Then inject 1 to 2 mL of lidocaine with epinephrine into the mucosa of the anterior tonsillar pillar using a 25-gauge needle The drainage needle should penetrate no more than 1 cm because the internal carotid artery usually lies laterally and posterior to the posterior edge of the tonsil.

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