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1566 SECTION 19: Eye, Ear, Nose, Throat, and Oral Disorders anteriorly or inferiorly. The pars tensa, the largest area of the TM, is only a few cell layers thick and thus is easily torn. Symptoms are acute onset of pain and hearing loss, with or with out bloody otorrhea. There may also be associated vertigo or tinnitus, but this is usually transient unless there has been injury to the inner ear or rupture of the round or oval windows. The TM should be completely visualized and the canal must be cleared of blood and debris. Most TM perforations heal spontaneously. Patients with perforations secondary to blunt or noise trauma that are isolated injuries can be safely discharged and referred to a specialist for further evaluation and a formal audiogram as soon after the injury as possible. Patients should be instructed not to allow water to enter the canal of the ear. Topical or systemic antibiotics are not needed unless foreign material is suspected of remaining in the canal or in the middle ear. Perforations in the pos terosuperior quadrant or those secondary to penetrating trauma have a greater likelihood of ossicular chain damage and should be referred to an otolaryngologist within 24 hours. COMPLICATIONS OF COCHLEAR IMPLANTATION Cochlear implantation functions through electronic stimulation of the auditory nerves in the cochlea in patients with bilateral moderate to severe sensorineural hearing loss. Common complications include vestibular complaints, device failure, and infection. 34 Infections include skin infection, OM, mastoiditis, and meningitis.34-39 If infection is a concern, then a CT with IV contrast is needed to evaluate position of the implant, fluid collections, bony involvement, and subperiosteal abscess. Recur rent OM in patients with cochlear implants can result in meningitis. Meningitis can occur days to years after implantation, with the greatest risk in the first 2 months. 34-42 The most common complication is dizziness or vestibular symp toms, which occur in close to 4% of patients. 34,40,41 Facial nerve weak ness is rare but can present acutely or as a delayed complication. 34 Device failure is the next most common complication and may require CT and device integrity testing. 34,43 Other rare complications include cholesteatoma, seroma, hematoma, cerebrospinal fluid leak, and TM perforation. REFERENCES The complete reference list is available online at www.TintinalliEM.com. FIGURE 242-5. Different-shaped ear scoops and loops are useful to remove cerumen from an impacted ear. Miniature alligator forceps can be used to extricate foreign bodies from the external ear canal. Face and Jaw Emergencies Stephanie A. Lareau Corey R. Heitz INTRODUCTION This chapter will discuss facial infections and disorders involving the mandible. Bell’s palsy is discussed in Chapter 172, “ Acute Peripheral Neurologic Disorders. ” Trigeminal neuralgia is discussed in Chapter 38, “Chronic Pain. ” Nonfacial cellulitis and erysipelas are discussed in Chapter 152, “Soft Tissue Infections. ” Impetigo in children is discussed in Chapter 142, “Rashes in Infants and Children. ” Orbital cellulitis is discussed in Chapter 241, “Eye Emergencies.

sorders. ” Trigeminal neuralgia is discussed in Chapter 38, “Chronic Pain. ” Nonfacial cellulitis and erysipelas are discussed in Chapter 152, “Soft Tissue Infections. ” Impetigo in children is discussed in Chapter 142, “Rashes in Infants and Children. ” Orbital cellulitis is discussed in Chapter 241, “Eye Emergencies. ” FACIAL CELLULITIS, ERYSIPELAS, AND IMPETIGO The differential diagnosis of facial infections is provided in Table 243-1.1  CELLULITIS Cellulitis is a superficial soft tissue infection that lacks anatomic con straints.2-4 Facial cellulitis is caused most commonly by Streptococcus species,5 including Streptococcus pyogenes (group A β-hemolytic) and group G Streptococcus, and Staphylococcus aureus ,4 with an increasing predominance of methicillin-resistant S. aureus.6 An important consideration for facial cellulitis is the potential for an odontogenic source of the infection in the midface. Anaerobic bacteria account for 24% to 62% of the odontogenic infections. 4,7 Methicillin-resistant S. aureus is the most common cause of purulent cellulitis, identified by purulent drainage, purulent bulla, or suspected abscess. 3 Methicillin-resistant S. aureus also is suspected when risk factors are present (see Chapter 152, “Soft Tissue Infections”). Less commonly, cellulitis may represent extension from deep space infections (see “Masticator Space Infection” section later in this chapter). Bedside US can exclude or identify facial abscess (Figure 243-1). CT can identify deep-seated infections incompletely imaged by US. Treatment options organized by infection type are provided in Table  243-2. 3,6-12 The selection of an antibiotic for cellulitis is based on differentiation of purulent from nonpurulent forms. 3,10 Duration of therapy is incompletely studied, but recommendations range from 5 to 7 days, 3,6,7,10-12 extended to 10 to 14 days for immunocompromise or inadequate response.3,10 Treatment failures range from 15% to 20% for β-lactams (amoxicillin-clavulanate, cephalexin, and dicloxacillin) as well as for the anti–methicillin-resistant S. aureus therapies 13 due to the failure to cover methicillin-resistant S. aureus and streptococcal species, respectively. In selected cases, traditional β-lactam therapy may be added to anti–methicillin-resistant S. aureus therapy, but this strategy does not improve outcome. 14 Include coverage for anaerobic bacteria when sus pecting an odontogenic source ( Table 243-2).4,7,9 Incision and drainage is the most effective treatment for abscess (see Chapter 152, “Soft Tissue Infections”). Antibiotic dose recommendations are listed in Table 243-3.  ERYSIPELAS Erysipelas is most common in the lower extremities (66% to 76%) 15-17 but is classically described as a disease of the face (see Figure 152-3). Erysipelas is caused by group G S. pyogenes, group C and group G Streptococcus, and S. aureus.3,15 Bullous erysipelas is a more severe form of the disease and most commonly is caused by methicillin-resistant S. aureus. 18 Penicillin is the antibiotic treatment of choice for presumed non–methicillin-resistant S. aureus infections3,17 but is chosen as empiric therapy in a minority of cases. 8,15-17 If the suspicion exists of a staphylo coccal infection (i.e., bullae, trauma, or the presence of a foreign body), include coverage for methicillin-resistant S. aureus (Table 243-2).  IMPETIGO Impetigo is a discrete, superficial bacterial epidermal infection charac terized by amber crusts (nonbullous) or fluid-filled vesicles (bullous) CHAPTER Tintinalli_Sec19_p1523-1606.indd 1566 8/2/19 3:06 PM

or the presence of a foreign body), include coverage for methicillin-resistant S. aureus (Table 243-2).  IMPETIGO Impetigo is a discrete, superficial bacterial epidermal infection charac terized by amber crusts (nonbullous) or fluid-filled vesicles (bullous) CHAPTER Tintinalli_Sec19_p1523-1606.indd 1566 8/2/19 3:06 PM CHAPTER 243: Face and Jaw Emergencies 1567 (see Figure 142-15). It is most common in children. S. aureus alone or in combination with S. pyogenes (group A β-hemolytic) is the most common cause of nonbullous impetigo. 19,20 Bullous impetigo is typi cally caused by S. aureus.21,22 Treatment should cover streptococcal and staphylococcal species. Topical therapy is sufficient for uncomplicated patients with nonbullous lesions. 22 Mupirocin, retapamulin, or fusidic acid ointment is recommended; however, some resistance exists. 22-24 Consider oral antibiotics for extensive lesions or lesions that do not respond to topical therapy alone. There is no clear preference between macrolides, β-lactamase–resistant penicillins, and cephalosporins. 3,21 Preferred choices are penicillinase-resistant penicillins (dicloxacillin, amoxicillin-clavulanic acid) or first-generation cephalosporins (cepha lexin). 3 For methicillin-resistant S. aureus, treat with trimethoprimsulfamethoxazole or clindamycin 3 (Table 243-3). In endemic regions (e.g., areas of Australia), scabies infestation frequently coexists with impetigo. 25 Consider adding ivermectin, 200 micrograms/kg, single dose, in addition to antibacterial therapy for impetigo.26 SALIVARY GLAND INFECTIONS There are three groups of salivary glands: the parotid, submandibular, and sublingual. The facial nerve passes through the superficial por tion of the parotid gland, and the parotid (Stensen’s) duct opens into the mouth opposite the upper second molar. The submandibular and sublingual glands lie below the plane of the tongue. The submandibular ducts open into the mouth at either side of the frenulum of the tongue. The multiple sublingual ducts open into the sublingual fold or directly into the submandibular duct. Signs of salivary gland infections are unilateral or bilateral facial swelling. Recurrent symptoms, dry mouth and eyes, or joint symptoms suggest etiologies such as immunologic or collagen vascular disorders. Other medical conditions, such as nutritional disorders, toxic exposures, diabetes, dehydration, medication usage (e.g., phenothiazines), preg nancy, and obesity, can result in salivary gland enlargement.

ptoms, dry mouth and eyes, or joint symptoms suggest etiologies such as immunologic or collagen vascular disorders. Other medical conditions, such as nutritional disorders, toxic exposures, diabetes, dehydration, medication usage (e.g., phenothiazines), preg nancy, and obesity, can result in salivary gland enlargement. On physical examination, determine the location of the swelling to identify the gland TABLE 243-1 Differential Diagnosis of Superficial Facial Infection Historical Features Onset/Timing Risk/Inciting Factors Physical Findings Infectious Cellulitis Gradual Skin breaks, foreign bodies, prostheses, immunosuppression Diffuse erythema without clear borders, pain Impetigo Acute Infants, children Discrete vesicles or bullae; patches of crusty skin Erysipelas Acute Elderly, infants and children, immune deficiency, diabetes, alcoholism, skin ulceration, impaired lymphatic drainage Well-defined, raised area of erythema, pain Viral exanthem Often acute Preceding or concurrent viral illness, fever Variable Parotitis Gradual Dehydration, diabetes, immunosuppression Swollen angle of mandible, potentially visible sialolith Necrotizing fasciitis Rapid Trauma, may be minor or not apparent Crepitus, skin necrosis, may be subtle Cutaneous anthrax Gradual Animal contact Black eschar with surrounding erythema Herpes zoster Acute Elderly, immunosuppression Exquisitely tender erythematous or vesicular rash following a dermatome Malignant otitis externa Gradual Diabetes, water exposure Ear pain with drainage, facial swelling, tragal tenderness Inflammatory Insect envenomation Acute Environment supporting insect life Diffuse, red, puffy Apical abscess with secondary buccal swelling Gradual Usually associated dental pain/caries Similar to cellulitis; may have intraoral/gingival findings Contact dermatitis Gradual or acute Often identifiable exposure Variable; maculopapular, itchy rash Immunologic Systemic lupus erythematosus Gradual Female-to-male ratio, 9:1 Erythema in classic “malar” distribution Angioneurotic edema Acute Exposure to angiotensin-converting enzyme inhibitor, allergen Lip, oral mucosal swelling, sometimes facial Vancomycin flushing reaction Acute Recent exposure to vancomycin Facial erythema, warmth FIGURE 243-1. Cellulitis versus abscess. The image on the left shows the cobblestoned appearance of cellulitis, while the one on the right shows a heterogenous fluid collection of abscess. [Photo contributed by R. Gordon, MD.] Tintinalli_Sec19_p1523-1606.indd 1567 8/2/19 3:06 PM

re to vancomycin Facial erythema, warmth FIGURE 243-1. Cellulitis versus abscess. The image on the left shows the cobblestoned appearance of cellulitis, while the one on the right shows a heterogenous fluid collection of abscess. [Photo contributed by R. Gordon, MD.] Tintinalli_Sec19_p1523-1606.indd 1567 8/2/19 3:06 PM 1568 SECTION 19: Eye, Ear, Nose, Throat, and Oral Disorders involved. Multiple gland involvement suggests infection. A palpable tender mass may be a sign of tumor or obstruction by a stone. The differ ential diagnosis of salivary gland swelling is provided in Table 243-4.27,28  VIRAL PAROTITIS (MUMPS) Viral parotitis is an acute infection of the parotid glands, characterized by unilateral or bilateral parotid swelling. It is most often caused by the paramyxovirus and may be caused less commonly by influenza, parainfluenza, coxsackie viruses, echoviruses, lymphocytic choriomeningitis virus, and even human immunodeficiency virus. 28 It is most common in children under the age of 15 years old, but since November 2014, clusters of mumps have been reported in adult members of professional hockey teams. The virus is spread by airborne droplets, incubates in the upper respiratory tract for 2 to 3 weeks, and then spreads systemically. Vaccine protection is not 100%, and outbreaks occur in settings of close contact, such as schools, colleges, sports teams, and camps. After a period of incubation, one third of patients experience a prodrome of fever, malaise, headache, myalgias, arthralgias, and anorexia during a 3- to 5-day period of viremia. 28 The classic salivary gland TABLE 243-2 Antibiotic Therapy for Facial Infections Infection Type Recommended Antibacterial Therapy Nonpurulent cellulitis Oral therapy: dicloxacillin, cephalexin, amoxicillin-clavulanate, clindamycin Parenteral therapy: nafcillin, cefazolin, clindamycin Total duration 5–7 d, extend if slow to respond or immunocompromised Purulent cellulitis (MRSA predominate) Oral therapy: trimethoprim-sulfamethoxazole, doxycycline, minocycline, clindamycin, linezolid Parenteral therapy: vancomycin, daptomycin, linezolid, ceftaroline Total duration 5–7 d, extend if slow to respond or immunocompromised Facial cellulitis of odontogenic origin Oral therapy: amoxicillin-clavulanate, clindamycin, β-lactam drug plus metronidazole Parenteral therapy: ampicillin-sulbactam, piperacillin-tazobactam, clindamycin, β-lactam drug plus metronidazole Total duration 5–7 d, extend if slow to respond or immunocompromised Erysipelas

ed Facial cellulitis of odontogenic origin Oral therapy: amoxicillin-clavulanate, clindamycin, β-lactam drug plus metronidazole Parenteral therapy: ampicillin-sulbactam, piperacillin-tazobactam, clindamycin, β-lactam drug plus metronidazole Total duration 5–7 d, extend if slow to respond or immunocompromised Erysipelas Oral therapy: amoxicillin or penicillin (only if MRSA is unlikely) Methicillin-sensitive Staphylococcus aureus suspected: amoxicillinclavulanate, cephalexin, dicloxacillin Bullous erysipelas (or MRSA suspected): trimethoprim-sulfamethoxazole, clindamycin, doxycycline, or minocycline Parenteral therapy: vancomycin, nafcillin, clindamycin Total duration 5–7 d, extend if slow to respond or immunocompromised Impetigo Topical: mupirocin or retapamulin ointment alone or with oral therapy Oral therapy: dicloxacillin, amoxicillin-clavulanate, cephalexin Alternative: azithromycin MRSA suspected: clindamycin or trimethoprim-sulfamethoxazole Total duration 5–7 d, extend if slow to respond or immunocompromised Suppurative parotitis

Oral therapy: amoxicillin or penicillin (only if MRSA is unlikely) Methicillin-sensitive Staphylococcus aureus suspected: amoxicillinclavulanate, cephalexin, dicloxacillin Bullous erysipelas (or MRSA suspected): trimethoprim-sulfamethoxazole, clindamycin, doxycycline, or minocycline Parenteral therapy: vancomycin, nafcillin, clindamycin Total duration 5–7 d, extend if slow to respond or immunocompromised Impetigo Topical: mupirocin or retapamulin ointment alone or with oral therapy Oral therapy: dicloxacillin, amoxicillin-clavulanate, cephalexin Alternative: azithromycin MRSA suspected: clindamycin or trimethoprim-sulfamethoxazole Total duration 5–7 d, extend if slow to respond or immunocompromised Suppurative parotitis Oral therapy: amoxicillin-clavulanate, clindamycin, or cephalexin with metronidazole Parenteral therapy: nafcillin, or ampicillin-sulbactam; if penicillin allergic, clindamycin or the combination of cephalexin with metronidazole, or vancomycin with metronidazole Hospital acquired or nursing home patients: consider vancomycin Total duration: 10–14 d Masticator space infection Parenteral therapy: IV clindamycin, ampicillin-sulbactam, piperacillintazobactam, or the combination of ampicillin with metronidazole Oral therapy: clindamycin or amoxicillin-clavulanate Total duration: 10–14 d Abbreviation: MRSA = methicillin-resistant Staphylococcus aureus. TABLE 243-3 Antibiotic Doses for Facial Infections Antibiotic Dosage Oral Antibiotics Amoxicillin/clavulanate 875/125 milligrams twice per day Azithromycin 500 milligrams first day, 250 milligrams 4 more days Cephalexin 500 milligrams four times per day Clindamycin 300 milligrams three or four times per day Dicloxacillin 500 milligrams four times per day Doxycycline 100 milligrams twice per day Metronidazole 500 milligrams every 8 h Minocycline 100 milligrams twice per day Penicillin V 500 milligrams four times per day Trimethoprim-sulfamethoxazole 1 double-strength tablet twice per day Parenteral Antibiotics Ampicillin-sulbactam 1.5–3.0 grams every 6 h Piperacillin-tazobactam 3.375 grams every 6 hours Clindamycin 600 milligrams every 8 h Ceftaroline 600 milligrams IV every 12 h (with CrCl >50 mL/min) Cefazolin 1 gram every 8 h Daptomycin 4 milligrams/kg IV every 24 h (with CrCl >30 mL/min) Linezolid 600 milligrams IV every 12h Metronidazole 1 gram loading dose, then 500 milligrams every 8 h Nafcillin 1–2 grams every 4 h Penicillin G 2–3 million units every 6 h Vancomycin 15 milligrams /kg every 12 h with adjustment for renal function Abbreviation: CrCl = creatinine clearance. TABLE 243-4 Differential Diagnosis of Salivary Gland Swelling Historical Features Disorder Onset Risks/Inciting Factors Clinical Features Infectious Viral parotitis (mumps) Gradual Nonimmunized Prodromal illness, unilateral tense swelling, absent warmth/erythema Buccal cellulitis Gradual Haemophilus influenzae infection in nonimmunized Erythematous, tender Suppurative parotitis Rapid Dehydration, immunosuppression, chronic illness, recent anesthesia Painful buccal swelling, fever, pus expression from Stensen’s duct Masseter space abscess Gradual Dental infection, post trauma Trismus, posterior inferior facial swelling Tuberculosis Gradual Exposure, immunosuppression Chronic crusting plaques Immunologic Sjögren’s syndrome Gradual — Dry mouth, eyes, sclerosis Systemic lupus Gradual Female sex, Asian or African American race No signs of infection Sarcoidosis Gradual Female sex, African American race No signs of infection Other Neoplasm Gradual — No erythema, warmth Sialolithiasis Gradual Dehydration, chronic illness Swelling, tenderness, no signs of infection Tintinalli_Sec19_p1523-1606.indd 1568 8/2/19 3:06 PM

ian or African American race No signs of infection Sarcoidosis Gradual Female sex, African American race No signs of infection Other Neoplasm Gradual — No erythema, warmth Sialolithiasis Gradual Dehydration, chronic illness Swelling, tenderness, no signs of infection Tintinalli_Sec19_p1523-1606.indd 1568 8/2/19 3:06 PM CHAPTER 243: Face and Jaw Emergencies 1569 swelling then follows. Unilateral swelling is typically followed by bilat eral parotid involvement. The gland is tense and painful, but erythema and warmth are notably absent. Stensen’s duct may be inflamed, but no pus can be expressed. Diagnosis is clinical and treatment is supportive. Salivary gland swelling typically lasts from 1 to 5 days. The patient is contagious for 9 days after the onset of parotid swelling, and children with mumps should be excluded from school or day care for this interval. Mumps is usually benign in children but can be severe in adults. Unilateral orchitis affects 20% to 30% of males (with a predisposition of ≥8 years of age), whereas oophoritis affects only 5% of females. Other complications of the mumps virus include mastitis, pancreatitis, aseptic meningitis, sensorineural hearing loss, myocarditis, polyarthritis, hemolytic anemia, and thrombocytopenia. 28 Immunocompetent patients with isolated viral parotitis or orchitis can be managed as outpatients. Admit patients with systemic complications.  SUPPURATIVE PAROTITIS Suppurative parotitis is a serious bacterial infection of the parotid gland that occurs in patients with compromised salivary flow. It is caused by the retrograde migration of oral bacteria into the salivary ducts and parenchyma. 28 Predisposing factors include recent anesthesia, dehy dration, prematurity or advanced age, sialolithiasis, oral neoplasms, salivary duct strictures, tracheostomy, and ductal foreign bodies. Medications that cause either systemic dehydration or decreased salivary flow specifically can cause parotitis. These include diuretics, antihistamines, tricyclic antidepressants, phenothiazines, β-blockers, and barbiturates. 28 Several chronic illnesses also predispose patients to suppurative parotitis, such as human immunodeficiency virus, hepatic or renal failure, diabetes mellitus, hypothyroidism, malnutrition, Sjögren’s syndrome, depression, anorexia, bulimia, hyperuricemia, and cystic fibrosis. Most cases of suppurative parotitis are caused by S. aureus, with Streptococcus pneumoniae, S. pyogenes, and Haemophilus influenzae as more infrequent pathogens. 3,28 Anaerobes such as Bacteroides species, peptostreptococci, and fusobacteria are common. 30,31 In the immunocompromised host, gram-negative organisms such as Escherichia coli and Pseudomonas may be seen.30,31 The onset of suppurative parotitis is rapid, and the skin over the parotid gland is red and tender. Pus may be expressed from the Stensen’s duct. There is often fever and trismus. Suppurative parotitis is diagnosed clinically, with evidence of puru lent drainage from Stensen’s duct. Cultures of Stensen’s duct drainage can guide therapy in the patient not responding to first-line antibiotics. Imaging is not helpful unless an abscess is suspected, in which case US or CT is diagnostic. Because suppurative parotitis is caused by states of decreased salivary flow, treatment should optimize salivary flow. Hydrate the volumedepleted patient. Massage and apply heat to the affected gland. Stimulate salivation using sialagogues, such as lemon drops. When possible, dis continue drugs that cause dry mouth, and attempt to correct underlying medical problems. 30,31 Treat patients with oral antibiotics if they can tolerate oral liquids and have no evidence of systemic illness.

pply heat to the affected gland. Stimulate salivation using sialagogues, such as lemon drops. When possible, dis continue drugs that cause dry mouth, and attempt to correct underlying medical problems. 30,31 Treat patients with oral antibiotics if they can tolerate oral liquids and have no evidence of systemic illness. Admit for parenteral antibiotics patients who have trismus and cannot tolerate oral liquids, are immu nocompromised or incapable of complying with an outpatient treatment regimen, or have not shown improvement after 48 hours of outpatient treatment. 30,31 Antimicrobial therapy consists of agents that cover both staphylococcal and streptococcal species (Tables 243-2 and 243-3). The initial choice for oral therapy includes amoxicillin-clavulanate; in penicillin-allergic patients, use clindamycin or a combination of cephalexin with met ronidazole. 3,30,31 When parenteral therapy is indicated, choices include nafcillin, ampicillin-sulbactam, or a combination of vancomycin with metronidazole. In hospitalized or nursing home patients, the possibility of methicillin-resistant S. aureus, for which vancomycin is appropriate, must be considered. In neonates, treat with gentamicin and antistaphy lococcal antibiotics combined with hydration. If there is no improve ment in 24 to 48 hours, surgical drainage is required.  SIALOLITHIASIS Sialolithiasis is the development of a calcium carbonate and calcium phosphate stone (sialolith) in a stagnant salivary duct. Salivary cal culi can develop in any age group, but usually are symptomatic in men between the third and sixth decades. 28 More than 80% of stones occur in the submandibular gland, with most of the remainder in the parotid. The symptoms of pain, swelling, and tenderness may resemble those of parotitis. It may be hard to distinguish parotitis from sialolithiasis, and the two conditions may coexist. Sialolithiasis is typically unilateral. The pain and swelling of sialolithiasis are colicky and exacerbated by meals. The diagnosis is clinical. A stone may be palpated within the duct, and the gland is firm. 28 Intraoral radiographs are more sensi tive than extraoral films in identifying salivary calculi. The calculi are radiopaque in about 70% of cases. US and thin-cut CT also will identify sialoliths but are usually obtained only if abscess is in the differential diagnosis. ED bedside US has been shown to be a useful diagnostic tool to determine number, size, and location of stones (Figure 243-2). 32 A conservative course of treatment should precede imaging studies. Occasionally on CT, the diagnosis of sialolithiasis is made by the typically glandular swelling and inflammatory changes (signifying ductal obstruction) without an obvious stone seen in the duct (Figure 243-3). Treatment is outpatient therapy with analgesics, antibiotics if there is concurrent infection, massage, and sialagogues, such as lemon drops. Palpable stones in the distal duct may be digitally “milked” from the duct. Complications of salivary duct obstruction include recurrent or persistent obstruction, strictures, infection, and gland atrophy. FIGURE 243-2. US image of sialolithiasis (the bright hemi-circular structure). [Photo contributed by R. Gordon, MD.] Tintinalli_Sec19_p1523-1606.indd 1569 8/2/19 3:06 PM

lked” from the duct. Complications of salivary duct obstruction include recurrent or persistent obstruction, strictures, infection, and gland atrophy. FIGURE 243-2. US image of sialolithiasis (the bright hemi-circular structure). [Photo contributed by R. Gordon, MD.] Tintinalli_Sec19_p1523-1606.indd 1569 8/2/19 3:06 PM 1570 SECTION 19: Eye, Ear, Nose, Throat, and Oral Disorders MASTICATOR SPACE INFECTION The masticator space consists of four potential spaces bounded by the muscles of mastication ( Figure 243-4). These spaces include the mas seteric (or submasseteric), superficial temporal, deep temporal, and pterygomandibular spaces. 33 The spaces are all contiguous. Bacteria may gain entry to the space from dental infections, trauma, surgery, or injections. Infections of the masticator space are polymicrobial and generally anaerobic, although aerobic oral streptococcal species may pre dominate briefly. 4,33 Typical organisms include species of Streptococcus, Peptostreptococcus, Bacteroides, Prevotella, Porphyromonas, Fusobacterium, Actinomyces, Veillonella, and anaerobic spirochetes.4,33 The most frequent acute clinical findings are trismus associated with facial swelling, pain, and erythema. When infection occurs in the masseteric space, there is facial swelling posteriorly and inferiorly, with mild to moderate trismus. If the temporal space is infected, there is soft tissue swelling over the temporalis muscle and trismus. Trismus without swelling suggests pterygomandibular space abscess. In chronic infection, the patient can be afebrile but may complain of intermittent trismus. Constitutional signs may include fever, malaise, dehydration, dysphagia, nausea, or vomiting. In more advanced cases, systemic signs of sepsis are present. The differential diagnosis includes other sources of lateral facial pain and swelling (Table 243-4). Ultrasonography is helpful in differentiating abscesses from cellulitis (Figure 243-1), for the diagnosis of lymphadenitis, and to identify internal jugular thrombosis. However, contrast-enhanced CT is the preferred diagnostic tool for masseteric and related deep space infections. 33-35 CT can define the extent of the abscess and distinguish cellulitis from abscess in all spaces except the retropharyngeal. 33 MRI can be consid ered if infection is thought to reach the skull base. 34 The patient’s condition determines therapy. Because all the subor dinate spaces of the masticator space communicate with each other and ultimately with the tissue planes that extend down the neck to the mediastinum, the extent of the infection should be defined efficiently and treatment begun promptly. Airway compromise is rare in unilateral masticator space infection. Administer antibiotics in the ED (Table 243-3), resuscitate for sepsis when present, and admit the patient. IV clindamycin is recommended, with alternatives including ampicillin-sulbactam, piperacillin-tazobactam, or the combination of penicillin with metronidazole. 4,33 Antibiotics are continued for 10 to 14 days. Consult otolaryngology for surgical intervention and management. TEMPOROMANDIBULAR JOINT DISORDERS The temporomandibular joint combines both a hinge and gliding action. The articular surfaces of the joint are separated by the articular disk, or meniscus, which assists in the hinge action between the mandibular condyle and the disk and in the gliding action between the disk and temporal bone.  TEMPOROMANDIBULAR JOINT DYSFUNCTION Temporomandibular joint dysfunction causes pain of the joint and its surrounding anatomic structures. Assess for temporomandibular joint injury when evaluating direct jaw trauma or acute dental injury.

ndyle and the disk and in the gliding action between the disk and temporal bone.  TEMPOROMANDIBULAR JOINT DYSFUNCTION Temporomandibular joint dysfunction causes pain of the joint and its surrounding anatomic structures. Assess for temporomandibular joint injury when evaluating direct jaw trauma or acute dental injury. 37 Most studies have found no significant correlation between occlusal parame ters or bruxism and signs or symptoms of temporomandibular joint disorders.38 Over time, degenerative joint disease (osteoarthritis) may result from chronic internal derangement or occur secondary to systemic disease such as rheumatoid arthritis or systemic lupus erythematosus. The chief complaint is usually pain localized to one of the muscles of mastication or pain with chewing in one or both temporomandibular joints. The masseter muscle is the most frequently identified painful area, followed by the temporalis, sternocleidomastoid, splenius capitis, and trapezius muscles. 38 Physical findings may include limitation in the range of motion of the mandible. Palpate the muscles of mastication to find areas of sensitivity, induration, rigidity, and swelling. Palpate the condylar heads with the teeth together and then with the teeth apart. The differential diagnosis of temporomandibular joint dysfunction includes jaw trauma, including fracture and dislocation; odontogenic pain, including from abscess, caries, or trauma; otologic referred pain, including from otitis media, otitis externa, and foreign body; and tem poral arteritis. Temporomandibular joint dysfunction is diagnosed by history and physical examination. Isolated temporomandibular joint clicking with out pain or other dysfunction is not diagnostically sufficient. 38 For acute trauma, the panoramic radiograph view of the mandible (panorex) identifies most fractures. 39 CT is appropriate in the assessment of potentially complex fractures, infections, and neoplastic disease. CT is often Right submandibular gland showing marked swelling and inflammatory changes without abscess Enlarged reactive cervical lymph node FIGURE 243-3. Marked enlargement of the right submandibular gland. This contrasted CT image shows marked enlargement of the right submandibular gland and surrounding inflammatory changes without an obvious stone or abscess formation. [Image used with permission of John Wightman, MD.] Temporalis muscle Temporal fascia Zygomatic arch Masseteric space Masseter muscle Mandible Deep temporal space Sphenoid bone Infratemporal space Hamular process Pterygomandibular space Medial pterygoid muscle Superficial temporal space FIGURE 243-4. Masticator space. Tintinalli_Sec19_p1523-1606.indd 1570 8/2/19 3:06 PM

Temporalis muscle Temporal fascia Zygomatic arch Masseteric space Masseter muscle Mandible Deep temporal space Sphenoid bone Infratemporal space Hamular process Pterygomandibular space Medial pterygoid muscle Superficial temporal space FIGURE 243-4. Masticator space. Tintinalli_Sec19_p1523-1606.indd 1570 8/2/19 3:06 PM CHAPTER 243: Face and Jaw Emergencies 1571 the imaging modality of choice in the ED as panorex is typically not available. The oral maxillofacial surgeon manages fractures and should be consulted for trismus, significant mandible displacement, and open fractures. For nontraumatic conditions, give simple analgesics, including NSAIDs. 40 Advise the patient to eat soft foods until definitive treatment is provided. The management of chronic temporomandibular dysfunc tion may ultimately require referral to a dentist, maxillofacial surgeon, or pain specialist. MANDIBLE DISLOCATION The mandible can be dislocated in an anterior, posterior, lateral, or superior direction. Anterior dislocation is most common and occurs when the mandibular condyle is forced in front of the articular eminence. Muscular spasm then traps the mandible in anterior dislocation, and the mandible is elevated before retraction. Spasm of the temporalis and lateral pterygoid muscles tends to prevent reduction once dislocation has occurred. Dislocations are usually bilateral but can be unilateral. Posterior dislocations are rare. They follow a blow that may or may not break the condylar neck. In posterior dislocation, the mandibular condyle is thrust backward against the mastoid, and the condylar head may prolapse into the external auditory canal. 36 Lateral dislocations are often associated with mandibular fracture. With a lateral dislocation, the condylar head is forced laterally and then superiorly into the temporal space. Superior dislocations occur from a blow to the partially open mouth that forces the condylar head upward. Associated injuries include cerebral contusions, facial nerve palsy, and deafness. Acute jaw dislocation causes severe pain, difficulty in speaking or swallowing, or malocclusion after a blow to the jaw or a seizure or, sometimes, spontaneously. There may be loose or missing teeth and areas of sensory deficit at the chin or mouth. With anterior dislocation, pain is localized anterior to the tragus. Symptoms may develop after extreme mouth opening from laughing, yawning, vomiting, taking a large bite, or trauma, or iatrogenically during dental extraction, general anesthesia, and tonsillectomy. 36 With anterior dislocations, the lower jaw is promi nent appearing, and there is visible and palpable preauricular depression from the displacement of the mandibular condyle. There also will be difficulty with jaw movement. If the dislocation is unilateral, there is deviation of the jaw away from the dislocation. When a posterior dislocation is considered, examine the external auditory canal. Confirm that hearing is at baseline. With lateral dislocations, the condylar head is palpable in the temporal space, and there are always signs of jaw fracture (e.g., malocclusion). Posterior, lateral, or superior dislocations result from severe trauma. The differential diagnosis includes mandibular fracture, traumatic hemarthrosis, acute closed locking of the temporomandibular joint meniscus, and temporomandibular joint dysfunction. In the cooperative patient with a spontaneous atraumatic anterior dislocation, the diagnosis is clinical. In other dislocations, including any traumatic dislocation, obtain radiographs. The panoramic view (pan orex) or a maxillofacial CT should be obtained for any significant trauma. Perform reduction in the ED for closed anterior dislocations without fracture.

us atraumatic anterior dislocation, the diagnosis is clinical. In other dislocations, including any traumatic dislocation, obtain radiographs. The panoramic view (pan orex) or a maxillofacial CT should be obtained for any significant trauma. Perform reduction in the ED for closed anterior dislocations without fracture. 36 A short-acting IV muscle relaxant (e.g., midazolam) may help to decrease muscle spasm. Appropriate airway and hemodynamic monitoring should be initiated. Full procedural sedation may be required. 41 Alternatively, local anesthetic can be placed into the joint space. Using aseptic technique, place a 21-gauge needle into the pre auricular depression just anterior to the tragus and inject 2 mL of 2% lidocaine 42 (Figure 243-5).  REDUCTION OF ANTERIOR TEMPOROMANDIBULAR JOINT DISLOCATION Most publications concerning techniques of mandibular joint relocation are descriptive or case reports.37,42,43 A single randomized controlled trial of 90 patients found that the wrist pivot method was most successful (96.7% vs. 86.7% for the conventional method and 66.7% for the extra oral method). 44 In addition, the authors found that the extraoral method was more difficult for the provider and the patient. The three methods are described in the following sections. Conventional Method The most commonly used technique requires the patient to be firmly seated with the head against the wall or chair back, positioned so that the examiner’s flexed elbow is at the level of the patient’s mandible. Apply a few layers of gauze (or plastic syringes) over gloved thumbs for protection, in case the mandible snaps closed after reduction. Facing the patient, place gloved thumbs in the patient’s mouth, over the occlusal surfaces of the mandibular molars, as far back as possible. Curve your fingers beneath the angle and body of the mandible. Using the thumbs, apply pressure downward and backward (toward the patient). Slightly opening the jaw may help disengage the condyle from the anterior eminence (Figure 243-6). When the dislocation is bilateral, it may be easier to relocate one side at a time. In an alternative version of the conventional method, with the patient recumbent and supine, stand at the head of the bed, place the thumbs on the molars, and apply downward and backward pressure (toward the stretcher) (Figure 243-7). FIGURE 243-5. Site for injection of local anesthesia for reduction of dislocated mandible. Place a 21-gauge needle into the preauricular depression just anterior to the tragus and inject 2 mL of 2% lidocaine. FIGURE 243-6. Reduction of dislocated mandible technique in a seated patient. The thumbs are placed over the molars, and pressure is applied downward and backward. Tintinalli_Sec19_p1523-1606.indd 1571 8/2/19 3:06 PM