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CHAPTER 245: Oral and Dental Emergencies 1579 similar to a common cold or viral upper respiratory infection, but symptom duration ranges from 7 days to up to 12 weeks and may present after a recent viral upper respiratory tract infection.40 American Academy of Otolaryngology guidelines recommend reserving the diagnosis of acute bacterial sinusitis for patients with symptoms persistent for 10 days or more. 38 Experts acknowledge that the evidence proving symptom duration alone can identify a bacterial etiology is weak. 42 However, the guideline panel considered this limitation on the diagnosis as appropriate, acknowledging the low specificity of the criteria. 38,42 If a complication of rhinosinusitis is suspected by clinical presentation or duration of symptoms, CT scan (with contrast) is helpful to identify or rule out intracranial extension. 38 The differential diagnosis of rhinosinusitis includes migraine headache, craniofacial neoplasm, foreign body retention, and dental caries. TREATMENT Supportive treatment is the most common and effective treatment for acute uncomplicated rhinosinusitis. Nasal saline irrigation alone or in conjunction with other adjunctive measures, such as nasal decon gestants, may decrease symptom severity. 38 Restrict the use of topical decongestants such as oxymetazoline to approximately 3 days to avoid rebound mucosal congestion or edema (rhinitis medicamentosa). Topical (intranasal spray) corticosteroids may shorten the duration of illness. In a 2014 Cochrane database systematic review analyzing the effi cacy of antibiotic therapy, the authors concluded that antibiotics may provide a small treatment effect in patients with symptoms of rhino sinusitis lasting >7 days. 37 However, because 80% of patients treated with placebo also improved within 2 weeks, it is unclear whether the treatment effect is clinically significant. In general, antibiotics should be reserved for patients with purulent nasal secretions and severe symptoms for ≥7 to 10 days. 36-38 If antibiotics are prescribed, amoxicillin is recommended as first-line therapy for most adults, 36 at a dose of 500 milligrams PO three times per day. Patients with penicillin allergies may receive macrolide antibiotics, cephalosporins, or fluoroquinolones. 36,41 For patients who have received antibiotics within the past 4 to 6 weeks, consider a fluoroquinolone or high-dose amoxicillin-clavulanate. 37 Use caution in selection of antibiotics in patients who are on oral anticoagulation. 21 In the aforementioned Cochrane review, comparisons between different classes of antibiotics showed no significant difference. 37 Follow-up with a primary care provider is advised. Patients with subacute, chronic, or recurrent rhinosinusitis should be evaluated for conditions that modify management, such as allergy, cystic fibrosis, or immunocompromise. Outpatient CT of the sinuses can evaluate for invasion of neighboring tissues and neoplasms. 37 ENT follow-up is advised.40,44 COMPLICATIONS Complications of rhinosinusitis are mostly related to extension of the infection beyond usual anatomic boundaries. Meningitis, cavernous sinus thrombosis, and intracranial abscesses are rare but important complications associated with contiguous spread of sinus disease. Up to 75% of cases of orbital cellulitis, which can lead to blindness through venous congestion and ischemia of the optic nerve, are attributable to disease of the sinuses.

is, cavernous sinus thrombosis, and intracranial abscesses are rare but important complications associated with contiguous spread of sinus disease. Up to 75% of cases of orbital cellulitis, which can lead to blindness through venous congestion and ischemia of the optic nerve, are attributable to disease of the sinuses. 40 Frontal sinusitis can lead to osteomyelitis of the frontal bone with a doughy swelling of the forehead called Pott’s puffy tumor and can also be associated with an extradural or subdural empyema. In general, patients with these deeper infec tions usually appear systemically ill or have focal neurologic signs and require admission and IV antibiotics. REFERENCES The complete reference list is available online at www.TintinalliEM.com. Oral and Dental Emergencies Ronald W. Beaudreau INTRODUCTION Oral emergencies generally can be divided into two broad categories: (1) nontraumatic orofacial pain and (2) orofacial trauma, specifically dentoalveolar trauma. Dental pain is a common ED chief complaint, so emergency providers should be familiar with normal oral and dental anatomy to appropriately differentiate and manage dental and nondental causes of dental pain.  ORAL AND DENTAL ANATOMY The normal adult dentition consists of 32 permanent teeth. The adult dentition has four types of teeth: 8 incisors, 4 canines, 8 premolars, and 12 molars. The primary or deciduous dentition consists of 20 teeth of three types: 8 incisors, 4 canines, and 8 molars. Figure 245-1 shows the eruptive pattern of both the primary and permanent dentition. Figure 245-2 illustrates the most commonly used tooth numbering system; however, description of the tooth type and location is also appropriate.  ANATOMY OF THE TEETH A tooth consists largely of dentin, which surrounds the pulp, the tooth’s neurovascular supply (Figure 245-3). Dentin is a homogeneous material produced by pulpal odontoblasts throughout life. Dentin is deposited as a system of microtubules filled with odontoblastic processes and extracellular fluid. The crown, or the visible portion of tooth, consists of a thick enamel layer overlying the dentin. Enamel, the hardest substance in the human body, consists largely of hydroxyapatite and is produced by ameloblasts before eruption of the tooth into the mouth. The root portion of the tooth extends into the alveolar bone and is covered with a thin layer of cementum. CHAPTER Age of primary tooth eruption Patient’s right Patient’s left Age of permanent tooth eruption 7–8 yr. 8–9 yr.

ly of hydroxyapatite and is produced by ameloblasts before eruption of the tooth into the mouth. The root portion of the tooth extends into the alveolar bone and is covered with a thin layer of cementum. CHAPTER Age of primary tooth eruption Patient’s right Patient’s left Age of permanent tooth eruption 7–8 yr. 8–9 yr. 11–12 yr. 10–11 yr. 10–12 yr. 6–7 yr. 12–13 yr. 11–13 yr. 6–7 yr. 11–12 yr. 10–12 yr. 9–10 yr. 7–8 yr. 6–7 yr. 8–12 mo. 9–11 mo. 16–22 mo. 13–19 mo. 25–33 mo. 23–31 mo. 14–18 mo. 17–23 mo. 10–16 mo. 6–10 mo. FIGURE 245-1. Normal eruptive patterns of the primary and permanent dentition. mo. = month; yr. = years. Tintinalli_Sec19_p1523-1606.indd 1579 8/2/19 3:07 PM

12–13 yr. 11–13 yr. 6–7 yr. 11–12 yr. 10–12 yr. 9–10 yr. 7–8 yr. 6–7 yr. 8–12 mo. 9–11 mo. 16–22 mo. 13–19 mo. 25–33 mo. 23–31 mo. 14–18 mo. 17–23 mo. 10–16 mo. 6–10 mo. FIGURE 245-1. Normal eruptive patterns of the primary and permanent dentition. mo. = month; yr. = years. Tintinalli_Sec19_p1523-1606.indd 1579 8/2/19 3:07 PM 1580 SECTION 19: Eye, Ear, Nose, Throat, and Oral Disorders  THE NORMAL PERIODONTIUM The periodontium, or attachment apparatus, is essential for maintain ing the integrity of the dentoalveolar unit. The attachment apparatus consists of a gingival component and a periodontal component. The gingival component includes the junctional epithelium, gingival tissue, and gingival fibers and primarily functions to maintain the integrity of the periodontal component. The periodontal component includes the periodontal ligament, alveolar bone, and cementum of the root of the tooth and forms most of the attachment apparatus. Disease states such as gingivitis and periodontal disease weaken and destroy the attachment apparatus, resulting in tooth mobility and tooth loss. Gingival tissue is keratinized stratified squamous epithelium. It can be divided into the free gingival margin and the attached gingiva. The free gingiva is the portion that forms the 2- to 3-mm-deep gingival sulcus in the disease-free state. The attached gingiva adheres firmly to the underlying alveolar bone. The nonkeratinized alveolar mucosa extends from the attached gingiva to the vestibule and floor of the mouth. The mucosal tissue of the cheeks, lips, and floor of the mouth is also composed of nonkeratinized squamous epithelium.  OROFACIAL PAIN Table 245-1 lists common causes of orofacial pain. Pain of dental origin may be diffuse in nature, presenting as a headache, sinus pain, eye pain, or jaw or neck pain, or may be localized to a single tooth. Remember to consider myocardial infarction as a cause of jaw pain. Use a systematic approach for examination of the oral cavity. If not contraindicated, examine the patient in the sitting position with the head supported. First, evaluate the general condition of the patient, including speech, ability to swallow oral secretions, and any obvious swelling or asymmetry of the head and neck. Next, examine the oral soft tissue using a tongue depressor to expand your view, looking specifically at the inner lips, the buccal and labial mucosa, the hard and soft palate, and the tongue and floor of the mouth. Ask the patient to extend the tongue, and gently grasp it with a piece of dry gauze, further extending it to the right and to the left, to expose each base. The floor of the mouth should be palpated with a finger in the mouth and one externally under the chin to check for a mass or lesion. Examine the teeth visually, and then gently percuss the suspected teeth with a firm clean object to determine if a specific tooth is the source of pain. If the patient has experienced trauma, test each tooth for mobility and tenderness with gentle pressure and percussion. Check that all the teeth occlude as nor mal for the patient. Assess the degree of opening of the mouth. Palpate for potential fractures of the mandible or maxilla. Finally, evaluate the temporomandibular joint by placing your index fingers in the ears and feeling for crepitance or popping while the mandible is fully opened and closed. PAIN OF ODONTOGENIC ORIGIN  TOOTH ERUPTION AND PERICORONITIS Discomfort is commonly associated with the eruption of primary or deciduous teeth in infants. Gingival irritation (86.18%), irritability (68.19%), and drooling (55.72%) are commonly associated findings. Teething infants may have a mildly elevated temperature, but it is rarely high enough to be characterized as fever.

S Discomfort is commonly associated with the eruption of primary or deciduous teeth in infants. Gingival irritation (86.18%), irritability (68.19%), and drooling (55.72%) are commonly associated findings. Teething infants may have a mildly elevated temperature, but it is rarely high enough to be characterized as fever. 2 Eruption of permanent teeth, especially third molars, or wisdom teeth, may cause pain. Gingival irritation and inflammation associated with tooth eruption are common and must be distinguished from pericoronitis. Pericoronitis is inflammation of the operculum: the gingival tissue overlying the occlusal surface of an erupting tooth. Impaction of food and debris beneath the operculum results in a severe inflammatory response. Without intervention, this progressive inflammatory process will result in localized infection. Because of the close proximity of the mas ticator space (composed of the masseteric space, pterygomandibular space, and the superficial and deep temporalis space) to third molars, this infection can cause trismus. If the infection spreads into the connecting parapharyngeal spaces, it can be life threatening. Treatment of mild to moderate pericoronitis without associated systemic symptoms consists of appropriate oral antibiotic therapy; local irrigation of food and debris from underneath the operculum; saline mouth rinses; and analgesia with NSAIDs and opiates as appropriate. See Table 245-2 for appropriate antibiotics for outpatient treatment of dental and oral Permanent maxillary right first molar Permanent mandibular right third molar Permanent maxillary left second premolar Permanent mandibular left canine Primary Teeth Primary maxillary right first molar Primary maxillary left second molar Primary mandibular left caninePrimary mandibular right lateral incisor 7 89 222324252627 D E F G MNOPQ Permanent Teeth Patient’s right Patient’s left FIGURE 245-2. Tooth numbering system. Crown Root Enamel Dentin Pulp Cementum Periodontal ligament Alveolar bone Apex FIGURE 245-3. The dental anatomic unit and attachment apparatus. Tintinalli_Sec19_p1523-1606.indd 1580 8/2/19 3:07 PM

ncisor 7 89 222324252627 D E F G MNOPQ Permanent Teeth Patient’s right Patient’s left FIGURE 245-2. Tooth numbering system. Crown Root Enamel Dentin Pulp Cementum Periodontal ligament Alveolar bone Apex FIGURE 245-3. The dental anatomic unit and attachment apparatus. Tintinalli_Sec19_p1523-1606.indd 1580 8/2/19 3:07 PM CHAPTER 245: Oral and Dental Emergencies 1581 infections. More severe cases may require IV antibiotics and admis sion; see masticator space infections in Chapter  243, “Face and Jaw Emergencies, ” for more information. For outpatient management, referral to a general dentist or an oral and maxillofacial surgeon within 24 to 48 hours is appropriate. 3,4  DENTAL CARIES AND PULPITIS Dental caries is the loss of integrity of the tooth enamel from hydroxy apatite dissolution by prolonged exposure to the acidic metabolic by-products of plaque bacteria. Caries most commonly occur in areas where plaque accumulates such as pits and fissures of the occlusal sur face, interproximally, and along the gingival margins. When a sufficient breach of enamel integrity occurs, and the dentin is involved, caries spread along dentinal microtubules. Direct communication between the oral environment and the vital dental pulp is established, and sensitivity to cold or sweet stimulus may result. The pulpal inflammatory process is initially reversible, but with con tinued stimuli, the pulp’s ability to respond and repair is compromised. Irreversible pulpitis can be distinguished from reversible pulpitis by the duration of symptoms. In reversible pulpitis, the duration of pain is short, lasting seconds, as compared with irreversible pulpitis, in which the pain may last for minutes to hours. The most common stimulus is heat or cold, although sweet or sour stimuli also can elicit pain. Irre versible pulpits may also present as spontaneous tooth pain; however, this is more commonly associated with pulpal necrosis. 3 Authors of a systematic review published in 2016 concluded that there is insufficient evidence to determine if antibiotics reduce pain when used to treat irreversible pulpitis, in the absence of obvious infection. 5 A local anesthetic block, as discussed in this chapter’s section on dental local anesthesia, greatly reduces pain and should be considered for short-term pain management. NSAIDs with or without acetaminophen as an adjunct are recommended by the American Dental Association over narcotics for managing dental pain because NSAIDs offer the most favorable balance between pain reduction and potential harms. 6 The definitive treatment for irreversible pulpitis and pulpal necrosis is root canal therapy or dental extraction.  CRACKED TOOTH SYNDROME Cracked tooth syndrome is an incomplete fracture of a tooth that may extend into the vital pulp. Molars are most commonly affected. The patient experiences sharp pain on chewing that resolves when chewing ceases. Cold and sweet stimuli may also evoke pain. NSAIDs are fre quently effective at temporarily controlling pain. 3,4 The patient should avoid chewing on the affected side and see a dentist for definitive treatment.  PERIRADICULAR PERIODONTITIS Acute periradicular periodontitis is the extension of pulp disease, inflammation, or necrosis into the tissues surrounding the root and apex of the tooth (deepest portion of the tooth socket). Occasionally it can be due to occlusal trauma. Periradicular lesions appear as a slight widen ing of the periodontal ligament space, a thinning of the lamina dura, or a radiolucent area associated with the root apex on a periapical dental radiograph. A panorex is not typically useful for periradicular periodontitis but can be important in identifying other painful osseous pathology (Figure 245-4).

slight widen ing of the periodontal ligament space, a thinning of the lamina dura, or a radiolucent area associated with the root apex on a periapical dental radiograph. A panorex is not typically useful for periradicular periodontitis but can be important in identifying other painful osseous pathology (Figure 245-4). Pain on percussion of the suspected tooth with a light metal instru ment, such as a handle of a dental mirror, helps to identify the offending tooth. Radiographically and clinically indistinguishable from perira dicular periodontitis, a periapical abscess by definition contains a col lection of pus. A small swelling of the gingiva with a draining fistula adjacent to the affected tooth is known as a parulis and can help identify the involved tooth ( Figure 245-5). If a dental abscess erodes through the cortical bone but does not drain spontaneously, then subperiosteal extension results in intraoral or facial swelling and fluctuance that should be incised and drained. Treat dental abscesses or other periapi cal lesions with appropriate antibiotics 3,7 (Table 245-2). NSAIDs with TABLE 245-1 Differential Diagnosis of Orofacial Pain Nontraumatic Causes of Potential Dental Pain Odontogenic origin Tooth eruption Cracked tooth syndrome Pericoronitis Periradicular periodontitis Dental caries Periapical abscess/facial space infection Dentinal sensitivity/cervical erosion Postextraction discomfort Reversible pulpitis Postextraction alveolar osteitis Irreversible pulpitis Postrestorative pain Periodontal pathology Gingivitis Periodontal abscess Periodontal disease Acute necrotizing gingivostomatitis Gingival abscess Peri-implantitis Neurogenic/neurophysiologic syndromes Trigeminal neuralgia Bell’s palsy Other cranial neuralgias Temporomandibular disorder Nondental infections Oral candidiasis Hand-foot-and-mouth disease Herpes simplex types 1 and 2 Sexually transmitted infections Varicella-zoster Herpangina Mumps Sinusitis Sialadenitis Parotitis Malignancies Squamous cell carcinoma Leukemia Kaposi’s sarcoma Melanoma Lymphoma Other etiologies Aphthous ulcers Pyogenic granuloma Traumatic ulcers Lichen planus Stomatitis and mucositis Cicatricial pemphigoid Uremia Pemphigus vulgaris Vitamin deficiency Erythema multiforme Radiation/chemotherapy related Crohn’s disease Benign migratory glossitis Behçet’s syndrome Orofacial Trauma Dental fractures Alveolar ridge fractures Subtle enamel cracks/infractions Facial bone fractures Dental crown and/or root fractures Oral soft tissue lacerations Dental luxations and avulsions TABLE 245-2 Appropriate Oral Antibiotics for Management of Dental and Oral Infections Antibiotic Adults Dosage Pediatric Dosage Amoxicillin 500 milligrams 3 times daily for 7 d 22.5 milligrams/kg 2 times daily Augmentin 875 milligrams 2 times daily for 7 d 22.5 milligrams/kg 2 times daily Clindamycin 300 milligrams 4 times daily for 7 d 7–10 milligrams/kg 3 times daily Metronidazole 500 milligrams 3 times daily for 7 d 5–10 milligrams/kg 3 times daily Doxycycline 100 milligrams 2 times daily for 7 d 2 milligrams/kg 2 times daily (not recommended <8 y old)Tintinalli_Sec19_p1523-1606.indd 1581 8/2/19 3:07 PM

ndamycin 300 milligrams 4 times daily for 7 d 7–10 milligrams/kg 3 times daily Metronidazole 500 milligrams 3 times daily for 7 d 5–10 milligrams/kg 3 times daily Doxycycline 100 milligrams 2 times daily for 7 d 2 milligrams/kg 2 times daily (not recommended <8 y old)Tintinalli_Sec19_p1523-1606.indd 1581 8/2/19 3:07 PM 1582 SECTION 19: Eye, Ear, Nose, Throat, and Oral Disorders or without supplemental acetaminophen are preferred over opiates by the American Dental Association for pain relief. 6 Refer to a dentist for definitive treatment.  FACIAL SPACE INFECTIONS Spread of odontogenic infections into the various facial spaces is relatively common. Buccal extension of a periapical infection of the mandibular teeth will involve the buccinator space. Maxillary labial extension of infection primarily will involve the infraorbital space. Perforation through the lingual cortical bone of mandibular molars, particularly the second and third molars, usually occurs below the mylohyoid ridge and involves the submandibular space. Lingual spread of periapical infec tions associated with mandibular anterior teeth will affect the lingual space. The submandibular space and lingual space communicate with each other at the posterior border of the mylohyoid muscle. Cellulitis of bilateral submandibular spaces and the lingual space is called Ludwig’s angina and is potentially life threatening. As these spaces and the masticator space communicate directly with the parapharyngeal space, airway compromise is the immediate concern. For detailed discussion, see Chapter 243, “Face and Jaw Emergencies, ” and Chapter 246, “Neck and Upper Airway. ” Infection of the infraorbital space may have a potentially devastating outcome if retrograde spread through the ophthalmic veins occurs and the cavernous sinus becomes involved.  POSTEXTRACTION PAIN Immediate postoperative pain is most commonly related to the trauma of surgery. Postoperative edema, such as with extraction of third molars, peaks within the first 24 to 48 hours and is best managed with ice packs and elevation of the head of the bed to 30 degrees. NSAIDs are preferred over oral narcotics for pain. 6 Trismus, common immedi ately after extraction, is usually the result of postoperative inflamma tion. It can also be caused by direct trauma to the temporomandibular joint or the muscles of mastication during the surgical procedure or during administration of the inferior alveolar injection. Trismus peaks in the first 24 hours and usually decreases thereafter unless infection develops. Progressively worsening trismus is concerning for a postop erative infection.  POSTEXTRACTION ALVEOLAR OSTEITIS (DRY SOCKET) Postextraction alveolar osteitis , or dry socket, usually occurs on the second or third postoperative day and is associated with exquisite oral pain. Total or partial displacement of the clot from the socket or fibrinolytic dissolution of the clot results in exposure of the alveolar bone and initiates a localized osteomyelitis of the exposed bone. Risk factors for developing postextraction alveolar osteitis include smoking, preexist ing pericoronitis or periodontal disease, a traumatic extraction, a prior history of alveolar osteitis, and hormone replacement therapy. 8-10 The incidence of postextraction alveolar osteitis is 1% to 5% of all extractions but is considerably higher (up to 30%) among impacted third molar extractions. It is generally agreed that the goal of treatment of alveolar osteitis is pain management until healing occurs. Gentle irrigation of the socket with warmed saline or chlorhexidine 0.12% oral rinse to remove debris is recommended.

extractions but is considerably higher (up to 30%) among impacted third molar extractions. It is generally agreed that the goal of treatment of alveolar osteitis is pain management until healing occurs. Gentle irrigation of the socket with warmed saline or chlorhexidine 0.12% oral rinse to remove debris is recommended. Intrasocket placement of various available medica ments is controversial, and two systematic reviews concurred that there is insufficient evidence to support one method of treatment over another. 8,9 Antibiotics may be indicated if there are systemic signs of infection (Table 245-2).10 Refer for dental follow-up.8-10  POSTEXTRACTION BLEEDING Postextraction bleeding is not uncommon. Displacement of the clot may result in recurrent or continued bleeding. Generally, firm pres sure applied to the extraction site is adequate to control bleeding. This is best accomplished by folding a 2 × 2–inch gauze pad and placing it over the extraction site and applying firm pressure by clenching with FIGURE 245-5. A parulis ( arrow) superior to the maxillary molar. [Image used with permission of David E. Beaudreau.] FIGURE 245-4. The radiographic appearance of a healthy tooth with a normal periodontal ligament space and distinct lamina dura ( A) compared with the radiographic appearance of periapical radiolucency (arrows) consistent with periradicular periodontitis, a periapical abscess, or periradicular cyst (B). [Image used with permission of Gary M. Beaudreau.] Tintinalli_Sec19_p1523-1606.indd 1582 8/2/19 3:07 PM

ligament space and distinct lamina dura ( A) compared with the radiographic appearance of periapical radiolucency (arrows) consistent with periradicular periodontitis, a periapical abscess, or periradicular cyst (B). [Image used with permission of Gary M. Beaudreau.] Tintinalli_Sec19_p1523-1606.indd 1582 8/2/19 3:07 PM CHAPTER 245: Oral and Dental Emergencies 1583 the opposing teeth. Pressure must be held firmly, not a chewing action, for 20 minutes or until hemostasis is complete. If direct pressure is not successful, then apply an absorbable gelatin sponge (Gelfoam ®, Pfizer Inc., New Y ork, NY), microfibrillar collagen (Avitene ®, Davol, Inc., Warwick, RI), or regenerated cellulose (Surgicel ®, Ethicon, Inc., Somerville, NJ) into the socket to provide a matrix for clot formation. Pressure can also be applied with a gauze pad soaked with tranexamic acid. When using any of these agents, continue to maintain pressure for 20 to 30 minutes. Sutures can be used for holding such agents in place or to loosely close the gingiva over the socket. Do not suture the gingiva tightly because this may cause necrosis of the gingival flap. If the above techniques are not successful, careful injection of the soft tissue surrounding the extraction with lidocaine with epinephrine may control the bleeding. Careful cautery with silver nitrate can also be useful. If bleeding continues, then oral and maxillofacial surgical consultation is necessary.  POSTRESTORATIVE PAIN Postrestorative pain can result from normal trauma from mechanical instrumentation of the tooth or direct exposure of the pulpal tissue during instrumentation. Pain associated primarily with mastication may be the result of improper occlusion of the new dental restoration or filling. After endodontic therapy, buildup of pressure in the pulpal chamber can cause severe pain. Provide NSAIDs or narcotic analgesia and refer to the patient’s dentist. Temporary prolonged pain relief can also be obtained using 0.5% bupivacaine with epinephrine and the appropriate dental anesthetic block as discussed in the dental local anesthesia technique section of this chapter. Follow up with the dentist the next day.  ORTHODONTIC APPLIANCES The most common emergency is a broken or bent wire that is irritating or lacerating the cheek or lip. This wire needs to be bent back away from soft tissue. This can easily be accomplished with dental instruments, or something soft such as a pencil eraser can be used to gently bend the wire. Cutting the wire is generally not indicated because it makes the end sharper. The broken portion of the wire can be removed in its entirety by removing the rubber ligatures from each orthodontic bracket, but this generally is not necessary. The patient should follow up as soon as possible with the orthodontist. PERIODONTAL PATHOLOGY Periodontal disease is a continuum of disease that begins with gingival inflammation and bleeding, or gingivitis, and can progress to destruction of the periodontal attachment apparatus, deepening of the normal gingival sulcus, periodontal pocket formation, bone loss, tooth mobility, and ultimately loss of teeth. 1 Besides oral hygiene, many factors including hormonal variations, medications, and systemic disease can also influence periodontal health. Periodontal disease usually progresses painlessly but may present as swollen gingival tissue or gingival bleeding. Treatment is directed at slowing or arresting the progression of disease primarily by the removal of plaque and its by-products. 1 Antibiotics may play a role in treatment. Referral to a dentist for definitive treatment is indicated because the treatment involves extensive dental cleaning, instruction and improve ment in oral hygiene, and in some cases, periodontal surgery.

ssion of disease primarily by the removal of plaque and its by-products. 1 Antibiotics may play a role in treatment. Referral to a dentist for definitive treatment is indicated because the treatment involves extensive dental cleaning, instruction and improve ment in oral hygiene, and in some cases, periodontal surgery.  GINGIVAL AND PERIODONTAL ABSCESS A gingival abscess is an acutely painful swelling confined to the mar gin of the gingiva or interdental papilla. It usually rapidly enlarges over 24 to 48 hours, and purulent exudate can frequently be expressed from the orifice. The most common etiology is the entrapment of foreign matter such as a popcorn kernel, piece of meat, toothbrush bristle, or piece of food in the gingiva. Treatment includes identifying and removing the embedded foreign body and irrigating with normal saline. Continued home irrigation is beneficial, and symptoms resolve quickly. 1,3 When plaque and debris are entrapped in the periodontal pocket, a periodontal abscess may form, resulting in severe pain. Small periodontal abscesses respond to local therapy with warm saline rinses and systemic antibiotics (Table 245-2). Larger periodontal abscesses require incision and drainage. Chlorhexidine 0.12% mouth rinses twice daily are useful in the short term. 1,3,4 Provide analgesia with NSAIDs, which are pre ferred over narcotics.6  ACUTE NECROTIZING ULCERATIVE GINGIVITIS Acute necrotizing ulcerative gingivitis is an aggressively destructive process (Figure 245-6). Also known as Vincent’s disease or trench mouth, it is part of a spectrum of disease ranging from localized ulcer ation of the gingiva to fatal noma (cancrum oris), in which localized ulceration and necrosis spread to the adjacent tissues of the cheeks, lips, and underlying facial bones. 1,3,4,11,12 The diagnostic triad includes pain, ulcerated or “punched out” interdental papillae, and gingival bleeding. Secondary signs include fetid breath, pseudomembrane formation, foul metallic taste, tooth mobility, lymphadenopathy, fever, and malaise. 1,3,11,12 The differential diagnosis for acute necrotizing ulcerative gingivitis is quite extensive, but herpes gingivostomatitis is the most difficult to dif ferentiate. Herpes gingivostomatitis usually has smaller vesicular erup tions, less bleeding, more systemic signs, and lack of interdental papilla involvement. 1,3,11,12 The cause is still poorly understood. Acute necrotizing ulcerative gingivitis appears to be an opportunistic infection in a host with low ered resistance. Anaerobic bacteria such as Treponema, Selenomonas, Fusobacterium, and Prevotella invade otherwise healthy tissue, resulting in an aggressively destructive disease process.1,3,11,12 The most important predisposing factors are human immunodeficiency virus infection and a previous episode of necrotizing gingivitis. Other contributing factors include poor oral hygiene, unusual emotional stress, poor diet and malnutrition, inadequate sleep, Caucasian descent, young age (early 20s), poor socioeconomic status, recent illness, alcohol use, and tobacco use. 1,3,11,12 Treatment consists primarily of bacterial control. Chlorhexidine 0.12% oral rinses twice a day and professional debridement and scal ing are the mainstay of treatment. Adjunctive antibiotic therapy with metronidazole (Table 245-2) is reserved for the immunocompromised or those with signs of systemic infection. Reduction in pain can be expected within 24 hours of institution of this regimen. Identification and resolution of the predisposing factors and supportive therapy with a soft diet rich in protein, vitamins, and fluids are important in establish ing and maintaining a disease-free state. 1,3,11,12, FIGURE 245-6. Acute necrotizing ulcerative gingivitis. [Image used with permission of Philip J.

regimen. Identification and resolution of the predisposing factors and supportive therapy with a soft diet rich in protein, vitamins, and fluids are important in establish ing and maintaining a disease-free state. 1,3,11,12, FIGURE 245-6. Acute necrotizing ulcerative gingivitis. [Image used with permission of Philip J. Hanes.] Tintinalli_Sec19_p1523-1606.indd 1583 8/2/19 3:07 PM

regimen. Identification and resolution of the predisposing factors and supportive therapy with a soft diet rich in protein, vitamins, and fluids are important in establish ing and maintaining a disease-free state. 1,3,11,12, FIGURE 245-6. Acute necrotizing ulcerative gingivitis. [Image used with permission of Philip J. Hanes.] Tintinalli_Sec19_p1523-1606.indd 1583 8/2/19 3:07 PM 1584 SECTION 19: Eye, Ear, Nose, Throat, and Oral Disorders  PERI-IMPLANTITIS Osseointegrated dental implants have become common over the past 30 years, allowing for a dental implant to replace a tooth. Pathologic changes around an implant are all given the general term of periimplant disease . Patients who present with peri-implantitis, a general term describing postprocedure pathologic changes, manifest similar symptoms to a periodontal abscess and require similar treatment. Gentle removal of the plaque and debris from around the implant and irrigation with normal saline or 0.12% chlorhexidine solution should be done. Give analgesia as needed and refer to a dentist for definitive care. 3,4,13 SPECIAL CONSIDERATIONS: NEUROGENIC AND NEUROPHYSIOLOGIC SYNDROMES See Chapter 172, “ Acute Peripheral Neurologic Disorders, ” for management of Bell’s palsy.  CRANIOFACIAL NEURALGIAS Trigeminal neuralgia is the most common of the craniofacial neuralgias. Other significantly less common neuralgias of the craniofacial region include glossopharyngeal neuralgia, vagal neuralgia, and superior laryn geal neuralgia involving the respective nerve distributions. Post–herpes zoster–related neuralgia is also a cause of acute facial pain and may become chronic in nature. See Chapter 165, “Headache, ” for further discussion.  TEMPOROMANDIBULAR DISORDER Temporomandibular disorder is a common cause of facial pain and headache representing a group of signs and symptoms that involve the muscles of mastication or the temporomandibular joint. See Chapter  243, “Face and Jaw Emergencies, ” for management.  CAVERNOUS SINUS THROMBOSIS Cavernous sinus thrombosis may present in association with an odon togenic infection with the additional symptoms of headache with or without vomiting, or the patient may rapidly deteriorate with meningeal signs, sepsis, and coma. Contrasted CT imaging may facilitate early recognition. See Chapter 174, “Central Nervous System and Spinal Infections, ” for management.  SOFT TISSUE LESIONS OF THE ORAL CAVITY RECURRENT APHTHOUS STOMATITIS Recurrent aphthous stomatitis, or ulceration, is one of the most com mon oral lesions ( Figure 245-7). Recurrent aphthous stomatitis by definition is idiopathic; therefore, other underlying causes such as trauma, vesiculobullous disease, medications, nutritional deficiencies, hematologic disorders, and fever syndromes must be considered. The etiology is multifactorial, involving physiologic interactions between the immune system and genetic and environmental factors. Aphthous ulceration involves the nonkeratinized epithelium, especially the labial and buccal mucosa, and begins as an erythematous macule that ulcerates and forms a central fibropurulent eschar. Aphthous stomatitis occurs in three forms. Minor aphthae usually measure <10 mm in diameter, are painful, and frequently are multiple. They usually resolve spontaneously in 10 to 14 days. Major aphthae have larger (>10 mm), deeper ulcers that take significantly longer to heal. The third form, called herpetiform aphthae, has up to 100 ulcers, each 1 to 2 mm in diameter. They tend to coalesce, creating much larger ulcers that require 10 to 14 days to heal. Treatment is primarily symptomatic. Several medications are effective in decreasing pain and increasing the rate of healing. Topical agents such as chlorhexidine 0.2% mouth rinse, anesthetic agents, and steroids applied topically or as a mouth rinse should be the first-line therapy.

that require 10 to 14 days to heal. Treatment is primarily symptomatic. Several medications are effective in decreasing pain and increasing the rate of healing. Topical agents such as chlorhexidine 0.2% mouth rinse, anesthetic agents, and steroids applied topically or as a mouth rinse should be the first-line therapy. Com mercially available bioadhesive pastes such as Orobase ® (Colgate Oral Pharmaceuticals, Canton, MA), which contains both corticosteroids and anesthetic agents, are effective. In more resistant cases, systemic steroids are indicated. HERPES ZOSTER AND OTHER INFECTIONS Herpes zoster frequently occurs along the distribution of the trigeminal nerve (see Chapter 154, “Serious Viral Infections, ” for management). Isolated intraoral lesions can occur but are not common. Involvement of the ophthalmic branch of the trigeminal nerve requires urgent ophthalmologic consultation (see Chapter 241, “Eye Emergencies”). 1,15 Other common infections such herpes simplex types 1 and 2, her pangina, hand-foot-and-mouth disease, and varicella-zoster virus cause painful ulcerative lesions of the oral cavity and perioral region. These conditions are adequately discussed in Chapter 124, “Mouth and Throat Disorders in Infants and Children. ” Many sexually transmitted infec tions can affect the oral cavity. In general, the appearance of oral lesions is similar in appearance to that of their genital counterpart. Treatment of sexually transmitted diseases of the oral cavity is the same as for genital involvement. 1,15 See Chapter 153, “Sexually Transmitted Infections, ” for detailed discussion. TRAUMATIC ULCERS Traumatic ulcers are a result of direct trauma to epithelial tissue. Com mon sources of trauma include rough or jagged edges on teeth or restorations, ill-fitting dentures, oral hygiene mishaps, and burns to the hard or soft palate secondary to hot foods. Removal of persistent sources of trauma is essential; otherwise, treatment is palliative. MEDICATION-RELATED SOFT TISSUE ABNORMALITIES Gingival hyperplasia is associated with many commonly used medi cations (Figure 245-8). Three classes of drugs have been identified as causal: anticonvulsants, calcium channel blockers, and immuno suppressants. Phenytoin, nifedipine, and cyclosporine exhibit the strongest association. Concomitant use of two such medications results in accelerated gingival proliferation. Enlargement begins in the interdental papillae. Regardless of medication, the clinical and histologic characteristics of gingival hyperplasia appear to be identi cal. The clinical appearance of the gingival tissue depends on oral hygiene and secondary inflammation. In the absence of inflamma tion, gingival proliferation results in dense tissue, normal in color ation, with a smooth, stippled, or granular texture. Inflammation FIGURE 245-7. Aphthous stomatitis. [Image used with permission of Baldev Singh.] Tintinalli_Sec19_p1523-1606.indd 1584 8/2/19 3:07 PM

secondary inflammation. In the absence of inflamma tion, gingival proliferation results in dense tissue, normal in color ation, with a smooth, stippled, or granular texture. Inflammation FIGURE 245-7. Aphthous stomatitis. [Image used with permission of Baldev Singh.] Tintinalli_Sec19_p1523-1606.indd 1584 8/2/19 3:07 PM CHAPTER 245: Oral and Dental Emergencies 1585 causes edematous changes and an erythematous coloration. Inflamed tissue bleeds readily. Histologically, an increase in collagen fibers, fibroblasts, and glycosaminoglycans is seen. Epithelial acanthosis also occurs. Although the cause of drug-related gingival hyperplasia is unclear, poor oral hygiene clearly increases its likelihood and sever ity. Treatment includes fastidious oral hygiene to slow the hyperplasia and gingivectomy in advanced cases. Many other medications and diseases are known to cause abnormalities of the oral mucosa or dental structures. Allergic mucositis, erythema multiforme, and fixed drug-type reactions are examples. Xerostomia and associated mucosal alterations are a side effect of many medica tions such as anticholinergics, antidepressants, and antihistamines. Stomatitis and mucosal ulcerations from chemotherapeutic agents are also common. 3,16 LESIONS OF THE TONGUE Many systemic conditions and local stimuli affect the appearance of the tongue. Various vitamin deficiencies and iron deficiency anemia cause atrophy of the filiform papillae, resulting in a smooth erythematous appearance. Occurrence of ectopic thyroid tissue on the midline poste rior portion of the tongue is called a lingual thyroid and is a common finding. Some common conditions affecting the tongue are discussed in the following sections.  BENIGN MIGRATORY GLOSSITIS Geographic tongue, or benign migratory glossitis, is a common benign finding on oral examination, occurring in 1% to 3% of the population. Typically, multiple areas of erythema on the tongue, caused by atrophy of the filiform papillae, are surrounded by well-demarcated zones of hyperkeratotic plaques. The lesions concentrate on the tip and dorso lateral aspect of the tongue and heal in several days, only to quickly reappear in other areas. These lesions usually are asymptomatic; how ever, a burning sensation or sensitivity to hot or spicy foods has been described. The cause is unknown, but an association with psoriasis, allergies, stress, diabetes, and anemia is reported. Generally, treatment is not indicated because this entity is benign. Reassurance of patients is usually sufficient. In patients in whom discomfort is a major factor, oral topical steroids such as fluocinonide gel applied several times daily may provide relief.  STRAWBERRY TONGUE Strawberry tongue is associated with erythrogenic, toxin-producing Streptococcus pyogenes. Clinically, the tongue has prominent red spots on a white-coated background. Microscopically, the fungiform papillae are hyperemic with a smooth, glossy surface. Treatment is with antibiotics directed at group A streptococci. LEUKOPLAKIA AND ERYTHROPLAKIA Leukoplakia is a white patch or plaque that cannot be scraped off and cannot be classified as any other disease. Leukoplakia is the most com mon oral precancer. Up to 7% of lesions exhibit dysplastic changes, with an overall risk of malignant transformation of 2% to 3% per year. The cause is unknown, but tobacco, alcohol, ultraviolet radiation, candidia sis, human papillomavirus, tertiary syphilis, and trauma have all been implicated. Lesions can occur on any intraoral mucosal site but commonly affect the buccal mucosa, tongue, and floor of the mouth. Biopsy is mandatory for all persistent leukoplakic lesions. Leukoplakic lesions of the floor of the mouth, tongue, and vermilion border are most likely associated with malignancy.

all been implicated. Lesions can occur on any intraoral mucosal site but commonly affect the buccal mucosa, tongue, and floor of the mouth. Biopsy is mandatory for all persistent leukoplakic lesions. Leukoplakic lesions of the floor of the mouth, tongue, and vermilion border are most likely associated with malignancy. Lesions demonstrating dysplastic changes warrant removal at follow-up by an oral surgeon or otolarygologist. 15,17 Erythroplakia is defined as a red patch that similarly cannot be clinically or pathologically characterized as any other disease. Although erythroplakia is far less common than leukoplakia, it has a greater potential for dysplastic changes; refer for removal as with leukoplakia. ORAL CANCER Oral cancer accounts for 2% to 4% of the cancers in the United States. More than 90% of all oral malignancies are squamous cell carcinoma (Figure 245-9). Lymphomas, Kaposi’s sarcoma, and melanoma com pose most of the remainder. Extrinsic risk factors include tobacco use, especially chewing tobacco or snuff; excessive alcohol consumption; and sunlight exposure. Intrinsic factors include immunosuppression, lichen planus, chronic oral candidiasis, human papilloma virus infection, human immunodeficiency virus infection, chronic inflammation, and nutritional deficiencies and general malnutrition. 15,17 Oral squamous cell carcinoma has four common morphologic presentations. Lesions can be exophytic, with an irregular surface; ulcerative, with irregular depressions and rolled borders; malignant leukoplakic; or erythroplakic. The most common site involved in oral cancer is the tongue, particularly the posterolateral and ventral sur face, accounting for 50% of the oral cancers in the United States. 15,17 Cancer of the floor of the mouth accounts for nearly 35%. Cancer of the lips is common and usually secondary to sunlight exposure. Oral cancer is generally painless, and patients are often unaware of the pres ence of a mass until it is advanced. Oral cancer lesions are usually firm, may bleed from ulceration, and have a history of poor healing. There may be associated firm lymphadenopathy. Early diagnosis is the key to successful treatment of oral squamous cell carcinoma. All ulcers, erythroplakic lesions, and leukoplakic lesions of the oral cavity that do not respond to palliative treatment in 10 to 14 days warrant biopsy by otolaryngology. Treatment depends on site of involvement and stage of disease. FIGURE 245-8. Gingival hyperplasia (overgrowth) secondary to phenytoin (Dilantin ®). [Used with permission of Philip J. Hanes.] FIGURE 245-9. Oral squamous cell carcinoma of the hard palate. [Image used with permission of H. Anthony Neal.] Tintinalli_Sec19_p1523-1606.indd 1585 8/2/19 3:07 PM

ement and stage of disease. FIGURE 245-8. Gingival hyperplasia (overgrowth) secondary to phenytoin (Dilantin ®). [Used with permission of Philip J. Hanes.] FIGURE 245-9. Oral squamous cell carcinoma of the hard palate. [Image used with permission of H. Anthony Neal.] Tintinalli_Sec19_p1523-1606.indd 1585 8/2/19 3:07 PM 1586 SECTION 19: Eye, Ear, Nose, Throat, and Oral Disorders  DENTOALVEOLAR TRAUMA Management of dentoalveolar trauma depends on the extent of tooth and alveolar involvement, the degree of development of the apex of the tooth, and the age of the patient. In injuries in younger patients, especially those who are <12 years of age, the pulp of anterior teeth is quite large, and dental fractures involving the pulp are common. Fortunately, in this age group, the apex of the root also is usually incompletely formed, allowing for a greater pulpal regenerative capability. As one ages, more dentin is formed. Thus, in older patients, the pulp chamber may be very small and pulpal exposure highly unlikely. Involvement of the root of the tooth compromises the attachment apparatus and makes it difficult to restore the tooth to function. DENTAL FRACTURES The International Association of Dental Traumatology system divides dental trauma into eight categories: enamel infraction, enamel fracture, enamel-dentin fracture, enamel-dentin-pulp fracture, crown-root frac ture without pulp exposure, crown-root fracture with pulp exposure, root fracture, and alveolar bone fracture ( Figure 245-10). The International Association of Dental Traumatology has developed guidelines to aid dentists and other healthcare professionals in the management of each these categories. 18,19 The goal of the emergency treatment of a fractured tooth is maintaining pulpal vitality and completion of the formation of the root and apex of the tooth. The proximity of the fracture to the pulp and the length of time before treatment, as well as other associated injuries, are most important in determining outcome. Treatment is aimed at sealing the dentinal tubules and creating a barrier between the dental pulp and the oral environment. Because pulpal necrosis is a process, it can occur at any time after trauma, and serial follow-up with a dentist is recommended. 18,19 A fracture of the crown of the tooth can involve any part of the enamel, dentin, and pulp of the tooth. Infraction is the least serious type of dental injury and essentially is a crack in the enamel of the tooth without loss of structure. This can be obvious or quite subtle. No emergency treatment is needed.  ENAMEL FRACTURES Enamel fractures (Ellis class I fractures) do not extend into the dentin of the tooth ( Figure 245-11). Generally, no emergency treatment is indi cated, except to smooth sharp corners that may irritate the tongue or mucosa. If the enamel fragment is recovered and kept moist, the patient’s dentist can bond it back in place. If the fragment was not recovered, soft tissue radiographs of any oral lacerations are necessary to rule out foreign bodies. Referral to a general dentist for aesthetic repair depends on the degree of cosmetic concern of the patient. 18,19  ENAMEL-DENTIN FRACTURES Enamel-dentin fractures (Ellis class II fractures) involve the dentin of the tooth and require intervention ( Figure 245-11). Generally, patients experience sensitivity to hot or cold stimuli as well as air passing over the exposed surface during breathing. The enamel-dentin fracture can be identified both by the patient’s symptoms and visualization of exposed dentin, which is a creamy yellow color compared with the whiter enamel. Because dentin is microtubular in structure, communication with the oral environment or desiccation from mouth breathing initiates an inflammatory response in the dental pulp.

e identified both by the patient’s symptoms and visualization of exposed dentin, which is a creamy yellow color compared with the whiter enamel. Because dentin is microtubular in structure, communication with the oral environment or desiccation from mouth breathing initiates an inflammatory response in the dental pulp. The thickness of remain ing dentin determines the rate of pulpal contamination. Greater than 2 mm of remaining dentin is felt to offer some protection to the pulpal tissue. A delay in treatment of >24 to 48 hours increases the likelihood of pulpal necrosis. The ED goal is the identification of a fracture. If definitive treatment cannot be ensured in 1 to 2 days, then cover the exposed dentin to decrease likelihood of pulpal injury. This is best achieved using glass ionomer dental cement that is easily mixed according to the Ellis class I Ellis class II Alveolar fracture Ellis class III FIGURE 245-10. The International Association of Dental Traumatology classification of dental fractures. FIGURE 245-11. International Association of Dental Traumatology classification for fractures of teeth (clinical). A. Enamel fracture (Ellis class I). B. Enamel-dentin fracture (Ellis class II) of the central incisor on the left in the photograph (notice the pink blush of the pulp through the thin layer of dentin), and an enamel-dentin-pulp fracture of the central incisor on the right in the photograph. [Image used with permission of Felicity K. Hardwick.] Tintinalli_Sec19_p1523-1606.indd 1586 8/2/19 3:07 PM

of the central incisor on the left in the photograph (notice the pink blush of the pulp through the thin layer of dentin), and an enamel-dentin-pulp fracture of the central incisor on the right in the photograph. [Image used with permission of Felicity K. Hardwick.] Tintinalli_Sec19_p1523-1606.indd 1586 8/2/19 3:07 PM CHAPTER 245: Oral and Dental Emergencies 1587 manufacturer’s instructions and carefully applied to the dried exposed dentin (DenTemp®, Majestic Drug Co., South Fallsburg, NY; and oth ers). If the dentin layer is <0.5 mm and the pulp can be seen as a pink area without bleeding, then first place a thin layer of calcium hydroxide base (Dycal ®, Dentsply International, Y ork, PA) followed by glass ionomer, as described earlier, to further protect the dental pulp. Referral to a dentist for definitive treatment is important. 18,19  ENAMEL-DENTIN-PULP FRACTURES In enamel-dentin-pulp fractures (Ellis class III fractures), exposure of the pulp has occurred (Figure 245-10). On wiping the fractured surface dry with sterile gauze, blood originating from the pulp of the tooth is easily identified. After carefully controlling pulpal bleeding with sterile gauze or a cotton pellet, cover the exposed pulp with a calcium hydroxide base (Dycal ®, Dentsply International, Y ork, PA), and then cover this and the remaining exposed dentin with glass ionomer cement as in enameldentin fractures until urgent dental evaluation can occur. If the pulpal exposure is extremely small, placing a calcium hydroxide base and glass ionomer is adequate until dental evaluation. For all but the smallest pulpal exposures, definitive treatment is some kind of endodontic or root canal therapy. Oral analgesics should be prescribed and topical analgesics avoided. 18,19 Crown-root fractures and root fractures are an uncommon conse quence of dental trauma. The coronal segment of the tooth may be displaced or simply mobile. Tenderness to percussion is usual. With any dental trauma, careful attention must be paid to identifying fractures of the root, as they can be clinically obscure, and dental radiographs from several angles may be necessary to identify these fractures. This, however, is beyond the scope of most EDs. Crown-root fractures may or may not involve the pulp. Emergency treatment consists of stabiliz ing the coronal segment until definitive treatment can be arranged. In isolated root fractures, the pulp is always involved. Healing of stabilized root fractures has been reported; thus, current recommendations are to reposition the coronal segment to its original position, confirm that position by radiograph, if available, and then stabilize with a flex ible splint as described below for luxation injuries. Dental follow-up within 24 to 48 hours is important, because splinting for a minimum of 4 weeks is required. In the ED, where oral surgical or dental consultation may not be readily available, extraction of an extremely mobile coronal segment of the tooth may be required to prevent possible aspiration. 18-20 LUXATION INJURIES The same forces that cause dental fractures may result in loosening of a tooth from the attachment apparatus. Careful evaluation of the teeth for tenderness, malpositioning, or mobility must be performed. There are six types of luxations: concussion, subluxation, extrusive luxation, lateral luxation, intrusive luxation, and avulsion. 18,19 Concussion is injury to the supporting structures of a tooth with clinical tenderness to percussion but no mobility. Subluxation is injury resulting in mobility without clinical or radiographic evidence of dislodgement of the tooth. Extrusive luxation is partial or total disruption of the periodontal ligament resulting in a partial dislodgement of a tooth from the alveolar bone.

with clinical tenderness to percussion but no mobility. Subluxation is injury resulting in mobility without clinical or radiographic evidence of dislodgement of the tooth. Extrusive luxation is partial or total disruption of the periodontal ligament resulting in a partial dislodgement of a tooth from the alveolar bone. Lateral luxation is displacement of a tooth labially (toward the lip) or lingually (toward the tongue) with concomitant fracture of the alveolar bone. Intrusive luxation is displacement of a tooth into its socket with associated periodontal ligament damage and alveolar bone contusion and fracture. Treatment of luxations depends on the tooth involved, the severity of injury, and the presence of associated root fracture and/or significant associated alveolar fracture. 18,19  CONCUSSIONS A concussive injury to a tooth is minor. The degree of tenderness to percussion determines the treatment. Stabilizing the tooth by splinting it to adjacent teeth is not indicated. Management of pain with NSAIDs, soft diet, and referral to a dentist to confirm the diagnosis and exclude more severe injury constitute the most appropriate course of action for the emergency physician. 18,19  LUXATIONS Subluxation represents a more significant injury than concussion and is associated with a higher incidence of subsequent pulpal necrosis. Clini cally, tooth mobility and some bleeding along the gingiva may be noted. A subluxed tooth generally does not require splinting. 18,19 An extrusive luxation requires repositioning the tooth to its original position and splinting to stabilize the tooth during healing. Ideally, dental radiographs should be obtained prior to repositioning the tooth to ensure that there is not a fracture of the root of the tooth, but in most EDs, this may not be possible, and repositioning and stabilizing should be attempted regardless. Repositioning the tooth may require local anesthesia. Firm, gentle pressure usually will reposition the tooth. If a clot has formed apical to the tooth, then more aggressive manipulation may be required. Splints made with flexible wire, nylon line, or bond able fiber mesh ribbon provide ideal stabilization. 18,19,21 If unavailable in the ED, a temporary splint with a noneugenol zinc oxide periodontal dressing (Coe-Pak , GC America Inc., Alsip, IL; or ZONE Periopak ®, DUX Dental, Oxnard, CA) ( Figure 245-12) is acceptable. Avoid excess material placement, especially on the occlusal surface, because interfer ence in occlusion will place stress on the tooth during mastication. The patient should see a dentist or oral and maxillofacial surgeon within 24 hours. A lateral luxation represents a more extensive injury and is associ ated with fracture of the surrounding alveolar bone. Repositioning of the tooth is generally more difficult. It usually can be accomplished by manipulating the displaced tooth with the thumb and forefinger. Once the apex has been dislodged from its locked-in position labially, apically directed axial pressure will reposition the tooth. Intra-arch stabilization is necessary for a minimum of 4 weeks. Temporary splinting with a periodontal dressing is acceptable if a minimal associated alveolar fracture occurred. Otherwise, splinting by an oral and maxillofacial surgeon or general dentist in the ED is mandatory. 18,19,21 Intrusive luxations are the most serious because significant dam age to the alveolar socket and periodontal ligament occurs. Root Splint material FIGURE 245-12. Temporary stabilization of a replanted or repositioned tooth. A. Tooth is repositioned back into its original position in the socket. B. Splint material is mixed thoroughly. C. Splint material is shaped and made ready for application. D. Packing is molded over repositioned tooth and two adjacent teeth to each side.

12. Temporary stabilization of a replanted or repositioned tooth. A. Tooth is repositioned back into its original position in the socket. B. Splint material is mixed thoroughly. C. Splint material is shaped and made ready for application. D. Packing is molded over repositioned tooth and two adjacent teeth to each side. Tintinalli_Sec19_p1523-1606.indd 1587 8/2/19 3:07 PM

12. Temporary stabilization of a replanted or repositioned tooth. A. Tooth is repositioned back into its original position in the socket. B. Splint material is mixed thoroughly. C. Splint material is shaped and made ready for application. D. Packing is molded over repositioned tooth and two adjacent teeth to each side. Tintinalli_Sec19_p1523-1606.indd 1587 8/2/19 3:07 PM 1588 SECTION 19: Eye, Ear, Nose, Throat, and Oral Disorders Medial Distal Facial Palatal resorption is common as a result of damage to the periodontal liga ment. Recommended treatment is allowing the tooth to erupt on its own or to orthodontically extrude the tooth if no eruption is noted by 3 weeks. 18,19,21 All patients who sustain luxation injuries should be instructed to maintain a soft diet for at least 2 weeks. Meticulous oral hygiene is essential. Twice-daily rinsing with chlorhexidine 0.12% mouth rinse is helpful. Referral to a dentist for close follow-up is indicated.  AVULSIONS Tooth Replantation and Care at the Scene Total displacement of a tooth from its socket, or avulsion, is a true dental emergency. 22,23 Replantation at the scene is the treatment of choice because the longterm prognosis for the replanted tooth is highly time dependent. Ide ally, the patient or a healthcare provider at the scene should perform this procedure. Handling only the crown portion of the tooth, gently rinse the tooth for a maximum of 10 seconds with sterile normal saline or tap water to remove debris. Then replace it immediately into the socket. Anterior teeth are most commonly affected. Figure 245-13 illustrates the morphology of the maxillary central incisor to assist replantation in the proper orientation. Early improper replantation holds a higher success rate for tooth salvage than delayed replantation resulting from waiting for arrival at the ED or for an oral and maxil lofacial surgeon. 22,23 If immediate replantation is not possible, then transport the tooth with the patient to the ED. Acceptable transport media include isotonic solutions such as Hank’s balanced salt solution, organ transport media, sterile saline, milk, and saliva. Commercial preparations of Hank’s balanced salt solution such as Save-A-Tooth ® (Phoenix-Lazerus, Inc., Pottstown, PA) and EMT Tooth Saver (Smart Practice, Phoenix, AZ) are available and come with a useful transport container as part of the system. Survival of the periodontal ligament fibers that remain attached to the root of an avulsed tooth is key to successful replantation. Milk is an acceptable storage medium because of its osmolarity and essential con centration of calcium and magnesium ions, and compares favorably with Hank’s balanced salt solution, which maintains periodontal ligament cell viability for up to 4 to 6 hours. Tooth Replantation in the ED In the ED, before replantation, rinse the tooth root clean of dirt and debris with sterile saline or, preferably, TABLE 245-3 Specific Recommendations for Replantation of Avulsed Teeth Clinical Scenario Treatment Moist tooth stored in acceptable media, and/or <60 min extra oral dry time 1. Gently irrigate the tooth root clean with sterile saline. 2. Administer local anesthesia. 3. Remove coagulum from the socket with a stream of saline. 4. Examine the socket. If there is a fracture of the socket wall, reposition it with an appro priate instrument. 5. Firmly replant tooth and verify the tooth position clinically and radiographically, if possible. 6. Flexible splint for up to 2 weeks. Extra oral dry time >60 min or other reason suggesting nonviable cells 1. Remove from tooth attached necrotic soft tissue carefully with gauze. 2. Administer local anesthesia. 3. Remove coagulum from the socket with a stream of saline. 4. Examine the socket. If there is a fracture of the socket wall, reposition it with an appro priate instrument. 5.

other reason suggesting nonviable cells 1. Remove from tooth attached necrotic soft tissue carefully with gauze. 2. Administer local anesthesia. 3. Remove coagulum from the socket with a stream of saline. 4. Examine the socket. If there is a fracture of the socket wall, reposition it with an appro priate instrument. 5. Firmly replant tooth and verify the tooth’s position clinically and radiographically, if possible. 6. Flexible splint for up to 4 weeks. Hank’s balanced salt solution. Do not scrub the root of the tooth, and do not disrupt existing periodontal fibers. Handle only the crown of the tooth. If an avulsed tooth with an open apex has been dry for <20 minutes, then the prognosis for reestablishing a vital pulp is good. If the tooth has been dry from 20 to 60 minutes regardless of apices, soak the tooth in a physiologic solution while preparing to replant the tooth. Physiologic solution decreases the chance of ankylosis (fixation of the tooth to the underlying bone). For an avulsed tooth that has been dry for >60 minutes, the periodontal cells are dead, and the goal is to maintain alveolar bone contour and aesthetics; however, ankylosis, root resorp tion, and eventual tooth loss are the expected outcome. Table 245-3 provides specific recommendations. 22.23,25 Dentists manage avulsed immature permanent teeth (patients age 5 to 15 years) differently than avulsed mature permanent teeth, but care of avulsed teeth in the ED prioritizes rapid replacement to preserve function. If the avulsed tooth was not recovered, obtain radiographs to ensure that the tooth was not aspirated. 22-24 Prepare the socket by carefully removing the clot and gently irrigat ing with sterile normal saline. Avoid socket manipulation if possible. However, any fracture of the socket wall should be carefully reposi tioned with an appropriate instrument. Local anesthesia is usually required. Replantation is accomplished with firm pressure. Having the patient bite on gauze until more permanent stabilization can be arranged is acceptable. Stabilization of the tooth in the ED with a flexible splint or temporary splinting such as a periodontal dressing (Figure 245-12) is necessary until follow-up with an oral and maxil lofacial surgeon. 21-23 Treatment with systemic antibiotics is controversial but still recom mended because experimental studies show benefit. Doxycycline is the preferred antibiotic choice. For children <12 years old, amoxicillin is acceptable (Table 245-2). Tetanus prophylaxis is necessary if the tooth has been contaminated by soil and the tetanus status is uncertain. Post treatment instructions for most dental trauma are essentially the same. Patient should be instructed to maintain a soft diet for 2 weeks, brush carefully with a soft toothbrush after each meal, and use chlorhexidine FIGURE 245-13. Illustration of a maxillary left central incisor in two views. Note that the part of the tooth facing medially comes to more of a right angle at the incisal edge (biting edge) than occurs distally. The facial portion of the tooth is more convex. Tintinalli_Sec19_p1523-1606.indd 1588 8/2/19 3:07 PM

xidine FIGURE 245-13. Illustration of a maxillary left central incisor in two views. Note that the part of the tooth facing medially comes to more of a right angle at the incisal edge (biting edge) than occurs distally. The facial portion of the tooth is more convex. Tintinalli_Sec19_p1523-1606.indd 1588 8/2/19 3:07 PM CHAPTER 245: Oral and Dental Emergencies 1589 0.12% mouth rinse twice a day.22,23,25 Follow-up should be facilitated with a dentist in 1 week. SPECIAL CONSIDERATIONS WITH LUXATION INJURIES  SEQUELAE OF LUXATION INJURIES Posttraumatic sequelae are variable. Pulp canal obliteration, pulpal necrosis, internal and external resorption of the root, and ankylosis may occur. The severity of luxation or avulsion is the most important deter mining factor in sequela occurrence. Transient apical breakdown occurs with all types of luxations, but is especially common with extrusive and lateral luxations and avulsions. Extrusive luxated teeth commonly undergo pulpal necrosis within 1.5 years of the traumatic event. Close dental follow-up is essential for early identification of these sequelae.  ALVEOLAR RIDGE FRACTURES Significant force must occur to dislodge or fracture teeth; conse quently, associated alveolar ridge fracture is common. Care to ensure the integrity of the maxilla and mandible is also important. Stabiliza tion of repositioned alveolar segments and associated teeth is essential for optimal results. This is best accomplished with flexible fixation placed by a general dentist or oral surgeon. Stabilization is maintained for up to 4 weeks depending on the severity of the involvement of alveolar bone. With significant alveolar ridge fracture, segments may require intermaxillary stabilization for up to 6 weeks in order to ensure adequate healing. 22,23  LUXATION INJURIES OF PRIMARY TEETH Avulsion or luxation injuries of primary teeth are treated differently from those of permanent teeth. In patients age 6 to 12 years old, dentition is mixed, so it is very important to distinguish primary from permanent teeth. Avulsed primary teeth are never replanted. Most luxation injuries in children require no treatment and heal spontaneously. However, severe luxations of primary teeth generally require extraction of the tooth. Repositioning or replanting primary teeth risks injuring the underlying permanent teeth and thus is avoided. Intruded primary teeth are generally left alone to reerupt into normal position. Because of the risk of damage to the permanent dentition, unless there is occlusal interference or the risk of aspiration, a dentist should manage most complicated luxation injuries of primary teeth. Referral to a dentist for follow-up is essential to ensure optimal long-term outcome. 26.27 SOFT TISSUE TRAUMA  ORAL CAVITY MUCOSAL LACERATIONS Traumatic injuries to the soft tissue of the oral cavity are common and can involve any of the soft tissues of the mouth. Appropriate treatment remains an area of controversy. Generally, because of the vascularity of the oral tissue, lacerations of the mouth heal quickly. See the “Intraoral Mucosal Lacerations” section of Chapter 42, “Face and Scalp Lac erations, ” for management recommendations. Lacerations involving the cheek or buccal mucosa must be examined carefully for involvement of Stensen’s duct, which drains the parotid salivary gland (the duct opens into the mouth opposite the upper second molar). If Stensen’s duct is compromised, repair by an oral and maxillofacial surgeon or otolar yngologist is indicated. Likewise, lacerations to the floor of the mouth require careful evaluation for involvement of Wharton’s duct of the submandibular salivary glands.

duct opens into the mouth opposite the upper second molar). If Stensen’s duct is compromised, repair by an oral and maxillofacial surgeon or otolar yngologist is indicated. Likewise, lacerations to the floor of the mouth require careful evaluation for involvement of Wharton’s duct of the submandibular salivary glands.  LIP LACERATIONS Lip lacerations are a potential cosmetic problem, so careful closure is essential (see Chapter 42, “Face and Scalp Lacerations, ” for management recommendations).  FRENULUM LACERATIONS Laceration of the maxillary labial frenulum, unless unusually large, does not require repair. Because such lacerations can be very painful, sched uled NSAIDs are recommended. 6 Because of the vascularity of adjacent tissue, lacerations to the lingual frenulum of the tongue may need repair. An absorbable suture such as 4-0 chromic gut or Vicryl ® is appropriate.  TONGUE LACERATIONS Lacerations of the tongue require special consideration because bleed ing and delayed swelling can compromise the airway. Simple linear lacerations <1 cm involving the central portion of dorsal surface of the tongue and that do not gape open heal well without repair. Except for the most extensive tongue lacerations, suturing does not necessarily improve outcome or reduce morbidity. All lacerations that bisect the tongue require repair. Partial amputations can be successfully replanted with the appropriate microsurgical techniques. Local anesthesia can be obtained by local infiltration or topically by placing 4% lidocaine-soaked gauze for 5 minutes on the laceration. Bilateral lingual nerve blocks can be used for lacerations of the anterior two thirds of the tongue that cross the midline. Repair of the tongue, especially in children, presents a special challenge, and many adjuncts such as a dental bite block or a Molt mouth prop can be helpful in keeping the mouth open. A piece of 4 × 4 gauze can be used to grasp the tongue. When laceration repair is warranted, absorbable sutures such as 4-0 chromic gut or Vicryl should be used. Sutures should be placed so as to include the muscular layer and the superficial mucosal layers of the tongue. Wound edges should be approximated and closed very loosely to allow for swelling of the tongue, which can be significant. Placing a closed hemostat between the suture and the tongue while tying can help prevent overtightening of the suture. The constant motion of the tongue quickly unties sutures in the mouth, so sutures should be tied with at least four square knots. If feasible, the sutures can also be placed so that the knots are buried into the wound. All patients should be instructed to rinse several times daily with a saline or chlorhexidine 0.12% mouth rinse.  DENTAL LOCAL ANESTHESIA TECHNIQUES Competence in dental local anesthesia is a useful skill for the emergency provider. The maxillary teeth can be anesthetized using local infiltra tive or supraperiosteal techniques, which are simple to do. (See Video: Periapical Dental Block). ANATOMY The trigeminal nerve is the largest cranial nerve, and although it has important motor functions, it is primarily a sensory nerve ( Figure 245-14). It divides into three main branches: the ophthalmic nerve, maxillary nerve, and mandibular nerve. The maxillary nerve provides sensory innervation to the maxilla and associated structures including the maxillary teeth and gingiva and oral mucous membranes. The third division, or mandibular nerve, is the largest of the three branches. The mandibular nerve has three main divisions. The first is the long buccal nerve that provides sensory innervation to the mucosa of cheek and buccal gingiva of the mandibular molars.

he maxillary teeth and gingiva and oral mucous membranes. The third division, or mandibular nerve, is the largest of the three branches. The mandibular nerve has three main divisions. The first is the long buccal nerve that provides sensory innervation to the mucosa of cheek and buccal gingiva of the mandibular molars. The second is the lingual nerve that runs superficial to the internal pterygoid muscle and innervates the anterior two thirds of the tongue, lingual gingiva, and floor of the mouth. Finally, the largest branch is the inferior alveolar nerve, which accompanies the inferior alveolar vein and artery in a neurovascular bundle passing between the ramus of the mandible and the sphenomandibular ligament to enter the mandibular canal. It divides at the region of the premolars, with the mental nerve exiting the mental foramen to innervate the soft tissue of the lip and chin and the incisal nerve continuing within the mandibular canal to innervate the teeth and gingiva. Tintinalli_Sec19_p1523-1606.indd 1589 8/2/19 3:07 PM

o enter the mandibular canal. It divides at the region of the premolars, with the mental nerve exiting the mental foramen to innervate the soft tissue of the lip and chin and the incisal nerve continuing within the mandibular canal to innervate the teeth and gingiva. Tintinalli_Sec19_p1523-1606.indd 1589 8/2/19 3:07 PM 1590 SECTION 19: Eye, Ear, Nose, Throat, and Oral Disorders  EQUIPMENT Specialized equipment is useful when giving dental injections, especially the inferior alveolar nerve block. Equipment includes: • A monojet aspirating dental syringe • Dental cartridges of anesthetic solution • Disposable 27-gauge, 32-mm needle • Topical anesthetic, if possible If an aspirating dental syringe is not available, any 3-mm aspirating syringe can be used. With larger syringes, the inferior alveolar nerve block is difficult because the syringe barrel interferes with the proper positioning of the needle. Position the patient in a dental chair or stretcher in a semi-reclined position with the head firmly against the headrest. Anticipate sudden movement of the patient. An overhead light is essential because dental injections require good visibility and control at all times to ensure safety of both the patient and the physician. If available, topical anesthetic can be applied to mucosa prior to injection to lessen the discomfort. First, dry the mucosal surface with gauze; then apply the topical gel for at least 1 minute prior to proceeding.  MAXILLARY INJECTIONS Supraperiosteal Infiltration Maxillary cortical bone is thin and porous enough to allow the diffusion of anesthetic solution to reach the apex of the root and effectively anesthetize the tooth. Figure 245-15 illustrates the supraperiosteal infiltration technique. The upper lip or cheek, depending on which tooth you are anesthetizing, is pulled up and taut. With the bevel facing toward the bone, the needle is inserted at the height of the buccal fold adjacent to the tooth. The needle should be directed along the long axis of the tooth and inserted to the height of or slightly above the apex of the tooth. In most cases, the needle only needs to be inserted a few millimeters. Aspirate, and if negative, then slowly inject 0.5 to 1 mL of anesthetic solution. It is important to remember that the root of the canine is significantly longer than that of other teeth and that, in general, the roots of teeth are inclined in a distal direction. The goal is to deposit the anesthesia at or above the apex of the desired tooth. 29-31 Palatal Injection Supraperiosteal infiltration of the maxillary teeth provides adequate anesthesia for pain control for a toothache, but not for procedures such as management of a dry socket or avulsed tooth. This may also require anesthesia of the palatal tissue, which can simply be accomplished by local infiltrative anesthesia. With a fine-gauge needle, puncture the palatal mucosa about halfway up the palate adjacent to the target tooth (Figure 245-16). Inject 0.1 mL of anesthetic solution. Blanching of the surrounding tissue is common, and this injection is usually quite uncomfortable. If a larger area of anesthesia is required, anesthesia of the anterior portion of the palate can be obtained by injecting anesthesia over the incisive foramen. The landmark is the incisive papilla. Anesthesia to the unilateral posterior portion of the palate can be obtained by injecting a small amount of anesthesia over the greater palatine foramen. 29-31  MANDIBULAR INJECTIONS In contrast to the maxilla where the cortex of overlying bone is relatively thin and infiltrative anesthesia is usually effective, the mandibular boney cortex is relatively thick and the inferior alveolar nerve block is usually required to gain adequate anesthesia of the mandibular molars and premolars.

ULAR INJECTIONS In contrast to the maxilla where the cortex of overlying bone is relatively thin and infiltrative anesthesia is usually effective, the mandibular boney cortex is relatively thick and the inferior alveolar nerve block is usually required to gain adequate anesthesia of the mandibular molars and premolars. A mental nerve block, as described in Chapter 36, “Local and Regional Anesthesia, ” can provide anesthesia for the premolars, canines, and incisors, as well as soft tissue of the lip and chin, when properly administered. The bone adjacent to the canines and incisors is thinner and more amenable to infiltrative anesthesia. Also, soft tissue anesthesia of the tongue can be obtained using the basics of the inferior alveolar nerve block. Injection of the long buccal nerve may be neces sary for incision and drainage of dental abscesses in the mandibular molar region, and this technique will be described. (See Video: Mental Nerve Block.) Inferior Alveolar Nerve Block (Direct Technique) The patient should be instructed to open the mouth widely to ensure good visu alization of anatomic landmarks ( Figure 245-17). First, the physician needs to palpate the greatest depth of the anterior border of the ramus Middle superior alveolar n. Posterior superior alveolar n. Supraorbital n. Lacrimal n. Nasociliary n. Ophthalmic division Trigeminal nerve Ophthalmic n. Maxillary n. Mandibular n. Maxillary division Mandibular division Long buccal n. Lingual n. Inferior alveolar n. Infraorbital n. Anterior superior alveolar n. FIGURE 245-14. The trigeminal nerve and its three main divisions. Tintinalli_Sec19_p1523-1606.indd 1590 8/2/19 3:07 PM

ic division Trigeminal nerve Ophthalmic n. Maxillary n. Mandibular n. Maxillary division Mandibular division Long buccal n. Lingual n. Inferior alveolar n. Infraorbital n. Anterior superior alveolar n. FIGURE 245-14. The trigeminal nerve and its three main divisions. Tintinalli_Sec19_p1523-1606.indd 1590 8/2/19 3:07 PM CHAPTER 245: Oral and Dental Emergencies 1591 Middle superior alveolar nerve Posterior superior alveolar nerve Anterior superior alveolar nerve FIGURE 245-15. The supraperiosteal infiltration. A. The maxillary nerve and innervation of the maxillary teeth by the posterior superior alveolar nerve, the middle superior alveolar nerve, and the anterior superior alveolar nerve. B. With the lip or cheek pulled taut, the needle is inserted at the height of the buccal fold. Note: The two to three concentric circles of dotted lines around the needle tip indicate the area where the anesthesia is deposited. C. The needle is directed along the long axis of the tooth, and anesthesia is deposited just superior to the area of the root apex. D. Clinical photograph depicting a supraperiosteal infiltration of the maxillary lateral incisor. Tintinalli_Sec19_p1523-1606.indd 1591 8/2/19 3:07 PM

ea where the anesthesia is deposited. C. The needle is directed along the long axis of the tooth, and anesthesia is deposited just superior to the area of the root apex. D. Clinical photograph depicting a supraperiosteal infiltration of the maxillary lateral incisor. Tintinalli_Sec19_p1523-1606.indd 1591 8/2/19 3:07 PM 1592 SECTION 19: Eye, Ear, Nose, Throat, and Oral Disorders or coronoid notch with the index finger or thumb. Then with that finger or thumb, the tissue is retracted toward the cheek, revealing the pterygotemporal depression that is between the raised ridge of mucosa (pterygomandibular raphe) medially and coronoid notch laterally. With the syringe directed from the opposite premolar area, the needle is inserted into the pterygomandibular depression at a point 1 to 1.5 cm above the occlusal plane. This is approximately at the level of index fin ger or thumb. The needle is then slowly advanced until bone is contacted (about 20 to 25 mm). Once bone has been contacted, the needle should be withdrawn about 1 to 2 mm and then aspirated. If no blood is aspi rated, then about 1.5 mL of anesthetic solution should be slowly injected. The needle then should be withdrawn about half of the distance, and the remainder of the dental carpule injected. This will ensure the anes thesia of the lingual nerve. 29-31 With experienced operators, the direct technique has about a 20% to 25% failure rate. Most commonly, failure is due to using too low of a point of injection. This places the anesthesia below the sphenomandibular ligament, which impedes its flow toward the inferior alveolar nerve. Repositioning the syringe higher above the occlusal plane will usually result in a successful injection. (See Video: Inferior Alveolar Nerve Block.) Lingual Nerve Block If only lingual nerve anesthesia is desired, then the above technique can be followed, except the needle need only be initially inserted about 10 mm, aspirated, and then the anesthetic agent instilled. This will provide anesthesia to the ipsilateral half of the ante rior two thirds of the tongue (Figure 245-18). 29-31 Long Buccal Injection If buccal soft tissue anesthesia is required, then this injection should be used. The needle is inserted into the mucosa in the buccal vestibule adjacent to the second or third mandibular molars (Figure 245-18). 29-31  INJECTION COMPLICATIONS The normal vasovagal symptoms, such as syncope, that can occur with any injection may occur during or after a dental injection. Flushing and elevation of the heart rate can also occur. Mild to severe allergic reac tions are possible. Due to the close proximity of the inferior alveolar artery and vein and the pterygoid plexus, a potential complication of inferior alveolar nerve block is traumatic hematoma formation. These are usually self-limiting and treated with ice to the face, but can be quite uncomfortable and an aesthetic issue for more than a week. Due to the superficial nature of the lingual nerve relative to the inferior alveolar nerve, inadvertent injury to the lingual nerve with subsequent temporary or permanent paresthesia can occur. This not only can affect sensation to the anterior two thirds of the affected side but also may affect taste because taste fibers run with the lingual nerve. Postinjection trismus, due to local trauma to the muscles of mastication, can occasionally occur. Needle breakage, although uncommon, has been reported, especially with improper technique such as bending the needle prior to use or redirecting the needle while injecting. Finally, unintentional injection too posteriorly may result in injection into the parotid region and can cause temporary facial nerve palsy. Nasopalatine nerve Incisive foramen 1 cm Greater palatine nerve Greater palatine foramen FIGURE 245-16. Palatal infiltration. A.

to use or redirecting the needle while injecting. Finally, unintentional injection too posteriorly may result in injection into the parotid region and can cause temporary facial nerve palsy. Nasopalatine nerve Incisive foramen 1 cm Greater palatine nerve Greater palatine foramen FIGURE 245-16. Palatal infiltration. A. The innervation to the soft tissue of the hard palate. The posterior portion of the palate is innervated by bilateral greater palatine nerves after they each exit their respective greater palatine foramens (see blue shaded area). The anterior portion of the hard palate is innervated by the nasopalatine nerve after exiting the incisive foramen. Injection over the incisive foramen (shown) will result in anesthesia to the purple shaded area. A similar injection over the area of the greater palatine foramen or the incisive foramen will provide anesthesia to its respective zone. B. A fine-gauge needle is inserted into the palatal tissue about 1 cm below the gingival margin, and a small amount of anesthesia is injected. Blanching of the palatal tissue surrounding the injection site is noted. This will provide anesthesia to the tissue adjacent to area injected as shown. C. Clinical photograph depicting a palatal infiltration. Tintinalli_Sec19_p1523-1606.indd 1592 8/2/19 3:07 PM

ival margin, and a small amount of anesthesia is injected. Blanching of the palatal tissue surrounding the injection site is noted. This will provide anesthesia to the tissue adjacent to area injected as shown. C. Clinical photograph depicting a palatal infiltration. Tintinalli_Sec19_p1523-1606.indd 1592 8/2/19 3:07 PM CHAPTER 245: Oral and Dental Emergencies 1593 Inferior alveolar nerve Lingual nerve Long buccal nerve Inferior alveolar nerve Lingual nerve Coronoid notch Long buccal nerve Mental nerve Coronoid notch A B Inferior alveolar vein Inferior alveolar artery Inferior alveolar nerve Sphenomandibular ligament Medial pterygoid muscle Superior constrictor muscle Lingual nerve Pterygomandibular raphe Buccinator muscle Masseter muscle Lingula Ramus Temporalis tendon Parotid gland Lateral Medial Anterior Posterior FIGURE 245-17. Inferior alveolar nerve block (direct technique). A. The anatomy of the inferior alveolar nerve as it enters the mandibular foramen in the pterygomandibular space. The lingual nerve lies superficial and medial to the inferior alveolar nerve. The coronoid notch is noted. B. The area of anesthesia obtained with a successful inferior alveolar nerve block. Usually the lingual nerve is also blocked, which provides anesthesia to the floor of the mouth, lingual gingiva, and the anterior two thirds of the tongue. C. The syringe should be directed from the contralateral premolar area about 1 to 1.5 cm above the mandibular plane. It is inserted about 20 to 25 mm until bone is touched in an area above the lingula. The needle should then be withdrawn 1 to 2 mm and aspirated for blood before injecting anesthesia. The sphenomandibular ligament attaches to the lingula and prevents the anesthesia from reaching the inferior alveolar nerve if the injection is too low. D. Clinical photograph of the direct technique. Note the point of injection in the pterygomandibular depression just lateral to the pterygomandibular raphe. E. A diagram of a transverse section of the pterygomandibular fossa at the level of an inferior alveolar nerve injection. Note that the needle passes through the buccinator muscle to an area just superior to the lingula. Tintinalli_Sec19_p1523-1606.indd 1593 8/2/19 3:07 PM