• Avulsed primary teeth should not be replaced. Avulsed permanent teeth should be reimplanted as soon as possible. Always consider aspiration when a tooth/tooth fragment cannot be located.
• Maintain a high index of suspicion for carotid injury in a patient with trauma to the oropharynx.
• Uncomplicated dental infections are treated on an outpatient basis. Deep fascial space infections often require hospitalization, IV antibiotics, and surgical drainage.
• Suppurative complications of pharyngitis include peritonsillar abscess (PTA), Lemmiere postanginal sepsis, and Ludwig angina.
• Needle aspiration can aid in differentiating between peritonsillar cellulitis and PTA. Aspiration, incision and drainage, or tonsillectomy may provide definitive treatment.
• Airway assessment is important in suspected cases of PTA, retropharyngeal abscess (RPA), and Ludwig angina. Definitive management of unstable airways is best achieved in the operating room with the assistance of an anesthesiologist or an ENT specialist.
Emergencies pertaining to the oral cavity and neck can be broadly divided into four categories: dental trauma, oropharyngeal trauma, dentoalveolar infections, and soft-tissue infections. Traumatic injuries are described in Section V.
ORAL AND DENTAL ANATOMY
Eruption of the 20 primary teeth begins with the lower central incisors between 6 and 10 months of age and is typically complete by 33 months. Eruption of the 32 secondary (permanent) teeth begins with the lower central incisors at approximately 6 years of age and is usually completed by 21 years of age. A tooth is composed of a neurovascular center, or pulp, which is surrounded by dentin (Fig. 96-1). The exterior surface of the tooth, or crown, is covered by enamel. The root of the tooth is protected by cementum and is attached to alveolar bone by the periodontal ligament (PDL). The oral cavity is bordered by the hard and soft palate superiorly, the tongue and its supporting structures inferiorly, and the cheeks which are supported by buccinator muscles. The vestibule is the space between the cheeks/lips and teeth. Gingiva covers the alveolar surfaces of the maxilla and mandible.
FIGURE 96-1. Dental anatomy.
Falls are the most common cause of injury in the preschool and school-age group. Among older children and teenagers, males are twice as likely to suffer dental trauma commonly resulting from motor vehicle collisions, sports-related injuries, and altercations.1 The most commonly injured dental structure is the maxillary central incisor.2 Dental trauma may be a marker for child abuse.
Luxations are injuries resulting from damage to the supporting structures of the teeth (PDL and alveolar bone) and are defined in terms of the lie of the tooth (see Table 96-1 for distinct types). Dental fractures may involve the tooth and/or supporting structures. Classification of dental fractures, adopted from the World Health Organization’s Application of the International Classification of Diseases to Dentistry and Stomatology, are listed in Table 96-2.3
Dental Fracture Terminology
Although dental trauma is rarely life-threatening, associated maxillofacial injuries and complications thereof may result in airway compromise, injury to surrounding nerves and blood vessels, penetration of anatomic planes of the neck with subsequent subcutaneous emphysema, pneumomediastinum, or mediastinitis.
Trauma to the primary teeth may result in a number of complications including: tooth infection, pulp necrosis with subsequent discoloration, displacement, premature loss, or problems with root resorption. Intrusion injuries to primary teeth are particularly concerning because of their anatomic proximity to the permanent teeth and frequency of anomalous permanent tooth development.4 Injuries to permanent teeth, including avulsion, can also result in pulp necrosis with subsequent color change, as well as abscess formation. The prognosis for avulsed permanent teeth is inversely proportional to the extraoral dry time. If the extraoral dry time is more than 60 minutes, the prognosis for saving the tooth is poor because of necrosis of the PDL.
All but the most minor cases should be referred to a dentist for evaluation and radiographic documentation as most EDs lack equipment for dental radiography (panoramic, periapical, and bitewing radiographs). Analgesia is indicated for all dentoalveolar injuries. NSAIDs are as effective as narcotics for the treatment of dental pain. Definitive treatment is dependent upon the type of tooth involved.
Primary teeth. Enamel and enamel–dentin fractures are treated with smoothing of sharp edges and dental referral. Complicated crown fractures benefit from capping with calcium hydroxide, pain management, and dental referral. Treatment of root, crown-root, and alveolar fractures is individualized requiring prompt dental referral. Luxation injuries generally heal without any treatment. Removal of severely loosened teeth is indicated if there is a high risk of aspiration. Reimplantation of an avulsed primary tooth is not recommended.
Permanent teeth. Uncomplicated crown fracture should be covered with glass ionomer. Reattachment of the tooth fragment can be performed on an outpatient basis. Complicated crown fractures require prompt capping with calcium hydroxide if available, analgesia, and prompt dental referral. The goal in treatment of luxation injuries is to maintain the integrity of the PDL. Concussion injuries require no treatment. All other luxation injuries should be repositioned, splinted, and referred to dental services for definitive care. Avulsion injuries of the permanent teeth require immediate reimplantation or placement in a nutritive storage media (milk, saliva, or Hanks balanced salt solution). Gently rinse the tooth handling it by the crown only, irrigate and suction the socket providing anesthesia as needed, reinsert into the empty socket, splint in place or have the patient hold the tooth in place and notify dental services. Gingival lacerations should be sutured. Guidelines for the management of traumatic dental injuries recommend antibiotic prophylaxis for patients with reimplantation of an avulsed permanent tooth.5 Tetanus status should be assessed and updated when indicated.
Soft palate or lateral pharyngeal wall trauma may present as avulsions, lacerations, and impalement. Deep space infections and carotid artery injury may complicate oropharyngeal trauma warranting thorough assessment. Injuries to the oropharyngeal soft tissues may present with bleeding, erythema, swelling, visible breaches in mucosal integrity, or presence of foreign bodies. Much of the data on the diagnostic evaluation of oropharyngeal injury are derived from small case series. There is no definitive diagnostic protocol. Carotid angiography is considered the gold standard for diagnosis of carotid injury but is invasive. Carotid ultrasound, CT scan, and MRA are other imaging modalities that can be considered; their utility in detecting thrombosis in the asymptomatic patient has not been demonstrated.6
Most soft-tissue oropharyngeal injuries heal without complications. Severe complications of seemingly innocuous injuries have been reported. Oral cavity microbes may contaminate the wound and spread to the nearby retropharyngeal space, mediastinum, or brain. Carotid artery injury, presumably arising from compression of the vessel, may result in an intimal tear with subsequent carotid and cerebrovascular thrombosis. Neurologic signs may take up to 60 hours to appear. The size of the lesion does not correlate with vascular injury, and there are no reliable clinical factors to identify patients at increased risk for neurologic sequelae.6,7
Most oropharyngeal injuries will heal spontaneously. Large, avulsed or hanging flaps require surgical exploration and repair.8 Antibiotic prophylaxis is controversial but evidence to support its utility is lacking. There is no consensus on the evaluation, diagnosis, and treatment of carotid injuries. Consultation with neurosurgery and/or vascular surgery is advised. (See Fig. 96-2 for management of palatal injuries.)
FIGURE 96-2. Algorithm for management of palatal injury. (Adapted with permission from Randall DA, Kang DR. Current management of penetrating injuries of the soft palate. Otolaryngol Head Neck Surg. 2006;135(3):356–360.)
Dentoalveolar infections include infections of the teeth and/or supporting structures (periodontium, bone). Dental abscesses may be classified as endodontic or periodontic. Endodontic (periapical) abscesses are located at the apex of the tooth and typically originate from dental caries which result in acute inflammation (pulpitis) followed by necrosis of the pulp. Untreated necrosis may lead to cellulitis and/or bacterial invasion of surrounding bone. Endodontic abscesses are the most common type of dental abscess in children. Periodontal abscesses, more common in adults, involve supportive tooth structures (PDL or alveolar bone) and form following infection of the periodontal tissues. This infection may occur from trauma, foreign body such as food debris, and surrounding gingival disease. Dentoalveolar infections are characteristically polymicrobial in nature.9 Infections less than 3 days in duration tend to be caused by penicillin-sensitive aerobic streptococci, those longer than 3 days tend to be caused by anaerobes, and those involving fascial planes involve an average of two to six organisms.10
Pulpitis presents as pain in response to thermal stimulation. Extension of the infection to the periapical tissues manifests with exquisite pain on chewing or percussion of the teeth. Fever, lymphadenopathy, tooth mobility, or edema of the soft tissues suggests the presence of a periapical abscess. An erythematous, fluctuant mass (parulis) extending toward the buccal side of the gum overlying the affected tooth may be seen. Deep space involvement is common in patients with delayed presentations of odontogenic pain. Swelling of deep spaces may represent simple cellulitis or abscess. Periapical, bitewing, or panoramic radiography may demonstrate radiolucencies where abscesses are located. In patients with signs and symptoms of local extension, a CT scan with intravenous (IV) contrast may be necessary to differentiate deep space cellulitis from abscess.
Most complications of dentoalveolar infections result from direct spread of infection to deep spaces. Spread to osseous structures, most commonly the mandible, may result in osteitis or osteomyelitis. Sequelae such as maxillary sinusitis and orbital cellulitis are reported. Ludwig angina is an extensive, life-threatening cellulitis of the submandibular, sublingual, and submental spaces. Patients present with erythema and a characteristic brawny, board-like swelling of the anterior neck, associated pain, edema, and elevation of the tongue. These patients often appear toxic and dehydrated because of inability to swallow. Indirect spread via lymphatic or hematogenous routes may also occur and result in painful regional lymphadenopathy. Deep fascial spread may also result in cavernous sinus thrombosis.
Simple, uncomplicated dental caries require analgesia and dental referral. NSAIDs are as effective as narcotics for treating dental pain.9 Pulpitis is treated by removal of infected pulpal tissue. Periapical and periodontal abscesses are treated by drainage achieved by incision and drainage (I&D), root canal therapy, or tooth extraction. Antibiotics are indicated in cases where local or systemic spread of infection is suspected. Penicillin or amoxicillin are effective against most endodontic infections. If anaerobic agents are suspected (e.g., infection for more than 3 days) prescribe clindamycin or penicillin plus metronidazole.
Admission to the hospital for airway monitoring, IV antibiotics, and surgical drainage is indicated for systemically ill patient with infections of deep fascial planes. Involve anesthesia and otolaryngologic specialists for patients with spread to the floor of the mouth.
INFECTIONS OF THE ORAL SOFT TISSUE
Oral mucosal infections may be a sign of systemic disease and should be carefully evaluated. Oral candidiasis and angular cheilitis are the most common oral manifestations of children with HIV infection. Viruses are the predominate cause of oral lesions. Primary herpetic gingivostomatitis is caused by herpes simplex virus type 1, with 30% to 40% of infected patients developing recurrent symptoms.11
Herpangina causes small vesicular lesions and punched-out ulcers in the posterior pharynx. Posterior pharyngeal ulcers likely represents coxsackievirus. Buccal and lingual vesicles with vesicles on the hands and feet (hand-foot-mouth disease) are also caused by enteroviruses (coxsackie A5, 10, and 16). Primary herpetic gingivostomatitis usually manifests with a prodrome of fever followed by lymphadenopathy and painful vesicles on a red swollen base which may become confluent. The stomatitis of candida produces curdy or velvety white plaques on the tongue and/or oral mucosa. Laboratory evaluation is generally not indicated.
Treatment of soft-tissue infections of the oral mucosa is largely symptomatic; oral analgesics and cold, soothing food such as ice pops. Children with stomatitis, ulcers, or severe sore throat benefit from gargling or oral administration of Kaopectate or Maalox combined with diphenhydramine ±viscous lidocaine (with caution for overtreatment with viscous lidocaine which can result in toxicity). Prescribe oral nystatin for candida infection. Oral acyclovir suspension may reduce duration of symptoms, improve healing of oral lesions, and reduce transmission.12 Acyclovir (15–30 mg/kg/d in three divided doses for 7–14 days) is recommended for herpes simplex infections in immunocompromised hosts.
Pharyngitis is defined as inflammation of the mucous membranes and underlying structures of the throat. The peak incidence occurs in children aged from 4 to 7 years, and approximately 10% of children seek medical care for pharyngitis annually. Most cases occur during colder months of the year when viruses are prevalent, and spread among family members is a prominent feature.13 Although bacteria, spirochetes, Chlamydia, Mycoplasma, mycobacteria, fungi, and parasites can all cause pharyngitis, 40% to 60% of cases are viral. Commonly involved viruses include adenovirus, parainfluenza virus, rhinovirus, herpes simplex, respiratory syncytial virus, Epstein–Barr virus, influenza virus, Coxsackie virus, echo virus, coronavirus, and cytomegalovirus.
Group A β-hemolytic Streptococcus (S. pyogenes, GAS) is the most common bacterial cause of pharyngitis in children, responsible for 15% to 30% of cases.13 Other, less common bacterial causes to consider include groups C and G streptococci, Mycoplasma pneumoniae, and Corynebacterium diphtheriae. Corynebacterium hemolyticum causes pharyngitis accompanied by a scarlatiniform rash similar to GAS. Pneumococcus, Staphylococcus aureus, Neisseria meningitides, and Haemophilus influenzae are thought to cause pharyngitis, usually after a viral upper respiratory infection. Fusobacterium necrophorum(FN) is both part of the normal oral flora and a pharyngeal pathogen implicated in Lemmiere syndrome.14 Consider Neisseria gonorrhoeae, Chlamydia trachomatis, and syphilis in sexually active adolescents.
Noninfectious causes of pharyngitis include postnasal drip, sinusitis, and respiratory irritants such as tobacco smoke or caustic ingestions. Agranulocytosis, lymphoma, and lymphocytic leukemia, though rare, can present with pharyngeal inflammation and symptoms.
Uvular inflammation may result from bacterial infection, trauma (usually medical instrumentation), and allergy. Uvulitis is most worrisome when associated with epiglottitis or angioneurotic edema, both potentially life-threatening conditions. GAS, H. influenzae type B, and Streptococcus pneumoniae can cause uvulitis.
Children with acute GAS pharyngitis commonly present with sore throat, fever, odynophagia, and tonsillopharyngeal erythema with or without exudate. Headache, vomiting, abdominal pain, and scarlatiniform rash (fine, erythematous, sandpaper-like) commonly accompany streptococcal pharyngitis. Non-GAS infections have a similar presentation. Rhinorrhea, cough, hoarseness, or mucosal ulcers, suggest a viral etiology. Epstein–Barr virus and cytomegalovirus infection present with fever, pharyngitis, and lymphadenopathy. Fatigue, abdominal pain, splenomegaly, and bilateral upper eyelid edema may also be noted. Low-grade fever, follicular conjunctivitis, sore throat, and cervical lymphadenopathy characterize pharyngoconjunctival fever. Pharyngitis accompanied by rash, joint pain, and urethral or vaginal discharge may indicate gonorrhea. Syphilis in the primary stage may present with diffuse pharyngeal erythema and a chancre. Secondary syphilis may manifest with gray oropharyngeal patches and a rash. Diphtheria presents as an adherent, grayish pharyngeal membrane with bull neck and toxic appearance.
Scoring systems for the diagnosis of GAS have not demonstrated adequate sensitivity or specificity in children. Testing for GAS by rapid antigen detection tests (RADT) is recommended except when overt viral features are present.14 False-positives with RADT are uncommon, however negative RADT should be confirmed by throat culture. The Infectious Diseases Society of America does not recommend GAS testing in children younger than 3 years.15 Diagnosis of infectious mononucleosis is largely clinical although viral capsid antigen IgM level may be helpful. Syphilis screening tests and/or cultures for N. gonorrhoeae are indicated for unusual presentations or recurrent disease.
Suppuration can spread to contiguous tissues causing PTA, Lemmiere postanginal sepsis (aerobic or anaerobic bacteremia from septic thrombophlebitis of the tonsillar vein), and Ludwig angina. Hematologic spread may result in mesenteric adenitis, meningitis, brain abscess, cavernous sinus thrombosis, suppurative arthritis, endocarditis, osteomyelitis, sepsis, and septic embolization to the lung.
Nonsuppurative complications of GAS include scarlet fever, acute rheumatic fever (ARF), and glomerulonephritis (PSGN). ARF typically begins 1 to 5 weeks after GAS infection and is suggested by clinical features outlined in the Jones criteria (see Chapter 110). PSGN tends to occur in outbreaks associated with virulent strains of GAS. Symptoms typically appear 1 to 3 weeks after pharyngitis, and 3 to 6 weeks after scarlet fever or impetigo. The most common presentation is dark urine, edema, and hypertension. Treatment of GAS pharyngitis within 10 days of the illness can prevent ARF, however, there is no evidence that treatment prevents PSGN.
Current recommendations for GAS pharyngitis support treatment of cases where clinical suspicion is high or the diagnosis is confirmed by RADT or culture. Penicillin (oral or IM) is the first-line agent. Advanced macrolide antibiotics, clindamycin, or first-generation cephalosporins may be used in penicillin-allergic patients.15 Treatment of group C and G streptococci should be considered in patients with severe symptoms and negative RADT culture. FN is treated with penicillin and metronidazole. Other bacterial causes require specific and supportive management. If diphtheria is suspected, diphtheria antitoxin is given along with penicillin or erythromycin to eradicate the organism.
PTA is the most common deep infection of the head and neck, typically seen in children older than 12 years.16 PTA usually begins as an episode of acute tonsillitis. Occlusion of tonsillar crypts and bacterial invasion of the peritonsillar area results in peritonsillar cellulitis. Pus collection in the supratonsillar fossa results in PTA. Most PTAs are polymicrobial infections. GAS predominate; Peptostreptococcus, FN and other normal mouth flora, including anaerobes, may also be detected.17 Uncommonly, H. influenzae, S. pneumoniae, and S. aureus are cultured.
Patients with PTA usually present with fever, pharyngeal discomfort, ipsilateral otalgia, and trismus. Drooling is not unusual. The voice has a muffled “hot potato” quality, and patients often appear toxic. Examination of the oropharynx may sufficiently distinguish peritonsillar cellulitis from an abscess. Cellulitis is commonly associated with diffuse swelling and edema in the peritonsillar region. Trismus may result from mass effect and involvement of the internal pterygoid muscle. Inferomedial displacement of the tonsil, contralateral shifting of the uvula, and ipsilateral cervical adenopathy are typically identified in patients with PTA.
The white blood cell count may be elevated. RADT may demonstrate GAS infection. However, needle aspiration of purulent material is the diagnostic gold standard and useful for directing antibiotic therapy. CT scan of the neck with contrast can be used to differentiate PTA from peritonsillar cellulitis and delineate extension of the disease to adjacent structures. The reported sensitivity and specificity of CT scan for PTA are 100% and 75%, respectively.18Intraoral ultrasound has also been used but has demonstrated a lower sensitivity than CT scan.18
Most complications of PTA result from direct spread and invasion of adjacent tissue. Septicemia, parapharyngeal abscess, glottic edema, and airway obstruction are reported. The lateral pharyngeal recess provides a natural communication to the anterior chest which could result in mediastinitis, lung abscess, thrombophlebitis, or necrotizing fasciitis.
Patients with PTA should receive IV hydration and parenteral antibiotics. Penicillin is the drug of choice. Clindamycin or a second- or third-generation cephalosporin are recommended in cases involving β-lactamase organisms. Steroids may improve swallowing and disease resolution, however, trials in children do not exist. Similar cure rates have been documented in patients managed by I&D or 3-point per mucosal needle aspiration. Needle aspiration and antibiotic therapy is effective in 85% to 90% of cases. Needle aspiration has several advantages. It can be performed safely in cooperative patients by emergency personnel, provides immediate relief of symptoms, and confirms diagnosis with minimal trauma. I&D has been documented to be more effective in rapidly relieving symptoms and may prevent recurrence of the disease.19
The retropharyngeal space is a pocket of connective tissue that extends from the base of the skull to the tracheal carina. It lies posterior to the pharynx and is bordered anteriorly by the buccopharyngeal fascia, posteriorly by the prevertebral fascia, and laterally by the carotid sheaths. It harbors two paramedian chains of lymphoid tissue that drain the nasopharynx, adenoids, and posterior paranasal sinuses. The lymphatic chains begin to atrophy around the third or fourth year of life.
RPA is a local infection with accumulation of pus in the prevertebral soft tissue of the neck; commonly seen in children aging between 2 and 6 years.20 RPA frequently originates from infection of the nose, paranasal sinuses, or nasopharynx with subsequent spread to retropharyngeal lymph nodes. RPA can also result from direct inoculation of the space from penetrating oropharyngeal trauma or spread from contiguous spaces (parapharyngeal and submandibular).
S. aureus and GAS are the most common pathogens. H. influenzae and anaerobes (Bacteroides, Peptostreptococcus, and Fusobacterium spp.) are also implicated. β-lactamase production is not rare.
A prodrome of nasopharyngitis progressing to an abrupt onset of high fever, dysphagia, refusal of feeding, severe throat pain, and neck pain or torticollis is typical. Irritability, fever, and decreased appetite are described in infants and toddlers. Respirations may be labored, and drooling or stridor may be present. Stiff neck with sore throat, dysphagia, stridor, and “hot potato” voice suggests retropharyngeal space infection. Meningismus may result from irritation of the paravertebral ligaments. Airway obstruction by RPA may mimic epiglottitis or croup, PTA, and infectious mononucleosis.
An elevated white cell count with a left shift is noted, but is unnecessary for therapeutic decisions. Soft-tissue lateral neck radiography may demonstrate a retropharyngeal mass (Fig. 96-3). In children younger than 15 years, the prevertebral space is normally <7 mm anterior to C2 and <14 mm anterior to C6 or <40% of the anteroposterior diameter of the C3 or C4 vertebral bodies. Neck flexion during plain radiography can cause false-positive results. IV contrast-enhanced CT scan of the neck is sensitive for RPAs and provides further information on local structures. Cultures and Gram stain of purulent material obtained from I&D is essential.
FIGURE 96-3. Retropharyngeal abscess.
The most serious acute complications are airway obstruction and aspiration. The abscess may rupture into the esophagus, mediastinum, or lungs resulting in pneumonia, empyema, and mediastinitis. Blood vessels may be eroded resulting in severe hemorrhage. Spread of infection to adjacent spaces and structures may also occur resulting in mediastinitis, osteomyelitis, and jugular vein thrombosis. Inadequate drainage can result in reformation of the abscess.
A standard approach to airway maintenance is vital since airway obstruction and aspiration can occur at any time. Hospitalization for hydration, IV antibiotics, and analgesia may be required. The optimal antibiotic regimen has not been established. Most resources recommend penicillinase-resistant penicillin with addition of clindamycin, metronidazole, and/or a third-generation cephalosporin for additional gram-negative coverage. Duration of treatment remains controversial. The need for surgical intervention is unclear. Several retrospective analyses suggest the utility of inpatient observation with IV antibiotic therapy.21,22 However, cases with signs of airway obstruction or multiple abscess sites typically require surgical drainage.23
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