Jeffrey G. Norvell
FACIAL INFECTIONS
IMPETIGO
Impetigo is a superficial epidermal infection that can be divided into bullous and nonbullous presentations.
Bullous impetigo is caused by Staphylococcus aureus, and it presents as vesicles that rapidly enlarge to form bullae with clear yellow fluid.
Nonbullous impetigo is caused by Streptococcus pyo-genes and Staph. aureus, and it presents as vesicles that break and form the characteristic honey crusts.
Mupirocin ointment 2% applied topically tid is the treatment of choice for localized infections.
Oral antibiotics are indicated for more diffuse infections and for infections that do not respond to topical therapy (Tables 152-1 and 152-2).
TABLE 152-1 Antibiotic Therapy for Facial Infections
TABLE 152-2 Antibiotic Doses for Facial Infections
ERYSIPELAS
Erysipelas is a superficial form of cellulitis involving the epidermis, upper levels of the dermis, and the lymphatic system.
Most common on the lower extremities, but also described on the face.
Erysipelas is most commonly caused by Strep. pyogenes and rarely Staph. aureus. Staphylococcus aureus is commonly found in bullous erysipelas.
Clinical features include a painful, red, raised, puffy appearance with a sharply defined, palpable border.
The diagnosis is clinical.
Patients are usually treated with oral antibiotics. Hospitalization and parenteral antibiotics should be considered for failed outpatient therapy, immunocom-promise, or evidence of systemic illness. Antibiotic recommendations are listed in Tables 152-1 and 152-2.
CELLULITIS
Cellulitis is a soft tissue infection that involves the skin and subcutaneous tissues.
Risk factors for cellulitis include violation of the skin barrier, immunosuppression, systemic disease (eg, diabetes), vascular compromise, and foreign bodies.
The pathogen usually is Strep. pyogenes or Staph. aureus, with an increasing predominance of methicillin-resistant Staph. aureus. Less commonly, cellulitis may represent extension from a deeper facial infection.
Cellulitis is characterized by erythema, edema, pain, warmth, and loss of function. A well-defined, palpable border is absent.
The diagnosis of cellulitis is clinical.
Laboratories and blood cultures may be needed for severe illness, immunocompromise, or significant comorbidities. Ultrasound and computed tomography may be used to evaluate for abscess.
Most patients can be treated with oral antibiotics (Tables 152-1 and 152-2).
Consider hospitalization and parenteral antibiotics for signs of systemic illness, failed outpatient therapy, or significant comorbidities (Tables 152-1 and 152-2).
SALIVARY GLAND DISORDERS
VIRAL PAROTITIS
Mumps, a paramyxovirus infection, is the most common cause of viral parotitis in children under age 15 years.
Other viral etiologies include influenza, parainflu-enza, coxsackie viruses, echoviruses, lymphocytic choriomeningitis virus, and HIV.
The virus is spread by airborne droplets.
Symptoms begin after an incubation period of 2 to 3 weeks and consist of fever, malaise, headache, myalgias, arthralgias, and anorexia.
Prodromal symptoms continue for 3 to 5 days and are followed by parotid gland enlargement.
Bilateral parotid enlargement occurs in 75% of cases and lasts up to 5 days. The gland is tense and painful, but erythema and warmth are absent and no pus can be expressed from Stensen’s duct.
Diagnosis is clinical. Viral serology can be obtained, but it will not affect acute management.
Treatment is supportive and consists of analgesics and antipyretics.
The patient is contagious for approximately 9 days after the onset of parotid gland swelling.
Epididymo-orchitis is the most common extra-salivary gland involvement in postpubertal males, affecting 20% to 30% of patients. It can precede or follow parotitis.
Oophoritis occurs in only 5% of females.
Other systemic complications include pancreatitis, aseptic meningitis, hearing loss, myocarditis, arthritis, hemolytic anemia, and thrombocytopenia.
SUPPURATIVE PAROTITIS
Suppurative parotitis is a serious bacterial infection that occurs in patients with diminished salivary flow.
Retrograde transmission of oral bacteria leads to infection.
Factors and conditions that lead to decreased salivary flow include recent anesthesia, dehydration, prematurity, advanced age, sialolithiasis, medications (eg, diuretics, ß-blockers, antihistamines, phenothiazines, tricyclic antidepressants), and certain disorders (eg, diabetes, HIV, hypothyroidism, Sjögren’s syndrome).
Suppurative parotitis is usually causedby Staph. aureus and less often by Streptococcus pneumoniae, Strep, pyogenes, and Haemophilus influenzae. Anaerobes such as Bacteroides species, Peptostreptococcus, and Fusobacteriumare found in 43% of isolates.
Clinical features may include rapid onset, fever, tris-mus, erythema, and pain over the parotid gland.
In contrast to mumps, pus may be expressed from the Stensen’s duct.
The diagnosis is clinical. Ultrasound or CT may be ordered if abscess is suspected.
Treatment consists of hydration, local massage, heat, sialogogues (eg, lemon drops, orange juice), and oral antibiotics (Tables 152-1 and 152-2).
Hospitalization and parenteral antibiotics (Tables 152-1 and 152-2) should be considered for trismus, inability to tolerate oral intake, immunocompromise, or failure of outpatient therapy.
SIALOLITHIASIS
Sialolithiasis is the development of stones is a stagnant salivary duct.
Eighty percent of salivary calculi occur in the sub-mandibular duct and most of the remainder in the parotid duct.
Patients present with unilateral pain, swelling, and tenderness of the involved gland that is exacerbated by meals.
Diagnosis is clinical. The stone may be palpable and the gland will be firm.
CT is usually only ordered if abscess is in the differential diagnosis.
Treatment initially consists of analgesics, massage, and sialogogues. If concurrent infection is suspected, treatment with antibiotics is indicated.
Palpable stones can be milked from the duct.
Persistently retained calculi can be removed electively by an otolaryngologist.
MASTICATOR SPACE ABSCESS
The masticator space consists of four contiguous potential spaces bounded by the muscles of mastication. These spaces include the masseteric, pterygomandibu-lar, superficial temporal, and deep temporal spaces.
Infections in these spaces, commonly associated with an odontogenic source, are polymicrobial. Typical organisms include species of Streptococcus, Peptostreptococcus, Bacteroides, Prevotella, Porphyromonas, Fusobacterium, Actinomyces, Veillonella, and anaerobic spirochetes.
Abscesses in these spaces result in swelling over the buccal, submandibular, or sublingual areas. Patients may also have fever, pain, erythema, and trismus.
Contrast-enhanced CT can help differentiate cellulitis from abscess, and if an abscess is present, its extent can be detailed.
Since these spaces ultimately communicate with the tissue planes that extend into the mediastinum, early treatment is imperative.
Airway compromise is rare, but it should be considered.
Emergency department treatment includes stabilization, antibiotics (Tables 152-1 and 152-2), otolaryn-gology consult, and hospitalization.
MANDIBLE DISORDERS
TEMPOROMANDIBULAR JOINT DYSFUNCTION
The temporomandibular joint (TMJ) combines a hinge and gliding movement. Anatomic internal derangement or systemic disease can cause dysfunction of this joint.
Patients present with dull pain in the region of the TMJ or pain localized over one of the muscles of mastication. Tenderness to palpation over the condylar head may be present when opening and closing the mouth and range of motion may be limited.
The diagnosis is usually clinical. For patients with trauma, imaging with CT or panoramic tomorgraphy (Panorex) may be warranted.
Treatment for nontraumatic conditions consists of warm compresses, soft diet, analgesics, NSAIDs, and referral to a dental specialist.
An oral-maxillofacial surgeon manages fractures.
MANDIBLE DISLOCATION
The mandible can be dislocated in an anterior, posterior, lateral, or superior direction.
Anterior dislocation is most common.
Patients with acute mandible dislocations present with severe pain, difficulty swallowing, and malocclusion.
In anterior dislocations, pain is localized anterior to the tragus and a history of extreme mouth opening is typical.
All other mandibular dislocations require significant trauma.
The diagnosis of a nontraumatic anterior dislocation is made clinically.
In other dislocations or if there is a history of trauma, imaging with mandibular radiographs, Panorex, or CT is needed.
Reduction may be attempted in closed anterior dislocations without fracture. Reduction may be facilitated with analgesia, muscle relaxants, or procedural sedation.
One technique to reduce anterior dislocations involves the patient in the sitting position and the provider applies downward and posterior pressure to the patient’s lower molars as shown in Fig. 152-1. Tape a few layers of gauze over the provider’s gloved thumbs for protection.
Patients with open or nonreducible dislocations, associated fractures, or nerve injury should be emergently referred to an oral-maxillofacial surgeon.
After successful reduction, patients are placed on a soft diet and instructed not to open their mouths more than 2 cm for 2 weeks.
FIG. 152-1. Reduction of dislocated mandible technique in a seated patient. The thumbs are placed over the molars, and pressure is applied downward and backward.
For further reading in Tintinalli’s Emergency Medicine: A Comprehensive Study Guide, 7th ed., see Chapter 238, “Face and Jaw Emergencies,” by Corey R. Heitz.