Chapter 243: Face and Jaw Emergencies

Cellulitis and erysipelas are discussed in detail in the chapter 147, "Soft Tissue Infections." Impetigo is discussed in the chapter 136, "Rashes in Infants and Children." The differential diagnosis of facial infections is provided in Table 243-1.¹

Cellulitis is a superficial soft tissue infection that lacks anatomic constraints.^2,3,4 Facial cellulitis is caused most commonly by Streptococcus pyogenes (group A β-hemolytic) and Staphylococcus aureus,⁴ with an increasing predominance of methicillin-resistant S. aureus.⁵ Less commonly, cellulitis may represent extension from deep space infections (see "Masticator Space Infection" section below). In children, buccal cellulitis from Haemophilus influenzae is now very uncommon if children have received the H. influenzae type b vaccine.⁶

Bedside US can exclude or identify facial abscess (Figure 243-1). CT can identify deep-seated, extensive infections that involve the soft tissues of the neck or pharynx.

Treatment is provided in Table 243-2. Duration of therapy is not well studied, but recommendations range from 7 to 14 days.^3,5,7,8 Treatment failures range from 15% to 20% for β-lactams (cephalexin, dicloxacillin, and amoxicillin-clavulanate) as well as for the anti–methicillin-resistant S. aureus therapies⁹ due to the failure to cover methicillin-resistant S. aureus and streptococcal species, respectively. Cephalexin appears to be the most cost-effective therapy based on a probability of 37% for infection with S. aureus and a 27% methicillin-resistant S. aureus prevalence.¹⁰ In selected cases, traditional β-lactam therapy may be added to anti-methicillin-resistant S. aureus therapy, but this strategy increases cost and potential for adverse effects of the medication.

Erysipelas is most common in the lower extremities (66% to 76%)^11,12,13 but is classically described as a disease of the face (see Figure 152-3). The nasopharynx is typically the source of bacteria.¹⁴ In the majority of cases, erysipelas is caused by S. pyogenes.^3,4 Bullous erysipelas is a more severe form of the disease, and half of the infections reported in a 2004 case series were due to methicillin-resistant S. aureus.¹⁵ Penicillin is the antibiotic treatment of choice^3,13 but is chosen as empiric therapy in a minority of cases.^11,12,16,17 If the suspicion exists of a staphylococcal infection (i.e., bullae, trauma, or the presence of a foreign body), alternatives include dicloxacillin, amoxicillin-clavulanate, or a cephalosporin³ (Table 243-2). One randomized, prospective trial compared the use of a macrolide, roxithromycin, with penicillin and found no difference in efficacy.¹⁸

Impetigo is a discrete, superficial bacterial epidermal infection, characterized by amber crusts (nonbullous) or by fluid-filled vesicles (bullous) (see Figures 141-14 and 141-15). It is most common in children. S. aureus alone or in combination with S. pyogenes (group A β-hemolytic) is the most common cause of nonbullous impetigo. Bullous impetigo is always caused by S. aureus.^3,19,20 Treatment should cover streptococcal and staphylococcal species. Topical therapy is sufficient for uncomplicated patients with only a few nonbullous lesions.²¹ Mupirocin, retapamulin, or fusidic acid ointment is recommended; however, some resistance is developing.^3,20,22,23 Consider oral antibiotics for extensive lesions or lesions that do not respond to topical therapy alone. Erythromycin and cloxacillin are superior to penicillin, but there is no clear preference between macrolides, β-lactamase–resistant penicillins, and cephalosporins.^3,19 Preferred choices are penicillinase-resistant penicillins (cloxacillin, dicloxacillin, amoxicillin-clavulanic acid) or first-generation cephalosporins (cephalexin).³ For methicillin-resistant S. aureus, treat with trimethoprim-sulfamethoxazole or clindamycin³ (Table 243-3).

There are three groups of salivary glands: the parotid, submandibular, and sublingual. The facial nerve passes through the superficial portion of the parotid gland, and the parotid (Stensen's) duct opens into the mouth opposite the upper second molar. The submandibular and sublingual glands lie below the plane of the tongue. The submandibular ducts open into the mouth at either side of the frenulum of the tongue. The multiple sublingual ducts open into the sublingual fold or directly into the submandibular duct.²⁴

Signs of salivary gland infections are unilateral or bilateral facial swelling. Recurrent symptoms, dry mouth and eyes, or joint symptoms suggest etiologies such as immunologic or collagen vascular disorders. Other medical conditions, such as nutritional disorders, toxic exposures, diabetes, dehydration, medication usage (i.e., phenothiazines), pregnancy, and obesity, can result in salivary gland enlargement. On physical examination, determine the location of the swelling to identify the gland involved. Multiple gland involvement suggests infection. A palpable tender mass may be a sign of tumor or obstruction by a stone. The differential diagnosis of salivary gland swelling is provided in Table 243-4.²⁴

VIRAL PAROTITIS (MUMPS)

Viral parotitis is an acute infection of the parotid glands, characterized by unilateral or bilateral parotid swelling. It is most often caused by the paramyxovirus and may be caused less commonly by influenza, parainfluenza, coxsackie viruses, echoviruses, lymphocytic choriomeningitis virus, and even human immunodeficiency virus.²⁵ It is most common in children under the age of 15 years old, but since November 2014, clusters of mumps have been reported in adult members of professional hockey teams. The virus is spread by airborne droplets, incubates in the upper respiratory tract for 2 to 3 weeks, and then spreads systemically. Vaccine protection is not 100%, and outbreaks occur in settings of close contact, such as schools, colleges, sports teams, and camps.²⁶

After a period of incubation, one third of patients experience a prodrome of fever, malaise, headache, myalgias, arthralgias, and anorexia during a 3- to 5-day period of viremia.²⁵ The classic salivary gland swelling then follows. Unilateral swelling is typically followed by bilateral parotid involvement. The gland is tense and painful, but erythema and warmth are notably absent. Stensen's duct may be inflamed, but no pus can be expressed.²⁵

Diagnosis is clinical and treatment is supportive. Salivary gland swelling typically lasts from 1 to 5 days. The patient is contagious for 9 days after the onset of parotid swelling, and children with mumps should be excluded from school or day care for this interval.

Mumps is usually benign in children but can be severe in adults. Unilateral orchitis affects 20% to 30% of males (with a predisposition of ≥8 years of age), whereas oophoritis affects only 5% of females. Other complications of the mumps virus include mastitis, pancreatitis, aseptic meningitis, sensorineural hearing loss, myocarditis, polyarthritis, hemolytic anemia, and thrombocytopenia.²⁵ Immunocompetent patients with isolated viral parotitis or orchitis can be managed as outpatients. Admit patients with systemic complications.

Suppurative parotitis is a serious bacterial infection of the parotid gland that occurs in patients with compromised salivary flow. It is caused by the retrograde migration of oral bacteria into the salivary ducts and parenchyma.²⁵ Predisposing factors include recent anesthesia, dehydration, prematurity or advanced age, sialolithiasis, oral neoplasms, salivary duct strictures, tracheostomy, and ductal foreign bodies.²⁵ Medications that cause either systemic dehydration or decreased salivary flow specifically can cause parotitis. These include diuretics, antihistamines, tricyclic antidepressants, phenothiazines, β-blockers, and barbiturates.²⁵ Several chronic illnesses also predispose patients to suppurative parotitis, such as human immunodeficiency virus, hepatic or renal failure, diabetes mellitus, hypothyroidism, malnutrition, Sjögren's syndrome, depression, anorexia, bulimia, hyperuricemia, and cystic fibrosis.²⁵

Most cases of suppurative parotitis are caused by S. aureus, with S. pneumoniae, S. pyogenes, and H. influenzae as more infrequent pathogens.^3,25 Anaerobes such as Bacteroides species, peptostreptococci, and fusobacteria may be found in up to 43% of isolates. In the immunocompromised host, gram-negative organisms such as Escherichia coli and Pseudomonas may be seen.

The onset of suppurative parotitis is rapid, and the skin over the parotid gland is red and tender. Pus may be expressed from the Stensen's duct. There is often fever and trismus.

Suppurative parotitis is diagnosed clinically, with evidence of purulent drainage from Stensen's duct. Cultures of Stensen's duct drainage can guide therapy in the patient not responding to first-line antibiotics.²⁷ Imaging is not helpful unless an abscess is suspected, in which case US or CT is diagnostic.

Because suppurative parotitis is caused by states of decreased salivary flow, treatment should optimize salivary flow. Hydrate the volume-depleted patient. Massage and apply heat to the affected gland. Stimulate salivation using sialagogues, such as lemon drops. When possible, discontinue drugs that cause dry mouth, and attempt to correct underlying medical problems.²⁷

Treat patients with oral antibiotics if they can tolerate oral liquids and have no evidence of systemic illness. Admit for parenteral antibiotics patients who have trismus and cannot tolerate oral liquids, are immunocompromised or incapable of complying with an outpatient treatment regimen, or have not shown improvement after 48 hours of outpatient treatment.²⁷

Antimicrobial therapy consists of agents that cover both staphylococcal and streptococcal species (Tables 243-2 and 243-3). The initial choice for oral therapy includes amoxicillin-clavulanate; in penicillin-allergic patients, use clindamycin or a combination of cephalexin with metronidazole.^3,27 When parenteral therapy is indicated, choices include nafcillin, ampicillin-sulbactam, or a combination of vancomycin with metronidazole. In hospitalized or nursing home patients, the possibility of methicillin-resistant S. aureus, for which vancomycin is appropriate,²⁷ must be considered. In neonates, treat with gentamicin and antistaphylococcal antibiotics combined with hydration. If there is no improvement in 24 to 48 hours, surgical drainage is required.

Sialolithiasis is the development of a calcium carbonate and calcium phosphate stone (sialolith) in a stagnant salivary duct. Salivary calculi can develop in any age group but usually are symptomatic in men between the third and sixth decades.²⁸ More than 80% of stones occur in the submandibular gland, with most of the remainder in the parotid.

The symptoms of pain, swelling, and tenderness may resemble those of parotitis. It may be hard to distinguish parotitis from sialolithiasis, and the two conditions may coexist. Sialolithiasis is typically unilateral. The pain and swelling of sialolithiasis are colicky and exacerbated by meals.

The diagnosis is clinical. A stone may be palpated within the duct, and the gland is firm.²⁸ Intraoral radiographs are more sensitive than extraoral films in identifying salivary calculi. The calculi are radiopaque in about 70% of cases. US and thin-cut CT also will identify sialoliths but are usually obtained only if abscess is in the differential diagnosis. ED bedside US has been shown in a case report to be a useful diagnostic tool to determine number, size, and location of stones (Figure 243-2).²⁹ A conservative course of treatment should precede imaging studies. Occasionally on CT, the diagnosis of sialolithiasis is made by the typically glandular swelling and inflammatory changes (signifying ductal obstruction) without an obvious stone seen in the duct (Figure 243-3).

Treatment is outpatient therapy with analgesics, antibiotics if there is concurrent infection, massage, and sialagogues, such as lemon drops.²⁸ Palpable stones in the distal duct may be digitally "milked" from the duct. Complications of salivary duct obstruction include recurrent or persistent obstruction, strictures, infection, and gland atrophy.²⁸

The masticator space consists of four potential spaces bounded by the muscles of mastication (Figure 243-4). These spaces include the masseteric (or submasseteric), superficial temporal, deep temporal, and pterygomandibular spaces.³⁰ The spaces are all contiguous. Masticator space infections occur when one or more bacterial agents invade all of these spaces. Bacteria may gain entry to the space from dental infections, trauma, surgery, or injections. Infections of the masticator space are polymicrobial and generally anaerobic, although aerobic oral streptococcal species may predominate briefly.^4,30 Typical organisms include species of Streptococcus, Peptostreptococcus, Bacteroides, Prevotella, Porphyromonas, Fusobacterium, Actinomyces, Veillonella, and anaerobic spirochetes.^4,30

The most frequent acute clinical findings are facial swelling, pain, erythema, and trismus. When infection occurs in the masseteric space, there is facial swelling posteriorly and inferiorly, with mild to moderate trismus. If the temporal space is infected, there is soft tissue swelling over the temporalis muscle and trismus. Trismus without swelling suggests pterygomandibular space abscess. In chronic infection, the patient can be afebrile but may complain of intermittent trismus.³¹ Constitutional signs may include fever, malaise, dehydration, dysphagia, nausea, or vomiting. In more advanced cases, systemic signs of sepsis are present. The differential diagnosis includes other sources of lateral facial pain and swelling (Table 243-4).

Ultrasonography is helpful in differentiating abscesses from cellulitis (Figure 243-1), for the diagnosis of lymphadenitis, and to identify internal jugular thrombosis.²⁹ Contrast-enhanced CT is the preferred diagnostic tool for masseteric and related deep space infections.^30,31,32 CT can define the extent of the abscess and distinguish cellulitis from abscess in all spaces except the retropharyngeal.³⁰ MRI can be considered if infection is thought to reach the skull base.²⁹

The patient's condition determines therapy. Because all the subordinate spaces of the masticator space communicate with each other and ultimately with the tissue planes that extend down the neck to the mediastinum, the extent of the infection should be defined efficiently and treatment begun promptly. Airway compromise is rare in unilateral masticator space infection. Treatment is airway control, stabilization, and treatment of infection. Administer antibiotics in the ED (Table 243-3), and admit the patient. IV clindamycin is recommended, with alternatives including ampicillin-sulbactam, cefoxitin, or the combination of penicillin with metronidazole.^4,30 Antibiotics are continued for 10 to 14 days. The macrolides (e.g., erythromycin) are generally no longer used for masticator space infections.³⁰ Otolaryngology consultation is recommended.

The temporomandibular joint combines both a hinge and gliding action. The articular surfaces of the joint are separated by the articular disk, or meniscus, which assists in the hinge action between the mandibular condyle and the disk and in the gliding action between the disk and temporal bone.³³

TEMPOROMANDIBULAR JOINT DYSFUNCTION

Temporomandibular joint dysfunction causes pain of the joint and its surrounding anatomic structures. Assess for temporomandibular joint injury when evaluating direct jaw trauma or acute dental injury.³⁴ Most studies have found no significant correlation between occlusal parameters or bruxism and signs or symptoms of temporomandibular joint disorders.^35,36 Over time, degenerative joint disease (osteoarthritis) may result from chronic internal derangement or occur secondary to systemic disease such as rheumatoid arthritis or systemic lupus erythematosus.³⁴

The chief complaint is usually pain localized to one of the muscles of mastication or pain with chewing in one or both temporomandibular joints. The masseter muscle is the most frequently identified painful area, followed by the temporalis, sternocleidomastoid, splenius capitis, and trapezius muscles.³⁵ Physical findings may include limitation in the range of motion of the mandible. Palpate the muscles of mastication to find areas of sensitivity, induration, rigidity, and swelling. Palpate the condylar heads with the teeth together and then with the teeth apart. The differential diagnosis of temporomandibular joint dysfunction includes jaw trauma, including fracture and dislocation; odontogenic pain, including from abscess, carie, or trauma; otologic referred pain, including from otitis media, otitis externa, and foreign body; and temporal arteritis.

Temporomandibular joint dysfunction is diagnosed by history and physical examination. Isolated temporomandibular joint clicking without pain or other dysfunction is not diagnostically sufficient.³⁵ For acute trauma, the panoramic x-ray view (Panorex) of the mandible is usually the initial imaging of choice. Panorex also provides information about the teeth and other parts of the jaw that may be contributing to pain.³⁷ CT is appropriate in the assessment of potentially complex fractures, infections, and neoplastic disease.

The oral maxillofacial surgeon manages fractures and should be consulted for trismus and significant mandible displacement. Otherwise, for uncomplicated fractures and nontraumatic conditions, give simple analgesics, including nonsteroidal anti-inflammatory drugs and, if necessary, narcotics. Advise the patient to eat soft foods until definitive treatment is provided. The management of chronic temporomandibular dysfunction may ultimately require referral to a dentist, maxillofacial surgeon, or pain specialist.

Trigeminal neuralgia, or tic douloureux, is characterized by facial pain in the distribution of cranial nerve V. The cause is not known. Some postulate there is peripheral nerve injury or disease that increases afferent firing or a failure of central inhibition. Compression of the nerve by vessels, tumors, or inflammation is also a potential cause.³⁸

Trigeminal neuralgia is characterized by paroxysms of severe unilateral pain in the trigeminal nerve distribution lasting only seconds, with normal findings on neurologic examination. There is no pain between paroxysms. Trigeminal neuralgia is divided into two categories. Classic trigeminal neuralgia includes idiopathic cases and cases due to microvascular compression. Secondary, or symptomatic, trigeminal neuralgia is due to tumor, multiple sclerosis, or other structural abnormalities.

The history is key for diagnosis. Pain is a severe, shocking or stabbing, and brief, lasting seconds to minutes. Complete resolution occurs between episodes. Pain is clearly in the distribution of cranial nerve V. Classically, the pain is unilateral, although it can be bilateral. Triggers include light touch, chewing, or a light breeze. Pain can be accompanied by facial spasms. Physical exam is unremarkable.

Treatment is most often medical, but severe cases may require surgical intervention. Carbamazepine, started at 100 milligrams PO twice a day and then increased in dosage as needed, is an effective treatment. Baclofen has also been shown to be successful.³⁹ Patients with trigeminal neuralgia may present to the ED because symptoms are of recent onset or recurrent and should be started or restarted on carbamazepine. Pain control is rarely an issue because the paroxysms are so brief. Refer patients to a neurologist.

Bell's palsy is the most common cause of unilateral facial paralysis. The cause, however, is not clear. A leading theory is that as the facial nerve exits the temporal bone, edema and ischemia result in compression of the nerve. Inflammatory, demyelinating, or compressive processes have all been suggested, including infections (herpes simplex virus, herpes zoster, Lyme disease, syphilis, Epstein-Barr virus, cytomegalovirus, human immunodeficiency virus, mycoplasma), microvascular disease (diabetes and hypertension), and medications, including chemotherapeutics.⁴⁰

Symptoms of Bell's palsy include acute onset of unilateral upper and lower facial paralysis, posterior auricular pain, decreased tearing, hyperacusis (oversensitivity to certain frequency and volumes), and otalgia. Some of these symptoms may develop prior to the classic facial paralysis. Onset is typically sudden, with a peak of symptoms in 48 hours.⁴⁰

Diagnosis is confirmed by thorough history and physical exam. Examination reveals weakness and/or paralysis of both the upper and lower portion of the face on the affected side. Flattening of the forehead and nasolabial folds on the affected side is present. Careful neurologic exam is useful in ruling out other conditions, such as stroke. In addition, examine the ear to ascertain presence of cranial herpes zoster, which along with stroke and Guillain-Barré syndrome accounts for >85% of misdiagnoses.⁴¹ Laboratory studies are not needed.

There is much controversy surrounding the treatment for Bell's palsy. Goals of emergency care include increasing the chances of recovery of facial nerve function and protection of the eye. The American Academy of Neurology guidelines state that steroids are highly likely to be effective and increase the likelihood of recovery.⁴² When initiated within the first 72 hours of symptom onset, steroids improve chances of full recovery. The recommended dosing is 1 milligram/kg up to 60 milligrams/d for 6 days, followed by a 10-day taper. Use of antivirals, such as acyclovir or valacyclovir, is controversial. According to the American Academy of Neurology's 2012 guidelines, benefits from antivirals have not been established and are thought be modest at best.⁴¹ A variety of other therapies including physical therapy, acupuncture, and surgical decompression have also been used with variable success. Cessation of the offending agent is indicated if the medications or chemotherapy is implicated. Apply ocular lubricants to protect against corneal abrasions, and it may be necessary to tape the patient's eyelid, especially during sleep.

MANDIBLE DISLOCATION

The mandible can be dislocated in an anterior, posterior, lateral, or superior direction. Anterior dislocation is most common and occurs when the mandibular condyle is forced in front of the articular eminence. Muscular spasm then traps the mandible in anterior dislocation, and the mandible is elevated before retraction. Factors that predispose patients to symptomatic anterior dislocation include a shallow glenoid fossa, increased muscle tone (such as during a seizure), and a loss of joint capsule tone from previous trauma. Spasm of the temporalis and lateral pterygoid muscles tends to prevent reduction once dislocation has occurred. Dislocations are usually bilateral but can be unilateral.³³ Posterior dislocations are rare. They follow a blow that may or may not break the condylar neck. In posterior dislocation, the mandibular condyle is thrust backward against the mastoid, and the condylar head may prolapse into the external auditory canal.³³ Lateral dislocations are often associated with mandibular fracture. With a lateral dislocation, the condylar head is forced laterally and then superiorly into the temporal space. Superior dislocations occur from a blow to the partially open mouth that forces the condylar head upward. Associated injuries include cerebral contusions, facial nerve palsy, and deafness.

Acute jaw dislocation causes severe pain, difficulty in speaking or swallowing, or malocclusion after a blow to the jaw or a seizure or, sometimes, spontaneously. There may be loose or missing teeth and areas of sensory deficit at the chin or mouth. With anterior dislocation, pain is localized anterior to the tragus. Symptoms may develop after extreme mouth opening from laughing, yawning, vomiting, taking a large bite, or trauma, or iatrogenically during dental extraction, general anesthesia, and tonsillectomy.³³ With anterior dislocations, the lower jaw is prominent appearing, and there is visible and palpable preauricular depression from the displacement of the mandibular condyle. There also will be difficulty with jaw movement. If the dislocation is unilateral, there is deviation of the jaw away from the dislocation. When a posterior dislocation is considered, examine the external auditory canal. Confirm that hearing is at baseline. With lateral dislocations, the condylar head is palpable in the temporal space, and there are always signs of jaw fracture (e.g., malocclusion). Posterior, lateral, or superior dislocations result from severe trauma. The differential diagnosis includes mandibular fracture, traumatic hemarthrosis, acute closed locking of the temporomandibular joint meniscus, and temporomandibular joint dysfunction.³³

In the cooperative patient with a spontaneous atraumatic anterior dislocation, the diagnosis is clinical. In other dislocations, including any traumatic dislocation, obtain radiographs. The panoramic (Panorex) view usually demonstrates the pathology and excludes other mandibular injury. In patients with more serious trauma, where there may be a superior dislocation or intracranial injury, CT will provide more information.

Perform reduction in the ED for closed anterior dislocations without fracture.³³ A short-acting IV muscle relaxant (e.g., midazolam) may help to decrease muscle spasm. Appropriate airway and hemodynamic monitoring is required. Procedural sedation has been used successfully.⁴³ Alternatively, local anesthetic can be placed into the joint space. Using aseptic technique, place a 21-gauge needle into the preauricular depression just anterior to the tragus and inject 2 mL of 2% lidocaine⁴⁴ (Figure 243-5).

REDUCTION OF ANTERIOR TEMPOROMANDIBULAR JOINT DISLOCATION

The most commonly used technique requires the patient to be firmly seated with the head against the wall or chair back, positioned so that the examiner's flexed elbow is at the level of the patient's mandible. Apply a few layers of gauze over gloved thumbs for protection, in case the mandible snaps closed after reduction.³³

Facing the patient, place gloved thumbs in the patient's mouth, over the occlusal surfaces of the mandibular molars, as far back as possible. Curve your fingers beneath the angle and body of the mandible. Using the thumbs, apply pressure downward and backward (toward the patient). Slightly opening the jaw may help disengage the condyle from the anterior eminence (Figure 243-6). When the dislocation is bilateral, it may be easier to relocate one side at a time.

In the second technique, with the patient recumbent and supine, stand at the head of the bed, place the thumbs on the molars, and apply downward and backward pressure (toward the stretcher) (Figure 243-7).³³

In addition to the above common methods, other approaches include the ipsilateral, in which the thumb is externally used to apply downward pressure on the displaced condyle; the wrist pivot method, in which the healthcare provider's thumbs are placed on the mentum, applying upward force, while the fingers apply downward force on the body of the mandible (Figure 243-8); and the gag reflex approach. In the gag reflex method, the provider stimulates the patient's soft palate with a tongue blade or dental mirror, thereby producing muscle relaxation and descent of the mandible, resulting in relocation of the condyle.³³

After successful reduction, the patient should be able to close his or her mouth immediately. Postreduction radiographs usually are not needed unless the procedure was difficult or traumatic or there is significant postreduction pain. Complications from the reduction itself are unusual but can include iatrogenic fracture or avulsion of the articular cartilage.

Dislocations that are open, superior, associated with fracture, have any nerve injury, or are irreducible by closed technique should be referred urgently to an otolaryngologist or maxillofacial surgeon.

Following successful reduction of an acute dislocation, patients may be discharged home, placed on a soft diet, and cautioned against opening their mouths >2 cm for the following 2 weeks.³³ Advise patients to support the mandible with a hand when they yawn. Nonsteroidal analgesics may help the initial discomfort. Elective referral to an oral maxillofacial surgeon is recommended. In severe cases, intermaxillary fixation may be required to control jaw motion during healing. Chronic dislocations may require operative intervention.