Maxillofacial Disorders

Published on 14/03/2015 by admin

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30 Maxillofacial Disorders

Temporomandibular Disorders

Pathophysiology

TMD is probably due to excessive strain on the muscles of mastication with resultant strain on the capsular ligaments of the TMJ.4 The result is that the mandibular condyle does not articulate properly in its joint. The patient feels pain and senses an occlusal disturbance.

Patients with TMJ dislocation are unable to close their mouth. With normal function, when the mandible is open, the mandibular condyle moves anteriorly and inferiorly. When the mandible closes, the condyle moves posteriorly and superiorly and returns to its original location (Fig. 30.1). TMJ dislocation results when the mandibular condyle moves anterior to the temporal eminence (the anterior portion of the mandibular fossa) (see Fig. 30.1). Once the dislocation occurs, the muscles of mastication spasm, which results in trismus and inability of the patient to return the mandibular condyle to its anatomic position. The dislocation usually results from excessive opening of the mouth, such as occurs with yawning or laughing. TMJ dislocation can also be the result of trauma, seizure, or dystonic drug reactions.

Presenting Signs and Symptoms

Unilateral pain in the region of the TMJ and clicking or crepitance that is exacerbated by chewing are the classic complaints of a patient with TMD (Box 30.1). The dull or throbbing pain is localized to the preauricular region or to the muscles of mastication and typically worsens with movement of the mandible, such as when eating or talking. Pain may be most severe in the morning if bruxism is an issue.5 If a click is present, the patient hears it when jaw opening is initiated. The pain may also radiate to the neck, ears, mandible, or temporal region.

Physical examination should include evaluation of the muscles of mastication by intraoral and external palpation. Palpation may reveal muscular spasm and tenderness. Palpation of the TMJ or muscles of mastication may reproduce the patient’s symptoms and trigger significant pain. The patient may have great pain with any attempt at jaw range of motion. Physical findings are also notable for reduced jaw opening and possible lateral deviation of the jaw.

An inability to close the mouth following extreme jaw opening, such as yawning, is the classic manifestation of TMJ dislocation. If the dislocation is unilateral, the mandible will deviate away from the side of the dislocation (Box 30.2).

Treatment

Temporomandibular Disorders

Management of TMD is primarily directed at improving the patient’s comfort, which is accomplished with analgesia, muscle relaxation, and behavioral modifications. In the absence of trauma, there is no indication for emergency imaging of the TMJ.

Pain should be addressed with antiinflammatory agents (e.g., ibuprofen, 600 mg by mouth every 6 hours, or naproxen, 500 mg by mouth every 12 hours) and narcotic pain medications (e.g., oxycodone, 5 to 10 mg by mouth every 6 hours as needed). Warm compresses should also be applied to the TMJ region for 15 minutes three times per day. Benzodiazepines are used to relieve masseter muscle spasm (e.g., diazepam, 5 mg by mouth every 8 hours as needed). Behavioral modifications include minimizing masseter muscle use through a soft diet and cessation of gum chewing. Reassurance is important because up to 40% of patients will experience resolution of their TMD symptoms with little or no treatment (Box 30.3).6

If bruxism is suspected, dental follow-up should be arranged, and a bite appliance can be considered. To date, experimentation with the use of botulinum toxin to reduce masseter muscle contractility and strength has yielded mixed results.7

Temporomandibular Dislocation

TMJ reduction is performed in the emergency department (ED) and is usually readily accomplished. Controlling the patient’s pain and masseter spasm facilitates the procedure. Analgesics (e.g., morphine, 5 mg intravenously as needed) and antispasmodics (e.g., diazepam, 5 to 10 mg intravenously titrated to the patient response) should be administered before reduction is attempted. Atraumatic TMJ dislocations do not require imaging.

Once the patient is comfortable, the clinician faces the patient and grasps the mandible inferiorly with the fingers of both hands. The clinician’s thumbs should be heavily wrapped in gauze for protection and then placed on the occlusive surfaces of the mandibular molars. Downward pressure is applied to move the mandibular condyle inferior to the temporal eminence. The mandible is then pushed posteriorly (Fig. 30.2). Once the condyle is posterior to the temporal eminence and pressure is released, the condyle returns to its anatomic position in the mandibular fossa. At the time of reduction, the masseter muscles may contract forcefully and cause the patient to inadvertently clench the jaw. The clinician must be aware of this possibility and ensure that the thumbs are guarded during the procedure and remove the thumbs from the occlusive surface of the molars as quickly as possible. If this method does not work, both thumbs may be placed simultaneously on the dislocated side and the reduction reattempted.8

In an effort to minimize risk to the practitioner, an extraoral approach to TMJ reduction was proposed by Chen et al. in 2007.9 The physician faces the patient and places a thumb on the palpable coronoid process that is displaced anteriorly. The fingers of that hand are placed on the mastoid process for stability. On the nondislocated side, the thumb is placed on the zygoma and the fingers hold the mandible angle. The nondisplaced side of the mandible is pulled anteriorly while concomitant pressure is applied posteriorly to the displaced coronoid process. Although this approach is less successful than the traditional approach, there is no risk of injury to the practitioner.

When reduction of the TMJ has been accomplished, the patient needs to avoid excessive mouth opening to prevent recurrent dislocation and may be discharged home. Postreduction pain can be treated with analgesics and antispasmodics. Advising a soft diet for 2 weeks will also minimize the patient’s discomfort. The patient should be evaluated by an oromaxillofacial surgeon within 2 weeks.

Epistaxis

Pathophysiology

The nasal mucosa is a highly vascular area, and any disruption of the mucosa can result in bleeding. Although epistaxis can be caused by trauma, this is not the most common cause. Bleeding more commonly results from upper respiratory infections (URIs), a dry environment, nasal foreign bodies, allergic rhinitis, nasal mucormycosis, topical nasal medications (including antihistamines and corticosteroids), and drugs taken intranasally such as cocaine (Box 30.4). Additionally, epistaxis may be the initial symptom of a primary or secondary systemic bleeding disorder. One study found that 45% of patients with bleeding severe enough to warrant hospitalization had an associated systemic disorder that may have contributed to the epistaxis.12

The relationship of hypertension to epistaxis is controversial. It is unclear whether elevated blood pressure is the cause or the effect of epistaxis; therefore, hypertension alone is not known to be an independent risk factor for nasal hemorrhage.1315

The Kiesselbach plexus is located at the anterior portion of the nasal septum and is the source of bleeding in patients with anterior epistaxis. The plexus is supplied by branches of the internal and external carotid arteries via the sphenopalatine, ethmoidal, and superior labial arteries. Another name for the Kiesselbach plexus is the Little area. The posterior nasal septum and lateral nasal wall are supplied by the sphenopalatine artery, which is the source of bleeding for posterior epistaxis.

Functionally, epistaxis is considered anterior when the site of bleeding can be visualized in the anterior portion of the nasopharynx. Posterior nasal hemorrhage cannot be directly visualized and occurs in the posterior or lateral parts of the nose.

Presenting Signs and Symptoms

Epistaxis may be manifested as minor bleeding with small quantities of blood dripping from the nares or as major bleeding with the patient vomiting blood. Approximately 90% of cases of epistaxis are anterior and the bleeding source is unilateral. Many patients, however, have blood flowing from both nares because blood from the unilateral bleeding source travels around the septum posteriorly and exits on the other side.

Patients with epistaxis may arrive at the ED with various home treatments in progress. All foreign bodies (cotton, tissues, tampons) should be removed from the nose after the patient arrives to better assess the location and quantity of bleeding.

Important historical elements include the duration of the bleeding, laterality, estimated blood loss, recent trauma, and other associated symptoms.

Obtaining a detailed history is often the key to determining the cause of the patient’s epistaxis. The clinician must know whether the patient has recurrent epistaxis, easy bruising, or other sources of bleeding, such as when shaving or brushing the teeth, or is taking a platelet inhibitor or anticoagulant medication. The past medical history is important in a patient who has hepatic disease, atherosclerosis, Osler-Weber-Rendu disease (hemorrhagic telangiectasia), diabetes mellitus, or cancer with ongoing chemotherapy treatment because each of these conditions is a risk factor for epistaxis.16 Women are more prone to epistaxis during pregnancy.

Trauma, nose picking, recent otorhinolaryngologic surgery, nasal foreign body, URI, nasal polyps, and exposure to a low-humidity environment all predispose to epistaxis and should be addressed in the patient’s history. The family medical history may reveal recurrent epistaxis in multiple family members. In the absence of a hereditary bleeding disorder, such a history suggests familial idiopathic epistaxis. A social history must also be obtained to identify alcoholism, intranasal drug use, or domestic violence.

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