Infections of the maxillofacial regions



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INFECTIONS OF THE MAXILLOFACIAL REGIONS
Dental infections arise from pulpal and periodontally involved teeth. The former tend to be more aggressive, with the necrotic contents of a nonvital tooth extending through the apical foramen of the root into the surrounding alveolar bone. The fate of the infection then depends on the virulence of the bacteria, host resistance factors, and regional anatomy. Patients with systemic disease are a population subset at increased risk of a dental infection. Odontogenic infections may arise from an in situ infected tooth or after extraction of a tooth. In the latter instance, infection may occur despite the oral administration of antibiotics. The interval for the development of the infection may be less than 1 day to as long as 1 to 3 weeks.

Odontogenic infections arise from bacteria that reside in the oral cavity and are often polymicrobial. Among the gram-positive organisms, Streptococci are isolated most often in odontogenic infections, with incidences reported as high as 50% to 65%. Anaerobic bacteria involved in odontogenic infections include both gram-positive cocci (Peptostreptococcus, Gemella) and gram-negative rods (Bacteroides).

The resultant infectious processes can be broadly divided by location into those localized to the dentoalveolar process; those that extend along fascial planes to various regions of the face, neck, and beyond; and those with systemic dissemination by the development of a bacteremia.

CLINICAL PRESENTATION


Pulpally involved teeth demonstrate percussion tenderness, increased pain to heat, and a diminished or absent response to electrical vitality testing. Initially, no evidence of osseous change may be seen on radiographic examination. Later, widening of the periodontal membrane space surrounding the tooth may develop as well as rarefaction of the periapical bone (Fig 1). With an indolent infection, a condensing osteitis in the bone about the root apex may occur. A radicular cyst may form gradually after months or years as a result of inflammation-induced proliferation of epithelial rests present in the periodontal membrane or suspensory ligament of the tooth. It should be noted that the severity of the infection, that is, whether it remains localized to the alveolus, forms a deep-space infection, or becomes disseminated, does not correlate with the extent of the radiographic findings.
The infection may remain localized within the medullary space of the mandible or maxilla, or it may perforate the cortical plates to become extraosseous. After the infection is in the soft tissues, it may take the form of a diffuse cellulitis, or a walled-off abscess cavity involving the labial or buccal gingiva (parulis) (FIG 2.) or the alveolar mucosa to form a vestibular space infection. Anteriorly, it may cause enlargement of the lip (macrocheilia), which may be mistaken for angioneurotic edema if the infectious nature of the process is not recognized. Localized dental pain and referred pain are present when the pulpal necrotic contents are under pressure and when the periosteum over the bone is being elevated or perforated; however, it may subside or completely disappear when the soft-tissue component of the infection occurs.


FIG. 3.

In the maxilla, the root ends are close to the labial and buccal plates (left).
In the mandible, the dental roots are closer to the lingual cortex posteriorly, and extraosseous spread may involve the floor of the mouth; however, in most cases, infections of both anterior and posterior mandibular teeth tend to spread buccally(right).

In the maxilla, the root ends are close to the labial and buccal plates. This positioning, combined with a thick block of alveolar bone interposed between the root ends and the hard palate, almost always produces extension buccally. Moreover, the dense attachment of the palatal mucosa to the underlying bone limits the spread of infection in cases that burrow medially, producing a localized, tender, unilateral palatal mass. Occasionally, the abscess is nontender and simulates a neoplasm. In the mandible, the dental roots are closer to the lingual cortex posteriorly, and extraosseous spread may involve the floor of the mouth; however, in most cases, infections of both anterior and posterior mandibular teeth tend to spread buccally.

In some cases, the infectious process perforates the overlying mucosa to form a fistula, generally intraoral at the apex of the root of the affected tooth. Infrequently, it may drain through the facial skin to produce a dentocutaneous fistula. In most instances, periodontal infections remain localized to the alveolus. The abscess cavity that forms tends to involve the gingiva of the affected tooth, which becomes loose and tender and is bathed by purulent secretions.
Pericoronitis

Pericoronitis represents an infection around the crown of an impacted, partially erupted, third molar tooth. The mandible is generally involved as limited space exists for the tooth to erupt, and the overlying gingiva is traumatized by the opposing maxillary molar. The infection (generally mixed flora) begins under the flap (operculum) covering the tooth. Clinically, it is first seen with localized pain, swelling, and trismus. Management is with antibiotics, irrigations, prevention of occlusal contact with the soft tissue flap, followed by tooth extraction. The mandibular molars are situated in the alveolus closer to the lingual cortical plate, with the thinner bone favoring extension of infections medially. Consequently, pericoronitis is a potentially dangerous infection, as anatomically, it is close to several anatomic spaces from which the infectious process can spread by extension along fascial planes.

The maxillary and mandibular teeth show different patterns of spread because of their anatomic location and relation to fascial spaces. The maxillary teeth tend to spread upward into potential spaces in the face created by the attachments of the mimetic muscles to the facial skeleton. However, the molar teeth are in proximity to and can readily involve the masticator space. The paranasal sinuses are another potential route of extension as the root apices of the posterior teeth abut and even protrude into the maxillary sinus. However, once a cervicofacial space is involved (e.g., masticator space), extension into an adjacent pharyngeal space (principally the parapharyngeal space) permits extension downward into the neck and mediastinum.

Infections of the mandibular teeth tend to spread downward into the neck. Extension out of the mandible medially, or laterally, into the soft tissues is determined by the position of the tooth in the dental arch where the buccal and lingual thickness of the bone varies anteroposteriorly. Once it is in the soft tissues, the infection spreading is determined by the fascial planes.


Canine Space Abscess

The levator of the upper lip (quadratus labii superioris) originates from the face of the maxilla by several heads to insert into the angle of the mouth. Medially, a potential space exists between the infraorbital and zygomatic heads, as well as between it and the caninus muscle arising from the bone above the canine fossa. This represents a plane along which an infection from the canine tooth can track superiorly. Clinically, a firm or fluctuant mass appears along the lateral border of the nose adjacent to the medial canthus of the eye (Fig 4). Treatment is by dependent drainage intraorally or percutaneously if the abscess is pointing there. As with all infections from pulpally involved teeth, extraction or root-canal therapy also is necessary.



Buccal Space Abscess

This space is bounded by the buccinator muscle and buccopharyngeal fascia medially, the cheek skin laterally, the lip muscles anteriorly, the pterygomandibular raphe posteriorly, the zygomatic arch superiorly, and the lower aspect of the mandible inferiorly. Infections of maxillary and mandibular bicuspid and molar teeth have access to this space when their necrotic pulpal contents extend through the buccal cortical plates above or below the attachments of the buccinator muscle on the alveolar processes, respectively. Extension of dental infection between the mucosa and the buccinator muscle leads to the intraoral formation of a vestibular abscess. Clinically, the buccal-space infection produces a tender swelling of the cheek that extends medially to the middle of the upper lip, where it is stopped by the fibers of the orbicularis oris muscle that form the philtrum and involves one third of the lower lip where the fibers of the depressor anguli oris run from the skin to the oral mucosa (Fig 5). Posteriorly, it extends over the ramus of the mandible to the border of the parotid gland. Superiorly, it may close the eye entirely by producing circumferential eyelid edema; however, the orbital contents are protected because the infection remains superficial to the orbital septum and tarsal plates of the eyelids. In all cases of periorbital infection producing eye closure, the eyelids must be forced open to determine whether a postseptal component is present that is placing the orbital contents and vision at risk. Generally, no intraoral component to this infection is present. Treatment is by percutaneous drainage because the plane of the infection is beneath the skin. In the preantibiotic era, midfacial infections were considered potentially life threatening because septic thrombophlebitis of the angular blood vessels represented a pathway of intracranial extension into the cavernous sinus. Cavernous sinus thrombosis from infections of dental origin by this route is essentially a rarity at present.



Sublingual Space Abscess

The sublingual space is bounded anteriorly and laterally by the mandible, superiorly by the floor of mouth and tongue, inferiorly by the mylohyoid muscle, posteriorly by the hyoid bone, and medially by the genioglossus, geniohyoid, and styloglossus muscles. This space communicates freely with that of the opposite side because no true fascial separation exists between them. The sublingual space also communicates anteriorly with the submental space below through dehiscences in the mylohyoid muscle and raphe. The mylohyoid ridge to which the muscle attaches to the inner aspect of the mandible slopes downward anteriorly; consequently, infections from the anterior teeth as well as the bicuspids and first molar tooth tend to remain above the mylohyoid shelf and enter into the sublingual space. Early infections produce unilateral elevation of the floor of the mouth adjacent to the offending tooth. Advanced infections spread anteriorly beyond the midline to the opposite side and posteriorly to produce elevation of the base of the tongue. Treatment is by intraoral drainage.


Submandibular Space Abscess

The submandibular space is separated superiorly from the sublingual space by the mylohyoid, hyoglossus, and styloglossus muscles medially and by the body of the mandible laterally. The lateral border is the overlying skin, superficial fascia, platysma muscle, and the superficial layer of the deep cervical fascia. Its inferior boundary is formed by the anterior and posterior bellies of the digastric muscle. Anteriorly, the space communicates freely with the submental space and posteriorly with the pharyngeal space. The contents of this space are the submaxillary gland, Wharton's duct, the lingual and hypoglossal nerves, the facial artery, and some lymph nodes and fat. Involvement of the submandibular space is produced principally by infections of the second and third mandibular molar teeth because of the higher position of the mylohyoid ridge on the mandible posteriorly, which places their root apices beneath the mylohyoid muscle. Clinically, a tense, ill-defined swelling is generally present below the mandible, which makes palpation of its inferior border difficult. Management is by an external cervical incision placed beneath the mandibular nerve to avoid injury to it and to provide adequate dependent drainage.


Submental Space Abscess

The submental space is a triangular space positioned in the midline beneath the mandible, with the symphysis as its superior border and its lateral margins, the anterior bellies of the digastric muscle. The floor of the space is the mylohyoid muscles, and the roof is the overlying skin, superficial fascia, and platysma muscle. Its contents are a few scattered lymph nodes and fibrofatty tissue. Its source of infection is by drainage from the mandibular incisor teeth as well as their gingiva and the central portion of the lower lip. Entry into the space also can occur from an infection in the adjacent sublingual and submandibular spaces. Infrequently, a posterior mandibular tooth may produce infection in the space without involvement of the adjacent submandibular space. Clinically, a firm, tense swelling is present beneath the chin. Management is by a small upper cervical incision placed in the midline to gain dependent drainage of the contents of the space.


Ludwig Angina

The term Ludwig angina refers to the collective involvement of the submandibular and sublingual spaces bilaterally and the submental space. Cases of dental origin arise from infections of the mandibular molar teeth, with the bicuspids rarely the source. The rapid spread of infection from one space to another demonstrates the facility with which virulent organisms can move through the compartments of the head and neck.

Clinically, a collar of brawny edema extends across the entire upper anterolateral neck with elevation and progressive induration of the floor of the mouth. As the sublingual spaces become progressively more involved, the tongue becomes posteriorly displaced with kinking of the supraglottic area, producing airway obstruction. The causative organisms include a variety of aerobic and anaerobic gram-positive cocci and gram-negative rods. Not infrequently, a mixed microbial flora is isolated.

After the diagnosis of Ludwig angina is made, the first priority is maintenance of the airway through an elective tracheotomy with the patient under local anesthesia. One should not wait for dyspnea or cyanosis to develop because these are late signs and signal impending airway closure.

Although this infection is characterized as a brawny cellulitis, in some cases, pockets of suppuration develop that require drainage through an external cervical approach. Intraoral drainage carries the risk of aspiration in patients with severe edema of the oral cavity and oropharynx. Systemic antibiotic therapy is not a substitute for tracheostomy except in early cases with minimal floor of the mouth swelling, which can be continuously observed. After massive edema has developed, it may take 1 week or more for it to subside with antibiotic therapy; therefore, control of the airway by tracheostomy is essential.


Masticator Space Abscesses – masseteric, pterygomandibular, temporal

Whereas the anterior layer of deep cervical fascia invests the muscles of mastication, connective tissue subdivisions create separate masseteric, temporal, and pterygoid spaces, all of which freely intercommunicate. The masseteric compartment is bound by the masseter muscle laterally and the ramus of the mandible medially. The pterygoid compartment has the pterygoid muscles medially and the mandibular ramus laterally as its borders. The temporal compartment itself is subdivided into two portions. The superficial portion is between the superficial temporal fascia and the temporalis muscle; the deep portion is between this muscle and the periosteum of the temporal bone. The greatest space is present between the pterygoid and temporal compartments. Anteriorly, the space is bounded by the pterygomandibular raphe, and posteriorly, its connective tissue envelops the parotid gland to form the combined parotidomasseteric fascia. In addition to the muscles of mastication, the masticator space contains fibrofatty tissue, the internal maxillary artery, and the mandibular nerve.

Infections of the masticator space tend to involve all the muscles. The hallmark is severe trismus with minimal external swelling. Fullness over the ramus of the mandible may be present from myositis or external displacement of the masseter muscle, or swelling may be present about the zygomatic arch from extension into the infratemporal space. More prominent facial swelling is seen with involvement of the temporal space. Intraoral palpation along the ramus of the mandible or behind the maxillary tuberosity may elicit fullness, tenderness, and fluctuance. The source of infection of this space is principally from mandibular and maxillary molar teeth (principally the former). Confirmation of the diagnosis is by computed tomography (CT), which delineates the muscles and fascial planes exceedingly well. Management is by surgical drainage intraorally. With large abscesses that extend toward the lateral pharyngeal space, external drainage is necessary. The major difficulty in treating these cases is in establishing the airway for the induction of general anesthesia, which may be accomplished by awake nasoendotracheal intubation but often requires preliminary tracheotomy under local anesthesia.

Deep Neck Abscesses

The majority of deep neck infections are of odontogenic origin. Consequently, the initiating dental focus must be identified and treated. The mandibular teeth are the principal source because of their proximity to cervical fascial planes.


Parapharyngeal Space Abscess

The parapharyngeal (also called pharyngomaxillary or lateral pharyngeal) space is cone shaped, with its apex below at the lesser cornu of the hyoid bone. It is bound medially by the pharynx and laterally by the ascending ramus of the mandible, the pterygoid muscles, and the capsule of the parotid gland. Superiorly, it extends to the skull base. Inferiorly, it extends to about the level of the hyoid bone, where it is interrupted by the fascia of the submandibular gland, the stylohyoid muscle, and the posterior belly of the digastric muscle. The space is divided into prestyloid and poststyloid compartments. The prestyloid compartment contains the internal maxillary artery and the inferior alveolar, lingual, and auriculotemporal nerves. The posterior wall is the carotid sheath. The poststyloid compartment is traversed by the internal jugular vein, the carotid artery, cranial nerves IX, X, and XI, and cervical sympathetic nerves. Clinically, the patient with a parapharyngeal space abscess is initially seen with an intraoral bulge of the tonsil and lateral pharyngeal wall as well as external swelling of the soft tissues over the mandible and the parotid region). Symptoms include pharyngeal pain, dysphagia, muffled voice, trismus, and fever. Purulence in the posterior compartment produces fewer and less focal findings. CT scanning can demonstrate whether cellulitis, an abscess cavity, or enlarged lymph nodes are present. Patients with deep neck infections are hospitalized for observation of the airway, the administration of intravenous antibiotics, and fluid replacement. The cellulitis may resolve on conservative therapy alone, but many patients require surgical drainage. Tracheostomy may be necessary when signs of airway obstruction develop and when trismus makes oral intubation impossible. Surgical exploration and drainage should be performed when a patient does not improve within 24 hours, an abscess is detected on imaging, or the patient deteriorates while under observation. The parapharyngeal space is drained by a lateral cervical incision, following the posterior belly of the digastric and stylohyoid muscles into its center.

The complications of parapharyngeal space infections are associated with the structures that run through or adjacent to it. These include hoarseness, or aspiration related to vagal injury, Horner syndrome related to sympathetic nerve injury, sternocleidomastoid or trapezius weakness from accessory nerve injury, decreased pharyngeal sensation related to glossopharyngeal nerve injury, and tongue paresis from hypoglossal nerve injury. Infrequently, direct injury to the cervical spine, including erosion and atlantoaxial subluxation, develops.

Infection adjacent to the internal jugular vein may induce septic thrombophlebitis with spiking fevers, engorged optic disks, and possibly elevated cerebrospinal fluid (CSF) pressure. In these cases, not only should the parapharyngeal space be drained, but the thrombophlebitic section of the internal jugular also should be ligated and the infected part excised. One of the most dreaded complications is the development of a mycotic aneurysm of the carotid artery from erosion of its wall by purulent material present within its sheath. The eroded segment of artery

requires ligation to prevent a catastrophic event.


Retropharyngeal Space Abscess

The retropharyngeal space is sandwiched between the pharyngeal constrictor muscles and their fascia and the alar layer of the prevertebral fascia. The space contains the retropharyngeal lymphatics, which drain the posterior two thirds of the nose, the nasopharynx, the paranasal sinuses, the soft palate, and the eustachian tube. It extends from the skull base at the pharyngeal tubercle downward behind the pharynx and esophagus, communicates with the pretracheal space, and ends in the mediastinum at about the level of the carina. Consequently, suppuration in this space may drain into either the anterior or posterior mediastinal compartments. This space has been thought of as the highway to the mediastinum. Directly behind the retropharyngeal space is the danger space between the alar and prevertebral layers of the deep cervical fascia, which leads into the posterior mediastinum, and behind it the prevertebral space, which extends to the sacrum. These spaces all intercommunicate (including the parapharyngeal and paramandibular) and carry the potential for distant spread of an infection.

The spread of infection into the deep neck spaces often causes pain and limitation of jaw, or neck, motion. Diffuse swelling with pitting edema of the neck may be present; however, fluctuance is a rare physical finding. Infection of the retropharyngeal space may cause dysphagia, odynophagia, drooling, and aspiration. Patients also may have dyspnea and stridor with a “hot potato” voice. Examination of the pharynx usually shows fullness and erythema of the posterior pharyngeal wall, often with a central furrow produced by the midline raphe. Patients with deep neck infections are usually toxic, with spiking fevers. A lateral radiograph of the neck reveals marked thickening of the prevertebral soft tissues in the involved segmentThe retropharyngeal space is best drained from an external approach. Intraoral drainage carries the risk of pulmonary complications from aspiration and is generally used only in children. The use of intravenous antibiotics is mandatory.

The retropharyngeal abscess may be complicated by spontaneous rupture into the pharynx, with the aspiration of pus producing pneumonia and possibly a lung abscess. The abscess also may dissect into the mediastinum, with the patient having relief of throat pain and onset of shortness of breath, chest pain, and tachycardia. Mediastinitis carries a high mortality rate and requires immediate drainage of the mediastinum. Delayed diagnosis and inadequate surgical drainage are the primary causes of lethal descending mediastinitis. CT of the chest is invaluable for early diagnosis, and its routine use in all patients with deep neck infections is essential.


Complications

  • Extension of infection from local to regional spaces

  • Orbital complications (blindness, ophthalmoplegia)

  • Jugular vein thrombosis

  • Septicemia

  • Metastatic abscesses

  • Airway compromise

  • Aspiration

  • Carotid artery rupture

  • Mediastinitis

  • Osteomyelitis

  • Cutaneous fistula

  • Cranial nerve deficits

  • Cavernous sinus thrombosis

  • Necrotizing fasciitis

  • Maxillary sinusitis, oroantral fistula

  • Septic shock

Sialoadenitis and sialolithiasis
Eighty percent of salivary calculi occur in the submandibular gland, whereas less than 20% occur in the parotid and approximately 1% in the sublingual gland. Minor salivary gland calculi are uncommon, with a predilection for the upper lip and buccal mucosa. In 75% of calculi involving the major glands, only a single calculus is found. Multiple gland involvement occurs in approximately 3%, and there is a slight male preponderance, with most occurring in middle age. Calculi commonly occur in patients with chronic sialadenitis. Most calculi are calcium phosphate with small amounts of magnesium, ammonium, and carbonate. A mixture of carbohydrates and amino acids form the organic matrix of these calculi. Despite their similar chemical makeup, 90% of submandibular calculi are radiopaque (Fig ), whereas 90% of parotid calculi are radiolucent with standard facial x-rays. Essentially all are detectable with CT. Ultrasonography is underused in this country. In Europe, it is widely available, relatively inexpensive, and accurate in trained hands. Magnetic resonance imaging will not detect calculi. However, in time, improvements in magnetic resonance sialography may allow the detection of stones.

A probable prerequisite for calculus formation is the presence of a nidus of material allowing the precipitation of salts, almost certainly coupled with salivary stasis. The submandibular duct is believed to be more susceptible to calculus formation because its saliva is more alkaline and has a higher concentration of calcium and phosphate and a higher mucus content. Furthermore, the duct is longer and has an antigravity flow. Submandibular calculi usually arise within the duct, whereas those in the parotid are at the hilum or within the parenchyma.



Most patients present with a history of recurrent swelling and pain in the involved glands, often associated with eating. Infections may or may not occur with repeated episodes of obstruction and swelling. Occasionally, calculi are discovered incidentally, and occasionally they appear as acute suppurative sialadenitis. The calculus may be palpable in the involved duct, and the gland may be diffusely enlarged and mildly tender. Massage of the gland demonstrates decreased flow of a cloudy or mucopurulent saliva. Plain x-ray films frequently reveal submandibular calculi but less so for parotid. Sialography is essentially 100% effective in making the diagnosis. Ultrasound and CT are also excellent for detecting calculi.

Complications of sialolithiasis include acute suppurative sialadenitis, ductal ectasia, and stricture. Treatment depends on the location of the calculus. Those at or near the orifice of the duct may be removed transorally, whereas those within the hilum of the gland often require complete excision of the gland.


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