Complex Odontogenic Infections

Introduction

Orofacial infections are the most common reason that patients present to the dentist or dental specialist; the infections are primarily due to dental caries, with inflammatory periapical pathology manifesting clinically as pain and swelling. However, periapical lesions involving the root apex may extend to, and beyond, the bone of the maxilla or mandible, then spreading to the adjacent and distant soft tissues. In general, odontogenic infections are managed adequately with caries control, endodontic therapy, scaling and root planning, and/or tooth extraction. If the infection extends outside of the alveolus and basal bone of the jaws into the surrounding soft tissues, the most prudent management is prompt surgical incision and drainage to prevent significant patient morbidity and airway compromise. Moreover, if the infection extends outside of, or distal to, the vestibule, it is usually best managed by an oral and maxillofacial surgeon who has extensive training in the management of the airway and the surgical management of head and neck infections. Infections that extend to the deep fascial spaces of the neck can result in significant edema, dysphonia, dysphagia, inability to handle secretions, systemic symptoms, and in the most severe cases, airway compromise. These urgent or emergent clinical scenarios require immediate attention and management. The objectives of this chapter are to review the relevant anatomy of the head and neck, etiology of complex orofacial infections, the clinical presentation signs and symptoms, diagnostic methods, and surgical and nonsurgical management of odontogenic infections, and discuss other infections of the head and neck region.

Anatomy

Management of infections of the head and neck requires the clinician to have a sound fundamental knowledge of head and neck anatomy—in particular, an understanding of the potential deep spaces created by the fascial planes of the head and neck through which infections can progress. In general, the regional anatomy of the head and neck can be regionalized on classifications based upon (1) the “triangles” of the neck, (2) those developed related to anatomy affected by penetrating neck trauma, and (3) infections of the head and neck.

The cervical fascial layers of the head and neck determine the boundaries of deep space neck infections. A thorough knowledge of the anatomy of these spaces will assist the practitioner in assessing the clinical and radiographic findings in the diagnosis of oral and maxillofacial infections. In addition, knowledge of the fascial spaces of the head and neck, and the vital structures that are contained within these spaces, will assist the clinician in providing adequate surgical access and drainage while avoiding iatrogenic injury and further potential patient morbidity. Furthermore, a clear knowledge of the muscular and fibrous soft tissue attachments to the maxillomandibular complex is critical to understanding the path of spread of an orofacial infection. An example of this is the significance of the position of the mylohyoid muscle attachment in relation to an infected mandibular tooth apex regarding whether the infection will extend into the sublingual space or the submandibular space. It is important to note that, prior to spreading to the deep fascial spaces of the neck, most oral infections will penetrate the facial cortical bone of the maxilla or mandible leading initially to a vestibular space abscess prior to further dissemination of the infection.

The deep spaces of the head and neck are fascia-lined spaces containing loose areolar connective tissue. Their purpose is to cushion and protect the nerves, muscles, vessels, and other important structures that run through them. These are “potential” spaces, only existing when invaded by bacteria or other material that leads to edema opening the space followed by a cellulitis phase and then an abscess stage ( Table 17.1 ).

The cervical fascia of the head and neck is divided into superficial and deep layers. The superficial fascia lies immediately deep to the skin surface, envelopes the platysma muscle as well as the muscles of facial expression, and consists mainly of subcutaneous tissue and connective tissues. It contains predominately superficial nerves and veins ( Fig. 17.1 ). The deep layer of cervical fascia can be divided into the superficial, middle, and deep layers. Furthermore, the middle layer of the deep cervical fascia can be divided further into the muscular and visceral layers, whereas the deep layer can be divided into the posterior prevertebral and anterior alar layers ( Figs. 17.2 and 17.3 ). The superficial layer of the deep cervical fascia (SLDF) originates posteriorly at the nuchal ridge and extends laterally and anteriorly, dividing to envelop the trapezius muscle and sternocleidomastoid muscle and attaching to the hyoid bone anteriorly. It envelops both the parotid and submandibular glands, then fusing with the fascia surrounding the anterior bellies of the digastric and mylohyoid muscles to form the inferior margin of the submandibular space. At the level of the mandible, the fascia splits and the internal layer covers the medial surface of the pterygoid muscles extending superiorly to the base of the skull. The external layer extends superiorly to envelope the masseter muscle and inserts into the zygomatic arch. Inferiorly, the SLDF inserts into the clavicles, sternum, and acromion process of the scapula. This forms the outer (superficial) layer of most deep fascial space neck infections. The muscular layer of the deep cervical fascia surrounds the buccinator, pharyngeal constrictor, sternothyroid, sternohyoid, and thyrohyoid muscles. It inserts on the hyoid bone and thyroid cartilages and then fuses with alar division of deep cervical fascia, forming an anterior wall of retropharyngeal space. The visceral aspect of the middle cervical fascia envelopes the trachea, thyroid, and esophagus and then extends inferiorly to join the pericardium. The deep layer of the cervical fascia is divided into the anterior alar fascia and the posterior prevertebral division, which is adherent to anterior aspect of vertebral bodies from the base of the skull to the vertebrae. It surrounds the muscles of the deep neck in the posterior triangle, enveloping the brachial plexus and subclavian vessels; this helps prevent posterior extension of infections into the mediastinum. The “danger space” is a potential space that lies between the alar and prevertebral fascia.

It is important to note that the deep fascial spaces of the head and neck are only potential spaces, and they are established only when invaded by space-occupying masses such as tumors, inflammation, or infection. The lubricating loose areolar protective tissue border is susceptible to invasion by the host inflammatory mediators such as macrophages, lymphocytes, and polymorphonuclear leukocytes, thereby becoming edematous within their interstitial space. Further progression of this cellulitis can lead to liquefactive necrosis within the fascial planes with fluid formation consisting of white blood cells and products of tissue necrosis and limitation of vascularity to the region due to increased hemostatic pressure, resulting in abscess formation.

As mentioned previously, the relationship between the anatomic boundaries where an odontogenic infection penetrates the outer cortex of the alveolar bone and spreads into the surrounding muscle and fascial attachments is critical to the path of spread of the infection via the path of least resistance. Usually the root apices are cephalad to the muscle attachment; therefore, when they penetrate the alveolar bone, they present as a vestibular space abscess, and, in some instances, a buccal space infection ( Fig. 17.4 ). Initially these represent an infection of the space of the body of the mandible (which is confined by the periosteum of the mandible). These infections can also travel to the subcutaneous tissues and subsequently the skin, leading to an orocutaneous fistula (or, more appropriately termed, sinus tract). This may happen commonly via the buccal space with borders determined by the maxilla, masseter muscle, mandible, buccinator muscle, and the muscles of facial expression and associated fascia. Whether the infection travels to the buccal space as opposed to remaining adherent to the maxilla or mandible depends on the level of cortical perforation with relation to the attachment of the buccinator muscle. If cephalad to the buccinator muscle attachment in the maxilla and caudal to the muscle attachment in the mandible, the infection may travel to the buccal space. However, if the root apex and location of cortical penetration is superior and inferior to the buccinator muscle attachment in the maxilla and mandible, respectively, the infection will likely present as a vestibular space infection. In this subperiosteal plane, vestibular space infections may then travel to the canine space, followed by infraorbital space in the maxilla, and from the space of the body of the mandible to a submandibular space infection in the mandible that then has the potential to rapidly propagate to deeper fascial spaces ( Table 17.2 ).

It is paramount to correctly diagnose the specific spaces involved in orofacial infections, because this is critical in determining the need for urgent surgical management. For example, buccal space infections may be drained intraorally or transcutaneously, especially if the infection is located in a superficial position below the skin surface ( Fig. 17.5 ). In an extraoral drainage procedure the incision and drainage site should be placed in a position inferior to the area of spontaneous drainage, rather than directly in the area of maximum edema with tissue necrosis, to allow for dependent drainage of the infection, as well as to allow for optimal cosmesis of the scar following resolution of the infection. However, for a vestibular space, canine space, or space of the body of the mandible infection, surgical drainage is best performed via an intraoral approach if dependent drainage can be achieved and because these spaces follow the paths of least resistance by which the infection would most likely spread ( Fig. 17.6 ). Infection may then progress from these so-called primary spaces to the secondary spaces, or deep fascial spaces of the neck, such as the pterygomandibular space, parapharyngeal spaces (lateral and retropharyngeal), carotid space, and pretracheal spaces (space of Burns).

Microbiology and Antibiotic Management

Most oral and maxillofacial and deep space neck infections are polymicrobial in nature; only 5% of bacterial organisms can be identified as aerobic, whereas 25% are identified as anaerobic in nature. Anaerobic-related bacterial infections are fastidious and often difficult to culture effectively because the specimens obtained are generally exposed to oxygen when collected. The most common aerobic bacterial species identified in head and neck infections are Streptococcus and Staphylococcus species. The most common anaerobic species found in head and neck infections are Bacteroides , Fusobacterium , Peptostreptococcus, Pigmented Prevotella, and Porphyromonas species. Despite advances in antimicrobial therapy, the primary antibiotic indicated in the treatment of oral and maxillofacial infections is penicillin (beta-lactam antibiotic) or clindamycin (if an allergy to penicillin exists). Alternatively, cephalosporin antibiotics (e.g., cefoxitin), a carbapenem antibiotic (e.g., imipenem, meropenem), or a macrolide antibiotic (e.g., azithromycin) may be used.

As an example of orofacial infections and antibiotic management, because the etiology of maxillary sinusitis is often odontogenic in nature from maxillary teeth, optimal antibiotic management should be initiated promptly. The treatment of maxillary sinusitis, which may progress beyond the boundaries of the sinus, usually includes a beta-lactam antibiotic with a beta-lactamase inhibitor (e.g., ampicillin/sulbactam), with or without metronidazole, that has a spectrum that includes the normal sinus flora (e.g., Streptococcus pneumoniae , Haemophilus influenzae , and Moraxella catarrhalis ). Seventy percent of odontogenic-related maxillary sinusitis bacterial isolates are susceptible to amoxicillin clavulanate, and 80% of Staphylococcus species cultured are capable of producing beta-lactamase, an enzyme that renders beta-lactam antibiotics (penicillin) ineffective, and increases the likelihood of spread of the infection to adjacent spaces. However, 50% of all maxillary sinusitis pathogens have been found to be resistant to clindamycin, making this specific antibiotic not ideal for antimicrobial therapy (see Chapter 16 ). Whereas odontogenic infections are bacterial in nature and often benefit greatly from antibiotic therapy, it is important to remember that the mainstay of treatment of odontogenic infections is surgical management and that antibiotics should only be used as adjuvant therapy.

Medical Comorbidities

The role of systemic disease cannot be understated with regard to an increased susceptibility to the development of head and neck infections of any microbial origin. Patients with one or more medical comorbidities, or those who are immunocompromised, are more likely to be affected by bacterial and fungal sources of orofacial infection. Patients who have impaired neutrophil function, such as those who have human immunodeficiency virus disease, diabetes mellitus, elderly, or those on chronic hemodialysis have inherent decreased phagocytosis and host bactericidal mechanisms. Furthermore, patients undergoing systemic chemotherapy may be neutropenic, and therefore unable to mount a “normal” host immune response to an odontogenic infection. These patients will often not present with an abscess due to their impaired neutrophil function or decreased number of circulating neutrophils (neutropenia). Diabetic patients are especially susceptible to infection due to an increased level of glycosylated hemoglobin (HbA1c), decreased vascularity and peripheral vascular disease, and decreased ability to resolve uncomplicated infections. Chronic hyperglycemia also affects other aspects of the host immune system, including white blood cell dysfunction. Patients with diabetes mellitus may be more prone to the development of an infection; when this occurs, these patients may have an increased severity of the infection, a higher rate of associated complications, increased morbidity, prolonged intensive care and hospital length of stay, and require more aggressive medical and surgical therapies. It is critical for the treating provider to manage and optimize the patient medically (e.g., obtain optimal blood glucose control as reflected in the HbA1c levels), as well as surgically, to promptly and aggressively resolve infections in this group of patients. In addition, diabetics are more susceptible to rare or unusual bacterial and fungal infections, which may present a diagnostic challenge when choosing the most appropriate antibiotic and antifungal medications.

Deep Fascial Space Infections

Infections Arising From Any Tooth

The spaces most commonly affected by odontogenic infections, and therefore the most common space involvement seen on clinical examination by the dentist or dental specialist, are the vestibular, buccal, and subcutaneous spaces. Infections of the maxillary and mandibular teeth almost always begin as a vestibular space abscess based upon the spread via the path of least resistance through the buccal or lingual plates of bone. Secondarily, these vestibular infections commonly spread to the canine/infraorbital space in the maxilla and the space of the body of the mandible in the mandible. The buccal space, which may be commonly involved in infections originating from the maxillary and mandibular teeth, is contiguous with the subcutaneous space. Therefore buccal space infections most commonly drain spontaneously via the skin at the inferior border of the mandible as an orocutaneous fistula, or sinus tract. If left untreated, these relatively simple-to-treat infections can spread to the deep fascial spaces of the neck, which are associated with significant patient morbidity ( Fig. 17.7 ).

Infections Arising From Maxillary Teeth

The maxilla is different from the mandible in that, unlike the mandible that is U-shaped, the bony palate forces infections arising from palatal cusps of maxillary teeth into the palatal space. This space, formed by the bone of the palate and the overlying periosteum, is often a drainage point for infections arising from the apices of the palatal roots of maxillary teeth. The lingual apices of the mandibular teeth, however, will usually drain to the sublingual space or submandibular space, depending upon whether they are cephalad or caudal to the mylohyoid muscle, respectively.

For those infections originating from the buccal roots of teeth, or from teeth with root apices positioned more buccally, the usual path of spread is to the vestibular space, and then to the canine and infraorbital space in the maxilla. The canine or infraorbital space is bounded by the quadratus labii superioris and levator anguli oris muscles, the nasal cartilages, and the oral mucosa. This space is affected most by infections arising from the particularly long root of the maxillary canine tooth. When infections originating from the apex of the maxillary canine root perforate the alveolar bone superior to the attachment of the levator anguli oris muscle and inferior to the origin of the levator labii superioris muscle, the canine space will become involved. Alternatively, this space may become infected by extension from an adjacent buccal space infection. Similarly, infraorbital space infections may spread directly into the buccal space. The space inferior to the canine space (caudal to the levator anguli oris muscle) is the vestibular space that often drains spontaneously into the oral cavity. Conversely, an abscess of the infraorbital space will often drain at points near the medial and lateral canthi of the eye because these areas lie medial and lateral to the attachment of the levator labii superioris muscle to the inferior orbital rim and represent the paths of least resistance in this region. On clinical examination of a canine space infection, the nasolabial fold with be obliterated or flattened by the tissue edema below this specific facial landmark.

The buccal space is bounded superficially by the overlying skin and subcutaneous tissues and deeply by the buccinator muscle. Maxillary molars are most commonly associated with buccal space infections because infections arising from their buccal root apices perforate the alveolar bone immediately superior to the attachment of the buccinator muscle on the alveolar process ( Fig. 17.8 ). Clinically there may be skin irregularities over the zygomatic arch, because the fascial layers superficial to the arch are tightly bound to the bone of the arch and become edematous superficially. Therefore, if there is no extension into adjacent spaces, the zygomatic arch and inferior border of the mandible usually remain palpable clinically in the setting of buccal space abscesses.

The infratemporal space is a potential fascial space that may be involved in the spread of maxillary odontogenic infections. It is a space that lies posterior to the maxilla and is continuous laterally and superiorly with the deep temporal space; therefore infections involving one of these spaces usually involve the other space. The infratemporal space is bordered medially by the lateral pterygoid plate of the sphenoid bone and superiorly by the base of the skull. Vital structures within this space include, but are not limited to, branches of the internal maxillary artery and pterygoid venous plexus. The pterygoid plexus is unique in that it provides emissary veins that travel through foramina in the base of skull and connect with intracranial dural sinuses. Infections reaching the pterygoid plexus may travel directly to the cavernous sinus because the veins of the head and neck lack valves to prevent retrograde propagation of bacteria. Infections of maxillary third molars most commonly contribute to bacterial spread to the infratemporal space. Due to the deep location, infections in the infratemporal space are difficult to examine adequately in the clinical setting, although temporal fullness may be visible.

The spread of periapical infections from maxillary teeth may erode superiorly and penetrate the floor of the maxillary sinus, causing maxillary sinusitis, and perhaps also spread to neighboring sinuses. Of note, odontogenic infections are implicated in 10% to 40% of cases of maxillary sinusitis and up to 75% of unilateral cases of maxillary sinusitis. However, maxillary teeth, as a source of sinusitis, are often overlooked clinically; in fact, patients will often be treated with medical and surgical management for chronic rhinosinusitis without assessing the dental disease as a potential contributory factor. Causes of maxillary sinusitis include iatrogenic, implant-related, traumatic, periapical osteitis, endodontic foreign bodies, restorative materials, bone grafting materials, and retained tooth or bone fragments. Any violation of the Schneiderian membrane may precipitate maxillary sinusitis, either from the spread of a periapical infection or penetration by a dental implant or an iatrogenic injury from sinus membrane elevation for placement of a bone graft. The most common clinical findings in maxillary sinusitis include facial pain, postnasal discharge, and congestion. The most common anaerobic gram-negative bacteria found associated with odontogenic-related maxillary sinusitis include Streptococcus , Peptostreptococcus , and Fusobacterium species. Aerobes include Streptococcus and Staphylococcus species, with these organisms present in 75% of cases of odontogenic sinusitis and acute infection. Less common but more difficult to treat etiologies include Aspergillus species. Acute sinusitis from odontogenic origin can propagate through the ethmoid sinus and spread to the periorbital space. Preseptal cellulitis—that is, an infection of the eyelid structures anterior to the orbital septum—will occasionally lead to an orbital cellulitis. Infections may travel freely (because there are no valves in the veins of the head and neck) either from the infraorbital vein into the infraorbital space, or the inferior ophthalmic vein, or via the sinuses to join with the common ophthalmic vein through the superior orbital fissure, which can then travel to the cavernous sinus (cavernous sinus thrombosis) and can be fatal even with optimal medical and surgical management. Surgical management of the sinus in odontogenic-related maxillary sinusitis includes open or functional endoscopic-assisted sinus surgery.