Infections of the oral cavity, neck, and head

Table II.

Common Causative Organisms	Antimicrobial Regimens
	Normal Host	Immunocompromised Host
Normal hosts: cover both aerobic and anaerobic bacteria    • Aerobic or facultative: Streptococcus mutans, viridans and other streptococci;    • Anaerobic: Peptostreptococcus spp., Bacteroides spp., Porphyromonas spp., Prevotella spp. and other oral anaerobesImmunocompromised hosts: cover facultative gram-negative bacilli (including Pseudomonas aeruginosa) in addition to above	Penicillin G 2-4 MU IV q 4-6h, plusmetronidazole 500 mg IV q 6h; or	Cefotaxime 2 g IV q 6h, orceftriaxone 1 g IV q 12h, orcefepime 2 g IV q 12h; each plus metronidazole 500 mg IV q 6h; or
	Ampicillin-sulbactam 2 g IV q 4h; or	Ciprofloxacin 400 mg IV q 12hplus eithermetronidazole 500 mg IV q 6hor clindamycin 600 mg IV q 6h; or
	Clindamycin 600 mg IV q 6h; or	Piperacillin-tazobactam 4.5 g IV q 6h;or
	Doxycycline 200 mg IV q 12h; or	Imipenem 500 mg IV q 6h; orMeropenem 1 g IV q 8h
	Moxifloxacin 400 mg IV q 24h

Whereas the causative microorganisms in odontogenic orofacial space infections were universally susceptible to penicillin in the past, this is no longer the case. β-lactamase production among oral anaerobes is increasingly recognized, particularly among Fusobacterium spp. and pigmented Prevotella spp. Treatment failure with penicillin alone has been well documented. Thus, penicillin monotherapy is no longer recommended. Penicillin plus metronidazole or a β-lactam-β-lactamase inhibitor combination (e.g., ampicillin-sulbactam) is recommended. Clindamycin, doxycycline, or moxifloxacin is an alternative for penicillin-allergic patients. Erythromycin and tetracycline are not recommended because of their lack of optimal anaerobic activity and increasing resistance among some strains of streptococci.

In immunocompromised hosts, broad-spectrum coverage for facultative gram-negative bacilli should be included. Combination therapy with a third or fourth generation cephalosporin plus metronidazole, or monotherapy with piperacillin-tazobactam, or a carbapenem (imipenem or meropenem) is indicated. In addition, patients with risk factors for methicillin-resistant Staphylococcus aureus (MRSA) infection should be treated empirically with vancomycin (15-20 mg/kg IV q 12h) or linezolid (600 mg IV q 12h). Risk factors for MRSA include history of intravenous drug abuse, comorbid disease (e.g., diabetes mellitus), and residence in a community or hospital with substantial incidence of MRSA.

Other treatment modalities include:

• Surgical incision and drainage of loculated space infection

• Dental extraction and restorative treatment

• Hyperbaric oxygen treatment of osteomyelitis of the jaw, if poor response to antibiotics alone

Complications

• Deep fascial space infections (e.g., Ludwig’s angina, lateral and retropharyngeal space infections, etc.)

• Osteomyelitis of the jaws

• Cavernous sinus thrombosis

• Hematogenous dissemination (brain, lung, heart valves)

• Association of poor oral health with cardiovascular diseases (stroke, myocardial infarction)

Prognosis

• Good if orofacial space infection is superficial (e.g., buccal, canine, submental)

• Poor if orofacial space infection is deep with potential for spread to lateral or retropharyngeal spaces (e.g., submandibular, sublingual, masseteric, infratemporal)

• Life-threatening if airway is compromised (e.g., Ludwig’s angina, lateral or retropharyngeal space involvement)

Pathogenesis

• Both dental caries and periodontal disease are initiated by dental plaques composed of unique ecosystems of microorganisms embedded in a biofilm on the tooth surface

  Plaque on the tooth surface above the gingival margin (supragingival plaque) consists of acidogenic (acid-producing) and aciduric (able to grow at low pH) bacteria, which cause dental caries and may invade the pulp (pulpitis or endodontic infection); infection eventually perforates the alveolar bony (periapical abscess) and spread into orofacial fascial spaces.

  Plaque on the tooth surface below the gingival margin (subgingival plaque) consists of proteolytic and histotoxic bacteria, which cause periodontal infection (gingivitis, periodontitis, or periodontal abscess); such infections may eventually penetrate into the deeper fascial spaces of the face and mouth.

Clinical manifestations of specific odontogenic orofacial space infections

The local anatomic barriers of bone, muscle, and fascia predetermine the routes of spread, extent, and clinical manifestations of many orofacial infections of odontogenic origin.

• If pus perforates through either the maxillary or mandibular buccal plate inside the attachment of the buccinator muscle, infection will be intraoral; if the perforation is outside this muscle attachment, infection will be extraoral (see Figure 1A). Thus, infection of the upper and lower molars, lower incisors, and lower canine teeth is often accompanied by extraoral manifestations.

• When a mandibular infection perforates lingually, it presents in the sublingual space if the apices of the involved teeth lie above the attachment of the mylohyoid muscle (e.g., mandibular incisor, canines, premolars, and first molars) and in the submandibular space if below the attachment of the muscle (e.g., the second and third molars; see Figure 1B)

• Other superficial odontogenic orofacial space infections include the buccal, submental, masticator, canine, and intratemporal spaces (see Figure 2).

Unique clinical presentations of superficial odontogenic orofacial space infections include:

• Buccal space infections – These arise primarily from mandibular or maxillary bicuspid or molar teeth, the apices of which lie outside of the buccinator muscle attachments. They are readily diagnosed because of marked cheek swelling but with minimal trismus or systemic symptoms (see Figure 4).

• Canine space infections – These originate from the maxillary incisors and canines and manifest as dramatic swelling of the upper lip, canine fossa, and frequently the periorbital tissues (see
  Figure 5). Pain is usually moderate, and systemic signs are minimal. Occasionally, direct extension of infection into the adjoining antrum leads to purulent maxillary sinusitis.

• Submental space infections – These originate from a mandibular incisor that perforates below the mentalis muscle. The chin appears grossly swollen and is firm and erythematous.

• Masticator space infections – These infections typically originate from the third molar tooth to involve the masticator spaces consisting of the masseteric, pterygoid, and temporal space components (see Figure 6). These spaces intercommunicate with each other, as well as the buccal and deeper peripharyngeal fascial spaces (see Figure 2). The clinical hallmark of infection is trismus with pain in the area of the body or ramus of the mandible (see Figure 7). Swelling may not be prominent since the infection is beneath large muscle masses. When present, swelling tends to be brawny and indurated, suggesting the possibility of cervicofacial actinomycosis or mandibular osteomyelitis.

• Temporal space infections – These infections typically originate from the posterior maxillary molar teeth. Swelling may be limited to the preauricular region and an area over the zygomatic arch (see Figure 8). As infection progresses, the cheek, eyelids, and whole side of the face may be involved. Infection may extend directly into the orbit via the inferior orbital fissure and produce proptosis, optic neuritis, and abducens nerve palsy (see Figure 9).

• Infratemporal space infections – An infratemporal space infection usually originates from the third maxillary molar tooth. Clinically, marked trismus and pain are present, but very little swelling is observed early in the course. Late manifestations are similar to those of temporal space infections, including extension into the orbit through the inferior orbital fissure. Infection may also extend internally to involve an area close to the lateral pharyngeal wall, resulting in dysphagia.

Figure 4.

Figure 5.

Figure 6.

Figure 7.

Figure 8.

Figure 9.

Additional imaging studies for complications

• Technetium bone scanning (may be combined with gallium or indium-labeled white blood cell scanning) to assess acute or chronic osteomyelitis of the jaw from odontogenic infection ($$$)

• MRI for investigation of deep fascial space infections, such as submandibular, infratemporal, or orbital space involvement ($$$)

Prevention

• Promote good oral hygiene and regular visits to dental professionals

• Rigorous brushing with fluoridated toothpaste and dental flossing after each meal

• Dietary counseling to reduce sugar-rich foods or beverages

• Modification of risk factors for dental caries such as tobacco smoking

• Early detection and treatment of dental caries and advanced periodontitis

WHAT'S THE EVIDENCE for specific management and treatment recommendations?

Although an independent association between periodontal disease and atherosclerotic vascular disease is well recognized, a causal relationship has not been established. Even though periodontal interventions result in a reduction in systemic inflammation and endothelial dysfunction in short-term studies, no evidence exists that they prevent the development of atherosclerotic vascular disease or its outcomes in the long term.

Chow, AW, Roser, SM, Brady, FA. “Orofacial odontogenic infections”. Ann Intern Med. vol. 88. 1978. pp. 392-402. (This is a landmark paper correlating the microbiology, clinical presentation, and anatomic inter-relationships of orofacial odontogenic infections.)

Loesche, W. “Dental caries and periodontitis: contrasting two infections that have medical implications”. Infect Dis Clin N Am. vol. 21. 2007. pp. 471-502. (This source contrasts the clinical manifestations, pathogenesis, and management of dental caries and periodontal disease.)

DRG CODES and expected length of stay

Expected length of hospital stay is 3-7 days.

Suppurative parotitis

Major symptoms and physical findings

Major symptoms include:

• fevers and chills

• sudden onset of painful swelling (pre- and postauricular)

• no dysphagia or trismus

Prominent physical findings include:

• high fever and systemic toxicity

• unilateral swelling and tenderness extending to angle of mandible (see Figure 10)

• fluctuance is generally not appreciated due to dense fascia overlying the parotid gland

• purulent discharge from opening of Stensen’s duct (opposite upper second molar; see Figure 11)

• ipsilateral facial nerve palsy in some patients

Figure 10.

Figure 11.

Epidemiology

• Elderly

• More common in male than female patients (2:1)

• Nursing home or outpatient setting

• Postoperative (dehydrated and intubated)

• Unique association with Klebsiella pneumoniae infection among diabetic patients in Southeast Asia

Predisposing factors

• Sialolithiasis

• Malnutrition

• Diabetes mellitus

• Anticholinergic medications (decrease salivary flow)

• Oral neoplasms obstructing Stensen’s duct

Laboratory investigation

• Blood cultures

• Complete blood count (CBC) with differential, erythrocyte sedimentation (ESR), C-reactive protein

• Serum electrolytes and renal function

• Elevated serum amylase in absence of pancreatitis

• Gram stain, cultures, and susceptibility testing of purulent exudate from opening of Stensen’s duct

• Needle aspiration of loculated pus from parotid gland

Imaging studies

• Ultrasound to detect frank abscess or stones within Stensen’s duct or parenchyma

• CT to detect stones and differentiate suppurative cellulitis from abscess or solid tumor

• MRI to detect extension of infection into the deep peripharyngeal structures

Indication for consultation

• Intensive care for sepsis and hypotension

• Respirology or Anesthesiology for impending airway obstruction

• Oral Surgery for surgical drainage

Therapeutic considerations

Treatment includes hydration and intravenous antibiotics. Since suppurative parotitis may invade deep fascial spaces of the head and neck and is potentially life-threatening, outpatient management with oral antibiotics is not advised.

Initial empirical antimicrobial regimens are based on the expected microbiology and host factors, such as comorbid conditions and immunosuppression (see Table III). The microbiology is quite variable and often polymicrobial involving both aerobic and anaerobic bacteria. S. aureus (including MRSA) is the most frequent isolate (about one-third of patients) followed by viridans streptococci. Facultative gram-negative organisms, such as Enterobacteriaeae, H. influenzae, Eikenella corrodens, and other gram-negative bacilli, are often seen in hospitalized patients. Pigmented Prevotella and Porphyromonas spp., Fusobacterium spp., and Peptostreptococcus spp. are the most common anaerobes.