Infectious Diseases

Infections of the oral cavity, neck, and head

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OVERVIEW: What every practitioner needs to know

This is a broad subject area. The topics to be covered include odontogenic orofacial "space" infections; suppurative parotitis; peritonsillar abscess; and deep neck space infections, including submandibular (Ludwig's angina), lateral pharyngeal, and retropharyngeal space infections. Although rare in the post-antibiotic era, deep space infections of the head and neck are potentially life-threatening. A clear understanding of their inter-relationships, anatomic routes of potential spread, and salient clinical presentations is critical to successful management and prevention of these infections.

Odontogenic orofacial space infections

Major symptoms and physical findings

Major symptoms include:

  • antecedent toothache

  • facial swelling and pain

  • fever and chills

  • halitosis

  • bleeding gums with minor trauma

Prominent physical findings include:

  • dental plaques, tooth decay (caries), gingivitis or periodontal pockets

  • facial or neck swelling and tenderness

  • inability to open the jaw (trismus)

  • difficulty in swallowing (dysphagia)

  • dyspnea with inspiratory stridor

Odontogenic orofacial infections arise either from dental caries or periodontal infections that have extended beyond the alveolar bone to involve the fascial spaces around the face and oral cavity. These infections tend to spread along planes of least resistance from the supporting structures of the affected tooth. In the maxilla, the alveolar bone is weakest on the buccal side throughout. In the mandible, the alveolar bone is weakest in the lingual aspect posteriorly affecting the molar teeth, and on the buccal side more anteriorly involving the incisors and canine teeth. Thus, location of the affected tooth predicts the route of spread and which orofacial spaces become infected (see Figure 1).

Figure 1.

Routes of spread of odontogenic orofacial infections along planes of least resistance. A, coronal section in the region of the first molar tooth: a, maxillary antrum; b, nasal cavity; c, palatal plate; d, sublingual space (above the mylohyoid muscle); e, submandibular space (below the mylohyoid muscle); f, intraoral presentation with infection spreading through the buccal plates inside the attachment of the buccinator muscle; g, extraoral presentation to buccal space with infection spreading through the ubccal plates outside the attachment of the buccinator muscle. B, lingual aspect of the mandible: a, apices of the involved tooth above the myohyoid muscle, with spread of infection to the sublingual space; b, apices of involved tooth below the mylohyoid muscle, with spread of infection into the submandibular space.

The fascial spaces around the mouth and face, which are most commonly implicated in odontogenic infections, are shown in Figure 2. Other non-odontogenic sources of infection include suppurative parotitis, peritonsillar abscess, sinusitis, and mastoiditis.

Figure 2.

Fascial spaces around the mouth and face. A, horizonal section at the level of the occlusal surface of the manibular teeth. B, frontal view of the face.

The main clinical presentation of various orofacial odontogenic infections are summarized in Table I. The location of these space infections can be helpful in identifying the underlying infected tooth and suggests the potential pathways for spread into deeper fascial space infections of the head and neck (see Figure 3).

Table I.

Clinical Features of Superficial Odontogenic Orofacial Space Infections
Orofacial space infections Usual dental source Clinical features
Pain Trismus Swelling Dysphagia Dyspnea
Masticator
Masseteric & pterygoid Molars (especially 3rd) + +++ May not beevident (deep) - -
Temporal Posterior maxillary molars + - Face, orbit (late) - -
Buccal Bicuspids, molars ± ± Cheek (marked) - -
Canine Maxillary canines, incisors ++ - Upper lip, canine fossa - -
Infratemporal Posterior maxillary molars + - Face, orbit (late) ± ±
Submental Mandibular incisors ++ - Chin (firm) - -

Figure 3.

Potential pathways of spread into deep fascial space infections of the head and neck.

Epidemiology

  • Both dental caries and periodontal disease are common conditions. According to the National Health and Nutrition Examination Survey during1999-2004:

    • 42% of children and adolescents and 90% of adults had dental caries in their primary teeth.

    • Prevalence of moderate to severe periodontal disease was 5% among those 35-49 years of age, 11% among 50-64 years of age, 14% among 65-74 years of age, and 20% among those older than 75 years of age.

  • Both are important causes of tooth loss after 65 years of age.

    • About 25% of all adults older than 60 years of age have lost all their teeth (edentulous), one-half from dental caries and one-half from severe periodontitis.

    • Dental caries are a more important cause of tooth loss before 35 years of age.

    • Periodontal disease is more important after 35 years of age.

  • The prevalence of orofacial space infections as a complication of dental caries or periodontal disease is unknown.

Predisposing factors

  • Poor oral hygiene

  • Advancing age

  • Tobacco use

  • Sugar-rich diet (dental caries)

  • Hormonal effects, such as puberty, menstruation, and pregnancy (periodontal disease)

  • Underlying disease (i.e., diabetes mellitus, rheumatoid arthritis, steroids, neutropenia)

Laboratory investigation

The diagnosis is primarily clinical and based on the history and physical examination. Cultures obtained intraorally are of little value because of contamination by the resident oral microflora.

  • Blood cultures, aerobic and anaerobic

  • Gram stain, aerobic and anaerobic cultures, and susceptibility testing of extraoral specimens obtained by needle aspiration

Imaging studies

  • Orthopantomogram or AP radiograph of teeth to assess periapical abscess or advanced periodontal disease ($)

  • CT of face and neck to assess source and extension of orofacial space infections ($$)

Indication for consultation

  • Dentistry - oral hygiene and dental extractions

  • Oral surgery - surgical drainage of orofacial space infections

Therapeutic considerations

Although surgical drainage of loculated pus and dental extraction are the mainstay of therapy, antibiotic treatment is required to halt local spread of infection and prevent hematogenous dissemination.

Anti-infective agents are generally indicated if fever and regional lymphadenopathy are present or when infection has perforated the bony cortex and spread into surrounding soft tissues. Severely immunocompromised patients are particularly at risk for rapidly spreading orofacial infections and bacteremia. Empiric antimicrobial therapy should be initiated promptly in such patients.

The choice of specific antimicrobial regimens for odontogenic orofacial infections is empirical based on anticipated causative pathogens and immune status of the host. This is because specimens obtained extraorally to avoid contamination by the oral commensal flora are rarely available. Odontogenic orofacial space infections are usually polymicrobial involving both strict anaerobes and facultative bacteria within unique ecosystems of the dental plaque and gingival crevice.

The most prevalent anaerobic bacteria include gram-positive cocci, such as Peptostreptococcus spp., and gram-negative rods, such as Bacteroides spp., Fusobacterium spp., Prevotella spp. and Porphyromonas spp. The most prevalent aerobes are facultative gram-positive cocci such as Streptococcus mutans, and viridans streptococci. Facultative gram-negative bacilli and S. aureus (including MRSA) are uncommon in immunocompetent hosts but may be more important in immunocompromised patients. The choice of initial antimicrobial regimens directed at these pathogens in the normal or immunocompromised hosts are shown in Table II.

Table II.

Common Causative Organisms and Initial Empirical Antimicrobial Regimens for Odontogenic Orofacial Space Infections
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.

Buccal space infection demonstrating marked swelling but no trismus or systemic toxicity.

Figure 5.

Canine space infection with dramatic swelling of the upper lip, canine fossa, and eyelid.

Figure 6.

Masticator space infections originating from the 3rd molar tooth. Horizontal view of the mouth showing ramus of the mandible, and the pterygoid and masseter muscles which are involved in mastication. Infection may spread to 1, peritonsillar space; 2, pterygoid space; 3, masseteric space; 4, buccal space; 5, intraorally

Figure 7.

Masticator space infection involving the right mandibular 3rd molar, showing marked swelling of the face and neck

Figure 8.

Temporal space infections. The temporal space is divided by the temporalis muscle into a superficial component enclosed by the masseter muscle and a deep component enclosed by the medial pterygoid muscle

Figure 9.

Deep temporal space infection with spread to the right parotid space and the orbit. This patient developed right optic neuritis with permanent loss of vision. A, frontal view; B, lateral view showing pre-auricular swelling.

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.

Patient with suppurative parotitis and gross swelling over the parotid and angle of the jaw.

Figure 11.

Purulent exudate discharging from the opening of the Stensen's duct opposite the second maxillary molar in a patient with suppurative parotitis.

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.

Table III.

Common Causative Organisms and Initial Empirical Antimicrobial Regimens for Suppurative Parotitis
Common Causative Organisms Antimicrobial Regimens
Normal host Immunocompromised Host
Normal hosts: cover both aerobic and anaerobic bacteria    •Aerobic or facultative: S. aureus, viridans and other streptococci    •Anaerobic: Peptostreptococcus spp., Bacteroides spp., Porphyromonas spp., Prevotella spp., Fusobacterium spp. and other oral anaerobesImmunocompromised hosts: cover MRSA and facultative gram-negative bacilli (including Pseudomonas aeruginosa) in addition to above Nafcillin 1.5 g IV q 4-6h plus eitherMetronidazole 500 mg IV q 6hor Clindamycin 600 mg IV q 6h; or Vancomycin 1 g IV q 12hor Linezolid 600 mg IV q 12h plus Cefotaxime 2 g IV q 6hor
Vancomycin 1 g IV q 12h plus either Metronidazole 500 mg IV q 6hor Clindamycin 600 mg IV q 6h Vancomycin 1 g IV q 12hor Linezolid 600 mg IV q 12h each plus Cefepime 2 g IV q 12hand Metronidazole 500 mg IV q 6-8hor
Vancomycin 1 g IV q 12hor Linezolid 600 mg IV q 12h,each plus Piperacillin-tazobactam 4.5 g IV q 6h; or
Vancomycin 1 g IV q 12hor Linezolid 600 mg IV q 12heach plus either Imipenem 500 mg IV q 6h or Meropenem 1 g IV q 8h

Oral step-down regimens

Step down therapy may be considered once the patient has improved and surgical management is deemed unnecessary. The choice of oral regimens for step-down therapy should ideally be guided by culture and susceptibility data.

Possible regimens include:

  • Clindamycin 450 mg PO q 8h plus ciprofloxacin 500-750 mg PO q 12h

  • Amoxicillin-clavulanate (875 mg PO q 12h) with or without linezolid 600 mg PO q 12h (depending on whether MRSA is present)

  • Linezolid 600 mg PO q 12h plus moxifloxacin 400 mg PO q 24h

Surgical incision and drainage should be implemented if there is no clinical response after 48 hours of treatment with empirical intravenous antibiotics.

Complications

  • Extension of infection into the lateral pharyngeal space (see Figure 12)

  • Facial nerve palsy

  • Parotid fistula

  • Recurrent parotid infections

Figure 12.

Cross section view of the mouth at the level of the mandibular molar teeth, showing proximity of the parotic and peritonsillar spaces to the lateral or parapharyngeal space and structures.

Prognosis

  • Relatively poor due to co-morbidity (e.g. diabetes mellitus)

  • Life-threatening if lateral pharyngeal space is involved

Pathogenesis

  • Obstruction of Stensen`s duct by calculi or tumor leads to retrograde seeding and suppurative infection of parotid gland.

  • Abscess may also develop by hematogenous seeding to the parotid.

Differential diagnosis

  • Lymphoma

  • Cervicofacial actinomycosis

  • Mumps parotitis

  • Mycobacterium tuberculosis and non-tuberculous mycobacteria (e.g., M. avium-intracellulare) infection

Additional imaging studies for complications

  • MRI with gladolinium enhancement ($$$)

  • CT sialography and fistulography ($$)

Prevention

  • Promote good oral hygiene

  • Avoid dehydration

  • Avoid anti-cholinergic medications and drugs that decrease salivary flow

  • Effective glycemic control for diabetes mellitus

DRG Codes and expected length of stay

Expected length of hospital stay is 7-10 days.

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

Brook, I. "Acute bacterial suppurative parotitis: microbiology and management". J Craniofac Surg. vol. 14. 2003. pp. 37-40.

(This is a comprehensive review with up-to-date microbiology.)

Cohen, MA, Docktor, JW. "Acute suppurative parotitis with spread to the deep neck spaces". Am J Emerg Med. vol. 17. 1999. pp. 46-9.

(This source illustrates the life-threatening nature of suppurative parotitis with spread to the deep fascial spaces.)

Peritonsillar Abscess (Quinsy)

Major symptoms and physical findings

Major symptoms include:

  • fever and chills

  • severe sore throat (unilateral)

  • ipsilateral neck swelling and pain

  • muffled voice ("hot potato" quality)

  • drooling

  • symptoms of obstructive sleep apnea (e.g. snoring)

  • trismus (irritation and reflex spasm of internal pterygoid muscle)

Prominent physical findings include:

  • high fever and systemic toxicity

  • inflamed pharynx

  • swollen, erythematous and fluctuant tonsil with exudate within tonsillar pillars (see Figure 13)

  • uvular deviation to opposite side

  • fullness or bulging of posterior soft palate near tonsil

  • ipsilateral cervical and submandibular lymphadenopathy

Figure 13.

Peritonsillar abscess. A large unilateral abscess is visible in the pharynx with prominent swelling of the soft palate and anterior pillar.

Epidemiology

  • Estimated annual incidence: 15-30 per 100,000

  • Accounts for about50% of deep neck infections in children and adolescents

  • Most common in adolescents and young adults, less common in young children

Predisposing factors

  • Recurrent tonsillitis or pharyngitis

  • Smoking

Laboratory investigation

  • Complete blood count (CBC) and differential, ESR, C-reactive protein

  • Serum electrolytes and renal function

  • Throat culture for group A streptococcus (S. pyogenes)

  • Gram-stain, cultures, and susceptibility testing of abscess fluid obtained by needle aspiration

Imaging studies

Imaging is not necessary to make the diagnosis of peritonsillar abscess but may be helpful in differentiating cellulitis from abscess and other deep neck space infections and to assess possible complications (e.g., airway compromise, extension to lateral pharyngeal space, etc.).

  • Lateral neck radiograph to exclude epiglottitis

  • Intraoral ultrasound (sensitivity 89-95%, specificity 79-100%)

  • CT with contrast (preferred) reveals hypodense mass with ring enhancement within peritonsillar space

  • MRI to evaluate extension of infection into deeper structures (better soft tissue delineation)

  • Magnetic resonance angiography (MRA) to evaluate vascular complications (e.g., Lemierre's syndrome)

Indication for consultation

  • Intensive care if airway obstruction suspected

  • Otolaryngology for needle aspiration or incision and drainage

  • Oral surgery for recurrent infection and tonsillectomy

Therapeutic considerations

  • The first step is upper airway management to treat respiratory distress and prevent aspiration of abscess contents.

  • Needle aspiration should be attempted to decompress abscess and obtain pus for Gram stain, cultures, and susceptibility testing. This is performed in Trendelenburg position with topical anesthesia and under ultrasound guidance.

  • Trial of empirical antibiotic therapy before definitive surgery if no evidence of airway compromise, severe trismus, or other complications.

Antimicrobial therapy

Peritonsillar abscess is usually polymicrobial. Group A streptococcus (S. pyogenes), S. aureus, and mixed respiratory anaerobes (Peptostreptococcus spp., Bacteroides spp., Fusobacterium spp, Prevotella spp., Porphyromonas spp., Veillonella spp.) are the most common isolates. Choices of initial empiric antimicrobial regimens are shown in Table IV. Subsequent therapy should be guided by culture data and susceptibility testing.

Table IV.

Common Causative Organisms and Initial Antimicrobial Regimens for Peritonsillar Abscess
Common Causative Organisms Antimicrobial Regimens
Normal Host Immunocompromised Host
Normal host: cover Group A streptococcus & mixed anaerobes      (± S. aureus)Immunocompromised host: cover MRSA 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, plusMetronidazole 500 mg IV q 6h, plusVancomycin 1 g IV q 12h
Ampicillin-sulbactam 2 g IV q 4h; or Ceftriaxone 1 g IV q 12h, plusMetronidazole 500 mg IV q 6h, plusVancomycin 1 g IV q 12h
Clindamycin 600 mg IV q 6h
Linezolid 600 mg IV q 12h

Oral step-down regimens

Step down therapy may be considered once the patient has improved and surgical management is deemed unnecessary. The choice of oral regimens for step-down therapy should be guided by culture and susceptibility data.

Possible regimens include:

  • Clindamycin 450 mg PO q 8h

  • Amoxicillin-clavulanate (875 mg PO q 12h) with or without linezolid 600 mg PO q 12h (depending on whether MRSA is present)

Surgical management

  • Surgical drainage by needle aspiration, incision and drainage, or tonsillectomy

  • Needle aspiration is better tolerated and the preferred procedure

  • "Quinsy tonsillectomy" - aspiration followed by tonsillectomy in single procedure is an option

  • Indications for interval tonsillectomy include:

    • Significant upper airway obstruction or other complications

    • Failure of abscess resolution despite other drainage procedures

    • Recurrent pharyngitis or tonsillitis

Complications

Peritonsillar abscess may compromise the upper airway or spread into surrounding structures, including the masseter and pterygoid muscles, the lateral pharyngeal space, and the carotid sheath (see Figure 12). Spontaneous rupture of the abscess may cause asphyxiation or aspiration pneumonia.

Other complications include:

  • upper airway obstruction

  • aspiration pneumonia

  • lateral pharyngeal space infection

  • septic jugular thrombophlebitis (Lemierre's syndrome; see Figure 14)

  • carotid sheath invasion and hemorrhage

  • necrotizing mediastinitis

Figure 14.

Contrast-enhenced axial CT of the neck in a young adult with jugular venous thrombosis associated with a lateral pharyngeal space infection secondary to a right peritonsillar abscess. The common carotid arteries (C) are normal but the right internal jugular vein (J) is enlarged with a dense or enhancing wall surrounding the more lucent intraluminal clot (arrow).

Prognosis

  • Most cases resolve without sequelae with early and appropriate treatment.

  • Recurrence may occur in 10-15% of cases (40% with history of recurrent tonsillitis).

Pathogenesis

  • Invasion by pathogenic bacteria (e.g., Group A Streptococcus and mixed aerobes and anaerobes) to cause pharyngitis and tonsillitis with progression to synergistic cellulites and abscess formation in the peritonsillar space

  • Rarely, peritonsillar abscess may also develop by hematogenous seeding of the salivary glands in the soft palate (Weber glands), which directly communicate with the tonsils.

Differential diagnosis

  • Acute epiglottitis (no trismus)

  • Retropharyngeal abscess (prominent neck stiffness but minimal or no trismus)

  • Lateral pharyngeal space infection due to spread from a parotid or submandibular space infection (bulging behind posterior tonsillar pillar rather than superior to the tonsil)

  • Severe tonsillopharyngitis (e.g., Epstein-Barr mononucleosis, coxsackie virus herpangina, tonsillar diphtheria, etc.)

Prevention

  • Early and appropriate treatment of tonsillitis or pharyngitis

  • Tonsillectomy for recurrent tonsillitis or pharyngitis

DRG codes and expected length of stay

Expected length of hospital stay is 3-5 days.

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

Use of steroids (methylprednisolone 2-3 mg/kg single dose IV) in peritonsillar abscess remains controversial. A single double-blind randomized clinical trial in 2004 showed significant improvement in symptoms (ability to swallow) and length of hospital stay in the steroid group compared to placebo. Confirmation with a larger study is needed before this can be routinely recommended.

Ozbek, c, Aygenc, E, Tuna, EUl, Selcuk, A, Ozdem, C. "Use of steroids in the treatment of peritonsillar abscess". J Laryngol Otol. vol. 118. 2004. pp. 439-42.

(This is a prospective study of use of steroids for peritonsillar abscess.)

Powell, J, Wilson, JA. "An evidence-based review of peritonsillar abscess". Clin Otolaryngol. vol. 37. 2012. pp. 136-45.

(This source provides the most up-to-date evidence-based review of peritonsillar abscess management.)

Safak, MA, Haberal, I, Kilic, D, Gocmen, H. "Necrotizing fasciitis secondary to peritonsillar abscess: a new case and review of eight earlier cases". Ear Nose Throat J. vol. 80. 833. pp. 824-30.

(This is a review of necrotizing fasciitis secondary to peritonsillar abscess.)

Deep neck space infections

Deep neck space infections most commonly originate from a septic focus in mandibular molars, tonsils, parotid gland, deep cervical lymph nodes, paranasal sinuses, or mastoids. These infections occupy three important spaces embedded within different layers of the deep cervical fascia: the submandibular space (see Figure 15), the lateral pharyngeal (also known as parapharyngeal or pharyngomaxillary) space (see Figure 16), and the retropharyngeal space (see Figure 17). Although rare in the post-antibiotic era, deep neck space infections are potentially life-threatening because of their proximity to the airway and vascular structures with potential spread into the carotid sheath, cavernous sinus, cranium, and the mediastinum (see Figure 3).

Figure 15.

Anatomic relationships in submandibular space infections.

Figure 16.

Lateral pharyngeal space and its contents. A, cross-section; B, sagittal view.

Figure 17.

Relationship of the retropharyngeal and danger spaces to various layers of the deep cervical fascia.

Major symptoms and physical findings

Deep neck space infections share some typical clinical features (Table V):

  • septic presentation with systemic toxicity

  • signs of airway obstruction and difficulty in swallowing

  • other manifestations are dependent on the primary source (i.e., odontogenic, rhinogenic, oropharyngeal, or otogenic).

Table V.

Comparative Clinical Features of Deep Neck Space Infections
Deep Fascial Space Infections Common Source Clinical Features
Pain Trismus Neck Swelling Dysphagia Dyspnea
Submandibular (submylohyoid & sublingual) Mandibular molar tooth ++ Minimal Mouth floor; submylohyoid Present if bilateral involvement Present if bilateral involvement
Lateral pharyngeal
    • Anterior (prestyloid or muscular) odontogenic, parotid, tonsil, mastoid +++ Prominent Anterior lateral pharynx; angle of jaw Present Occasional
    • Posterior (retrostyloid or neurovascular) + Minimal Posterior lateral pharynx (hidden) Present Severe
Retropharyngeal (and danger) Esophagus, lateral pharyngeal extension, retropharyngeal lymph nodes + Minimal Posterior pharynx Present Present
Parotid Parotid abscess or suppurative parotitis +++ None Angle of jaw Absent Absent
Peritonsillar Peritonsillar cellulitis or abscess +++ Present Anterior tonsillar pillar and soft palate Prominent Occasional

Clinical manifestations unique to specific sites of infection:

  • Oropharyngeal, peritonsillar, parotid, and submandibular abscesses include:

    • sore throat and trismus

    • unilateral erythema and swelling of face and neck

    • purulent oral or pharyngeal exudate

    • pooling of saliva

    • asymmetry of the oropharynx

    • submandibular or cervical lymphadenopathy

  • Trismus is due to pressure or infection of the muscles of mastication (masseter and pterygoids).

  • Dysphagia and odynophagia are secondary to inflammation of the cricoarytenoid joints.

  • Dysphonia and hoarseness indicate involvement of the tenth cranial nerve.

  • Unilateral tongue paresis indicates involvement of the twelfth cranial nerve.

  • Stridor and dyspnea signify airway obstruction and may indicate spread of infection to the mediastinum.

  • Unexplained bruising or bleeding in the neck, oral cavity, nose, or ear may suggest carotid sheath involvement with mycotic aneurysm of the internal carotid artery.

Epidemiology

  • Linked to primary source of infection

  • May occur at any age but more common in young adults

Predisposing factors

  • Linked to primary source of infection (i.e., odontogenic versus oropharyngeal versus rhinogenic or otogenic)

  • Penetrating trauma to floor of mouth (e.g., instrumentation)

  • Esophageal perforation (from chicken bones or cancer)

Laboratory investigation

  • Blood culture

  • Complete blood count (CBC) and differential, ESR, C-reactive protein

  • Serum electrolytes and renal function

  • Aspirate from loculated pus for Gram stain, cultures and susceptibility testing

Imaging studies

  • Lateral neck radiograph to assess airway and retropharyngeal soft tissues (normally about 5 mm deep, less than 1/3 the diameter of C4 vertebra; with retropharyngeal space infection, the pharynx or upper airway is displaced anteriorly by more than 1/2 the wide of C4 vertebra; see Figure 18).

  • CT with contrast to assess edema, swelling, and air-fluid levels involving deep neck spaces and to differentiate retropharyngeal from prevertebral space infections

  • MRI with angiography to assess vascular complications (e.g., cavernous sinus thrombosis, carotid sheath infection with septic jugular thrombophlebitis, or carotid artery mycotic aneurysm)

Figure 18.

Lateral radiograph of the neck. A, normal lateral cervical view; B, expansion of the retropharyngeal soft tissues due to spread from a lateral pharyngeal space infection.

Indication for consultation

  • Dentistry for odontogenic source of infection

  • ENT for clinical evaluation and needle aspiration of peripharyngeal space infections

  • Intensive care and Anesthesiology for airway and life support

  • Radiology for imaging studies

  • Oral Surgery for definitive evacuation of loculated space infections and removal of primary source

Therapeutic considerations

Appropriate antibiotics in conjunction with surgical drainage of loculated infection are essential for successful outcome.Antimicrobial therapy

  • Choice of antimicrobial regimens is empirical, dependent on the primary source (e.g., odontogenic or oropharyngeal versus rhinogenic or otogenic), anticipated causative microorganisms, and immunity of the host.

  • Maximum doses should be administered to optimize tissue penetration and bactericidal activity.

  • Selection of subsequent antibiotics should be guided by culture data and susceptibility testing.

In immunocompromised hosts, broad-spectrum coverage for facultative gram-negative bacilli, as well as oral aerobes and anaerobes, should be included. 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 (Table VI).

Table VI.

Common Causative Organisms and Initial Antimicrobial Regimens for Deep Neck Space Infections
Primary Source Common Causative Organisms Antimicrobial Regimens
Normal Host Immunocompromised Host
Odontogenic (Lugwig's angina or submandibular space infections) 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 4-6hplusmetronidazole 500 mg IV q 6hor Cefotaxime 2 g IV q 6horceftriaxone 1 g IV q 12horcefepime 2 g IV q 12h each plusmetronidazole 500 mg IV q 6hor
Ampicillin-sulbactam 2 g IV q 4hor Ciprofloxacin 400 mg IV q 12h plus eithermetronidazole 500 mg IV q 6horclindamycin 600 mg IV q 6hor
Clindamycin 600 mg IV q 6hor Piperacillin-tazobactam 4.5 g IV q 6hor
Doxycycline 200 mg IV q 12hor Imipenem 500 mg IV q 6horMeropenem 1 g IV q 8h
Moxifloxacin 400 mg IV q 24h
Oropharyngeal (peritonsillar abscess or quinsy) see section on peritonsillar abscess see section on peritonsillar abscess see section on peritonsillar abscess
Rhinogenic or Otogenic (purulent sinusitis or chronic mastoiditis) Normal hosts: cover both aerobic and anaerobic bacteria    •Aerobic or facultative: Streptococcuspneumoniae, Haemophilus influenzae, 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 Ampicillin-sulbactam 3 g IV q 6hor Same as for odontogenic space infections
Ciprofloxacin 400 mg IV q 12hplusMetronidazole 500 mg IV q 6hor
Ciprofloxacin 400 mg IV q 12hplusClindamycin 600 mg IV q 6h

Timely surgical management

  • The primary pathology in deep neck space infection is a cellulitis that involves the connective tissues, fasciae, and muscles; surgical drainage should be implemented only if the cellulitic process has localized into a discrete abscess (as confirmed by CT or MRI).

  • Premature incision into an area of cellulitis area may actually worsen the situation by breaking down the natural barriers and hastening the spread of infection.

Complications

  • Carotid sheath involvement is a complication of lateral pharyngeal space infection with potential for carotid artery erosion or septic jugular thrombophlebitis (see Figure 12). Carotid artery mycotic aneurysm arises from arteritis due to contiguous inflammation, resulting eventually in formation of a false aneurysm, which may rupture. Characteristic clinical features include:

    • insidious onset with fever of unknown origin

    • recurrent "herald bleeds" from the nose, mouth, or ear

    • hematoma formation in the surrounding tissues

    • choice of antibiotics is the same as for lateral pharyngeal space infections from odontogenic or oropharyngeal sources (see Table VI)

  • Septic jugular thrombophlebitis (Lemierre's syndrome) is a complication of lateral pharyngeal space infection from odontogenic, parotid, or peritonsillar space infections (see Figure 14) and should be suspected in patients with antecedent pharyngitis, septic pulmonary emboli, and persistent fever despite antibiotic therapy. Choice of antimicrobial regimens is the same as for lateral pharyngeal space infections from odontogenic or oropharyngeal sources.

  • Suppurative cavernous sinus thrombosis is a complication of sphenoid or ethmoid sinusitis and any septic foci of the face and head due to rich vascular supply and retrograde venous spread (see Figure 19). Major clinical findings include:

    • abrupt onset with diplopia, photophobia, orbital edema, and progressive exophthalmos

    • ophthalmoplegia (cranial IV and VI involvement)

    • midposition fixed pupil (cranial III involvement)

    • loss of corneal reflex and diminished sensation over the upper face (cranial V involvement)

    • papilledema, retinal hemorrhage, and loss of vision due to obstruction of venous flow from the retina and optic neuritis

  • Acute necrotizing mediastinitis is a complication of retropharyngeal or "danger" space infection with direct extension into the posterior mediastinum.

    • It may result in spread to the pleura or pericardium, resulting in empyema or pericardial tamponade.

    • Primary source of infection may be odontogenic, peritonsillar, or parotid abscess.

    • Antimicrobial treatment depends on the primary source (odontogenic or rhinogeic; see Table VI).

  • Suppurative intracranial infection is a complication of lateral and retropharyngeal space infections of rhinogenic or otogenic origin; hematogenous or contiguous spread to the cranium may cause brain abscess, subdural empyema, epidural abscess, or septic intracranial sinus thrombosis.

Figure 19.

Computed tomgraphic scan of the head of a patient with cavernous sinus thrombosis secondary to sphenoid sinusitis. Arrow indicates thrombus in the right cavernous sinus.

Prognosis

  • Guarded because of life-threatening nature of infection

  • Mortality varies from less than 1% to 25%, depending on age, underlying disease, prompt diagnosis, and appropriate treatment.

Pathogenesis

  • Deep neck space infections are typically polymicrobial, with propensity to break down normal barriers and spread along fascial planes.

  • Primary pathology is a synergistic cellulitis that involves the connective tissues, fasciae, and muscles, frequently undergoing necrosis and eventually abscess formation.

  • Potential pathways of extension from one space to another are illustrated in Figure 3.

Clinical manifestations of specific deep neck space infections

  • Submandibular space infections (Ludwig's angina)

    • This typically arises from the submylohyoid space (where apices of the molar teeth are located) with subsequent spread to the sublingual space (see Figure 15).

    • Infection is bilateral (due to contiguous spread).

    • High fever, chills, mouth pain, stiff neck, drooling, dysphagia, and muffled voice are seen.

    • There is a characteristic "woody" or brawny cellulitis (with or without crepitus) in the submandibular region and neck (see Figure 20).

    • The tongue may enlarge to 2-3 times normal size because of swelling and protrude out of the mouth or distend posteriorly into the hypopharynx and palate.

    • Posterior extension directly involves the epiglottis causing obstruction of the upper airway (patient frequently leans forward to maximize the airway diameter).

    • Trismus is unusual, unless there is spread into the lateral pharyngeal space.

Figure 20.

Early appearance of a patient with Ludwig's angina showing boardlike, brawny swelling in the submandibular region and the neck.

  • Lateral pharyngeal (also known as parapharyngeal or pharyngomaxillary) space infections (see Figure 16)

    • Symptoms and signs are dominated by primary source of infection (i.e., odontogenic or oropharyngeal versus rhinogenic or otogenic).

    • Anterior (prestyloid or muscular) compartment is more commonly involved than posterior (poststyloid or neurovascular) compartment containing the carotid sheath (enclosing common carotid artery, internal jugular vein, and cranial nerves IX to XII).

    • Cardinal clinical features are:

      • systemic toxicity with fever and rigors

      • induration and swelling below the angle of the mandible

      • medial bulging of the pharyngeal wall

      • trismus

    • Dyspnea may be prominent because of edema and swelling of the epiglottis and larynx.

    • Neurological signs (e.g., Horner syndrome, hoarseness, unilateral tongue paresis) indicate cranial nerve involvement (IX to XII) in the neurovascular compartment.

  • Retropharyngeal or "danger" space infections

    • The retropharyngeal space communicates directly with the lateral pharyngeal space (see Figure 16)

    • The "danger" space lies posterior to the retropharyngeal space and extends from the base of the skull to the diaphragm via the entire length of the posterior mediastinum.

    • Sore throat or difficulty in swallowing or breathing may be the first indication of infection.

    • Diagnosis may be delayed because of trismus from primary sources of infection (e.g., odontogenic sepsis or peritonsillar abscess), which makes direct examination of the posterior pharyngeal wall difficult.

    • Differential diagnosis includes prevertebral space infection associated with vertebral osteomyelitis.

Additional imaging studies for complications

  • CT to assess cavernous sinus thrombosis, intracranial suppuration, and necrotizing mediastinitis

  • MRI angiography to assess vascular complications (septic jugular thrombophlebitis, carotid artery mycotic aneurysm, cavernous sinus thrombosis)

Prevention

  • Oral hygiene and dental treatment to prevent caries and advanced periodontal disease

  • Tonsillectomy for recurrent tonsillitis or peritonsillar abscess

  • Avoid dehydration and anticholinergic medications that decrease salivary flow

  • Appropriate treatment of acute or chronic sinusitis, mastoiditis, or middle ear infections

DRG codes and expected length of stay

  • Expected hospital stay is variable.

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

Barakate, MS, Jensen, MJ, Hemli, JM, Graham, AR. "Ludwig's angina: report of a case and review of management issues". Ann Otol Rhinol Laryngol.. vol. 110. 2001. pp. 453-6.

(This is a good review of management issues for Ludwig's angina.)

Chow, AW, Mandell, GL, Bennett, JE, Dolin, R. "Infections of the oral cavity, neck and head". Principles and practice of infectious diseases. Elsevier Churchill Livingstone. 2010. pp. 855-71.

(This source is an in-depth review of deep fascial space infections of the oral cavity, head, and neck.)

Reynolds, SC, Chow, AW. "Severe soft tissue infections of the head and neck: a primer for critical care physicians". Lung. vol. 187. 2009. pp. 271-9.

(This is a practical overview of the diagnosis and management of deep fascial space infections of the head and neck.)
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