136 Head and Neck Infections
Normal Head and Neck Flora
Huge numbers of bacteria reside in the oral cavity in health, with the bacterial load exceeding 1011/mL in the gingival crevices of patients with teeth.1 The main bacterial species are anaerobes including Bacteroides, Fusobacterium, Prevotella, and Peptostreptococcus. Other common oral inhabitants include Streptococcus mutans, Staphylococcus aureus, Actinomyces spp., and Eikenella corrodens. Pharyngeal colonization and subsequent infection with organisms such as Streptococcus pneumoniae, Neisseria meningitidis, and Streptococcus pyogenes may also occur.
In acute illness, an additional modifying factor is the decreased production of oral mucosal fibronectin. This is of relevance to the clinician because fibronectin in normal physiologic amounts will preferentially bind gram-positive bacteria (such as S. mutans); however, when the production of fibronectin is decreased, there is rapid colonization of the oral cavity with gram-negative organisms, including species such as Pseudomonas aeruginosa.2 These gram-negative organisms may then participate in head and neck infections of oral or odontogenic origin, necessitating broad nosocomial-type gram-negative antibiotic coverage when the patient has been recently hospitalized or acquired the infection in the intensive care unit (ICU).
Sites of Deep Head and Neck Infection
Serious infection of the head and neck can involve the following general anatomic areas:
Some of these anatomic areas are connected via actual or potential spaces. Thus infection beginning in one space may spread rapidly to involve others, with potential resultant damage or destruction of vital structures. Such connections are discussed in the following sections, and differentiating features are highlighted in Table 136-1.
TABLE 136-1 Differentiating Features of Deep Neck Infections
| Space | Clinical Features* |
|---|---|
| Submandibular space (“Ludwig’s angina”) | Woody submental induration, protruding swollen/necrotic tongue, no trismus, rotted lower molars commonly present |
| Lateral pharyngeal space (anterior) | Fever, toxicity, trismus, neck swelling |
| Lateral pharyngeal space (posterior) | No trismus, no swelling (unless ipsilateral parotid is involved), cranial nerve IX-XII palsies, Horner’s syndrome, carotid artery erosion |
| Retropharyngeal space (retropharynx) | Neck stiffness, decreased neck range of motion, soft-tissue bulging of posterior pharyngeal wall, sore throat, dysphagia, dyspnea |
| Retropharyngeal space (“danger space”) | Mediastinal or pleural involvement |
| Retropharyngeal space (prevertebral) | Neck stiffness, decreased neck range of motion, cervical instability, possible spread along length of vertebral column |
| Jugular vein septic thrombophlebitis (Lemierre syndrome) | Sore throat, swollen tender neck, dyspnea, chest pain, septic arthritis |
Clinical Syndromes
Sinusitis
Acute bacterial sinusitis accounts for a high proportion of physician visits in the primary care setting.5 In the ICU, patients who are critically ill, with nasogastric tubes or endotracheal or nasotracheal tubes in place, may develop acute sinusitis caused by resistant nosocomial organisms (e.g., methicillin-resistant S. aureus [MRSA], P. aeruginosa) and anaerobes.3 Treatment involves the use of broad-spectrum antimicrobial agents (Table 136-2) and close collaboration with an otolaryngologist to determine if drainage is needed. In addition, application of topical vasoconstrictors and steroids to the nasal mucosa is often recommended to help the sinus secretions drain.
TABLE 136-2 Therapeutic Options for Sinusitis, Pharyngitis, Epiglottitis
| Syndrome | Likely Flora | Antibiotic Options* |
|---|---|---|
| Sinusitis (community-acquired) | Haemophilus influenzae, Streptococcus pneumoniae, Staphylococcus aureus | |
| Sinusitis (ICU-acquired) | Pseudomonas aeruginosa Escherichia coli and related coliforms Methicillin-resistant S. aureus (MRSA) | |
| Sinusitis (fungal) | Aspergillus spp. Mucorales spp. | |
| Pharyngitis | Corynebacterium diphtheriae | |
| Epstein-Barr virus (with airway compromise) | ||
| Epiglottitis | H. influenzae type b Streptococcus pyogenes (group A strep) |
* Antibiotic choices listed are examples, since for most infections, multiple different antibiotics are effective, and individual choice will be influenced by patient factors (allergies, etc.), local hospital bacterial resistance rates, and microbiological culture results.
Complications of nosocomial sinusitis are related to the local anatomy. Spread via the diploic veins can result in meningitis, brain abscess, contiguous osteomyelitis, or cavernous sinus thrombosis. Spread from the ethmoid sinuses can result in frontal lobe brain abscesses, whereas sphenoid sinus infection can spread to involve the surrounding pituitary gland, optic chiasm, internal carotid artery, cavernous sinus, or temporal lobe of the brain.1
In patients with diabetic ketoacidosis, high-dose steroid treatment, severe neutropenia, or history of desferrioxamine treatment, rhinocerebral mucormycosis or aspergillosis can develop. This infection can be rapidly fatal if the underlying problem cannot be corrected. The general teaching has been that high-dose antifungal therapy (see Table 136-2) plus extensive surgery is always required for any hope of survival. However, the need for major surgery in all cases has come into question recently.4 Close collaboration with appropriate surgeons and infectious disease colleagues is required in such cases.
Pharyngeal Infections
Life-threatening pharyngeal infections include acute anaerobic pharyngitis (Vincent’s angina) caused by a combination of oral anaerobes and spirochetes. The clinical manifestations of this entity in the critically ill host include acute ulcerations and necrosis of the oral mucosa and gums. Secondary bacteremia with sepsis syndrome can complicate matters. Treatment involves adequate oral débridement and administration of antibiotics with both aerobic and anaerobic activity (see Table 136-2).1
Quinsy (peritonsillar abscess) can complicate prior tonsillitis and is most common among young adults. Presenting symptoms include fever, pharyngeal pain, and unilateral pharyngeal swelling. If not adequately drained, the infection can spread into the lateral pharyngeal space, which was the commonest cause of mortality due to quinsy in preantibiotic days. Infection with anaerobes can result in a higher rate of recurrence of quinsy.5 Fusobacterium necrophorum is currently the most commonly encountered organism in peritonsillar abscesses in Denmark.6
Diphtheria is now rare thanks to mass vaccination. It presents as a sharply demarcated adherent dark gray nasal or pharyngeal membrane. Clinical illness is due to release of a bacterial toxin that inhibits translocase (via inhibition of elongation factor 2). Myocardial dysfunction and central nervous system toxin-mediated injury may occur late, but fulminant infections can be complicated by death from acute respiratory obstruction or circulatory failure (bull-neck diphtheria).1 Culture of the organism (Corynebacterium diphtheriae) requires the use of specific Loeffler medium.
Epiglottitis
Acute epiglottitis is primarily a disease of children who have not received the Haemophilus influenzae type b (Hib) vaccine and is thus rare at present.7 Acute epiglottitis presents as an acute febrile illness usually of less than 12 hours duration, with the child characteristically sitting forward, drooling saliva, and taking shallow and apprehensive breaths (deeper breathing draws the epiglottis over the airway and produces obstruction). The diagnosis is made clinically, although lateral neck radiography (if the child is stable enough to go for x-ray) characteristically shows enlargement of the epiglottis 30% to 57% of the time. Attempts to visualize the classically described edematous cherry red epiglottis directly may precipitate acute airway obstruction and should not be attempted unless the ability to secure an airway immediately is certain. Blood and epiglottis cultures usually grow H. influenzae type b. However, since the introduction of mass vaccination against H. influenzae type b, the incidence of infection with non–type b strains is increasing.7
Antibiotic options for epiglottitis are outlined in Table 136-2. There is no clear consensus on the role of exogenous corticosteroids to decrease epiglottic edema. Rifampin prophylaxis should be administered for 4 days to close household and hospital contacts of patients (especially those younger than 4 years) with invasive H. influenzae type b disease.
Full access? Get Clinical Tree
