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Head and neck infections
Infections of the head and neck range in severity from minor to life threatening. A scoring system reflecting the need for hospitalization of such patients has been proposed. The intensivist is called upon to manage such patients either when they are critically ill or when airway compromise has occurred or is imminent. Besides airway management and control of sepsis, the intensivist must also be aware of the local anatomy and relevant microbiology. This knowledge will help guide the choice of antimicrobial agents and allow the clinician to anticipate the potential for spread of infection to related anatomic spaces and subsequent complications.
Normal head and neck flora
Huge numbers of bacteria reside in the oral cavity in health, with the bacterial load exceeding 10 11 /mL in the gingival crevices of patients with teeth. 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 . 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
Knowledge of the local anatomy is critical to the understanding and management of these infections. This has recently been reviewed. Serious infection of the head and neck can involve the following general anatomic areas:
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Sinus
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Pharynx
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Epiglottis
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Retropharyngeal space
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Submandibular space (Ludwig angina)
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Lateral pharyngeal space (anterior and posterior)
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Internal jugular vein (Lemierre syndrome)
Some of these anatomic areas are connected via actual (e.g., retropharyngeal) or potential (e.g., danger) 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 116.1 .
TABLE 116.1
Differentiating Features of Deep Neck Infections
| Space | Clinical Features * |
|---|---|
| Submandibular space (Ludwig 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 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 |
Predisposing factors for the development of deep neck infection include uncontrolled dental infection, spread of infection from other local structures (tonsils, vertebrae), local intravenous (IV) catheter placement or injection drug use, diabetes, human immunodeficiency virus (HIV) infection, and local trauma (e.g., the use of laryngeal mask anesthesia). , The use of cetuximab in combination with either radiation or chemotherapy for locally advanced head and neck cancer is associated with increased risk of local infection, as is the use of rituximab. A poor level of education and living far from a tertiary care center have also been shown to increase the risk of development of severe deep neck space infection.
Clinical syndromes
Sinusitis
Acute bacterial sinusitis accounts for a high proportion of physician visits in the primary care setting. In the ICU, patients who are critically ill with nasogastric, 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. Treatment involves the use of broad-spectrum antimicrobial agents ( Table 116.2 ) and close collaboration with an otolaryngologist to determine if drainage is needed. In addition, application of topical vasoconstrictors and inhaled topical steroids to the nasal mucosa is often recommended to help the sinus secretions drain.
TABLE 116.2
Therapeutic Options for Sinusitis, Pharyngitis, and Epiglottitis
| Syndrome | Likely Flora | Antibiotic Options * |
|---|---|---|
| Sinusitis (community acquired) | Haemophilus influenzae, Streptococcus pneumoniae, Staphylococcus aureus |
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|
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| Sinusitis (ICU acquired) | Pseudomonas aeruginosa, Escherichia coli and related coliforms, methicillin-resistant S. aureus (MRSA) |
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| Sinusitis (fungal) |
|
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| Liposomal amphotericin B (5–10 mg/kg/day IV) | ||
| Voriconazole (6 mg/kg q12h × 2 doses, then 4 mg/kg q12h) | ||
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||
| Pharyngitis | Corynebacterium diphtheriae | IV penicillin or erythromycin plus diphtheria antitoxin |
| Epstein-Barr virus (with airway compromise) | No antiviral therapy effective IV steroids |
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| Epiglottitis | H. influenzae type b | Ceftriaxone (1–2 g IV q24h) |
| Streptococcus pyogenes (group A strep) | Ampicillin-sulbactam (3 g IV q6h) | |
| Rifampin prophylaxis (600 mg orally q24h) for close contacts for 4 days |
* Antibiotic choices listed are examples, because for most infections, multiple different antibiotics are effective; individual choice will be influenced by patient factors (e.g., allergies), local hospital bacterial resistance rates, and microbiologic 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.
In patients with diabetic ketoacidosis, high-dose steroid treatment, severe neutropenia, or history of desferrioxamine treatment, rhinocerebral mucormycosis (most commonly Rhizopus spp.) 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 116.2 ) plus extensive surgery are always required for any hope of survival. However, the need for major surgery in all cases has come into question recently. Close collaboration with appropriate surgeons and infectious disease colleagues is required in such cases.
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