Head and Neck Infections

Published on 22/03/2015 by admin

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136 Head and Neck Infections

Infections of the head and neck range in severity from minor to life threatening. 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 as well as allow the clinician to anticipate the potential for spread of infection to related anatomic spaces and subsequent complications.

image 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).

image 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

* Fever and signs of systemic toxicity are common to all.

image 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

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