Head and Neck Infections

Manon Kwon

Infections of the head and neck are both common and potentially life-threatening. Knowledge of the fascial layers and the potential spaces of the neck are important to clinical practice because of the potential complications that may arise.

CLINICAL PRESENTATION

The signs, symptoms, and complications of the infectious disorders of the head and neck are determined largely by the anatomic compartment of origin. The fascial layers serve as important barriers to infection and often determine the path of the spread of infection. In addition, comorbidities frequently found in severe presentations are diabetes mellitus, old age, alcohol abuse, systemic disease, and immunosuppressed states (such as in patients with AIDS or in those undergoing chemotherapy).

Patients with deep neck infections can present in a variety of ways with the most common signs and symptoms being fever, pain, swelling, and a variable period ranging from 1 day to several weeks. Decreased oral intake can result in mild to severe dehydration, and swelling may lead to airway compromise.

Deep neck infections may occur at any age, but there appears to be a somewhat bimodal distribution. Overall there is a predominance in patients over 50 with a higher prevalence in the lower socioeconomic groups mainly due to poor oral hygiene and lack of dental care (2–4,6,7). In pediatric patients, these infections can occur at any age, but most commonly occur between 3 to 5 years of age with a slight male predominance (5).

The most common etiologic sites of infection are the teeth and tonsils. Other common causes are postsurgical and trauma that disrupts the skin and soft tissues. Intravenous drug users can present with jugular vein infections from contaminated injections. Other less common causes include foreign bodies, sialolithiasis, parotid obstruction, osteomyelitis, and epiglottitis. In patients with recurrent deep neck infections, consider underlying congenital anomalies (branchial cleft cysts, lymphangiomas, and thyroglossal duct cysts) (2–7,19).

Although mortality from head and neck infections has decreased significantly since the emergence of antibiotics, resistant organisms are spreading into the community. Most infections are polymicrobial including anaerobic and facultative oral bacteria (5). The most commonly isolated organisms in the head and neck infections are gram-positive aerobes followed by anaerobes, gram-negative aerobes and fungi. Streptococcus viridans and Staphylococci species dominate the gram positives, while Klebsiella pneumoniae and Neisseria species are frequently the gram-negative culprits (6). Emergency physicians must also be cognizant that the onset may be insidious secondary to partial treatment with antibiotics.

Facial cellulitis of odontogenic origin usually involves the upper half of the face when the maxillary teeth are the source. Involvement of the middle and lower part of the face and neck suggests a mandibular origin. These infections are generally well contained, but in a compromised host there may be rapid spread of infection, which can be fatal (24,25). Infections that affect the midface are commonly caused by a dental abscess of the anterior maxillary molar teeth and the buccal space. Infections in these areas can lead to cavernous sinus thrombosis because of the pattern of venous drainage, airway compromise, and mediastinal extension (1). Odontogenic sinusitis refers to the secondary infection of the paranasal sinuses originating from dental infection. Although most paranasal sinus infections result from an upper respiratory tract infection, direct spread of the infection from the teeth and associated oral tissues can result in secondary sinusitis. Based on proximity, the maxillary sinuses are most often involved. Symptoms include headache, foul discharge, fever, weakness, and drainage. Osteomyelitis may complicate odontogenic infection typically involving the premolar soft tissues, maxillary sinuses, infratemporal fossa, or the periorbital region.

Ludwig Angina

Ludwig angina is defined as an infection involving the submandibular, sublingual, and submental spaces with marked elevation of the tongue (2,4,10). A characteristic brawny edema, induration, or board-like swelling is present on the floor of the mouth. Tender and firm anterior neck edema without fluctuance is appreciated on physical examination. Patients may also complain of stridor, drooling, difficulty talking, tachypnea, and tender tongue with abnormal protrusion.

Ludwig angina typically begins as an infection of the second and third mandibular molars (odontogenic), progressing rapidly into tissues that cover the small muscles between the larynx and the floor of the mouth. Hemolytic Streptococcus sp is the most commonly identified organism. Mixed flora can also cause an overgrowth of gas-producing organisms such as Bacteroides fragilis. Although Ludwig angina is a cellulitis with diffuse infiltration, subsequent abscess formation is not uncommon. The mode of spread is typically direct and not lymphatic. Thus the infection is classically bilateral, but not always obvious on initial presentation. Ludwig angina may result in a life-threatening airway compromise and obstruction, and these patients tend to be quite toxic.

Mediastinitis

Although the most common cause of acute mediastinitis is esophageal rupture (due to instrumentation, foreign body, or trauma), descending necrotizing fasciitis from the retropharyngeal space, prevertebral space, or other anterior visceral spaces can also spread into the mediastinum. Symptoms include increased respiratory difficulty, tachycardia, chest pain, back pain, erythema/edema of the neck and chest, crepitus, and shock. It is important to have a low threshold for further workup in patients with these symptoms (12,13,14,16). Comorbid conditions such as diabetes and immunocompromised patients are at higher risk for this severe infection. Mediastinitis may also result from direct extension from an adjacent source of infection, including osteomyelitis of the sternoclavicular joint, pulmonary infections, and spread of granulomatous disease from mediastinal lymph nodes.

Salivary Infections

Salivary infections can develop in three ways: (a) retrograde migration into the duct from the oral cavity, (b) contagious spread of a local infection, or (c) as a suppurative complication of salivary stasis secondary to an obstructing stone. New literature suggests that the infection is polymicrobial, consisting of Streptococcus sp, Staphylococcus sp, aerobes, anaerobes, or viral etiology (mumps, AIDS, influenza, coxsackieviruses) (2,3). Sialoadenitis is a suppurative inflammation of the Stensen duct or the Wharton duct. Infectious parotiditis is often seen in elderly, dehydrated, diabetic, or patients with granulomatous disease. This entity is usually bilateral and associated with fever and a toxic appearance. Drugs with anticholinergic and diuretic properties can contribute to the development of sialoadenitis (6,25).

Lemierre Syndrome

Lemierre syndrome is a form of septic thrombophlebitis, with or without metastatic abscesses, typically involving the internal jugular vein ipsilateral to a neck or throat infection. First described in 1936, however most cases have occurred in the postantibiotic era, and it was termed in 1984 as the “forgotten disease.” However, recent reviews of the literature suggest an increasing incidence. The offending organism is most commonly a Fusobacterium anaerobic gram-negative bacillus, which is part of the normal flora of the mouth. Predisposing factors include trauma, edema, anoxia, or tissue destruction after dental disease (18,20).

Cavernous Sinus Thrombosis

The cavernous venous sinuses are bilateral structures that communicate with the pterygoid plexus as well as the superior ophthalmic vein. Because these sinuses anastomose with facial veins which have no valves, paranasal sinus, odontogenic, and facial infections may spread into the cavernous sinus. Patients with cavernous venous sinus thrombosis often have a history of midface infection for the past 5 to 10 days. Presenting signs and symptoms include headache, fevers, and cranial nerve deficits, specifically CN III to VI. The patient may have orbital pain, visual disturbances, and fullness with periorbital edema or discrete abscess. Other symptoms include confusion, drowsiness, and coma as a result of central nervous system involvement and/or sepsis.

DIFFERENTIAL DIAGNOSIS

In addition to the processes discussed above, the differential diagnosis of head and neck infections is broad and includes simple pharyngitis, dental infections, and referred pain. Tumors may present as nonspecific swelling and can be difficult to differentiate from advanced primary infections. Viral infections involving the salivary glands (e.g., mumps) can present as facial swelling. Less common infections include tuberculous cervical lymphadenitis (scrofula), cytomegalovirus, catscratch disease, and actinomycosis. Failure to respond to conventional therapy should lead the clinician to suspect a complication or an alternative diagnosis. Certain fungal infections, such as mucormycosis, although rare, are more common in the head and neck regions and should be considered in the immunocompromised patient. Autoimmune diseases such as Sjögren syndrome and Mikulicz disease can also lead to facial swelling caused by enlargement of the salivary glands. Trauma-induced swelling (vascular and nonvascular), can also mimic facial infections (4).

ED EVALUATION

The initial evaluation must focus on an assessment of the ABC’s, as some patients with a deep neck infection present in septic shock and require emergent airway management. The patient’s alertness, posture, work of breathing, stridor, and quality of voice may be assessed in the first few seconds. Once this assessment has been made, more stable patients may have a more detailed physical examination and diagnostic testing.

Protective eyewear, mask, and gloves should be worn when evaluating the oral cavity. Positioning the patient is also important, ideally at a 45-degree angle. Consider examining children on a parent’s lap for patient comfort. It is important to have the following equipment readily available: a good light source, a tongue blade, gauze, suction, and a dental mirror. Providing topical anesthesia of the oropharynx may facilitate the examination in some cases. A MacIntosh laryngoscope blade is an excellent tongue depressor and light source for examination and or procedure.

Patients with dental pain should be examined for the presence of infection and localized dental pain. Pain to percussion with a tongue blade indicates involvement at the apex of the tooth (such as a periapical abscess). Tender swelling of the gingiva adjacent to a tooth may indicate either a periodontal abscess or extension of a periapical abscess through the cortex of bone into the subperiosteal space.

The EM physician should evaluate for facial swelling which can be subtle in some cases as well as adenopathy and other signs of infection. In patients with sialoadenitis, pus may be expressed from the meatus of the salivary duct with gentle pressure to the gland or “milking” along the duct. In severe head and neck infections such as Ludwig angina, trismus, the inability to open the mouth because of involvement of the internal pterygoid or masseter muscle, may be present. Overall, this sign is present in less than 20% of patients even in advanced head and neck infections. More commonly in severe infections, patients will have a toxic presentation or appear in respiratory distress with impending upper airway obstruction or concomitant pneumonia. Other significant clinical signs include torticollis from sternocleidomastoid (SCM) inflammation, neck pain with neck movement, drooling of secretions, stridor, otalgia, headache, and vocal quality changes (2–7,19). Advanced infections may also extend down to the mediastinal area or present as facial cellulitis with closure of the eye indicating potential spread of infection to the periorbital spaces.

Imaging studies provide important information in identifying infection, discerning abscess versus edema, mass, or lymphadenopathy, guiding drainage procedures, and diagnosing complications. Computed tomography (CT) scanning with intravenous contrast is the most helpful and readily available advanced imaging study in most hospitals. Depending on the soft tissues involved, one should consider a maxillofacial CT with 1-mm cuts and/or a neck CT with intravenous contrast. MRI may be superior to CT in assessing the origin of infection and it is less prone to interference from dental artifacts. However most studies note that CT venography seems to be superior to MR venography in the identification of the cerebral venous sinuses and at least equivalent in the diagnosis of cerebral venous sinus thrombosis (1,2,5,9,11). Overall, CT remains the advanced imaging study of choice in most instances.

A lateral soft tissue radiograph of the neck may be a helpful screening tool for deep space infections since it may reveal a thickened prevertebral stripe, enlarged epiglottis, or soft tissue gas. However it gives little information on abscess, and CT is preferred. For patients with chest symptoms, a plain chest radiograph or a chest CT may be indicated to search for evidence of mediastinitis. For patients with evidence of cellulitis or phlegmon by CT but no definitive abscess, IV antibiotics alone are effective. Patients with Ludwig angina can develop complications including internal jugular thrombophlebitis, intracranial extension, and carotid hemorrhage. Findings on CT for sinusitis may include thickening of sinus walls, sclerosis, and perforation (12–16). Since most stones are radiopaque, CT is likely to demonstrate sialolithiasis and its infectious complications if present. The salivary gland demonstrates enlargement, hypodensity on precontrast scan, and avid postcontrast enhancement, with adjacent inflammatory stranding and fascial thickening. The salivary duct may be dilated and thick walled due to a stone obstructing the duct. MR imaging can display inflammation and edema, but is poor in detecting the actual stone. In Lemierre’s, CT scan with contrast demonstrates enlargement and thrombosis of the internal jugular vein, with enhancement of the walls of the vein and perivenular soft tissues.