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Deep neck space infections in adults

Deep neck space infections in adults
Author:
Anthony W Chow, MD, FRCPC, FACP
Section Editor:
Marlene L Durand, MD
Deputy Editor:
Milana Bogorodskaya, MD
Literature review current through: Dec 2022. | This topic last updated: Aug 04, 2022.

INTRODUCTION — Deep neck space infections most commonly arise from a septic focus of the mandibular teeth, tonsils, parotid gland, deep cervical lymph nodes, middle ear, or sinuses. These deep cervical space infections have become relatively uncommon in the post-antibiotic era. Consequently, many clinicians are unfamiliar with these conditions. In addition, with widespread use of antibiotics and/or profound immunosuppression, the classic manifestations of these infections, such as high fever, systemic toxicity, and local signs of erythema, edema, and fluctuance, may be absent.

Deep neck space infections often have a rapid onset and can progress to life-threatening complications [1]. Thus, clinicians must be aware of such infections and should not underestimate their potential extent or severity.

The relevant anatomy, microbial etiology, clinical manifestations, diagnosis, and treatment of certain deep neck space infections in adults will be reviewed here. Peritonsillar abscesses, submandibular space infections (Ludwig angina), and suppurative parotitis are discussed in detail separately:

(See "Peritonsillar cellulitis and abscess".)

(See "Ludwig angina".)

(See "Suppurative parotitis in adults".)

ANATOMIC CONSIDERATIONS — Knowledge of the cervical compartments and interfascial spaces is essential for understanding the pathogenesis, clinical manifestations, and potential routes of spread of infections involving these spaces.

Cervical fascia — The muscles, vessels, and visceral structures of the neck are enveloped by the cervical fascia, which has a superficial and deep component (figure 1). The superficial cervical fascia consists of the subcutaneous tissues of the neck, which completely enclose the head and neck and are continuous with the platysma anteriorly.

The deep cervical fascia has three layers: superficial, middle, and deep, which can be thought of as defining a series of cylindrical compartments that extend longitudinally from the base of the skull to the mediastinum (figure 1):

The superficial or investing layer of the deep cervical fascia encloses all of the deeper parts of the neck, beginning at the nuchal line and extending anteriorly, dividing to enclose the trapezius, sternocleidomastoid, and strap muscles, as well as the submaxillary and parotid glands.

The middle or pretracheal fascia encloses the cervical viscera including the pharynx, esophagus, larynx, trachea, thyroid, and parathyroid glands.

The deep or prevertebral fascia arises from the nuchal ligament and encloses the vertebral column and muscles of the spine. The prevertebral fascia originates posteriorly on the spinous processes and encircles the splenius, erector spinae, and semispinalis muscles (figure 1). Prior to completing its circle anterior to the vertebral bodies, it fuses to the transverse processes. At this point, it is split into two layers: the alar fascia anteriorly and the prevertebral fascia posteriorly.

All three layers of the deep cervical fascia contribute to the carotid sheath, which forms a neurovascular compartment that encloses the carotid artery, the internal jugular vein, and the vagus nerve.

Fascial spaces — There are three spaces between the planes of the deep cervical fascia that are of major clinical importance, the submandibular, parapharyngeal, and retropharyngeal spaces [2]:

Submandibular space – Mandibular anatomy is comprised of multiple potential spaces, including the submandibular, sublingual, and submental spaces [3].The submandibular space is bordered anteriorly by the mandible, superiorly by the mylohyoid muscle, inferiorly by the hyoid bone, medially by the anterior belly of the digastric muscles, and laterally by the mandible as well. The sublingual space is superior to the submandibular space and separated by the mylohyoid muscle. However, the posterior portions of the spaces are in communication with each other, which allows for the contiguous spread of infection within the fascial spaces (figure 2). Infection within the sublingual space results in gross swelling of the tongue that can result in acute airway obstruction. It is this space that is primarily involved in Ludwig angina.

Parapharyngeal space – Also known as the lateral pharyngeal or pharyngomaxillary space, the parapharyngeal space is located in the lateral aspect of the neck and is shaped like an inverted cone, with its base at the skull and its apex at the hyoid bone (figure 3). It lies deep to the pharyngeal constrictor muscle and is contiguous medially with the pretracheal fascia of the visceral compartment and laterally with the superficial fascia (which invests the parotid gland), the internal pterygoid muscle, and the mandible.

The parapharyngeal space is divided into an anterior (prestyloid or muscular) compartment and a posterior (retrostyloid or neurovascular) compartment by the styloid process and its attached muscles, the stylomandibular ligament, and the insertion of these structures into the hyoid bone (figure 3).

The anterior compartment contains no vital structures, only fat, lymph nodes, connective tissue, and muscle. It is the compartment most closely related to the tonsillar fossa and the internal pterygoid muscle. The posterior compartment contains the 9th to 12th cranial nerves superiorly and the 10th cranial nerve more inferiorly, the carotid sheath and its contents, and the cervical sympathetic trunk. The carotid sheath, which runs in the posterior aspect of the parapharyngeal space, pierces the cone at its apex to enter the mediastinum (figure 3).

Infection of the parapharyngeal space may result from pharyngitis, tonsillitis, parotitis, otitis, or mastoiditis, as well as odontogenic infections, especially if the masticator space is involved. (See "Complications, diagnosis, and treatment of odontogenic infections".)

Retropharyngeal space – The retropharyngeal space is bound anteriorly by the buccopharyngeal fascia, which closely surrounds the constrictor muscles of the neck, and posteriorly by the alar layer of the deep cervical fascia where they are adjoined at T1 or T2. It is situated behind the hypopharynx and the esophagus, and lies between the alar fascia posteriorly and the posterior aspect of the pretracheal fascia anteriorly (figure 1 and figure 4). It communicates with the parapharyngeal space laterally where the carotid sheaths reside.

Other spaces arising from the cervical fascia with potential for deep neck infections include: the "danger" space, the prevertebral space, the pre-tracheal space, the peritonsillar space, and the parotid space.

Danger space – Posterior to the retropharyngeal space is the danger space, which is bound by the alar fascia anteriorly and the prevertebral fascia posteriorly (figure 1 and figure 4). It extends from the base of the skull and descends freely through the entire posterior mediastinum to the level of the diaphragm (T11 to T12). Thus, the danger space provides the most important anatomic route for contiguous spread between the neck and the chest.

Prevertebral space – The prevertebral space is bound by the prevertebral fascia, which originates posteriorly on the spinous processes and encircles the splenius, erector spinae, and semispinalis muscles (figure 1 and figure 4). Prior to completing its circle anterior to the vertebral bodies, it fuses to the transverse processes. At this point, it is split into two layers: the alar fascia anteriorly and the prevertebral fascia posteriorly. The prevertebral space extends from the base of the skull to the coccyx, thus allowing organisms to spread as far down as the psoas muscle sheath.

Pretracheal space – The pretracheal space comprises the anterior portion of the visceral compartment and completely surrounds the trachea and esophagus (figure 1). It is contiguous with the carotid sheath laterally and with the superior mediastinum inferiorly.

Peritonsillar space – The peritonsillar space lies between the capsule of the palatine (faucial) tonsil medially, the superior constrictor muscle laterally, and the tonsillar pillars anteriorly and posteriorly (figure 5). A dreaded complication of a peritonsillar abscess (quinsy) is to rupture through the superior constrictor muscle and extend directly into the parapharyngeal space, which lies posterior to the tonsillar bed.

Parotid space – The parotid space is formed by the splitting of the investing fascia at the level of the stylomandibular ligament to enclose the parotid gland within a superficial capsule and a deep capsule (figure 6). The superficial capsule is thick and strong, tightly adherent to the superficial pole of the parotid gland. The deep capsule adjacent to the dorsal lobe of the parotid gland, however, is thin and infection in the gland can easily penetrate through this capsule and extend through the stylomandibular tunnel into the parapharyngeal space. The stylomandibular ligament effectively separates the parotid space from the submylohyoid space.

The masticator space, which lies lateral and anterior to the parapharyngeal space and consists of the masseteric, pterygoid, and temporal spaces, is described in detail elsewhere; infection of the masticator space arises most frequently from molar teeth, particularly the third molars (ie, wisdom teeth). (See "Complications, diagnosis, and treatment of odontogenic infections".)

Lymph nodes — The lymph nodes of the head and neck can be divided into 10 principal groups (figure 7). Six of these (occipital, mastoid, parotid, maxillary [facial], submandibular, and submental nodes) form a collar at the junction of the head and neck. Within this collar, the sublingual and retropharyngeal nodes lie near the base of the tongue. The anterior and lateral cervical nodes form a chain along the front and side of the neck, respectively. The lateral cervical chain serves as a common root for drainage. The final conduit from all lymphatics in the head and neck is the large deep chain situated along the carotid sheath. When inflamed, these nodes become adherent to the fascial sheath of the vessels; thus, a suppurative infection of the cervical lymph nodes may frequently invade the bloodstream.

In addition to the regional lymph nodes of the head and neck, both the nasopharynx and the oropharynx are richly endowed with mucosa-associated lymphoid tissues similar to the bronchus-associated lymphoid tissues and the gut-associated lymphoid tissues. In particular, the aggregation of lymphoid tissues surrounding the nasopharynx is known as Waldeyer's ring and comprises the palatine, lingual, adenoidal, and tonsillar lymphoid tissues. Acute inflammation involving these tissues, such as during acute tonsillopharyngitis, croup, otitis media, retropharyngeal abscess or Epstein-Barr virus mononucleosis, may result in acute airway compromise and constitutes a medical emergency [4,5].

Potential routes of spread — The deep cervical fascial spaces are normally bound together by loose connective tissue and intercommunicate to varied degrees. The potential pathways of extension from one space to another are illustrated in the accompanying figure (figure 8). A thorough understanding of the potential anatomic routes of infection not only provides valuable information on the nature and extent of infection but also suggests the optimal surgical approach for effective drainage.

COMMON CLINICAL CONCEPTS

Microbiology — Deep neck space infections are typically polymicrobial and represent the normal resident flora of the contiguous mucosal surfaces from which the infection originated. Due to the close anatomic relationships, the resident flora of the oral cavity, upper respiratory tract, and certain parts of the ears share many common organisms (figure 9) [6].

Although deep neck space infections are all caused by typical oral cavity flora, the specific organisms vary depending on the origin of the infection.

Odontogenic head and neck infections − Although as many as 50 to 100 bacterial species may be present on the oral mucosal surface, the typical deep neck space infection includes, on average, five or six bacterial types [7,8]. Anaerobes generally outnumber aerobes on all mucosal surfaces of the oral cavity by a factor of 10:1 [9]. Studies employing molecular techniques have demonstrated that the microbiome of odontogenic infections is extremely complex and routine clinical cultures are inadequate in fully characterizing the precise microbiology of these infections [10,11]. It is likely that these molecular methods will be incorporated into the routine clinical microbiology laboratory in the future.

In general, the most common organisms isolated from odontogenic deep neck space infections are viridans streptococci, reflecting their abundance in the mouth [12-15]. Streptococcus anginosus group (formerly called the Streptococcus milleri group) are types of viridans streptococcus that are part of the normal oral flora and are notorious for causing abscesses in the head and neck. Most abscesses originating from the teeth also harbor oral anaerobes, including Parvimonas micra (formerly Peptostreptococcus micros), other Peptostreptococcus species, Fusobacterium nucleatum, pigmented Prevotella species such as Prevotella melaninogenica (formerly Bacteroides melaninogenicus), and Actinomyces species [16-18].

Oropharyngeal infections − Infections arising from the pharynx frequently contain oral anaerobes and facultative streptococci, particularly Streptococcus pyogenes (see "Complications of streptococcal tonsillopharyngitis"). In a study of 847 patients with peritonsillar abscess, Fusobacterium necrophorum was the most commonly detected species (23 percent), followed by S. pyogenes (17 percent), and group C or G streptococci (5 percent) [19]. Haemophilus influenzae may also be a pathogen in parapharyngeal or retropharyngeal abscesses [20].

Otogenic head and neck infections − In addition to streptococci and obligate anaerobes, Staphylococcus aureus and facultative gram-negative rods, including Pseudomonas aeruginosa can be involved, as with chronic otitis media and mastoiditis [15,21]. (See "Chronic otitis media, cholesteatoma, and mastoiditis in adults".)

Sinogenic infections − Complications of suppurative sinusitis may involve the typical organisms that cause acute bacterial rhinosinusitis, such as Streptococcus pneumoniae, H. influenzae, Moraxella catarrhalis, and S. aureus (table 1) [16]. In addition, obligate anaerobes are commonly implicated in head and neck infections originating from chronic sinusitis [22]. (See "Acute sinusitis and rhinosinusitis in adults: Clinical manifestations and diagnosis", section on 'Acute bacterial rhinosinusitis'.)

Prevertebral space infections − Infections of the prevertebral space usually originate from contiguous spread of a cervical spine infection (such as discitis or vertebral osteomyelitis), by local instrumentation of the trachea or esophagus, or by hematogenous seeding. Thus, the microbiology of prevertebral space infections is quite different from that of retropharyngeal or odontogenic deep neck infections, and is discussed separately. (See 'Microbiology' below.)

P. aeruginosa and other drug-resistant organisms, such as extended-spectrum beta-lactamase-producing Enterobacteriaceae, may also be more likely in patients with certain risk factors. Immunocompromised hosts (eg, patients with chemotherapy-induced neutropenia) are particularly likely to harbor such pathogens, but those with diabetes mellitus, postoperative infection, or trauma are also at increased risk. Klebsiella pneumoniae has been frequently isolated from deep neck space infections in Taiwan, particularly from patients with diabetes mellitus. This species is a more common pathogen in various infections in Southeast Asia than in most other regions [23-25]. (See "Clinical features, diagnosis, and treatment of Klebsiella pneumoniae infection".)

General clinical features — Although the primary source of infection (ie, odontogenic versus oropharyngeal, otogenic, or sinogenic) determines the initial clinical presentation, deep neck space infections share some typical clinical features. They are often associated with sore throat and/or trismus (the inability to open the jaw). Trismus indicates pressure or infection affecting the muscles of mastication (the masseter and the pterygoids) or involvement of the motor branch of the trigeminal nerve. Dysphagia and odynophagia may be secondary to inflammation in several locations, including the cricoarytenoid joints. Because of the dense superficial layer of the deep cervical fascia and its musculofascial planes, a fluctuant mass is not readily appreciated by external palpation of patients with deep neck space infections. When possible, palpation of the oral cavity may instead help in identifying such a mass or focal tenderness. The characteristic signs of deep pus are pitting or a doughy feeling on firm deep palpation.

Stridor and dyspnea signify airway obstruction and may be manifestations of local pressure or spread of infection to the mediastinum. Dysphonia and hoarseness are late findings in neck infections and may indicate involvement of the 10th cranial nerve. Unilateral tongue paresis indicates involvement of the 12th cranial nerve.

Specific patient factors (such as comorbid disease, hospitalization, antecedent surgery or trauma, or immunocompromised state) can also impact the clinical presentation of deep neck space infections. As an example, in patients who have undergone radical neck surgery or radiation to the neck for cancer, diffuse cellulitis and lymphedema may be prominent clinical features. Similarly, in patients who have undergone tracheostomy and prolonged mechanical ventilation, a tracheo-esophageal fistula may develop with spread of infection into the mediastinum. Patients in the intensive care unit with prolonged internal jugular central venous catheters may develop suppurative thrombophlebitis of the internal jugular vein (variant of Lemierre syndrome).

Specific manifestations of the major deep neck space infections are discussed in greater detail below or in separate topic reviews. (See 'Prevertebral space infections' below and 'Parapharyngeal and retropharyngeal space infections' below and 'Other specific deep neck space infections' below.)

Clinical suspicion and urgent imaging — Any signs or symptoms suggesting a deep neck space infection should prompt urgent investigation with imaging studies to diagnose a deep neck space infection, identify the precise site of infection, and evaluate for potential spread. Such signs or symptoms include severe unilateral sore throat; bulging of the pharyngeal wall, soft palate, or floor of the oropharynx; neck pain or swelling; torticollis (wry neck) due to muscle spasm; stiff neck; presence of crepitus; or signs suggesting airway obstruction (eg, muffled voice, drooling or pooling of saliva, stridor, or other signs of respiratory distress). If airway obstruction is suspected, such patients should first be promptly assessed for intubation and possible surgical intervention. (See 'Airway management' below.)

Computed tomography (CT) is generally the imaging modality of choice to diagnose and evaluate the site and extent of deep neck space infections [26]. CT allows the critical evaluation of soft tissues and especially bone from a single exposure (image 1). In addition, the axial imaging format of CT is particularly well suited to the head and neck. Because CT can localize a process and define its extent, particularly extension into the mediastinum or the cranial vault, it is also an invaluable tool for planning and guiding aspiration for culture or open drainage.

Magnetic resonance imaging (MRI) is useful for assessing the extent of soft tissue involvement and for delineating vascular complications. In a study of 15 patients with deep neck space infections who underwent both CT and MRI, MRI was superior to CT for anatomic discrimination, lesion conspicuity, extension of the lesion, and number of spaces involved in odontogenic infections [27]. MRI was particularly helpful for patients in whom distinction between a mass lesion and the surrounding soft tissue structures is poor on CT. However, MRI takes significantly longer than CT to obtain good quality images, which may cause discomfort or claustrophobia [26]. In addition, individuals with certain implanted devices cannot undergo MRI. (See "Principles of magnetic resonance imaging".)

Additional imaging to evaluate the vasculature may be warranted in particular cases. As an example, CT angiography may be indicated if other imaging or clinical features suggest involvement of the neurovascular compartment within the carotid sheath [26].

Plain radiography is of limited utility for the evaluation of deep neck space infections; if performed, it is sometimes helpful for detecting retropharyngeal swelling or epiglottitis in lateral views of the neck [26]. Focused ultrasound, which determines the ratio of tongue thickness to oral cavity height, is a reliable method for assessing airway impairment and has been validated by comparison with CT scanning [28,29].

General management issues

Principles of antimicrobial therapy — Appropriate antibiotics in conjunction with surgical drainage of loculated infection are essential for a successful outcome of deep neck space infections. The primary pathologic finding in deep neck space infections is cellulitis that involves the connective tissues, fasciae, and muscles, and frequently undergoes necrosis. This necrotizing cellulitis results in a serosanguinous, putrid infiltration of the cervical tissues, usually with little or no frank pus present. During this stage of infection, treatment is primarily medical with antibiotics, directed at eradicating the causative microorganisms and preventing local or systemic spread of infection. Surgical drainage should be implemented only if the cellulitic process has localized into a discrete abscess. Premature incision into a cellulitic area may actually worsen the situation by breaking down the natural defenses and hastening the spread of infection.

Blood cultures should be obtained on all patients who present with a deep neck space infection regardless of whether fever is present.

Empiric regimens are based upon the expected microbiology and immune status of the host, and coverage should be narrowed if microbiologic data become available. The choice of antimicrobial regimens for the treatment of deep neck space infections has not been evaluated in clinical trials. Maximum doses of systemic antimicrobials should be administered in order to optimize tissue penetration.

Airway management — All patients with deep neck space infection should undergo an assessment for possible airway obstruction. For those who have evidence of airway impingement, maintenance of an adequate airway is a primary and urgent management issue. (See "Clinical presentation, diagnostic evaluation, and management of malignant central airway obstruction in adults".)

The use of glucocorticoids for symptomatic relief in nonallergic patients with head and neck infections remains controversial; the evidence regarding its benefits is too limited to support routine use of glucocorticoids for this purpose. However, a systematic review of the role of corticosteroids in cervicofacial infections suggested that short-term high-dose corticosteroids may be beneficial in some head and neck infections, particular in cases with impending airway obstruction [30]. (See "Peritonsillar cellulitis and abscess", section on 'Glucocorticoids'.)

PARAPHARYNGEAL AND RETROPHARYNGEAL SPACE INFECTIONS

Clinical presentation and complications

Parapharyngeal space infections — Since the clinical presentation may be dominated by the symptoms and signs of the primary source of infection, the diagnosis of parapharyngeal space involvement is often delayed. Dental infections are the most common underlying source, followed by peritonsillar abscess, and rarely parotitis, otitis, or mastoiditis (Bezold abscess).

Presenting clinical features – The cardinal clinical features of parapharyngeal space infections are similar to the general findings of deep neck space infection (see 'General clinical features' above) and consist of:

Trismus (ie, the inability to open the jaw)

Induration and swelling below the angle of the mandible

Medial bulging of the pharyngeal wall

Systemic toxicity with fever and rigors

Dyspnea can occur but is not prominent unless edema and swelling involve the epiglottis and larynx.

Findings on physical examination include swelling of the face and neck, erythema, and purulent oral discharge. Swelling and displacement of the parotid gland is usually seen. There may be pooling of saliva in the mouth and asymmetry of the oropharynx. Swelling of the pharyngeal wall, if present, will be behind the palatopharyngeal arch and is easily missed clinically. Lymphadenopathy is usually present.

These findings are prevalent with infection of the anterior compartment of the parapharyngeal space, which is more common than involvement of the posterior compartment. An abscess localized to the posterior neurovascular compartment of the parapharyngeal space may present with minimal trismus or pain and instead with sepsis and neurologic signs indicating cranial nerve involvement (eg, Horner syndrome, hoarseness, unilateral tongue paresis). The posterior tonsillar pillar may be displaced. Parotid gland swelling can occur with posterior compartment infection as well as anterior.

Complications – Parapharyngeal space infections are potentially life-threatening because of the possibility of involving the carotid sheath and its vital contents (eg, common carotid artery, internal jugular vein, vagus nerve), propensity for airway impingement, and bacteremic dissemination. Suppuration may also advance quickly to other spaces, particularly to the retropharyngeal and "danger" spaces, possibly reaching the mediastinum inferiorly or the base of the skull superiorly. (See 'Retropharyngeal space infections' below.)

Carotid sheath involvement – Involvement of the carotid sheath is a dreaded complication of parapharyngeal space infections because of the potential for carotid artery erosion and suppurative jugular thrombophlebitis [31]. The carotid sheath abuts all three layers of the deep cervical fascia. Thus, infection may arise by spread from the parapharyngeal space, submandibular space, or suppuration of the deep cervical lymph nodes [32].

There are no characteristic symptoms or signs of a carotid sheath infection. A history of sore throat is usually but not always present and may be mild or unilateral; there may be a latent period of up to three weeks before development of obvious manifestations of a deep neck space infection. The patient presents either in a toxic condition or insidiously with a fever of undetermined origin. Trismus is absent, and signs of local suppuration may be subtle initially because of the tight connective tissue around and within the carotid sheath. In some patients, there is diffuse swelling along the sternocleidomastoid muscle with marked tenderness and torticollis to the opposite side.

Carotid artery mycotic aneurysms have a mortality rate of approximately 20 percent [33]. Erosion of the carotid artery is a potentially devastating complication. This complication arises from an arteritis due to contiguous inflammation, resulting eventually in the formation of a false aneurysm, which may rupture. Erosion and rupture of the carotid artery may be heralded by recurrent small hemorrhages from the nose, mouth, or ear (ie, "herald bleeds"). This is followed by hematoma formation in the surrounding tissues, a protracted clinical course, and eventually the onset of shock due to exsanguination. Ligation of the carotid artery may be necessary in cases of major hemorrhage, but the mortality rate remains high, and the risk of stroke is significant [1]. (See "Overview of infected (mycotic) arterial aneurysm".)

Suppurative jugular thrombophlebitis – Suppurative jugular thrombophlebitis (also known as Lemierre syndrome or postanginal sepsis) should be suspected in patients with antecedent pharyngitis, septic pulmonary emboli, and persistent fever despite antimicrobial therapy. It is caused most commonly by F. necrophorum, which is often present in the bloodstream [34]. (See "Catheter-related septic thrombophlebitis".)

Retropharyngeal space infections

Presenting clinical features – The clinical features of a retropharyngeal space infection depend on the primary source of the infection. Sore throat, difficulty swallowing, or difficulty breathing can be prominent features when the infection is caused by local spread, which is usually secondary to penetrating trauma (eg, from chicken bones or following instrumentation of the esophagus or trachea). Fever and systemic toxicity may also be present. Examination of the oropharynx may demonstrate midline or unilateral swelling or bulging of the posterior pharyngeal wall. (See 'General clinical features' above.)

Retropharyngeal space infection can also spread from local extension of a parapharyngeal infection or from more distant infections (eg, odontogenic infections) by involvement of the retropharyngeal lymph nodes. In such cases, trismus may be prominent and prevent direct examination of the posterior pharyngeal wall. (See 'Parapharyngeal space infections' above.)

Complications – Retropharyngeal abscesses are among the most serious of deep space infections, since infection can extend directly into the anterior or posterior regions of the superior mediastinum, or into the entire length of the posterior mediastinum via the danger space (figure 1 and figure 4).

Acute necrotizing mediastinitis is the most feared complication of a retropharyngeal space infection. An infection in the "danger" space between the alar and prevertebral fasciae may drain by gravity into the posterior mediastinum, resulting in mediastinitis and empyema [35]. In the past, 70 percent of cases of mediastinitis were the result of infection spread in this manner. However, with the introduction of antibiotics, mediastinal extension has become uncommon, and most cases of acute mediastinitis result from esophageal perforation [36].

Clinically, the onset of acute necrotizing mediastinitis is rapid and is characterized by the following:

Widespread necrotizing process extending the length of the posterior mediastinum, occasionally into the retroperitoneal space

Rupture of mediastinal abscess into the pleural cavity with empyema or development of loculations

Pleural or pericardial effusions, frequently with tamponade

The mortality of acute necrotizing mediastinitis in adults is high (25 percent), even when appropriate antibiotics are administered.

Aspiration pneumonia is another potential complication of retropharyngeal space infection [37]. Pneumonia may result from impairment of swallowing or spontaneous rupture of the abscess into the airway. (See "Aspiration pneumonia in adults".)

Diagnosis — The diagnosis of a parapharyngeal or retropharyngeal space infection is suspected based on clinical presentation and established by imaging (typically computed tomography [CT]) (see 'Clinical suspicion and urgent imaging' above). In addition to imaging, blood cultures should be obtained on all patients with a parapharyngeal or retropharyngeal space infection regardless of whether fever is present to identify potential pathogens.

General CT findings of deep neck space infections include loss of definition between the anatomic spaces in the neck, stranding in the subcutaneous tissues (image 2), tissue enhancement, and frank abscess formation [38]; the location of the findings indicates whether it is a parapharyngeal or retropharyngeal space infection (image 1).

Occasionally, necrotic lymph nodes (eg, from malignant metastatic disease) can be similar in appearance to an abscess on CT (peripheral enhancement with central low attenuation); in such cases magnetic resonance imaging (MRI) can be helpful to differentiate the two [38].

Although CT or MRI is preferred over plain radiographs, certain findings from a plain radiograph, if performed, can also suggest a retropharyngeal space infection. These include increased thickness of the prevertebral soft tissues, air or air-fluid levels, and foreign bodies. There may be cervical lordosis with swelling and gas collections in the retropharyngeal space causing anterior displacement of the larynx and trachea (image 3). In the presence of a retropharyngeal space infection, the pharynx or upper airway is displaced anteriorly by more than one-half the width of the fourth cervical vertebral body (C4; normally, the soft tissues of the posterior wall of the hypopharynx are about 5 mm deep, less than one-third the diameter of C4). Focused ultrasound measuring the tongue thickness to oral cavity height ratio is a reliable method of assessing airway impairment [28].

Longus colli tendinosis due to deposition of calcium hydroxyapatite crystals in the longus colli tendons can elicit an inflammatory response and mimic an infectious process in the retropharyngeal space. However, the fluid collection is noninfectious in nature, and typical CT findings include calcification within the tendon and a simple fluid collection without peripheral enhancement [39]. (See 'Prevertebral space infections' below.)

Treatment

Indications and methods for drainage — For patients who have a dental source of infection, we recommend early removal of that source [40]. Additional initial decisions on drainage for parapharyngeal or retropharyngeal space infections depend upon whether local suppuration has developed or whether only the initial phase of diffuse cellulitis is present. Abscess formation is often difficult to determine clinically but can be identified on imaging studies. This differentiation is important because drainage should be delayed in the cellulitis stage, whereas loculated abscesses should be drained. (See 'Principles of antimicrobial therapy' above.)

Open surgical drainage has been the traditional approach to abscess management. For patients with well-defined deep neck space infections without airway compromise, ultrasound-guided needle aspiration is an effective alternative and is associated with decreased hospital stay and improved cost savings [41,42]. In retropharyngeal space infection complicated by acute necrotizing mediastinitis, surgical drainage of the mediastinum is required and may be performed by either the cervico-mediastinal or the transthoracic approach. Although the cervical approach may be effective in early mediastinitis, thoracotomy is generally indicated once the necrotizing process has entered the "danger" space.

Endoscopic drainage is contraindicated owing to the proximity of the great vessels.

Antibiotic therapy

Community-acquired infection — Initial empiric antimicrobial treatment of parapharyngeal or retropharyngeal space infections in immunocompetent patients with community-acquired infections depends in part on the probable site of origin of the infection:

For immunocompetent patients with a probable oral or odontogenic (ie, from the teeth) source, we suggest a regimen that has activity against streptococci (including clindamycin-resistant viridans streptococci), H. influenzae, and anaerobic bacteria (see 'Microbiology' above). We do not routinely include coverage against methicillin-resistant S. aureus (MRSA), but do so if there are risk factors for MRSA infection or colonization, as below.

Example empiric regimens include:

Ampicillin-sulbactam (3 g intravenously [IV] every six hours) or

Ceftriaxone (2 g IV every 24 hours) or levofloxacin (750 mg IV every 24 hours)

plus

Metronidazole (500 mg IV every eight hours) or clindamycin (600 mg IV every eight hours)

For immunocompetent patients with a probable otogenic (ie, from the ear or mastoids) source, we suggest a regimen that has activity against streptococci (including clindamycin-resistant viridans streptococci), H. influenzae, and anaerobic bacteria as well as facultative gram-negative coverage, including P. aeruginosa (see 'Microbiology' above). We do not routinely include coverage against MRSA, but do so if there are risk factors for MRSA infection (table 2) or colonization.

Example empiric regimens include:

Cefepime (2 g IV every 8 hours) plus metronidazole (500 mg IV every eight hours) or

Piperacillin-tazobactam (4.5 g IV every six hours)

Imipenem (1 g IV every six hours) or meropenem (2 g IV every eight hours)

For immunocompetent patients with a probable sinogenic (ie, from the sinuses) source, we suggest a regimen that has activity against S. pneumoniae, M. catarrhalis, S. aureus (including MRSA), and anaerobic bacteria. (See 'Microbiology' above.)

Example empiric regimens include:

Vancomycin (table 3) plus ampicillin-sulbactam (3 g IV every six hours) or

Vancomycin (table 3)

plus

Ceftriaxone (2 g IV every 24 hours) or levofloxacin (750 mg IV every 24 hours)  

plus

Metronidazole (500 mg IV every eight hours) or clindamycin (600 mg IV every eight hours)

As above, we include coverage against MRSA for infections of oral/odontogenic or otogenic source when the patient has risk factors for MRSA infection or colonization and for infections of sinogenic source. This is usually achieved with the addition of vancomycin (table 3) or linezolid (600 mg orally or IV every 12 hours) to the regimen.

The antibiotic doses are intended for patients with normal renal function; dosing of many of these agents must be reduced in patients with renal dysfunction.

Empiric antibiotic therapy can be adjusted once culture results are available. (See 'Directed therapy and duration' below.)

Health care-associated infection or immunocompromised host — For patients who are immunocompromised or have a health care-associated infection (eg, residents of long-term care facilities, those with recent hospitalization), we suggest a broad-spectrum regimen that provides coverage against MRSA and P. aeruginosa, in addition to other gram-positive and gram-negative aerobes and anaerobes (see 'Microbiology' above). Examples include:

Vancomycin (table 3) or linezolid (600 mg IV every 12 hours) plus one of the following:

Cefepime (2 g IV every 8 hours) plus metronidazole (500 mg IV every eight hours) or

Imipenem (1 g IV every six hours) or

Meropenem (2 g IV every eight hours) or

Piperacillin-tazobactam (4.5 g IV every six hours)

The antibiotic doses are intended for patients with normal renal function; dosing of many of these agents must be reduced in patients with renal dysfunction.

Empiric antibiotic therapy can be adjusted once culture results are available. (See 'Directed therapy and duration' below.)

Directed therapy and duration — Antibiotic therapy can be adjusted to a narrower regimen if informative culture results are available; however, anaerobic coverage is generally maintained even if anaerobes are not isolated. Therapy should generally be continued for two to three weeks until fever and leukocytosis have resolved and local tenderness and swelling have subsided. Longer courses may be warranted when complications involving bone or vascular structures are present.

We generally favor intravenous antibiotics for the entire duration of treatment; however, antibiotics that have excellent oral bioavailability, such as linezolid, levofloxacin, and metronidazole, may be administered orally once the patient is improving, provided absorption is normal.

Other management issues — In patients who are recovering, it is important to restrict all oral intake until any swallowing impairment, which may have a prolonged course, has resolved completely.

PREVERTEBRAL SPACE INFECTIONS

Microbiology — The microbiology of prevertebral space infections is quite different from that of other deep neck infections. Infections of the prevertebral space usually originate from contiguous spread of a cervical spine infection (such as discitis or vertebral osteomyelitis), by local instrumentation of the trachea or esophagus, or by hematogenous seeding. There is a predominance of gram-positive organisms, the most common being S. aureus. Less common organisms include various facultative gram-negative bacilli (including P. aeruginosa), mycobacteria, and fungi.

One study of cervical osteomyelitis and prevertebral abscess occurring in 14 injection drug users found that S. aureus caused 71 percent of cases, while coagulase-negative staphylococci (14 percent), viridans streptococci (7 percent), and Pseudomonas (7 percent) caused the remaining cases [43]. Methicillin-resistant S. aureus (MRSA) is an increasingly common cause of vertebral osteomyelitis, particularly in patients with risk factors for MRSA colonization. Injection drug users, for example, have a 16-fold higher incidence of invasive MRSA infections of any type than non-users [44].

Risk factors — Risk factors of prevertebral space infections are essentially the same as those for vertebral osteomyelitis. Specifically, intravenous drug use, immunosuppression, alcohol use disorder, and diabetes mellitus are known risk factors [45,46]. (See "Vertebral osteomyelitis and discitis in adults", section on 'Epidemiology'.)

Clinical presentation and complications — The clinical manifestations of prevertebral space infections vary, depending on location of the primary source of infection (eg, cervical spondylodiscitis and osteomyelitis) and whether there is associated spinal epidural abscess or cord compression. In one small series of 11 patients, the most common presenting signs and symptoms were neck pain (100 percent), odynophagia (54 percent), dysphagia (36 percent), neck rigidity (36 percent), fever (27 percent), and back pain (9 percent) [47].

Physical examination of the oropharynx can reveal a bulge in the posterior pharyngeal wall in some patients. Examination of the cervical spine may also demonstrate swelling or erythema.

Complications of prevertebral space infections are mainly related to spinal epidural collections that cause cord compression. Among patients with spinal epidural abscess, approximately one-third have neurologic deficits ranging from nerve root pain to paralysis [48].

Irreversible paralysis has been reported to occur in 4 to 22 percent of patients with spinal epidural abscess. Spread of infection to or from the disc or vertebrae may cause local destruction with mechanical instability of the spine. (See "Spinal epidural abscess", section on 'Prognosis'.)

Since the prevertebral space extends from the base of the skull down to the coccyx and is contiguous with the psoas muscle sheath, seemingly distant abscesses can form within the psoas muscle in a patient who has a prevertebral space infection [49]. A cervical prevertebral space infection presumed secondary to upward spread from an infected pancreatic pseudocyst has also been reported [50].

Diagnosis — The diagnosis of a prevertebral space infection is made by characteristic findings on imaging in patients with symptoms of deep neck space infection (see 'Clinical suspicion and urgent imaging' above) or suspected cervical osteomyelitis. In addition to imaging, blood cultures should be obtained on all patients with a paravertebral space infection regardless of whether fever is present to identify potential pathogens.

In prevertebral space infections, enhancing phlegmon or abscess can be visualized in the prevertebral space [26]. Imaging also often demonstrates associated spondylodiscitis or vertebral osteomyelitis.

Management — Treatment of prevertebral space infections consists of expeditious drainage of any abscess and broad-spectrum antibiotics.

Drainage — Drainage should be attempted on all prevertebral space infections in which there is a clear abscess or loculated fluid collection. Ultrasound-guided percutaneous drainage is an effective and safe alternative to traditional surgical incision and drainage for some patients [42].

In the case of prevertebral space infection associated with cervical osteomyelitis, debridement of necrotic bone may also be warranted. (See "Vertebral osteomyelitis and discitis in adults", section on 'Surgery'.)

Antibiotic therapy

Initial regimen selection — For patients with prevertebral space infections, we suggest an initial antibiotic regimen that has activity against S. aureus (including MRSA), gram-negative bacilli, and anaerobes (see 'Microbiology' above). Examples include:

Vancomycin (table 3) plus one of the following:

-Cefepime (2 g IV every 8 hours) plus metronidazole (500 mg every eight hours) or

-Piperacillin-tazobactam (4.5 g IV every six hours) or

-Ciprofloxacin (400 mg IV every 12 hours) plus metronidazole (500 mg IV every eight hours)

Linezolid (600 mg IV every 12 hours) or daptomycin (6 mg/kg IV every 24 hours) are other MRSA-active agents that can be substituted for vancomycin in patients intolerant of vancomycin; IV linezolid is preferred initially but may be substituted with oral therapy if the clinical condition stabilizes.

For patients with health care-associated infections or with risk factors for infection with an extended-spectrum beta-lactamase-producing organism, empiric treatment with a MRSA-active agent (eg, vancomycin) plus a carbapenem (imipenem 1 g IV every six hours or meropenem 2 g IV every eight hours) is appropriate.

We include coverage for anaerobes (eg, adding metronidazole to cefepime or ciprofloxacin) during early empiric therapy because of the potential uncertainty of a prevertebral versus retropharyngeal infection or the possibility of extension of a prevertebral space infection from a retropharyngeal site. Once it is established that a prevertebral space infection is related to vertebral osteomyelitis, continuation of specific anaerobic coverage is not routinely necessary. (See "Vertebral osteomyelitis and discitis in adults", section on 'Empiric therapy'.)

The antibiotic doses below are intended for patients with normal renal function; dosing of many of these agents must be reduced in patients with renal dysfunction.

Directed therapy and duration — Antibiotic therapy can be adjusted to a narrower regimen if informative culture results are available. For uncomplicated prevertebral space infections without evidence of discitis or osteomyelitis, two to three weeks of therapy is likely adequate. However, most prevertebral space infections are due to spread of infection from discitis or vertebral osteomyelitis, in which case a longer duration of therapy is typically recommended [51]. (See "Vertebral osteomyelitis and discitis in adults", section on 'Duration of therapy and follow-up'.)

We generally favor intravenous antibiotics for the entire duration of treatment; however, antibiotics that have excellent oral bioavailability, such as linezolid, ciprofloxacin, and metronidazole, may be administered orally once the patient is improving, provided absorption is normal.

OTHER SPECIFIC DEEP NECK SPACE INFECTIONS

Peritonsillar abscess (quinsy) — Peritonsillar abscess, also known as quinsy, is a suppurative complication of acute tonsillitis with extension into the peritonsillar space. The latter consists of loose areolar tissue overlying the tonsil and is surrounded by the superior pharyngeal constrictor muscle and the anterior and posterior tonsillar pillars. Peritonsillar abscesses may affect patients of all ages but are most common among young adults between 15 and 30 years of age. The infection begins as a cellulitis and progresses to abscess formation, most commonly near the superior pole of the tonsil. Patients complain of high fever, odynophagia, unilateral sore throat, and otalgia. Classic signs include a muffled voice, trismus, unilateral deviation of the uvula towards the unaffected side, and soft palate fullness or edema. The oral airway may be compromised, and drooling may occur. Peritonsillar abscesses are often polymicrobial. The predominant bacterial species are S. pyogenes (group A streptococcus), Streptococcus anginosus group, and oral anaerobes such as Fusobacterium necrophorum. Peritonsillar abscess is discussed in greater detail separately. (See "Peritonsillar cellulitis and abscess".)

Parotid space infections — Acute suppurative parotitis is characterized by the sudden onset of unilateral induration and erythema that extends from the cheek to the angle of the jaw. The parotid gland becomes swollen and extremely tender. Purulent discharge may be expressed by gentle compression around the orifice of the parotid duct (Stensen's duct). Although a stone obstructing the salivary duct may predispose to bacterial infection, inspissated secretions and/or stasis are more common predisposing features. Three factors that predispose to suppurative parotitis are acutely diminished salivary flow, poor oral hygiene, and increased susceptibility to infection [52]. Thus, acute suppurative parotitis is typically seen in older, debilitated, and/or dehydrated patients who may be diabetic or taking anticholinergic medications that decrease salivary flow.

The microbiology of acute suppurative parotitis is quite variable and is often polymicrobial. S. aureus is by far the most frequently isolated pathogen, but anaerobes are also common. Acute suppurative parotitis is discussed in more detail elsewhere. (See "Suppurative parotitis in adults".)

Ludwig angina — Ludwig angina is a bilateral infection of the submandibular, sublingual, and submental spaces that begins in the floor of the mouth, most commonly related to the second or third mandibular molar teeth. It is typically a polymicrobial infection involving the flora of the oral cavity (table 4) [53]. It is an aggressive, rapidly spreading "woody" or brawny cellulitis without lymphadenopathy (picture 1). Airway compromise is a potential complication and requires careful monitoring and rapid intervention to prevent asphyxia and aspiration pneumonia [54]. Ludwig angina is discussed in greater detail separately. (See "Ludwig angina".)

Pretracheal space infections — Pretracheal space infections most commonly arise as a consequence of perforation of the anterior esophageal wall, occasionally through contiguous extension from a retropharyngeal space infection, or as a consequence of prolonged tracheostomy [55]. The clinical presentation is characterized by severe dyspnea, but hoarseness may be the first complaint. Swallowing may be difficult, and fluids may be regurgitated through the nose. A pretracheal space infection is always serious because of impending airway obstruction and possible extension into the mediastinum. Prompt surgical drainage is critical to prevent such complications.

SUMMARY AND RECOMMENDATIONS

Overview – Deep neck space infections most commonly arise from a septic focus of the mandibular teeth, tonsils, parotid gland, deep cervical lymph nodes, middle ear, or sinuses. Since these infections often have a rapid onset and may progress to life-threatening complications, clinicians must be aware of such infections and should not underestimate their potential extent or severity. (See 'Introduction' above.)

Anatomy – The deep cervical fascia has three layers, superficial, middle, and deep, which can be thought of as defining a series of cylindrical compartments that extend longitudinally from the base of the skull to the mediastinum (figure 1). This anatomy informs potential routes of spread of infections involving these spaces. (See 'Anatomic considerations' above and 'Potential routes of spread' above.)

Microbiology – Deep neck space infections are typically polymicrobial and represent the normal resident flora of the contiguous mucosal surfaces from which the infection originated. The most common organisms isolated from oral or odontogenic sources of infection are streptococci, in particular viridans streptococci, reflecting their abundance in the mouth. Most abscesses originating from the teeth or throat also harbor oral anaerobes. Haemophilus influenzae may also be a pathogen. Infections of otogenic or sinogenic source have slightly different microbiology. (See 'Microbiology' above.)

Clinical features – Clinical features of deep neck space infections depend on the site of infection and generally include severe neck or throat pain and swelling with fever and systemic toxicity. In parapharyngeal and retropharyngeal infections, bulging of the pharyngeal wall may be observed. Complications include carotid sheath involvement with parapharyngeal space infections, extension into the mediastinum with retropharyngeal space infections, and spinal epidural abscesses with prevertebral space infections associated with cervical osteomyelitis. (See 'General clinical features' above and 'Parapharyngeal and retropharyngeal space infections' above and 'Prevertebral space infections' above.)

Diagnosis – Patients with suspected deep neck space infections should undergo prompt imaging to confirm the diagnosis (image 2 and image 1), identify the precise site of infection, and evaluate for potential spread. Computed tomography (CT) is the imaging modality of choice. Magnetic resonance imaging (MRI) is useful for assessing the extent of soft tissue involvement and for delineating vascular complications. (See 'Clinical suspicion and urgent imaging' above and 'Parapharyngeal and retropharyngeal space infections' above and 'Prevertebral space infections' above.)

Management – Management of deep neck space infections includes antibiotic therapy and aspiration or surgical drainage of loculated collections. Empiric antibiotic regimen selection depends upon the source of infection and certain patient features. (See 'Principles of antimicrobial therapy' above.)

Parapharyngeal and retropharyngeal infections – Among those with parapharyngeal and retropharyngeal infection, we suggest the following empiric coverage. Regimen examples are found above. Antibiotic therapy can be adjusted to a narrower regimen if informative culture results are available (although anaerobic coverage is generally maintained even if anaerobes are not isolated). Duration of therapy is generally two to three weeks, but complications may warrant longer courses. (See 'Antibiotic therapy' above.)

-For immunocompetent patients with a community-acquired infection and a probable oral or odontogenic source, we suggest an empiric regimen with activity against streptococci (including clindamycin-resistant viridans streptococci), H. influenzae, and anaerobic bacteria (Grade 2C).

-For immunocompetent patients with a community-acquired infection and a probable otogenic source, we suggest an empiric regimen with activity against streptococci (including clindamycin-resistant viridans streptococci), H. influenzae, and anaerobic bacteria, as well facultative gram-negative bacilli, including Pseudomonas aeruginosa (Grade 2C).

-For immunocompetent patients with a community-acquired infection and a probable sinogenic source, we suggest a regimen that has activity against Streptococcus pneumoniae, Moraxella catarrhalis, Staphylococcus aureus (including methicillin-resistant S. aureus [MRSA]), and anaerobic bacteria (Grade 2C).

-For immunocompromised patients or those with a health care-associated infection, we suggest an empiric broad-spectrum regimen with activity against MRSA and P. aeruginosa in addition to other gram-positive and gram-negative aerobes and anaerobes (Grade 2C).

Prevertebral space infections – Infections of the prevertebral space usually originate from contiguous spread of a cervical spine infection (such as discitis or vertebral osteomyelitis), by local instrumentation of the trachea or esophagus, or by hematogenous seeding. S. aureus is the most common pathogen; others include streptococci, gram-negative bacilli, including P. aeruginosa, and anaerobes. For initial treatment of patients with prevertebral space infections, we suggest an antibiotic regimen that has activity against S. aureus (including MRSA), gram-negative bacilli, and anaerobes (Grade 2C). Duration of therapy of isolated prevertebral space infection is usually two to three weeks but is longer if osteomyelitis is also present. (See 'Prevertebral space infections' above.)

Other deep neck space infections – Management of other deep neck space infections, including peritonsillar abscess, parotid space infections, and submandibular space infections, are discussed in detail elsewhere. (See "Peritonsillar cellulitis and abscess" and "Suppurative parotitis in adults" and "Ludwig angina".)

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