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Infections of Deep Neck Spaces
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Infections of Deep Neck Spaces Blake W. Hansen MD , Stanislav Ryndin DO , Katherine M. Mullen MD PII: DOI: Reference:
S0887-2171(19)30064-2 https://doi.org/10.1053/j.sult.2019.10.001 YSULT 890
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Seminars in Ultrasound CT and MRI
Please cite this article as: Blake W. Hansen MD , Stanislav Ryndin DO , Katherine M. Mullen MD , Infections of Deep Neck Spaces, Seminars in Ultrasound CT and MRI (2019), doi: https://doi.org/10.1053/j.sult.2019.10.001
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Title: Infections of Deep Neck Spaces Authors: 1. Blake W. Hansen, MD ([email protected]) 2. Stanislav Ryndin, DO ([email protected]) 3. Katherine M. Mullen, MD ([email protected]) Authors Affiliation: UMMS-Baystate Radiology 759 Chestnut Street Springfield, MA 01199 USA Corresponding Author: Blake W. Hansen, MD ([email protected]) Abstract: Identifying infections of the deep neck spaces and understanding how they spread can be a diagnostic challenge that is complicated by complex anatomy and far-reaching clinical implications. Deep neck infections have the potential to quickly spread throughout the neck and chest, leading to widespread disease that can be rapidly fatal and resistant to treatment. This article provides a foundation for evaluating deep neck infections through a review of essential anatomy and a discussion of important diseases that interact with these spaces.
Keywords: Sialadenitis, Ludwig Angina, Lemierre Syndrome, Peritonsillar abscess, Odontogenic Abscess
Infections of Deep Neck Spaces Identifying infections of the deep neck spaces and understanding how they spread can be a diagnostic challenge that is complicated by complex anatomy and far-reaching clinical implications. Deep neck infections have the potential to quickly spread throughout the neck and chest, leading to widespread disease that can be rapidly fatal and resistant to treatment. Appropriate diagnosis of deep neck space infections involves first identifying the correct anatomic location as this will provide clues to the origin of the disease, determine which structures are at risk, and guide treatment. Secondly, deep spaces that communicate with the area of infection should be closely evaluated to rule out additional spread of disease and to expand the differential diagnosis as prominent areas of infection may be sequelae of a more subtle primary infection. Equipped with an understanding of which deep neck spaces are involved and how they interact, a more accurate evaluation of potential etiologies, clinical risks and appropriate treatment can be formulated. In this article, we provide a foundation for evaluating deep neck infections through a review of essential anatomy and a discussion of important diseases that interact with these spaces.
Deep Neck Anatomy The deep neck spaces are primarily divided by the layers of the deep cervical fascia and are commonly organized by suprahyoid and infrahyoid spaces (specifically the superficial layer, middle layer, and deep layer of the deep cervical fascia). Different deep neck spaces are susceptible to different pathologies and the spread of disease is constrained by the fascial layers. Understanding the anatomy of the deep neck spaces allows the likely path of spread and potential origin of disease to be determined and more closely evaluated (Figure 1).
Spaces of the Suprahyoid Neck Oral Mucosal and Pharyngeal Mucosal Spaces The oral mucosal and pharyngeal mucosal spaces are not true fascia-enclosed spaces, but rather continuous sheets of suprahyoid mucosa that are typically included to allow for a complete spatial mapping of the suprahyoid neck. The oral mucosal space extends from the lips to the circumvallate papillae and the posterior border of the hard palate and contains minor salivary glands and mucosal surface tissue, including the buccal mucosa lining the cheeks and lips, hard palate, and anterior two thirds of the tongue. The pharyngeal mucosal space is composed of the nasopharynx, oropharynx, and hypopharynx. Important contents include the pharyngeal mucosal surface, Waldeyer’s lymphatic ring (adenoids, palatine tonsils, and lingual tonsils), minor salivary glands, muscle, and the torus tubarius (cartilaginous end of the eustachian tube).[1] Asymmetry of the pharyngeal mucosal space is common and does not necessarily indicate pathology.[1] However, tonsillar and peritonsillar abscesses are common infections of this space, which may then spread to the nearby parapharyngeal, masticator, and submandibular spaces.[2]
Parapharyngeal Space (Prestyloid) The parapharyngeal space is a suprahyoid region extending from the skull base to the superior cornua of the hyoid bone. It is bounded by the pharyngeal mucosal space medially and the superficial layer of the deep cervical fascia laterally. Posteriorly, it is bounded by both the carotid sheath and buccopharyngeal fascia (middle layer of the deep cervical fascia). It contains fat, minor salivary glands, the internal maxillary artery, ascending pharyngeal artery, and part of the pterygoid venous plexus.[1] The suprahyoid component of the carotid space is sometimes included in the anatomic description of the parapharyngeal space and referred to as the poststyloid parapharyngeal space, with the anterior region (referred to here as the parapharyngeal space) delineated using the term prestyloid parapharyngeal space. In this article, the suprahyoid component of the carotid space is included in the carotid space section below. Most parapharyngeal space lesions spread from adjacent spaces. Primary parapharyngeal space lesions are rare.[1] Infections typically spread to the parapharyngeal space from the pharyngeal mucosal space, masticator space, parotid space, and carotid space. Inferiorly, there is no fascia separating the submandibular space from the parapharyngeal space, allowing parapharyngeal disease to spread to the submandibular space. The most common infections of this space include tonsillar and peritonsillar abscesses.[2]
Peritonsillar abscess Peritonsillar abscess (PTA) is the most common infection of the deep head and neck. Most cases are sequelae of chronic or recurrent bacterial tonsillitis, leading to abscess in the parapharyngeal space or pharyngeal mucosal space. It is most common in patients 20 - 40 years of age, without predilection to gender. Although occurrence in children is relatively rare, PTA has an increased risk for airway obstruction in a pediatric population as compared to adults. Patients may present with odynophagia, voice changes, trismus, drooling, dysphagia, and systemic symptoms such as fever, chills, and malaise.[3] Each palatine tonsil is bordered by the palatoglossal arch anteriorly and palatopharyngeal arch posteriorly, and is covered by a fibrous capsule laterally. Peritonsillar abscesses tend to form between the tonsil and the fibrous capsule, with potential to spread to surrounding structures.[3] The most commonly used and most practical modality for evaluation of tonsillar pathology is computed tomography, (CT), which will typically show fluid density with peripheral enhancement adjacent to an inflamed tonsil (Figure 2). CT is considered 100% sensitive for identification of PTA.[4] However, it is only 75% specific as approximately 25% of cases with the aforementioned characteristics will be phlegmonous, and therefore non-drainable.[5] Ultrasonographic evaluation for PTA is used less frequently due to its limitations with patient body habitus, operator skill and a relatively limited assessment of surrounding structures. Advantages of ultrasonography include lack of ionizing radiation and the ability to guide aspiration if performed by a physician or qualified mid-level provider. Most commonly, the tonsil is evaluated by inserting an endocavity ultrasound probe intraorally with the help of a tongue blade, as this position often allows for abscess aspiration. Alternatively, a high-frequency probe may be positioned in the submandibular region and directed superiorly. An abscess is seen as a hypoechoic or anechoic focus with lowlevel internal echoes, which sometimes has a relatively hyperechoic periphery and increased peripheral vascularity on color Doppler.[6]
Masticator Space The masticator space is a paired suprahyoid region bounded by the superficial layer of the deep cervical fascia, extending from the top of the parietal bone to the inferior mandible. This space contains muscles of mastication, the posterior body and ramus of the mandible, trigeminal nerve (CN V3), and maxillary artery.[1] Most masticator space infections originate from odontogenic infection, leading to cellulitis, phlegmon, or abscess. Consequently, when a masticator space infection is identified, special attention should be given to imaging of the oral space as the infected teeth will need to be identified and treated to prevent recurring infection. [2] Masticator space infections tend to spread to adjacent spaces, including the sublingual space (which runs along the medial body of the mandible), buccal space, parotid space, and parapharyngeal space.[7]
Odontogenic Masticator Space Abscess Odontogenic masticator space abscesses begin with mandibular molar infections or dental manipulation, followed by trismus and nonspecific signs of infection such as fever, leukocytosis, and tenderness. [2] As they grow, they have the ability to spread to the sublingual space, parapharyngeal space, parotid space, and beyond.[7] Masticator space abscesses are best evaluated with contrast-enhanced CT, allowing evaluation of pyogenic collections in the soft tissues, molar tooth erosion, mandibular osseous changes, and related signs of inflammation (see Figures 3-4). Cortical destruction of the mandible with periosteal elevation suggests mandibular osteomyelitis. A masticator space abscess will present with a focal fluid-density collection in the muscles of mastication and
compression of the parapharyngeal space from anterolateral to posteromedial. Other differential considerations include cellulitis, phlegmon, and myositis.[2] Treatment of masticator space abscesses begins with extraction of the decayed molar, eliminating the source of the infection. From this point, treatment depends on the extent of the infection. If diagnosed early, aggressive IV antibiotics may be sufficient; however, most patients will require both IV antibiotics and surgical drainage. If mandibular osteomyelitis has developed, placement of a subperiosteal drain and prolonged IV antibiotics may be needed.[2]
Parotid Space The parotid space is a paired suprahyoid region located posterior to the masticator space, bounded by the superficial layer of the deep cervical fascia and extending from the external auditory canal or mastoid tip to the parotid tail (inferior to the angle of the mandible). Its contents include parotid glands, intraparotid lymph nodes, the extracranial facial nerve (CN VII), external carotid artery, retromandibular vein, parotid duct, and accessory parotid glands.[1] Potential infections found in the parotid space include acute or chronic parotitis (sialadenitis) (Figure 5), reactive lymphadenopathy, and necrotizing lymphadenopathy.[2] See the submandibular section for additional information regarding sialadenitis.
Submandibular / Submaxillary Space The submandibular space, also known as the submaxillary space, is a horseshoe-shaped suprahyoid region with lateral components that communicate posteriorly. It is bounded by mylohyoid sling and platysma muscle, extending from the mylohyoid sling to the hyoid bone. It contains the submandibular glands, level I lymph nodes, the caudal loop of CN XII, anterior belly of digastric muscles, facial vein, and sometimes includes the tail of the parotid gland.[1] Infections in the submandibular space often spread to the contralateral submandibular space, sublingual space, along the styloglossus muscle into the parapharyngeal space, and through loose areolar tissue into the retropharyngeal space (Figure 6). Common infections include submandibular space sialadenitis with ductal calculus, diving ranula, and reactive or suppurative adenopathy. This is also one of the spaces that may be involved in potentially life threatening Ludwig angina.[1] See the sublingual section for additional information regarding Ludwig angina.
Sialadenitis Sialadenitis, or inflammation of salivary glands, is a multi-cause process which may be acute or chronic. Acute sialadenitis most commonly occurs secondary to a bacterial infection in the setting of sialolithiasis and less commonly may be due to viruses, dehydration, and pharmaceuticals. Bilateral parotitis in pediatric population is seen in mumps. Chronic sialadenitis may be due to autoimmune conditions such as Sjogren and Mikulicz syndrome, but is also frequently associated with sialolithiasis.[8] Other causes of salivary gland inflammation may be due to iodine-131 administration and post-radiation.[9] Patients typically present with swelling of the affected salivary gland, and when acute, frequently complain of postprandial pain.[10] If the cause is bacterial, purulent drainage may be seen at the ostium of the duct. Salivary duct stones are present in sialadenitis involving 80-90% of submandibular glands (see Figure 7) and about 10-20% of parotid glands, resulting in duct obstruction and upstream dilatation. Since salivary duct obstruction plays a significant role in sialadenitis, most cases occur in submandibular glands, which have a higher rate of sialolithiasis.[10]
CT is one of the main modalities for evaluation for sialadenitis and may demonstrate an enlarged salivary gland with increased attenuation, increased enhancement (on CECT) poorly defined borders, surrounding fat stranding, lymphadenopathy, and thickening of platysma and adjacent cervical fascia. Occasionally, an associated fluid collection with a peripherally-enhancing rim of soft tissue may be seen, indicating an abscess. Although less sensitive for visualization of stones and salivary duct ectasia than CT, ultrasound may provide useful information without exposure to ionizing radiation.[11] Typically, a high-frequency 7-12 MHz probe is used for the examination. Ultrasound appearance varies depending on the stage of the disease. In the acute form, an inflamed salivary gland appears enlarged, hypoechoic (or may have hypoechoic foci within the gland), heterogenous, with increased intrinsic vascularity on color Doppler. In the chronic stage, the affected gland usually appears small, irregular, and hypoechoic.[12,13] Occasionally, a dilated salivary duct may be visualized in cases of recurrent and/or chronic sialadenitis (Figure 8).[13] MRI may be able to differentiate acute and chronic sialadenitis. In the acute phase, the affected gland may appear hypointense on T1 and hyperintense on T2. In the chronic phase, the gland will be heterogeneously hypointense on T1 and of low or intermediate intensity on T2.[14,15] T2 hyperintense signal of surrounding tissues may be evident, indicating surrounding edema. A T2-hyperintense, T1-hypointense focus with peripheral enhancement and restriction on DWI indicates an associated abscess.
Sublingual Space The sublingual space represents bilateral submucosal, non-fascial lined regions extending between the mucosa at the floor of the mouth and the mylohyoid muscular ring. It contains the hypoglossal nerve, lingual nerve, glossopharyngeal nerve, submandibular ganglion, and sublingual and submandibular glands and ducts.[1]
Ludwig Angina Ludwig angina is a necrotizing cellulitis of the floor of the mouth, with mortality rates of up to 10%. It carries a high risk of airway compromise, sometimes progressing rapidly and necessitating endotracheal intubation or tracheostomy. Patients may present with trismus, dysphagia, odynophagia, tender non-fluctuant induration in the submandibular space, neck swelling, stridor, and elevation of the tongue. It is primarily a clinical diagnosis, but imaging helps to assess the extent of cellulitis, the degree of airway obstruction, the presence of soft tissue gas to suggest gas-forming organisms, and the possibility of an abscess. Infection typically involves the submandibular, sublingual, and submental spaces, but may extend into other spaces of the face and neck, and even further inferiorly into the mediastinum. Hence, cross-sectional imaging, primarily contrast-enhanced CT, is paramount in determining the extent of disease. About 90% of Ludwig angina cases occur from the spread of an odontogenic infection, most commonly from second or third mandibular molars (see Figure 9). Other potential primary sites are peritonsillar abscess, parapharyngeal abscess, epiglottitis, or trauma resulting in penetration of the mouth floor. Thus, CECT is often instrumental in determining the primary cause of infection. Apart from the aforementioned findings, CECT may also demonstrate loss of submandibular space fat planes, muscle swelling, skin thickening and fat stranding.[16-18] Although not used as frequently due to limited availability, longer acquisition times, and increased cost, MRI may also be used to detect the aforementioned findings, albeit with decreased accuracy for visualization of associated destructive bony lesions and soft tissue emphysema. Treatment involves intravenous antibiotics, intravenous steroids to decrease oropharyngeal edema, incision and drainage of abscesses, and occasionally surgical debridement and decompression of submandibular space[17].
Buccal Space The buccal space is a small area located between buccinator muscle and zygomatic muscles, extending inferiorly to the masticator space (Figure 10). It contains the buccal fat pad, buccal branch of the facial nerve (CN VII), buccal branch of the mandibular nerve (CN V3), distal parotid duct, accessory parotid tissue, minor salivary gland tissue, and lymph nodes.[1]
Spaces of Both Suprahyoid and Infrahyoid Neck Carotid Space (including the poststyloid parapharyngeal space) The carotid space is bounded by the carotid sheath, which is composed of elements from all layers of the deep cervical fascia. It extends from the jugular foramen and carotid canal to the aortic arch, spanning the suprahyoid and infrahyoid neck, and containing the carotid arteries, internal jugular veins, and cranial nerves IX-XII.[1] In the suprahyoid neck, the carotid sheath is sometimes referred to as the poststyloid parapharyngeal space. Carotid space disease often presents with hoarseness due to involvement of the recurrent laryngeal nerve (branch of CN X). Potential infections include carotid space cellulitis, abscess, and postpharyngeal venous thrombosis (Lemierre Syndrome) [2]
Lemierre Syndrome (Suppurative Jugular Thrombophlebitis) One of the potentially lethal complications of an oropharyngeal infection is distant spread via venous drainage. Through hematogenous seeding, an infection can spread to any organ or tissue, most commonly affecting the lungs.[19] When embolic spread of an oropharyngeal infection is demonstrated associated with internal jugular vein thrombosis, it is termed Lemierre Syndrome.[20] Patients may present with neck fullness, trismus, pain posterior to the jaw angle, and systemic signs and symptoms including fever, chills, malaise, bacteremia, and leukocytosis. Contrast-enhanced CT is the modality of choice for many practitioners due to its accessibility, rapidity, the ability to visualize thrombosis of internal jugular veins and their tributaries, and the ability to evaluate local extent of primary infection as well as distal spread through septic emboli. A CECT will show a filling defect within an internal jugular vein, with or without surrounding fat stranding.[21] Occasionally, internal jugular vein tributaries, such as a facial vein, may be involved (Figure 11).[22] Ultrasonography is occasionally used for evaluation of the neck in the setting of suspected infection and may reveal a hyperechoic (or less often iso- or hypoechoic) filling defect within IJV (Figure 12) and its tributaries, as well as decrease or absence of color flow. Loss of cardiac pulsatility and respiratory phasicity may indicate a nonvisualized thrombus more proximally.[23] Ultrasound may also visualize local pharyngeal infectious foci such as a peritonsillar abscess or cervical adenitis, although CECT remains superior due to its ability to image larger areas with greater tissue penetration.
Retropharyngeal Space and Alar / Danger Space The retropharyngeal space and alar space (more commonly known as the danger space) are indistinguishable on most imaging studies, and disease infecting one space will often spread to the other. These spaces are therefore commonly discussed together or even treated as a single entity.[1]
The retropharyngeal space is a posterior midline suprahyoid and infrahyoid structure bounded anteriorly by the buccopharyngeal fascia (middle layer of the deep cervical fascia) and posteriorly by the alar fascia, starting as high as the skull base and ending between the C6-T6 vertebral body levels.[1] The danger space is located immediately posterior to the retropharyngeal space, being bounded anteriorly by the alar fascia and posteriorly by the prevertebral fascia. One important difference is that the danger space extends considerably more inferior, passing through the mediastinum and extending to the diaphragm. This allows infections of the danger space to spread from the neck to the mediastinum and chest, often with fatal results. Consequently, detection of infections in the retropharyngeal or danger spaces should be followed with a high degree of suspicion for mediastinal or thoracic spread of disease, and may necessitate further imaging.[1] The retropharyngeal space is divided medially by the median raphe, allowing pathology to present either symmetrically or asymmetrically, whereas the alar space does not have a midline division and should always present with symmetric pathology.[1] The danger space primarily contains fat, while the retropharyngeal space contains both fat and lymph nodes. These lymph nodes can be seeded by pharyngitis, leading to suppurative adenopathy, retropharyngeal abscess, phlegmon, or cellulitis.[1] Retropharyngeal space infections tend to spread posteriorly to the danger space, and laterally to the carotid space. Infections in the danger space frequently spread to the retropharyngeal space, mediastinum, and chest.[2]
Retropharyngeal Abscess Retropharyngeal abscess (RPA) is a potentially lethal infectious process that requires prompt recognition and treatment. Abscesses in the retropharyngeal space typically occur as secondary infections when a primary infection (most notably, infections of nasopharynx, middle ear, or sinuses) spread to draining retropharyngeal lymph nodes, leading to suppuration of lymph nodes and formation of abscesses (Figure 13). The most commonly affected population is children under 5 years of age due to the increased frequency of nasopharyngeal, sinus, and middle ear infections.[24] Patients may present with fever, malaise, neck swelling, and signs of laryngeal obstruction such as drooling and stridor. A similar presentation may be seen with retropharyngeal cellulitis or phlegmon, without a drainable collection.[24] Radiographs are limited in evaluation of retropharyngeal abscesses, but may show widening of the prevertebral soft tissue stripe if the abscess is large enough. This finding is not specific for RPA, but may be sufficient to warrant further investigation with adequate supportive clinical findings (Figure 14). The most often utilized modality is contrast-enhanced CT, which can be rapidly performed and allows for sufficient spatial resolution to determine the extent of an abscess and involvement of other nearby tissues. It will show a hypodense collection with peripheral enhancement, often with displacement of nearby tissues and surrounding edema. It should be noted that CT has a significant false-positive rate of approximately 10% and a false-negative rate of approximately 13%.[25] A high false-positive rate could be partially attributed to retropharyngeal cellulitis, which may occasionally have a similar appearance (Figure 15). MRI is a more accurate test for RPA due to increased tissue contrast and the availability of diffusion weighted sequences. An RPA will demonstrate hypointense to intermediate intensity T1 signal, T2 hyperintensity, restricted diffusion, and peripheral enhancement on postcontrast T1 sequences (Figure 16).
Treatment of a retropharyngeal abscess includes a combination of intravenous antibiotic coverage and transoral drainage. One of the major complications of retropharyngeal abscess is extension of infection through the conjoined danger space into the mediastinum, which may require surgical intervention (Figure 13).[26]
Perivertebral Space The perivertebral space is a midline suprahyoid and infrahyoid space bounded externally by the deep layer of the deep cervical fascia, and consisting of tissues that surround the vertebral column. It is further divided into a prevertebral (anterior) component and bilateral paraspinal (posterior) components. The prevertebral component extends from the skull base to the level of T4. The paraspinal components extend along the length of the spine to the sacrum.[1] The prevertebral component contains vertebral bodies, prevertebral muscles, scalene muscles, brachial plexus roots, the phrenic nerve, vertebral artery, and vertebral vein. The paraspinal components contain paraspinal muscles and vertebral columns.[1] Most perivertebral space lesions originate in the vertebral bodies or discs. Common infections include pyogenic vertebral body osteomyelitis and tuberculous vertebral body osteomyelitis.[2] Infections in the prevertebral component are most likely to spread out from the perivertebral space through the neural foramina, and into the epidural space, leading to spinal epidural abscess.[1]
Posterior Cervical Space The posterior cervical space is a suprahyoid and infrahyoid region with complex fascial boundaries, extending from the posterior mastoid tip to the clavicle. This space contains fat, the spinal accessory nerve (CN XI), spinal accessory nodal chain, pre-axillary brachial plexus, and dorsal scapular nerve.[1] The most common infection found in the posterior cervical space is suppurative lymphadenopathy.[2]
Spaces of the Infrahyoid Neck Visceral Space The visceral space is a midline infrahyoid space bounded by the middle layer of the deep cervical fascia, extending from the hyoid bone to the upper mediastinum. It contains the larynx, trachea, hypopharynx, esophagus, recurrent laryngeal nerves, thyroid, parathyroid glands, and lymph nodes.[1] Visceral space infections may present in the form of laryngitis, infected larygocele, tracheobronchitis, or suppurative thyroiditis.[2]
Conclusion While infections of the deep neck spaces can be diagnostic challenges, an anatomy-focused approach helps to simplify the process and increase diagnostic accuracy. Identifying the correct deep neck space will allow the Radiologist to better evaluate likely routes of spread, understand clinical risks, and determine probable causes.
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Figure 1 Deep spaces of the head and neck.
Figure 2 A 29-year-old male presented with a sore throat and malaise. Contrast-enhanced CT (CECT) demonstrating bilateral peritonsillar abscesses (left greater than right).
Figure 3 An 84-year-old female presented with painful facial swelling following attempted extraction of wisdom teeth. Contrast-enhanced CT demonstrating a left masticator space abscess.
Figure 4 (A and B) Contrast-enhanced CT demonstrating a left masticator space abscess secondary to odontogenic infection in a 51-year-old male.
Figure 5 Contrast-enhanced CT demonstrating right-sided parotitis.
Figure 6 A 34-year-old female presented with painful swelling of the neck. (A and B) Contrast-enhanced CT demonstrating a right submandibular space abscess.
Figure 7 A 74-year-old male presented with left-sided neck pain and swelling. CECT demonstrated left submandibular gland, which is enlarged and relatively hyperdense, with associated soft tissue stranding and thickening of left platysma (A). There were several stones in Wharton’s duct, indicated by the arrow (B).
Figure 8 A 45-year-old male presented with left-sided neck swelling. Ultrasound demonstrated enlarged and heterogeneous submandibular gland (A) with mildly increased vascularity and dilatation of left Wharton’s duct (B).
Figure 9 A 60-year-old male with history of diabetes presented with pain and swelling of face and mouth. CECT demonstrated a submandibular fluid collection with peripheral enhancement, consistent with an abscess, along with extensive submandibular, sublingual, and submental edema, and partial effacement of the oropharynx (A and B). Also seen is a lucency surrounding the root of the third mandibular molar, indicated by the arrow (C), suggesting an odontogenic source for this infectious process.
Figure 10 (A and B) Contrast-enhanced CT demonstrating buccal phlegmon.
Figure 11 A 24-year-old male with a sore throat and hoarseness. CECT shows a right peritonsillar abscess (A), thrombus extending from right facial vein into the internal jugular vein, indicated by an arrow (B), and left lower lobe consolidation with a pleural effusion (C).
Figure 12 Ultrasonographic appearance of IJV thrombus.
Figure 13 Contrast-enhanced CT images of a 33-year-old male with an odontogenic infection that (A, B) resulted in retropharyngeal abscess phlegmonous extension to the danger space. (C) Infection further spread inferiorly, causing pulmonary abscess and mediastinal infection. (D, E) This was followed by worsening infection and soft tissue emphysema several days later. (F) Post-operative images of the same patient following extensive incision and drainage.
Figure 14 A 6-year-old male with sore throat, neck stiffness, fever and leukocytosis. XR showed a widened prevertebral soft tissue stripe (1.5 cm), suspicious for an RPA, which was confirmed to be an abscess on a follow-up CT.
Figure 15 (A-C) A 4-year-old male presented with right-sided neck swelling. A right-sided retropharyngeal abscess was seen on CT, for which he has undergone transoral incision and drainage, after which he markedly improved and was discharged on oral antibiotics.
Figure 16 A 64-year-old male with retropharyngeal phlegmon, C5-C6 epidural abscess, and left longus coli abscess (not visualized). He improved on IV antibiotics. (A) STIR. (B) T1. (C) T1 post contrast.
Infections of Deep Neck Spaces Blake W. Hansen MD , Stanislav Ryndin DO , Katherine M. Mullen MD PII: DOI: Reference:
S0887-2171(19)30064-2 https://doi.org/10.1053/j.sult.2019.10.001 YSULT 890
To appear in:
Seminars in Ultrasound CT and MRI
Please cite this article as: Blake W. Hansen MD , Stanislav Ryndin DO , Katherine M. Mullen MD , Infections of Deep Neck Spaces, Seminars in Ultrasound CT and MRI (2019), doi: https://doi.org/10.1053/j.sult.2019.10.001
This is a PDF file of an article that has undergone enhancements after acceptance, such as the addition of a cover page and metadata, and formatting for readability, but it is not yet the definitive version of record. This version will undergo additional copyediting, typesetting and review before it is published in its final form, but we are providing this version to give early visibility of the article. Please note that, during the production process, errors may be discovered which could affect the content, and all legal disclaimers that apply to the journal pertain. © 2019 Published by Elsevier Inc.
Title: Infections of Deep Neck Spaces Authors: 1. Blake W. Hansen, MD ([email protected]) 2. Stanislav Ryndin, DO ([email protected]) 3. Katherine M. Mullen, MD ([email protected]) Authors Affiliation: UMMS-Baystate Radiology 759 Chestnut Street Springfield, MA 01199 USA Corresponding Author: Blake W. Hansen, MD ([email protected]) Abstract: Identifying infections of the deep neck spaces and understanding how they spread can be a diagnostic challenge that is complicated by complex anatomy and far-reaching clinical implications. Deep neck infections have the potential to quickly spread throughout the neck and chest, leading to widespread disease that can be rapidly fatal and resistant to treatment. This article provides a foundation for evaluating deep neck infections through a review of essential anatomy and a discussion of important diseases that interact with these spaces.
Keywords: Sialadenitis, Ludwig Angina, Lemierre Syndrome, Peritonsillar abscess, Odontogenic Abscess
Infections of Deep Neck Spaces Identifying infections of the deep neck spaces and understanding how they spread can be a diagnostic challenge that is complicated by complex anatomy and far-reaching clinical implications. Deep neck infections have the potential to quickly spread throughout the neck and chest, leading to widespread disease that can be rapidly fatal and resistant to treatment. Appropriate diagnosis of deep neck space infections involves first identifying the correct anatomic location as this will provide clues to the origin of the disease, determine which structures are at risk, and guide treatment. Secondly, deep spaces that communicate with the area of infection should be closely evaluated to rule out additional spread of disease and to expand the differential diagnosis as prominent areas of infection may be sequelae of a more subtle primary infection. Equipped with an understanding of which deep neck spaces are involved and how they interact, a more accurate evaluation of potential etiologies, clinical risks and appropriate treatment can be formulated. In this article, we provide a foundation for evaluating deep neck infections through a review of essential anatomy and a discussion of important diseases that interact with these spaces.
Deep Neck Anatomy The deep neck spaces are primarily divided by the layers of the deep cervical fascia and are commonly organized by suprahyoid and infrahyoid spaces (specifically the superficial layer, middle layer, and deep layer of the deep cervical fascia). Different deep neck spaces are susceptible to different pathologies and the spread of disease is constrained by the fascial layers. Understanding the anatomy of the deep neck spaces allows the likely path of spread and potential origin of disease to be determined and more closely evaluated (Figure 1).
Spaces of the Suprahyoid Neck Oral Mucosal and Pharyngeal Mucosal Spaces The oral mucosal and pharyngeal mucosal spaces are not true fascia-enclosed spaces, but rather continuous sheets of suprahyoid mucosa that are typically included to allow for a complete spatial mapping of the suprahyoid neck. The oral mucosal space extends from the lips to the circumvallate papillae and the posterior border of the hard palate and contains minor salivary glands and mucosal surface tissue, including the buccal mucosa lining the cheeks and lips, hard palate, and anterior two thirds of the tongue. The pharyngeal mucosal space is composed of the nasopharynx, oropharynx, and hypopharynx. Important contents include the pharyngeal mucosal surface, Waldeyer’s lymphatic ring (adenoids, palatine tonsils, and lingual tonsils), minor salivary glands, muscle, and the torus tubarius (cartilaginous end of the eustachian tube).[1] Asymmetry of the pharyngeal mucosal space is common and does not necessarily indicate pathology.[1] However, tonsillar and peritonsillar abscesses are common infections of this space, which may then spread to the nearby parapharyngeal, masticator, and submandibular spaces.[2]
Parapharyngeal Space (Prestyloid) The parapharyngeal space is a suprahyoid region extending from the skull base to the superior cornua of the hyoid bone. It is bounded by the pharyngeal mucosal space medially and the superficial layer of the deep cervical fascia laterally. Posteriorly, it is bounded by both the carotid sheath and buccopharyngeal fascia (middle layer of the deep cervical fascia). It contains fat, minor salivary glands, the internal maxillary artery, ascending pharyngeal artery, and part of the pterygoid venous plexus.[1] The suprahyoid component of the carotid space is sometimes included in the anatomic description of the parapharyngeal space and referred to as the poststyloid parapharyngeal space, with the anterior region (referred to here as the parapharyngeal space) delineated using the term prestyloid parapharyngeal space. In this article, the suprahyoid component of the carotid space is included in the carotid space section below. Most parapharyngeal space lesions spread from adjacent spaces. Primary parapharyngeal space lesions are rare.[1] Infections typically spread to the parapharyngeal space from the pharyngeal mucosal space, masticator space, parotid space, and carotid space. Inferiorly, there is no fascia separating the submandibular space from the parapharyngeal space, allowing parapharyngeal disease to spread to the submandibular space. The most common infections of this space include tonsillar and peritonsillar abscesses.[2]
Peritonsillar abscess Peritonsillar abscess (PTA) is the most common infection of the deep head and neck. Most cases are sequelae of chronic or recurrent bacterial tonsillitis, leading to abscess in the parapharyngeal space or pharyngeal mucosal space. It is most common in patients 20 - 40 years of age, without predilection to gender. Although occurrence in children is relatively rare, PTA has an increased risk for airway obstruction in a pediatric population as compared to adults. Patients may present with odynophagia, voice changes, trismus, drooling, dysphagia, and systemic symptoms such as fever, chills, and malaise.[3] Each palatine tonsil is bordered by the palatoglossal arch anteriorly and palatopharyngeal arch posteriorly, and is covered by a fibrous capsule laterally. Peritonsillar abscesses tend to form between the tonsil and the fibrous capsule, with potential to spread to surrounding structures.[3] The most commonly used and most practical modality for evaluation of tonsillar pathology is computed tomography, (CT), which will typically show fluid density with peripheral enhancement adjacent to an inflamed tonsil (Figure 2). CT is considered 100% sensitive for identification of PTA.[4] However, it is only 75% specific as approximately 25% of cases with the aforementioned characteristics will be phlegmonous, and therefore non-drainable.[5] Ultrasonographic evaluation for PTA is used less frequently due to its limitations with patient body habitus, operator skill and a relatively limited assessment of surrounding structures. Advantages of ultrasonography include lack of ionizing radiation and the ability to guide aspiration if performed by a physician or qualified mid-level provider. Most commonly, the tonsil is evaluated by inserting an endocavity ultrasound probe intraorally with the help of a tongue blade, as this position often allows for abscess aspiration. Alternatively, a high-frequency probe may be positioned in the submandibular region and directed superiorly. An abscess is seen as a hypoechoic or anechoic focus with lowlevel internal echoes, which sometimes has a relatively hyperechoic periphery and increased peripheral vascularity on color Doppler.[6]
Masticator Space The masticator space is a paired suprahyoid region bounded by the superficial layer of the deep cervical fascia, extending from the top of the parietal bone to the inferior mandible. This space contains muscles of mastication, the posterior body and ramus of the mandible, trigeminal nerve (CN V3), and maxillary artery.[1] Most masticator space infections originate from odontogenic infection, leading to cellulitis, phlegmon, or abscess. Consequently, when a masticator space infection is identified, special attention should be given to imaging of the oral space as the infected teeth will need to be identified and treated to prevent recurring infection. [2] Masticator space infections tend to spread to adjacent spaces, including the sublingual space (which runs along the medial body of the mandible), buccal space, parotid space, and parapharyngeal space.[7]
Odontogenic Masticator Space Abscess Odontogenic masticator space abscesses begin with mandibular molar infections or dental manipulation, followed by trismus and nonspecific signs of infection such as fever, leukocytosis, and tenderness. [2] As they grow, they have the ability to spread to the sublingual space, parapharyngeal space, parotid space, and beyond.[7] Masticator space abscesses are best evaluated with contrast-enhanced CT, allowing evaluation of pyogenic collections in the soft tissues, molar tooth erosion, mandibular osseous changes, and related signs of inflammation (see Figures 3-4). Cortical destruction of the mandible with periosteal elevation suggests mandibular osteomyelitis. A masticator space abscess will present with a focal fluid-density collection in the muscles of mastication and
compression of the parapharyngeal space from anterolateral to posteromedial. Other differential considerations include cellulitis, phlegmon, and myositis.[2] Treatment of masticator space abscesses begins with extraction of the decayed molar, eliminating the source of the infection. From this point, treatment depends on the extent of the infection. If diagnosed early, aggressive IV antibiotics may be sufficient; however, most patients will require both IV antibiotics and surgical drainage. If mandibular osteomyelitis has developed, placement of a subperiosteal drain and prolonged IV antibiotics may be needed.[2]
Parotid Space The parotid space is a paired suprahyoid region located posterior to the masticator space, bounded by the superficial layer of the deep cervical fascia and extending from the external auditory canal or mastoid tip to the parotid tail (inferior to the angle of the mandible). Its contents include parotid glands, intraparotid lymph nodes, the extracranial facial nerve (CN VII), external carotid artery, retromandibular vein, parotid duct, and accessory parotid glands.[1] Potential infections found in the parotid space include acute or chronic parotitis (sialadenitis) (Figure 5), reactive lymphadenopathy, and necrotizing lymphadenopathy.[2] See the submandibular section for additional information regarding sialadenitis.
Submandibular / Submaxillary Space The submandibular space, also known as the submaxillary space, is a horseshoe-shaped suprahyoid region with lateral components that communicate posteriorly. It is bounded by mylohyoid sling and platysma muscle, extending from the mylohyoid sling to the hyoid bone. It contains the submandibular glands, level I lymph nodes, the caudal loop of CN XII, anterior belly of digastric muscles, facial vein, and sometimes includes the tail of the parotid gland.[1] Infections in the submandibular space often spread to the contralateral submandibular space, sublingual space, along the styloglossus muscle into the parapharyngeal space, and through loose areolar tissue into the retropharyngeal space (Figure 6). Common infections include submandibular space sialadenitis with ductal calculus, diving ranula, and reactive or suppurative adenopathy. This is also one of the spaces that may be involved in potentially life threatening Ludwig angina.[1] See the sublingual section for additional information regarding Ludwig angina.
Sialadenitis Sialadenitis, or inflammation of salivary glands, is a multi-cause process which may be acute or chronic. Acute sialadenitis most commonly occurs secondary to a bacterial infection in the setting of sialolithiasis and less commonly may be due to viruses, dehydration, and pharmaceuticals. Bilateral parotitis in pediatric population is seen in mumps. Chronic sialadenitis may be due to autoimmune conditions such as Sjogren and Mikulicz syndrome, but is also frequently associated with sialolithiasis.[8] Other causes of salivary gland inflammation may be due to iodine-131 administration and post-radiation.[9] Patients typically present with swelling of the affected salivary gland, and when acute, frequently complain of postprandial pain.[10] If the cause is bacterial, purulent drainage may be seen at the ostium of the duct. Salivary duct stones are present in sialadenitis involving 80-90% of submandibular glands (see Figure 7) and about 10-20% of parotid glands, resulting in duct obstruction and upstream dilatation. Since salivary duct obstruction plays a significant role in sialadenitis, most cases occur in submandibular glands, which have a higher rate of sialolithiasis.[10]
CT is one of the main modalities for evaluation for sialadenitis and may demonstrate an enlarged salivary gland with increased attenuation, increased enhancement (on CECT) poorly defined borders, surrounding fat stranding, lymphadenopathy, and thickening of platysma and adjacent cervical fascia. Occasionally, an associated fluid collection with a peripherally-enhancing rim of soft tissue may be seen, indicating an abscess. Although less sensitive for visualization of stones and salivary duct ectasia than CT, ultrasound may provide useful information without exposure to ionizing radiation.[11] Typically, a high-frequency 7-12 MHz probe is used for the examination. Ultrasound appearance varies depending on the stage of the disease. In the acute form, an inflamed salivary gland appears enlarged, hypoechoic (or may have hypoechoic foci within the gland), heterogenous, with increased intrinsic vascularity on color Doppler. In the chronic stage, the affected gland usually appears small, irregular, and hypoechoic.[12,13] Occasionally, a dilated salivary duct may be visualized in cases of recurrent and/or chronic sialadenitis (Figure 8).[13] MRI may be able to differentiate acute and chronic sialadenitis. In the acute phase, the affected gland may appear hypointense on T1 and hyperintense on T2. In the chronic phase, the gland will be heterogeneously hypointense on T1 and of low or intermediate intensity on T2.[14,15] T2 hyperintense signal of surrounding tissues may be evident, indicating surrounding edema. A T2-hyperintense, T1-hypointense focus with peripheral enhancement and restriction on DWI indicates an associated abscess.
Sublingual Space The sublingual space represents bilateral submucosal, non-fascial lined regions extending between the mucosa at the floor of the mouth and the mylohyoid muscular ring. It contains the hypoglossal nerve, lingual nerve, glossopharyngeal nerve, submandibular ganglion, and sublingual and submandibular glands and ducts.[1]
Ludwig Angina Ludwig angina is a necrotizing cellulitis of the floor of the mouth, with mortality rates of up to 10%. It carries a high risk of airway compromise, sometimes progressing rapidly and necessitating endotracheal intubation or tracheostomy. Patients may present with trismus, dysphagia, odynophagia, tender non-fluctuant induration in the submandibular space, neck swelling, stridor, and elevation of the tongue. It is primarily a clinical diagnosis, but imaging helps to assess the extent of cellulitis, the degree of airway obstruction, the presence of soft tissue gas to suggest gas-forming organisms, and the possibility of an abscess. Infection typically involves the submandibular, sublingual, and submental spaces, but may extend into other spaces of the face and neck, and even further inferiorly into the mediastinum. Hence, cross-sectional imaging, primarily contrast-enhanced CT, is paramount in determining the extent of disease. About 90% of Ludwig angina cases occur from the spread of an odontogenic infection, most commonly from second or third mandibular molars (see Figure 9). Other potential primary sites are peritonsillar abscess, parapharyngeal abscess, epiglottitis, or trauma resulting in penetration of the mouth floor. Thus, CECT is often instrumental in determining the primary cause of infection. Apart from the aforementioned findings, CECT may also demonstrate loss of submandibular space fat planes, muscle swelling, skin thickening and fat stranding.[16-18] Although not used as frequently due to limited availability, longer acquisition times, and increased cost, MRI may also be used to detect the aforementioned findings, albeit with decreased accuracy for visualization of associated destructive bony lesions and soft tissue emphysema. Treatment involves intravenous antibiotics, intravenous steroids to decrease oropharyngeal edema, incision and drainage of abscesses, and occasionally surgical debridement and decompression of submandibular space[17].
Buccal Space The buccal space is a small area located between buccinator muscle and zygomatic muscles, extending inferiorly to the masticator space (Figure 10). It contains the buccal fat pad, buccal branch of the facial nerve (CN VII), buccal branch of the mandibular nerve (CN V3), distal parotid duct, accessory parotid tissue, minor salivary gland tissue, and lymph nodes.[1]
Spaces of Both Suprahyoid and Infrahyoid Neck Carotid Space (including the poststyloid parapharyngeal space) The carotid space is bounded by the carotid sheath, which is composed of elements from all layers of the deep cervical fascia. It extends from the jugular foramen and carotid canal to the aortic arch, spanning the suprahyoid and infrahyoid neck, and containing the carotid arteries, internal jugular veins, and cranial nerves IX-XII.[1] In the suprahyoid neck, the carotid sheath is sometimes referred to as the poststyloid parapharyngeal space. Carotid space disease often presents with hoarseness due to involvement of the recurrent laryngeal nerve (branch of CN X). Potential infections include carotid space cellulitis, abscess, and postpharyngeal venous thrombosis (Lemierre Syndrome) [2]
Lemierre Syndrome (Suppurative Jugular Thrombophlebitis) One of the potentially lethal complications of an oropharyngeal infection is distant spread via venous drainage. Through hematogenous seeding, an infection can spread to any organ or tissue, most commonly affecting the lungs.[19] When embolic spread of an oropharyngeal infection is demonstrated associated with internal jugular vein thrombosis, it is termed Lemierre Syndrome.[20] Patients may present with neck fullness, trismus, pain posterior to the jaw angle, and systemic signs and symptoms including fever, chills, malaise, bacteremia, and leukocytosis. Contrast-enhanced CT is the modality of choice for many practitioners due to its accessibility, rapidity, the ability to visualize thrombosis of internal jugular veins and their tributaries, and the ability to evaluate local extent of primary infection as well as distal spread through septic emboli. A CECT will show a filling defect within an internal jugular vein, with or without surrounding fat stranding.[21] Occasionally, internal jugular vein tributaries, such as a facial vein, may be involved (Figure 11).[22] Ultrasonography is occasionally used for evaluation of the neck in the setting of suspected infection and may reveal a hyperechoic (or less often iso- or hypoechoic) filling defect within IJV (Figure 12) and its tributaries, as well as decrease or absence of color flow. Loss of cardiac pulsatility and respiratory phasicity may indicate a nonvisualized thrombus more proximally.[23] Ultrasound may also visualize local pharyngeal infectious foci such as a peritonsillar abscess or cervical adenitis, although CECT remains superior due to its ability to image larger areas with greater tissue penetration.
Retropharyngeal Space and Alar / Danger Space The retropharyngeal space and alar space (more commonly known as the danger space) are indistinguishable on most imaging studies, and disease infecting one space will often spread to the other. These spaces are therefore commonly discussed together or even treated as a single entity.[1]
The retropharyngeal space is a posterior midline suprahyoid and infrahyoid structure bounded anteriorly by the buccopharyngeal fascia (middle layer of the deep cervical fascia) and posteriorly by the alar fascia, starting as high as the skull base and ending between the C6-T6 vertebral body levels.[1] The danger space is located immediately posterior to the retropharyngeal space, being bounded anteriorly by the alar fascia and posteriorly by the prevertebral fascia. One important difference is that the danger space extends considerably more inferior, passing through the mediastinum and extending to the diaphragm. This allows infections of the danger space to spread from the neck to the mediastinum and chest, often with fatal results. Consequently, detection of infections in the retropharyngeal or danger spaces should be followed with a high degree of suspicion for mediastinal or thoracic spread of disease, and may necessitate further imaging.[1] The retropharyngeal space is divided medially by the median raphe, allowing pathology to present either symmetrically or asymmetrically, whereas the alar space does not have a midline division and should always present with symmetric pathology.[1] The danger space primarily contains fat, while the retropharyngeal space contains both fat and lymph nodes. These lymph nodes can be seeded by pharyngitis, leading to suppurative adenopathy, retropharyngeal abscess, phlegmon, or cellulitis.[1] Retropharyngeal space infections tend to spread posteriorly to the danger space, and laterally to the carotid space. Infections in the danger space frequently spread to the retropharyngeal space, mediastinum, and chest.[2]
Retropharyngeal Abscess Retropharyngeal abscess (RPA) is a potentially lethal infectious process that requires prompt recognition and treatment. Abscesses in the retropharyngeal space typically occur as secondary infections when a primary infection (most notably, infections of nasopharynx, middle ear, or sinuses) spread to draining retropharyngeal lymph nodes, leading to suppuration of lymph nodes and formation of abscesses (Figure 13). The most commonly affected population is children under 5 years of age due to the increased frequency of nasopharyngeal, sinus, and middle ear infections.[24] Patients may present with fever, malaise, neck swelling, and signs of laryngeal obstruction such as drooling and stridor. A similar presentation may be seen with retropharyngeal cellulitis or phlegmon, without a drainable collection.[24] Radiographs are limited in evaluation of retropharyngeal abscesses, but may show widening of the prevertebral soft tissue stripe if the abscess is large enough. This finding is not specific for RPA, but may be sufficient to warrant further investigation with adequate supportive clinical findings (Figure 14). The most often utilized modality is contrast-enhanced CT, which can be rapidly performed and allows for sufficient spatial resolution to determine the extent of an abscess and involvement of other nearby tissues. It will show a hypodense collection with peripheral enhancement, often with displacement of nearby tissues and surrounding edema. It should be noted that CT has a significant false-positive rate of approximately 10% and a false-negative rate of approximately 13%.[25] A high false-positive rate could be partially attributed to retropharyngeal cellulitis, which may occasionally have a similar appearance (Figure 15). MRI is a more accurate test for RPA due to increased tissue contrast and the availability of diffusion weighted sequences. An RPA will demonstrate hypointense to intermediate intensity T1 signal, T2 hyperintensity, restricted diffusion, and peripheral enhancement on postcontrast T1 sequences (Figure 16).
Treatment of a retropharyngeal abscess includes a combination of intravenous antibiotic coverage and transoral drainage. One of the major complications of retropharyngeal abscess is extension of infection through the conjoined danger space into the mediastinum, which may require surgical intervention (Figure 13).[26]
Perivertebral Space The perivertebral space is a midline suprahyoid and infrahyoid space bounded externally by the deep layer of the deep cervical fascia, and consisting of tissues that surround the vertebral column. It is further divided into a prevertebral (anterior) component and bilateral paraspinal (posterior) components. The prevertebral component extends from the skull base to the level of T4. The paraspinal components extend along the length of the spine to the sacrum.[1] The prevertebral component contains vertebral bodies, prevertebral muscles, scalene muscles, brachial plexus roots, the phrenic nerve, vertebral artery, and vertebral vein. The paraspinal components contain paraspinal muscles and vertebral columns.[1] Most perivertebral space lesions originate in the vertebral bodies or discs. Common infections include pyogenic vertebral body osteomyelitis and tuberculous vertebral body osteomyelitis.[2] Infections in the prevertebral component are most likely to spread out from the perivertebral space through the neural foramina, and into the epidural space, leading to spinal epidural abscess.[1]
Posterior Cervical Space The posterior cervical space is a suprahyoid and infrahyoid region with complex fascial boundaries, extending from the posterior mastoid tip to the clavicle. This space contains fat, the spinal accessory nerve (CN XI), spinal accessory nodal chain, pre-axillary brachial plexus, and dorsal scapular nerve.[1] The most common infection found in the posterior cervical space is suppurative lymphadenopathy.[2]
Spaces of the Infrahyoid Neck Visceral Space The visceral space is a midline infrahyoid space bounded by the middle layer of the deep cervical fascia, extending from the hyoid bone to the upper mediastinum. It contains the larynx, trachea, hypopharynx, esophagus, recurrent laryngeal nerves, thyroid, parathyroid glands, and lymph nodes.[1] Visceral space infections may present in the form of laryngitis, infected larygocele, tracheobronchitis, or suppurative thyroiditis.[2]
Conclusion While infections of the deep neck spaces can be diagnostic challenges, an anatomy-focused approach helps to simplify the process and increase diagnostic accuracy. Identifying the correct deep neck space will allow the Radiologist to better evaluate likely routes of spread, understand clinical risks, and determine probable causes.
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Figure 1 Deep spaces of the head and neck.
Figure 2 A 29-year-old male presented with a sore throat and malaise. Contrast-enhanced CT (CECT) demonstrating bilateral peritonsillar abscesses (left greater than right).
Figure 3 An 84-year-old female presented with painful facial swelling following attempted extraction of wisdom teeth. Contrast-enhanced CT demonstrating a left masticator space abscess.
Figure 4 (A and B) Contrast-enhanced CT demonstrating a left masticator space abscess secondary to odontogenic infection in a 51-year-old male.
Figure 5 Contrast-enhanced CT demonstrating right-sided parotitis.
Figure 6 A 34-year-old female presented with painful swelling of the neck. (A and B) Contrast-enhanced CT demonstrating a right submandibular space abscess.
Figure 7 A 74-year-old male presented with left-sided neck pain and swelling. CECT demonstrated left submandibular gland, which is enlarged and relatively hyperdense, with associated soft tissue stranding and thickening of left platysma (A). There were several stones in Wharton’s duct, indicated by the arrow (B).
Figure 8 A 45-year-old male presented with left-sided neck swelling. Ultrasound demonstrated enlarged and heterogeneous submandibular gland (A) with mildly increased vascularity and dilatation of left Wharton’s duct (B).
Figure 9 A 60-year-old male with history of diabetes presented with pain and swelling of face and mouth. CECT demonstrated a submandibular fluid collection with peripheral enhancement, consistent with an abscess, along with extensive submandibular, sublingual, and submental edema, and partial effacement of the oropharynx (A and B). Also seen is a lucency surrounding the root of the third mandibular molar, indicated by the arrow (C), suggesting an odontogenic source for this infectious process.
Figure 10 (A and B) Contrast-enhanced CT demonstrating buccal phlegmon.
Figure 11 A 24-year-old male with a sore throat and hoarseness. CECT shows a right peritonsillar abscess (A), thrombus extending from right facial vein into the internal jugular vein, indicated by an arrow (B), and left lower lobe consolidation with a pleural effusion (C).
Figure 12 Ultrasonographic appearance of IJV thrombus.
Figure 13 Contrast-enhanced CT images of a 33-year-old male with an odontogenic infection that (A, B) resulted in retropharyngeal abscess phlegmonous extension to the danger space. (C) Infection further spread inferiorly, causing pulmonary abscess and mediastinal infection. (D, E) This was followed by worsening infection and soft tissue emphysema several days later. (F) Post-operative images of the same patient following extensive incision and drainage.
Figure 14 A 6-year-old male with sore throat, neck stiffness, fever and leukocytosis. XR showed a widened prevertebral soft tissue stripe (1.5 cm), suspicious for an RPA, which was confirmed to be an abscess on a follow-up CT.
Figure 15 (A-C) A 4-year-old male presented with right-sided neck swelling. A right-sided retropharyngeal abscess was seen on CT, for which he has undergone transoral incision and drainage, after which he markedly improved and was discharged on oral antibiotics.
Figure 16 A 64-year-old male with retropharyngeal phlegmon, C5-C6 epidural abscess, and left longus coli abscess (not visualized). He improved on IV antibiotics. (A) STIR. (B) T1. (C) T1 post contrast.