Critical infections in the head and neck: A pictorial review of acute presentations and complications

Abstract

Non-traumatic head and neck emergencies include several disease processes such as infectious, inflammatory, and malignant. Infections are among the most common pathological processes that affect the head and neck, and are particularly important due to their acute, severe, and potentially life-threatening nature. Radiologists need to be well acquainted with these entities because any delay or misdiagnosis can lead to significant morbidity and mortality. Having a general understanding of such diseases is crucial, their prevalence, clinical presentation, common causative pathogens, route of spread, potential complications, and multimodality radiological appearance. Furthermore, understanding the relevant anatomy of the region, including the various fascial planes and spaces, is essential for radiologists for accurate image interpretation and assessment of potential complications. Our aim is to review the most common severe infections affecting the head and neck as well as other rare but potentially life-threatening infections. We will also describe their imaging features while focusing on the anatomy of the regions involved and describing their potential complications and treatment options.

Introduction

Head and neck imaging often can be challenging for radiologists because of the complex anatomy and various pathological processes. A lack of knowledge of serious conditions affecting this region can lead to a delay in diagnosis causing considerable morbidity and mortality. Therefore, timely and proper imaging interpretation are pivotal to patient care.^1–4

Infections are the most common causes of head and neck emergencies compared to inflammatory and neoplastic causes. ⁵ They are mostly initiated by streptococci and perpetuated by anaerobes. Respiratory pathogens such as Hemophilus influenzae and nosocomial infections, mainly Staphylococcus aureus and Enterobacteriaceae are also common culprits. In immunosuppressed patients, mycobacterial infections and fungal infections, such as mucormycosis and aspergillus infections, may also occur. Empiric antibiotic treatment depends on the location of infection and the underlying risk factors with surgery sometimes being required in some extensive infections and for abscess drainage. ⁶

High-risk infections usually occur in immunocompromised and older patients and those with diabetes but can also occur in healthy individuals.^5,7 Infections can lead to vascular complications, can compromise airway patency, and may spread to the spine, mediastinum, or intracranially. ⁸ Despite the availability of antibiotic therapy and early surgical intervention, head and neck infections still cause a significant burden on clinical centers.^1–4,9 Therefore, radiologists should be familiar with these conditions, their radiological appearance, and potential complications.

Understanding the anatomy of the region and the routes of spread of infection is crucial for proper diagnosis and treatment. Although infections can involve multiple areas, the head and neck anatomy can be organized into five sections based on the origin of the infection: the oral cavity and pharynx, the neck (including the spine), the sinuses, the orbits, and the ears. The neck is further divided by fascial planes that provide specific routes of dissemination of an infectious process once a disease process is established. The neck is enclosed by the superficial fascia and the deep cervical fascia, the latter is further divided into three layers: the superficial, middle, and deep layers. These layers divide the neck into multiple spaces. The neck spaces are further divided into the suprahyoid and infrahyoid spaces with some spaces spanning the hyoid bone, namely, the carotid, retropharyngeal, and prevertebral spaces.^8,10,11 Radiologists should be aware of these spaces for proper interpretation of images and detection of potential complications.

Regarding imaging modalities of the head and neck, infectious diseases are best evaluated with cross-sectional imaging (CT and MRI) with some role for ultrasound in the evaluation of superficial infections like cervical lymphadenitis, parotitis, and infected congenital (branchial cleft and thyroglossal duct) cysts. Conventional radiographs, though easy to obtain, are often inadequate, but do have a role for evaluation of dental pathology, retropharyngeal abscess, epiglottitis, and laryngotracheobronchitis (croup). ¹²

In this pictorial essay, we will be reviewing the most common severe infections affecting the head and neck as well as other rare but potentially life-threatening infections as we describe the relevant anatomy, imaging features, their potential complications, and treatment options.

Malignant otitis externa

Malignant otitis externa (MOE), also known as necrotizing otitis externa, is a severe infection of the external ear that is most commonly caused by Pseudomonas aeruginosa. The infection usually occurs in diabetics. Other less common risk factors include AIDS, post-transplant immune suppression, and hematologic malignancies. Presenting symptoms include pain and ear discharge. ¹³

The infection usually starts at the bone–cartilage junction of the external auditory canal then progresses to chondritis and osteomyelitis. ¹⁴ The infection can then spread posteriorly into the mastoid, anteriorly into the temporomandibular joint, medially into the petrous apex and remainder of the skull base, or inferiorly to the soft tissues below the temporal bone.

Findings on cross-sectional imaging include soft tissue thickening with or without bone erosion in the external auditory canal. With further progression of the infection, there may be opacification/fluid within the mastoid and middle ear, thickening of the ipsilateral nasopharynx, and infiltration of the parapharyngeal space fat (Figure 1). ¹⁴ Tc-99m bone scan can help differentiate MOE from typical external otitis by demonstrating temporal bone and skull base involvement. Gallium-67 and Indium-111 can be used to assess response to treatment. ¹⁵

Figure 1.

Malignant otitis externa in a 65-year-old diabetic female presenting for 4-month history of right facial swelling, otalgia, and right hearing loss. Axial (A) and coronal (B) post-contrast, T1 weighted fat sat images showing right otitis externa with extension into the masticator space, parapharyngeal space, parotid space, and temporomandibular joint with enhancement of the right mandibular condyle (red arrow), suggestive of osteomyelitis. There is also cortical erosion of the tegmentum tympani and dural enhancement along the floor of the right middle cranial fossa (green arrow) with no brain parenchymal involvement.

The major differential diagnosis for MOE on imaging is squamous cell carcinoma of the external ear. The clinical context should aid in differentiating between the two entities. When present, soft tissue infiltration and inflammatory changes with or without fluid collections can help point to the diagnosis of MOE as opposed to squamous cell carcinoma.

The mainstay of treatment is antibiotics with fluoroquinolones being the usual first-line agents. Indications for surgical intervention include biopsy to exclude malignancy and to obtain material for culture and debridement of necrotic tissue. ¹⁶

Coalescent mastoiditis

Coalescent mastoiditis (CM) is a suppurative infection of the mastoid air cells causing erosion of the mastoid septae. It is a rare complication occurring in less than 1% of all cases of otomastoiditis. ¹⁷ Although the incidence has markedly decreased with the advent of antibiotics, the rarity of this condition nowadays has, on occasions, led to a delay in its recognition. ¹⁸ The mortality rate from intracranial complications of CM has been reported to be as high as 10%. ¹⁹ The pathogenesis is related to formation of granulation and pus under pressure with hyperemia and subsequent bony resorption. ²⁰

Risk factors include age below 2 years and incomplete pneumatization of the mastoid air cells. ²⁰ The most common pathogens that cause mastoiditis are S. pneumoniae, H. influenza, and group A streptococcus pyogenes. Patients usually present with fever, otalgia, and post-auricular erythema and swelling. ⁴

Regarding diagnostic imaging, contrast enhanced CT or MRI are the main modalities used to assess for CM. Findings on cross-sectional imaging include opacification of the mastoid air cells, ill definition and destruction of the bony septae, and erosion of the mastoid cortex, the latter two features are better appreciated on CT scan, but once the diagnosis of coalescent mastoiditis is established, MR is superior in the detection of intracranial complications such as cerebritis prior to formation of a frank abscess (Figure 2).

Figure 2.

Bilateral coalescent mastoiditis with right sigmoid sinus thrombosis in a 6-year-old boy presetting for severe headache. Contrast enhanced axial CT scan (A bone window, B soft tissue window) showing bilateral opacification of the air cells (yellow arrows), more so on the right, with destruction of some bony septae. There is also a filling defect within the right sigmoid sinus indicative of sigmoid sinus thrombosis (blue arrow).

The main differential diagnosis for coalescent mastoiditis is simple mastoiditis secondary to otitis media which should not produce destruction of the mastoid septae. Patients with CM, unlike those with simple mastoiditis, will appear obviously ill with systemic signs such as high fever and local signs such as mastoid tenderness, protruding pinna, and copious ear discharge. Other imaging features which can favor CM over simple acute mastoiditis or mastoid effusion include mastoid enhancement, restricted diffusion, and intermediate T2W signal intensity (which suggest purulence of the mastoid fluid), complete rather than partial mastoid opacification, greater than 50% middle ear cavity opacification, and peri-mastoid dural enhancement. ²¹ Sterile mastoid effusion/trapped fluid is commonly seen and should not be overcalled as mastoiditis without specific radiologic or clinical evidence. If unilateral mastoid opacification is noted, especially in an elderly patient, one should be alerted to evaluate the ipsilateral nasopharynx for presence of a mass causing obstruction of the Eustachian tube. Other differential diagnoses of mastoid opacification include acquired cholesteatoma (which unlike CM usually presents with chronic ear drainage). An encephalocele should be suspected when there is non-dependent soft tissue associated with a defect in the tegmen and can be confirmed with MR, especially high-resolution T2W imaging.

Complications of CM include subperiosteal abscess, Bezold abscess, epidural or subdural empyema, venous sinus thrombosis (usually the sigmoid sinus), cerebritis/cerebellitis and brain abscess (in the temporal lobe or cerebellum), facial neuritis, and labyrinthitis. The latter can be diagnosed on imaging by finding abnormal enhancement in the inner ear bony labyrinth. ²⁰

Surgical treatment options of mastoiditis include incision and drainage, myrigotomy (with or without tympanostomy tube), and mastoidectomy. Indications for surgical intervention include intracranial complication, subperiosteal abscess, failure of medical therapy, and development of cholesteatoma. ²²

Petrous apicitis

Petrous apicitis (PA), also known as apical petrositis, is a rare and potentially life-threatening infection, generally considered as a form of osteitis developing from infected and obstructed air cells in a pneumatized apex of the petrous temporal bone. Due to its rarity, its incidence in adults today is largely unknown, and it is considered less common due to the early use of antibiotics for acute otomastoiditis.^23,24 However, mortality rates without antibiotic treatment can approach up to 20% of cases. ²⁵

Clinical presentation depends on whether PA is isolated or is a complication of acute otomastoiditis. The classical presentation of petrous apicitis is known as Gradenigo’s syndrome and consists of a triad of paresis of the abducens nerve (due to involvement of Dorello’s canal), deep facial pain in the distribution of the trigeminal nerve (due to inflammation of the dura and trigeminal nerve in Meckel’s cave), and acute suppurative otitis media. However, the complete classic triad is only present in a minority of cases. Presentation may also be due to extension beyond the petrous apex leading to dural venous sinus thrombosis or intracranial extension manifesting as meningitis, epidural abscess, subdural empyema, and cerebral abscess. ²⁵

Early diagnosis of PA requires high clinical suspicion and availability of proper imaging modality. In PA, CT imaging shows erosive lysis with ill-defined irregular edges at the apex of the petrous temporal bone with associated dural thickening and enhancement. MRI shows abnormal, sometimes peripheral enhancement with fluid signal.^9,26,27 Thus, we expect to see low to intermediate T1 fluid signal, hyperintense T2 signal, and peripheral enhancement on T1 with gadolinium (Figure 3). Thickening of the dura of Meckel’s cave and the cavernous sinus should not be overlooked, as well as for findings suggestive of cavernous sinus thrombosis.^25,27

Figure 3.

In a 55-year-old male being initially treated for otitis media later presented with left temporal headache, photophobia, and left eye droop. Post-contrast T1 (A) and T2 (B) weighed images showing high signal on T2 (blue arrow) and enhancement of the left petrous apex (yellow arrow). There is in addition abnormal enhancement in the left aspect of the clivus.

Differential diagnosis of PA includes trapped fluid/effusion in the petrous apex (no enhancement or restricted diffusion and no septal erosion on CT), cholesterol granuloma (typically a round expansile petrous apex mass with high signal intensity on T1W and T2W), and encephalocele (should be suspected when there is non-dependent soft tissue associated with a skull base defect). Cholesteatoma may mimic infection due to septal/bone erosion and presence of restricted diffusion but is typically associated with chronic symptoms like ear drainage (when acquired), in addition, cholesteatoma whether acquired or congenital is non-enhancing.

Asymmetric petrous apex pneumatization is a normal variant that should not be mistaken for pathology, the non-pneumatized side demonstrates relatively higher signal on MR but it is typically of similar intensity to bone marrow, CT can resolve the issue if there is a doubt as to whether the asymmetry is due to difference in pneumatization.

As for treatment options, most of the cases only require antibiotics; however in some severe cases, surgical drainage may be needed. ²⁵

Bezold abscess

Bezold abscess is a complication of coalescent mastoiditis, resulting from inflammation and necrosis of the mastoid tip. The inflammatory process extends deep to the superficial fat planes that surround the sternocleidomastoid muscle, and therefore do not produce an obvious palpable abnormality which may prevent early detection. The original description of Bezold’s abscess entailed erosion of the mastoid at the level of insertion of the posterior belly of the digastric muscle (digastric groove) with spread of the infection along the course of the digastric anteriorly (Figure 4).

Figure 4.

Bezold abscess in an 8-year-old male patient presenting with fever, bilateral earache, and left-sided swelling over the mastoid bone. Axial CT scan, bone window(A), and soft tissue window(B) showed left otitis media and coalescent mastoiditis with a low density rim peripherally enhancing lesion (blue arrow) seen along the tip of the left mastoid in the retro-auricular area displacing the external ear anteriorly. Finding consistent with Bezold abscess.

Pneumatization of the mastoid tip is a predisposing factor, due to thinning of the cortex. ²⁸ For this reason, Bezold abscess is more common in adults than in children. ²⁹ Other risk factors include presence of a cholesteatoma and prior mastoidectomy. ³⁰ It is important to distinguish a Bezold abscess from a subperiosteal abscess which is due to extension of the infection through erosion of the lateral mastoid cortex. This abscess is easily palpable in contrast to a Bezold abscess. ²³ In addition, Bezold abscess is more likely to spread to the deep spaces of the neck including the carotid, prevertebral, danger, and retropharyngeal spaces.

Presenting signs and symptoms include fever, otalgia, neck pain, decreased neck range of motion, and facial paralysis secondary to CN VII involvement. Early surgical drainage is generally required for treatment. ³¹

Ludwig’s Angina

Ludwig’s angina is cellulitis of the floor of the mouth involving the sublingual, submental, and submandibular spaces. It is a rapidly progressive infection that could be life-threatening due to sublingual edema causing elevation and posterior displacement of the tongue leading to airway compromise, and, in neglected cases, infection may spread to the mediastinum causing descending mediastinitis.^9,32,33 Although it is mostly caused by mandibular tooth infection and pericoronitis, some cases originate from infection in the pharynx, sinuses, ^32,34,35 or secondary to submandibular sialadenitis.

Patients typically present with pain and swelling of the floor of the mouth and rarely present with chest pain due to involvement of the mediastinum. ⁹

Imaging is useful for assessing dental infection or abscess and to assess airway patency (Figure 5). Contrast-enhanced CT and MR images show a phlegmonous process with distortion and swelling of the floor of the mouth with thickening and enhancement of adjacent soft tissues. Enlargement of the submental and/or submandibular lymph nodes, thickening of the platysma muscle, and infiltration of the subcutaneous fat are also frequently seen. Pus or gas formation may be present in late presentations^10,36; however, an abscess need not be present to make the diagnosis.

Figure 5.

Ludwig angina with abscess formation in a 37-year-old female with a history of recent tooth extraction presenting for painful swelling of the left side of the face with radiated pain to the left ear. Axial (A), coronal, (B) and sagittal (C), contrast enhanced CT scan of the neck showing left sublingual space abscess (blue arrows) containing gas bubbles with a phlegmon in the left sublingual space and fat stranding in the submandibular space (image C) consistent with cellulitis.

After securing the airway, intravenous antibiotics are the go-to treatment. Surgical drainage of the abscesses might be needed. ³⁷

The differential diagnosis of Ludwig’s angina includes angioedema which can be hereditary, due to allergy, induced by ACE-inhibitors or idiopathic. Angioedema is associated with swelling of the face, lips, and tongue, and laryngeal edema and stridor may be present.

Epiglottitis (also known as supraglottitis)

Epiglottitis is acute inflammation of the epiglottis and adjacent supraglottic structures that could be life threatening due to potential airway obstruction.^38,39 Epiglottitis has become more common in adults than in children and less prevalent overall since the emergence of antibiotic therapy and the introduction of the Haemophilus influenzae type B vaccine.^39,40 Epiglottitis can be caused by extension of infections from other head and neck regions, such as dental infection, skin cellulitis, laryngopyocele, tonsillitis, and even from non-infectious processes such as sarcoidosis. ⁸

Although it is rapidly progressive with high risk of airway obstruction in children, in adults, the larger size of airway makes epiglottis relatively less critical and more slowly progressive.^38,39 Thus, whereas acute epiglottitis in children presents with signs of airway compromise like stridor and tripod posturing, in adults it presents with more usual upper respiratory tract symptoms like sore throat and dysphagia. ⁴¹

Diagnosis is clinical but is confirmed by nasopharyngoscopy. ⁴² The classic “thumbprint” sign may be seen on lateral soft-tissue neck radiographs, but this imaging modality has poor sensitivity. ⁴² Bedside ultrasound, CT may also be considered as adjunctive testing to rule out other possible diagnosis such as retropharyngeal abscesses. ⁴³ Contrast-enhanced CT scan generally shows thickened, edematous, and enhancing epiglottis and aryepiglottic folds with narrowing of the airway (Figure 6).

Figure 6.

Epiglottitis in a 30-year-old male with 3 days history of productive cough, presenting for sudden onset dysphonia, globus sensation, and stridor. Axial (A) and sagittal (B), contrast enhanced CT scan of the neck showing enlarged and thickened epiglottis (yellow arrows) and aryepiglottic folds with edema and mucosal enhancement.

Antibiotics are the mainstay of initial treatment with steroids considered potential adjuncts. Intubation or tracheostomy is sometimes required to secure the airway. ⁴⁴

Parapharyngeal space abscess

A potentially life-threatening infection that most commonly develops secondary to tonsillitis/peritonsillar abscess or odontogenic infection. ⁴⁵ Direct spread from sources in other neck spaces or by direct inoculation from penetrating trauma (such as a foreign body in the oropharynx) are less common causes. Presenting symptoms include fever, sore throat, dysphagia/odynophagia, and fluctuant neck swelling.

Due to the proximity of the parapharyngeal space to several vital structures, there are a number of serious complications that can develop including airway compromise due to mass effect or reactive laryngeal edema, internal jugular vein thrombosis, carotid pseudoaneurysm and blowout, spread to the retropharyngeal space, and subsequent mediastinitis.

The imaging modality of choice in the acute setting is CT scan of the neck. A small abscess is relatively easy to localize to the PPS, as the abscess becomes larger, this may become more challenging, and attention should be paid to the pattern of displacement of the other neck spaces.

The differential diagnosis on imaging includes an infected lymphatic malformation (look for insinuation into adjacent spaces without significant mass effect) and a necrotic tumor. MRI can be helpful to rule out the latter by demonstrating abnormal restricted diffusion in the center of the abscess indicating presence of pus (Figure 7). Whereas in necrotic tissue, there is restricted diffusion in the solid hypercellular peripheral component of the tumor. Tumors that involve the parapharyngeal space include salivary gland tumors (benign mixed tumor being the most common, arising either from minor salivary gland rests or from extension from the deep lobe of the parotid gland), nerve sheath tumors (most commonly Schwannoma), paragangliomas, and lipomas. ⁴⁶

Figure 7.

Parapharyngeal space abscess in a one-year-old female presenting with fever, dyspnea, and left neck mass. Contrast enhanced, coronal CT scan of the neck (A) and contrast enhanced T1 weighted MRI image of the neck (B) showing a rim enhancing, left parapharyngeal abscess (yellow arrow). It shows diffusion restriction on DWI (C) corresponding to the non-enhancing/fluid component indicating presence of pus.

Parapharyngeal abscess should be distinguished from a peritonsillar abscess (quinsy). The latter arises between the tonsillar capsule and the constrictor muscles while a parapharyngeal abscess lies lateral to the constrictor muscles.

Treatment is with antibiotics, image-guided aspiration, and surgical drainage (transoral or transcervical). ⁴⁷

Retropharyngeal abscess with descending mediastinitis

Retropharyngeal abscess (RPA) is caused by either the spread of infection from a site that drains into the retropharyngeal lymph nodes leading to suppurative lymphadenopathy and subsequent LN rupture or direct inoculation of the retropharyngeal space typically by an ingested sharp foreign body that penetrates the posterior wall of the pharynx like a fishbone. A major complication of RPA is acute mediastinitis. It is important to understand the anatomy of the deep cervical fascia in order to accurately diagnose an RPA. The deep cervical fascia is composed of three layers: the superficial, middle, and deep layers. These layers divide the neck into multiple spaces.^11,27 The superficial layer covers the entire neck deeper than the platysma. The middle layer encloses all the visceral organs and forms the visceral space in the infrahyoid neck. The deep layer encases the paravertebral muscles and forms the perivertebral space. The deep layer splits into two leaves, the ventral leaf which is called the alar fascia and the dorsal leaf is the prevertebral fascia. The space between the posterior aspect of the middle layer and the alar fascia is called the retropharyngeal space which extends from the skull base to the thoraco–cervical junction between the C6 and T4 vertebra. The space between the alar fascia and the prevertebral fascia (the two leaves of the deep layer of the cervical fascia) is called the danger space; it extends from the skull base to the mediastinum. Finally, the space between the prevertebral fascia and the spine is called the prevertebral space (Figure 8).^11,26,27

Figure 8.

Sagittal T2 weighted image of the neck illustrating the extent of the retropharyngeal space (green line) terminating at around C7 vertebral body with the danger space (red line) and the prevertebral space (blue line) extending beyond the field of view to the mediastinum.

The retropharyngeal space contains deep cervical lymph nodes that drain the upper respiratory tract, the middle ear, and the paranasal sinuses.

An infection in the retropharyngeal space can bypass the alar fascia because the latter ends laterally at C1, creating a gap between C1 and the skull base; thus, providing a potential point of entry into the danger space. ⁴⁸ If infection spreads to the danger space, it can extend inferiorly to the mediastinum and cause descending mediastinitis which has a high mortality rate due to its non-specific symptoms and clinical findings leading to delayed diagnosis (Figure 9). ¹¹ Although infections most commonly spread through the danger space to the mediastinum,^38,49 they also may spread through the carotid sheaths and visceral space.

Figure 9.

Retropharyngeal abscess with extension into the mediastinum in a 63-year-old male patient presenting for dysphagia and odynophagia. CT scan of the neck (A, B, C) and thorax (D) showed multiple fluid collections, with enhancing rim at the level of the oropharynx (yellow arrow) extending inferiorly to the hypopharynx, posteriorly to the retropharyngeal and the danger spaces reaching the posterior mediastinum (red arrow). This is secondary to spread of a left submandibular abscess (A) which in turn is presumably caused by an odontogenic infection in this patient who had recently had extraction of a left mandibular molar tooth.

Patients usually present with sore throat, neck pain with limited range of motion, cough, and fever. CT and MR are needed for abscess localization and to help distinguish a true abscess from mimics like retropharyngeal edema, cellulitis, and suppurative retropharyngeal lymph nodes. ⁵⁰ A true abscess appears as a rim-enhancing hypoattenuating collection that expands the retropharyngeal space and may contain foci of air as well as fluid.^38,49 while unruptured suppurative lymph nodes while demonstrating similar central low attenuation and rim enhancement are usually localized to the lateral aspect of the retropharyngeal space. Some retropharyngeal abscesses are presumably caused by rupture of a suppurative lymph node. Imaging is also useful for assessment of the potential complications, such as descending mediastinitis. Other complications include extension to the spine and epidural space, airway compromise, and involvement of the major cervical vessels. Small RPAs are treated with intravenous antibiotics. Treatment of larger abscesses is generally via incision and drainage.^3,51

Differential diagnosis of retropharyngeal edema in addition to early infection includes reactive edema in the setting of spondylodiscitis or spine trauma and central venous obstruction.

Cervical spine infection

Cervical spondylodiscitis is most commonly due to hematogenous seeding, and less commonly direct inoculation from spinal surgery or penetrating trauma, or direct extension from an adjacent infection. ⁵² Risk factors for pyogenic spondylodiscitis are infective endocarditis, chronic kidney disease, intravenous drug use, degenerative disease, diabetes, and immunocompromised states.^53–55 The most common infecting organism in pyogenic spondylodiscitis is staphylococcus aureus.^52–56 Atypical pathogens causing spondylodiscitis like Tuberculosis, Brucella, and fungal infection are much less common but are important to recognize. ⁵² Patients usually present with neck pain and elevated inflammatory markers with or without fever and other constitutional symptoms.^52–55

Pyogenic spondylodiscitis usually involves one spinal segment: endplates and intervening disc. On CT, there may be endplate irregularities and erosions, prevertebral inflammatory changes, and epidural phlegmon that progresses to abscess formation in later stages. ⁸ It is important to scrutinize the perivertebral soft tissues as changes such as soft tissue infiltration and epidural phlegmon may precede visible bone changes on CT scan as illustrated in Figure 10. MRI is more sensitive for early detection of spondylodiscitis and evaluation of epidural abscesses. ⁵⁷ On MRI, there is high signal intensity on T2WI/fluid signal intensity in the disc and enhancement post-administration of gadolinium (Figure 10(c) and (d)). Fat-suppressed images are helpful to reveal the contrast enhancement. FDG-PET/CT, bone scan, or gallium scan would be considered if MRI cannot be obtained. ⁵⁶

Figure 10.

73-year-old male presenting for neck pain. Contrast enhanced CT, soft tissue window (A) and bone window (B) show prevertebral soft tissue thickening (red arrow) and anterior epidural phlegmon (yellow arrow) at C4–C5 with no appreciable endplate changes except for subtle disk space narrowing. Sagittal T2WI and contrast enhanced T1WI (C and D) show end-plate edema (green arrows) and enhancement (blue arrows) at the same level again with the anterior epidural thickening and enhancement (orange arrow). Findings are consistent with acute spondylodiscitis.

Patients are usually treated conservatively.^52,57 Surgical intervention is reserved for patients with neurological deficit, spinal cord compression, spinal instability, progressive deformity, and infection or abscess not responding to medical treatment. ⁵⁶

Spinal tuberculosis has a more indolent clinical presentation and most commonly involves the thoracic spine.^52,58–61 Differentiation of pyogenic and tuberculous spondylitis may be difficult. In contrast to pyogenic infection, tuberculosis tends to involve multiple vertebral levels (three or more levels), involvement of the anterior vertebral bodies with subligamentous spread, relative disc sparing, thin-wall abscesses, large cold paraspinal abscesses, and intact dorsal meningo-vertebral ligament. (Figure 11).^52,58–62 Gibbus deformity is a known complication of tuberculosis.^58,59 Brucellar spondylitis, a zoonotic infection, may present with diffuse spondylitis with intact vertebral architecture. Paraspinal collections in brucellosis are smaller than tuberculosis.^52,59,60

Figure 11.

Cervical spondylodiscitis in a 31-year-old male presenting for cough and neck swelling and found to have positive PPD test. Enhanced CT scan of the neck, axial (A) and corona l (B) soft tissue window and sagittal bone window (C), show multiple retropharyngeal and prevertebral collections and cystic lesions representing necrotic lymph nodes (the largest shown in image A and B) (yellow arrow). There is associated multilevel bone destruction of several vertebral bodies (C) (green arrow). Epidural extension (red arrow) was seen at T1–T3 with obliteration of the spinal canal and compression of the spinal cord (better seen on the soft tissue window not shown here). Culture of the lesion was positive for Mycobacterium tuberculosis complex.

Aspergillus spondylitis occurs almost exclusively in the immunocompromised patients. ⁶³ Serrated appearance of the vertebral endplates, subchondral T2 hypointensity, and preserved nuclear cleft are features of Aspergillus spondylitis. Similar to tuberculosis, multilevel involvement and subligamentous spread may be seen. ⁶³

Neuropathic spondyloarthropathy may simulate spondylodiscitis.^52,64 Clinical context, involvement of both anterior and posterior elements, vacuum phenomenon, bone sclerosis, malalignment, paraspinal soft tissue masses, or fluid collections containing bone debris are clues for neuropathic spondyloarthropathy. ⁶⁴ If diagnosis remains uncertain, biopsy and culture may be necessary. ⁶⁴

Septic arthritis of the atlanto-axial or facet joints, like any other joint, present with joint effusion, expansion, rim-enhancement, bone marrow edema, and inflammatory changes in the surrounding tissues.^65–67

Acute invasive fungal rhinosinusitis

Acute invasive fungal rhinosinusitis (AIFR) is a life-threatening disease with a high mortality rate (24–61%).^68–72 The primary risk factor for AIFR is neutropenia and neutrophil dysfunction, and it occurs almost exclusively in immunocompromised patients, whether due to hematologic malignancies, chemotherapy, immunosuppressive medications, diabetes, or acquired immunodeficiency syndrome.^68–72 Early diagnosis is crucial to improve outcome and limit morbidity.^68,72,73 Aspergillus species are the most common causative agents in neutropenic patients; in diabetics, Zygomycetes fungi (Mucor, Rhizopus, Rhizomucor, and Absidia) are the most common.^68,74

Initially, patients usually present with non-specific symptoms such as fever, nasal congestion, and rhinorrhea.^68,69,72 More worrisome and specific features such as vision changes, proptosis, and cranial neuropathy usually occur in advanced cases.^68,69,72 Therefore, a high clinical index of suspicion is needed for early detection. Other clinical features are facial pain, headache, facial swelling, epistaxis, and altered mental status.^68,69 Endoscopic findings may range from edema, ulcer to frank necrosis involving the turbinates, nasal septum, and nasal floor. ⁶⁹ Necrosis is a specific endoscopic finding in AIFR. ⁶⁹ Biopsy is performed to confirm the diagnosis. The disease may be limited to the nasal cavity which has relatively a better prognosis. Orbital and intra-cranial extension carries a much worse prognosis.

Imaging plays an important role in diagnosis and evaluation of disease extent.^74–76 CT is often the first imaging modality used. However, MRI is superior to CT in detecting early changes of AIFS and in evaluating orbital and intracranial extension. ⁷⁵ Early findings are unilateral nasal soft tissue, mucosal thickening, nasal turbinate ulcer and mucosal non-enhancement, periantral fat infiltration, and soft tissue in the pterygopalatine fossa, nasolacrimal duct, or lacrimal sac (Figures 12 and 13).^75,76 In immunocompromised patients, radiologists should diligently look for these findings. Late findings are bone destruction, orbital invasion, and intracranial extension through the superior orbital fissure, foramen ovale, and rotundum. (Figure 14).^75,76

Figure 12.

Early mucormycosis findings in a 13-year-old immunocompromised patient. There is a non-enhancing necrotic ulcer in the nasal septum (green arrow) consistent with mucormycosis. Patient underwent localized resection of the affected part of the septum (B).

Figure 13.

Coronal enhanced CT image (A) shows asymmetric soft tissue thickening and enhancement in the right nasal cavity and opacification of the right maxillary sinus (yellow arrow), soft tissue in the nasolacrimal duct (red arrow) and intra-orbital fat stranding. Axial CT image (B) shows subtle right peri-antral fat stranding and increased density in the right pterygo-palatine fossa (PPF) (green arrow).Axial T1 weighted fat-sat post-contrast image (C) shows non-enhancing mucosal disease and peri-antral inflammatory changes.

Figure 14.

Rhino-cerebro-orbital mucormycosis. Axial and coronal T1WFS post-gadolinium images (A) and (B) respectively, axial diffusion weighted (C) and axial unenhanced CT (D). There is necrosis of the right side of the palatal mucosa and right middle turbinate not enhancing after contrast administration (B). The infection extends from the right PPF, through the foramen rotundum into Meckel’s cave (yellow arrow) meanwhile involving the trigeminal nerve and right aspect of the pons (green arrow). On a later non-enhanced brain CT (D) the patient developed hemorrhage in the right temporal lobe (red arrow).

A retrospective case–control study ⁷⁶ of 42 patients with AIFR and preexisting risk factors showed that the presence of one of the following seven CT findings (periantral fat, bone dehiscence, orbital invasion, septal ulceration, pterygopalatine fossa, nasolacrimal duct, and lacrimal sac opacification) has 87% positive predictive value, 95% negative predictive value, 95% sensitivity, and 86% specificity. The same study showed that the presence of two findings has 88% sensitivity, 100% specificity, and 100% positive predictive value. On MRI, salient features include low signal intensity on T2W imaging within the sinus cavity due to presence of paramagnetic substances like iron and magnesium (although this can also be seen with non-invasive fungal infections) and lack of enhancement on post-gadolinium images corresponding to necrosis. ⁷⁴

Although the radiologic features of AIFR are generally similar across the different causative organisms, one series found that Mucor species (as opposed to Aspergillus) demonstrated a higher degree of bilateral involvement. ⁷⁷

The complications are vascular thrombosis, cavernous sinus thrombosis, carotid pseudoaneurysm, perineural spread, cerebritis, cerebral abscess, orbital cellulitis, and osteomyelitis.^68,78 The mainstay of treatment is aggressive surgical debridement with systemic antifungal therapy along with correction of the underlying comorbidities. Surgical debridement correlates with mortality and should be considered in all cases despite advanced disease and patients comorbidities. ⁶⁸

Orbital cellulitis

Orbital cellulitis also known as post-septal cellulitis is a life-threatening orbital infection of the soft tissue posterior to the orbital septum. ⁷⁹ Orbital cellulitis can be located: 1—within the cone (intraconal), which consists of the extraocular muscles encased by an intermuscular membrane; 2—outside the muscular cone (extraconal) between the intermuscular membrane and the orbital walls; and 3—subperiosteal locations (Figure 15).

Figure 15.

Normal ocular anatomy. Axial contrast enhanced CT scan of the orbit and the globe (yellow circle) with soft tissue and bone window reformats. The dotted lines indicate the expected location of the orbital septum, which separates the preseptal and post-septal spaces. The figure highlights the extraconal space (green asterisks), intraconal space (red asterisks), the lateral rectus muscle (black arrow), medial rectus muscle (red arrow), the optic nerve (pink arrow), the lamina papyracea (green arrow), superior orbital fissure (yellow arrow,) and zygomatic bone (blue arrow).

Orbital cellulitis is typically secondary to paranasal sinusitis but may also be seen after penetrating orbital injury or ocular surgery. Complications include vision loss, superior ophthalmic vein and cavernous sinus thrombosis, meningitis, and intracranial abscess formation. ⁸⁰ CT findings include sinus opacification, retrobulbar fat stranding, and extraconal/intraconal fluid collections, with mass effect on the extraocular muscles and proptosis. Tenting of the posterior globe and stretching of the optic nerve can be seen with more severe degrees of proptosis and is an important sign that can be predictive of visual compromise. Abscesses might not necessarily demonstrate peripheral enhancement especially in early presentation (Figure 16).^81–83 The differential diagnosis of orbital cellulitis includes inflammatory conditions such as idiopathic orbital inflammation (also known as orbital pseudotumor), Wegener’s granulomatosis, IgG4-related disease, and Sarcoidosis as well as thyroid orbitopathy. ⁸⁴ Some neoplasms that extend from the sinuses to the orbit may mimic an aggressive infection.

Figure 16.

Orbital cellulitis in a 48-year-old male patient presenting with diplopia. Early CT scan (A) showed acute sinusitis in the left ethmoid air cells. There is left post-septal cellulitis with an intraorbital extraconal subperiosteal abscess along the lamina papyracea (blue arrow). On late images (B) there was an increase in the left proptosis with tenting of the left globe (green arrow) and stretching of the optic nerve, a sign of increased orbital tension.

Treatment is with intravenous antibiotics. In case of high risk of vision loss, poor response to initial treatment, and/or presence of large intraconal or subperiosteal abscess, surgical drainage may be necessary. ⁸⁵

Cavernous sinus thrombosis

The cavernous sinuses lie on either side of the sella turcica, they are venous spaces formed (like the other dural venous sinuses) by the splitting of the inner meningeal and outer periosteal layers of the dura. They receive blood from the orbit via the superior ophthalmic vein and the brain via cerebral veins and the sphenoparietal sinus, and they drain posteriorly into the superior and inferior petrosal sinuses. There are also intercavernous sinuses which serve as a communication between the two cavernous sinuses. The cavernous sinuses contain the internal carotid artery (ICA) and cranial nerve (CN)VI within the lumen of the sinus itself and CN III, IV, V1, and V2 within its lateral wall.

Cavernous sinus thrombosis is a serious condition associated with high morbidity and mortality for which early diagnosis and treatment are crucial. The most common cause of cavernous sinus thrombosis is sinusitis, specifically of the sphenoid sinuses and ethmoid air cells. ⁸⁶ Facial, nasal, pharyngeal, odontogenic, and orbital infections are less common causes of CST. Non-infectious causes of CST as with other dural venous include hyper-coagulable states such as pregnancy, dehydration, OCP use, and malignancy.

Presenting symptoms include headache, fever, proptosis, chemosis, periorbital swelling, and painful ophthalmoplegia.

The diagnosis is generally made nowadays on CT and MRI with contrast. Findings include a filling defect/non-opacification of the sinus with or without enlargement with loss of the normal concavity which is best appreciated on the coronal images. Secondary signs related to venous congestion including dilatation of the superior ophthalmic vein, proptosis, and periorbital edema (Figures 17–19). A large thrombus may extend into the superior ophthalmic vein or petrosal sinuses. On imaging, the differential diagnosis includes cavernous sinus neoplastic lesions such as Schwannoma, meningioma, lymphoma, cavernous hemangioma, and perineural tumor spread as well as inflammatory and granulomatous conditions such as Tolosa-Hunt syndrome, sarcoidosis, and tuberculosis. These neoplastic and infiltrative processes generally show some degree of enhancement as opposed to CST. Carotid-cavernous fistula, similar to CST, causes enlargement of the sinus and dilatation of the superior ophthalmic vein and can be confused with CST on unenhanced CT or MRI, but on an enhanced study, CC fistula causes early opacification of the sinus rather than a filling defect.

Figure 18.

Coronal (A) and axial (B) T1WFS MRI images done 4 days later showing lack of enhancement of the left cavernous sinus consistent with cavernous sinus thrombosis (red arrow). There is also lack of enhancement in the sphenoid sinus mucosa (yellow arrow), laterally and inferiorly suggestive of ischemic mucosa with extension of abnormal signal intensity into the sphenoid bone and left side of the clivus indicative of osteomyelitis (not shown). Moreover, there is abnormal dural enhancement and thickening in the left middle cranial fossa (green arrow) as well as abnormal enhancement in the left masticator space (B) denoting spread of infection.

Figure 17.

Cavernous sinus thrombosis in a 35-year-old female patient with recurrent pseudomonas sinusitis presenting with left cranial nerve VI palsy. CT scan showed enlargement and non-enhancement within the left cavernous sinus (blue arrow), associated with enlargement of the left superior ophthalmic vein (not shown), in keeping with left-sided cavernous sinus thrombosis. Note the changes of sphenoid sinusitis (green arrow).

Figure 19.

At one month follow-up, TOF MRA of the intracranial vessels (C) shows absence of flow-related enhancement in the left internal carotid artery denoting occlusion of the left internal carotid artery. There is flow related enhancement in the left MCA, left PCA, and left ACA, filling through the circle of Willis.

The differential diagnosis based on the clinical presentation includes orbital cellulitis (another cause of painful ophthalmoplegia), preseptal cellulitis, and orbital apex syndrome.

Lemierre syndrome

Also known as septic thrombophlebitis of the internal jugular vein (IJV) and post-anginal sepsis is a rare but potentially life-threatening disease that is typically a complication of tonsillar/pharyngeal infection. It most commonly affects young adults. ⁸⁷

The non-spore forming anaerobic bacteria Fusobacterium necrophorum is the most common causative organism accounting for more than 80% of cases. ⁸⁸

The severity of the disease lies in the propensity of the infected IJV thrombus to cause septic emboli, most commonly to the lungs. Less common sites of systemic sepsis like septic arthritis, osteomyelitis, splenic and hepatic abscesses, and meningitis have also been reported. ⁸⁹ The presenting symptoms include symptoms of acute pharyngitis, fever, neck pain, tenderness and swelling, hoarseness, and dysphagia which can occur due to involvement of CN IX and X in the carotid space. ⁹⁰

The diagnosis can be made on CT or MRI with contrast showing the thrombosis of the IJV with thrombus (Figure 20). US can also be used for this purpose by showing a non-compressible thrombosed vein with or without expansion .Although US can miss thrombi located proximally at the skull base or other difficult areas to access such as behind the clavicle, the presence of indirect signs, namely, loss of respiratory variability and cardiac pulsatility on spectral Doppler exam may suggest the diagnosis. CT scan is superior to chest x ray in demonstrating the presence of septic emboli and resultant pulmonary infarcts which appear as predominantly peripheral opacities with cavitation. A vessel leading to the pulmonary opacity (feeding vessel sign) and reduced central enhancement can also be observed and relatively specific.^90–92

Figure 20.

Seven-month-old girl presenting with coughing, intermittent fevers, and dyspnea then developed right neck stiffness and pain. Contrast enhanced CT neck with coronal reconstruction (A), MRV (B), and CT chest (C) revealed nonopacification of the right internal jugular vein (yellow arrow), sigmoid and transverse sinuses (blue arrows) indicative of thrombosis, and bilateral cavitating lung lesions due to septic emboli (red arrows). Findings are characteristic of septic thrombophlebitis of the internal jugular vein. (Case courtesy of David Yousem).

Treatment is with IV antibiotics with good anaerobic coverage. Anticoagulation should be considered in certain cases. ⁹⁰

Necrotizing fasciitis

Necrotizing fasciitis (NF) of the head and neck is a rare but life-threatening condition. NF more commonly affects the lower extremities, trunk, and perineum. In the head and neck, the initial cause is usually dental or pharyngeal infection. ⁹³

It is characterized by a rapidly spreading infection that initially involves the superficial fascia with extensive necrosis then may extend to the deep fascia and other deep soft tissues, usually with associated systemic toxicity. When it involves the neck, it can spread caudally into the mediastinum (Figure 21(c)), resulting in pulmonary complications that may lead to death. ⁹³

Figure 21.

Necrotizing fasciitis in a 65-year-old male. Axial (A and C) and sagittal reconstructed (B) CT-scan shows significant soft tissue edema, fat streaking and fluid with extensive soft tissue emphysema seen mainly in the left masticator space (yellow arrow) and infratemporal fossa, left TMJ, retropharyngeal spaces (green arrow), subcutaneous soft tissues anterior to the larynx and extending down to the mediastinum (red arrow).

Presenting symptoms include rapidly spreading erythema, tenderness, and pain, the latter is described as extreme, thought to be due to neural involvement, ⁹³ ; its disproportionate nature is a helpful specific clinical clue to the diagnosis. ⁹⁴

The usual causative organisms are obligate anaerobes, Enterobacteriaceae, non-group A streptococcus, and group A streptococcus. ⁹⁵

Imaging findings include skin thickening, fascial thickening, and edema, in particular in the deep intermuscular fascia, inflammatory changes involving multiple compartments and later on development of areas of non-enhancement denoting necrosis.^96,97 Soft tissue gas which is best seen on CT scan is highly supportive of the diagnosis (Figure 21). The differential diagnosis on imaging includes cellulitis and erysipelas. Diffuse edema in the superficial and deep fat planes can be seen in the setting of central venous obstruction (internal jugular vein or superior vena cava) and should not be mistaken for necrotizing fasciitis. NF should also not be confused with iatrogenic soft tissue emphysema, in particular when caused by tooth extraction using compressed air-driven drill, ⁹⁸ as this can be an unrecognized entity. The lack of inflammatory changes on imaging despite the extensive emphysema tracking along the deep spaces of the neck and lack of local and systemic signs and symptoms should aid in the differentiation.

Early recognition of NF is crucial to prevent the high morbidity and mortality of this condition. The treatment is surgical debridement of necrotic tissues and antibiotic coverage.

ORCID iD

Tamara El Annan https://orcid.org/0000-0002-0394-597X