Pictorial ReviewTuberculosis in the head and neck — a forgotten differential diagnosis
Introduction
Tuberculosis (TB) is a scourge in underdeveloped and some developing countries. The World Health Organization (WHO) Statistical Information System (WHOSIS) reported that India has the highest incidence of TB in the world, with an incidence of 168/100,000 (approximately 42 times the incidence in North America, which stands at 4/100,0001). Extra-pulmonary TB constitutes a high percentage of these lesions (approximately 25%), of which 10–35% are found in the head and neck region.1, 2 The prevalence of human immunodeficiency virus (HIV) infection concomitant with TB is 8.8% and this increases the mortality of the disease by 33%. TB is also a great mimic and remains a diagnostic dilemma. Therefore, it is imperative for residents and radiologists to be familiar with the laboratory tests and imaging appearances of TB.
This study presents the imaging spectrum of tuberculous involvement in the following head and neck regions: oral cavity and oropharynx; larynx; salivary glands; mastoid–middle ear complex; petrous apex; sino-nasal region; skull base and cranio-vertebral (CV) region; thyroid gland; neck spaces; lymph nodes; and skeletal system with associated soft tissues. The pathogenesis, imaging findings, and differential diagnosis of tuberculous involvement in the head and neck region will be discussed.
TB may mimic or co-exist with other conditions in the head and neck; therefore, tissue confirmation is mandatory. All cases included in this manuscript were confirmed using fine-needle aspiration cytology, biopsy, or histology following surgery. Ultrasound and Doppler examinations were carried out on a Philips SD 5000 SonoCT system using high-frequency linear array probes (7.5–12 MHz). High-resolution computed tomography (HRCT) was performed on a Philips Brilliance 40-slice MDCT system and magnetic resonance imaging (MRI) studies were performed on a Philips Achieva 1.5 T MRI system using parallel imaging and surface coil technology whenever necessary.
Section snippets
Pathogenesis
Primary infection by inhaling tubercle bacilli is rare. Secondary infection following pulmonary TB may be either via an exogenous route (infected sputum) involving crypts and presenting as unilateral tonsillar enlargement, or via an endogenous route (haematogenous spread) involving germinal centres and presenting as bilateral tonsillar enlargement.3 It may be associated with laryngeal/hypopharyngeal tubercular foci especially in miliary TB.3, 4, 5, 6
Imaging findings
Tubercular lesions present as a diffuse
Pathogenesis
Primary involvement is rare and occurs by direct infection of the mucosa via aerosolized particles.7 Secondary involvement occurs via expectoration of highly infectious sputum from the tracheo-bronchial tree, via haematogenous spread from sites other than lungs,7, 8 or via lymphatic spread, which is rare.3 There is no age or gender predilection9, 10; however, children with laryngeal TB may not show chest radiographic abnormalities.7 TB and SCCa may coexist in the same patient, hence
Pathogenesis
Tubercular involvement of the salivary glands is rare. The source of infection is secondary and several theories are postulated12: (1) trans-oral spread with retrograde extension along the salivary ducts from the oropharynx, oral cavity or oral mucosa; (2) haematogenous spread from primary disease elsewhere in the body; or (3) lymphatic spread from infected tonsils or, in the case of the parotid gland, from the external auditory canal.13
Imaging findings
At ultrasonography tubercular involvement of the salivary
Pathogenesis
In this region primary involvement is more common than secondary.16 Primary infection occurs by direct implantation through the external auditory canal and a perforated tympanic membrane. Secondary involvement occurs either by aspiration of infected mucus from the upper respiratory tract, with retrograde transmission through the eustachian tube, or by haematogenous spread from an infective focus elsewhere in the body. Complications include hearing loss, facial palsy, abscesses, external or
Pathogenesis
The petrous apex may be extensively pneumatized and rich in bone marrow making it susceptible to haematogenous spread (through venous plexuses) of TB. It may also be infected by retrograde transmission of infection via cell tracts from the mastoid.
Imaging findings
HRCT demonstrates loss of aeration and septa within the mastoid with replacement by soft-tissue density lesions (Fig. 7). On MRI the soft tissue within the petrous apex is hypointense on T1-weighted imaging, hyperintense on T2 and short-tau inversion
Pathogenesis
Sinonasal involvement is nearly always secondary to pulmonary TB, wherein the infection reaches the sinuses by direct extension or via the bloodstream.18 However, the incidence of primary TB of nose and paranasal sinuses has risen in the recent past without any associated clinical or laboratory manifestation of pulmonary TB in the patient.19
Imaging findings
Three imaging stages of the disease have been described5: Stage 1: nasal soft-tissue nodules/paranasal sinus involvement, with periosteal thickening. Stage
Pathogenesis
The skull base and CV junction are secondarily involved by direct extension of disease from the cranial vault, paranasal sinus, or mastoid–middle ear complex, and rarely due to meningitis. Intracranial complications include meningitis, subdural empyema, sellar abscess,5 multiple cranial neuropathies, jugular vein thrombosis, ventral medullary compression, and paraparesis secondary to anterior spinal artery involvement.20 Predisposing factors include immunocompromised hosts and diabetic patients.
Pathogenesis
Tuberculous involvement of the thyroid is rare21 and is due to secondary involvement either by haematogenous spread, via the lymphatic route, or by contiguous spread from adjacent infected larynx and cervical lymph nodes.22 Tubercular thyroid involvement is rare because21 the thyroid gland is enveloped by a tough capsule protecting it from contiguous spread of infection and the high iodine concentration within the gland which acts as a natural antiseptic. Additionally, increased blood flow
Pathogenesis
Secondary lymphatic involvement is common due to acute tubercular pharyngitis/mastoiditis or chronic tuberculous infection of cervical spine or cervical lymph nodes. It commonly occurs in the retropharyngeal space mostly due to persisting infection in the retropharyngeal nodes. Complications include airway obstruction, jugular vein thrombophlebitis, descending suppurative mediastinitis, and vascular occlusions.23
Imaging findings
CT and MRI show variable-sized transpatial, ill-defined, thick-walled masses with
Pathogenesis
This is the most common form of primary head and neck TB constituting 5% of cervical lymphadenopathy with predominant involvement of the posterior triangle, supraclavicular, and internal jugular group of nodes bilaterally.5
Secondary involvement of the cervical lymph nodes is seen following pulmonary TB (the inferior group of nodes in the neck is primarily involved).5
Imaging findings
Ultrasonography24 demonstrates predominantly hypoechoic nodes with or without echogenic hilus (Fig. 12) with a heterogeneous echo
Pathogenesis
Secondary involvement of the spine is via haematogenous spread from a primary source with seeding of septic emboli through small penetrating end arteries subjacent to the vertebral endplate. Disc involvement is by contiguous spread and neurovascular proliferation. Subligamentous extension may produce abscesses in pre- and perivertebral spaces and intra-spinal extension may lead to neural compression.25
Imaging findings
Typical MRI and CT findings include anterior vertebral involvement, narrowing of the disc
Pathogenesis
This is a rare site for involvement of tubercular arthritis, because of peculiarity of blood supply to this joint.29, 30
Imaging findings
CT and MRI demonstrate osteolytic lesions involving the opposing articular surfaces of the sterno-clavicular joint (Fig. 14a) and narrowing of the joint space with subsequent bony ankylosis (Fig. 14b). Other imaging findings include associated soft-tissue inflammatory changes with cold abscess formation.
Differential diagnosis
Low-grade pyogenic infection, rheumatoid arthritis, neoplasm, multiple
Pathogenesis
Calvarial involvement is either secondary to haematogenous spread from pulmonary TB or by contiguous spread from paranasal sinuses and orbits.
Imaging findings
Imaging findings on CT and MRI include osteolytic lesions in the calvarium with associated soft-tissue inflammatory changes, cold abscess formation, and intracranial, extradural, peripherally enhancing, centrally liquefied lesions.
Differential diagnosis
Pyogenic infection and metastases are among the differential diagnoses.
Conclusion
Tuberculous infection affects many sites in the head and neck, and has a variety of imaging appearances, mimicking benign and malignant lesions. The diagnosis of TB can be suggested based on specific imaging features, in the right clinical setting. Early commencement of treatment prevents debilitating complications and morbidity from disseminated disease.
TB should be included in the differential diagnosis of lesions in the head and neck if the patient has history of active TB or a history of
References (31)
- et al.
Laryngo-pharyngeal tuberculosis
Rev Bras Otorrinolaringol
(2007) - et al.
US neck nodes, review abnormal nodes, part II
Clin Radiol
(2003) WHO report 2008: global tuberculosis control — surveillance, planning, financing. Core Health Indicators
- et al.
A clinical review of 128 cases of head and neck tuberculosis presenting over a 10-year period in Bradford, UK
J Laryngol Otol
(2007) - et al.
Concurrent tuberculosis of the larynx and the tonsil
Yonsei Med J
(1988) - et al.
Tonsillar tuberculosis associated with pulmonary and laryngeal foci
Intern Med
(2002) - et al.
CT and MR imaging of head and neck tuberculosis
RadioGraphics
(1997) - et al.
Pseudo tumoral laryngeal tuberculosis
India Paediatr
(2003) - et al.
Tuberculosis of the aryepiglottic fold and sinus pyriformis
Mount Sinai J Med
(2006) - et al.
Laryngeal tuberculosis: CT findings
AJR Am J Roentgenol
(1996)