Elsevier

Clinical Radiology

Volume 65, Issue 1, January 2010, Pages 73-81
Clinical Radiology

Pictorial Review
Tuberculosis in the head and neck — a forgotten differential diagnosis

https://doi.org/10.1016/j.crad.2009.09.004Get rights and content

The aim of the present review is to illustrate the pathogenesis and imaging findings of tuberculosis in specific head and neck regions to avoid pitfalls in diagnosis. It is imperative to be aware of, and provide an early diagnosis for, extra-pulmonary tubercular lesions in the head and neck. A high index of suspicion combined with an appropriate clinical setting serves as an important background to diagnose tubercular lesions in the head and neck region and differentiate them from malignancy and other disease entities. Early diagnosis and treatment can prevent irreversible and debilitating complications and mortality from disseminated tuberculosis.

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)

  • L.C. Barbosa de Sa et al.

    Laryngo-pharyngeal tuberculosis

    Rev Bras Otorrinolaringol

    (2007)
  • A.T. Ahuja 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

  • K. Menon 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)
  • H.P. Kee et al.

    Concurrent tuberculosis of the larynx and the tonsil

    Yonsei Med J

    (1988)
  • K. Yamamoto et al.

    Tonsillar tuberculosis associated with pulmonary and laryngeal foci

    Intern Med

    (2002)
  • W.K. Moon et al.

    CT and MR imaging of head and neck tuberculosis

    RadioGraphics

    (1997)
  • K. Singh et al.

    Pseudo tumoral laryngeal tuberculosis

    India Paediatr

    (2003)
  • M. Unal et al.

    Tuberculosis of the aryepiglottic fold and sinus pyriformis

    Mount Sinai J Med

    (2006)
  • W.K. Moon et al.

    Laryngeal tuberculosis: CT findings

    AJR Am J Roentgenol

    (1996)
  • M.M. Lindell et al.

    Laryngeal tuberculosis

    AJR Am J Roentgenol

    (1977)
  • P.K.Y. Lam et al.

    Medialisation thyroplasty for unilateral vocal fold paralysis associated with chronic pulmonary tuberculosis

    Hong Kong Med J

    (2007)
  • L. Alex et al.

    Tuberculosis of parotid gland — a case report

    India J Radiol Imaging

    (2006)
  • M. Seeley et al.

    Two cases of parotid tuberculosis

    J NZ Med Assoc

    (2007)
  • F. Alyas et al.

    Diseases of the submandibular gland as demonstrated using high resolution ultrasound

    Br J Radiol

    (2005)
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