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18F-Fluorodeoxyglucose-Positron Emission Tomography/Computed Tomography in Tuberculosis: Spectrum of Manifestations
Address for correspondence: Dr. Rakesh Kumar, Department of Nuclear Medicine, Division of Diagnostic Nuclear Medicine, All India Institute of Medical Sciences, New Delhi - 110 029, India. E-mail: rkphulia@yahoo.com
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Abstract
The objective of this article is to provide an illustrative tutorial highlighting the utility of 18F-fluorodeoxyglucose-positron emission tomography/computed tomography (18F-FDG-PET/CT) imaging to detect spectrum of manifestations in patients with tuberculosis (TB). FDG-PET/CT is a powerful tool for early diagnosis, measuring the extent of disease (staging), and consequently for evaluation of response to therapy in patients with TB.
Keywords
Fluorodeoxyglucose-positron emission tomography/computed tomography
positron emission tomography/computed tomography
tuberculosis
Introduction
Tuberculosis (TB) is contagious and airborne infectious disease. It ranks as the second leading cause of death from a single infectious agent, after the human immunodeficiency virus. Over past two decades, TB remains a worldwide emergency despite substantial improvement in health service. Patients with sputum-negative pulmonary TB (PTB) and extra-PTB (EPTB) are difficult to diagnose and may be missed at all points of care. Imaging for diagnosis of TB is challenging because it can mimic other diseases such as sarcoidosis or neoplasm.
Various radiopharmaceuticals used in positron emission tomography (PET) imaging have shown potential utility in TB. The most commonly used PET radiotracer in the management of TB is 18F-fluorodeoxyglucose (18F-FDG). FDG is a surrogate marker for glucose metabolism and has consistently been shown to have increased concentration in areas of inflammation associated with active TB. 18F-FDG-PET/computed tomography (CT) though unable to differentiate between TB and other diseases may still have a role in TB diagnosis in conjunction with other modalities. Increasingly, PET/CT is being used to accurately define the full extent of systemic involvement, yield material for culture and sensitivity studies (to allow an early diagnosis of drug-resistant TB), or potentially to monitor the healing process. PET/CT scans may suggest the sites of safe high-yield biopsies, thus yielding confirmatory histopathology, cultures, or polymerase chain reaction samples.[12]
Fluorodeoxyglucose-Positron Emission Tomography/computed Tomography Findings in Tuberculosis
Pulmonary tuberculosis
Parenchymal involvement:
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18F-FDG-PET/CT showed tracer uptake in areas of lung consolidation ± cavitations surrounded by micronodules and mild uptake within lymph nodes. 18F-FDG-PET is able to differentiate active PTB from old or inactive disease as active tuberculoma has significantly higher maximum standardized uptake value compared with inactive tuberculoma.[3] 18F-FDG-PET/CT has the potential to become a tool for monitoring the treatment response in selected cases of EPTB or multidrug resistance. PET/CT scans can guide accurate targeting of active sites of disease for biopsy, from the thoracic cavity as well [Figures 1–4]
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Lymphadenopathy: FDG avidity with necrosis and calcification may be seen in involved lymph nodes with or without parenchymal lung involvement [Figure 5]. On CT, the enlarged nodes typically show central low attenuation, which represents caseous necrosis, and peripheral rim enhancement, which represents the vascular rim of the granulomatous inflammatory tissue
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Pleural effusion: Pleural effusion may be associated with parenchymal lung involvement or may be present independently. Pleural effusion is usually unilateral and on the same side as the primary focus of TB. The effusion may be large and occur in patients without evidence of parenchymal disease on chest radiographs. The effusion may show mild FDG uptake.
Cardiac tuberculosis
Cardiac TB usually presents as pericardial involvement in the form of pericardial thickening [Figure 3]. Effusions are reportedly less common. Myocardial involvement may be difficult to discern due to physiological FDG uptake and may potentially benefit from dietary preparation aimed at reducing physiological myocardial FDG uptake.[4]
Musculoskeletal tuberculosis
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Bone involvement: Skeletal TB usually occurs secondary to hematogenous spread from other lesions. Spinal TB forms the most common form of skeletal TB forming approximately 50% cases of skeletal TB [Figure 6]. Paradiscal FDG avid lesions with associated cold abscess are the most frequent. Vertebral compression, collapse, and associated deformity may occur. Hip and knee joints form other commonly involved sites of skeletal TB. Involvement of the ankle, shoulder, and elbow may also occur, though far rarer. Involvement of the small bones of the hands and feet may lead to dactylitis. Tubercular osteomyelitis in the absence of arthritis is rare. It has been described as a poorly defined lytic lesion with peripheral sclerosis on imaging[5]
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Muscle involvement: Muscle involvement may occur either as contiguous involvement from adjacent focus of TB or as an independent focus of infection in the muscle. Involvement is usually in the form of an FDG avid cold abscess. The lesions tend to spread along the route offering least resistance and thus track along the fascial planes [Figures 3, 7, and 8].
Tuberculosis involving central nervous system
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Meningeal involvement: Usually seen as involvement of the basal cisterns in the form of basal exudates. Involved areas show contrast enhancement on contrast-enhanced CT. FDG uptake may be seen in involved areas. Choroid plexus enhancement with ventricular enlargement on imaging is highly suggestive of TB meningitis
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Parenchymal involvement: Parenchymal involvement may occur in the form of a tuberculoma, visualized as a ring-enhancing lesion with increased peripheral FDG uptake [Figure 9]. Other forms of involvement include focal cerebritis visualized as a region of increased FDG uptake in brain parenchyma. Cerebritis may progress to form an abscess. Miliary nodules may be seen cases of diffuse miliary TB.[6]
Head and neck tuberculosis
Head and neck TB occurs in about 15% of EPTB:
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Lymph node involvement: Most common location of head and neck TB is within neck nodes. They present as painless cervical lymphadenitis. The involved nodes are homogeneous with central necrosis and calcification. In FDG-PET/CT, they show peripheral increased tracer uptake [Figures 3 and 10]
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Extranodal tuberculosis: Extranodal TB is very rare. The most common affected sites are larynx, temporal bone, and pharynx.
Abdominal tuberculosis
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Lymphadenopathy: Lymphadenopathy is the most common presentation of abdominal TB. In TB, the mesenteric, mesenteric root, celiac, porta hepatis and peripancreatic lymph nodes are most commonly involved, reflecting the lymphatic drainage of the small bowel. Caseating lymph nodes are seen as having hypodense centers and peripheral rim enhancement and increased tracer uptake on FDG-PET/CT [Figures 2, 3 and 8]
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Tuberculous peritonitis: Can be visualized as diffusely FDG avid peritoneal thickening and nodules on fused PET/CT images.[7] Omental thickening is seen often as an omental cake appearance. A fibrous wall can cover the omentum, developing from long-standing inflammation and is called omental line
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Bowel tuberculosis: Better visualized with PET/CT enterography and usually seen as areas of focal FDG uptake with associated thickening/ulceration. Most common site is the ileocaecal region followed by gastroduodenal, colonic, and anorectal region. In early disease, there is symmetric circumferential thickening of cecum and terminal ileum. Later, the ileocaecal valve and adjacent medial wall of the cecum are asymmetrically thickened. In more advanced disease, gross wall thickening, adherent loops, large regional nodes, and mesenteric thickening can together form a soft tissue mass centered around the ileocaecal junction. CT scan can also pick up ulceration or nodularity within the terminal ileum, along with narrowing and proximal dilatation. Other areas of small and large bowel involvement manifest as circumferential wall thickening, narrowing of the lumen, and ulceration. In the colon, involvement around the hepatic flexure is common. Physiological FDG uptake in the gut must be taken into account during any interpretation[8]
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Adrenal gland involvement: Asymmetrical enlargement with foci of increased FDG uptake. Later on, atrophy of the gland with calcifications can be seen [Figure 1][9]
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Hepatosplenic tuberculosis: Can occur as involvement in the form of FDG avid nodules or diffuse involvement which may be visualized as a “hot” liver/spleen [Figure 4][10]
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Urinary system tuberculosis: Usually in the form of Ulcerative and cavitary lesions showing FDG uptake. Complications such as papillary necrosis, scarring, and strictures may be seen. Postdiuretic imaging may aid visualization of lesions in the bladder and pelvicalyceal system[1112]
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Genital tuberculosis: Testicular TB usually occurs due to direct extension from the urinary tract. Epididymal extension may occur secondary to urinary TB or may occur hematogenously in children. Physiological FDG uptake in testis must be taken into consideration while evaluating involvement. Prostate can have TB through direct hematogenous extension.
Female genital TB most commonly occurs in the form of tubo-ovarian abscess which may be unilateral or bilateral [Figure 11]. Involvement of the uterus may also occur. Physiological uterine and ovarian uptake must be taken into account during evaluation of disease status.[1213]
Assessment of Treatment Response
One of the principal areas of interest and relative strength of FDG-PET/CT lies in its potential utility for response evaluation in TB [Figures 12–14]. FDG-PET/CT imaging allows for both interim and end-of-treatment evaluations. Interim treatment response evaluations may facilitate estimation of the efficacy of treatment regimen and may potentially aid clinical decisions regarding treatment protocols and regimens. End-of-treatment evaluations are primarily aimed at searching for residual disease which may require further treatment.[1415] This is more so true in the case of tubercular infections requiring long treatment durations (e.g., skeletal TB) in which drug toxicities are a greater concern.
Financial support and sponsorship
Nil.
Conflicts of interest
There are no conflicts of interest.
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