DOI: 10.1148/radiol.2381031758
(Radiology 2006;238:366-370.)
© RSNA, 2006
Case 90: Disseminated Tuberculosis1
David Pérez-Solís, MD,
Luis H. Luyando, MD,
Azucena Callejo-Ortea, MD and
Manuel Crespo-Hernández, MD, PhD
1 From the Departments of Pediatrics (D.P., A.C., M.C.) and Radiology (L.H.L.), Hospital Universitario Central de Asturias, Celestino Villamil, s/n, 33006 Oviedo, Spain. Received October 29, 2003; revision requested January 20, 2004; revision received February 5; accepted March 18.
Correspondence: Address correspondence to D.P. (e-mail: david.perez{at}sespa.princast.es).
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HISTORY
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A 10-year-old girl who was perinatally infected with human immunodeficiency virus (HIV) was admitted to the hospital with an axillary temperature of up to 39°C (102.2°F) of 12-hours duration. This fever was preceded by asthenia and anorexia of 3-weeks duration. The patient had persistent hepatomegaly and splenomegaly since 9 years of age. Antiretroviral treatment was started at 7 years of age with zidovudine; during the past year, she had been taking stavudine, lamivudine, and ritonavir. The results of a tuberculin skin test 9 months earlier were positive, so she had been taking isoniazid for 6 months. Physical examination at admission showed pallor, inguinal and lateral cervical adenopathies, and hepatosplenomegaly; none of these findings had changed since her most recent outpatient visit, which occurred 8 weeks earlier. Laboratory data revealed white blood cell count of 4500/mm3 (4.5 x 109/L) (normal range, 4500–13 500/mm3 [{4.5–13.5} x 109/L]), hematocrit level of 24.0% (0.24) (normal range, 35%–45% [0.35–0.45]), hemoglobin level of 7.9 g/dL (79 g/L) (normal range, 11.5–15.5 g/dL [115–155 g/L]), and erythrocyte sedimentation rate of 142 mm/h (normal range, 0–10 mm/h). Her CD4 cell count was 208/mm3 (0.208 x 109/L) (normal range, 450–1400/mm3 [0.45–1.4 x 109/L]) and her HIV RNA level was 1 200 000 copies per milliliter. A chest radiograph was obtained. Blood, urine, stool, throat, and gastric aspirate cultures were obtained, and empiric therapy with cefotaxime was started.
The patient was still febrile 10 days after admission, and splenomegaly had increased. Transverse ultrasonography (US) of the abdomen was performed, and at that time, the results of blood and stool cultures showed Klebsiella pneumoniae and Candida albicans with regular bacterial flora, respectively. Cefotaxime was then substituted for tobramycin and amphotericin B; however, the symptoms persisted 1 week later. Thus, a second chest radiograph was obtained, and computed tomography (CT) of the abdomen was performed.
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IMAGING FINDINGS
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At admission, chest radiography revealed no abnormal findings (Fig 1). Transverse abdominal US (Fig 2) depicted an enlarged spleen with multiple small hypoechoic round lesions. A small amount of ascites, which was not visible on the image, was also detected. The second chest radiograph (Fig 3), which was obtained 18 days after the first chest radiograph, revealed a reticulonodular pattern, which was more apparent on the right side of the patient's body. CT images of the abdomen obtained with intravenously administered contrast material (Clarograf; Schering, Berlin, Germany) (Fig 4) showed multiple round hypoattenuating splenic lesions, most of which were smaller than 1 cm in diameter. There were also multiple enlarged nodes in the left paraaortic and right retrocrural regions; some of these nodes had a low-attenuation center and a contrast material–enhanced rim.
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Figure 2: Transverse US image of the abdomen. There are multiple small nodules (arrows) in an enlarged spleen. The lesions are hypoechoic and round. These lesions have different sizes but are all less than 1 cm in diameter.
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Figure 4a: Transverse abdominal CT images obtained after administration of intravenous contrast material. (a) Multiple small subcentimetric hypoattenuating lesions are located in the spleen. There is also a right retrocrural enlarged node with a hypoattenuating central area (arrow). (b) Multiple hypoattenuating splenic lesions and two enlarged nodes with a low-attenuation center and a contrast-enhanced rim in the left paraaortic region (arrows).
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Figure 4b: Transverse abdominal CT images obtained after administration of intravenous contrast material. (a) Multiple small subcentimetric hypoattenuating lesions are located in the spleen. There is also a right retrocrural enlarged node with a hypoattenuating central area (arrow). (b) Multiple hypoattenuating splenic lesions and two enlarged nodes with a low-attenuation center and a contrast-enhanced rim in the left paraaortic region (arrows).
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DISCUSSION
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Culture of gastric aspirate performed at admission yielded Mycobacterium tuberculosis 40 days after admission. Antituberculosis treatment with isoniazid, rifampin, pyrazinamide, and streptomycin was initiated after the second chest radiograph was obtained. After 4 weeks of this therapy, however, the patient remained febrile, and her general condition had not improved. A surgical approach was then proposed. Splenectomy was performed, and some affected lymph nodes and a small portion of the pancreas were removed. Two days after splenectomy, the patient's fever disappeared and her condition improved; 10 days after splenectomy, she was discharged from the hospital. Antituberculosis treatment was continued for 9 months, and she remained asymptomatic 24 months after discharge. Pathologic analysis revealed chronic splenitis, pancreatitis, and lymphadenitis, with caseated granulomata and presence of acid-fast bacilli.
In patients without HIV, more than 80% of tuberculosis (TB) cases are only pulmonary in nature; however, among patients with HIV, up to two-thirds of those patients with TB have extrapulmonary involvement (1). In contrast to adults, who usually are infected with TB before they contract HIV, most children are already infected with HIV when TB infection occurs; thus, primary infection predominates over reactivation in children.
Abdominal TB is a disease that predominantly occurs in young adults, with peak incidence occurring between 20 and 40 years of age. Almost all cases are caused by M tuberculosis; however, with the increased number of HIV infections, Mycobacterium avium-intracelulare has become a major pathogen. The most common abdominal TB manifestations are TB lymphadenopathy, peritonitis, and gastrointestinal TB. Solid organ involvement (ie, involvement of the liver, spleen, or pancreas) occurs less frequently (2,3).
Patients with disseminated TB may have splenic involvement, but splenic TB is rarely the main feature in patients with disseminated TB. Splenic TB has been reported in immunocompetent patients (2,4–6), but it is more commonly associated with patients infected with HIV (7–12). Patients with splenic TB usually have a fever and a constitutional syndrome, and splenic TB should be expected in patients with symptoms (eg, fever, asthenia, night sweats) indicative of TB disease and splenomegaly. In rare cases, splenic TB is associated with spontaneous splenic rupture (11) or hypersplenism syndrome (6).
In patients infected with HIV, antituberculosis drugs should be selected carefully, and drug interactions with antiretroviral agents should be taken into account. Glucocorticoids may be effective in patients who respond slowly to antituberculosis therapy (12). In certain cases, splenectomy may be indicated (7,9).
Diagnosis of splenic TB may be difficult. In areas with a low prevalence of TB, many patients have negative findings at chest radiography and skin testing; however, in areas with a high prevalence of TB, incidence of abnormal chest radiographs and positive skin tests is high in patients without abdominal TB (2). Miliary nodules may not be visible on chest radiographs during the first weeks of the illness; thus leading to a delay in diagnosis (13). Microbiologic staining has a low sensitivity, and culture analysis is a slow process. US and CT are both useful in the detection of ascites, solid organ involvement, lymphadenopathy and bowel thickening, although some of these findings may be missed with US because of overlying gas, operator dependence, and the meticulous technique needed (14).
Splenic TB usually occurs in the miliary form, with nodules that range from 0.5 to 2.0 mm in diameter and cannot be detected on US or CT images (15). Macronodular involvement is uncommon, but it may be detected with these imaging techniques. Reports of splenic TB repeatedly describe US images of splenomegaly with small multiple hypoechoic lesions. In a series of 278 patients with acquired immunodeficiency syndrome who underwent abdominal US, 22 (7.9%) had focal splenic lesions; 18 of these 22 patients had numerous round or oval hypoechoic lesions that were 0.5–2.0 cm in diameter, and all of the hypoechoic lesions were caused by disseminated M tuberculosis infections (10). CT images of splenic TB usually demonstrate low-attenuation lesions that may be single or multiple, may show ring enhancement with administration of intravenous contrast material, and may become calcified (2). The most closely associated CT findings are small multiple hypoattenuating lesions (16), and Salazar et al (12) suggest initiation of empiric antituberculosis treatment in patients with these characteristic findings. CT evidence of focal splenic lesions is seen more frequently in patients with disseminated M tuberculosis infection than in patients with M avium-intracellulare infection (16).
The differential diagnosis of patients with fever, splenomegaly, and multiple hypoechoic hypoattenuating splenic lesions includes splenic abscesses that may be bacterial, fungal, or granulomatous in nature. Pyogenic abscesses are usually solitary. On US images, they appear as small irregular hypoechoic lesions that may evolve into a poorly defined heterogeneous mass. On CT images, they typically appear as single irregularly marginated hypoattenuating lesions. The presence of intralesional gas is pathognomonic of pyogenic infection, although it occurs infrequently. Multiple splenic abscesses, usually smaller than 2 cm in diameter, are commonly associated with nonbacterial infections (ie, fungal and granulomatous infections). Fungal abscesses, when visible, characteristically appear on US images as round hypoechoic lesions with a central hyperechoic area (ie, "bull's-eye" or "target" appearance) that corresponds to inflammatory cells with a surrounding hypoechoic band of fibrosis. The "wheel-in-a-wheel" pattern is seen when the central portion becomes necrotic and hypoechoic. Contrast-enhanced CT typically depicts fungal splenic abscesses as multiple small low-attenuation lesions. Patients with cat-scratch disease may also develop splenomegaly and splenic microabscesses (17).
Neoplasms that involve the spleen—such as lymphoma (both Hodgkin and non-Hodgkin lymphoma), leukemia, metastasis, or even Langerhans cell histiocytosis—may manifest as focal hypoechoic hypoattenuating lesions. Sarcoidosis, which is a systemic granulomatous disease of unknown origin, may also have abdominal involvement with lymphadenopathy and hypoattenuating nodules in the liver and spleen (17,18).
It is generally impossible to differentiate visceral TB lesions from fungal infections, lymphoma, or metastasis—unless they are associated with other typical abdominal TB findings, such as lymph node or bowel involvement (15). Abdominal TB lymphadenopathy has most commonly been reported in the lesser omental, mesenteric, and upper paraaortic regions, whereas in patients with lymphoma, the lower paraaortic lymph nodes are predominantly involved. CT typically depicts enlarged nodes with a low-attenuation center and a contrast-enhanced rim, which correlate with central caseation surrounded by reactive inflammation, whereas the lymphoma lymphadenopathy enhancement pattern is usually homogeneous (19). The involved nodes occasionally show calcification. These characteristic patterns are not pathognomonic, and they may be seen in metastasis from testicular tumors, Whipple disease, and lymphoma after radiation therapy; however, integration with other clinical, laboratory, and imaging findings helps in the differentiation of these findings from TB findings (2,15). In our patient, evidence of contact with TB (ie, positive skin test), characteristic splenic lesions, and low-attenuation enhancing appearance of the retroperitoneal adenopathy made disseminated TB the most likely diagnosis. This was even more evident after the miliary pattern was detected on the second chest radiograph.
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FOOTNOTES
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| Part one of this case appeared 4 months previously and may contain larger images.
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References
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- Andronikou S, Welman CJ, Kader E. The CT features of abdominal tuberculosis in children. Pediatr Radiol 2002;32:75–81.[CrossRef][Medline]
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- Suri S, Gupta S, Suri R. Computed tomography in abdominal tuberculosis. Br J Radiol 1999;72:92–98.[Abstract]
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Congratulations to the 91 individuals and three resident groups who submitted the most likely diagnosis (disseminated tuberculosis) for Diagnosis Please, Case 90. The names and locations of the individuals and resident groups, as submitted, are as follows:
Individual responses
- Hisashi Abe, Osaka, Japan
- Gholamali Afshang, MD, Tinley Park, Ill
- Oguz Akin, MD, New York, NY
- Herminia Tyminski Al-Saffar, MD, Manama, Bahrain
- Canan Altay, MD, Izmir, Turkey
- Albert J. Alter, Madison, Wis
- Dr Juan Ramón Ayuso, Barcelona, Spain
- Ken Baliga, Rockford, Ill
- Sanjay Bhat, Temple, Tex
- Jorge Brito, MD, Coimbra, Portugal
- Marcos Nogueira Chagas, MD, Brasilia, Brazil
- Haris Chrysikopoulos, MD, Kerkyra, Greece
- Y. S. Cordoliani, MD, Paris, France
- Anil Kumar Dasyam, Pittsburgh, Pa
- Thaworn Dendumrongsup, MD, Songkla, Thailand
- Jackson U. Dy, Makati City, Philippines
- Francis Flaherty, MD, Ridgefield, Conn
- Ángeles Franco, Madrid, Spain
- Irwin M. Freundlich, MD, Tucson, Ariz
- Akira Fujikawa, Tokyo, Japan
- Ann S. Fulcher, MD, Richmond, Va
- Douglas Gardner, MD, Windsor, Ontario, Canada
- Gilles Genin, MD, Annecy, France
- Paulo Gil Agostinho, Coimbra, Portugal
- Yves Goël, MD, Lausanne, Switzerland
- Mark Goldshein, MD, Andover, Mass
- Francisco J. Gonzalez, MD, Cantabria, Spain
- Daniel Gridley, MD, Phoenix, Ariz
- Flavius Guglielmo, MD, Basking Ridge, NJ
- Yukihiro Hama, MD, PhD, Bethesda, Md
- Srinivasan Harish, Hamilton, Ontario, Canada
- Ronald J. Homer, MD, Weston, Conn
- Suzanne Yoon Homer, MD, Weston, Conn
- Alfred L. Horowitz, MD, Asheville, NC
- Felix A. Hughes, III, MD, Virginia Beach, Va
- Kiriakos Kalampoukas, Konzai, Greece
- Hung-Wen Kao, MD, Taipei, Taiwan, Republic of China
- Ajit Singh Kashyap, MD, Pune, India
- Ravinder Kaur, MD, Chandigarh, India
- Craig D. Kesack, Doylestown, Pa
- P. Kiely, MB, Limerick, Ireland
- Myeong-Jin Kim, MD, PhD, Seoul, Korea
- Takuji Kiryu, MD, Gifu, Japan
- Yu-Ting Kuo, MD, Kaohsiung, Taiwan
- Stefanos Lachanis, MD, Athens, Greece
- Mario Laguna, West Allis, Wis
- John T. Lim, MD, Newport Coast, Calif
- Dr Kamonporn Limchawalit, Bangkok, Thailand
- David A. Lisle, Brisbane, Australia
- Marina Lucchesi, Buenos Aires, Argentina
- N. B. S. Mani, MD, Nassau, Bahamas
- John A. Mattingly, MD, Belleville, Ill
- Frank McKowne, MD, Vancouver, Wash
- Jonathan Meyer, MD, Chicago, Ill
- Ari Mintz, MD, Lake Forest, Ill
- Sankar Ranjan Mondal, MD, Nassau, Bahamas
- Tammam Nehme, East Wenatchee, Wash
- Cesar Higa Nomura, São Paulo, Brazil
- Edward S. Oh, Tucson, Ariz
- Michael T. O'Loughlin, MD, West Hartford, Conn
- Sanford M. Ornstein, MD, Phoenix, Ariz
- Ann B. Owen, MD, Murfreesboro, Tenn
- Victor A. Pérez-Candela, MD, Las Palmas de Gran Canaria, Spain
- Krishna Mohan Pottala, Atlanta, Ga
- Mauricio C. Ramos, MD, El Paso, Tex
- Venkateswar Rao Surabhi, MBBS, MD, Hyderabad, India
- Mathieu H. Rodallec, Paris, France
- Dr Luc Roussel, Sijsele, Belgium
- Recep Savas, Izmir, Turkey
- Matt Shapiro, MD, Charlottesville, Va
- Niall Sheehy, MD, Dublin, Ireland
- Grady Shue, Bethesda, Md
- Ken Simmons, Sydney, Australia
- Darrin S. Smith, MD, Visalia, Calif
- Scott D. Steenburg, MD, Mount Pleasant, SC
- Marius Stellmann, MD, Stade, Germany
- Kouichi Sugiyama, Hamamatsu, Japan
- Norio Takahashi, MD, Fukui, Japan
- Satoru Takahashi, MD, PhD, Nijmegen, the Netherlands
- Douglas L. Teich, MD, Brookline, Mass
- Eugene Tong, MD, Austin, Tex
- Meriç Tüzün, Ankara, Turkey
- Unni K. Udayasankar, Atlanta, Ga
- Lalendra Upreti, MD, New Delhi, India
- Ricardo Videla, Cordoba, Argentina
- Christopher Vittore, MD, Rockford, Ill
- Dr Silvio Alejandro Vollmer, Rio Negro, Argentina
- Sasan Yasharpour, MD, Staten Island, NY
- Stanko Yovichevich, MD, Sydney, Australia
- Joe Yut, Olathe, Kan
- Yu Zhang, San Francisco, Calif
Resident group responses
- Hospital Italiano de Cordoba Radiology Residents, Cordoba, Argentina
- Hospital of the University of Pennsylvania Radiology Residents, Philadelphia, Pa
- Oregon Health & Science University Radiology Residents, Portland, Ore
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J. Ahualli
Regarding "Case 90: Disseminated Tuberculosis"
Radiology,
January 1, 2007;
242(1):
318 - 318.
[Full Text]
[PDF]
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M. K. Demir, D. P. Solis, and L. H. Luyando
Diagnosis Please Comment
Radiology,
January 1, 2007;
242(1):
319 - 319.
[Full Text]
[PDF]
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TOP
HISTORY
IMAGING FINDINGS
