Extrapulmonary tuberculosis - Imaging Features Outside the Chest · 2019-08-26 · tuberculosis...

Extrapulmonary tuberculosis - Imaging Features Outside theChest

Poster No.: C-1978

Congress: ECR 2015

Type: Educational Exhibit

Authors: S. C. S. Silva, D. N. Silva, R. Amaral, D. Garrido, I. C. S. P. Basto;Ponta Delgada/PT

Keywords: Musculoskeletal spine, Abdomen, Lymph nodes, CT, MR,Diagnostic procedure, Infection, Abscess, Education and training

DOI: 10.1594/ecr2015/C-1978

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Learning objectives

• Recognize imaging manifestations of tuberculosis (TB) affecting various organsystems outside the chest;

• Expose how TB imaging can mimic a variety of other entities;• Illustrate this review with some cases from our institution.

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Background

The recent growing of tuberculosis (TB) prevalence increased general concern about thispathology.

Diagnosis of extrapulmonary tuberculosis is often difficult, this disease can involve anyorgan system, can demonstrate several clinical/radiologic features, and has tendency fordissemination from its primary site. Tuberculosis can mimic numerous other pathologies.

In immunocompromised patients this entity usually comprises multiple extrapulmonarysites like the skeleton, genitourinary tract, and central nervous system [1].

During this review we will talk about common manifestations of TB, likegenitourinary tuberculosis and lymphadenopathy (which are referred as the commonestextrapulmonary ones), and spinal involvement (which is known as the commonest siteof skeletal manifestations).

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Findings and procedure details

Central nervous system tuberculosis is beyond the scope of this poster, but we still haveto mention possible manifestations like meningitis, tuberculoma, abscess, cerebritis, andmiliary tuberculosis.

GENITOURINARY TUBERCULOSIS: is the most common manifestation ofextrapulmonary tuberculosis [2].

Renal Tuberculosis- Mycobacterium tuberculosis reaches the kidneys, by thehematogenous route from the lungs and is often a primary site of genitourinary TB [2].

• The earliest urographic sign, is a "moth-eaten" calix due to erosion, whichis followed by papillary necrosis. The dilatation of the pelvicaliceal system,often with irregular margins and containing caseous debris, usually resultsfrom distal stricture and can compromise the renal function, focal or globally[1]. Destructive dilatation or localized hydrocalycosis, may also be seen [3].Incomplete opacification of the calix, also known as phantom calix, may resultfrom infundibular stenosis [1];

• Within the renal parenchyma there may be cavitations usually detected asirregular pools of contrast material;

• Contracture of the cicatricial fibrotic parenchyma may result in caliceal or renalpelvic traction, which may progress to end-stage fibrosis - strictures of thepelvicaliceal system produce luminal narrowing, either directly or by causingkinking of the renal pelvis (Kerr kink) - and subsequent autonephrectomy;

• Calculi may also be found within the renal collecting system;• Calcifications may be amorphous, granular, curvilinear, or lobar in end-stage

tuberculosis (putty kidney) [1];• Extension of the disease into the extrarenal space should also be excluded [1].

Ureteral Tuberculosis - May be involved by ascent or descent route.

• This type of involvement is seen in half of patients with genitourinary TB [1];• The earliest signs of ureteral tuberculosis are the dilatation and ragged

irregular appearance of the urothelium [3];

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• Ureteric walls may become thickened, usually at points of normal anatomicnarrowing, such as the ureteropelvic junction, pelvic brim and vesicouretericjunction [2];

• In advanced states, ureteral calcifications, strictures, shortening and fillingdefects may be seen [3]. Chronic fibrotic strictures may manifest as beadedor corkscrew appearance [1] and chronic thickening as foreshortened pipe-stem ureter;

• Wall calcifications are rare findings with this entity;• Periureteral inflammatory changes should also be excluded [1].

Bladder Tuberculosis - May become infected by ascent or descent route.

• Restriction of bladder capacity is the most common finding in this cystitis, withwall thickening, ulceration and luminal filling defects, resulting in a shrunkenand calcified bladder;

• Advanced bladder involvement may be complicated by vesicoureteral refluxdue to fibrosis involving the ureteral orifice, and a diminutive and irregularbladder (thimble bladder) [1];

• Wall calcifications are infrequent with this entity [1].

Female Genital Tuberculosis - Salpingitis may be caused by hematogenousdissemination.

• Fallopian tubes (often bilateral) are involved in about 94% of womenwith genital tuberculosis. This entity manifests as multiple strictures andobstruction;

• Endometrial involvement results in adhesions causing deformity and possibleobliteration of the endometrial cavity;

• Advanced tuberculous endometritis may result in an Asherman-like syndrome;• Calcified lymph nodes may be seen in the adnexal region;• A tubo-ovarian abscess that extends through the peritoneum into the

extraperitoneal space is highly suggestive of tuberculosis [3].

Male Genital Tuberculosis - The prostate and seminal vesicles are often primary sites.The testicle may become involved by direct extension from an epididymal infection,hematogenous spread is rare.

• Tuberculous prostatitis, or similar seminal vesicles infection, may lead tonecrosis, calcification, caseation, and cavitation;

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• Tuberculous involvement of the testicles usually manifests at ultrasonographyas focal or diffuse areas of decreased echogenicity with epididymalinvolvement [1];

• The most common finding of tuberculous prostatitis at transrectal US, arehypoechoic areas with an irregular pattern in the peripheral zone;

• Contrast-enhanced CT may reveal hypoattenuating prostatic lesions, whichrepresent foci of caseous necrosis and inflammation [3].

LYMPHATIC TUBERCULOSIS: is more prevalent among children, and it is one of themost common abdominal manifestations of TB [1]. Cervical and supraclavicular nodesare the most commonly involved [3].

• Imaging of TB lymphadenitis is similar in patients with and without AIDS [1];• Contrast-enhanced CT reveals nodes with peripheral enhancement and low

attenuation centers - highly suggestive but not pathognomonic [3];• Lymphadenopathy is the most common manifestation of abdominal

tuberculosis usually multiple and large, averaging 2-3 cm in diameter. Themesenteric and peripancreatic groups are the most commonly affected [3].

GASTROINTESTINAL TUBERCULOSIS: Abdominal tuberculosis is usually secondaryto pulmonary tuberculosis, even though radiologic evaluation often shows no evidenceof lung disease [1]. TB rarely affects the GI tract [2] but ileocecal region is themost commonly involved segment - present in 80%-90% of patients with abdominaltuberculosis [3]. This fact is attributed to the abundance of lymphoid tissue [1].

• Thickening of ileocecal valve lips or widening of the valve with narrowingof the terminal ileum (the Fleischner sign) is characteristic of tuberculosis.Early barium studies demonstrate spasm and hypermotility with edema of theileocecal valve, followed by thickening of the ileocecal valve [1]. A narrowterminal ileum with fast emptying of the affected segment across a gapingileocecal valve into a shortened, rigid, obliterated cecum (Stierlin sign) mayalso be seen [1].

• Double-contrast barium may show shallow linear or stellate ulcers withcharacteristically elevated margins [3]. Literature also describes these ulcersas larger (linear/stellate), in opposition to those related with Crohn's disease,which are described as rounder, as the first ones tend to follow the orientationof lymphoid follicules [1]. Moreover, tuberculosis is associated with greaterthickening of the bowel wall and fistulas/sinus tracts are rare [3].

• Cecal amputation is also classically described [3] and as the diseaseprogresses the cecum becomes conical, shrunken, and elevated out in the

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iliac fossa due to fibrosis due to mesocolic retraction [1,2]. Some authors alsodescribe exophytic extension of cecal medial wall, engulfing the terminal ileum[1].

• In advanced stages, GI tract involvement by TB has some typicalmanifestations like annular "napkin ring" stenosis, obstruction, shortening,retraction, and pouch formation [3].

TUBERCULOUS PERITONITIS: Peritoneal involvement in tuberculosis is rare andis usually caused by hematogenous spread [2], although frequently associated withgastrointestinal forms of TB. Three types of tuberculosis peritonitis are described [3]:

• The wet type (the most common): large amount of free or loculated viscousfluid [1,3], that has high CT attenuation due to its rich protein and cellularcontent [1];

• The fibrotic-fixed type: characterized by large omental masses, matted loopsof bowel and mesentery, and possibly loculated ascites;

• The dry/plastic type (the less common): consists of caseous nodules,fibrotic peritoneal reaction and dense adhesions.

Inflammatory extension through the peritoneum into the extraperitoneal compartmentsuggests tuberculosis and can be helpful in the differential diagnosis.

HEPATOSPLENIC TUBERCULOSIS: this manifestation is most likely secondary tohematogenous dissemination from another primary site [1]. Manifestations generally fittwo different types:

• micronodular /miliary form (most common): often occurs in associationwith miliary pulmonary tuberculosis. Hepatosplenic ultrasound may revealdiffusely hyperechogenicity, or less common multiple hypoechoic nodules andoccasional hyperechoic nodules. On CT scans this form usually expresses asmultiple <10mm, low attenuation foci on CT, but it can also be occult and onlymanifest as diffusely enlarged liver or spleen [2].

• macronodular /tuberculoma form (rare): manifests as ill-definedhypoattenuating lesions 1-3 cm in diameter or a single mass within a diffusehepatosplenomegaly [3]. Early in the development of this lesions, contrast-enhanced images may reveal central enhancement, whereas more advancedlesions may demonstrate calcification [1].

• MR imaging shows hypointense and minimally enhancing honeycomblikelesions on T1-weighted images. On T2-weighted images, the lesions arehyperintense with a less intense rim relative to the surrounding liver.

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ADRENAL TUBERCULOSIS: Bilateral asymmetric involvement is common and it's seenin up to 6% of the patients with active tuberculosis.

• In early stages this lesions manifest as soft-tissue masses with a nonspecificappearance, namely rim enhancement and central low attenuation on CT [1];

• The gland may shrink and calcify in advanced stages of disease [3], leadingto the development of Addison disease [1].

MUSCULOSKELETAL LOCALIZATIONS: this kind of involvement usually occurs inpatients with extrapulmonary TB (25%) [2]. In children, lesions are symmetric and areless sclerotic, and typically seen in the peripheral skeleton, while in adults lesions arepredominantly sclerotic and have an axial predilection for skeleton involvement [4].

• Spinal involvement (the most common skeletal manifestations, representingabout 50% of these ones) [3]. The most common extrathoracic locationis L1. The disease process can affect multiple vertebral bodies and diskspaces (Tuberculous Spondylitis (Pott Disease [1]), or manifest as single-level involvement, with sparing of adjacent disc spaces. CT and MR are veryimportant form the demonstration of small focus of bone infection and in theeffort of evaluating the extension of the disease [3].

• Vertebral body involvement often progress from the anterior segment,adjacent to the end plate and can ultimately result in selective collapse andwedging, leading to the characteristic angulation and gibbus formation [1,2]- tuberculous kyphosis [3]. Less often, posterior elements of the spine maybecome involved [1]. End plate demineralization results in loss of densemargins. Although a well-defined margin of destruction is usually present,reactive sclerosis or periosteal reaction in the adjoining vertebral body istypically absent.

• Disk space may then become involved via several routes (along the anterioror posterior longitudinal ligament or penetrating subchondral bone in the endplate).

• Paraspinal extension from the vertebra and disk through adjoining ligamentsand soft tissues is frequently seen and usually occurs anterolaterally,with possible progression to a psoas abscess. This abscess can producesignificant paraspinal soft-tissue opacity and when healed may havecalcifications, which are virtually pathognomic, and may extend into the groinand thigh [1,3].

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• Extraspinal tuberculous osteomyelitis: usually hematogenous in origin,and most commonly involves femur and tibia (generally epiphysis)[1], andsmall bones of the hands and feet [3]. In children, metaphyseal foci can involvethe growth plate [1]. Cystic tuberculosis, a rare form of skeletal tuberculosis, ismore common in children [1] and is characterized with disseminated lesions,well-defined, areas of hyperlucency with variable amounts of sclerosis, seenin patients with good resistance and acquired immunity [4];

• Tuberculous dactylitis (involving short tubular bones): especially frequent inchildren. The most common radiographic findings are related to the fusiformsoft-tissue swelling and periostitis [3]. These findings are followed by gradualbone destruction and possible sequestrum formation [1]. With the destructionof the underlying bone, a cystlike cavity may form, ballooning out the remainingbone ("spina ventosa") [1,3];

• Tuberculous arthritis: possibly secondary to direct invasion from acontiguous focus of tuberculous osteomyelitis or may result fromhematogenous dissemination [1]. This entity is characteristically monoarticularand hip and knee are most frequently involved articulations [3]. Thetypical Phemister triad assembles juxtaarticular osteoporosis, peripherallylocated osseous erosions, and gradual narrowing of the interosseous space.Occasionally, wedge-shaped areas of necrosis (kissing sequestra) may beseen on both sides of the affected joint [1]. If tuberculous arthritis is leftuntreated, complete joint obliteration may ultimately culminate in fibrousankylosis of the joint [1,3].

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Images for this section:

Fig. 1: Coronal contrast-enhanced CT image shows several cervical enlarged lymphnodes, and one necrotic lymph node - tuberculous lymphadenitis.

© HDES, Hospital do Divino Espírito Santo de Ponta Delgada - Ponta Delgada/PT

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Fig. 2: Axial contrast-enhanced CT image shows nonuniform, low-attenuation lesionswithin the liver - Hepatic tuberculosis - and an adenopathy projected over thegastrohepatic ligament.


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Fig. 3: Coronal contrast-enhanced CT image shows multiloculated pelvic abscesses dueto genital tuberculosis.


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Fig. 4: Image courtesy of MD Mukesh G. Harisinghani. Lateral radiograph demonstrateserosion of the anterior margin of the vertebral body (arrow) caused by subligamentousspread of spinal tuberculosis.

© Harisinghani MG, McLoud TC, et al. Tuberculosis from Head to Toe. Radiographics2000; 20:449-470;

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Fig. 5: Image courtesy of MD Mukesh G. Harisinghani. Retrograde pyelogram showsfilling of the dilated hydronephrotic lower and middle pole of the right kidney. Thecollecting system has irregular margins (straight solid arrow) and shows irregular fillingdefects (curved arrow) from necrosis of the parenchyma. Upper pole calcification is alsoseen (open arrow) - Tuberculous pyonephrosis.


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Fig. 6: Image courtesy of MD Mukesh G. Harisinghani. Axial contrast-enhanced CTscan demonstrates concentric thickening of the cecum (straight solid arrow). Smallbowel dilatation (curved arrow), ascites in the greater peritoneal space, and thickeningof the peritoneum (open arrow) are also seen - Ileocecal tuberculosis and peritonealtuberculosis (wet type).


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Conclusion

The tuberculosis prevalence has increased in the last years. The radiologist has animportant function to contribute to accurate diagnosis, recognizing the imagiologicalfindings of extrapulmonary tuberculosis. This disease can affect any organ system, havea variety of clinical and radiologic features and mimic numerous of other diseases.

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References

[1] Harisinghani MG, McLoud TC, et al. Tuberculosis from Head to Toe. Radiographics2000; 20:449-470;

[2] MacLean KA, Becker AK, et al. Extrapulmonary Tuberculosis: Imaging FeaturesBeyond The Chest. Canadian Association of Radiologists Journal 2013; 64: 319-324;

[3] Engin G, Acunas B, et al. Imaging of Extrapulmonary Tuberculosis. Radiographics2000; 20:471-488;

[4] Malik S, Joshi S, et al. Cystic Bone Tuberculosis in Children -A Case Series. IndianJ Tuberc 2009; 56: 220-224.

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