Tropical Medicine Central Resource

Fig. 5.44 A-H. Tuberculosis affects the cecum in different ways, but the end result is almost always contraction and considerable distortion. These figures illustrate eight different cases from different parts of the world. A Early mucosal ulceration and edema, with shrinkage. The infection has caused ulceration of the proximal half of the transverse colon. B Mucosal edema and ulceration of the right side of the colon and of the terminal ileum, which is beginning to dilate. The appendix is also infected. C The cecum is contracted, grossly edematous, and ulcerated, and the terminal ileum is dilated. D Gross and extensive mucosal edema with nodulation and spiculation of the cecum and ascending colon. The ileocecal valve is patent and the terminal ileum is also edematous and nodular. E-H Four different examples of shrinkage of the tuberculous cecum. In E and F the terminal ileum is not affected or even obstructed, but the cecum is much reduced in size. In G there is some ulceration of the terminal ileum, but only minimal obstruction and mild dilatation. In H the cecum is very small, and the ileum is dilated and almost seems to hang from the small narrow cecum.

Fig. 5.45. Tuberculosis often affects more than one part of the bowel. This patient had a palpable mass in the right iliac fossa which clinically suggested malignancy. The barium enema showed that the cecum was displaced upwards and both the cecum and terminal ileum had edematous, swollen mucosa. However, there were marked mucosal changes in the sigmoid colon also, which led to the alternative diagnosis of amebiasis. Tuberculosis was not considered but the combination of fixation of the ileocecal junction, the contracted cecum, and small bowel adhesions is typical of tuberculosis. The palpable mass was due to enlarged lymph nodes.

Fig. 5.46 A-F Scanning, both ultrasonography and CT, can demonstrate the type of mass shown in Fig. 5.45 but can also be used to show thickening of the bowel wall and ascites. A-C Sonograms showing thick-walled bowel, groups of thickwalled bowel matted together, and distended small bowel with echogenic walls and ascites. D-F scans of children showing the thick walls of ileum (arrows) filled with contrast, contrast-enhanced mural thickening, and a thickened irregular contrast-filled cecum (arrow). The patients shown in D-F all had ascites. (From Cremin and Jamieson 1995).

Fig. 5.47 A-H. Tuberculous colitis can affect any part of the large bowel. A Tuberculosis affecting the cecum, ascending colon and much of the transverse colon. B Tuberculosis affecting the cecum, apparently sparing the ascending colon but involving the transverse colon. C Tuberculosis affecting the left half of the colon. In each of these patients there is spasm, saw-tooth distortion of the bowel wall, mucusal ulceration, and edema. In A and C there is excess mucus which is better seen in B, in which the edema is so acute that there is thumb-printing. This patient had active pulmonary tuberculosis. D Mucosal ulceration in the sigmoid colon of a child: the lower part of the colon is straight because of the peritoneal thickening. It would be difficult by any imaging method to distinguish any of these cases from amebiasis. E The irregular saw-tooth appearance of tuberculous mucosal ulceration (descending colon). F Spasm and mucosal edema affecting the whole of the descending and proximal sigmoid colon of a 53-year-old African patient. The cecum and ascending colon were also affected, but could not be filled with the barium enema because of the spasm and discomfort. G Skip ulcers encircling and constricting the ascending colon of a 42-year-old Arab female. H Extensive transverse ulceration without any narrowing in the sigmoid colon of a 38-year-old Arab female. (C AMP 229499; E from Cremin and Jamieson 1995).

The rectum is the least common site for tuberculosis in the gastrointestinal tract. There may be ulcerating procitis, fistulas and even stricture (Fig. 5.49). Any chronic ischiorectal abscess in the tropics should raise the possibility of underlying tuberculosis. A chest x-ray is often requested in patients who have a perianal or ischiorectal abscess but who are otherwise in good health. The majority of these will be negative. Imaging with barium, ultrasonography, or CT may demonstrate the abscess but it can be very difficult to demonstrate any fistula or connection between the abscess and deeper tissues. The differential diagnosis will include lymphogranuloma venereum, schistosomiasis, amebiasis, and rarely, actinomycosis or Crohn's disease.

Enteroliths

Intestinal calculi are not seen very frequently, but may occur above any chronic bowel stricture. They seem to be more common in India than elsewhere, but isolated cases have been noted from many countries where tuberculosis is common. When the stricture is high within the small bowel, the enteroliths are composed of choleic acid and are usually radiographically nonopaque but may be seen as a dense mass on ultrasonography or CT. In the lower bowel, where there is a greater alkaline content and a higher concentration of calcium salts, enteroliths often become radiographically opaque (Fig. 5.42 G). Some are completely opacified, but others have translucent centers with a ring of calcification. These calcified enteroliths may be found in the lower ileum or colon in up to 3%-4% of cases of intestinal tuberculosis. They vary from multiple small stones to a single large laminated calculus. Massive nontuberculous enterolithiasis has been associated with ileal dysgenesis: the enteroliths were located in the distal ileum and there was an ileo-transverse-colonic fistula. Enteroliths must also be differentiated from calcified granulomatous lymph nodes, renal stones, gallstones, or less commonly, vesical stones. Cross-sectional imaging with ultrasonography or CT is an ideal way to localize them accurately. Barium studies may not always be successful because of the bowel stricture which is the underlying cause.

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Fig. 5.48 A-E. Tuberculosis can cause local narrowing in any part of the bowel at any age. The differential diagnosis is then very difficult. A Stricture in the ascending colon of a 40-year-old man. B A very tight stricture just proximal to the hepatic flexure in a young woman. C A constriction with ulceration in the sigmoid colon of a middle-aged man; these tuberculous strictures resemble localized amebomas, and carcinoma would have to be considered, although it is rare in some parts of the tropics. D A tight stricture in the proximal transverse colon. E Two elongated strictures in the transverse colon of a child: there is also ulceration and thickening of the descending colon. These patients come from three different continents: all had normal chest radiographs and in each the diagnosis of tuberculosis was confirmed histologically. (E from Cremin and Jamieson 1995).

Tuberculosis of the Peritoneum and Abdominal Lymph Nodes

Tuberculous peritonitis occurs at any age and in both sexes, and in some series accounts for 30% of all nonpulmonary tuberculosis and for at least 20% of all cases of ascites. In most countries about half the cases of abdominal tuberculosis will be due to peritoneal infection, but in children and young adults the frequency is even higher. In almost every case there is associated abdominal lymphadenopathy; the infection may originate from a primary intestinal or gynecological source, or be blood borne; it is seldom possible to locate the primary focus.

The major clinical symptoms are abdominal distention and abdominal pain, vomiting and diarrhea are less common, occurring in under 30% of patients. Nonspecific findings, such as weight loss and tiredness, are difficult to evaluate in the tropics, but occur consistently in tuberculous peritonitis.

Clinical examination shows that 30% of the patients are afebrile, but almost all have ascites; which is clinically detectable in only about one-third. The tuberculin skin reaction varies geographically, but is often negative (Nigeria 70%, Ethiopia 23%), and the chest radiograph is often normal (India 60%, Ethiopia 50%, Iran 40%). Over 30% of the patients will have lymphadenopathy elsewhere, most commonly cervical. On palpation the abdomen has an ill-defined "doughy" feeling, and in 15% or more of patients there will be palpable abdominal masses. The liver and spleen are often enlarged. There is a very reliable laboratory test for tuberculous peritonitis. If the fluid is examined and the adenosine deaminase (ADA) level is over 32.3 u/l, there is a 98% sensitivity and 95% specificity for tuberculosis.

Laparoscopy is one way to obtain a tissue biopsy because even culture of the ascitic fluid may be negative. It is useful to exclude other causes of ascites, such as carcinomatosis, lymphoma, or even worms. However, laparoscopy is not without risk, and in tuberculous patients carries a mortality of 3%-12%.

The course of the disease may be relatively benign (except in AIDS patients), and the response to antituberculous therapy quite rapid. The ascites may persist, even when the patient is improving clinically. Histological examination shows that the majority of the infected abdominal lymph nodes will be caseating and necrotic. These nodes may rupture into the peritoneum, disseminating small tubercles all over the peritoneal cavity and occasionally causing an acute clinical reaction and hemorrhagic exudate. When this happens, the protein content of the ascitic fluid will be high (over 45 g/l) and the fluid/ blood glucose ratio will be below 0.96, with marked lymphocytosis. The tubercle bacilli can be seen on direct staining of the fluid or subsequently on culture. Another initially rare complication is intestinal obstruction, which increases in frequency as the fluid is absorbed and adhesions form. At autopsy, cecal or ileal ulceration may occasionally be found.

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Fig. 5.49 A-E. Sigmoid and rectal tuberculosis. A Sigmoid colitis extending into the upper part of the rectum, with edema, ulceration, and mural thickening. B The possible end result: the sigmoid is smooth, lacking normal haustration or mucosal pattern. In both the acute and chronic stages, tuberculosis resembles amebiasis or any other ulcerating colitis. C, D The rectum is narrowed, ulcerating, and thickened. There is minimal obstruction at this stage, but if untreated the rectum will narrow and the sigmoid will dilate. E A different lateral projection of the same patient shows two fistulae which may connect with the skin in the perineum. Only biopsy will differentiate tuberculosis from lymphogranuloma venereum or amebiasis. Schistosomiasis can cause the same mucosal changes but fistulae are much less common. (A AFIP 682419-4; B AFIP 29499-185).

Tuberculous Peritonitis

Ultrasonography is the method of choice for imaging tuberculous peritonitis. There are three imaging patterns. There may be ascites (the "wet" form), there may be multiple caseous nodules and adhesions (the plastic or "dry" form), or there may be a combination in which loops of bowel, omentum, or mesentery have clumped together, often becoming palpable and associated with ascites.

When there is ascites, it can be free, localized or loculated (Figs. 5.50, 5.51). When free, it is either clear fluid or contains multiple thin strands, septa, or floating debris. These strands may be mobile and quite delicate or relatively thick so that adhesions occur. Fluid may be trapped between the thickened loops of bowel, producing alternating echoic and echo-free bands (the "sandwich" appearance). Both on ultrasonography and CT the density of tuberculous ascites is variable; when clear, it is a transudate in the early stage and becomes thickened later. There may be progression to an abscess, seen on Ultrasonography as well-defined localized fluid collections, septate and with internal echoes. Aspiration of this thick fluid can be difficult or even impossible due to its consistency and the multiple septate divisions. But even at this stage, there can be good response to antituberculous therapy.

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Fig. 5.50 A-F. Tuberculous peritonitis A An Ethopian patient with tense ascites. (Courtesy of Dr. Richter) B Multiple loops of dilated bowel, with fluid levels, floating in ascites. It can be very difficult to decide whether this is due to obstruction or ileus. C, D Dilated loops of small bowel with thick edematous walls. This is still an ileus, but obstruction may develop later because of adhesions. C is an African and D a patient from India. E A sonogram showing thickened bowel walls and ascites due to tuberculosis in a 44-year-old African from Zimbabwe. B bowel; AS ascites; BL urinary bladder. (Courtesy of Dr. Sam Mindel) F A sonogram of a South African child showing echogenic bowel loops radiating from the mesenteric root, with ascites. (From Cremin and Jamieson 1995).

Computed tomography can demonstrate the ascites and the plastic changes, but preliminary oral contrast should be used within the bowel so that the thickening of the bowel wall, the omentum, and the lymph nodes can be differentiated. CT may be better than ultrasonagraphy for the anatomical localization of the fluids and to show where it is loculated or has been walled off into thick abscess. In patients with AIDS the progress is similar but exaggerated.

In the dry form of peritonitis, ultrasonagraphy will demonstrate irregular echo-free or echo-poor, nodular or laminar thickening of the peritoneum. The nodules are poorly echogenic and occur almost anywhere on the peritoneal surface. Histologically they are caseating granulomas. The mesenteric thickening may lead to fixation of the bowel and, when there is fluid, these loops of bowel and mesentery have been described as "radiating from the mesenteric root in a stellate configurating." This is more clearly seen with CT. On MRI performed with gadolinium enhancement, lymphadenopathy can be demonstrated. However, there is seldom any great advantage in using either CT or MRI compared with ultrasonagraphy.

Routine supine and erect radiographs of the abdomen will show free fluid and multiple distended loops of small bowel, often with thickened intestinal walls. There may be scattered fluid levels in the erect position, but the findings are those of an ileus rather than obstruction. The amount of fluid in the abdomen may make the details of the bowel somewhat hazy. The proximal colon may be involved and also dilated to the same extent.

As healing occurs, the degree of dilatation lessens and the wall of the gut is less thickened. Adhesions may form and there may be subacute obstruction with fluid levels. At this stage, barium contrast gastrointestinal studies may be helpful and careful fluoroscopy with palpation will make it possible to decide whether the loops of bowel are fixed or mobile. However, apart from adhesions, the majority of cases will have a normal radiological examination of the small intestine without any obvious bowel involvement.

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Fig. 5.51 A-F. With scanning it is possible to identify lymphadenopathy and peritoneal fluid: it is not always possible to be sure of the etiology. A, B Ultrasonography shows multile enlarged tuberculous lymph nodes (LN/N) and ascites. C, D Loculated peritoneal fluid, a very common finding in tuberculous peritonitis. (A-D are all patients from Zimbabwe, courtesy of Dr. S. Mindel.) E A contrast-enhanced CT scan (with contrast also in the bowel) shows the thickened intestinal loops and a large omental mass (X). There is loculated low-density ascites. F Contrast-enhanced CT showing rim-enhancing para-aortic lymph nodes (arrows). (E and F are children from South Africa, from Cremin and Jamieson 1995).

Tuberculous Abdominal Lymph Nodes

At least one-third of patients with tuberculous peritonitis will have lymphadenopathy, and in some countries, e. g., India, the frequency of lymph node involvement may be as high as 70%. Lymphadenopathy may occur without detectable bowel involvement. All groups of nodes within the abdomen can be infected, particularly those around the pancreas, portal region, aorta, and vena cava. On ultrasonography the enlarged nodes are usually hypoechoic (Fig. 5.51 A, B), and some display central echogenic areas where caseation has started. Some nodes will be discrete, while others adhere together into large masses. Both CT and ultrasonography can demonstrate nodal calcification before it can be seen on a plain radiograph. On CT, most nodes are of low density with some peripheral rim enhancement (Fig. 5.51 F). It is probable that some of the abscesses (cold abscesses) within the peritoneum result from extensive caseation of lymph nodes; they have a very variable ultrasound and CT appearance depending on the degree of caseation, central necrosis, and septation.

Enlargement of the abdominal lymph nodes may cause direct pressure on various parts of the gut; there may be distortion of the pyloric antrum, duodenal loop, and upper jejunum in particular. If the nodes are very large and swollen, the bowel may become adherent to them and involved in the tuberculous process. This results in a spiky irregular outline of the intestinal mucosa, localized edema, and ileus. Rupture of enlarged nodes into the intestine has been reported, but only happens when this adhesive process has occurred. It can present as a communicating diverticulum.
Calcification of the mesenteric nodes may be seen on healing, but is not as common as might be expected. It will be detected earlier by CT scanning. Although the presence of caseation and calcification suggest tuberculosis, metastatic malignancy and histoplasmosis can occasionally also calcify. When healing, tuberculous calcification may be seen as discrete lines on both CT and ultrasonography. Radiographically visible abdominal nodal calcification due to tuberculosis is uncommon in Africa and many parts of the tropics despite the frequency of the infection. (However, calcification in nodes elsewhere, such as the neck, mediastinum, and inguinal region, is quite common.)

Lymphangiography has been used for the evaluation of lymph nodes in abdominal tuberculosis, using pedal injections. Sharply outlined central filling defects, extending in some cases to the periphery, have been described as a feature of tuberculous lymphadenitis. As would be expected, the bunching of the lymph nodes together in an adherent mass can also be seen. The central filling defects are probably tuberculous caseation. In some lymph channels there is obstruction to the flow. Most of the changes described on lymphangiography can also be seen in lymphoma and metastatic disease. Ultrasonography and CT scanning have replaced lymphangiography for diagnosis in most countries (which is probably appreciated by the patient).

A rare tuberculous involvement of a large giant cystic lymphangioma has occurred in an Ethiopian male immigrant to Israel. His father had tuberculosis. The patient had a draining right axillary sinus, a large fluctuating abdominal mass, and an equally large reducible right inguinal hernia. There was no palpable lymphadenopathy. Imaging showed this to be one cystic mass extending from the posterior mediastinum into the pelvis, and aspiration of the fluid was positive for M. tuberculosis. The mass responded to antituberculous therapy and fluid aspiration. Two similar injections have been reported in cystic hygromas of the hand.

Tuberculosis of the Liver, Spleen, and Pancreas

Hematogenous, disseminated tuberculosis can result in small (miliary) tuberculous nodules in any organ. Clinically, generalised hepatomegaly and less often splenomegaly may be palpated when there is abdominal tuberculosis. Isolated tuberculomas of the spleen have also been reported.

There may be multiple small tuberculous granulomas (tubercles) in the liver (Fig. 5.52 A-F) or spleen (Fig. 5.53) which on ultrasonography have a granular echoic or hypoechoic appearance. The granulomas can become macronodular, depending on the stage of development. Some will have central, more echogenic areas. If a tuberculous abscess develops, the hypoechoic center will be surrounded by a hyperechoic rim. One or more areas of caseous necrosis may develop. This is less common in the spleen. In some tuberculous granulomas there will be calcification, seen on plain radiographs or causing acoustic shadowing on ultrasonography.

Large tuberculous masses are unusual, but have been reported. One such mass was 3.5x5.5 cm, and situated in the left lobe of the liver (Fig. 5.52 G-I). On CT the mass was hypodense and showed peripheral enhancement with contrast. Celiac arteriography in this case showed stretched hepatic vessels and some neovascularity, which suggested that the mass was inflammatory rather than neoplastic in origin.

Only very rarely will a solitary hepatic, splenic, or pancreatic abscess or tuberculoma be the presenting evidence of tuberculosis. Almost always there will be marked tuberculous lymphadenopathy within the abdomen, and often in peripheral nodes also.

Pancreatic tuberculosis may be nodular or (less commonly) form an abscess, usually of complex echogenicity but with less surrounding pancreatitis than a pyogenic abscess. The nodular pattern is less easily recongized. Pancreatic lesions are unlikely to be seen in children. In adults they are probably going to become more common in patients with AIDS.

All tuberculous granulomas may calcify and then be demonstrated by any method of imaging (Fig. 5.53 A, B). Many cases of splenic or, less often, hepatic calcified tuberculous granulomas are chance findings.

The differential diagnosis can be difficult because of the rarity of active infection in the liver, pancreas, or spleen. A chest x-ray may be normal, but the tuberculin skin test is usually positive. Most of these tuberculous lesions in solid organs will be nonenhancing, although there may be rim enhancement at some stage. If noncalcified, they can be mistaken for hydatid disease, amebic abscesses, or, more commonly, malignancy. Image-guided aspiration can be used to make the diagnosis and, in some cases, for instillation of drugs. When lesions are calcified their etiology can be more difficult to identify, since they may resemble a collapsed hydatid cyst, an old pyogenic or mycotic infection, or even a calcified hematoma following trauma (especially in the spleen). For noncalcified, active granulomas or abscesses, imaging can be used to follow treatment, and prolonged follow-up is advisable because recurrence of tuberculosis from these isolated abscesses has been recorded.

Fig. 5.52A-I. Tuberculosis of the liver. A, B Ultrasonography showing hypoechoic granulomas and a granuloma with an echogenic center in the livers of two children. C In another child there are hypoechoic lymph nodes with echoic calcification at the porta hepatis. D A contrast-enhanced CT shows multiple nonenhancing granulomas in a child's liver. E In a different child there are rim-enhancing nodes (arrow) at the porta hepatis. F A child from a Pacific Island has a similar granuloma in the liver. G Tuberculoma of the liver: A 3.5x5.5 cm hyperechoic mass in the lateral segment of the left lobe (sonogram). An isolated hyperechoic nodule with calcification was also found in the right lobe. H, I CT scans of the same patient show a large hypodense lesion almost filling the lateral segment of the left lobe of the liver. The other nodule in the right lobe, is hypodense with a central hyperdense focus. I After intravenous contrast, the lesion in the left lobe shows peripheral enhancement and central hypodensity; the nodule in the right lobe remains hyperdense. The patient was a 30-year-old male, a known hepatitis B carrier, complaining of right upper quadrant abdominal pain. His chest radiograph showed diffuse reticulonodulation and pleural thickening due to pulmonary tuberculosis and pleurisy. Ultrasoundguided liver biopsy showed acid-fast bacilli. After 9 months of antituberculous treatment the tuberculoma had almost disappeared. (A-E from Cremin and Jamieson 1995; F courtesy of Dr. Cheryl Sisler, Hawaii; G-I courtesy of Dr. T. C. R Tan et al. and Br J Radiol, 1997).

Fig. 5.53 A-E. Tuberculosis of the spleen. A, B Radiographs of a patient who was known to have tuberculosis of the spine: he presented with a fistula in the left loin. A Intravenous urography showed two calcified granulomas lying laterally to the kidney, in the splenic region. B A contrast sinogram through the fistula showed that it connected with the lower of the two splenic granulomas and that there was an extensive tuberculous abscess tracking along the twelfth rib to the infected vertebrae. C A sonogram of a child shows diffuse increased echogenicity in the spleen due to small widespread focal granulomas. (D) In another child there are enlarged lymph nodes at the splenic hilum. E A contrast-enhanced CT scan shows multiple nonenhancing granulomas in the spleen (the straight arrow points to a similar granuloma in the liver; the curved arrow shows adenopathy at the splenic hilum). (C-E from Cremin and Jamieson 1995).

The incidence of tuberculosis of the kidney varies throughout the tropics; wherever it occurs, it is more common in the higher socioeconomic groups, repeating the pattern of the disease in Europe. It is uncommon in tropical Africa, despite the fact that tuberculosis is prevalent in most other tissues. It occurs frequently in much of Asia and India, particularly in association with diabetes. There are often tuberculous foci in the chest and skeleton also.

Renal tuberculosis in the tropics is probably almost always bilateral, although it may be first identified on one side only, especially if contrast urography is used to make the diagnosis. It usually starts as a localized caseating lesion, most commonly in the upper pole of either kidney, although it may arise anywhere. Such foci are caused by hematogenous spread. Alternatively, it may present as pyelonephritis as the result of reflux from an infected bladder.

The nidus of infection in the renal parenchyma enlarges and ruptures into a neighboring calyx, discharging necrotic caseous material and distorting the calyx (Fig. 5.54). This can be demonstrated by intravenous or retrograde urography, ultrasonography, CT, or MRI. If there is a communication into the tuberculous cavity, it may fill during an intervenous contrast examination; the affected calyx becomes an ulcerated cavernous lesion. The infection spreads to involve the draining calyceal infundibulum, which may then develop a stricture and seal off the infected calyx. If the ulcer and stricture are located in the renal pelvis, there will be obstruction to the outflow of urine and the calyces will become clubbed. Later, a stricture of the renal pelvis can seal off the kidney, and fibrosis and calcification may follow. This may result in autoamputation of the kidney. If there is direct extension of the tuberculous infection into the rest of the kidney, the entire kidney becomes a bag of caseous necrotic pus.

Fig. 5.54 A-E. Tuberculosis of the kidney; appearance on excretory urograms. A Widening and distortion of the upper calyces of the right kidney, with a stricture just above the renal pelvis. B Destruction of the lower calyces in the left kidney (arrow) with the formation of crescents outlining the edges of the tuberculous abscess (cavity) C A tuberculous cavity in the lower pole of the kidney. D All the calyces in this left kidney are clubbed and distorted, and there is an abscess in the upper pole. E A more advanced infection in the right kidney with hydronephrosis and dilatation of the lower half of the right ureter. The left kidney and ureter are normal so far.

Ultrasonography is a very satisfactory way to image each step of this pathological process (Fig. 5.55). Although it is possible to demonstrate the irregular and dilated calyces and the connecting cavities by urography, ultrasonography gives a better image of the renal parenchyma and will show increased echogenicity and mixed echogenicity around the calyceal lesions. Focal parenchymal granulomas which cannot be seen radiographically may be identified by ultrasonography. (Scanning should always include both kidneys even when there is an obvious lesion on one side only. On ultrasonography a tuberculous abscess will appear as an echogenic, irregular mass, often containing debris. Local or general hydronephrosis can be imaged and in the end stage the kidney will become irregular in outline, with varying thickness of the cortex. Eventually there may be calcification in the granulomas or abscess, showing as bright areas on an ultrasound scan (Fig. 5.56). Punctute calcification of the upper pole and curvilinear calcification outlining the entire kidney are the two extremes of renal involvement. CT and MRI are alternative ways to scan.
Autoamputation, the end result of advanced tuberculosis, can cause remarkably little clinical disturbance, especially in patients who are malnourished and in ill health for other reasons. There can be complete nonfunction on contrast urography or scintigraphy, a finding noted in half the patients in one pediatric series. On ultrasonography or CT, the distorted renal mass can be accurately demonstrated, showing the ultrasonically echogenic fibrosis and contraction and the bright echoes of calcification.

In tuberculosis, the ureters are dilated proximally, with irregular granulomas which result in one or more strictures and which ultimately lead to hydronephrosis (Fig. 5.57). Eventually, spotty ureteric calcification develops; in extreme cases this may merge into extensive pipe calcification along the length of the ureters. Intravenous, or even better, retrograde pyelography is the most accurate way to delineate the full length of the ureters to demonstrate strictures or calcification. Although the echogenic irregularity and granulomatous masses, as well as the dilatation of the ureters, can be demonstrated by ultrasonography, it is not so easy to assess the peristalsis. CT and MRI are less reliable (and MRI particularly is not a good way to demonstrate calcification) and are both a more costly way of evaluatingthe ureters.

Differentiation from schistosomiasis is usually fairly reliable. In schistosomiasis calcification is first seen in the lower end of the ureters and the bladder and then extends up the ureters; it is most unusual to see much ureteric calcification without bladder calcification, and the nodular irregularity of the ureters as seen on contrast studies will be useful in making the differentiation. In tuberculosis, the calcification extends down the ureter and the bladder is very seldom calcified to the same extent as in schistosomiasis. The multiple strictures and nodules of ureteritis cystica are rare in the pattern of urinary tuberculosis in the tropics. Transitional cell carcinoma of the ureter is rare in much of the tropics but does produce irregular strictures with mucosal destruction and nodular masses, often with the characteristic goblet or champagne glass appearance.

Fig. 5.55 A-F. Scanning can show parenchymal tuberculosis and its progress more accurately than urography. A, B Ultrasonography shows echogenic foci in the renal parenchyma as well as irregular caliectasis. C More advanced destruction of the calyceal system in the right kidney, with some parenchymal foci. D A coronal T 1-weighed MR scan of the same patient showing the extent of the renal infection. E Ultrasonography of a different patient showing an abscess in the right kidney. F Angiography is useful in the differential diagnosis between a tumor and infection. The extent of the renal tuberculosis is well shown in this right renal series. (A-D from Cremin and Jamieson 1995; E courtesy of WHO: The manual of diagnostic ultrasound, Geneva, WHO, 1995; F courtesy of the University of Capetown Radiology Library).

Fig. 5.56 A-E. When renal tuberculosis heals, it usually calcifies. A A large parenchymal granuloma in the lower pole of the left kidney. B Fine scattered calcification in the upper pole of the left kidney and the lower pole of the right kidney with scarring and shrinkage of the renal parenchyma. C Almost complete calcification of the right kidney. (There is no contrast medium.) An African from Kenya. This is the end result of renal tuberculosis. As well as heavy calcification within the right kidney, linear calcification can be seen in the right ureter, but not in the bladder. The ureteric calcification is unlike the intermittent, spotty calcification seen in schistosomiasis and, if that were the cause, there would almost certainly by bladder calcification also and a comparatively normal kidney. D, E Auto-amputation shown by ultrasonography (D) and by contrast CT (E). In D there is also echogenic material blocking the renal pelvis. (C courtesy of Dr. S. Malik, Nairobi; D, E from Cremin and Jamieson 1995).

Fig. 5.57 A-D. Tuberculosis of the ureters. Strictures and dilatation can occur at almost any level along the ureter. A Hydronephrosis of the right kidney resulting from a stricture of the distal ureter in a child from South Africa. B A similar almost complete ureteric obstruction in an adult Kenyan African. It is difficult to know whether the kidney is also infected, or only obstructed. C Ultrasonography showing dilatation of the upper ureter and thickening of the ureteric epithelium, as well as parenchymal cavitation. D Advanced bilateral ureteric calcification. Unlike schistosomiasis, the bladder is not calcified. (A, C from Cremin and Jamieson 1995).

When tuberculosis affects the bladder there is gradual and usually localized thickening of the bladder wall, with increasing diminution of the bladder volume. Trabeculation of the mucosa may develop. The vesicoureteric orifices are affected by this progressive fibrosis and there will then be bilateral, often asymmetrical hydroureter and hydronephrosis. Both CT and ultrasonography will demonstrate the irregular and thick bladder wall caused by the tuberculous granulomas (Fig. 5.58). To show this clearly, the bladder must be full which, in some patients with tuberculosis, may cause considerable discomfort because chronic contraction is usual. Contrast radiography or cystography is likely to demonstrate reflux up to the dilated ureters because the orifices will usually be rigid and held open. Bladder calcification due to tuberculosis is very uncommon and, when it occurs, is patchy. Calcification in small granulomas may be seen more easily on ultrasonography or CT. When bladder calcification is seen on a radiograph, schistosomiasis is the diagnosis until proven otherwise. Spontaneous tumor calcification can occur in bladder neoplasm (particularly in India), and needs to be differentiated from tuberculosis (but only after schistosomiasis has been excluded).

Ultrasonography and CT (and MRI) have shown that adrenal tuberculosis is a little more common than previously suspected. It is usually bilateral, which is important in the differential diagnosis from adrenal hemorrhage in adults or from tumors (although metastases, especially from a lung primary, can also be bilateral).

Both ultrasonography and CT will shown enlargement of the adrenal glands: if it is easy to see the adrenals with ultrasonography they are probably enlarged (except in infants). On CT, there can be enhancement after contrast injection. When healing occurs, there will be calcification in the tuberculous granuloma and it can be diffuse, localized, or punctate: it is not always easy to recognize on plain radiograph. Tuberculous abscesses in the adrenal are initially well defined but later become complex.

The differential diagnosis is not difficult, particularly when there is calcification. Adrenal hemorrhage is not uncommon bilaterally during infancy but usually occurs on one side only in adults. Tuberculosis often causes bilateral enlargement and the enlargement may decrease but still persist after healing and calcification.

Fig. 5.58 A-F Tuberculosis of the bladder. A The small contracted, thick-walled bladder which is a common result of tuberculosis. Ultrasonography showing an irregular, thick-walled but contracted bladder and dilated ureters (arrows): B transverse and C sagittal projections. D Mural thickening and an irregular defect at the base of the bladder, particularly on the right side. There was also right renal tuberculosis. E A contrast-enhanced CT scan of a child (not the same patient as in D) with tuberculous thickening at the base of the bladder. F Speckled calcification throughout the bladder and the lower left ureter. There are calcified granulomas in the lymph nodes in front of the sacrum on the right. It is unusual for tuberculous calcification to be so extensive: it is more commonly present in one bladder segment only. This was proven to be tuberculosis, without any evidence of schistosomiasis. (B, C, E from Cremin and Jamieson 1995).

Fig. 5.59 A-E. Genital tuberculosis. A A sonogram of a tuberculous abscess in the testes: there is central necrosis with fluid and debris. Tuberculosis must be considered in the differential diagnosis of almost any testicular mass, even when there is no other evidence of tuberculosis. B Fallopian tuberculosis is a common cause of infertility but cannot be easily distinguished from any other infection. This patient from Kenya has bilateral hydrosalpinx and roughening of the contour of the cervix uteri. C, D This 13-year-old girl from Zimbabwe presented clinically with bilateral cystic abdominal masses. C Urography showed displacement upwards of both kidneys and medially of both ureters. The third and fourth lumbar vertebrae are both sclerotic, with loss of joint space between them. D The cystic masses were drained bilaterally and filled with contrast, showing two huge dilated fallopian tubes which were subsequently removed surgically. The infection in the spine responded to antituberculous therapy and a year later the urogram was almost normal. E A tuberculous abscess often forms a sinus or fistula. This histerosalpingogram shows a fistula between the left fallopian tube and the sigmoid colon. The uterine cavity is contracted and distorted and the right fallopian tube is dilated and blocked distally.

Tuberculosis can infect any part of the genital tract but most commonly it is the fallopian tubes which are affected (Fig. 5.59 B-E). Hydrosalpinx and pyosalpinx are fairly common and may be large. There may be calcification of the pyosalpinx.

Hysterosalpingography shows flask-shaped dilatation of the fallopian tubes due to obstruction at the fimbriae. Sometimes, the block is at the uterine opening, and then the tubes are not visualized. Tuberculous endometritis and cervicitis may show as synechiae, irregular uterine mucosal lining, or an elongated cervix with loss of differentiation at the uterocervical junction. Surprisingly, tuberculous endometritis is not a significant cause of sterility (2% or less), whereas fallopian tube blockage will be, whatever the cause. Both ultrasonography and CT can demonstrate these changes and show the anatomical relationship clearly. However, the overall picture provided by hysterosalpingography has some advantages, particularly in the investigation of sterility.

Tuberculous masses within the pelvis can be the result of tuberculous peritonitis, with matting of the omentum, mesentery, and bowel, or they can be due to tuberculous tubo-ovarian abscesses. Both types of mass can be large and have been mistaken for carcinoma of the ovary or, in males, for the large nodal ,mass of lymphoma. On ultrasonography, such masses will have mixed echogenicity and there will be mixed density on CT because almost all will have both solid and cystic components. At least one tuberculous abscess has involved the bladder and vagina. Tuberculous tubo-ovarian abscesses may calcify and be seen in either side of the pelvis (together or singly) as well-defined homogeneous circular masses, sometimes with areas of increased density, probably due to the granuloma. Serpiginous or linear calcification can occur in the fallopian tubes.

Tuberculosis can affect the testes, presenting clinically as a swollen testes with a hydrocele. Ultrasonography will show a mass of mixed echogenicity, often with a central cavity containing debris (Fig. 5.59A). It can be very difficult to differentiate tuberculosis from a tumor or other infection. Ultrasonography can also demonstrate the thickening due to edema caused by tuberculosis of the epididymis and vas deferens, both of which may eventually calcify and be seen on radiographs of the male pelvis. This must be differentiated from schistosomiasis and diabetes. Contrast studies of the vas and spermatic cord have not proven useful.

There are three important characteristics of bone and joint tuberculosis in the tropics which differ from the non-AIDS cases in North America and Europe: it is often an acute osteomyelitis or arthritis, it is often a destructive condition which can affect any and every bone in the skeleton, and it is frequently multifocal.

Bone and joint tuberculosis is extremely common in tropical countries; there is a tendency to focus on pulmonary tuberculosis as the major public health problem, but skeletal infection is a neglected and serious disease for which there are few accurate statistics. It is common in India; Asia, much of tropical Africa, and South America. It is fueled by malnutrition, inadequate housing, poor medical services, and, perhaps most importantly, lack of health education; to this list must now be added AIDS. Many patients report to the doctor only when the disease is advanced and when they are paraplegic, crippled, or deformed. The majority of cases are not due to bovine tuberculosis; they arise from hematogenous spread, but in many patients the original site of infection will not be identified. There are no accurate figures on the relationship of bone tuberculosis to diagnosed pulmonary tuberculosis. A normal chest radiograph does not exclude a tuberculous etiology for a bone or joint infection, but neither does pulmonary tuberculosis mandate the same etiology for any osteomyelitis or arthritis; pyogenic infections are as common as tuberculosis. Whatever the state of the lungs, when there is a skeletal infection in the tropics tuberculosis should be considered in the differential diagnosis, whether the patient is HIV negative or positive.

No age is exempt. Skeletal tuberculosis may occur in babies from 6 months upwards and become an advanced disease; the elderly are similarly affected. It is most common in children and young adults, but is not rare in any age group. It occurs most frequently in the spine; the hip is the most common joint affected, followed by the knee, ankle, elbow, wrist, and shoulder in decreasing frequency. Tuberculous osteoinyelitis can affect the skull, mandible, pelvis, ribs, and scapula. No bone escapes. Next to trauma it is the commonest cause of crippling and deformity and is such a common disease that it is cared for in general hospitals all over the tropical world. Drug therapy is usually effective, often dramatically so, but the late stage at which the patients appear necessitates skilled orthopedic correction which is not always available. Although the clinical presentation may be acute, the radiological findings often indicate that the infection has been present for a considerable time.

The majority of patients with skeletal tuberculosis (if they do not have AIDS) will be positive tuberuclin reactors, but a small percentage, perhaps less that 2%, will have negative skin tests. This can cause difficulty in diagnosis. Equally, because so many of the population will be positive reactors anyway, the finding of a positive tuberculin test in a patient with bone or joint infection is only really significant in infancy and the first few years of life. The diagnosis must be suggested by a high clinical index of suspicion, and confirmed by biopsy and culture. Unfortunately, not all biopsies will yield positive results; it may be necessary to treat the disease because of the clinical and radiological findings, despite a negative culture. A "sterile" culture is most likely to be tuberculosis and is useful in that it helps to exclude a pyogenic and typhoid etiology.

Because of poor host immunity, tuberculosis (even in those without AIDS) often behaves as an acute disease and must be treated in the same way. Surgical biopsy, even aspiration, is not a benign procedure and may result in widespread hematogenous dissemination and septicemia. A potentially tuberculous bone or joint should be treated with the same caution as a pyogenic dental abscess and surgery should be carried out under a therapeutic "umbrella" of antituberculous drugs; this rule should be violated only in cases of paraplegia due to an abscess or some similar acute emergency. The clinical and radiological diagnosis is surprisingly accurate in the majority of patients; biopsy will be confirmatory and provide a culture for the sensitivity of the organism, rather than being an immediate necessity. In the spine, removing the "pus" may be therapeutic also.

Tuberculous osteomyelitis and arthritis are often associated with marked peripheral lymphadenopathy (also tuberculous). This combination is particularly found in spinal tuberculosis and conversely, when children have gross lymphatic involvement, concomitant bone or joint disease should be carefully excluded. In one reported series from the Philippines, 7 out of 39 children with lymphatic tuberculosis were found, on radiological examination, to have spinal tuberculosis which had been clinically unsuspected. This combination occurs throughout the tropics, particularly in India and Africa; skeletal involvement can be remarkably silent in its early stages and may only become obvious because of a complication. In AIDS, skeletal tuberculosis becomes yet another part of the onslaught of infections.

The best way to image any part of the skeleton will depend very much on the site involved, but because tuberculous bone infections are so often multi-focal and may be present in different parts of the skeleton and yet be clinically silent, scintigraphy is a very valuable early investigation. However, when such a scan shows multiple active sites in the patient who is clinically ill and has lost weight, the possibility of malignancy will also have to considered. To make the differential diagnosis more difficult, the tumormarker CA 125 may be positive in destructive skeletal tuberculosis and even in tuberculous peritonitis.

Caries. Pott's disease. Pott's paraplegia. Ger: Pottparaplegie. Fr: paraplégie de Pott.

The description and statistics in this section refer to HIV-negative patients. For those with AIDS, the clinical and imaging findings are similar, but often more advanced, and the site incidence may be different. Tuberculosis in AIDS is "tropical tuberculosis;" but more progressive and often more advanced. In most tropical countries tuberculosis of the spine accounts for more than 50% of all cases of skeletal tuberculosis. Clinically, paraplegia is the commonest presenting symptom. It may be complete and acute, with bladder paralysis and inability to walk; depending on the level of the infection, it may present as quadriplegia. In other patients the symptomatology may be less severe, but neurological involvement occurs in half of those who have tuberculous spines. The remainder complain of the deformity, of pain, or of general weakness and ill health which bring them to the physician. Some will complain of a mass in the groin, which may be a hernia, but the possibility of a psoas abscess should be remembered in every such case. Whatever the presentation, a careful examination will reveal some neurological deficit (often unsuspected) in the majority of patients when first seen; yet they may have very gross spinal deformity but still be ambulatory.

If the radiological findings in tuberculosis of the spine are to be understood, it is important to have a clear idea of the underlying pathological changes. These were beautifully described in 1936 by Compere and Garrison, working at the University of Chicago. They made longitudinal whole-body sections of tuberculous spines and correlated these with radiological findings and the histological examination. Their autopsy research has since been confirmed at surgery by Hodgson and others in Hong Kong (1969). Now, in recent years, CT and especially MRI have imaged the pathophysiology, and provided three-dimensional confirmation. There are two basic premises: (a) cartilage resists destruction by tuberculosis and (b) there is no blood supply to the intervertebral disc, although there is a rich blood supply to the vertebrae. The vertebral blood supply does not cross the articular surface; the disc obtains its nutrition from lymphatics.

The intervertebral disc is a fibrocartilaginous ring, the annulus, blended with hyaline cartilage plates above and below and enclosing the nucleus pulposus. The nucleus is an interlacing matrix of fibrous tissue and fibrocartilage, with semigelatinous substance within the mesh; because this is liquid it is incompressible, and therefore narrowing of the disc can only take place when there is extrusion or destruction of the nucleus or, alternatively, dehydration. Tuberculosis commonly starts by hematogenous implant and more rarely by direct extension from infected lymph nodes. It is essentially a bonedestroying infection, with little evidence of repair in the early stages. When it occurs beneath cartilage, the cartilage is eventually destroyed but the annulus and nucleus tend to survive much longer. It is only when there is fissuring of the annulus that the infection can involve the disc proper. Even when the vertebral body has become caseous, wedged, and destroyed, careful histological search will nearly always show the nucleus, either intact or in part, having prolapsed into the softened bone or debris. Primary tuberculous invasion of the annulus has not been demonstrated. Narrowing of the disc space occurs when the annulus eventually becomes infected and fluid escapes, or when the nucleus is extruded. At this stage there will be loss of the disc space when imaged.

Compere and Garrison also showed very clearly the spread of tuberculous abscesses under the anterior or, more rarely, the posterior spinal longitudinal ligaments. When this occurs the infection involves the vertebral bodies and the disc remain intact for a considerable time. They illustrated pathologically what may be demonstrated by imaging, i. e., that multiple vertebrae can be involved above and below the original focus and yet the disc and the dura may remain intact. The cartilaginous plate of the vertebra is a barrier, more effective in children than in adults because it is thicker during childhood.

The studies of Compere and Garrison showed pressure on the spinal cord is likely to be from an epidural or subdural abscess, and sometimes from a prolapsed disc. Direct pressure from a collapsed vertebra is rare. Paraplegia thus results from the abscess, from the prolapsed disc or tuberculous debris, or occasionally from edema of the cord due the neighboring infection.

The same authors also pointed out that tuberculous peritonitis from direct spread of a spinal abscess is uncommon and that most cases of tuberculous spinal meningitis are hematogenous in origin.
Compere and Garrison showed that in pyogenic infections, invasion of the intervertebral disc occurs more rapidly, is seen earlier, and is more common. This is because the cartilaginous plate is destroyed by proteolytic enzymes and the nuclear substance is extruded more rapidly, with dissolution of the annulus. This occurs in all pyogenic infections, but particularly in brucellosis. The ability of the intervertebral disc to survive a tuberculous infection during the early stages is important in the differential diagnosis. It is particularly well illustrated in (Figs. 5.60 B, C, E and 5.61 A, and 5.66). The anterior spread of an abscess is well illustrated in (Fig. 5.71 B).

There are important general principles which guide the imaging of spinal tuberculosis:

1. Plain skeletal radiography provides a great deal of information, but it does not show the extent of the very important intradural abscess or of its paravertebral extension. It does not always demonstrate every locus of bone infection, nor does it show the nucleus palposus.

2. Because spinal tuberculosis is often multifocal, bone scintigraphy is a very valuable early examination; not only will other vertebral foci be seen, but early infection elsewhere in the skeleton may be discovered.

3. Ultrasonography is useful in demonstrating the paravertebral abscess and any associated lymphadenopathy. Beyond this, it does not provide useful information in most cases.

4. CT is excellent for demonstrating the exact extent of the skeletal disease, the deformity, and the size and position of the abscess (if any). It does not demonstrate intramedullary foci.

5. MRI provides very accurate information about both the soft tissue and bone involvement. It is accurate in the demonstration of bone lesions and is the only way to image focal myelitis in the cord. It is a poor method of imaging calcification as it occurs during healing.

Although the destructive process of spinal tuberculosis is best imaged by CT or MRI, plain radiography and standard tomography can provide useful information, particularly if the underlying pathological process is understood.

The original tuberculous focus may be marginal, central, or subperiosteal and is usually in the vertebral body (Fig. 5.60). Infection starting in a pedicle is not all that uncommon, and can be bilateral. In nontropical countries destruction of the pedicle suggests malignancy, either metastatic or lymphomatous, but in the tropics it may be tuberculous. It is not very uncommon for only the neural arch to be affected, the vertebral body remaining intact.

This can be difficult to detect with plain radiography, but is well seen by CT. The transverse processes are rarely involved except as part of the spread of infection; the spinous process is occasionally affected, but causes little deformity.

Many tuberculous spinal infections are multifocal: when suspected in any vertebra, the whole spine should be radiographed (if there has not been previous scintigraphy). Infection may be centered in one, two, three, or four contiguous vertebrae, or there may be normal vertebrae between other sites of infection, above or below that originally discovered. In some patients there will be more than two involved areas, each separated by normal vertebrae.

The degree of bone destruction when the patient is first radiographed is infinitely variable. There may be an area of increased lucency, occasionally localized by low-grade clinical pain and perhaps identified after radionuclide scanning. Standard tomography, CT, or MRI, may be necessary to find the defect within the vertebral body. Unfortunately, this is the least common presentation; most patients are first seen when the vertebral lesions are easily visible on routine films.

Fig. 5.60 A-I. Tuberculosis can affect any part of the vertebral body or neural arch. In the early stages, the intervertebral disc space may remain normal. A Destruction in the center of the vertebral without any change in shape. A patient from Tanzania. B This vertebral body has also maintained its shape but there is more advanced central destruction and the upper border will probably collapse. C The upper border of this vertebra is beginning to collapse and there is minimal lose of disc space. The central focus of infection was clearly visible only on torriography. D Similar infection in the lower half of the body. On the routine films, the loss of the cortical margin was visible but not the central destruction. E Central destruction of the lower half of the vertebral body, only seen on the anteroposterior view. The disc space is slightly narrowed. F Destruction of the right side of the vertebral body and the neural arch, with the remainder of the body maintaining its shape. The lower disc space is narrowed on the right side; the upper space is almost normal. A small lytic defect is present on the right side of the body below, and there is a small paravertebral abscess. The extent of the bony destruction is usually underestimated by plain radiography and is better seen by CT or MRI (see also Figs. 5.68, 5.69, 5.70). G, H Tuberculosis affecting the spinous process only. This is very unusual. I A CT scan of a child from South Africa, showing destruction of the neural arch on both sides, as well as of the vertebral body. Arrows, anterior spinal abscess. (A courtesy of Dr. Harold Jacobson; from Cremin and Jamieson 1995; I from Cremin and Jamieson 1995).

Because of the bone destruction the extent of the change in the vertebral shape is variable. The vertebra may be intact, with no change in its outline or there may be one or more peripheral defects; this can occur in any part of the vertebral body. Alternatively, collapse may be so complete that there is a "vertebra plans" (Fig. 5.61). In nontropical countries it is a diagnostic "rule" that vertebra plana is never tuberculous, but we have a personal series of more than 40 such cases, all of them proven tuberculosis, and many other radiologists in the tropics have seen similar cases. Tuberculosis in the tropics does not follow European and North American rules.

Fig. 5.61 A-D. Vertebra plana. Four different patients. A The vertebra has collapsed and yet the upper and lower margins remain intact and the disc spaces are clear. B More extensive collapse with small bilateral paravertebral abscesses. C This mid-thoracic vertebra has collapsed in the same way, with intact upper and lower margins, and dear disc spaces. However, there is some new bone on either side and there is some destruction of the left upper border of the vertebra below. There is a left paravertebral abscess, but none is visible on the right. D A pseudo-vertebra plana: the top half of the body is intact and becoming sclerotic. The disc space above is clear, but the anterior half of the lower margin has been destroyed although the posterior edge remains normal. These four patients were all Africans from Zimbabwe.

Wedge formation is the commonest finding and is a complex process with many variants. The majority of vertebrae collapse anteriorly; some demonstrate lateral collapse and only in a minority will the collapse first occur posteriorly. (This is said to be more common in pyogenic infections, but it can happen in tuberculosis.) The wedge may be formed of only one vertebral body which has collapsed on itself, either with both the upper and lower borders falling inwards towards the center, or with one or other border remaining intact and the wedging occurring onto it (Figs. 5.62, 5.63). However, the radiological appearance of a wedge can be misleading and what at first seems to be one vertebra may be a wedge formed of two or even more. The disc space may seem to be totally obliterated. In such cases, the upper border of the top vertebral body and the lower border of the one beneath remain intact but are no longer parallel, and the central parts of both vertebrae merge to become the wedge. The angulation can vary so that the wedge is around either the upper or lower vertebra, or both. The same destructive process can extend to involve three vertebrae or, rarely, four. When this happens the middle vertebral body disappears. It is thus essential to identify each pedicle when assessing, tuberculous wedging, and if possible also to localize the vertebral ends of the ribs to be sure of the number of vertebrae involved. A seemingly severely wedged small vertebral body may be all that is left of three or, at the most, four vertebrae. Fusion may be complete, the cortical margins may be reestablished, and there may be no trace of the original anatomy. The resulting spinal deformity is equally variable. There may . be little clinical abnormality, even when there is marked vertebral destruction; alternatively, there may be severe kyphosis (Fig. 5.64), and if two regions of the spine are infected, the curvature is often bizarre and myelography (see later) becomes a major problem. In the majority of patients the spinal cord manages to adapt to amazing curves, and paraplegia is seldom due to the bony deformity; it usually results from the abscess within the spinal canal. When paraplegia occurs without pus, it is due to vascular or toxic changes, or, as MRI has demonstrated, the intramedullary lesion; very rarely paraplegia is due to vertebral disc displacement. The disc is involved late in tuberculosis, and is more often displaced into the vertebral body than posteriorly into the cord. Even when most of the rest of the disc has disappeared, very late in the infection, MRI can often show the fluid in the nucleus.

Fig. 5.62 A, B. In early spinal tuberculosis, the commonest finding is decrease in the disc space and some destruction of the vertebral body. A Most of the upper part of the vertebral body has given way and the intervertebral disc has probably sunken into the necrotic bone. The vertebra above is intact, but the disc space is narrowed. B This vertebra has given away even more, so that the disc and the vertebra above have caused it to split. Yet the disc spaces above and below are normal and no other infected vertebrae are visible on this radiograph. (Though there is the possibility of other foci of infection above or below and these should be sought and excluded. Increasing kyphosis and, eventually, spinal cord damage are inevitable unless this is treated).

Fig. 5.63 A-H. The way in which wedge formation in tuberculosis occurs depends on the number of vertebrae involved. A Opposing surfaces of two thoracic vertebrate have been infected, and the disc space is no longer visible. B Twelve months later (with treatment) the bones are healing and fusing into one. C Thirty-one months after film A, there is a solid wedge made from two vertebral bodies, with well-defined edges. The disc spaces above and below the wedge are normal: there will probably be no further change until degenerative arthritis develops. Wedge formation can be more complicated. D One complete vertebral body has collapsed into a wedge, but with normal vertebrae above and below. E Two vertebrae have become wedged and the opposing surfaces of the vertebrae above and below are also infected. F, G There are three vertebrae at the center of this kyphosis and they will probably fuse into one solid wedge. If there is no abscess, this degree of curvature does not immediately cause neurological symptoms in children, but as their growth alters from age 12-13 years onward, there may be pressure on the cord. The end results may resemble H. This healed wedge formed from two vertebrae and fused with the vertebral body immediately below.

Fig. 5.64 A, B. Tuberculous kyphosis. Two African patients with severe kyphosis and infection of multiple vertebrae. A Eight vertebrae are infected. Three have become individual vertebrae plana. The wedge in the center is formed from the 12th thoracic and the first lumbar vertebrae combined. There is a large calcified psoas abscess extending anteriorly down into the pelvis. B Similar mid-thoracic infection involving multiple vertebrae which are now healed. There is a calcified abscess anteriorly. There is no vertebral rotation and the anteroposterior view showed there was very little scoliosis.

Healing of a tuberculous infection in the spine occurs in many different ways. The vertebral body may return to normal and be reconstituted with apparently normal margins and only slight increase in trabecular density to indicate the previous infection. When two vertebral bodies have fused, the resulting bone may also look almost normal, apart from the wedge shape. In other cases vertebrae sclerosis occurs, so that all or part of the vertebral body is increased in density (Fig. 5.65); this is evenly distributed and is seldom patchy. In temperate climates it is commonly said that tuberculosis does not cause sclerosis, but this is not applicable in the more accute pattern of the disease in the tropics. However, sclerosis does not always follow the expected distribution of the bone necrosis; it may be seen radiologically in parts of the vertebra which have up to then been considered normal. CT, MRI, or standard tomography of a tuberculous spinal infection usually demonstrates considerably more bone destruction than can be appreciated on routine films, and during healing the sclerosis may follow this distribution. (Except when affecting the upper thoracic vertebrae, the indication to scan or tomograph tuberculous vertebrae, particularly when the diagnosis has been firmly established, should be based more on the neurological examination than the radiographic appearances.) Bone sclerosis does not necessarily indicate secondary infection; it can occur as a result of tuberculosis without any complications.

Spinal tuberculosis in the tropics often heals with marked anterior and lateral bony bridging, to such an extent that it may resemble ankylosing spondylitis (Figs. 5.66, 5.67). It may be surprisingly symmetrical, but the normal sacroiliac joints in this pattern of tuberculosis may help to establish the correct diagnosis.

Fig. 5.65 A-F The healing of spinal tuberculosis. Sclerosis represents initial evidence of repair but it does not reliably indicate that the infection has healed completely. A Increased trabecular density occurring about 3 months after starting antituberculous treatment. B Increasing density in the lower part of a wedge of vertebrae. C Increased density of a whole vertebral body, which is irregular in outline and smaller than the two normal vertebrae above and below it. The disc spaces are surprisingly clear. D The lateral aspect of this vertebra had collapsed and the bone is increasing in density and will probably not wedge any further. The upper margins of the two vertebrae above are also slightly increased in density, suggesting that they were previously infected. E A well-healed sclerotic tuberculous focus in the lower anterior portion of a vertebral body, with decrease in disc space and some reactive sclerosis in the vertebra below. This was a young African man who had been treated for more than 2 years to reach this stage. F Healing can take place without increased bone density, but will then involve a lot of fibrosis. This could be mistaken for the result of trauma, but was proven tuberculosis. (C Courtesy of Dr. Harold Jacobson).

Fig. 5.66 A-E. Spinal tuberculosis heals with "bridge" formation between vertebrae until, in some patients, it may resemble the bamboo spine of ankylosing spondylitis. The bridges form surprisingly quickly. A Loss of joint space between the 12th thoracic and the first lumbar vertebrae. There is little other change except for some slight irregularity of the opposing surfaces. B Six weeks later there is new bone forming a bridge between the two vertebrae on the right side and, more surprisingly there are bridges on both sides of the normal space between the 11th and 12th thoracic vertebrae. C Three months later there is firm bridging between the 11th and 12th thoracic vertebrae and some increase in thickening of the partial bridges between the 12th thoracic and first lumbar vertebrae. There is now a faint bridge forming on the left side at this level and bridging has started between the first and second lumbar vertebrae, although that disc space is also normal. D, E The end result of healing. The sclerosis in the center of the body of the second lumbar vertebra and (in the lateral view) the healed focus of infection on the anterior edge of the 12th thoracic vertebrae show that this is post tuberculosis. The sacroiliac joints are normal. This African from Zimbabwe has been under treatment for spinal tuberculosis for 3 years. F It is difficult to recognize this as the end result of tuberculosis, but this African has also been treated and observed for more than 3 years. Although these patients (D-F) show bridging between most of their lumbar vertebrae, the process may be limited to only two or three and occur at any level (see Fig. 5.67).

Fig. 5.67. A Unilateral bridging around a focus of infection in the vertebral bodies. There is considerable variation in the lower corner of one vertebral body. B Small bilateral frequency of bridging and in some countries scierosis may be bridges across a narrow disc space, with marked sclerosis of less common.

Bone formation and bridging can be unexpectedly rapid or may occur slowly; it can be localized between one or two vertebrae, may be extensive at one side of the spine and not the other, may occur anteriorly and not laterally, or may occur in any combination. Many of the bony bridges are arched, leaving a clear space between the vertebrae. In many cases there is no vertebral collapse, which is a distinguishing feature from previous trauma. In others there is marked destruction.

There is some geographic variation in the pattern of tuberculosis of the spine and its healing. In most of Africa, bony bridging is relatively common; in Asia the process is much more destructive and there is much more rarefaction; this heals with either normal bone replacement or some increase in the trabecular density superimposed on the deformity.

One of the most difficult radiological problems is to assess the degree of healing; this can only be done after review of serial radiographs, preferably at 2-3 months intervals, to assess progress. Lack of further change may be the first sign of healing. The difficult surgical decisions are when to operate, to decompress, to use a bone graft, or only to immobilize. The "correct" treatment of spinal tuberculosis is still controversial. It was shown by Konstam in West Africa that a short preliminary period of drug therapy in hospitals could be followed by ambulatory care with a spinal cast. The results were excellent even when there was considerable neurological and urological deficit when the patient entered the hospital. His research was confirmed that the most important factor in the effective treatment of spinal tuberculosis is drug therapy. This must be continued, of course, for an adequate time and patients must be reviewed regularly. If the patient is in a cast, surgeons must be persuaded to change it at a review visit, so that the progress of the spine may be properly assessed radiologically; attempts at review when radiographs have been taken through the cast are highly unreliable. A more surgical approach was used by Roper in Zimbabwe, Kircaldy-Willis in East Africa, and Hodgson in Hong Kong, combining surgery, cast, and drug therapy. The results are usually excellent, but whether every case needs surgery is very much a matter of opinion. Ambulatory care is successful and thus of great importance in developing countries, where hospital beds and skilled nursing are in short supply.

Not every vertebra infected with tuberculosis will have a paraspinal abscess. Tuberculous abscesses present in many different ways:

1. There may be an abscess but no bone lesion (or a bone lesion but no abscess).

5. There may be a large abscess with no clinical symptoms or a small abscess with paraplegia.

6. Abscesses may surface almost anywhere on the skin but particularly in the inguinal region, in the thighs, in the loin, near the sternum, or in the neck. A retropharyngeal abscess may cause difficulty in swallowing. A psoas abscess may connect with any part of the intestine and present as a fecal fistula.

CT and MRI have radically altered our knowledge of these tuberculous abscesses by showing them, and bone foci, where they cannot be imaged on plain radiographs (Figs. 5.68-5.70). In particular, the full extent and position of any fluid can be demonstrated by CT or MRI.

Fig. 5.68 A-E Tuberculous abscesses. The best way to image an abscess around a tuberculous spinal infection is by scanning, particularly with CT and MRT. However, when these modalities are not available, abscesses can be seen with plain radiography or, occasionally, with contrast media. They are usually much larger than the plain radiographs suggest. A There is a large abscess in front of the cervical spine, displacing the trachea and esophagus anteriorly. B Another patient with a similar abscess a little lower in the cervical spine. Both these abscesses could have been demonstrated by ultrasonography, but radiography gives a better image of the spine as well. C This 5-year-old child was quadriparetic because of the anterior cord compression from a tuberculous abscess at the level of C5 (arrow) shown by T 1-weighted MRI. D T 2-weighted MR-scan in another child shows destruction of C2-4 with anterior and posterior abscesses. E with intravenous gadolinium there is peripheral enhancement but the necrotic content of the abscess does not enhance. (D, E from Cremin and Jamieson 1995).

Fig. 5.69 A-I. Tuberculosis of the thoracic spine. A-C These three different patients each had a large bilateral paravertebral abscess, seen through the mediastinum. Such abscesses can be large enough to compress the trachea, particularly in children. D CT-guided drainage of an anterior paravertebral abscess with the patient supine; there is destruction of the thoracic vertebral body. These are all African patients. E Similar mid-thoracic abscess in a child from the Pacific Islands. F, G The CT scan shows left upper cavitating pneumonia (F) and, at a lower level, destruction of the vertebrae with fluid on both sides (G). H The MR scan confirms the pneumonia and shows the size of the abscess and the destruction of the vertebrae. I The lateral MR scan shows the cord compression.