Hilar and Mediastinal Lymphadenopathy
The lungs may be normal but enlargement of the mediastinal lymph nodes may be the only presenting abnormality in tuberculosis, discovered on a radiograph of the chest taken because the patient is complaining of a cough, other pulmonary symptoms, tiredness, or weight loss (Figs. 5.9-5.12). Thoracic lymphadenopathy in tuberculosis occurs only in the primary (anergic nonimmune phase), and is not seen in the secondary (hyperergic immune) pattern.
The majority of patients with tuberculous hilar lymphadenopathy will have a positive tuberculin skin test; if it is negative it should be repeated after a short interval to exclude sarcoidosis, which is uncommon (although it does occur) in many parts of the tropics despite its frequency among Afro-Americans in the United States.
At any stage of the infection the nodes may enlarge sufficiently to rupture into a bronchus, causing an acute inhalation tuberculous bronchopneumonia. This may lead to severe clinical symptoms or, alternatively, may produce little clinical response. It should be suspected radiologically when fresh segments of patchy consolidation appear unexpectedly during any primary tuberculous infection (Fig. 5.8).
Enlarged mediastinal nodes can also rupture into the pericardium, causing acute tamponade or an acute tuberculous pericarditis. In some patients this causes sudden deterioration, but in others the clinical course is surprisingly benign.
Hilar and mediastinal lymphadenopathy may resolve completely, but this may take many months. There may be residual calcification, although the incidence of calcified nodes is variable in different parts of the tropics, possibly related to the state of nutrition. Statistically, in the tropics hilar calcification is more common in children than in adults, for which there are two possible explanations. Either calcification has occurred and subsequently been absorbed, or the background immunity and the state of nutrition of children and young adults is improving compared with their elder generation. AIDS may reverse this statistic, as it has many others.
diagnosis of enlarged mediastinal and hilar lymph nodes is largely dependent
on the local pattern of disease; in the tropics, tuberculosis usually
will be the most likely etiology, especially when the more peripheral
peribronchial and perihilar nodes are enlarged. Sarcoidosis occurs in
the tropics, but not commonly and with considerable variation geographically;
in sarcoidosis there is usually enlargement of the mediastinal and paratracheal
nodes in particular, as well as bilateral symmetrical hilar node enlargement.
Lymphoma, especially in children, may present with enlarged nodes in
the chest and elsewhere, and is indistinguishable from tuberculosis.
Similarly, Kaposi sarcoma in children in the tropics may present as
an acute lymphadenopathy with very few of the characteristic pigmented
skin nodules. (There is often lacrimal involvement.) But tuberculosis
is also a common cause of peripheral lymphadenopathy in the tropics:
for example, the majority of enlarged cervical nodes in Uganda in patients
under the age of 50 years are tuberculous. In adults, malignant disease
is often the initial diagnosis when mediastinal nodes are enlarged,
but it must be remembered that even old people may have "primary"
tuberculosis. When the patient is HIV-positive, intrathoracic lymphadenopathy
is as likely to be tuberculous as malignant; for example, in West Africa
over 80% of patients with combined TB and AIDS have mediastinal lymphadenopathy.
At any age, biopsy and histopathology may be necessary to establish
the correct diagnosis.
Fig. 5.9 A-D. Tuberculous lymphadenopathy. This is only found in the primary (anergic, nonimmune) phase. The pattern and density of the lymph nodes is very variable. A PA and B lateral radiographs of a 32-year-old woman who had been "unwell" for some weeks, without specific complaints or cough. Her PPD was positive and she had a mild evening pyrexia. There is marked bilateral peribronchial and perihilar lymphadenopathy. C Standard tomography of a different patient shows large lymph nodes around the main branch of the major bronchi on both sides. D Multiple calcified granulomas in both hilar and right paratracheal lymph nodes. There is a calcified complex in the left upper lobe. (D courtesy of Semin Roentgenol, 1979).
Fig. 5.10 A-F. Tuberculous lymph nodes may enlarge and cause pressure on different parts of the bronchial tree. A Marked enlargement of the peritracheal nodes: no lung focus is visible. Only biopsy or therapeutic trial could differentiate between tuberculosis and lymphoma. B Standard tomography shows compression of the right main and the right upper lobe bronchi. There is also compression of the intermediate and right middle lobe bronchi, but a little less marked than that of the upper lobe. There is a large thick-walled cavity beyond the almost blocked upper lobe bronchus: the tuberculin test was positive, but the sputum did not contain M. tuberculosis. The adenopathy was tuberculous but the cavity was pyogenic, the result of the blocked upper lobe bronchus. C, D Partial atelectasis accompanying infection of the right middle lobe, with markedly enlarged hilar and mediastinal lymph nodes. E, F Enlarged mediastinal lymph nodes (best seen in F) which have caused obstructive emphysema, with over-expansion of the left lung and displacement of the mediastinum to the right. This was a young patient from the Pacific Isles. (E, F courtesy of Dr. Cheryl Sisler, Hawaii).
Fig. 5.11. A A left parasternal ultrasound scan shows a large lymph node (arrow) adjacent to the aortic arch (A,D) below the left subclavian artery. B A CT scan shows calcification in the right lung parenchyma and mediastinal lymph nodes due to tuberculosis. C, D A frontal chest radiograph shows left hilar adenopathy; rim enhancement is seen on the contrast CT scan. E, F This child's chest radiograph shows a widened superior mediastinum which might be mistaken for the thymus; the contrast-enhanced CT scan shows large tuberculous lymph nodes, with rim-enhancement. (From Cremin and Jamieson 1995).
Fig. 5.12 A-D. MRI can also demonstrate both the pulmonary and nodal changes of tuberculosis. A The coronal T 1-weighted and B coronal gadolinium-enhanced T 1-weighted scans showing consolidation in the left upper lobe, which is enhanced, and nodal masses in the right superior mediastinum, right hilum, and below the carina, with rim-enhancement. There are also enlarged para-aortic nodes with rim-enhancement (arrows). C A coronal gadolinium-enhanced T 1-weighted scan showing rim-enhancing nodal masses in the left hilum. D An axial T 1-weighted scan showing superior mediastinal adenopathy and consolidation in the left upper lobe. (From Cremin and Jamieson 1995).
Fig. 5.13. The characteristic radiograph of a "destroyed lung" in a patient from Malawi. There is flattening of the left chest wall, with displacement of the mediastinum to the left. There are cavities in the fibrotic left lung. Some pleural thickening is present on the left. The right lung is over-expanded, but otherwise normal.
The Destroyed Lung
The "destroyed lung" describes the very characteristic radiographic appearance of a common end result of primary tuberculosis, or less often, of a nontuberculous mycobacterial infection, e. g., M. avium-intracellulare (Fig. 5.13).
The pathophysiology of the destroyed lung is easy to understand (Fig. 5.14). There are lymph nodes at the division of each major and segmental bronchus which are enlarged by a primary tuberculous infection. With such a close anatomical relationship, any swelling results in pressure on the bronchus, causing narrowing often to the extent of blockage. This may resolve as the nodes subside or the bronchial wall may be so involved and damaged that the cartilage is destroyed. If there is pressure or fibrosis sufficient to cause blockage of the bronchus, there may be collapse of the segment or even the lobe of the lung peripherally.
Enlarged tuberculous lymph nodes are the usual cause of the destroyed lobe or lung, which is a very common finding in Africa or India, but is also seen wherever tuberculosis is common (e. g., in the Australian aborigines). Statistically the left upper lobe is more frequently affected; in one extensive survey of admission chest x-rays in a large African hospital, left upper lobar pneumonia in young adults was more likely to be tuberculous. The right upper lobe is a little less often involved, and none of the other lobes escape. (The "right middle lobe syndrome" described in England results from similar lymph node fibrosis.) The outcome of the fibrosis and bronchial constriction is often secondary pyogenic infection of the atelectatic segments. Bronchiectasis then develops, often being both tuberculous and pyogenic in origin (Fig. 5.15). Because of the underlying lung collapse and fibrosis, the chest wall flattens, particularly over upper lobe disease, and the mediastinum is pulled by the fibrotic lung towards the same side. The lung damage is slowly progressive, with recurrent infection and further fibrosis. There may be cavity formation, and as the disease heals it is very difficult to decide clinically or radiologically whether a fresh cavity is the result of recurrent tuberculous infection or secondary infection or whether there are fibrotic bullae only. Although no longer commonly performed where CT scanning is available, bronchography in these patients is dramatic and demonstrates the extent and pattern of lung damage. When the underlying sequence of lymphadenopathy, atelectasis, infection, bronchiectasis, fibrosis, contraction, and scarring is understood, it is so characteristic that it is possible to look at the plain chest radiograph and describe the bronchogram or CT scan; (Figs. 5.14-5.16) without actually performing it (which is much appreciated by the patient).
During the process of healing, local pleural effusions frequently occur over the destroyed area of lung, especially over the apex. Such fluid is usually trapped by adhesion over the upper lobe, so that the costophrenic angles frequently remain clear. Fluid does not have any prognostic significance but may resemble a mass: CT or ultrasonography may help to distinguish between pleural fluid (mobile) and pleural thickening.
Subsequently, the major clinical problem in patients who have a "destroyed lung" is recurrent infection. This may be tuberculous or pyogenic, or even both, and can be contaminated by a fungus or other saprophyte. Examination of the sputum is very misleading; it almost always contains a multiplicity of organisms and it is difficult to identify tuberculous bacilli. Management of these patients presents a problem; some control of the pyogenic infection may be obtained by antibiotics, but such treatment is not always successful, the outcome depending on the extent of the fibrosis and on the drainage from the affected area. Surgery is sometimes attempted but can be extremely difficult because the pleura is thickened and adherent, and the underlying lung fibrotic and friable. The end result may be a disastrous tuberculous empyema. Localized thoracoplasty has helped to enhance the drainage in some patients, but masterly inactivity is another option.
In summary, a destroyed lung is easy to recognize and describe radiologically but there are no satisfactory criteria to distinguish the etiology of subsequent infections. Clinical recognition is equally straightforward, but treatment remains a recurring problem in some patients.
Fig. 5.14 A-F. The development of a "destroyed lung." A Primary left upper lobe tuberculous pneumonia. B Standard tomography shows the enlarged mediastinal and perihilar lymph nodes, compressing not only the apical posterior bronchus but also the other bronchi to the left lung. C Because of the compression and resulting obstruction, the left lung is shrinking and the mediastinum is moving to the left. The left chest wall is being flattened and there is some pleural reaction. D A bronchogram about a year later shows widespread bronchiectasis with overlying pleural thickening. There are adhesions along the diaphragm and widening of the lower half of the trachea. The right lung is over-expanded but is otherwise normal. E A similar destroyed lung, but on the right side. The mediastinum is shifted to the right and the right chest is contracted. F The bronchogram shows the underlying shrunken right lung, with bronchiectasis, and the overlying pleural thickening.
Fig. 5.15 A-E. Further examples of destroyed lungs. A The typical PA chest radiograph: the left lung is almost opaque, the trachea and mediastinum are shifted to the left, and the right lung is over-expanded. The left chest is smaller than the right side. This was an African child. B Same case as A. Bronchography shows the severe underlying bronchiectasis affecting the whole lung: the heart is displaced to the left and there is some pleural reaction which stretches up over the apex of the lung. C Another African child. As well as the gross bronchiectasis and shrinkage of the left lung, there is early dilatation of the right lower lobe bronchi, probably due to recurrent inhalation from the secondarily infected left lung. This child has marked pleural thickening on the left side. D In this case only the left upper lobe and the lingula are affected and there is very little bronchial thickening. E Bronchiectasis with slight mediastinal shift and pleural thickening, and adhesions tenting the left side of the diaphragm. The destroyed lung which results from primary (nonimmune) tuberculosis almost always affects only one lung. The other lung remains normal apart from over-expansion and occasional secondary infection, as in C. When bronchiectasis follows secondary (immune) tuberculosis, it is nearly always bilateral.
Fig. 5.16 A-F. CT of the destroyed lung. A Marked compression of the right lower lobe bronchus (arrow) by enlarged nodes. There is segmental consolidation and compensatory emphysema in the remainder of the right lung. B Severe compression of the trachea (arrow) due to mediastinal lymphadenopathy: there is right upper lobe consolidation. C-F Scans at different levels in the same patient showing destruction of the left lung, with volume loss, cavitation, and consolidation. There is early calcification in some of the left hilar and subcarinal nodes (C, D arrows). There is no gross pathology in the right lung. The patient eventually had a left pneumonectomy. (From Cremin and Jamieson 1995).
Pleural and Pericardial Effusions
Tuberculous pleural effusions at any age are usually a manifestation of primary, anergic (nonimmune) tuberculosis. The fluid may be serous, proteinaceous, bloody, or occasionally purulent (Fig. 5.17). Pleural biopsy and DNA fingerprinting are reliable methods of establishing the diagnosis. Mediastinal lymphadenopathy often can be demonstrated by CT or tomography, even when there is no radiologically visible pulmonary parenchymal lesion. The majority of tuberculous effusions will be unilateral, but bilateral effusions are not uncommon in tuberculosis in the tropics. (Whenever there is a bilateral effusion, a tuberculous infection of the thoracic spine should also be excluded.) Ultrasonography is an excellent way to localize fluid (Fig. 5.18) and exclude a subphrenic cause, such as an hepatic amebic abscess or ascites.
Tuberculous effusions may loculate anywhere, including over the upper zones of the lung or in the pleural fissures. The radiological appearance may then suggest local consolidation or a tumor, and decubitus radiographs and lordotic views may be necessary for differentiation. Ultrasonography will demonstrate the septate adhesions and pleural thickening.
Removal of a large amount of pleural fluid in a malnourished patient may cause sudden clinical deterioration. Aspiration should be controlled and guided by ultrasonography, so that only sufficient fluid is removed to permit a functioning lung volume; if the fluid is purulent, total and continuous drainage will be required. If this is not adequate, pleural thickening and lung encasement will follow. Most tuberculous pleural effusions respond well to appropriate drug therapy.
Pleural calcification may be the sequel to a tuberculous pleuritis (Fig. 5.19). The calcification may have a feathery or lacy pattern, or be linear around an encysted effusion. Calcification is not evidence of cure, and decalcification may occur, particularly if the infection becomes active again. Calcification in the diaphragm is almost always due to asbestosis, and not to tuberculosis. It must be distinguished from calcification of the diaphragmatic pleura; but this also is uncommon following tuberculosis and is much more likely to be due to asbestosis. Of course, asbestosis and tuberculosis may coexist, and in some parts of the world frequently do.
Tuberculous pericarditis (Fig. 5.20) may be a primary anergic tuberculous infection or may follow rupture of adjacent mediastinal lymph nodes into the pericardium. The posterior aspect of the pericardium is in close apposition to the mediastinal lymph nodes beneath the carina. Rupture of these nodes may cause an acute clinical crisis, with tamponade, or may be a subclinical event. Subsequent healing can be complete, leading to an apparently normal pericardium, or may result in severe thickening and calcification. Because both layers of the pericardium are involved, adhesions are frequent and may be extensive; the epicardium may be involved. When there is restrictive (constrictive) pericarditis there may be a need for surgical decompression; this procedure can be hazardous because the cardiac muscle and small epicardial coronary arteries can be damaged. Careful ultrasonography may delineate the extent of the fibrosis before surgery.
Constrictive pericarditis may exist without any radiologically visible calcification, and may be better recognized with CT, magnetic resonance imaging (MRI), or ultrasonography (Fig. 5.21). When the constriction is severe, it may present as cor pulmonale with a radiographically normal heart size. In many patients extensive pericardial calcification has little physiological effect on the heart, while in others, minimal calcification seen on a plain radiograph may be the only sign of extensive pericardial fibrosis.
A solitary pericardial tuberculoma has been reported, forming a small mass along the left heart border. It is not easy by any method to distinguish a pericardial tumor from pericardial thickening.
Cardiac tuberculosis see Chap. 25.
Fig. 5.17 A-F. Tuberculous primary (nonimmune) pleural effusion. A A young African man with a right-sided pleural effusion and right hilar adenopathy. With antituberculous treatment, the fluid resolved more rapidly than the lymph nodes, which eventually calcified. B A teenage girl with a left-sided pleural effusion which extends up into the interlobar fissure. There is probably left hilar adenopathy, partially obscured by the fluid. C Localized pleural effusion on the right side which has been present for years. No pleural effusion is "safe". This type of effusion may become reactivated quite unexpectedly. D An encapsulated effusion along the right chest wall. The central density over the right chest is due to pleural thickening and fluid lying posteriorly. There was no change over many years and the patient remained quite healthy. E Bilateral pleural effusions in a young African girl. The lateral views clearly showed mediastinal lymphadenopathy; tuberculosis was confirmed by pleural biopsy. F A large pleural effusion almost filling the left side of the chest and partially collapsing the underlying lung. Although this resembles a destroyed lung, the mediastinum is shifted away from the density and the left side of the chest has not collapsed significantly. The main left bronchi can be seen clearly and are not obstructed. (A, B, D courtesy of Semin Roentgenol, 1979).
Fig. 5.18 A-G. Ultrasonography in tuberculous pleural effusions. A Fluid in the left chest; this could be tuberculous or pyogenic. Aspiration and biopsy would be necessary to discover the etiology. B A multiseptate right-sided pleural exudate due to tuberculosis. A and B are patients from Zimbabwe (courtesy of Dr. Sam Mindel). C-E Three different patients with septate tuberculous pleural effusions: the serous bands are adherent to both the visceral and parietal pleura. F, G Many tuberculous pleural effusions will have multiple internal linear echoes, which move freely when the patient changes position. This is a characteristic of tuberculosis. These patients are from Uganda. [Courtesy of Dr. L. Belli, Turin, and Radiol Med (Torino), 1992].
Fig. 5.19 A-D. Pleural calcification is often the end result of tuberculous pleurisy and has many patterns. A, B This African patient had a pleural effusion many years previously which resulted in fibrotic shrinkage of the right chest and mediastinal shift to the right. The bronchogram showed the underlying contracted lung but there is no bronchial obstruction or saccular bronchiectasis as is found in a destroyed lung. The pleural fibrosis has caused the right side of the chest to contract. The left lung is emphysematous but otherwise normal. C Typical diaphragmatic calcification due to asbestosis, seen in a patient who has never had tuberculosis. This can be bilateral or unilateral, and is seldom symmetrical. Both costophrenic angles are clear; had the calcification been the result of a tuberculous effusion there would have been pleural thickening. D This Indian had a right pleural effusion which healed, leaving pleural thickening laterally and calcification posteriorly. Although the right chest is a little contracted, there is no mediastinal shift.
Fig. 5.20 A-D. Tuberculous pericarditis may be a primary tuberculous infection or follow rupture of an adjacent lymph node. A This African child had a right upper lobe primary tuberculous pneumonia and marked lymphadenopathy; she then developed a pericardial effusion and a left pleural effusion. B A huge cardiac outline which results from a large pericardial effusion. There is no evidence of cardiac failure or pleural fluid at this stage. C An African child from Zimbabwe with a large right pleural effusion and right lower lobe pneumonia. The right paramediastinal shadow is caused partly by pleural fluid and partly by enlarged lymph nodes. Other enlarged lymph nodes can be seen through the heart shadow around the left hilum. She had a pericardial effusion which needed to be removed, but which did not contain M. tuberculosis. However, the bacilli were present in her sputa. D Extensive calcification of the pericardium seen in a lateral view of the heart. The amount of pericardial calcification does not indicate the degree of pericardial constriction. This patient did not suffer from constrictive pericarditis. (A, C courtesy of Semin Roentgenol, 1979).
Fig. 5.21. A Ultrasonography is an excellent way to identify pericardial fluid, as in this child from southern Africa. B A loculated pericardial effusion with fibrous septa and marked thickening of the pericardium. There is some compression of the right ventricle (R.V). This was an African from Zimbabwe with known tuberculosis. C A 13-year-old Polynesian boy with a pericardial effusion and bilateral pleural effusions. There is mediastinal lymphadenopathy. D The CT scan of the same patient, confirming the pericardial fluid, bilateral pleural effusions, and moderate lymphadenopathy. E A large tuberculous pericardial effusion in a child from South Africa, shown by contrast-enhanced CT: there is a large tuberculous lymph node (arrow) and consolidation in the right middle lobe. F Pericardial calcification seen on a CT scan (arrows). There is a right pleural effusion and right middle lobe consolidation. G-I MRI of tuberculous pericarditis shows marked pericardial thickening. G T 1-weighted image showing the pericardium with the same signal intensity as the myocardium. H T 2-weighted image demonstrating low signal intensity on the inner surface of the thickened pericardium (arrowhead). The pericardial effusion also shows a low signal (arrow). I The lower scan is gadolinium enhanced, showing enhancement of thickened parietal and visceral pericardium (arrow). (A, E, F from Cremin and Jamieson 1995; B courtesy of Dr. Sam Mindel; C, D courtesy of Dr. Cheryl Sisler, Hawaii; G-I courtesy of H. Hayashi and Br J Radiol, 1998).
Miliary tuberculosis is an acute disseminated infection, the result of hematogenous spread; the primary focus may not be recognizable and may be extrapulmonary (Fig. 5.22). In other patients, miliary spread occurs during active pulmonary tuberculosis when there is rupture of a caseating lymph node or a cavity into a blood vessel. Even with good treatment there is a mortality of 13%-50%. Only about 30% of patients with miliary tuberculosis will have the bacillus in their sputum; up to 60% may have negative skin tests. Miliary tuberculosis is always evidence of a life-threatening infection. While it is usually easy to recognize the miliary pattern on a chest radiograph of a patient of any age, there is no correlation between the number or size of miliary nodules and the clinical health of the patient. Often those who are very ill show fewer nodules. The patient's general health and state of nutrition are very important factors.
Clinical correlation is essential to differentiate miliary tuberculosis from other causes of miliary nodulation, many of which may be found during the investigation of any debilitating illness. The initial chest radiograph may be normal, and reexamination of the chest should be requested "if symptoms persist", because miliary tuberculosis may only become apparent radiologically up to 10 days or more after the clinical illness has started; it may be recognized earlier, however, with high-resolution CT. There is also considerable variation in the "miliary" pattern radiologically, again with little correlation with the patient's clinical status. In some patients, at first there is only interlobular septal thickening, which can be very difficult to recognize, particularly on the chest x-ray of a small child: high-resolution CT is more reliable. The traditional miliary (millet seed) nodules are tiny, discrete, and all about the same size, less than 2 mm. These nodules may coalesce into patchy and more irregular opacities, and high-resolution CT will show even more variation (Fig. 5.23). The distribution of the nodules is not symmetrical and there are differences in size and density, which may represent different episodes. High-resolution CT may also show cavitation which has not been suspected on the chest radiographs. In some patients there may be hilar lymphadenopathy, but in others the miliary disease is so acute that the lymph nodes are normal.
Hepatosplenomegaly often occurs in association with miliary infection, and on ultrasonography is seen as a granular echoic appearance in the liver or spleen. In some patients there may be multiple small hypoechoic nodules, some of which have central echogenic necrosis. On CT the small nodules are of low density and usually do not enhance with contrast, except occasionally around the rim of the nodule. These granulomas may become confluent, appearing as hypoechogenic or echogenic masses up to 2 cm in size. Both hepatic and splenic nodules may calcify.
Miliary tuberculosis in the tropics may occur at any age, including in the elderly, even when the patients are HIV-negative. But patients who have altered immunity (e. g., from AIDS, malnutrition, recurrent infection, diabetes, leukemia, lymphoma or other malignancy) are at risk when exposed to tuberculosis and are particularly liable to develop miliary spread. The differential diagnosis includes the miliary pattern caused by the passage of larvae of various parasites through the lungs, during which there will in most cases be a peripheral blood eosinophilia; unfortunately, this can be misleading, because miliary tuberculosis may be superimposed on the parasitic background of the patients, and is not excluded by eosinophilia. Fortunately, in the majority of parasitic infections the radiological appearances change rapidly, whereas in miliary tuberculosis the nodules may become more apparent but the overall pattern does not fluctuate within a short period. Miliary tuberculosis may take 2 or 3 months to fade, even with adequate therapy. Only rarely does it result in miliary calcification.
There are many miners (for coal, tin, gold, etc.) throughout the tropical world in whom silicosis and silicotuberculosis must be considered in the differential diagnosis of miliary patterns in the lungs. Silicotuberculosis also occurs in women.
Fig. 5.22 A-E. Miliary tuberculosis. A, B Acute miliary tuberculosis in an African child. The lateral view shows enlarged mediastinal nodes. C, D This child was undergoing treatment for primary tuberculosis (C). There were enlarged lymph nodes in both hila and in the right paratracheal region, all showing early calcification. At no time was there a visible pulmonary lesion and the child had no symptoms. A few weeks later (D) for no apparent clinical reason, her general condition deteriorated and there was hematogenous spread to both lungs. There was also some patchy nodulation in the right lower lung suggesting that a lymph node had ruptured into a vessel and a bronchus. The calcification and the lymph nodes provided evidence only of local healing, and not of cure. E Miliary tuberculosis with cavitation in both upper lobes and enlarged hilar lymph nodes on both sides. This indicates a primary tuberculous infection in a 21-year-old African, whose only clinical complaint was a sore throat and ear ache. He was found to have a tuberculous right tonsil and mastoiditis. As so often happens in developing countries, at this stage the patient disappeared. (C, D courtesy of Semin Roentgenol, 1979).
Any pneumoconiosis, but silicosis in particular, carries an increased risk of tuberculosis. Routine chest radiography is required by law in many countries before anyone may work underground and is repeated every year. The increased risk of tuberculosis is such that many countries provide a pension, not only for silicosis but whenever a miner develops tuberculosis while at work or within 1 year of leaving the mines or high-risk occupation. The radiological differential diagnosis between silicosis and miliary tuberculosis can be extremely difficult, and depends on the distribution of the miliary nodules in the lung. In silicosis the nodules are almost invariably first recognized in the infraclavicular, upper midzone of the frontal chest film; over a period of months they become visible in the apices and the lower lung sequentially, and the original nodules become more prominent. Miliary tuberculosis has no such differential distribution and may occur everywhere (both lungs) at the same time. If both diseases occur together (silicotuberculosis) the radiologist is quite often unable to recognize the underlying pathological process and must resort to careful study of the preceding films and a sound clinical knowledge of the patient. High-resolution CT may help in the differential diagnosis. Lymphadenopathy can suggest tuberculosis, but also occurs in silicosis, developing a significant and almost unique "eggshell" pattern (sarcoidosis is the only other likely cause of this calcification). The development of a large, irregular, fibrotic "conglomerate mass" (massive fibrosis) in an upper zone is indicative of silicosis, but some authorities believe that there must also be infection before this occurs.
Silicosis can occur in unexpected places and persons, and not only in those who work in high-risk occupations, e. g., miners, quarriers, stone workers, and even sculptors in stone. In the Transkei in the Republic of South Africa, approximately half a million women developed silicosis because, from childhood onwards, the girls and women ground corn between two stones which had a high silica content (Fig. 5.24). The stones slowly disintegrated and as the women leaned over to add pressure to powder the corn finely, they inhaled large quantities of the silica-containing dust. Their children, strapped to their backs or running around the huts, were exposed to silica in the same way. The dust in these huts became full of silica of the correct particle size and characteristics to cause silicosis; as a result many of the young girls and women not only developed silicosis but there was an increased incidence of tuberculosis (more accurately, silicotuberculosis. This had a strange collateral effect; their husbands, many of whom worked underground in the gold mines of the Transvaal but under good health surveillance, went home and then returned to the mines from the rural areas with a higher incidence of tuberculosis than their fellow miners whose wives made flour by more modern methods! The whole population became at risk because of this domestic occupation. Moreover, even those who produced the grindstones were likely to suffer from silicosis as, for example, in a village north of Kano in Nigeria, West Africa, where sandstone is quarried in pits from which grindstones are hewn and then widely used throughout Nigeria for grinding guinea corn. A total of 126 workers were examined and 49 had silicosis, 17 of them in an advanced stage of massive fibrosis. Among these, seven also had pulmonary tuberculosis. No doubt similar hazards exist elsewhere in the tropical world for equally unexpected reasons (and elderly American Indian women have been shown to have faced the same hazards from grinding corn).
Fig. 5.23 A-D. Miliary tuberculosis. The miliary nodules vary considerably. A Fine nodulation in the right upper lobe, evenly distributed but with some nodules beginning to coalesce. B The left lower lobe of another patient with more numerous nodules varying a little in size. In this patient the nodules did not coalesce. C High-resolution CT showing small widespread nodules with interlobular septal and interstitial thickening. D High-resolution CT in another child from South Africa, with multiple nodules of two sizes, suggesting two episodes of hematogenous dissemination. Early diagnosis of hematogenous spread is important to reduce the high mortality. (C, D from Cremin and Jamieson 1995).
Fig. 5.24 A, B. Not every miliary pattern on a chest radiograph is due to tuberculosis. This African woman had been grinding corn between stones since she was 9 years old. She was under treatment for miliary tuberculosis until it was realized that the distribution of the miliary nodules within her chest was not compatible with this diagnosis, and there had been no response to antituberculous therapy. The sputum did not contain M. tuberculosis nor did her clinical condition suggest active miliary tuberculosis. She had silicosis and was lucky, because many of the women who ground corn in this way developed silicotuberculosis. The possibility of some alternative diagnosis must always be considered when the patient's clinical condition does not match the radiographic appearance. (Courtesy of S Afr Med J, 1967).
Primary, anergic or nonimmune tuberculosis occurs in any combination of the patterns described. This is significant in establishing the differential diagnosis; for example, it is unusual to see both lobar pneumonia and bronchopneumonia on the same chest radiograph in a pyogenic infection. Similarly, patchy bronchopneumonia with a small pleural effusion, or lobar pneumonia with pericarditis, is more likely to be tuberculous than pyogenic. Lobar pneumonia which does not clear in a few weeks is probably not pyogenic. Any chest infection at any age which does not respond appropriately to antibiotic therapy may be tuberculous, unless, particularly in adults, it is secondary to bronchiectasis or underlying neoplasm. Multiple cavities in young children may be tuberculous or staphylococcal. Enlarged hilar and mediastinal lymph nodes with any form of pneumonia, abscesses, or pleural or pericardial fluid should always suggest tuberculosis. Pleural effusions in young teenage patients, especially if bilateral and with no cardiac or renal disease, are probably tuberculous. Miliary lung disease, especially when accompanied by lymphadenopathy and effusions, also suggests tuberculosis.
It is very important to recognize that the lung changes in primary (nonimmune) tuberculosis go through a progressive spectrum, and that the first radiograph may be taken at any stage in the sequence. In some there may be lobar pneumonia and/or hilar lymphadenopathy, while in others there may be a healing peripheral focus or bronchogenic spread or pleural effusions; furthermore, there may be a combination of any of these events. Primary tuberculosis is not a static process, and the progress shown radiographically may provide the diagnosis when it is not clear on the initial film. Unlike a pyogenic infection, tuberculosis seldom simply fades away. The rate at which these changes develop and heal depends on what is called, in broad terms, the "resistance" of the individual patient, together with the success of any treatment. It is this whole repertoire of change which may allow the correct diagnosis, hopefully before it is too late for the patient.
Immune Tuberculosis (Also known as Secondary, Hyperergic, Reactivation, or Adult Tuberculosis)
The term "adult" tuberculosis is misleading because this pattern of disease can occur in any patient at almost any age beyond infancy. The majority of cases of "adult" pattern tuberculosis develop as a separate illness, or as a complication of other ill health, e. g., AIDS, diabetes, or malnutrition. There are a few patients whose immunity alters during the course of a primary tuberculous infection and an "adult" pattern develops without an interval. Whatever the sequence, the radiologist must not, therefore, hesitate to diagnose "adult" tuberculosis in a child, particularly one who has received BCG vaccination.
Secondary or immune tuberculosis is usually bilateral. In one survey only 4% of patients had unilateral disease. Cavitation is the rule rather than the exception, particularly during the active stage of the disease. When there is bilateral infection in the upper lobes, it is almost certainly due to tuberculosis; if it is bilateral and in the lower lobes, it may well be pyogenic bronchiectasis, following pertussis (whooping cough) or chronic sinus infection. If the infection involves one upper lobe and the opposite lower lobe, it is likely to be tuberculous. In Asia, all these appearances may also be due to paragonimiasis or to melioidosis.
The clinical symptoms of patients in the tropics are similar to those of patients in nontropical areas, but may be more severe. Hemoptysis, cough, fever, night sweats, and general debility are common. Many patients have clinical evidence of lung fibrosis, which causes asymmetrical flattening of the chest wall and shift of the trachea (mediastinum): there are often associated physical signs of cavitation. Clinically the differential diagnosis must include pyogenic pneumonia, chronic lung abscess, bronchiectasis, fungal infections, paragonimiasis or melioidosis (where appropriate), amebic infection of the lung (usually but not invariably associated with a large liver), and malignant disease.
In the majority of patients the radiological diagnosis of hyperergic secondary (immune) tuberculosis is not difficult. Tuberculosis is a necrotizing infection in which cavitation and fibrosis can occur together or separately; both are usually bilateral in the upper lobes, especially tending to involve the apical and posterior segments. The superior segment of a lower lobe is another common site, but no lung segment escapes. Any multilobar infection with fibrosis and cavitation is likely to be reinfection tuberculosis, or an atypical mycobacterial infection. If the fibrosis is sufficient to shift the mediastinum, tuberculosis is even more likely. The mediastinal and hilar lymph nodes are not usually enlarged and may or may not be calcified. Sometimes it is possible to identify a primary parenchymal granuloma (such granulomas are usually calcified), but failure to do so does not exclude tuberculosis. There will often be pleural thickening, particularly in the costophrenic angles or over the lung apices. The rate of progress is very variable, but is usually slow and insidious, except when tuberculosis complicates some other severe illness, such as AIDS.
The initial lesion of reactivation tuberculosis is usually an alveolar haze with a few small pulmonary nodules, from which there may be some interstitial lines, often radiating to the hilum (Fig. 5.25). Further ill-defined opacities develop, with commencing distortion of the interstitial pattern due to fibrosis. At this stage the appearances often change if the patient is radiographed each month, with further distortion of the normal vascular and interstitial patterns. Contraction can progress until the interlobar fissure and hilum are displaced, usually upwards until one or both hila are much higher than normal.
Fig. 5.25 A-D. The earliest evidence of immune (reactivation) tuberculosis is a soft alveolar haze, usually in the apex or upper lobe. This African man worked in a hospital and had routine chest radiograph which was normal 3 weeks before he became ill, with a cough, sputum, and minimal hemoptysis. His next radiograph (A) showed the clouding in the right apex with a few small tubercles. There were M. tuberculosis in the sputum. Although treatment was started, 12 weeks later (B) the infection had spread and was beginning to cavitate. The patient was found to be diabetic. C Another patient, who had lost weight and was unwell. There is a soft alveolar haze with small nodules in the periphery of the lung, probably in the anterior segment of the right upper lobe. The sputum contained M. tuberculosis and treatment was started: the patient improved clinically but after 7 months (D) the radiographic appearances seemed to have deteriorated.
Even without treatment, the infection may be arrested at any stage. This leaves residual scarring but in many cases the healing process is complicated by endobronchial involvement and there is stenosis or kinking of one or more peripheral bronchi. This results in secondary pyogenic infection and bronchiectasis, superimposed on the contracted fibrotic lung. In some patients this destructive process progresses to such an extent that it resembles the destroyed lung of primary infections (see previous section on "Destroyed Lung"). Unfortunately, at any stage the infection may be reactivated, sometimes after many years. Reactivation has been recorded from 35 to 51 years after the initial diagnosis. It is therefore not possible to describe any patient as being "cured." It may be better to report "probably old tuberculosis" or "apparently well healed." Unfortunately, clinicians are not much better at judging the future course of the disease.
Contrary to what is often taught, cavitation (Fig. 5.26) has diagnostic significance but no prognostic value, because necrosis and liquefaction are the normal course of tuberculosis. Cavities appear in 37%-75% of all cases of active secondary tuberculosis. They may be thick walled or thin walled and may be surrounded by a parenchymal reaction or appear to cause no local disturbance. They are more common in the upper lobes and the superior segments of the lower lobes than elsewhere, but may occur in any part of either lung. Cavities fluctuate considerably during treatment; radiographically, they may increase or decrease in size, may contain fluid, and may show a fluid level or apparently be empty, depending on the reabsorption, expectoration, or bronchial spread of the contents.
Fig. 5.26 A-F Many patients present with bilateral upper lobe infection, often as in A with asymmetrical cavitation on both sides. B Cavities are not a reliable way to judge the progress of healing: they are evidence of necrosis, which is part of the natural history of the infection. This cavity in the right upper lobe has developed within an area of consolidation. C This cavity has a thick wall and a fluid level, which means that it communicates with a bronchus. There is nodulation in the lung below it. D In another patient there is a much larger thin-walled cavity with less fluid, probably because some of the contents of the cavity have been coughed up. E The solid "mass" lying in this thin-walled cavity could be either a mycetoma or a large blood clot, or both. Hemorrhage into a cavity with subsequent infection occurs quite often. There are fibrotic changes throughout the right lung because this cavity appeared unexpectedly when the infection seemed to be quiescent. F In this patient there were several small cavities in the right upper lobe which must have communicated with the bronchi because there is now inhalation bronchogenic spread into the left lower lobe. This pattern, with infection of an upper and a lower lobe, is very common.
When there is obvious cavitation on standard radiographs, the sputum will be positive for bacilli in 80% of patients, but not always at the first examination; a negative sputum does not therefore exclude tuberculosis or indicate cure. Cavities may not disappear: 7%-10% of all cavities become bacteriologically sterile under treatment but remain patent. If, following surgery, cavities are examined histologically, part of the cavity wall may show healing while in another part there is active infection. Histopathologically, tuberculous cavities are abscesses and the wall of the cavity is lined with necrotic tissue. The only slight help which may be obtained in identifying active infection is when the inner wall of the cavity becomes radiographically ill-defined and the outer wall becomes less distinct. Unfortunately, a secondary infection, particularly fungal, can have exactly the same effect. Each and every radiological characteristic of the cavities can alter month by month, while the clinical condition of the patients may improve or worsen without any relationship to any radiological change in the cavities.
Unfortunately, space does not permit the illustration of all the vagaries of pulmonary tuberculosis in the tropics: the most important differences (between nontropical and tropical patients) are the rapidity with which tuberculosis may change or progress in the tropics, and how slowly it may heal even during adequate treatment. Equally important is the often acute and unexpected pattern of the infection, which may make it difficult to accept that it may be due to tuberculosis, whether in the primary (nonimmune) or in the secondary, reactivation (immune) phase.
The significance of cavitation has been overemphasized; it is but one event in the natural history of the disease. It is not even unique to human tuberculosis, air-fluid levels having been reported in the lungs of a tuberculous cockatoo!
there is hemoptysis, the hemorrhage may come either from the lining
of a cavity or from endobronchial disease, as when bronchoscopy shows
that the blood comes from a lung segment in which there is no radiologically
visible cavity. In tuberculosis, arteriography has not been a very satisfactory
method of diagnosing or treating the source of the hemorrhage, probably
because there is almost always a great deal of associated fibrosis and
scarring. A clot in a tuberculous cavity can mimic a mycetoma or become
infected by a fungus. It is only the reabsorption of the clot after
a relatively short period, 1 or 2 weeks, which can exclude a fungus
ball. Most cavities heal by obliteration, leaving a scar, but some remain
as thin-walled bullae.
Fibrosis is equally unrewarding prognostically (Figs. 5.27-5.29). Change is almost always slow, so that comparison with a radiograph taken a few weeks previously may show no alteration. It is essential always to compare findings with the very earliest film available. It is never possible to judge the status of the infection from one radiograph; even extensive pulmonary fibrosis may include active disease. The radiological assessment of activity is very unreliable (Fig. 5.30), and is often made more difficult by a secondary pyogenic infection in the fibrotic lung: clinically it may be some other concomitant illness, such as amebiasis or dysentery, which has led to deterioration in the patient's general health. When there is lung fibrosis it is impossible by any imaging technique to differentiate pyogenic infection from recurrent tuberculosis, or to exclude contamination by a saprophytic fungus (Fig. 5.31). The diagnosis has to be made clinically with the help of the bacteriologist; unfortunately, relapsing secondary infections are common.
However, to end this section on a more positive note, the majority of patients eventually heal or fibrose their tuberculosis into a state of inactivity provided they continue with adequate treatment.
Fig. 5.27 A-D. The success, and failure, of treatment for tuberculosis. This African patient had started treatment in November for active tuberculosis. A Two months later the sputum was still positive for tuberculosis. Cavitation and consolidation are still present in the right upper lobe, with some overlying apical fluid. Some shrinkage of the upper part of the right lung has occurred, with slight mediastinal shift to the right. Infection is present in the left lung, particularly in the lower lobe but also in the apex. B By June, after 7 months' treatment there has been remarkable improvement. The right upper lobe has contracted and become fibrotic. The cavity has disappeared and the fluid over the apex of the lung has been absorbed. The left lung has also improved, leaving some minimal fibrosis only. The sputum was now negative. C Unfortunately, 1 year later there has been a severe relapse; a tuberculous focus has probably ruptured into a bronchus, with resulting widespread bronchopneumonia in both lungs. There is now consolidation in the right lung and a huge cavity in the right upper lobe. There is active disease and cavitation in the left lung. The mediastinum is still shifted a little to the right because of the underlying fibrosis and the right side of the chest is smaller than the left. Treatment was continued with slow improvement until (D) 4 years after the original radiographs. A large emphysematous bulla is present in the right upper lobe and the right lower lobe is also emphysematous. The middle lobe is severely contracted. This lung is also fibrotic and shows some small bullae. The sputum had been negative for about a year, but the fibrotic contraction and formation of bullae had continued until the right lung was virtually destroyed. Though fibrotic, the left lung is the only functioning remainder. The right lung is bronchiectatic and will often be secondarily infected. From this stage onwards it will be very difficult to decide whether any clinical illness is evidence of further reactivation of the tuberculosis.
Fig. 5.28 A-C. In some patients the response to antituberculous treatment can be remarkable. A This African woman presented with severe bilateral cavitating tuberculosis: her sputum was positive for tuberculosis. She was started on treatment and 5 months later (B) there had been improvement in both lower lobes, but there were huge bullae almost replacing both upper lobes (the left in particular), and compressing the remainder of both lungs. She was clinically improved but very short of breath. Treatment was continued and (C) 11 months later there was remarkable improvement: the bullae had disappeared and both lungs were clear except for some upper lobe fibrosis. It is difficult to believe that these three chest radiographs are of the same patient. The change in her clinical condition was equally impressive.
Fig. 5.29 A-F. Tuberculosis heals by fibrosis. It may cause (A) a localized stricture in a small bronchus (arrow) and result in repeated segmental infection of (B) gross bronchiectasis and contraction. The appearance of "apical" fibrosis (C) may be misleading. A bronchogram in the same patient (D) shows that the right upper and middle lobes and the superior segment of the lower lobe are contracted upwards, with gross emphysema of the lower lobe. E Fibrosis also affects the pleura and it is often difficult to be sure whether the air-fluid level is in the lung or pleural space. F Standard tomography of the same patient shows the multiple fibrotic septa and thickening of the visceral pleura. It is not necessary to have a secondary pyogenic infection to produce this result.
Fig. 5.30. Severe bilateral chronic tuberculosis will remain unchanged radiographically for many years. In this 70-year-old patient no part of the lung has escaped. He occasionally produced sputum which contained a few M. tuberculosis bacilli and so remained a danger to his family, with whom he lived. Surgery was obviously impossible, but the success of continuing antituberculous therapy is doubtful.
Fig. 5.31 A, B. Reactivation tuberculosis must be included among the many causes of interstitial fibrosis, particularly in middle-aged patients. The clinical complaint is usually of dyspnea and general ill health. A Both lungs of this 50-year-old man showed severe interstitial fibrosis and honeycombing. The sputum was consistently negative for M. tuberculosis and the diagnosis was established by surgical biopsy. There was no radiographic change after 12 months of antituberculous therapy. B Lungs with interstitial fibrosis are fragile. An acute pneumothorax can develop after paroxysmal coughing, in this case bilaterally but much more severely on the left.
Histopathologically, a tuberculoma is a focus of caseating pneumonia, although this is an oversimplified definition using a controversial explanation. Radiologically, a tuberculoma is a nodular, usually circular opacity in the lung, from 1 to 10 cm in diameter. Tuberculomas may be dense or hazy: while most are well defined, a few are more irregular in outline. CT or careful radiography may demonstrate small satellite tubercles. About ten percent of tuberculomas have central cavitation (necrosis). Tuberculomas are usually solitary but may be multiple; sometimes several occur in one lung segment. They may be found in any part of the lung, most often towards the periphery. Calcification, if present, can be central or eccentric, granular or in the form of small scattered flecks best seen with CT. The majority of tuberculomas show no calcification, even on CT or tomography, and there is no hilar lymphadenopathy; there is seldom hilar calcification. Most tuberculomas do not have any surrounding parenchymal reaction, although occasionally there will be haziness of part of their outline, apparently due to some increased vascularity or lymphatic thickening directed toward the hilum; this may result from continued activity or reactivation.
A tuberculoma may be found in a patient of any age, sometimes by chance on a radiograph taken for some other reason. Other patients present with cough and loss of weight. The appearance of the tuberculoma may remain unchanged for weeks or months, or it may unexpectedly break down as the result of some alteration in the patient's immune status. This can cause bronchogenic infection, or local spread becoming an area of pneumonia. No tuberculoma is "safe;' even when unchanged for a long period.
diagnostic problems are considerable: many tuberculomas are only diagnosed
after surgical removal because a tumor has been suspected. If the patient
is young, malignancy is unlikely and in the tropics, tuberculosis will
be the most common etiology. A mycotic infection, such as histoplasmosis
or coccidiomycosis, is possible; an early pyogenic or amebic lung abscess
must be excluded. Unlike the majority of tuberculomas, lung abscesses
are progressive and seldom remain unchanged. The tuberculin skin test
will usually be positive, but this may not be a helpful differentiating
feature. A hytiatid cyst will have to be excluded, but this is usually
not too difficult. In adults, primary carcinoma of the lung must be
considered, although it is still uncommon in many parts of the tropics.
For the solitary nodule which strongly resembles primary or metastatic
lung carcinoma radiographically, and which is too small or inaccessible
for CT-guided biopsy, surgical excision may be the only way to establish
the diagnosis, but if tuberculosis is considered possible, it is a wise
precaution to give the patient adequate antituberculous therapy prior
to biopsy or surgery.
Fig. 5.32 A-J. Tuberculomas may appear in any part of the lung, at any age; they may be single or multiple and are of varying size. The sputum is almost always negative for M. tuberculosis. A Standard tomography of a small tuberculoma in the right lower lobe just above the diaphragm. B A larger smooth round tuberculoma in the right lower chest of a young woman. This did not change in spite of treatment over a period of many months. C A large ill-defined tuberculoma in the right lower lobe of an elderly patient. The initial diagnosis was carcinoma of the lung, but fortunately the sputum was positive for tuberculosis. D Some tuberculomas are lobulated or multiple. These two in the right middle lobe are well defined and could be mistaken for metastases. E A paramediastinal tuberculoma, clinically and radiologically suspected of being malignant. The diagnosis was made after surgical removal. F Standard tomograms of a lobulated tuberculoma in the left upper lobe, which was removed surgically. Even if tomography (including CT) demonstrates calcification, it is seldom possible to completely exclude malignancy by imaging unless the calcification is central in which case the vast majority of lesions will be benign. G Multiple well-defined tuberculomas in the left mid-lung. These closely resemble metastases, but in this young African patient there was no known primary. H Tuberculomas are not always quiescent and harmless. There is a small tuberculoma with satellite nodules in the left upper lobe: it had not changed over 4 months. The patient refused surgery because he was clinically well. I Six months later the outline had become indistinct and further nodules had spread throughout the upper lobe. He remained clinically well but antituberculous therapy was started. J Unfortunately in spite of treatment, the infection continued to spread and coalesced into a caviating area of pneumonia which eventually led to further bronchogenic spread into the left lower lobe.
Isoniazid is used in chemoprophylaxis, particularly to prevent development of tuberculosis in infected persons or those who have been in contact with patients who have sputum which is positive for tuberculous bacilli. It is also used for treatment, together with antibiotics. Prolonged therapy with isoniazid, apart from risking liver damage and peripheral neuropathy, may result in the development of thin-walled cysts (Fig. 5.33). Such cysts may regress or develop ball-valve obstruction due to blockage of the segmental bronchi. They may enlarge to resemble a single emphysematous bulla and may burst, causing an acute pneumothorax or pneumomediastinum. This can happen in children or in adults.
Chronic Pleural Disease
A pleural effusion during the reactivation stage of tuberculosis almost always means direct spread of the infection into the pleural cavity and is really an empyema. It is a different process to the primary pleural effusion which occurs in the nonimmune patient. If there is a spontaneous air-fluid level in the pleura, then a bronchopleural fistula has developed. Tuberculosis often causes adhesions between the parietal and visceral pleura, causing loculation of the pleural fluid, and, following aspiration, there may be loculated air-fluid levels within thick-walled pleural cavities. On a standard chest radiograph it can be very difficult to differentiate this from pulmonary cavitation; ultrasonography, CT, or standard tomography may be helpful, but intrapleural contrast examinations may be necessary to show the cavity and the connections if decortication is considered. Eventually, many, but not all, tuberculous effusions and pleuritis result in pleural calcification which may be extreme in some individuals, extending over half or more of the involved hemithorax.
Direct spread of tuberculosis from the lung or pleura to any part of the chest wall does occur, but is extremely uncommon. It is a little more frequent in atypical mycobacterial infections. When there is a tuberculous empyema the ribs can be directly involved (Fig. 5.34). Infection of the sternum, ribs or spine occurs in children, particularly during the progressive primary type of infection. Hematogenous dissemination accounts for other cases with skeletal involvement (see Fig. 5.89).
In many cases of spinal tuberculosis, there is no pulmonary infection, but an abscess from infected vertebrae can track around the intercostal space and surface alongside the sternum. The vertebral lesion may not be obvious radiologically and radioisotope bone scans or CT or MR may be advisable, or standard tomography where scanning is not available. Tuberculosis of the ribs or sternum follows the same pattern as skeletal tuberculosis elsewhere.
Infection of an infant within the uterus or during parturition is rare. However, many infants become infected from their mother within a few days after birth. There are about 150 recorded cases of undoubted congenital tuberculosis. The skin reaction to tuberculin is not always positive and the diagnosis can be difficult. About half these children will die within 3 or 4 weeks. It is not known whether this pattern or frequency of congenital infection will change in mothers who are HIV-positive. A chest radiograph of the infant will show a pattern of either miliary disease or primary tuberculosis, and progressive tuberculosis may develop. Some may be born with or develop primary skin tuberculosis. It is possible that the mother will have no radiological and little clinical evidence of tuberculosis.
Fig. 5.33 A-D. Large emphysematous bullae can develop in children and adults, and can occur spontaneously or in association with isoniazid therapy. A A large thin-walled air-containing cyst in the right lung, displacing the mediastinum to the left. It is very easy to mistake this for a pneumothorax and attempt to decompress it. This may result in a bronchopleural fistula, but in some patients the pressure is so severe that the risk has to be taken. B Spontaneous rupture of a similar cyst has caused subcutaneous emphysema and a pneumomediastinum. If the pressure increases, this may be fatal. C A lateral radiograph showing a similar large cyst in a child. This is quite thick walled, and there is tuberculous lymphadenopathy. However, this is not a tuberculous cavity. D Another child with a large bulla in the left mid-lung. The patients illustrated in C and D were both being treated with isoniazid.
Fig. 5.34 A, B. Tuberculosis of the chest wall is uncommon. A This patient had a tuberculous empyema and the fifth right rib became infected directly from the empyema.There is also periosteal reaction along the underside of the sixth right rib. B There is a lytic lesion in the anterior end of the first left rib which was found on biopsy to be tuberculous. The lung was not infected and no other source of tuberculosis was found. (See also Fig. 5.85).
Immunization with BCG
Many countries with a high incidence of tuberculosis recommend BCG vaccination (bacille Calmette-Guérin, an attenuated but live strain of M. tuberculosis), often during the first few days of life. The protection provided varies in different countries: it has been excellent in Haiti, but less successful in parts of India and Puerto Rico. The difference in results is not easily explained; sometimes it is due to technical problems with the vaccine and its administration. Another theory suggests that where environmental mycobacteria are common, people are already protected. However, where successful, the main benefit has been to reduce the risk of tuberculous meningitis and acute disseminated infections.
Protection following BCG immunization can last from 10 to 20 years; there are a few complications. Between 3 and 6 months after vaccination, children occasionally develop axillary (or inguinal) lymphadenitis on the same side (Fig. 5.35). This is probably no more than a classical primary complex, but in some children the nodal swelling is considerable and a very few nodes may suppurate: other children may be generally unwell and pyrexial, but the chest x-ray is almost invariably normal and remains so. Some countries use a more potent BCG vaccine when immunizing neonates, and this has been inadvertently used for older children. Although there was an increased skin reaction, which took longer to heal, there were no other complications and after 6 months the resulting scar was much the same as if the correct strength had been used.
The response to BCG vaccination is very dependent on the state of health and nutrition of the individual. When healthy, a positive reaction will be obtained in 85% of those vaccinated. The BCG response is grossly impaired in children and young adults with kwashiorkor (severe protein deficiency) and very depressed also when the patients are marasmic with kwashiorkor (combined protein and calorie deficiency.). However, if the individual is marasmic only (calorie deficient) the successful vaccination rate is the same as in healthy patients. This is important, because the pattern of tuberculosis which may develop in those who have been vaccinated is very dependent on the success or otherwise of the vaccination. After successful BCG vaccination the tuberculin skin reaction should be positive and, if active tuberculosis does develop some years later, it will follow the hyperergic (secondary immune) pattern.
BCG osteomyelitis has been recorded, it is rare. The lesion is usually
eccentric in the metaphysis of a long bone, breaking the cortex but
seldom causing a periosteal reaction. Generalized BCG tuberculosis and
tuberculous meningitis are even more rare; these complications may have
an increased incidence in HIV+ patients. Intravesical BCG has been used
successfully in the treatment of bladder carcinoma: subsequent miliary
tuberculosis (recognized on a chest radiograph) has been recorded in
two patients. The response to appropriate antituberculous therapy has
When an individual known to have a negative tuberculin skin test (PPD, Heaf or Mantoux) converts "spontaneously" to a positive reaction it is presumptive evidence of a tuberculous infection, although the site of the focus may never be found. A year of isoniazid or other therapy is often recommended. Several large series have shown that routine chest x-rays during this treatment are unnecessary, provided the patient takes the prescribed drugs correctly and continuously for at least 9 of the required 12 months. Only if treatment is discontinued or is inadequate should chest radiographs be taken regularly. Not all authorities agree with this regimen, and in the tropics the conversion may be due not to tuberculosis but to other mycobacteria. There is also some health risk from the chemotherapy, statistically about the same as for an otherwise healthy individual developing active tuberculosis after the tuberculin skin reaction has become positive. The risks of isoniazid-induced hepatitis are age dependent, and many authorities do not recommend its use in patients older than 40 years. Even if patients are not given active prophylaxis, repeated chest radiographs should not be routine but be taken only when indicated by the clinical condition of the individual.
Hypertrophic pulmonary osteoarthropathy, "clubbing" is not now usually associated with pulmonary tuberculosis (Fig. 5.36). It used to be more common and was a frequent finding in America and elsewhere before antituberculous therapy was available. However, it may still occur in up to one-third of African men with debilitating pulmonary tuberculosis. It seems to be more common in those who are undernourished but cannot be correlated with the extent of the findings on the chest x-ray or any other likely cause. Whether clubbing is increasing again in pulmonary tuberculosis in other regions is not yet recorded. It is important as a possible explanation for periosteal reaction on the clavicles, femora, digits, or elsewhere.
Fig. 5.35. The chest radiograph of a child who had had BCG vaccination 4 months previously. The chest is normal but the left axillary lymph nodes are considerably enlarged. It is very unusual for there to be any pulmonary abnormality following BCG vaccination.
Fig. 5.36 A, B. Clubbing is much less common in patients with pulmonary tuberculosis than in the past. A This middleaged patient with chronic tuberculosis, which has caused fibrosis of his left lung and pleura with flattening of the left chest wall, has (B) well-marked hypertrophic pulmonary osteoarthropathy. There is some apical fibrosis in his right lung, but he was not more dyspneic than would be expected, and there was no other reason for his clubbing. (There was no evidence of any bone foci.)
Nontuberculous mycobacterial infections (MOTT or "mycobacteria other than tuberculosis") cannot be distinguished clinically, radiologically, or pathologically from tuberculosis in the lungs or any other organ system, including bones. Some authorities state that there are about 40 different species; others recognize over 60 species. All agree that about half are potentially able to cause disease in humans. The distinction between M. tuberculosis and nontuberculous mycobacteria can only be made in the laboratory and requires selective culture, biochemical, DNA/polymerase chain reactions, and RNA sequencing, as well as serology. Differential skin testing is unreliable and cross-sensitivity occurs; almost all MOTT produce hypersensitivity to tuberculin and confuse the validity of the standard tuberculin skin tests (PPD, Heaf, or Mantoux reactions).
These nontuberculous mycobacteria are all common in the environment and all are acid-fast. The commonest human pathogens are:
Apart from M. ulcerans, all have low virulence and poor infectivity and seem to lack person-to-person transmission, but there is evidence that this may be altered by immunosuppression, since all the nontuberculous mycobacterial infections are being seen much more frequently because of the AIDS epidemic. The majority are resistant to most antituberculous drugs, but may be treated by multidrug regimens, often aided by surgery.
The frequency of MOTT in Europe and North America is 1%-3% of all new cases of tuberculosis. In Western Australia the frequency has increased to 16%. The prevalence of tuberculosis is not affected by other mycobacteria, nor do the MOTT bacilli give any protection against tuberculosis. Repeated isolation of the same mycobacterium is required before suggesting that this is the causal organism for any illness. If M. tuberculosis is also present, then this is likely to be the dominant organism. Although the incidence of MOTT disease is now showing a marked increase due to the AIDS epidemic, it has in the past been uncommon in most developing countries except when patients had preceding lung damage; for example, MOTT were cultured twice as often in African gold miners who had silicosis compared with those who did not. Despite AIDS, MOTT is still less common in the tropics than elsewhere. The MOTT bacteria may be more important as subliminal infections.
Many MOTT are low-grade pathogens and others exist as saprophytes. The known precipitating factors in infections are chronic lung damage, such as emphysema and bronchitis, industrial lung disease (both mining and agricultural), urban air pollution, and immunosuppression. All MOTT (except M. ulcerans) can rarely cause pulmonary lesions. M. scrofulaceum may cause cervical lymphadenitits in children under 12 years old. M. kansasii and M. aviumintracellulare often affect males over the age of 45. M. ulcerans infects mainly the panniculus; M. marinum (balnei) also affects the skin, as do M. fortuitum and M. chelonei.
There have been many descriptions of the radiological appearances of different MOTT pulmonary infections, and there are some small differences, but as already noted, it is not possible to distinguish radiologically between the mycobacteria. When an otherwise healthy patient with an apparently straightforward tuberculous infection fails to respond to adequate therapy, the commonest cause is drug resistance and the alternative is infection with a nontuberculous mycobacterium.
Mycobacterium paratuberculosis (Johne's bacillus). Within the M. avium-intracellulare complex is M. paratuberculosis, which is very common in the intestine of many animals, including cattle, sheep, and primates. It has been cultured from humans with chronic intestinal inflammation, resembling Crohn's disease. It is very difficult to recognize by culture and in some instances cannot be cultured at all. It is very resistant to most antituberculous drugs.
Its incidence in the tropics is not documented, but it has caused cervical lymphadenitis and chronic granulomas of the small intestine, closely resembling those found in the animal infection. Radiologically, a cobblestone appearance of the mucosa, with segmental narrowing of the terminal ileum, has been reported. Human infection is acquired from drinking infected milk from animals which may be apparently well and are subclinically infected. The AIDS epidemic, lowering the human immunity, opens the way to more widespread infection by this bacillus.
Despite the overall prevalence of tuberculosis in many parts of the tropics, there is no part of the world where tuberculosis commonly affects the gastrointestinal system. In the past, before drug therapy became available and patients died of advanced tuberculosis, about 80% were found to have abdominal tuberculosis at autopsy the more advanced the pulmonary tuberculosis, the more likely there was to be bowel infection. However, now that treatment has become possible, the correlation of pulmonary tuberculosis with abdominal tuberculosis has altered, and less than 50% (in some series 25%) of patients with abdominal tuberculosis have pulmonary tuberculosis also. This ratio may again alter significantly with AIDS; for example, already in Haiti patients with AIDS are 3.5 times more likely to have extrapulmonary tuberculosis than patients who are HIV-negative.
Tuberculosis in the bowel starts as a localized inflammation of the lymphoid tissue and progresses to necrosis. The reaction can be ulcerating or hypertrophic or both. Tuberculous ulcers in the bowel are often transverse and linear, rather than round. Throughout the alimentary tract, tuberculosis forms granulomas which may be demonstrated as a mass; as distortion due to fibrosis, or as a stricture. When the infection has healed, there may be a residual scar, adhesions, or an ulcer on the damaged tissue.
Except in tuberculous peritonitis (see section on Tuberculous Peritonitis) there are no clinical or laboratory criteria which are of any significance other than the histology. Stool culture for tuberculosis is unreliable. The symptomatology is vague and cannot be related satisfactorily to the abdominal lesions in the majority of patients. Ill health, vomiting, diarrhea (30%), and constipation (20%) are all generalized symptoms. Malabsorption is not uncommon. Analysis of the blood is normal except for anemia, which is very common in tropical countries and is more likely to indicate the presence of parasites rather than tuberculous bowel. There is no close relationship between pulmonary and alimentary tuberculosis. Many patients will have active lung disease, but a normal chest x-ray does not exclude tuberculosis in the alimentary tract.
The development of imaging by scanning (ultrasonography, CT, or MRI) has provided a better understanding of the pathophysiology and clinical pattern of tuberculosis in the abdomen. The diagnostic index of suspicion for tuberculosis has been raised, but unfortunately this is all that imaging can do; there are no specific changes for any form of intraabdominal tuberculosis. Nevertheless, all current methods of imaging provide very useful guidance and are invaluable in follow-up during or after treatment.
most common alimentary forms are peritoneal and cecal tuberculosis;
other sites are less frequently affected. But again, it is probable
that the incidence and pattern will change in AIDS patients, particularly
late in their disease, adding to the already difficult problem of differential
Tuberculosis of the Esophagus
There are three ways in which tuberculosis may present in the esophagus: (1) as a long stricture; (2) as gross dilatation above a narrow stricture, and (3) as ulceration, with or without a diverticulum. A tuberculous granuloma presenting as a mass in the esophagus does not appear to have been reported, but is a theoretical possibility.
The common site of infection is in the upper half of the esophagus (Fig. 5.37). The patient may present with difficulty in swallowing or with sudden impaction of food and acute dysphagia. Intrinsic tuberculosis of the upper third of the esophagus must be differentiated from the traction and fusiform pseudodiverticula which may be caused by fibrotic tuberculosis in the lung apices. In these patients the trachea is always deviated. Many texts state that traction diverticula in the mid-third of the esophagus are the result of adhesions from tuberculous mediastinal lymphadenopathy. None of the authors of this book, who together have considerable tropical and tuberculous experience, have ever seen this occur; it may happen, but it is not the cause of most esophageal diverticula.There are many thousands of patients with tuberculous mediastinal lymphadenopathy and very few with esophageal diverticula.
Tuberculosis may cause a hard nodular swelling in the thyroid, which often grows quite rapidly; it is only later in the disease that an abscess develops, either in the neck or, rarely, behind the sternum. A mediastinal tuberculous abscess spreading from nodal or vertebral infection also may cause pressure displacement of the esophagus but a pyogenic abscess or an intrathoracic goiter must also be considered. Tuberculous infection of the esophagus has been known to cause both bronchoesophageal fistulae and erosion into an aortic aneurysm. These complications may become more common with AIDS.
Long-segment esophageal strictures with irregular granulations on the surface have to be differentiated from caustic burns, inflammatory or fungal esophagitis, and malignancy (Fig. 5.38). Carcinoma of the esophagus in the tropics may be multifocal and extend over 15 cm (6 inches) or more. Short-segment tuberculous strictures involving the lower third of the esophagus have to be differentiated from achalasia, peptic esophagitis and neoplasm; tuberculosis is a rare cause, and such differentiation is often impossible radiologically.
Fig. 5.37. A Tuberculosis of the esophagus. A stricture in the upper third of the esophagus which has all the characteristics of a carcinoma: only the histology can provide the diagnosis. (Courtesy of Dr. J. Farman.) B Mucosal edema and ulceration in the upper third of the esophagus of an Indian: he suffered from pain and dysphagia. This type of tuberculosis may eventually perforate (C) into the mediastinum but will still heal satisfactorily with the correct treatment. D A similar infection which has formed a pseudodiverticulum posteriorly in the lower third of the esophagus.
Fig. 5.38. Tuberculosis of the lower end of the esophagus causing a stricture just above the cardia. The huge dilated esophagus lies on the right side of the mediastinum and closely resembles the esophagus in achalasia or Chagas' disease. The patient had active pulmonary tuberculosis and a left pleural effusion, but histological examination of the esophagus provided the correct diagnosis. (Courtesy of Ms. A.A. Whitmore, Harare).
Tuberculosis of the Stomach
Tuberculosis of the Stomach is a very uncommon form of tuberculosis, although it may become more frequent in AIDS patients. However, it is unlikely to become easier to diagnose either clinically or radiologically. The clinical history and the imaging appearance may suggest simple peptic ulceration, other granulomatous diseases, lymphoma, or carcinoma of the stomach. Even at surgery the macroscopic appearances can resemble malignancy and the differential diagnosis may only be made histologically.
Radiologically, tuberculosis of the stomach may present as shallow ulceration, (which can be extensive), a granulomatous mass or as fibrosis (Fig. 5.39). The most common of these is ulceration at the pylorus, which causes gastric outlet obstruction. It resembles and often cannot be distinguished from fibrosis following peptic ulceration or from malignancy. Tuberculosis is yet another cause of gastric dilatation, but is sufficiently rare as to be a surprise to both the radiologist and the surgeon when histology is obtained. Tuberculous gastric ulceration has been reported on both the greater and lesser curvatures off the stomach, usually surrounded by induration and therefore reducing peristalsis.
These ulcers are usually shallow but can be quite large. The likely mistaken radiological diagnosis will be lymphoma or carcinoma.
The tuberculous granulomatous mass in the stomach is the least common presentation of this uncommon form of tuberculosis. With such a mass, there is always associated mucosal ulceration and surrounding fibrosis. The ulcers are chronic and will be mistaken for malignancy.
The shape of the stomach (and duodenum) can be distorted by extrinsic pressure from enlarged tuberculous lymph nodes (Fig. 5.40, 5.41). These usually compress on the distal third of the stomach and in some cases are adherent. In one such patient there was a very large gastroesophageal mass at the cardia causing distortion, with an overlying gastric ulcer. Although ultrasonography, CT or MRI can demonstrate the lymphadenopathy, the correct diagnosis is not likely to be achieved by imaging.
Fibrotic tuberculosis can mimic linitis plastica, scirrhous carcinoma, infiltrating lymphoma, or even syphilis. To this differential diagnosis must be added Crohn's disease, which is rare in the tropics.
of the Duodenum and Small Intestine
The clinical presentation in most cases is of upper small bowel obstruction, but occasionally the obstruction is lower, in the ileum. There is usually a history of intermittent attacks of abdominal pain, with nausea and sometimes vomiting; when the small bowel is involved, malabsorption and malnutrition occur more frequently. Eventually the obstruction becomes persistent.
Abdominal radiographs in the supine and erect positions will show dilated loops of small bowel and fluid levels. In one series from India, there were dilated loops of bowel in 54% of patients with abdominal tuberculosis and, in over half of them, there were fluid levels on the erect radiographs. Tuberculosis causes different patterns of small bowel disease. Infiltrating tuberculous granulomas around the duodenum result in loss of normal mucosal pattern, rigidity, and narrow strictures; a stricture of the third part of the duodenum (particularly in India) should raise the suspicion of tuberculosis. In the ileum, the Peyer's patches are affected and transverse ulcers develop with typical undermined edges. In the early stages, when there is minimal dilatation of the ileal loops with excess fluid in the lumen and no significant stricture, the barium forms bubbles with ill-defined edges; later as the strictures become well established, the barium column is trapped proximal to the stricture, and outlines the stricture and dilated lumen. The dilated ileum can reach mammoth proportions. It may be necessary to introduce a peroral small intestinal tube for a selective small-bowel enema to demonstrate the stricture. These strictures are most common in the ileum but may be seen in the jejunum and even in the duodenum. Tuberculous strictures are not as long as those of regional enteritis, and in addition, as noted earlier, Crohn's disease is extremely rare in India and many other tropical countries. Occasionally in tuberculosis there are fistulae in addition to the strictures, and the differential diagnosis then becomes impossible without histological examination. Calcified enteroliths are commonly seen within dilated loops of small bowel proximal to tuberculous strictures, but are uncommon in any other chronic enteritis (Fig. 5.42 F).
When scanned by ultrasonography, CT, or MRI, the bowel lesions demonstrate the same imaging pattern. There is concentric bowel wall thickening, often with ulceration; this may be seen in any region of the small bowel or even into the colon. There is also narrowing of the lumen, which can be correlated with barium studies. It is not always easy to demonstrate such strictures by scanning. The bowel loops become matted together and adhesions, exudates, inter-loop fluid, or abscess may form complex masses. A "sandwich" appearance has been described when fluid collects close to the bowel wall and there is focal ascites; this results in alternating echogenic and echo-free layers through the wall of the bowel, showing the serosa, the fluid, and then the pattern of the adjacent bowel wall. Omental thickening (described as "caking") can also be demonstrated; a tuberculoma of the omentum has been recorded. Some loops of bowel will be dilated, others more normal or narrowed. Bowel wall thickness of more than 5 mm during contraction and 3 mm during distention is said to be abnormal, but whether this also applies in patients who have malabsorption or added parasitic infection is not known. In abdominal tuberculosis there is likely to be concomitant lymphadenopathy, and any part of the small bowel, but especially the duodenum and jejunum, can be distorted and displaced by enlarged tuberculous lymph nodes. Adhesions are frequent and the mucosal folds may be stretched over the nodes. It is unusual for complete obstruction to result from this type of extrinsic lesion.
Fig. 5.39 A-D. Tuberculosis of the stomach. A Mucosal ulceration and edema along the lesser curvature of the stomach of a patient from India. B Tuberculous gastritis causing thickening of the wall of the stomach and narrowing of the pyloric antrum of an African patient. C Granulomatous tuberculosis thickening and immobilizing the lesser curvature of the stomach from below the cardia down to the pylorus. In each of these patients the radiological diagnosis is likely to be carcinoma or lymphoma because tuberculosis of the stomach is rare. D Tuberculosis of the stomach resembling linitis plastica. The stomach would not distend beyond this size and peristalsis was absent. The radiological diagnosis was malignancy: it may be impossible even at surgery to distinguish tuberculosis without histological confirmation.
Fig. 5.40 A-F Pressure on the stomach and duodenum from tuberculous lymphadenopathy. A Displacement of the second part of the duodenum downwards and the third portion upwards. An African patient. B Distortion of both the lesser and greater curvature of the stomach and the pyloric antrum, with stretching of the pylorus and partial obstruction of the second and third parts of the duodenum. C Persistent pressure on the great curvature of the stomach which was thought to be due to carcinoma of the pancreas. The patient complained of abdominal swelling and pain. At surgery there was a large inoperative "tumor" which was found on histology to be due to active tuberculosis. Where it had originated remained undecided, but the patient responded to appropriate treatment. (Courtesy of the University of Capetown, Radiology Library.) D Intravenous gadolinium-enhanced T 1-weighted MR scan showing an enhanced nodal inflammatory mass (arrow) with areas of nonenhancing necrosis. E A contrast-enhanced CT scan showing multiple rim-enhancing nodes in the periaortic region. F A CT scan of a child from South Africa shows diffuse calcification in enlarged mesenteric lymph nodes. There is also some ascites (arrows). (D-F from Cremin and Jamieson 1995).
Fig. 5.41 A-H. The pressure from tuberculous lymph nodes may eventually cause obstruction in the duodenum. A A large duodenal bulb due to obstruction of the second part of the duodenum, caused by fibrosis following tuberculous lymphadenitis. B A stricture at the junction of the second and third parts of the duodenum of a 6-year-old child from India, which caused partial obstruction. This was the result of adhesions from previous tuberculous lymphadenitis. Both A and B could be misdiagnosed as the result of congenital bands (Ladd's syndrome). C Pressure on the second part of the duodenum and obstruction at the junction of the third and fourth parts by enlarged lymph nodes and tuberculous duodenitis. D Tuberculous mucosal ulceration and edema of the second, third, and fourth parts of the duodenum. This could be mistaken for lymphoma or even a severe parasitic infection. With proper treatment this condition may heal completely, or result in strictures. E Perforation of a tuberculous ulcer of the second part of the duodenum into the biliary tract, with reflux of bile. (There are two incidental duodenal diverticula.) F Intense spasm due to tuberculous ulceration of the first and second parts of the duodenum of an Arab patient. Tuberculosis was confirmed histologically. (The arrow points to an artefact.) G A funnel-shaped stricture in the proximal jejunum of a 12-year-old Arab female. H A CT scan shows pressure on the transverse duodenum from lymphadenopathy. There was also an ileal stricture which is not demonstrated.
Fig. 5.42 A-H. Tuberculosis of the small intestine. A The acute phase with loss of normal bowel pattern, excess fluid within the gut, and rapid transit of barium. B Multiple granulomatous strictures and dilated lengths of bowel. C Multiple lengths of dilatation and strictures with fistula formation, indistinguishable from regional enteritis except by histology. D A tuberculous duodenal-colic fistula in a 7-year-old child with malabsorption (incidental stomach rotation). E A narrow "apple core" stricture in the ileum (arrows). F Partial obstruction of the midileum due to tuberculous granulation tissue. G Enteroliths in the small bowel of a patient from India, with multiple strictures in the small bowel from tuberculosis. H Ultrasonography can be used to show the thick wall of tuberculous small bowel and will often demonstrate that the bowel loops are adherent of clumped together. This patient was an African male, aged 43 years, from Zimbabwe. (B courtesy of the University of Capetown Radiology Library; C AFIP 229499; D courtesy of Dr. D. Makanjuola and Eur J Radiol, 1998; H courtesy of Dr. Sam. Mindel).
Tuberculosis of the Cecum (Hyperplastic Tuberculosis of the GI Tract)
Tuberculosis of the cecum is one of the most common types of intra-abdominal tuberculosis, and in some series it accounts for up to 60% of all tuberculous bowel infections. (The other common sites are the peritoneum and lymph nodes.) The clinical symptoms are vague. There may be alternating diarrhea and constipation, changes in bowel habit, a palpable mass and vague crampy pain in the right iliac fossa, general ill health, and anemia, but all are nonspecific. When tuberculosis affects the cecum and distal ileum (Fig. 5.43), initially there will be intense ileocecal spasm seen on barium studies or small bowel examination (Stierlin's sign). Later, the lumen and size of the cecum are compromised as the granulomas form into a mass and undergo fibrosis. The mesocolon of the cecum contracts; the cecum is pulled up out of the right iliac fossa and shrinks (Figs. 5.44, 5.45), often drastically, culminating in the classical conical, pyramidal, or at times, pear-shaped configuration. The associated fibrosis causes a partial stricture at the ileocecal region and the dilated terminal ileum appears to be suspended from the cecum like a pendulum. There is restricted movement of the cecum on palpation, not only transversely but also in the craniocaudal axis. Sinus formation is uncommon unless there has been inadequate surgical interference; sinus formation and osteoinyelitis of the ilium suggest a mycotic infection, usually actinomycosis, not tuberculosis.
Scanning by any method, but particularly ultrasonography will show thickening of the bowel wall in the ileocecal region and in the ascending colon (Fig. 5.46). In many patients the right iliac fossa may be comparatively empty because the cecum has been drawn up by fibrosis. When thickening occurs, it is nearly always concentric but may be distorted by the peritoneal adhesions. Ulceration in the ileocecal area is always associated with bowel wall thickening and may be superficial or deep. The correlation between scanning and barium studies is good, but the typical appearance as shown by barium enema may be more diagnostically accurate. The irregular pattern of spicules and progressive narrowing, together with displacement of the cecum, is likely to be more marked than in amebiasis.In children in particular, the ileocecal valve may be so thick that it mimics a mass in the cecum; it remains patent because of the fibrosis. Oral contrast is helpful with CT scanning to show the thickness of the bowel wall and narrowing of the lumen. However, in many cases only histology will provide the correct diagnosis.
The differential diagnosis includes an appendiceal abscess, amebiasis, actinomycosis, granulomatous colitis, and malignancy. Tenderness on palpation is maximal with appendiceal abscess, tethering of the cecum is maximal in tuberculosis, and sinus formation and adjacent osteomyelitis are most common in actinomycosis. Reflux into the ileum due to loss of ileocecal sphincter action is easily demonstrated in amebiasis and malignancy, in spite of the tumor; reflux is less common in tuberculosis in the early stages because of spasm, and later because of fibrosis. Amebic infection can present as granulomatous disease also, but the fibrosis accompanying tuberculosis is more severe than that seen in amebiasis. Multiple granulomas and strictures may also occur in amebic infection, but in over 90% of patients with amebiasis only the last 6 inches of small bowel are involved, whereas in tuberculosis and Crohds disease the terminal ileum is involved in 45%-50% or more of patients with cecal disease. Lymphoma will have to be considered, but carcinoma, granulomatous colitis, and ischemic colitis are all rare in most tropical countries.
Fig. 5.43 A-E. Tuberculosis of the terminal ileum and cecum. A Dilatation, edema, and ulceration of the terminal ileum. B The contracted cecum which is the result of tuberculosis in a five-year-old child from India. There is marked adynamic dilatation of the terminal ileum, mucosal ulceration, and loss of the normal ileal pattern. C Gross dilatation of the terminal ileum above a long stricture proximal to a contracted tuberculous cecum. D The sonogram of the thickened cecum of a child from the Pacific Islands with ileocecal tuberculosis. E A tuberculous ulcer at the ileocecal junction, causing marked constriction and distortion, with resulting obstruction and dilatation of the ileum above it. (D courtesy of Dr. Cheryl Sisler, Hawaii).
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).
Tuberculosis of 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.
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.
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).
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.
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).
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.
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.
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.
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
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.
granulomas may calcify and then be demonstrated by any method of imaging
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).
Kidneys and Ureters
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.
is a very satisfactory way to image each step of this pathological process
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
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.
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.
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
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.
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
Tuberculosis of Bone
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.
Clinico-pathological-radiological Correlation: Spinal Tuberculosis
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.
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.
Imaging of Spinal Tuberculosis
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).
2. The abscess may be unilateral or bilateral.
3. The abscess may be lateral, or anterior, or both.
4. The abscess may appear below, or occasionally above, the obvious bone focus.
5. There may be a large abscess with no clinical symptoms or a small abscess with paraplegia.
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
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.
Fig. 5.70. A. A 25-year-old African complained of backache ans was found to have a left paravertebral abscess and erosion of the medial end of left tenth rib (arrowhead). B A T 1-weighted coronal MR scan showed bilateral abscesses and low-intensity signals from the marrow of T 8 and T 9. C The T 1-weighted sagittal MR scan showed the large abscess anteriorly and posteriorly, with destruction of the vertebral bodies and compression of the cord (arrow). D After 6 weeks of antituberculous treatment the abscess is much smaller and the cord is less compressed (arrow). It was realized more than 30 years ago (Konstam) that many of the neurological signs are caused by the abscesses rather than the spinal deformity. CT and MRI have confirmed this dramatically. (Courtesy of Dr. Peter Corr, Durban) E Apart from pressure on the cord from an abscess, there may be a tuberculoma, as shown at the level of C 4 in a different patient, a child. This is an intravenous gadolinium-enhanced T 1-weighted MR scan. (From Cremin and Jamieson 1995).
Wherever the abscess presents, there should be careful imaging of the whole spine, starting preferably with isotope scintigraphy. Paravertebral abscesses occur at all levels and may be present on one side only, on both sides symmetrically or asymmetrically, or only in front of the spine without any lateral extension. Some may be dumb-bell in shape, protruding wherever space permits. They vary considerably in size and shape. When there is an anterior spinal abscess, underneath the spinal ligaments, the anterior edge of the vertebral bodies may become concave because of the transmitted aortic pulsation. The vertebral cartilages are not affected and the pressure absorption of the body may be minimal or considerable, so that it resembles the concavity caused by an aortic aneurysm. MRI is the best way to demonstrate what is actually happening, and CT is also suitable for this purpose.
A psoas abscess may connect with any part of the bowel, may be extensive and surround the kidney or the liver, or may burst through the skin onto the surface almost anywhere (Fig. 5.71). In many cases sinography is required, but careful technique is essential. The examination should be carried out under aseptic conditions and under fluoroscopic control. The sinus should be blocked by using the largest catheter that can be inserted; a balloon catheter will often help in achieving a tight connection. Pus should be aspirated, if possible, and pressure on the surrounding tissue or the suspected site of the abscess may help this drainage. Contrast material should then be injected and considerable pressure may be required if the full extent of the abscess is to be visualized. The case illustrated in (Fig. 5.71A and B) was a patient who presented with a sinus in the left side of the lower abdomen, without any obvious etiology. The only organism cultured from it was E. coli. A barium enema and an upper gastrointestinal series with a follow-through examination did not show any connection to any part of the bowel.
Two limited sinograms were performed before the patient was referred to the author, who blocked the sinus and, using considerable pressure, showed the abscess extending up the left psoas and surrounding the left kidney, across the midline between T12 and L1, and then coursing down the right psoas to connect posteriorly with the cecum. This was, therefore, a sinus draining from the left lower abdomen and yet connected with the cecum on the opposite side through a tuberculous abscess of the spine. (A very similar case has been seen in an American who has never been near the tropics!)
Paravertebral tuberculous abscesses shrink and often show calcification as they heal and fibrose (Fig. 5.72). Unfortunately, calcification does not always indicate sterility. There may be active caseous material contained within the fibrotic bag.
Fig. 5.71 A-D. Psoas abscesses can be very extensive and have unexpected connections. This young African has a persistent left flank sinus contaminated with E. coli. A The sinogram from the left lower flank, close to the iliac crest, showed that the fistula was connected to an enlarged left perirenal tuberculous abscess, which had started in a tuberculous infection between the 12th thoracic and first lumbar vertebrae. The abscess had also drained down in the right psoas and connected with the cecum, which was the source of the E. coli infection. B The lateral view of the same patient shows contrast running in front of the vertebrae, above and below the infection. This demonstrates how anterior abscesses can transmit aortic pulsation and also the etiology of the anterior bone bridging which occurs when the periosteum and anterior spinal ligaments are lifted. The aortic pulsation can bow the front of the vertebrae, as is shown in C in a much older patient with advanced aortic athromatous calcification. A previous tuberculous infection has resulted in fusion and increased density of the two lower thoracic vertebrae. D Another African patient with a fistula connecting the terminal ileum with a paraspinal abscess, which originated in lower thoracic tuberculosis. It is not always possible to demonstrate these fistulae with a barium gastrointestinal series. E. coli contamination is usually sufficient proof, even if the actual fistula cannot be imaged. (C courtesy of Dr. Harold Jacobson).
Fig. 5.72 A-E. Tuberculous abscesses of the lower spine. Thoracic and lumbar abscesses track along the psoas and can present at the inguinal region. When they heal, they often calcify. A Well-defined, heavily calcified abscess starting at the lower thoracic region in a patient with severe kyphosis. B Bilateral loculated and less densely calcified psoas abscesses. C A unilateral calcified psoas abscess in the lumbar region. There is bridging between the upper lumbar vertebrae, well above the visible abscess. D, E Sonograms of a right psoas abscess, displacing the kidney, in an African patient from Zimbabwe. RK right kidney. (A courtesy of Dr. Harold Jacobson; D, E courtesy of Dr. Sam Mindel).
Fig. 5.73 A-D. Myelography in tuberculous paraplegia. Where scanning is not available, there is no contraindication to myelography under fluoroscopic control. A There is narrowing of the disc space between the second and third lumbar vertebrae, but the myelogram shows distortion not only at this level, but also one space above. B A patient with thoracic paraplegia. Myelography shows long irregular defects, between the tenth and 12th thoracic vertebrae. C Myelography in a kyphotic patient can be difficult. In spite of the angle, in this patient there was no obstruction on myelography: it can be difficult to retain the contrast at the level of the curve when it flows freely in either direction. D The myelogram may show complete block. (D courtesy of Dr. Harold Jacobson).
Fig. 5.74 A, B. Postoperative spinal tuberculosis. It is very difficult to assess healing, which may take years. These are the postoperative images of a 2-year-old girl from the Pacific Islands. A The lateral radiograph shows the graft across the infected and wedged thoracic vertebrae (T 9-11). B T 2-weighted MRI shows the residual abscess and granulation tissue and the exact extent of the bone destruction. (Courtesy of Dr. Cheryl Sisler, Hawaii).
Fig.5.75 A-G. The case history of spinal tuberculosis. A young man from Saudi Arabia had been complaining of pain between his shoulder blades for some months before he came to hospital one weekend, with rapidly developing'paraplegia. Plain radiography (A) showed wedging of two upper thoracic vertebrae. Myelography (B) showed almost complete block at this level and CT scan (C) showed destruction of the vertebra, particularly on the right side, and of the medial end of the rib at the same level. Fluid was present in the right side of the chest. D-G Pre- (D) and postgadolinium (E-G) MR scans show the full extent of the paraspinal abscess, and of the epidural granulomatous tissue. The findings on the CT scan are confirmed but shown more dearly. Subsequent surgical decompression revealed both caseation and granulomatous tissue with M. tuberculosis on direct smear microscopy. The patient made a good recovery. (Courtesy of Dr. Frank McGuiness, Ryadh).
Scanning, Paraplegia, and Myelography
As already mentioned, MRI is the ideal way to examine a patient with a tuberculous spine. A T 1-weighted scan shows tuberculous spondylitis as an area of low signal intensity where there is normally a higher intensity from the bone marrow, adjacent to the end plate of the vertebra. On a T 2-weighted scan these lesions have a high intensity. Liquid pus also yields a high-intensity signal on a T 2-weighted scan. MRI gives an accurate image of the spinal cord compression associated with intraspinal abscesses. At surgery, almost all patients with paraplegia will have at least a small abscess; even if it has not been visualized on plain radiography, it will probably be clearly seen on MRI (Fig. 5.73). Paraplegia indicates that there is about 50%-60% extradural compression above the conus, provided there is no vertebral instability. Peripheral nerves below the cauda or extraspinal nerves are not likely to be affected by compression. In some cases of paraplegia, the cord will appear to be intact, in which case there is likely to be a vascular deficit, a toxic reaction, or, as MRI can demonstrate (by showing a high-intensity focus on a T 2-weighted scan), damage to the cord, probably due to prolonged compression. This focal myelitis has a poor prognosis and the paraplegia is likely to be irreversible. However, as Konstam demonstrated, rest and drug therapy may relieve paraplegia which is of short duration, and simple decompression, either by needle aspiration or surgery, may be all that is needed in the early stages. Whenever any intervention is planned, it is a wise precaution to have the patient already on antituberculous therapy to obviate the risk of tuberculous septicemia.
Whatever method of imaging is used, it is essential that the whole cord or spinal canal is examined because the obstruction may not occur at the site of the obvious bone lesion, but rather be above or below it, depending on the extent of the fluid, necrotic tissue displacement, or granulation tissue.
If MRI is not available, myelography, with or without CT, is a very useful investigation and should be performed as early as possible and always before surgery to localize the exact site of any obstructions (Fig. 5.74). There are no contraindications to myelography although in some patients the kyphosis may make it extremely difficult. Where there is a double curve, careful manipulation of the patient (especially in the lateral decubitus position) may permit the column of contrast material to travel throughout the length of the spinal canal. Sometimes this is technically impossible, even when there is no blockage, because of severe spinal angulation. Fortunately, paraplegia is less often due to kyphosis or bony deformity than to an abscess or soft tissue pressure. The decision as to whether myelography needs to be repeated during treatment should be based on the clinical examination.
surgery in patients with spinal tuberculosis it is very difficult to
assess healing, which may take years. Again, MRI is the best method
for this purpose (Fig. 5.75).
Fig. 5.76 A-D. Skeletal tuberculosis. The pelvis. Infection of the sacroiliac joints can be destructive and then, as healing occurs, become sclerotic and fused. A Widening and irregularity of the left sacroiliac joint. B Sclerosis on the iliac side of the right sacroiliac joints. C In another patient there is infection on both sides of the sacroiliac joint, particularly the sacrum. D Extensive destruction of a right sacroiliac joint in a different African patient. The infection must have spread through the right ilium, which is becoming sclerotic. The joint is widened throughout its length. The right hip joint is narrowed and probably also infected. (A, C courtesy of Dr. Harold Jacobson).
Theoretically any type of bone infection may cause a paravertebral abscess. In practice, the majority of spinal abscesses in the tropics are tuberculous; if there is active pulmonary tuberculosis, the possibility of spinal infection also being tuberculous is enhanced. It is unusual for a pyogenic or typhoid infection to cause a large paravertebral abscess, and even less often do such abscesses point to the surface as occurs with tuberculosis. On MRI, pyogenic disc infection usually has a high intensity on T 2-weighted scans, but in tuberculosis less than one third show this. However, pyomyositis (tropical myositis) can present in this way, usually without any osseous lesion (see Chap. 30). Brucellosis may also produce a paravertebral abscess (see Chap. 32). There may be paravertebral thickening in lymphoma (particularly in Burkitt's lymphoma) which may resemble an abscess, and the bony destruction may also be very confusing because Burkitt's lymphoma may involve a vertebral body or a pedicle (see Chap. 41). Sometimes the differential diagnosis is impossible with any method of imaging, but in the majority of cases there will be other evidence of Burkitt's or other lymphoma to establish the correct diagnosis. Wedging, particularly wedging and fusion of two or three vertebrae, is very uncommon in any infection other than tuberculosis.
Because tuberculous osteomyelitis in the tropics (even in patients without AIDS) is often an acute disease, it is difficult to differentiate from other infections and the clinical condition of the patient may be very important when giving a radiological opinion. Nontuberculous spinal infections usually cause more severe clinical symptomatology than tuberculosis, with more systemic reaction, a higher pyrexia, and a raised white cell count, but none of these criteria are absolute and biopsy or aspiration and culture are essential.
The differential diagnosis of tuberculosis from acute trauma is seldom difficult, if only because of the clinical history. Trauma does not cause as much bone loss and destruction as tuberculosis. Long standing cases need serial review, both clinical and radiological. In the majority of such problem patients the etiology is of no immediate clinical significance, permitting a more cautious approach. Scintigraphy or other imaging survey of the rest of the spine may show other involved vertebrae and allow the differentiation between trauma and infection.
In all patients, the possibility of malignancy will have to be excluded, particularly when the bone destruction involves the pedicles. Many malignant tumors cause paravertebral swelling resembling an abscess; obtaining a tissue specimen, either through needle aspiration or biopsy, becomes essential. Most errors are made because the possibility of tuberculosis is overlooked in the elderly or in the very young.
Fig. 5.77 A-G. Tuberculosis of the ischium and symphysis pubis. In the early stages most tuberculous lesion in the ischium are ill-defined lucent areas; they later become sclerotic. A A lucent focus of infection in the left ischium, with some early surrounding sclerosis. B A more destructive lesion closer to the hip in another patient, with some loose bone fragments. C There are foci on both sides on the symphysis and in the left ischiurn. D Both sides of this symphysis have been infected, the joint is widened, and there is a central sequestrum. An African from Zimbabwe. E A different patient from the same country in which a similar infection has healed causing sclerotic fusion across the symphysis. F There is a lytic area of infection above the acetabulum in this child from South Africa, but the hip joint remains normal. G An isotope scan at the same patient shows that the iliac infection is more extensive than seen on the radiograph. Tuberculosis is the proven cause in all these cases. (A-C courtesy of Dr. Harold Jacobson; F, G from Cremin and Jamieson 1995).
A tuberculous infection of a joint can occur at any stage, but is more common in the younger age groups. Even babies from 6 months onwards may present with quite severe skeletal infection. The joints most affected in order of frequency are the hips, knees, ankles elbows, wrists, sacroiliac joints, and shoulders (Fig. 5.76, 5.77). In 98% of HIV-negative patients the tuberculin skin test will be positive. The way in which tuberculosis affects a joint depends on whether the original focus is in the synovium or in the adjacent bone. Spread of the infection from bone into a joint is more common and has a poorer prognosis.
Nontuberculous mycobacteria may cause arthritis and bone infection. This is uncommon, but may become more frequent in patients with AIDS. Mycobacterium kansasii has been known to infect knee joints, and M. intracellulare has infected the shoulder, the spine, and, in one patient, both wrists. The differential diagnosis will only be made by joint aspiration or synovial tissue culture.
Patients will first complain of either slight pain or stiffness in the affected joint, and of limitation of movement. In the early stages pain is minimal and it is only as the joint swells that it becomes significant. In many cases there will be a dull, ill-defined ache, often worse at night, but in developing countries such discomfort is often ignored, and it is not until the disease has progressed further that the patient seeks help.
In the beginning, it will be difficult to detect any clinical abnormality to account for the symptoms. Later there will be edema and swelling around the joint, with some limitation of passive movement and increase in local temperature; an effusion often develops early and aspiration of the fluid usually shows it to be clear or straw-colored with few cells; it is sterile on culture. The diagnosis may have to be presumptive, because it may not be possible to find any positive proof of tuberculosis. At this stage, scintigraphy is a reliable way of excluding bone infection; ultrasonography and MRI, and to a lesser extent CT, can be useful in demonstrating the soft tissue changes. Radiographically the joints may be entirely normal in the early stages, and it may take 2-6 weeks before there are positive radiological findings (Fig. 5.78).
The earliest change is loss of clarity of the bones forming the joint; their margins become hazy and difficult to define. There is a mild generalized osteoporosis but not localized bone destruction. The joint space may be widened because of the effusion. Progress of the infection is slow, but a little more rapid once the radiological changes have developed. The osteoporosis becomes more pronounced and there will be soft tissue swelling around the joint. It may be difficult to define any bone erosion because of the osteoporosis and the variable change in bone density. Eventually foci of bone destruction become more definite as the cartilage is destroyed. At this stage the radiological appearance is "ghost-like;" particularly when compared with the opposite normal side. If only the synovium is involved, and if treatment is adequate, the disease shows no further progress but slowly heals with a return of the joint towards normality. In the majority of cases, however, there is permanent damage to the cartilage and occasionally to the underlying bone which may lead to degenerative arthritis. When the synovial involvement has been severe, the joint may eventually ankylose.
Fig. 5.78 A-F. Tuberculosis of the hip. The earliest evidence of infection may be an effusion into the joint. A The CT scan did not show any bone lesion but there were M. tuberculosis in the effusion. B In other patients there may be soft tissue swelling, osteoporosis, and loss of bone definition, as can be seen by comparison with the normal left hip. C A different but similar infected hip in which the ill-defined, hazy appearance of the joint and the soft tissue swelling around the acetabulum, particularly medially, are clearly shown. D-F The same patient (an African from Zimbabwe) over a period of 3 years. D There is soft tissue swelling and an effusion in the hip joint with destruction of the acetabulum and femoral head. E Six months later there is less fluid and the bone density is improving: in spite of the bone destruction, there are no sequestra. F Two years later the joint has fused: there will be shortening of the limb and there is significant deformity of the right side of the pelvis. (A courtesy of Dr. Cheryl Sisler, Hawaii).
Scintigraphy is a very useful way of locating tuberculous bone infection and ensuring that it is not multifocal. In the majority of patients, tuberculous infection of a joint is due to spread from a focus within an adjacent bone. An effusion is evidence of this spread but may also occur before actual cartilage destruction has taken place. The bony focus may be close to the articular surface, a few millimeters away from it, or in the metaphysis. The very early bone focus (as well as the soft tissue involvement) can be shown by MRI, and the extent of marrow replacement can be assessed. Gadoliniumenhanced T 1-weighted images show differential rim enhancement. Such foci can be single or multiple, and although they are usually opposite one another on opposing sides of the joint, they need to be so closely related. On plain radiographs or CT, the lesion within the bone appears as an area of decalcification, without any definite edge and of no particular shape. This slowly spreads up the shaft, but also across the epiphysis into the joint. At this stage clinical symptoms will be minimal. Some patients may complain of a dull ache or "spasm" in the joint or occasionally some swelling. Careful clinical examination may show some restriction of movement, but this may be so slight that there is little suspicion of an underlying osteomyelitis.
As the infection bursts into the joint, there will be a considerable reaction, with fluid and tuberculous debris in the joint space. The sacroiliac joints can be the most difficult to assess on plain radiography. Scintigraphy can be helpful but the uptake ratio between the sacroiliac joint and the os sacrum can vary with age. In any joint, CT and MRI provide more definite evidence of bone destruction on either side of the joint, and of subsequent joint involvement. Clinically, at this stage, there is no doubt that a limb joint is abnormal. It will be painful, swollen, and immobile.
The disease progresses with further destruction and disorganization; the soft tissues, already swollen, become involved with the tuberculous process, best shown by MRI or CT. The joint may subluxate. In weight-bearing joints such as the hip (one of the most commonly affected: (Figs. 5.78, 5.79), involvement of the acetabulum may lead to rupture of the femoral head into the pelvis, particularly where treatment has been delayed and weight bearing has been continued. CT and MRI, and occasionally ultrasonography, can show a soft tissue mass within the pelvis when this occurs. There will usually be multiple, very small sequestra within the mass. The margin of the infected lesion in the bone will probably show reactive sclerosis. Angiography has been used to show the soft tissue mass, which is usually vascular, but it is unlikely that this will provide much useful information.
As healing occurs, the joint space usually narrows; the bones increase in density but do not remodel and the deformity persists. Ankylosis is almost inevitable and may in fact be beneficial because it often permits limited use of the limb. The entire process may take months, even with adequate drug therapy, and the principal imaging problem is to assess the progress of healing, because the changes occur slowly and are often minimal. Ankylosis may become complete, but because of fibrous tissue rather than bony fusion. In such cases the infection may be quiescent but not fully healed. As with all other types of tuberculosis, experience must be combined with careful clinical judgment and continuous observation of the patient to obtain the best end result.
either synovial or osteoarticular, may occur in any tuberculous joint
and the same pattern will be followed. Variations occur depending on
the type and location of the joint, whether or not it is weight bearing,
and how much it is used. For example, when foci oppose each other on
either side of a joint [usually the knee (Fig.
5.80), but also the elbow, shoulder, and hip, dense areas of
bone may be seen ("kissing sequestra"). There is some individual
variation depending on the host resistance, but this is more in terms
of the time taken for the changes to be complete rather than in the
pattern of the disease.
Fig. 5.79 A-F. Tuberculosis of the hip. In some patients the femoral head remains surprisingly intact, while in others it is eventually destroyed. A A cystic lesion in the acetabulum of a young African male: the hip joint is narrowed and irregular. There was also infection in the inferior pubic ramus. B There is destruction of the greater trochanter in this adult African and a cystic lesion in the neck of the femur, spreading into the femoral head. The joint space is not affected. C In this child there is central destruction of the upper end of the left femur, with a periosteal reaction along the shaft. The joint is infected and the femoral head has been dislocated and will never develop properly. D Advanced tuberculosis of the left hip and the left part of the pelvis. The hip joint is fused and there is dense sclerotic bone around the three lytic foci in the left iliac bone. This could be mistaken for a pyogenic infection. E The femoral head has disappeared, the acetabulum is irregular and sclerotic, and there are cystic changes both in the femoral neck and around the joint. The end result will be fusion, and there may be fixed fibrosis already. F The joint has been completely destroyed and dislocated and is surrounded by calcified debris. There will be marked shortening of the right leg and the hip is fixed. (Courtesy of the University of Cape Town Radiology Library).
Tuberculosis of Bones
Osteomyelitis due to the tubercle bacillus is a common condition and need not always involve a joint; in fact it can occur in virtually any bone in the skeleton (Figs. 5.81-5.85). It is most common in childhood but no age is immune; it is frequently multifocal. Scintigraphy is very helpful in identifying the possible multiple sites.
As with pyogenic organisms, the infection most commonly begins in the metaphysis. Its effect on the adjacent joint has already been described. Away from the joint the early changes, localized areas of osteoporosis without any surrounding bone reaction, are often more easily seen than delineated. They have no particular shape, but follow the contour of the bone; in the skull they may be large and apparently spreading. The initial lesion may be seen in the diaphysis, but this is rare. Multiple bones may be infected or the same bone may have foci in different places, not initially connected.
If there is a lesion close to the cortex, expansion is common and cortical thinning occurs. There will be an associated periosteal reaction with a fine lamellar pattern, spreading proximally and distally from the original focus. Ultrasound can identify the edema and the periosteal reaction and be used to guide aspiration biopsy to establish the diagnosis. Both CT and MRI can image the infection, but are unlikely to add much to the accuracy of the diagnosis. This type of reaction is most common in the smaller bones, such as the phalanges (tuberculous dactylitis) and is most frequently seen in children (Figs. 5.86, 5.87). The changes are more marked at this age because the cortex is relatively soft and expansion occurs more easily. The old descriptive term "spina ventosa" (spina=short bone; ventosa=inflated with air) is thus especially appropriate (Fig. 5.86 A).
The radiolucent areas are filled with tuberculous granulation tissue, which causes the expansion. As the cortex expands and thins, subperiosteal new bone is laid down on the outer aspect; this new bone may be layered, quite thick and dense, and sclerotic. Because there is the appearance of an involucrum, the possibility of a pyogenic infection should be considered. The differential diagnosis then depends largely on the patient's clinical condition. In tuberculosis the pain is not marked, pyrexia is minimal, and the whole condition is relatively benign. A pyogenic osteomyelitis causing such a reaction would be acutely painful, swollen, and inflamed, with a generalized systemic reaction which is often absent in the tuberculous variety.
detectable sequestration does not often occur in tuberculosis because
the blood supply has not been affected, but there are exceptions and
tuberculous sequestra do occur without any other associated infection
F). CT may detect very small sequestra when a bone lesion has
spread rapidly into the soft tissues, e. g., in the pelvis.
Fig. 5.80 A-H. Tuberculosis of the knee. A The earliest signs of infection may be a large joint effusion and mild generalized osteoporosis, without any visible bone defect. B, C Another African patient from Zimbabwe. The soft tissue swelling and effusion are marked but there is a lytic bone focus in the lower end of the femur and periosteal elevation around the full diameter of the femoral shaft. There is accentuated growth of both the femoral and tibial epiphyses. The lytic bone focus is important in the differential diagnosis, because nonarticular rheumatoid arthritis and hemophilia can both give similar appearances before there is any bone destruction. D Another patient with a lytic bone focus medially in the lower end of the femur, but also in the femoral epiphysis with a slight sclerotic margin. There is a joint effusion. E A tuberculous infection of the patella with a suprapatellar effusion. F, G The end stages of a tuberculous joint infection. In F there were foci on both sides of the joint; the lateral femoral and tibial condyles had been partially absorbed and destroyed. New bone is present on the lateral aspect of the joint with some fragmentation. There is angulation which may progress. The joint will probably fuse, with either fibrous tissue or bony anyklosis, but in some patients it may remain a lax unstable joint. H A healed but badly damaged joint, with partial destruction of the upper end of the tibia, and a lot of new bone and loose fragments. There is calcified debris in the supra-patellar bursa.
In Europe and North America, the same multifocal lytic lesions can occur, but they are better demarcated and cyst-like. They are most common in the long bones of children and young adults; sometimes they are symmetrical. Probably the difference between the tropical and nontropical pattern is related to immunity or more prompt treatment. The "tropical" pattern will be seen in AIDS anywhere and will often be more destructive and spread more rapidly.
In the skull, scapula, and ribs, as well as the long bones, there may be similar lytic foci without any bone response. In the skull this results in quite large, destructive lesions. Solitary skull foci also occur, sometimes with a reactive edge and a central "button" sequestrum. Because these solitary tuberculous foci are associated with a fluctant "cold" abscess they were named "a puffy tumor" by Sir Percival Pott in the eighteenth century.
In the ribs there may be quite a marked periosteal reaction and localized swelling (Fig. 5.85 E, F). Some care has to be taken to differentiate tuberculous osteomyelitis of a rib from a tuberculous abscess tracking around the intercostal space from its origin in the thoracic spine. Such as abscess will also cause swelling, and there may be some local periosteal reaction on adjacent ribs. Ultrasonography (or CT/MRI) may help to track the abscess more accurately and, like scintigraphy, will locate any intrinsic bone focus. Radiographically, in slender bones such as ribs it may not be easy to see the destructive areas within the bone itself, particularly when the periosteal reaction is marked; an exactly similar process can occur in the long bones. Periosteal new bone is not the "hallmark" of pyogenic infection; it can also be seen in tuberculosis.
In the tropics this type of "cystic" and periosteal tuberculous bone infection (Fig. 5.81) may be relatively slow and benign, or can be progressive, depending on the host resistance and the rapidity with which treatment is commenced. In young children the imaging changes may appear worse than the clinical condition. When tuberculous osteomyelitis occurs in adolescence and adults, it takes longer to heal and may be more significant. In the skull vault the infection usually spreads outwards; only rarely does it involve the meninges, leading to an intracerebral tuberculous abscess (Fig. 5.95).
follows the same slow pattern already described (Fig.
5.88). The bone density returns; the defect may be filled in
with new bone, or may persist for some time. The bone may be sclerotic,
heavily trabeculated, or relatively normal. Some areas may be dense,
resembling sequestra; the dense sclerosis in some bones, especially
in the diaphysis, may mimic a chronic pyogenic (Brodie's) abscess. Healing
is more rapid in the long bones and digits than in the flat bones and
tends to leave less deformity except when the epiphyseal place has been
involved, which commonly results in shortening. Almost all diaphyseal
lesions respond well to therapy.
Fig. 5.81 A-G. Tuberculosis in the lower leg. Many tuberculous foci in the long bones are cystic and are often multiple. There is nearly always periosteal reaction. A Multiple cystic foci in the tibia and lower femur. There is minimal periosteal reaction along the upper half of the tibia laterally. B Multiple similar cysts in the tibia and fibula of another patient, with a periosteal reaction in the fibula particularly. Some of the cystic foci have minimal sclerotic but incomplete borders. C A focus of infection in the center of the tibia with a layered periosteal reaction. D An expansile lesion in the fibula, with the ghost of the original shaft running through it. E Tuberculous foci may appear in more than one limb. In this African there is a periosteal reaction around the shafts of tibiae and the left fibula, with several faint foci of infection. G An African child from Kenya with tuberculous foci in both fibulae, the left tibia, and the lower ends of both femora. He also had similar foci in the right humerus, radius, and ulna. This type of tuberculous bone infection usually responds quite well to appropriate treatment (see Fig. 5.88). (B courtesy of Dr. Harold Jacobson ; A, C, D from Cremin and Jamieson 1995).
Fig. 5.82 A-F Tuberculosis around the ankle joint. A Very early infection. There is synovial thickening and a small effusion, as well as a minimal bone defect in the cortex of the upper surface of the talus posteriorly. B Infection of the lower end of the tibia, with an effusion into the ankle joint. There is marked soft tissue swelling. C A large defect medially and posteriorly in the lower end of the tibia with generalized osteoporosis and a small focus in the fibula. The ankle joint is decreased and a focus of infection is seen in the talus posteriorly. There is marked soft tissue swelling, and a joint effusion. D Collapse and destruction of the os calcis with marked soft tissue swelling and generalized osteoporosis. The infection is in the os calcis, but the whole joint will eventually be destroyed. E Cystic and sclerotic tuberculous infection in the posterior two-thirds of the os calcis, only affecting the cortex in one small area of the upper margin, near the tendo Achillis. F A more localized infection of the os calcis, with a sequestrum and extensive disruption of the upper surface. In D-F the differential diagnosis would include pyogenic and mycotic infections. (Courtesy of the University of Cape Town Radiology Library).
Fig. 5.83 A-D. The swollen ankle of a 7-year-old boy from the Pacific Islands. A There is generalized osteoporosis, but it is difficult to be sure that there is any bone focus. B-D MR scans show the joint effusion, and destruction of both the talus and the posterior part of the tibial epiphysis. The unfortunate child had tuberculous meningitis and miliary tuberculosis.
Fig. 5.84 A-H. Tuberculosis of the shoulder. A Acute tuberculosis with marked osteoporosis of all the bones around the shoulder. There is minimal periosteal elevation along the clavicle, but there is no bony defect. B A more chronic infection with multiple lytic areas in the head of the humerus, the clavicle, and the acromion process. The acromioclavicular joint is disrupted, but the shoulder joint is still relatively intact. C Considerable destruction of the head of the humerus in a child. There is left hilar lymphadenopathy. D Cystic tuberculosis in the right shoulder of a middle-aged African. The glenoid is almost destroyed, and filled with multiple cystic lesions. Next to it, the head of the humerus shows similar defects and there is destruction of the articular surface. The joint space is narrowed. The acromion was also affected. E Erosion of the glenoid and humeral head in a child; F, G two CT scans in the same patient showing the defect in the humeral head and the partial destruction of the glenoid (G). H The late stage of tuberculosis; there is calcified debris all around the joint, with partial destruction of the end of the clavicle. The acromion was also involved. The humeral epiphysis is very decalcified. The calcified masses could be mistaken for tumoral calcinosis, but the destruction of the clavicle and acromion provide evidence of infection. (E-G from Cremin and Jamieson 1995).
Fig. 5.85 A-G. Tuberculosis in the arm, scapula, and chest wall. A A lytic defect in the lower end of the humerus, will ill-defined edges, destruction of the cortex, and a minimal periosteal reaction. A similar but earlier lesion is suspected in the head of the radius. B A well-defined lytic focus in the upper end of the humerus, with a smaller, less clear focus in the middle of the shaft. C Periosteal reaction along the radius and ulna, with disruption of the lower end and widening of the upper end of the ulna and some lytic foci in the lower end of the radius. D Lytic destruction and minimal periosteal reaction in the lower part of the scapula. E, F Tuberculosis of the ribs. In E there is cortical destruction and periosteal reaction, and in F the infection is a little more advanced. There is also a pleural reaction. G A CT scan showing tuberculous infection of the left upper chest wall of a 4-year-old child from the Pacific Islands. He had widespread adenopathy, left upper lobe tuberculous infection, and tuberculous foci in the liver. (A progressive primary infection.) (D-F courtesy of Dr. Harold Jacobson; G courtesy of Dr. Cheryl Sisler, Hawaii).
Fig. 5.86 A-F Tuberculosis of the extremities. Infections of the hands and feet produce similar images. A The hand of an infact showing marked periosteal elevation and multiple lytic areas of bone destruction. There is a periosteal reaction along the ulna also. Lytic defects are present without periosteal reaction in some of the digits. B In this child there is also some epiphyseal damage and less periosteal reaction. The infection was by atypical mycobacteria, but this could not be recognized by looking at the images. C Destructive tuberculous osteomyelitis affecting the fourth left metacarpal. D The hand of an older patient with more advanced tuberculosis; the proximal phalanx of the fifth finger has been almost entirely replaced by granulation tissue and there are also multiple lytic foci in the phalanges of the third and fourth fingers. This is an unusual form of tuberculosis and it could be mistaken for multiple enchondromas or even metastases. E Osteomyelitis of the second right metatarsal and F the fibula of the same patient, a young African girl; her hand is shown in C. Her chest x-ray was normal and there were no other bone foci. (A courtesy of Dr. Harold Jacobson; C, E, F courtesy of the University of Cape Town Radiology Library).
Fig. 5.87 A-E. Tuberculosis of the carpal and tarsal bones in different patients. All show generalized osteoporosis, particularly at the ends of the digits and around the carpal and tarsal joints. No bone foci are visible because the disease is mainly synovial. Bone destruction is likely to occur eventually and fusion will be the end result. A Osteoporosis is well marked. B The wrist of another patient in which bone destruction has started, involving the radius and ulna as well as the metacarpals. The carpus is collapsing. C In this patient the cystic and destructive tuberculous infection could be mistaken for rheumatoid arthritis or even severe gout. D Similar changes in the tarsus: generalized osteoporosis particularly around the joints. There are a few bone foci in the metatarsals. E A more chronic infection at the proximal end of the right first metatarsal and the medial side of the tarsus. The cystic lesions are becoming sclerotic and the joints are fused. There is a periosteal reaction along the shaft of all the metatarsals, but this may be due to the soft tissue reaction rather than local bone infection. This African patient was treated for many months but there was no significant change in his foot. (B courtesy of Dr. Harold Jacobson).
Fig. 5.88 A-D. The healing of tuberculous bone foci. A Cystic changes in the lower end of the femur and the upper end of the tibia, including their epiphyses. Eighteen months following the completion of 6 months of antituberculous treatment, the changes have responded well. They will probably leave only small dense foci. C This young African child had been on treatment for 3 months and the large cystic focus was healing with sclerosis. The periosteal reaction along the medial aspect of the femur has also thickened. Unfortunately, there is considerable disruption of the normal growth pattern of the femoral epiphysis. D A longstanding lesion in the lower end of the femur of another child with a multicystic appearance, periosteal thickening, and widening of the lower end of the femur. In this case the epiphysis is small but otherwise appears normal.
The differential diagnosis of tuberculous bony lesions can be very difficult, particularly if this possible etiology is not considered early. The patient's clinical condition may help to differentiate tuberculosis from acute pyogenic infections, but even this may not ensure accuracy. The mycotic infections, such as North American blastomycosis, can simulate tuberculosis, particularly in their early stages. The multifocal destructive lesions of histoplasmosis duboisii (see Chapter 6) may resemble the aggressive form of tuberculosis.
In the early stage osteoporosis is more marked in tuberculosis compared with pyogenic infections, but tropical (or AIDS) tuberculosis (unlike tuberculosis in Europe or North America) may behave quite acutely and change can be rapid. Sequestration is not common in tuberculosis, but can occur. Spread of infection across an epiphyseal plate is uncommon in pyogenic infections, but is frequent in tuberculosis. Eosinophilic granuloma may mimic tuberculosis (or vice versa) and infections associated with sickle cell disease, such as typhoid osteomyelitis, may closely resemble tuberculosis in their early stages in the bones of the skull vault or in the spine. Later there tends to be more periosteal reaction and the clinical condition is more acute in nontuberculous infections. The frontoparietal lytic lesions of tuberculosis are usually ill defined, compared with the clearly beveled edge of histiocytosis. Syphilis can produce very similar osteolytic lesions.
Particularly in children it is important to differentiate early rheumatoid arthritis, especially the monarticular variety. Cystic lesions could be mistaken for hydatid disease of bone, but this is uncommon in the midshaft of long bones.
The pattern of tuberculosis is the same in the bones of the skull, and may be found in the sphenoid, mastoid, zygoma, as well as the calvarium (Figs. 5.89-5.95). The maxilla and the mandible can also be involved and the differential diagnosis can be extremely difficult.
Tropical tuberculosis affects the skeleton in many ways, and this possible etiology must be remembered when any bone infection, "acute" or "chronic", is being reviewed.
Fig. 5.89 A, B. Tuberculosis is very frequently multifocal, particularly in patients who have a depressed immune system for any reason. Although multifocal infection is seen most commonly in children as part of the progressive primary tuberculosis, it may also appear in adults, even in old age if the infection is reawakened. A This 10-month-old African baby had widespread skeletal tuberculosis. There are cystic lesions with marked periosteal reaction in almost all the long bones. In the right arm, the lower end of the humerus, the upper end of the radius, and the lower half of the ulna are affected. There is dactylitis of the fifth right metacarpal. There were similar lesions in the left arm. B There cystic lesions in both lower limbs, in each femur; the left is more severely affected and shows a greater periosteal reaction. In the lower legs only the right fibula seems to have escaped. Whenever there is multifocal disease, a radioisotope bone study may reveal unexpected foci. The only reason that this child was brought to a hospital was because of swelling of the left lower leg. (Courtesy of the University of Cape Town Radiology Library).
Fig. 5.90 A-C. Tuberculosis in the spine may be the clinical reason why a patient comes to hospital, but there are often foci of infection elsewhere. In this small African child there is destruction of the inner ends of the sixth and seventh ribs and the infection has spread along the seventh right rib (A). The right side of the sixth thoracic vertebra has collapsed, although so far the disc space has remained relatively intact. There is a large right paravertebral abscess and a smaller one on the left. It is probable that the rib became infected from the spinal foci, because there is a periosteal reaction along to the anterior ends of both the sixth and seventh right ribs. This child also had two tuberculous foci in the vault of the skull (B) and destruction of the condyle of the mandible (C).
Fig. 5.91 A, B. A young African from Zimbabwe being treated for pulmonary tuberculosis was found to have a swelling around the jaw. There were no local symptoms. There is destruction of the left side of the mandible with multiple granulomas and very little new bone periosteal reaction.
Fig. 5.92 A-C. This young African child had an overwhelming tuberculous infection and presented (A) with multiple cutaneous lesions covering the whole body. The only bone focus was in the upper end of the left humerus (B), seen on the chest radiograph. There was a large cavity almost replacing the right upper lobe, pneumonia, and multiple tuberculous foci throughout both lungs. Young children with lowered immunity may suffer from hematogenous miliary spread and present with papules, erythematous macules, or purpuric lesions over most of the body. The tuberculin skin test is usually negative and the prognosis is often poor, but this child improved after 2 months of treatment (C). The skin lesions are regressing, and there is a thick periosteal reaction around the upper end of the humerus, seen through the shadow of the shoulder.
Fig. 5.93 A-C. This African patient came to hospital with a complaint of frequency of micturition. An intravenous urogram showed that he had a tuberculous infection of the spine (A) with almost complete destruction of the 12th thoracic vertebra. There was a large left paravertebral abscess, and destruction and subluxation of the 12th left rib. A large lytic defect was present in the right 10th rib. The patient was started on antituberculous therapy but later complained of a pain in his foot where there was a similar destructive lesion in the third metatarsal (B). The urogram had also shown tuberculous swelling of the left side of the bladder (C) and another incidental finding was almost complete destruction of the right lower pubic ramus. Despite all these lesions, the patient's main complaint was still urinary!
Fig. 5.94 A-D. When the infection is tuberculosis, patients may only complain of part of the infection. This teenage African came to hospital with swollen right orbit (A, B) and was found to have a destructive bone infection of the right orbital margin. Standard tomography (B) showed not only the sclerotic thickening, but a sequestrum within a lytic area above the eye. His chest radiograph (C) showed a primary tuberculous infection, with lymphadenopathy and the lateral radiograph (D) showed that he also had a tuberculous sternum.
Fig. 5.95 A-D. Tuberculosis may affect any part of the skull. A, B Two different views of a lytic area in the frontal bone. C Multiple lytic areas across the skull vault. D Similar foci with surrounding bone reaction suggesting healing or a more chronic infection.
Fig. 5.96 A-H. Plain radiography of the skull may show calcification in tuberculomas or basal meninges. A normal skull radiograph does not, of course, exclude tuberculosis. A Multiple calcified tuberculomas with calcification of the meninges, probably also tuberculous. B Multiple calcified tuberculomas in a child. C Calcification of the basal meninges. D Curvilinear calcification in a tuberculoma in the left occipital region. E, F A calcified tuberculoma which was a chance finding in a patient who suffered a head injury. The depressed fracture had to be elevated and the tuberculoma was removed to confirm the histology. G, H Angiography is not usually helpful in making the diagnosis. However, it may indicate the size of the mass, if scanning is not available. A lateral radiograph (G) shows suture diastasis and a calcified mass. Arteriography (H) shows that this is a avascular and indicates that the size of the tuberculoma is much larger than the calcification would suggest. (G, H courtesy of Dr. L. Handler, Cape Town). None of these radiographs would pernut an accurate diagnosis of tuberculoma.
CT and MRI have changed our knowledge of the incidence and significance of tuberculosis of the central nervous system (CNS). It was not possible previously to image satisfactorily the different lesions caused by tuberculosis: plain radiography seldom gives much information or allows an accurate diagnosis (Fig. 5.96), and many foci that cannot be demonstrated with plain radiography are recognized on CT or MRI.
Tuberculomas of the brain probably have a variable geographic distribution, seemingly being more common in India and southern Africa. But this may also reflect the availability of imaging facilities and, particularly with the AIDS epidemic, CNS tuberculosis is likely to become more common. Tuberculosis involves the CNS by hematogenous spread, except in a few cases which result from rupture of cranial osteitis, e.g., from the mastoid or frontal bones. The tubercle bacilli may be seeded anywhere but are most common superficially over cerebral and cerebellar hemispheres and the ventricular system.
Tuberculosis of the central nervous system affects the meninges (which is probably the most important, because it carries a poor prognosis but if treated early may respond) and causes granulomatous masses (tuberculomas) which vary considerably in size and significance. Tuberculous abscesses are probably the result of central necrosis in a tuberculoma. Most tuberculomas respond to treatment, some may resolve spontaneously and the minority calcify. Plain radiography seldom gives much information or allows an accurate diagnosis. CT and MRI are the important imaging methods.
develops and caseates, involving the meninges, the infection can spread
to the subarachnoid space. The most extensive reaction is at the base
of the brain, where a thick exudate develops and surrounds the cranial
nerves, compressing blood vessels and blocking the foramina of the fourth
ventricle. The general inflammatory response also causes raised intracranial
1. Tuberculous meningitis
2. Parenchymal or meningeal mass lesions, tuberculoma
In some patients both varieties develop together, becoming a very complex infection.
meningitis as a presenting illness is most common in children and carries
a significant mortality and complication rate if not treated early.
It is often associated with progressive primary tuberculosis and will
also be seen in immunosuppressed patients. Cranial nerve damage may
occur and ischemic infarction can occur in any part of the brain: these
are the two most common causes of long-term complications. The incidence
of infarction is high, perhaps 40%-60%. As the blood vessels become
involved with the proliferative arachnoiditis, spasm and occlusion may
result in infarction.
Where available, CT and MRI are the most important imaging modalities (Figs. 5.97, 5.98). Following infarction, CT will show ill-defined hypodense areas, which may enhance with contrast. MRI is more accurate and a contrast enhanced T 2-weighted scan can demonstrate a mass effect and hyperintense areas. These may progress to show cavitation. On T 1-weighted scans these areas are well defined and hypointense.
Hydrocephalus develops in most cases of tuberculous meningitis unless treatment is started very promptly (Fig. 5.99). The obstruction is usually in the basal cisterns or the aqueduct. Immediate surgical shunting may be necessary. The end results, even with treatment, may be fibrosis and continued basal obstruction. Healing may be recognized by lack of contrast enhancement on CT but the end stage is difficult to judge. A small number of cases will resolve completely.
Cerebral arteriography during the active phase of meningitis may show vascular irregularity of the larger vessels basally, probably due to arteritis because of the surrounding inflammation. Sometimes complete obstruction of the vessel can be demonstrated. These findings correlate well with the CT images and it is doubtful whether arteriography is indicated during tuberculous meningitis. Occasionally tuberculous meningitis may form plaques or clusters of thickening around major cerebral vessels, demonstrated by CT. These have not been reported commonly from tropical patients, but this may represent infrequency of scanning rather than absence of the pathology.
It is important to note that the incidence of intracranial tuberculomas complicating tuberculous meningitis is 4%-28%: at least one such case has developed during adequate antituberculous treatment. The presence of an intracranial tuberculoma may be indicated by clinical deterioration and may be thought to be due to a resistant organism. When a clinical change occurs, MRI or CT scanning is indicated.
Fig. 5.97. A-E. Three important findings on CT scanning of tuberculous meningitis: A basal leptomeningeal enhancement (small arrows); B, C infarction in the basal ganglia (curved arrow) and hydrocephalus. D, E MRI with gadolinium enhancement in another child showing basal leptomeningeal enhancement, as well as a cavitated infarct deep in the left gray matter (arrow) and hydrocephalus. (From Cremin and Jamieson 1995).
Fig. 5.98 A-D. A 9-year-old girl from the Pacific Islands with tuberculous meningitis. A Contrast-enhanced CT scan shows edema in the right temporal lobe and inflammatory reaction in the basal cisterns and sylvian fissures, with has enhanced. B, C T 1-weighted MR images with contrast show similar enhancement of the basilar cisterns and the sylvian fissures, encasing the middle cerebral arteries. D Another child; a right carotid angiogram shows nearly complete occlusion of the artery as it traverses the meninges. An alternative collateral supply has been derived from the middle meningeal artery (long arrows), the ophthalmic artery (short arrows), and the posterior system (curved arrows). (A-C courtesy of Dr. Cheryl Sisler, Hawaii; D from Cremin and Jamieson 1995).
Any granuloma may develop into a tuberculoma, forming a mass anywhere on or within the meninges. A tuberculoma can be single and nodular, or there may be more than one (Fig. 5.100). Provided they are treated, almost all will resolve without residual imaging abnormality; untreated many will continue to become calcified granulomas (Figs. 5.96, 5.100 A, B). A few, during development, may become tuberculous cerebral abscesses. These have thin walls and are smooth but can be multiloculated. They are indistinguishable from pyogenic abscesses except histologically. Many have surrounding edema which can be demonstrated by CT (hypodense) and T 2-weighted MRI (hyperintense) (Fig. 5.101).
The tuberculoma without central necrosis is hypodense on CT and hyperintense on T 1-weighted MR scans. T 2-weighted scans show hypointensity. On both CT and MRI there is contrast enhancement. If there is central necrosis, this does not enhance and there will be a ring mass (Fig. 5.101 C, D). The central necrosis of tuberculoma may have two origins. The granulation tissue may undergo necrosis or it may result from cellular components which can be caseous or quite liquefied, more like pus. Both types of necrosis may be present in the same abscess and will react differently on CT and MRI. When due to a granuloma, the necrotic area does not enhance, is hyperdense on CT, and is hypointense on T 2-weighted MRI. When liquid, it is hypodense on CT and hyperintense on T 2-weighted MRI (Fig. 5.102).
Some tuberculomas under treatment may resolve in 3 or 4 months, but others may take over a year. Of those which are treated, about 5% probably calcify; this is a surprisingly small figure, because CT and MRI scans undertaken for other reasons have shown granulomas in patients with no previous history or knowledge of a CNS tuberculous infection: natural resistance must result in calcification more often than occurs with therapy.
Cerebral arteriography can demonstrate the mass lesion of a tuberculoma, depending on its size and situation. They are almost all avascular, but a small minority have a ring blush.
The differential diagnosis for tuberculous meningitis in the early stages includes any progenic infection. Tuberculomas can be mistaken for an intracranial neoplasm, or almost any other disease process causing mass lesions in the brain (such as subacute trauma, hemorrhage, pyogenic abscesses, or hydatid disease).
clinical history, the clinical examination, and a high index of suspicion
are very important. Mycotic infections can give rise to identical clinical
and imaging findings (see Chapter on Taeniasis, Cysticerosis).
These are the "puffy tumours" described by Sir Percival Pott. The soft tissue swelling can be quite significant. They can be imaged with ultrasonography, CT, or MRI. It is important to distinguish them from histiocytosis or a low-grade pyogenic infection. These and other tuberculous lesions within the bones of the skull have been described and shown in (Fig. 5.84-5.95).
Fig. 5.99 A-F Ventricular dilatation is common with tuberculous meningitis, but is not always permanent. A A 14-month-old boy from the Pacific Islands with tuberculous meningitis and positive CSF culture for M. tuberculosis; a nonenhanced CT shows ventricular enlargement. B With contrast there is enhancement of the basilar cisterns and sylvian fissures. C A 23-month-old girl, also from the Pacific Islands, was treated successfully for tuberculous meningitis when she was 6 months old. The enhanced CT scan shows persistent ventricular enlargement, but there is no enhancement of the basal cisterns. D The lateral, third and fourth ventricles, also enlarged, showing that there is communicating hydrocephalus. E This is ,the admission CT scan of another child with active tuberculous meningitis, already on treatment. F A repeat scan of the same child 1 month later. Another scan after 3 months did not show any significant change. (E, F from Cremin and Jamieson 1995).
Fig. 5.100 A-F. Tuberculous granulomas. A The lateral radiograph of the skull of a 35-year-old man from the Pacific Islands who had tuberculous meningitis when he was 19 year old. There is a group of calcified granulomas (arrows) which are better seen on the nonenhanced CT (B: arrows). There are more than would be expected from the plain radiograph. C The contrast-enhanced CT scan of another child from South Africa showing that the granuloma has a hypodense center and surrounding edema (arrow). D T 2-weighted MR scan of the same patient shows that the caseous necrotic center is T 2 hyperintense, the rim of the granuloma is hypointense (arrow), and the edema is T 2 hyperintense. E Several granulomas (arrows) are shown on a contrast-enhanced CT of another patient. There is also basal enhancement and hydrocephalus. F A gadolinium-enhanced T 1-weighted MR scan of another patient shows a cluster of granulomas in the left occipital lobe. (A, B courtesy of Dr. Cheryl Sisler, Hawaii; C-F from Cremin and Jamieson 1995).
Fig. 5.101 A-D. Some tuberculomas have been described as "gummatous" and become quite large. A T 2-weighted MR scan of a large tuberculoma. There is hyperintense edema surrounding a predominantly hypointense granuloma. B On a T 1-weighted MR scan, the tuberculoma is isointense. C, D Gadolinium enhanced MR scans of another patient show that the central necrosis is hypointense but there is strong rim enhancement. Both tuberculomas imaged in the same way. (From Cremin and Jamieson 1995).
Fig. 5.102 A-C. Tuberculous abscesses do not image in the same way as tuberculomas. A A contrast-enhanced CT scan shows rim enhancement with a hypodense center. There is also a group of enhancing granulomas posterior to the abscess. B A T 2-weighted MR scan without enhancement shows that the abscess has a hypointense rim and a hyperintense center. C A T 1-weighted MR scan of the same patient, with gadolinium enhancement, shows that the center of the ab scess is hypointense and the wall of the abscess enhances.(From Cremin and Jamieson).
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