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Pulmonary manifestations of tuberculosis in children clinical aspects
72
JOURNAL
OF
PULMONARY
THE
FACULTY
OF
RADIOLOGISTS
MANIFESTATIONS OF TUBERCULOSIS IN CHILDREN* CLINICAL ASPECTS BY A. MARGARET MACPHERSON, M.D., F.R.C.P.
IT is always difficult to give any definite limit to what is meant by the term tuberculosis in childhood. Infection by the tubercle bacillus takes place during childhood in a large number of cases, figures varying between 4 ° per cent and 8o per cent for positive tuberculin reactors at the age of 15 years. In this country the majority of tuberculous primary infections are pulmonary lesions, t \
I
~
_ _ _ _
MALES
..........
FEMALES
14oo t
1200
I
t
t
t
Iooo t.I
~oo
.~
600 \
/~oo 2.00
FI9~oV - ~ - t O - t s - z o - a s - S o - 3 . S - e ~ o "4 $ "~'o - ~ ' s - 6 o - h 5"..o~,e,. 65" Fig. I 1 5 . - - D e a t h s due to all forms of tuberculosis in E n g l a n d and Wales, z 946.
the bacilli being inhaled from infected persons. It is obvious that comparatively few children become ill as a result of primary infection. This statement, however, requires modification since infection taking place at different ages may have different results. Under 5 years of age, primary lesions are significant. This can be seen by comparing the mortality curves and the infectivity rates. The mortality rate at 5 years of age is comparatively high (Fig. ii5) , while the infectivity rate at this age is low compared with the rest of the childhood years, as shown in Fig. I 16. * Being papers given to the Faculty of Radiologists at the Summer Meeting at Sheffield, 1949.
TUBERCULOSIS
IN
CHILDREN
73
It is evident, therefore, that although fewer children are infected in infancy than in later childhood, the infection is serious in a high proportion. Between the ages of 5 and I z years primary lesions are of less serious import. When primary infection takes place over the age of I2 years, it appears that the primary lesion may again cause trouble, giving rise to symptoms and, in some cases, may be followed directly by tuberculous lesions of the adult type. T h e manifest lesions due to primary infection are found in the lungs, lymph-glands, and sometimes in the pleura also. T h e following brief description is typical of the average lesion. T h e pulmonary lesion is small and of little clinical significance. It may or may not be detected in the X-ray film ; frequently it is not visible until calcification has taken place. The position of the primary lung lesion varies. According to most observers, it is most frequently found in the right upper lobe and least often in the right middle lobe. Its occurrence in other lobes is variously estimated according to different authors. The lymph-gland lesion is nearly always more obvious than the pulmonary lesion, and
IO0 90
gO
¢ h
,¢; ~3
.,
. .
., :.~ ~ . , .~_,/ '.~ _
: 30 ~ 2d r~-r
I
=
~70 Y~.
C/RL~. ANDG/~I.,5
•
0
AdEO
. . . . .
80~
s
"l 5 ; ~ ~
9.,o,,,,,o,,,~
Fig. I 1 6 . - - T h e percentage of children attending the Out-Patients D e p a r t m e n t , Brompton, in I93 I, w h o reacted to the M a n t o u x Test.
this is specially so in younger children. These glands are frequently visible in the X-ray film but, in the typical case, are not accompanied by clinical manifestations. It is not often possible to know the exact time at which infection takes place, but it may be possible to estimate, by means of the change in tuberculin reaction, within a few weeks the time of infection, and in some of these cases it has been shown that there is a definite ' latent ' period between primary infection and the appearance of X-ray evidence of glandular enlargement, a period varying in length, no doubt, but sometimes extending into weeks. It follows that one negative film is not sufficient to exclude evidence of a primary lesion, and a further radiograph taken two or three months later may then show enlarged hilar glands. T h e lymph-glands involved may belong to more than one g r o u p ; the glands draining the area in which the primary lesion is situated are always affected and, more distally, other tracheobronchial or paratracheal glands are involved, and in some cases the glands on the opposite side are also infected. Although primary lesions are usually situated in the subpleural region or the lung, associated pleural effusion does not commonly occur in children. The pleural lesion is more often a localized pleural thickening, in some cases with localized effusion which may be interlobar.
74
JOURNAL
OF
THE
FACULTY
OF
RADIOLOGISTS
It is obvious from the above description that the occurrence of primary infection in children provides, as a rule, little clinical interest. It is the gross infection, or the complications resulting from primary lesions, which gives rise to definite illness and clinical signs.
SEVERE PRIMARY LESIONS AND COMPLICATIONS FOLLOWING PRIMARY LESIONS In some children the pulmonary lesion may be of clinical significance. There are three main causes for this being so. In the first place, the infection may be a gross one or may be a heavy infection frequently repeated. Secondly, the age at which infection takes place may modify the reaction to primary tuberculous infection. As already stressed, primary infection in infancy is not well tolerated, and in adolescence it may also lead to further tuberculous pulmonary lesions. Thirdly, the natural resistance to infection may be unusually low as a result of malnutrition, or other infections, such as measles ; or resistance may be decreased in certain races or families. If any of these conditions are present, the pulmonary lesion usually does not remain small, localized, and encapsuled, but instead there may be large areas of tuberculous bronchopneumonia. The clinical picture produced by this condition is varied. At the one extreme there is an acutely ill infant with physical signs of bronchopneumonia and a high swinging temperature, the condition at first being indistinguishable from a non-tuberculous bronchopneumonia. T h e following points may help to differentiate the condition : a history of contact with tuberculosis and a positive reaction to a tuberculin test in an infant suggests strongly a possible tuberculous aetiology ; lack of response to sulphonamides and to penicillin; rapidly developing emaciation, and, when obtainable, acidfast bacilli in stomach-washings or sputum clinch the diagnosis. At the other extreme is the child with local physical signs o]~ pneumonia and X-ray evidence of gross pulmonary disease, but with few toxic symptoms. T h e temperature chart of these children shows a slight evening rise, with bouts of higher temperatures lasting perhaps two to three days and occurring at irregular intervals. The child is not wasted but does not gain weight normally. Clinical and X-ray findings change very little over a period of months, then slowly regress, and usually clear completely, leaving no clinical evidence and in the X-ray films either no evidence or calcified lesions only. The lesion appears to heal completely and the child's condition returns to normal. Pleural Lesions.--Large effusions are not c o m m o n ; they may he transient, lasting as short a time as a week and clearing completely. As a rule the child is not acutely ill but has slight symptoms, such as general malaise or some pain in the chest. Pyrexia is variable and there are the usual signs of an effusion. The differential diagnosis between tuberculous and non-tuberculous effusions m a y not be easy or possible until the effusion clears and a primary complex becomes visible in the X-ray film. Lymph-gland Lesions are the commonest cause of clinical manifestations. Associated with a small pulmonary lesion may be large caseating glands around the hilum of the lung or in the paratracheal regions. These cannot be detected by physical signs, but certain general symptoms and signs are often significant. As with children who develop a subacute tuberculous bronchopneumonia, there is general malaise and unsatisfactory weight report. The temperature chart is also similar (Fig. Ii7). Diagnosis of the condition is 0nly possible by means of radiographs, when the large gland masses are seen. It must be remembered that when the affected glands are in the region of the carina or paratracheal, or if there is a slight asymmetry of position when the picture is taken, the glands may not be obvious in the postero-anterior films. These large glands not infrequently give rise to secondary lesions, the most important of which are occlusion of the lumen of a bronchus, bronchopneumonia, and h a~matogenous spread. A bronchus may become blocked as a result of pressure of the gland on the wall or following ulceration of the gland through the bronchial wall. If the occlusion is complete or almost complete, collapse
TUBERCULOSIS
IN
CHILDREN
75
of the lung beyond takes place. If a small bronchus is involved there will be no symptoms or abnormal signs. On the other hand, blocking of a main bronchus may give rise to symptoms such as spasmodic cough, wheezing, or breathlessness. On examining the child, rhonchi and a characteristic whistling respiration may be heard and sometimes there are signs of consolidation, but often these are masked by the emphysematous condition of the other lobes of the lung. It appears that a large number of these collapsed lobes re-expand and cause no further trouble. Some, however, remain collapsed and give rise to permanent atelectatis or to bronchiectasis, conditions which may declare themselves at once or which may not cause any trouble until many years later. Erosion of a gland into a bronchus may cause a segmental bronchopneumonia. This does not occur frequently, the eroding gland more often blocking the bronchus than spreading infection distally. The bronchopneumonia so produced is clinically similar to that produced by the spreading pulmonary lesion. H~ematogenous spread may take place from a tuberculous gland by erosion into a blood-vessel or through the large lymph-ducts and so into the blood-stream. ~ONTH
~-~L~f
DAY / 6
17! /6 19 2 0 21 3.3, ~
.F,d i ~P:':'
-3
Io~
:
:
:
:
: I : I:
I:
I:I
:
t
3.
:
:
:
:
ii;i;ii
: l :1 :I:
l;l
:
:
:
:I
:l
: I :I:I
:
i
! I:
i x7.--Temperature
I:1:1:
I :l:l:l:l:l:l chart
of
child
,4
~I
"'~'::
ii:
:
:
:I
:
:
:
i ii
:
:1 : I ~ I :
!
';i ~ /.. ,F',.:;',y "T ;( ! " / ' ~ !
3
: .............
1. !~ ~t,l!filil[litili.lil~lil]|]li:.l:]
)= ~ Fig.
"
...............
ili i i i : i
(~a ll~J : I
_~,_~
:
2/~ ~5" 3 6 3 7 ;IS 3.9 3 0
!
'
!
~2; /. "[ ~!] V '~)~] ': I :l:l:l;l:l:l:l
with
tuberculous
hilar
adenitis.
Pulmonary lesions may also produce blood-stream infection. This invasion of the blood-stream is probably more common than is usually supposed and stresses the fact that tuberculosis in childhood must always be considered as a general disease and not one localized to the pulmonary system alone. A heavy infection may produce acute generalized miliary tuberculosis and meningitis, with their serious and often fatal implications. Lesser infections will produce subacute miliary lesions. In the lung these may be seen in a child with little constitutional disturbance and may be difficult to differentiate from the very similar picture produced by lymphatic congestion associated with gross hilar adenitis. The subacute miliary lesions slowly regress and disappear from the picture. We still have no definite answer to the question--do they later become active and give rise to adult tuberculosis ? Miliary lesions develop on other parts of the body and may later, or at the time, cause lesions in bones or kidneys, etc. While the child is in bed having treatment for the more obvious thoracic lesions, lesions in the bones may be quite unobtrusive and may only be found accidentally or may not be found until the child begins to get up and be more active. As an example of this, there was a small child of a little over one year old who had had repeated radiographs of its lungs to show the primary complex, over a period of months ; and then by chance the X-ray picture included the right humerus, which showed a well-established tuberculous lesion which had not been suspected. Another child of 9 years, being treated in a sanatorium for gross primary lung lesion, quietly developed spinal caries, which was not apparent until a paravertebral shadow of a cold abscess was evident in the lung films.
76
JOURNAL
OF
THE
FACUI,TY
OF
RADIOLOGISTS
What can and should be done for primary lesions ? The first decision to make is whether they need treatment or not. Most children with uncomplicated primary lesions require no treatment. On the other hand, those with large caseating areas in lungs or glands must be given treatment
Fig. IX8.--July 3, 1937.
Fig. I I 9 . - - D e c . 18, I937. Increasing collapse, rightmiddlelobe.
Early primary lesion.
over a long period. T h e y should be rested in bed with as much fresh air and indirect sunlight as possible and given cod-liver oil or other forms of vitamins A and D and plenty of milk. This r~gime may have to be continued for six months or more, depending on the X-ray picture showing
Fig. I ~ o . - - M a r c h 5, I938.
Postero-anterior view. s y m p t o m s at this date.
First
Fig. I 2 I . - - M a r c h 5, 1938.
Lateral view.
definite evidence of healing. Calciferol is of doubtful value. Streptomycin has little effect on the caseating masses and should not be given at this stage because of the danger of the development of a resistant strain of tubercle bacilli which would make treatment of meningitis, should it
TUBERCULOSIS
IN
CHILDREN
77
develop subsequently, ineffective. When pulmonary collapse is present, time should be allowed for spontaneous re-expansion, which occurs in most cases within a year, before further measures such as bronchoscopy are considered. In many cases, when done in the active primary stage, bronchoscopy has little permanent effect, which is not surprising when one remembers that the bronchial lesion is produced by large active tuberculous lesions in the glands outside the bronchi which may reproduce pulmonary collapse after temporary clearing of the bronchus. In some cases bronchoscopy is followed by a spread of tuberculous lesions. Subacute miliary pulmonary tuberculosis should be treated with streptomycin, great care being taken in the first place that the diagnosis is correct and that the :case is one of true miliary lesion and not of lymphatic congestion. The outlook for acute miliary tuberculosis and meningitis
Fig. Iz2.--April I, I938.
Bronchogram showing blocking of middle-lobe bronchus.
Fig. IZ2.--Aug. I7, I939.
Bronchogram.
h'as been entirely altered with the introduction of streptomycin, the inevitably fatal prognosis being altered to a more hopeful one with a proportion of complete recoveries. The following case will illustrate many of the points I have tried to make. This child of two years, attending the Contact Clinic at the Brompton Hospital, was known, from previous tuberculin tests, to have become infected within three months of the taking of a film (Fig. i 18). At this time the child had a strongly positive reaction to a Mantoux test with O.T. i-iooo, and his mother, who had been a quiescent case, had recently had an exacerbation of symptoms. The radiographs showed an enlarged hilar shadow on the right and collapse of the right middle lobe. The child had no symptoms. Five months later the child was still free from symptoms and the radiograph showed more definite collapse (Fig. 119). Three months later, with little change in the radiograph (Figs. i2o, i2i), the child had developed a spasmodic cough, the first symptom. A bronchogram taken at this time demonstrated blocking of the middle-lobe bronchus (Fig. I22). During the next year, re-expansion took place. Fig. 123 shows a bronchogram taken two years after the original radiograph. Calcification was beginning to show itself at this stage, and in subsequent pictures taken during the next two years there was an increasing amount of calcification, Fig. 124, taken eleven years after the primary infection, shows
78
JOURNAL
OF
THE
FACULTY
OF
RADIOLOGISTS
the final result of the lesion, with a calcified primary lesion in the lower lobe and calcified glands in the right hilum, and re-expansion of the right middle lobe. This story of a primary lesion in X-ray pictures sums up most of the important factors in this condition ; the importance of a history of contact with an active tuberculous case and the effect of this on a young child ; the comparative insignificance in the X-ray picture of the pulmonary lesion compared with the lesions of the hilar glands; the secondary effect of this enlargement
Fig. I24.--Oct. 25, I948.
Calcified primary complex.
causing collapse of the lung ; the minimal clinical manifestations compared with the X-ray evidence and the delay of eight months in development of symptoms ; the re-expansion of the collapsed lobe and the final apparent healing of the Primary lesion. Perhaps most important of all, this case illustrates the slow rate at which these lesions alter; in this case changes in the X-ray pictures were taking place for at least five years before the picture of a ' h e a l e d ' focus became constant.
JOURNAL
OF
PULMONARY
THE
FACULTY
OF
RADIOLOGISTS
MANIFESTATIONS OF TUBERCULOSIS IN CHILDREN* CLINICAL ASPECTS BY A. MARGARET MACPHERSON, M.D., F.R.C.P.
IT is always difficult to give any definite limit to what is meant by the term tuberculosis in childhood. Infection by the tubercle bacillus takes place during childhood in a large number of cases, figures varying between 4 ° per cent and 8o per cent for positive tuberculin reactors at the age of 15 years. In this country the majority of tuberculous primary infections are pulmonary lesions, t \
I
~
_ _ _ _
MALES
..........
FEMALES
14oo t
1200
I
t
t
t
Iooo t.I
~oo
.~
600 \
/~oo 2.00
FI9~oV - ~ - t O - t s - z o - a s - S o - 3 . S - e ~ o "4 $ "~'o - ~ ' s - 6 o - h 5"..o~,e,. 65" Fig. I 1 5 . - - D e a t h s due to all forms of tuberculosis in E n g l a n d and Wales, z 946.
the bacilli being inhaled from infected persons. It is obvious that comparatively few children become ill as a result of primary infection. This statement, however, requires modification since infection taking place at different ages may have different results. Under 5 years of age, primary lesions are significant. This can be seen by comparing the mortality curves and the infectivity rates. The mortality rate at 5 years of age is comparatively high (Fig. ii5) , while the infectivity rate at this age is low compared with the rest of the childhood years, as shown in Fig. I 16. * Being papers given to the Faculty of Radiologists at the Summer Meeting at Sheffield, 1949.
TUBERCULOSIS
IN
CHILDREN
73
It is evident, therefore, that although fewer children are infected in infancy than in later childhood, the infection is serious in a high proportion. Between the ages of 5 and I z years primary lesions are of less serious import. When primary infection takes place over the age of I2 years, it appears that the primary lesion may again cause trouble, giving rise to symptoms and, in some cases, may be followed directly by tuberculous lesions of the adult type. T h e manifest lesions due to primary infection are found in the lungs, lymph-glands, and sometimes in the pleura also. T h e following brief description is typical of the average lesion. T h e pulmonary lesion is small and of little clinical significance. It may or may not be detected in the X-ray film ; frequently it is not visible until calcification has taken place. The position of the primary lung lesion varies. According to most observers, it is most frequently found in the right upper lobe and least often in the right middle lobe. Its occurrence in other lobes is variously estimated according to different authors. The lymph-gland lesion is nearly always more obvious than the pulmonary lesion, and
IO0 90
gO
¢ h
,¢; ~3
.,
. .
., :.~ ~ . , .~_,/ '.~ _
: 30 ~ 2d r~-r
I
=
~70 Y~.
C/RL~. ANDG/~I.,5
•
0
AdEO
. . . . .
80~
s
"l 5 ; ~ ~
9.,o,,,,,o,,,~
Fig. I 1 6 . - - T h e percentage of children attending the Out-Patients D e p a r t m e n t , Brompton, in I93 I, w h o reacted to the M a n t o u x Test.
this is specially so in younger children. These glands are frequently visible in the X-ray film but, in the typical case, are not accompanied by clinical manifestations. It is not often possible to know the exact time at which infection takes place, but it may be possible to estimate, by means of the change in tuberculin reaction, within a few weeks the time of infection, and in some of these cases it has been shown that there is a definite ' latent ' period between primary infection and the appearance of X-ray evidence of glandular enlargement, a period varying in length, no doubt, but sometimes extending into weeks. It follows that one negative film is not sufficient to exclude evidence of a primary lesion, and a further radiograph taken two or three months later may then show enlarged hilar glands. T h e lymph-glands involved may belong to more than one g r o u p ; the glands draining the area in which the primary lesion is situated are always affected and, more distally, other tracheobronchial or paratracheal glands are involved, and in some cases the glands on the opposite side are also infected. Although primary lesions are usually situated in the subpleural region or the lung, associated pleural effusion does not commonly occur in children. The pleural lesion is more often a localized pleural thickening, in some cases with localized effusion which may be interlobar.
74
JOURNAL
OF
THE
FACULTY
OF
RADIOLOGISTS
It is obvious from the above description that the occurrence of primary infection in children provides, as a rule, little clinical interest. It is the gross infection, or the complications resulting from primary lesions, which gives rise to definite illness and clinical signs.
SEVERE PRIMARY LESIONS AND COMPLICATIONS FOLLOWING PRIMARY LESIONS In some children the pulmonary lesion may be of clinical significance. There are three main causes for this being so. In the first place, the infection may be a gross one or may be a heavy infection frequently repeated. Secondly, the age at which infection takes place may modify the reaction to primary tuberculous infection. As already stressed, primary infection in infancy is not well tolerated, and in adolescence it may also lead to further tuberculous pulmonary lesions. Thirdly, the natural resistance to infection may be unusually low as a result of malnutrition, or other infections, such as measles ; or resistance may be decreased in certain races or families. If any of these conditions are present, the pulmonary lesion usually does not remain small, localized, and encapsuled, but instead there may be large areas of tuberculous bronchopneumonia. The clinical picture produced by this condition is varied. At the one extreme there is an acutely ill infant with physical signs of bronchopneumonia and a high swinging temperature, the condition at first being indistinguishable from a non-tuberculous bronchopneumonia. T h e following points may help to differentiate the condition : a history of contact with tuberculosis and a positive reaction to a tuberculin test in an infant suggests strongly a possible tuberculous aetiology ; lack of response to sulphonamides and to penicillin; rapidly developing emaciation, and, when obtainable, acidfast bacilli in stomach-washings or sputum clinch the diagnosis. At the other extreme is the child with local physical signs o]~ pneumonia and X-ray evidence of gross pulmonary disease, but with few toxic symptoms. T h e temperature chart of these children shows a slight evening rise, with bouts of higher temperatures lasting perhaps two to three days and occurring at irregular intervals. The child is not wasted but does not gain weight normally. Clinical and X-ray findings change very little over a period of months, then slowly regress, and usually clear completely, leaving no clinical evidence and in the X-ray films either no evidence or calcified lesions only. The lesion appears to heal completely and the child's condition returns to normal. Pleural Lesions.--Large effusions are not c o m m o n ; they may he transient, lasting as short a time as a week and clearing completely. As a rule the child is not acutely ill but has slight symptoms, such as general malaise or some pain in the chest. Pyrexia is variable and there are the usual signs of an effusion. The differential diagnosis between tuberculous and non-tuberculous effusions m a y not be easy or possible until the effusion clears and a primary complex becomes visible in the X-ray film. Lymph-gland Lesions are the commonest cause of clinical manifestations. Associated with a small pulmonary lesion may be large caseating glands around the hilum of the lung or in the paratracheal regions. These cannot be detected by physical signs, but certain general symptoms and signs are often significant. As with children who develop a subacute tuberculous bronchopneumonia, there is general malaise and unsatisfactory weight report. The temperature chart is also similar (Fig. Ii7). Diagnosis of the condition is 0nly possible by means of radiographs, when the large gland masses are seen. It must be remembered that when the affected glands are in the region of the carina or paratracheal, or if there is a slight asymmetry of position when the picture is taken, the glands may not be obvious in the postero-anterior films. These large glands not infrequently give rise to secondary lesions, the most important of which are occlusion of the lumen of a bronchus, bronchopneumonia, and h a~matogenous spread. A bronchus may become blocked as a result of pressure of the gland on the wall or following ulceration of the gland through the bronchial wall. If the occlusion is complete or almost complete, collapse
TUBERCULOSIS
IN
CHILDREN
75
of the lung beyond takes place. If a small bronchus is involved there will be no symptoms or abnormal signs. On the other hand, blocking of a main bronchus may give rise to symptoms such as spasmodic cough, wheezing, or breathlessness. On examining the child, rhonchi and a characteristic whistling respiration may be heard and sometimes there are signs of consolidation, but often these are masked by the emphysematous condition of the other lobes of the lung. It appears that a large number of these collapsed lobes re-expand and cause no further trouble. Some, however, remain collapsed and give rise to permanent atelectatis or to bronchiectasis, conditions which may declare themselves at once or which may not cause any trouble until many years later. Erosion of a gland into a bronchus may cause a segmental bronchopneumonia. This does not occur frequently, the eroding gland more often blocking the bronchus than spreading infection distally. The bronchopneumonia so produced is clinically similar to that produced by the spreading pulmonary lesion. H~ematogenous spread may take place from a tuberculous gland by erosion into a blood-vessel or through the large lymph-ducts and so into the blood-stream. ~ONTH
~-~L~f
DAY / 6
17! /6 19 2 0 21 3.3, ~
.F,d i ~P:':'
-3
Io~
:
:
:
:
: I : I:
I:
I:I
:
t
3.
:
:
:
:
ii;i;ii
: l :1 :I:
l;l
:
:
:
:I
:l
: I :I:I
:
i
! I:
i x7.--Temperature
I:1:1:
I :l:l:l:l:l:l chart
of
child
,4
~I
"'~'::
ii:
:
:
:I
:
:
:
i ii
:
:1 : I ~ I :
!
';i ~ /.. ,F',.:;',y "T ;( ! " / ' ~ !
3
: .............
1. !~ ~t,l!filil[litili.lil~lil]|]li:.l:]
)= ~ Fig.
"
...............
ili i i i : i
(~a ll~J : I
_~,_~
:
2/~ ~5" 3 6 3 7 ;IS 3.9 3 0
!
'
!
~2; /. "[ ~!] V '~)~] ': I :l:l:l;l:l:l:l
with
tuberculous
hilar
adenitis.
Pulmonary lesions may also produce blood-stream infection. This invasion of the blood-stream is probably more common than is usually supposed and stresses the fact that tuberculosis in childhood must always be considered as a general disease and not one localized to the pulmonary system alone. A heavy infection may produce acute generalized miliary tuberculosis and meningitis, with their serious and often fatal implications. Lesser infections will produce subacute miliary lesions. In the lung these may be seen in a child with little constitutional disturbance and may be difficult to differentiate from the very similar picture produced by lymphatic congestion associated with gross hilar adenitis. The subacute miliary lesions slowly regress and disappear from the picture. We still have no definite answer to the question--do they later become active and give rise to adult tuberculosis ? Miliary lesions develop on other parts of the body and may later, or at the time, cause lesions in bones or kidneys, etc. While the child is in bed having treatment for the more obvious thoracic lesions, lesions in the bones may be quite unobtrusive and may only be found accidentally or may not be found until the child begins to get up and be more active. As an example of this, there was a small child of a little over one year old who had had repeated radiographs of its lungs to show the primary complex, over a period of months ; and then by chance the X-ray picture included the right humerus, which showed a well-established tuberculous lesion which had not been suspected. Another child of 9 years, being treated in a sanatorium for gross primary lung lesion, quietly developed spinal caries, which was not apparent until a paravertebral shadow of a cold abscess was evident in the lung films.
76
JOURNAL
OF
THE
FACUI,TY
OF
RADIOLOGISTS
What can and should be done for primary lesions ? The first decision to make is whether they need treatment or not. Most children with uncomplicated primary lesions require no treatment. On the other hand, those with large caseating areas in lungs or glands must be given treatment
Fig. IX8.--July 3, 1937.
Fig. I I 9 . - - D e c . 18, I937. Increasing collapse, rightmiddlelobe.
Early primary lesion.
over a long period. T h e y should be rested in bed with as much fresh air and indirect sunlight as possible and given cod-liver oil or other forms of vitamins A and D and plenty of milk. This r~gime may have to be continued for six months or more, depending on the X-ray picture showing
Fig. I ~ o . - - M a r c h 5, I938.
Postero-anterior view. s y m p t o m s at this date.
First
Fig. I 2 I . - - M a r c h 5, 1938.
Lateral view.
definite evidence of healing. Calciferol is of doubtful value. Streptomycin has little effect on the caseating masses and should not be given at this stage because of the danger of the development of a resistant strain of tubercle bacilli which would make treatment of meningitis, should it
TUBERCULOSIS
IN
CHILDREN
77
develop subsequently, ineffective. When pulmonary collapse is present, time should be allowed for spontaneous re-expansion, which occurs in most cases within a year, before further measures such as bronchoscopy are considered. In many cases, when done in the active primary stage, bronchoscopy has little permanent effect, which is not surprising when one remembers that the bronchial lesion is produced by large active tuberculous lesions in the glands outside the bronchi which may reproduce pulmonary collapse after temporary clearing of the bronchus. In some cases bronchoscopy is followed by a spread of tuberculous lesions. Subacute miliary pulmonary tuberculosis should be treated with streptomycin, great care being taken in the first place that the diagnosis is correct and that the :case is one of true miliary lesion and not of lymphatic congestion. The outlook for acute miliary tuberculosis and meningitis
Fig. Iz2.--April I, I938.
Bronchogram showing blocking of middle-lobe bronchus.
Fig. IZ2.--Aug. I7, I939.
Bronchogram.
h'as been entirely altered with the introduction of streptomycin, the inevitably fatal prognosis being altered to a more hopeful one with a proportion of complete recoveries. The following case will illustrate many of the points I have tried to make. This child of two years, attending the Contact Clinic at the Brompton Hospital, was known, from previous tuberculin tests, to have become infected within three months of the taking of a film (Fig. i 18). At this time the child had a strongly positive reaction to a Mantoux test with O.T. i-iooo, and his mother, who had been a quiescent case, had recently had an exacerbation of symptoms. The radiographs showed an enlarged hilar shadow on the right and collapse of the right middle lobe. The child had no symptoms. Five months later the child was still free from symptoms and the radiograph showed more definite collapse (Fig. 119). Three months later, with little change in the radiograph (Figs. i2o, i2i), the child had developed a spasmodic cough, the first symptom. A bronchogram taken at this time demonstrated blocking of the middle-lobe bronchus (Fig. I22). During the next year, re-expansion took place. Fig. 123 shows a bronchogram taken two years after the original radiograph. Calcification was beginning to show itself at this stage, and in subsequent pictures taken during the next two years there was an increasing amount of calcification, Fig. 124, taken eleven years after the primary infection, shows
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the final result of the lesion, with a calcified primary lesion in the lower lobe and calcified glands in the right hilum, and re-expansion of the right middle lobe. This story of a primary lesion in X-ray pictures sums up most of the important factors in this condition ; the importance of a history of contact with an active tuberculous case and the effect of this on a young child ; the comparative insignificance in the X-ray picture of the pulmonary lesion compared with the lesions of the hilar glands; the secondary effect of this enlargement
Fig. I24.--Oct. 25, I948.
Calcified primary complex.
causing collapse of the lung ; the minimal clinical manifestations compared with the X-ray evidence and the delay of eight months in development of symptoms ; the re-expansion of the collapsed lobe and the final apparent healing of the Primary lesion. Perhaps most important of all, this case illustrates the slow rate at which these lesions alter; in this case changes in the X-ray pictures were taking place for at least five years before the picture of a ' h e a l e d ' focus became constant.