TB in the ED
Radiology Cases in Pediatric Emergency Medicine
Volume 4, Case 6
Craig T. Nakamura, MD
Kapiolani Medical Center For Women And Children
University of Hawaii John A. Burns School of Medicine
     This is a three-year old Korean male who presents 
to the emergency department with respiratory distress.  
Ten days ago, he had developed a cough, rhinorrhea, 
sore throat, and temperature of 39.4 degrees.  The 
cough, rhinorrhea, and sore throat resolved after a 
three day period.  However, he continued to spike 
fevers.  Three days ago, he was seen by his primary 
care physician.  A PPD was placed.  He was then 
started on oral cefuroxime.  He was previously exposed 
to a grandaunt who was treated for tuberculosis in 
Korea and a grandfather with a chronic cough within the 
household.  He has had a decreased oral intake and a 
two kilogram weight loss over the previous two weeks.
     Exam:  VS T39.2, P148, RR68, BP 104/69.  Oxygen 
saturation 90% in room air (100% on 5 liters O2 by 
nasal cannula).  He is alert with moderate respiratory 
distress.  HEENT Normal.  No lymphadenopathy.  Neck 
supple.  Heart regular without murmurs.  Moderately 
severe chest retractions noted.  Breath sounds are 
decreased on the right.  There is good aeration over the 
left lung fields.  No wheezing, rhonchi, or rales are 
heard.  There is dullness to percussion over the right 
base.  Abdomen soft, flat, bowel sounds active, without 
tenderness.  Extremities significant for a positive PPD.  
Capillary refill < 2 seconds.
     Laboratory studies:  CBC  WBC 9.2 with 41% 
lymphs, 43% segs, 14% monos, 1% eos, 1% basos.  
Hgb. 12.6, hct. 37.2.  Chemistry panel is normal.
     A chest radiograph is obtained.

View chest radiograph.

     If you can see vertical lines on the image 
(resembling stripes), these are due to an artifact of the 
radiographic "grid" used on the film.  This grid is very 
fine and only visible on very close inspection.  
Unfortunately, the scanning process enhances the 
visibility of this grid.  Ignore this artifact.

     A PA view is shown here.  His chest radiograph 
demonstrates a complete opacification of the right 
hemithorax with a shift of the mediastinal structures to 
the left.
     This patient presents with primary tuberculosis (TB) 
and a pleural effusion.  There are two types of 
pulmonary TB:  primary and postprimary.  In primary 
TB, the typical route of infection occurs by the 
inhalation of aerosolized (two to five micron) droplets 
laden with Mycobacterium tuberculosis from the cough 
of a person with active disease.  The mycobacteria 
usually deposit in the middle or lower lobes, where they 
undergo phagocytosis and multiply intracellularly.  As 
neutrophils arrive, tubercles are formed and the 
phagocytized tubercles are carried to regional lymph 
nodes.  During this stage, there are both lymphatic and 
hematogenous dissemination, as the primary focus of 
infection becomes encapsulated and eventually 
calcifies.  Hypersensitivity develops over a period of two 
to ten weeks.  In the majority of cases, surviving 
mycobacteria remain dormant.
     Postprimary TB involves the reactivation of dormant 
bacilli which occurs with episodes of 
immunosuppression, malnutrition, or debilitation, 
typically within two years following exposure.  It occurs 
in 5% to 15% of cases of TB.  Primary and postprimary 
TB differ clinically, pathologically, and radiologically.
     There are five distinct radiographic presentations of 
primary TB:
     1.  Parenchymal disease
     2.  Atelectasis
     3.  Lymphadenopathy
     4.  Pleural effusion
     5.  Miliary disease

     Parenchymal disease is seen as a unifocal 
consolidation, typically involving the right lung (there are 
conflicting reports as to the preference of which regions 
are affected within the lung).  The infiltrate is multilobar 
in approximately 25% of the cases.  These infiltrates 
are usually homogeneous with ill-defined borders.  
Lamont further subdivided the consolidations into six 
types:  linear interstitial, segmental or lobar 
consolidation, confluent, collapse, emphysema, and 
cavitation.  The most common consolidation type is 
linear interstitial.  Air bronchograms or associated 
lymphadenopathy may be present.  The infiltrates clear 
in about two-thirds of all cases.  After an initial 
paradoxical worsening of the consolidation, resolution 
occurs over a period of six months to two years.  In 
15% of the cases, a calcified scar may persist (the 
Ghon focus).  For evaluation of treatment efficacy, the 
parenchymal infiltrates should be followed every two to 
three months until stable or cleared.
     Lobar or segmental atelectasis occurs most 
frequently in children under two years of age.  The 
atelectasis is caused by either endobronchial disease 
or external bronchial compression due to hilar 
adenopathy.  It usually involves the anterior segment of 
the upper lobe or the medial segment of the middle 
lobe and will persist until the node or endobronchial 
lesion regresses.
     Hilar and mediastinal adenopathy can be seen in 
about 96% of children with primary TB, and is 
considered the radiological hallmark.  The most 
frequently involved nodes are the hilar and right 
paratracheal.  The involvement is usually unilateral and 
right-sided (bilateral in 25% to 30% of cases).  Often 
there is an associated parenchymal infiltrate or region 
of atelectasis.  The lateral chest radiograph is 
particularly beneficial in the evaluation of adenopathy 
and should be included in the investigation of children 
suspected of having TB or those in contact with adults 
with TB.  The adenopathy with primary TB usually 
resolves without sequelae, although nodal calcification 
may occur.  A nodal calcification associated with a 
Ghon focus is known as a Ranke complex.  The 
adenopathy should be monitored on an annual basis 
until stable or resolved.
     Pleural effusion, uncommon in infants and young 
children, can be seen in adolescents and adults.  It is 
usually unilateral and occurs in 6% to 12% of primary 
TB infections.  The effusion may mask underlying 
parenchymal disease.  However, with appropriate 
therapy, resolution is often rapid and without sequelae.
     During the hematogenous stage of primary TB, 
between 1% and 7% of patients will have radiographic 
evidence of miliary disease.  Children under two years 
of age are most commonly affected, usually within six 
months of infection.  When symptoms begin, the chest 
radiograph is typically normal.  Hyperinflation may occur 
during the first two weeks.  This can be followed by 
diffuse, small nodular opacities about six weeks after 
the onset of symptoms.  Left untreated, the nodules 
may enlarge to about five millimeters or may coalesce 
and cavitate.  With proper therapy, the nodules resolve 
within two to six months.  Miliary calcification is 

View miliary TB example.

     These PA and lateral chest radiograph views are 
taken in a 7-month old with miliary TB.  There are 
multiple small nodules throughout the lungs bilaterally.  
There is a focal consolidation in the right upper lobe.
      To illustrate how rapidly this can improve, examine 
the follow-up chest radiographs taken three weeks after 
anti-TB therapy is initiated.

View miliary TB follow-up.

     Note the substantial clearing of the multiple small 
nodular densities and the clearing of the right upper 
lobe consolidation.

     The radiologic patterns observed in postprimary TB 
can be divided into four categories:
     1.  Parenchymal disease and cavitation
     2.  Airway disease
     3.  Pleural disease
     4.  Other

     The first manifestation of parenchymal disease is a 
heterogeneous poorly defined infiltrate (the exudative 
lesion) within the apical/posterior segments of the upper 
lobe or the superior segment of the lower lobe.  This is 
thought to be secondary to a higher oxygen tension or 
decreased lymphatic clearance within these regions.  
This may progress to lobar or lung opacifications or 
may evolve into better-defined coarse reticular or 
nodular opacities (the fibroproliferative lesion).  The 
lesion may calcify.  Pleural thickening with subpleural 
atelectsis and fibrosis often leads to an "apical cap" in 
40% of the patients.  One important point is that 
disease activity cannot be assessed by radiologic 
     Inactive disease is defined as a stable chest 
radiograph for six months and repeatedly negative 
sputum cultures.  Cavitation may occur in 40% to 90% 
of those with parenchymal disease.  The cavities are 
often multiple and are between one and three 
millimeters.  They have thick and irregular walls, but 
can become emphysematous in nature.
     Airway TB manifests as bronchial stenosis, tracheal 
TB, or laryngeal TB.  Bronchial stenosis is the most 
common of the three, and occurs in 10% to 40% of 
cases of active TB.  This complication is visualized 
radiographically as persistent lobar or segmental 
collapse, hyperinflation, or mucoid impaction.  It may 
lead to bronchiectasis.
     The pleural disease of post primary TB occurs in 6% 
to 18% of cases.  These pleural effusions are often 
small (as opposed to the large effusions characteristic 
of primary TB) and associated with significant 
parenchymal disease.
     Other radiographic characteristics of postprimary TB 
include pseudoaneurysms which are seen as an 
enlarging mass or a rapidly appearing consolidation.  
Vertebral osteomyelitis may occur as well as paraspinal 
and prevertebral abscesses.

     Lamont AC, Cremin BJ, Pelteret RM.  Radiological 
patterns of pulmonary tuberculosis in the paediatric age 
group.  Pediatric Radiology 1986;16:2-7.
     Agrons GA, Markowitz RI, Kramer SS.  Pulmonary 
tuberculosis in children.  Seminars in Roentgenology 
     McAdams HP, Erasmus J, Winter JA.  Radiologic 
manifestations of pulmonary tuberculosis.  Radiology 
Clinics of North America 1995;33(4):655-676.
     Ghon A.  The Primary Lung Focus of Tuberculosis in 
Children.  London, JA Churchill, 1916.
     Smuts NA, Beyers N, Gie RP, et al.  Value of the 
lateral chest radiograph in tuberculosis in children.  
Pediatric Radiology 1994;24:478-480.
     Caffey J.  Primary pulmonary tuberculosis.  In:  
Silverman F (ed).  Pediatric X-Ray Diagnosis, 8th 
edition.  Chicago, Year Book, 1985, pp. 1210-1227.

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Web Page Author:
Loren Yamamoto, MD, MPH
Associate Professor of Pediatrics
University of Hawaii John A. Burns School of Medicine