Presentation1.pptx, pediatric tb diseaase

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Presentation1.pptx, pediatric tb diseaase

  1. 1. PEDIATRIC TUBERCULOSIS. Dr/ ABD ALLAH NAZEER. MD.
  2. 2. Prehistoric humans 8000 BC and Egyptian mummies from 2500 - 1000 BC revealed evidence of TB disease DNA studies of an Inca mummy around 700 AD showed evidence of Pott’s disease 1827–1892: Jean Antoine Villemin proved the infectious nature of TB. In 1882: Robert Koch identified the tubercle bacillus Early 20th century: The TB vaccine, BCG was developed by Calmette and Guérin. 1943: Streptomycin was discovered by Waksman Historical Facts.
  3. 3. T. B epidemiology. TB is a global health problem (1/3 infected with TB) 8.6 million incident cases of TB worldwide in 2012 122 per 100,000 population. TB burden: Asia (58%), Africa region (27%), Eastern Mediterranean (8 %), Europe (4 %), and America (3%) Common cause of death from any infectious agent worldwide. 1.3 million died from TB in 2012. TB and HIV co-infection has increased. 1.1 million (13 %) of new TB cases have HIV. Drug resistant TB (3.6% of new cases, 20% of previously treated).
  4. 4. T.B in children. 2012 TB burden in children (<15 years). 530,000 cases (6% of 8.6 million new cases in 2012) 64,000 deaths/year. Tuberculosis in children can be hard to diagnose. Most children have nonspecific symptoms. Culture is not routinely attempted in children. Tuberculin skin test, IGRA has false + / - Xpert MTB/RIF molecular test is unable to detect culture positive TB in 20-25%. Medical Imaging plays a very important role in diagnosis and follow up of TB in children.
  5. 5. Primary disease. In primary TB, the chest radiograph usually shows hilar lymphadenopathy and/ or pulmonary air space opacities. Primary TB may be seen in any age group but is most common in younger children, before the age of adolescence. A review of TB disease in teens found that only 10% had radiologic findings of primary disease with lymphadenopathy. Adolescents are more likely to have adult- like TB with cavitary disease. Lymphohematogenous spread following infection is typical and may progress to disseminated disease. In many cases, the primary lung focus will resolve undetected and the infection can remain dormant as LTBI. The risk of disease progression and disease severity depend on host factors including the age of the child when the infection occurs. Infants have the highest risk of disease progression as well as more severe forms of disease. Children 5 years of age and less and teenagers have a higher risk of progression of TB disease when compared to children infected between 6-10 years of age.(Table 1)
  6. 6. The radiographic appearance of primary TB typically includes enlargement of regional lymph nodes, with or without a small localized focus of air space consolidation. In the absence of clinical symptoms, the subtle changes of primary TB may be difficult to detect radiographically. Unlike adult reactivation disease, pediatric primary TB is characteristically pauci-bacillary and non-cavitary. The primary focus is reported in the right chest more commonly, although it may occur anywhere in the lungs. Due to the mediastinal lymphatic drainage, right sided adenopathy normally accompanies right lung primary opacities whereas bilateral lymphadenopathy is often seen with left sided opacities. Hilar lymphadenopathy is the hallmark of pediatric tuberculosis and is often the only radiographic finding.
  7. 7. Radiological Imaging. Radiograph (x-ray) most commonly used imaging test. Sensitivity of 38.8%, specificity of 74.4% for TB diagnosis. Normal CXR does not rule out TB. For lymphadenopathy, 67% sensitive; 59% specific Computed tomography (CT). More accurate than x-ray for lymphadenopathy. Assessment of disease extent and activity. Helpful for suspected TB with unequivocal CXR or without microbiologic proof. Ultrasound and MRI now plays an increasing role.
  8. 8. Primary infection. Primary infection is mostly seen in younger children. Mycobacteria are inhaled, settles in the lung, and causes inflammatory reaction (Ghon focus). Bacilli multiplies and spread via lymphatics causing Lymphadenopathy. Ghon complex: lung lesion, lymphadenopathy, and lymphangitis. Bacilli are dormant until re-activation (Latent TB infection) or progresses into active TB disease in some children. Radiographs usually show lymphadenopathy. Subtle lung changes (Ghon focus) may or may not be seen
  9. 9. A-P and Lateral view of Ghon focus.
  10. 10. Hilar lymphadenopathy.
  11. 11. Hilar and mediastinal lymphadenopathy on CT contrast enhanced.
  12. 12. Latent T.B infection(LTBI). A pre-clinical state: Absence of clinical symptoms. Usually positive tuberculin skin test or Quantiferon test .Chest x-ray are usually normal. Chest x-ray may also show residual changes of infection in the lungs (granulomas) and / or lymph nodes. The original focus of infection is eradicated within weeks or months but bacilli remain viable within dormant granulomas. Most children are identified during contact investigations or skin test screenings.
  13. 13. Calcified lymphadenopathy.
  14. 14. Failure of cell mediated immunity to contain or eradicate the infection leads to disease progression. At risk: immunocompromised, infants and children < 4 yrs, persons with untreated or inadequately treated TB disease. Symptoms depend on age and degree of dissemination. Some have few symptoms Spectrum of disease progression: Progression of primary pulmonary disease. Progression of lymphadenopathy. Progression of lung and lymph node disease with complications. Disseminated disease / hematogenous spread (virtually any organ). Primary progressive T.B disease.
  15. 15. T.B pneumonia.
  16. 16. TB with loculated pleural effusion.
  17. 17. CT of the T.B with pleural effusion (arrow) and bilateral lung consolidations
  18. 18. CT Scan shows anterior mediastinal low attenuation lymph nodes with peripheral enhancement (arrows), with a large area of adjacent lung consolidation.
  19. 19. LYMPHADENOPATHY.
  20. 20. Presents with barking cough, sputum production, hemoptysis and dyspnea. Result of an enlarged lymph node compression or erosion. Radiographic findings: Hyperaeration. Segmental or subsegmental atelectasis. Collapse / consolidation. CT with 3D and MPR. Highly accurate. Shows lymphadenopathy compressing the large airway. Shows associated small airways, lung, pleura, and bone disease. Trachiobronchial T.B disease in children.
  21. 21. Pleural Disease.
  22. 22. A consequence of primary or post primary disease. Younger children are more prone. Hematogenous dissemination, initially involving lung interstitium and ultimately the airspaces. Nodules measuring 2-3 mm in diameter are seen best on CT more in lower lung zones because of greater blood flow Clearing is usually from 7 to 22 months after treatment TB involvement of other organs is common Evaluation of other sites especially the brain is important. Military T.B disease.
  23. 23. Miliary TB.
  24. 24. Miliary TB.
  25. 25. Congenital Tuberculosis Congenital tuberculosis is a rare form of primary disease caused by prenatal transmission of TB from the mother to the fetus through the umbilical vein or amniotic fluid. For this to occur, hematogenous spread, disseminated disease or uterine involvement during pregnancy would be the most likely mechanisms. Infants with congenital TB may have clinical symptoms at birth but usually present within the first 2-3 weeks of life. Disease after 1 month of age is more likely to have been acquired post-natally. Chest radiographic findings may resemble other more common types of neonatal pneumonia. Findings of intrathoracic lymphadenopathy, evidence of liver involvement (usual site of entry), or a miliary pattern of pneumonia are all supportive of tuberculosis. Unless the mother has evidence of uterine, placental or disseminated TB disease, it can be difficult to distinguish congenital transmission from respiratory transmission soon after birth. In either case, TB in the neonatal period is often a rapidly progressive, disseminated, extensive and life threatening disease .
  26. 26. Congenital Tuberculosis.
  27. 27. Congenital TB with multiple lung consolidation, and left hilar lymph nodes. Several weeks later, the consolidation is resolved and replaced by large air fluid cyst.
  28. 28. Also referred to as Adult-type or Reactivation TB. After dormancy, organism are able to reactivate And proliferate leading to post primary. Most common form of TB in adults and older children. Imaging Features: Consolidation involving the upper lobes due to decreased lymph flow. Cavitation is common. Often associated with significant fibrosis. Lack of lymphadenopathy. Post-primary T.B disease.
  29. 29. Endobronchial spread of TB . Note the extensive linear and nodular opacities in the left upper lobe (“bronchopneumonia).
  30. 30. Latent TB infection. X-ray shows lymphadenopathy with or without lung disease. Radiographs could be normal. Primary Progressive TB Disease. Progressive lymph node and lung disease. Can affect intrathoracic & extrathoracic structures Post primary TB. Apical cavitary consolidation, fibrosis and atelectasis. There is overlap of radiographic manifestations. between primary and post-primary TB. Important imaging consideration.
  31. 31. Genitourinary TB is commonly encountered. Intestinal involvement in 55-90% of fatal cases. Hepatobiliary, lymphadenopathy and peritonitis A minority of patients ( <50%) with abdominal TB have abnormal chest radiographic findings. Clinical symptoms are diverse and non-specific Clinical presentation does not correlate with the severity and extent of imaging findings. ABDOMINAL TUBERCULOSIS.
  32. 32. Hematogenous dissemination. Imaging appearance. Micronodular. Macronodular. Mass – like. May contain calcifications. DDX: neoplasm, abscess, fungal infections. HEPATOSPLENIC TUBERCULOSIS.
  33. 33. Routes: -Ingestion of the tubercle bacilli. -Direct extension from an adjacent infected organ. -Hematogenous spread. -Presentation: abdominal pain, weight loss, anemia, and fever with night sweats, obstruction, palpable mass RLQ -Hemorrhage, perforation, and malabsorption. - Ileocecal involvement in 80 – 90%. Imaging: Inflammation causing mucosal thickening and irregularity, luminal narrowing, and obstruction. DDx: amebiasis, Crohn's disease, ileocecal malignancy. GASTROINTESTINAL TUBERCULOSIS.
  34. 34. T.B LYMPHADENOPATHY.
  35. 35. Abdominal TB lymphadenopathy. The same patient has a low attenuation center and a thin rim of peripheral enhancement, suggestive of an abscess.
  36. 36. Splenic lesions. The hypoechoic, round lesions of varying sizes seen on ultrasound may represent granulomas.
  37. 37. T.B PERITONITIS.
  38. 38. Wet Peritonitis.
  39. 39. Skeletal involvement in TB occurs in 1-3%. - Spondylitis, arthritis, osteomyelitis. Hematogenous spread, direct invasion. Children are more prone than adults. Concurrent intrathoracic TB is present in < 50% Associated soft tissue abscess. Arthritis: 25% of cases, usually monoarticular. - Phemister triad, usually affects hips and knees Oseomyelitis: unifocal or multifocal. - Cystic, infiltrative, erosive, spina ventosa. MUSCULOSKELETAL TUBERCULOSIS.
  40. 40. TB osteomyelitis with abscess formation.
  41. 41. Spine is most common site of bone involvement. Usually upper lumbar (L1) and lower thoracic. More than one vertebral body are typically affected. Begins in the anterior part of the vertebral body adjacent to endplates, spreads to into the disk space. Leads to vertebral collapse - Gibbus deformity. Paraspinal involvement usually the psoas. DDX: pyogenic vertebral osteomyelitis, metastasis, primary neoplasm (lymphoma, myeloma). TUBERCULOUS SPONDYLITIS(POTT,S DISEASE).
  42. 42. TB spondylitis with para-spinal abscess.
  43. 43. TB spondylitis. Bilateral paraspinal abscess . Note the calcified mediastinal lymph nodes (long arrow).
  44. 44. Hematogenous dissemination to brain and meninges. - Becomes clinically apparent 6 months after infection. Gelatinous exudate fills the meninges along the basal cisterns and along the walls of the meningeal vessels. - Vasculitis causing infarcts (50%). - Communicating hydrocephalus (50-77%). - Abnormal meningeal enhancement typically more pronounced in the basal cisterns. - Other manifestations: tuberculoma, cerebritis, abscess, miliary pattern, subdural epyema and atrophy. CNS TUBERCULOSIS.
  45. 45. TB meningitis.
  46. 46. Basal cisterns and midbrain, loculated abscess (arrows).
  47. 47. Multiple small ring enhancing lesions in the cerebellum represent tuberculomas
  48. 48. Tuberculous otomastoiditis.
  49. 49. TB of the skull with enhancing epidural abscess.
  50. 50. Brain infarcts secondary to TB mengitis.
  51. 51. TB of the sternum with abscess formation.
  52. 52. Tuberculous cervical lymphadenitis
  53. 53. Conclusion. Tuberculosis is an important disease worldwide and is sometimes difficult to recognize in children who do not follow the same patterns of disease as adults. In children the lungs, lymph nodes or central nervous system are more commonly involved. In general, radiographic findings may be suggestive but often are not specific c for TB. Characteristic patterns in children with TB include unilateral hilar lymphadenopathy with or without consolidation and miliary disease. Cavitary lesions are uncommon except in adolescents who may demonstrate findings similar to adult disease. Contrast CT and/or MRI are the best diagnostic imaging modalities for extra-pulmonary disease. Pediatric TB may present with confusing and difficult to interpret clinical information. Radiographic images are among the most important diagnostic tools.
  54. 54. Thank You.

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