local complications general complications physiological complication

1. COMPLICATIONS OF
TUBERCULOSIS
DR. ANKUR GUPTA
S.M.O. (NODAL DRTB CENTRE, DEPTT. OF
PULMONARY MEDICINE)

2. Complications of Tuberculosis can mimic other
disease entities. Therefore, recognition and
understanding of such thoracic and
extratoracic sequelae and are important to
facilitate diagnosis and institute proper
treatment

3. COMPLICATIONS
LOCAL
• Parenchymal
• Airway
• Vascular
• Mediastinal
• Pleural
• Chest Wall
GENERAL
• Physiologic
• Tuberculous enteritis and
Enteritis
• Secondary Amyloidosis
• Respiratory Failure
• Cor pulmonale

4. Parenchymal Complications
1. Tuberculoma and Thin-walled Cavity
2. Cicatrization and Destruction of the Lung
3. Aspergilloma
4. Bronchogenic Carcinoma

5. Tuberculoma and Thin-walled Cavity
• Tuberuloma - It is a round or oval granuloma
caused by AFB, lined by granulomatous
inflammatory tissue or connective tissue
– Central portion - caseation necrosis.
– Solitary or multiple
– Diameter from 0.5 to 4.0 cm or greater.
– Margins are smooth or sharply defined
– Satellite lesions are seen in up to 80%.
– Calcification is found in 20%–30%.

6. Tuberculoma

7. Tuberculoma and Thin-walled Cavity
• Thin-walled Cavity
– aka OPEN NEGATIVE SYNDROME OR INH CAVITIES
– Seen in both active and inactive disease
– May disappear after ATT
– Occasionally wall becomes paper-thin and an air-
filled cystic space remains
– Wall thickness 1 cm to 1 mm and may be smooth,
sometimes simulating an emphysematous bulla,
cyst or pneumotocele

8. Thin-walled Cavity

9. Cicatrization and Lung Destruction
• Cicatrization atelectasis is a common finding after
postprimary tuberculosis (40%)
• Marked fibrotic response manifests as
– Atelectasis of the upper lobe
– Retraction of the hilum
– Compensatory lower lobe hyperinflation and
– Mediastinal shift toward the fibrotic lung.
• Nonspecific fibrotic response
– Parenchymal bands,
– Fibrotic nodules and cavities
– Traction bronchiectasis

11. Aspergilloma (Mycetoma; “Fungas Ball”)
• Mobile, rounded mass surrounded by a
crescentic air shadow is noted inside a lung cavity
(air-crescent sign)
• Aspergilloma associated with chronic TB has been
reported to be 11%
• 25%–55% of patients with aspergilloma have a
history of chronic cavitary tuberculosis.
• Hemoptysis is the most common clinical
symptom (50%–90%),cough, weight loss, rarely
fever and dyspnea

12. Aspergilloma (Mycetoma; “Fungas Ball”)
• DD
– Organized hematoma
– Pus inside cavity
– Neoplasm,
– Hydatid cyst
• DX –
– Serum precipitins for aspergillus (100%),
– Sputum culture
– Skin test
– Bronchoscopy.
• Treatment –
– Systemic antifungal
– Local instillation of antifungal
– Surgery
– Wait and watch

14. Bronchogenic Carcinoma
• Bronchogenic carcinoma and PTB often coexist
• Manifestations of carcinoma may be obscured or
misinterpreted as progression of tuberculosis.
• TB may favor the development of bronchogenic
carcinoma by local mechanisms (scar cancer)
• Any predominant or growing nodule should be
suspicious for coexisting lung cancer in patients
with TB

16. Airway Complications
1. Bronchiectasis
2. TB Endobronchitis and Tracheitis
3. Tracheobronchial Stenosis
4. Broncholithiasis

17. Bronchiectasis
• Result of tuberculous involvement of the
bronchial wall and subsequent fibrosis.
• Bronchiectasis is seen in 30%– 60% of patients
with active postprimary tuberculosis and in
71%–86% of patients with inactive disease
• Bronchiectasis located in the apical and
posterior segments of the upper lobe is highly
suggestive of a tuberculous origin “DRY
BRONCHIECTASIS”

19. TB Endobronchitis and Tracheitis
• Occur in 1/3`rd of cases.
• AFB Implantation may be direct, via
circulation, or via lymphatics.
• CF- cough, hemoptysis, dyspnea, soreness or
constriction in substernal region.
• O/E – Localized wheeze.

21. • Rasmussen aneurysm is a rare phenomenon
caused by weakening of the pulmonary artery
wall from adjacent cavitary tuberculosis
• Progressive weakening of the arterial wall
occurs as granulation tissue replaces both the
adventitia and the media
• granulation tissue – replaced by fibrin -
thinning of the arterial wall –
pseudoaneurysm - rupture

22. Tracheobronchial Stenosis
• caused by 1. granulomatous changes in the
tracheobronchial wall
– erythema - lymphocytic infiltration(submucosa) -
tubercle formation – fibrosis)
• 2. extrinsic pressure from enlarged peribronchial
lymph nodes.
• Endobronchial involvement occurs in
approximately 2%–4%
• The left main bronchus is most frequently
involved.

23. Tracheobronchial Stenosis
• Active stage of stenosis
– Irregular luminal narrowing with wall thickening
– Enhancement
– Enlarged adjacent mediastinal nodes
• Fibrotic stage
– Concentric narrowing of the lumen
– Uniform thickening of the wall
– Involvement of a long bronchial segment

25. Broncholithiasis
• Defined as the presence of calcified or ossified material
within the lumen of the tracheobronchial tree.
• Uncommon complication.
• The calcific nidus in a tuberculous lymph node erodes
into the bronchial wall and may occlude the bronchus
• Symptoms - cough, hemoptysis, wheezing,recurrent
pneumonia
• Change in the position or disappearance of a calcific
focus on serial radiographs, development of airway
obstruction, resulting in lobar or segmental atelectasis,
mucoid impaction, or expiratory air trapping.

27. Vascular Complications
• Hemoptysis
– more common and potentially serious (30-35%)
– Initial manifestation, during treatment, after treatment.
• Cause –
– from cavity wall
– rupture of Rasmussen`s aneurysm
– direct erosion of capillaries
– d/t granulomatous inflamm
– d/t sec infetion
– d/t tubercular endobronchitis (bronchial circulation)
– d/t bronchiectasis (bronchial circulation)
– d/t aspergilomata
– d/t bronchioliths (bronchial circulation)
– d/t scar carcinoma

29. Mediastinal Complications
• Lymph Node Calcification and Extranodal
Extension.
• Esophagomediastinal Fistula.
• Pericardial Tuberculosis.
• Fibrosing Mediastinitis.

30. Lymph Node Calcification and
Extranodal Extension.
• Tuberculous mediastinal lymphadenitis is a frequent
manifestation of primary pulmonary tuberculosis.
• Enlarged nodes occur in 83%–96% of pediatric cases,
decrease with age.
• Caused by the formation of tuberculous caseating
granulomas in lymph nodes, commonly on right side .
• In the active stage, the nodes have central low
attenuation and peripheral rim enhancement at CT.
• Extranodal extension may occur into bronchus,
pericardium, and esophagus.

32. Esophagomediastinal Fistula
• Most common cause of esophageal
tuberculosis is secondary involvement from
adjacent Tuberculous Lymphadenitis.
• Rare complication.
• Symptoms - fever, cough, weight loss,
dysphagia, chest discomfort, or back pain.
• Esophageal involvement results in strictures,
tracheobronchial or mediastinal fistulas, and
traction diverticula

34. Pericardial Tuberculosis
• Caused by extranodal extension of TB lymphadenitis
into the pericardium (1% of cases of tuberculosis)
• Constrictive pericarditis characterized by fibrous or
calcific constrictive thickening of the pericardium,
which prevents diastolic filling of the heart (10%)
• CT findings
– pericardial thickening 3 mm with or without pericardial
effusion.
– RHF  Secondary dilatation of IVC
– acute angulation or interventricular septum,

36. Fibrosing Mediastinitis
• Fibrosing mediastinitis is presence of excessive fibrosis
in the mediastinum and is uncommon
• TB mediastinitis is rare (most common histoplasmosis)
• Symptoms – cough, fever, and symptoms d/t
compression of the SVC, esophagus, and
tracheobronchial tree
• CT findings
– mediastinal or hilar mass
– calcification in the mass
– tracheobronchial narrowing
– Pulmonary vessel encasement
– superior vena cava obstruction
– pulmonary infiltrates

38. Pleural Complications
1. Chronic Tuberculous Empyema and
Fibrothorax
2. Bronchopleural Fistula
3. Bronchopleural Fistula

39. Tubercular Empyema and Fibrothorax
• Pleural infection is usually caused by
– rupture of a subpleural caseous focus into the pleural
space
– hematogenous dissemination
– contamination by adjacent infected lymph nodes
• Chronic tuberculous empyema - persistent,
grossly purulent pleural fluid containing AFB
• CT scans - focal fluid collection with pleural
thickening and calcification and with or without
extrapleural fat proliferation

40. Tubercular Empyema and Fibrothorax
• Fibrothorax with diffuse pleural thickening but
without effusion on CT scans suggests
inactivity
• Chyliform or pseudochylous pleural effusion is
a high-lipid nonchylous effusion and is most
commonly caused by tuberculous empyema

42. Bronchopleural Fistula
• Bronchopleural fistula occurs due to an open
pathway between bronchus and pleura
established by tuberculosis
• BPF usually follows trauma, surgical procedure or
spontaneously
• Diagnosis –
– increasing amount of sputum production
– air in the pleural space
– a changing air-fluid level
– contralateral spread of pneumonic infiltration

43. Bronchopleural Fistula

44. Pneumothorax
• In severe and extensive pulmonary
involvement by the infectious process and the
onset of bronchopleural fistula and empyema.
• Occcurs in 5% of patients with postprimary TB.
• Pathogenesis
– pleural caseous infiltrates -> liquefaction -> pleural
necrosis and rupture.
• Tube drainage is the treatment of choice

45. Pneumothorax

46. Chest Wall Compliations
1. Chest Wall Tuberculosis
2. Tuberculous Spondylitis
3. Malignancy Associated with Chronic
Empyema

47. Chest Wall Tuberculosis
• CWTuberculosis characterized by bone or costal
cartilage destruction and soft tissue masses that
may demonstrate calcification or rim
enhancement
• Involves the sternum, the sternoclavicular joint,
or a rib osseous destruction and localized
abscess formation
• Occur by direct extension or by hematogenous
spread.
• When spontaneous discharge of empyema
through the parietal pleura into the chest wall
forms subcutaneous abscess, it is termed
empyema necessitatis

49. Tuberculous Spondylitis
• Aka Pott disease, is caused primarily by
hematogenous spread of pulmonary infection
and commonly affects the lower thoracic and
upper lumbar spine
• early features
– irregularity of the vertebral end plates
– Decreased height of the intervertebral disk space,
– sclerosis of the adjacent bone
• Late features
– Anterior wedging of the vertebral body -> kyphosis
– paravertebral abscess.

51. Malignancy Associated with Chronic
Empyema
• Rare complication. mean duration 25 years.
• The histopathologic diagnoses in reported cases
have been malignant lymphoma, SqCCa,
mesothelioma, malignant fibrous histiocytoma,
liposarcoma, rhabdomyosarcoma, angiosarcoma,
and hemangioendothelioma,
• Imaging clues –
– increased opacity in the thoracic cavity
– soft-tissue bulging and blurring of fat planes
– destruction of bone near the empyema
– extensive medial deviation of the calcified pleurae

53. COMPLICATIONS
LOCAL
• Parenchymal Lesions
• Airway Lesions
• Vascular Complication
• Mediastinal Lesions
• Pleural Lesions
• Chest Wall Lesions
GENERAL
• Physiologic changes
• Tuberculous Laryngitis
• Secondary Amyloidosis
• Respiratory Failure
• Cor pulmonale

54. Physiologic changes
• Airway obstruction – in 30-60% cases of PTB.
• Airway restriction – D/t effusion, thickening,
fibrothorax
• Mixed defect.
• Type of abnormality depends upon the type
and extend of involvement or residual damage
left out.

55. Respiratory Failure & Cor Pulmonale
1. Extensive destruction of pul. Parenchyma
greater V/Q mismatch.
2. Pleural pathology (thickening, fibrothorax).
3. Atropy or disuse of respiratory muscles
1+2+3 mechanical disadvantage -> Tachypnea,
Hypoxia, Hypercapnia  Respiratory Failure.
Cor Pulmonale – Enlargement of RV due to
increased RV afterload sec to pulmonary
disease

56. Tuberculous Laryngitis
• In 4 – 25 % of cases, via direct implantation,
lympahatics or blood vessels.
• CF-
– Soreness or pain in throat
– Dry, hacking cough and hoarseness of voice
• Laryngoscopy may reveal an ulcer, granuloma,
paresis or paralysis of VC, destruction of VC or
stenosis.
• Sputum is usually positive or AFB.

58. Secondary Amyloidosis
• Ctz by deposition of extracellular eosinophilic
substance in various organs – kidneys (100%),
spleen(75%), liver(63%), adrenals(21%) etc.
• Lag period is about 5 years in majority of
cases.
• Now a rare complication d/t modern ATT

59. • Any questions, suggestions, corrections please
mail me back at learningtbchest@gmail.com

60. QUESTIONS