RESPIRATORY SYSTEM: INTRODUCTION, ATELECTASIS, ARDS

1. INTRODUCTION
ATELECTASIS, ARDS
Dr Vijay Shankar S

2. RESPIRATORY SYSTEM

3. OVERVIEW
• Congenital anomalies,Neonatal lung
diseases
• Pulmonary infections
• Obstructive vs Restrictive lung diseases
COPDs & Penumoconiosis
• Pneumoconiosis
• Lung tumors

4. TODAY
• Anatomy and histology
• Functions
• Congenital anomalies
• Atelectasis and collapse
• Hyaline membrane disease
• ARDS

5. A 7-year-old boy accidentally inhales a small peanut, which lodges in
one of his bronchi. A chest x-ray reveals the mediastinum to be shifted
toward the side of the obstruction. Which of the following pulmonary
abnormalities is most likely present in this boy?
a. Absorptive atelectasis
b. Compression atelectasis
c. Contraction atelectasis
d. Patchy atelectasis
e. Hyaline membrane disease

9. _
1. Trachea
2. Bronchus (Right- or Left- Primary Bronchus)
3. Lobar Bronchus
4. Segmental Bronchus
5. Bronchus
6. Bronchiole
7. Terminal Bronciole
8. Respiratory Bronchiole
9. Alveolar Duct
10
.
Alveolar Sac / Alveolus

12. Normal histology of alveolar septa

18. Paediatric lung disease
• Congenital
• Bronchopulmonary sequestration
• Hyaline membrane disease(NRDS)

19. ATELESTASIS/ COLLAPSE
• Greek word τελήςἀ , "incomplete" + κτασις,ἔ
"extension"
• Defn: incomplete expansion of lung parenchyma
( neonatal/primary )
– Etiology
prematurity, cerebral birth injury, CNS
malformation and IUhypoxia
• Sec/acquired atelectasis – collapse of previously
expanded lung

20. IRREVERSIBLE

21. SIGNIFICANCE
• Reduces oxygenation and predisposes to
infection!
• Reversible except contraction type!

22. GROSS
• Small,
• dark blue,
• fleshy and non-crepitant ( looks like a
liver)

25. Histology
• Alveolar space in the affected area
– are small with thick interalveolar septa.
– Contain proteinaceous fluid with scattered epithelial
squames & meconium.
• Scattered aerated space

26. Neonatal respiratory distress
syndrome
• Hyaline membrane disease
• Characterised by hyaline membrane formation
• Begins with dyspnoea a few after birth with
tachypnoea, hypoxia and cyanosis and in severe
case death occurs in few hours.

27. • More common in LBW babies
• Etiology.
Preterm baby
Infants born to diabetic mothers
Delivery by caesarean section without
preceding labour
Excessive sedation
Birth asphyxia
Male preponderance

28. PREMATURITY
Reduced SURFACTANT synthesis, storage and release
Decreased alveolar surfactant
Increased alveolar surface tension
Atelectasis
Uneven perfusion Hypoventilation
HYPOXEMIA + CO2 RETENTION
Acidosis
Pulmonary Vasoconstriction
Pulmonary hypoperfusion
Endothelial damage + Epithelial damage
Plasma leak into alveoli
FIBRIN + NECROTIC CELLS
( HYALINE MEMBRANE)
Increased
diffusion
gradient

29. GROSS
• The lungs are normal in size ,
• Reddish purple in color.
• Are solid and airless so that they sink in
water.

36. Acute lung injury

37. • Spectrum of endothelial and epithelial lesions
• Manifestations:
congestion
surfactant disruption
atelectasis

38. Variable progression to:
• Pulmonary edema
• Acute respiratory distress syndrome
• Acute interstitial pneumonia

39. Microvascular injury
• Injury to endothelial or epithelial cells
• Leakage of fluids and proteins into the interstitial
space → alveoli
• Localized: symptoms of infection
• Diffuse: ARDS

40. Acute respiratory distress
syndrome
ARDS / DAD / shock lung

41. ARDS
• Clinical syndrome caused by diffuse alveolar
capillary damage
Clinically,
• Severe life threatening respiratory insufficiency
of rapid onset
• Cyanosis
• Severe arterial hypoxemia refractory to o2
• Progress to multisystem organ failure

42. Infection
Sepsis
Diffuse pulmonary infections –
viral mycoplasma, PCP, miliary
TB
Gastric aspiration
Physical injury
Mechanical trauma
Pulmonary contusions
Near drowning
Fractures with fat embolism
Burns
Ionizing radiation
Inhaled irritants
Oxygen toxicity
Smoke
Irritant gases & chemicals
Chemical injury
Heroin or methadone overdose
ASA
Barbiturate overdose
Hematological conditions
Multiple transfusions
DIC
Pancreatitis
Uremia, C-P bypass

43. PATHOGENESIS

44. Acute alveolar injury
Release of cytokines
By Macrophages
(IL1, 8, TNF)
By Activated neutrophils
(Protease, leukotrienes,
PAF, Oxidases)
Local tissue damage, intra alveolar edema loss of diffusion capacity and
damage to type II alveolar pneumocytes Surfactant inactivation
HYALINE MEMBRANE
STIFF LUNG

45. Clinical course
• Previously hospitalized pts develop tachypnea
and dyspnea
• Increasing cyanosis and hypoxemia
• Unresponsive to oxygen therapy
• Respiratory acidosis develops

46. Chest X ray
• Diffuse
alveolar
infiltration

47. Morphology - Acute stage:
• Heavy, firm, red and boggy
• Congestion, intra-alveolar edema, inflammation
and fibrin deposition
• Alveolar walls lined by waxy hyaline
membranes
• Fibrin rich edema fluid mixed with cytoplasmic
and lipid remnants of necrotic epithelial cells

48. Organizing stage
• Type II pneumocytes proliferate
• Organization of the exudate  intra alveolar
fibrosis
• Thickening of alveolar septa
• Proliferation of interstitial cells and deposition of
collagen
• Fatal cases  superimposed bronchopneumonia.

49. The blue arrows point to intralveolar macrophages and type II pneumocytes.
• The green arrow identifies brightly eosinophilic hyaline membranes.

50. • The blue arrows point to the type II pneumocytes which are very prominent;
their nuclei protruding into the alveolar space.
• The arrows highlight the thickened septum.
• The septum contains excess collagen, fibroblasts, and lymphocytes.
• Hyaline membranes are not present.

52. A 7-year-old boy accidentally inhales a small peanut, which
lodges in one of his bronchi. A chest x-ray reveals the
mediastinum to be shifted toward the side of the
obstruction. Which of the following pulmonary
abnormalities is most likely present in this boy?
• a. Absorptive atelectasis
• b. Compression atelectasis
• c. Contraction atelectasis
• d. Patchy atelectasis
• e. Hyaline membrane disease