INTRODUCTIONATELECTASIS, ARDS

Dr Vijay Shankar S

RESPIRATORY SYSTEM

OVERVIEW

• Congenital anomalies,Neonatal lung diseases

• Pulmonary infections• Obstructive vs Restrictive lung diseases

COPDs & Penumoconiosis• Pneumoconiosis• Lung tumors

TODAY

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

A 7-year-old boy accidentally inhales a small peanut, which lodges inone of his bronchi. A chest x-ray reveals the mediastinum to be shiftedtoward the side of the obstruction. Which of the following pulmonaryabnormalities is most likely present in this boy?

a. Absorptive atelectasisb. Compression atelectasisc. Contraction atelectasisd. Patchy atelectasise. Hyaline membrane disease

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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

Normal histology of alveolar septa

Paediatric lung disease

• Congenital • Bronchopulmonary sequestration• Hyaline membrane disease(NRDS)

ATELESTASIS/ COLLAPSE

• Greek word  ἀτελής, "incomplete" + ἔκτασις, "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

IRREVERSIBLE

SIGNIFICANCE

• Reduces oxygenation and predisposes to infection!

• Reversible except contraction type!

GROSS• Small, • dark blue,• fleshy and non-crepitant ( looks like a

liver)

Histology

• Alveolar space in the affected area– are small with thick interalveolar septa.– Contain proteinaceous fluid with scattered epithelial

squames & meconium.• Scattered aerated space

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.

• More common in LBW babies

• Etiology.Preterm babyInfants born to diabetic mothersDelivery by caesarean section without preceding labourExcessive sedationBirth asphyxiaMale preponderance

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 alveoliFIBRIN + NECROTIC CELLS ( HYALINE MEMBRANE)

Increased diffusion gradient

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

water.

Acute lung injury

• Spectrum of endothelial and epithelial lesions

• Manifestations:congestionsurfactant disruptionatelectasis

Variable progression to:

• Pulmonary edema• Acute respiratory distress syndrome• Acute interstitial pneumonia

Microvascular injury

• Injury to endothelial or epithelial cells• Leakage of fluids and proteins into the interstitial

space → alveoli

• Localized: symptoms of infection• Diffuse: ARDS

Acute respiratory distress syndrome

ARDS / DAD / shock lung

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

Infection SepsisDiffuse pulmonary infections – viral mycoplasma, PCP, miliary TBGastric aspiration

Physical injuryMechanical traumaPulmonary contusionsNear drowningFractures with fat embolismBurnsIonizing radiation

Inhaled irritantsOxygen toxicitySmokeIrritant gases & chemicals

Chemical injuryHeroin or methadone overdoseASABarbiturate overdose

Hematological conditionsMultiple transfusionsDIC

PancreatitisUremia, C-P bypass

PATHOGENESIS

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

Clinical course

• Previously hospitalized pts develop tachypnea and dyspnea

• Increasing cyanosis and hypoxemia• Unresponsive to oxygen therapy• Respiratory acidosis develops

Chest X ray

• Diffuse alveolar infiltration

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

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.

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

• 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.

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