RespPath-Lecture 4-Atelectasis, Pulmonary Congestion & Edema, and ARDS

Lecture 4
Prepared and presented by

Marc Imhotep Cray, M.D.
Photo: Colorized scanning electron micrograph of the lung, showing alveoli. Seeley’s Anatomy & Physiology. 10th ed. New York, NY: McGraw-Hill 2010
Respiratory Pathology
Lecture 4
Atelectasis
 Atelectasis refers to incomplete expansion of lungs or collapse of
previously inflated lung substance
 Produces areas of relatively airless pulmonary parenchyma
 Severe atelectasis significantly reduces oxygenation and predisposes

to infection
 Acquired atelectasis is generally encountered in adults and may be

divided into following categories:
 Obstruction (or resorption) atelectasis
 Compression atelectasis
 Patchy atelectasis
 Contraction atelectasis
 It is a reversible disorder (except that caused by contraction)

Marc Imhotep Cray, M.D. 2
Lecture 4
Four types of atelectasis

Obstruction atelectasis involves parts of lung distal to an obstructed
bronchus
 Compression atelectasis usually involves entire lung
 pleural space is filled with fluid compressing lung, which has retracted
toward hilum
o Similar findings can be produced by pneumothorax, except in
“pneumo” lung collapses because of entry of air into pleural space
 Patchy atelectasis involves small segments of all lobes
o Airless patches of lung parenchyma, which have collapsed because
of a deficiency of surfactant, are distributed irregularly and usually
are found in both lungs
 Contraction atelectasis usually occurs in subpleural areas and is typically
caused by interstitial fibrosis, which prevents the expansion of parenchyma
Lecture 4
Four types of atelectasis (2)

Obstruction atelectasis Compression atelectasis Patchy atelectasis Contraction atelectasis
Modified from: Damjanov I, Pathology Secrets 3rd ed. 2009

Lecture 4
Obstruction (or resorption) atelectasis

 Mechanism: An obstruction in airway impairs filling of Alveoli All air
in alveoli is eventually resorbed and alveoli collapse
 Causes of obstructive atelectasis: Aspirated foreign body, tumor, and

mucus (e.g., in chronic bronchitis and cystic fibrosis)
 Mediastinal shift: Toward source of atelectasis

Lecture 4
Compression atelectasis
 Mechanism: A condition or lesion external to lungs (i.e., in pleural
cavity) compresses lung and impairs filling of alveoli upon respiration
 Causes of compressive atelectasis: Blood in pleural cavity (i.e.,

hemothorax), air in pleural cavity (i.e., pneumothorax), and fluid in e
pleural cavity (e.g., pulmonary edema)
 Mediastinal shift: Away from source of atelectasis

Lecture 4
Compressive atelectasis (2)

 Photograph shows atelectasis as
result of a left-sided hemothorax
due to a gunshot wound
 blood in left pleural cavity
caused compressive
atelectasis of left lung
 Note smaller size of left lung and

its wrinkled pleural surface (due
to collapse), compared to smooth
pleural surface of right lung
Kemp WL, Burns DK and Brown TG. The Big Picture: Pathology,
2008

Lecture 4
Patchy(micro) atelectasis
The right lung of an infant is pale and
expanded by air; the left lung is collapsed.
 Mechanism: Loss of surfactant
 Causes: Prematurity, interstitial

inflammation, postsurgical
Rubin R and Strayer DS Eds. Rubin’s Pathology: Clinicopathologic

Marc Imhotep Cray, M.D. Foundations of Medicine, 6th Ed. 2012 8
Lecture 4
Pulmonary edema: Causes

 Hemodynamic disturbances
 most common mechanism is one attributable to increased hydrostatic
pressure left-sided congestive heart failure
 also occur as a consequence of decreased plasma oncotic pressure
 Direct increase in capillary permeability

 most common causes are infectious agents, inhaled gases, liquid aspiration,
and drugs
 edema results from primary injury to vascular endothelium or damage to
alveolar epithelial cells (with secondary microvascular injury)
 Lymphatic insufficiency
 Lymphangitic carcinomatosis
 Fibrosing lymphangitis (e.g., silicosis)
Lecture 4
Pathologic features of pulmonary

congestion and edema
Macroscopic features
 characterized by heavy, wet lungs
 Long-standing pulmonary congestion causes brown induration of
lungs (lungs are firm and brown), which predisposes to infection
Histologic features
 alveolar capillaries are engorged
 Proteinaceous material is located within alveoli; it appears pink in
hematoxylin and eosin-stained specimens
 In long-standing cases of pulmonary congestion, numerous heart
failure cells, as well as fibrosis and thickening of alveolar walls,
appear

Lecture 4
Pulmonary edema, PA chest

 Pulmonary passive congestion from
left-sided heart failure (cardiogenic
edema) increases interstitial
markings, and edema fluid spills into
alveoli, creating infiltrates
 Shows pulmonary congestion and

edema throughout all lung fields
 Pulmonary veins are distended near

hilum
 Left heart border is prominent
because of left atrial enlargement
 This patient had mitral stenosis

Klatt EC. Robbins and Cotran Atlas of Pathology, 3rd Ed. 2015
Lecture 4
Pulmonary edema, PA chest (2)

 PA chest radiograph shows
extensive congestion and edema
throughout all lung fields from
severe CHF from cardiomyopathy,
and edema obscures cardiac
silhouette
Lecture 4
Pulmonary edema, microscopic

 Alveoli filled with a smooth to
slightly floccular pink material ( )
characteristic of pulmonary
edema
 Capillaries within alveolar walls

are congested, filled with many
red blood cells (RBCs)
 Pulmonary congestion with

edema is common in patients
with heart failure and in areas of Klatt EC. Robbins and Cotran Atlas of Pathology, 3rd Ed. 2015
inflammation of lung
Results: Hypoxemic Acute Respiratory Failure
Respiratory failure with pO2 of <60 mm Hg
Lecture 4
Pulmonary edema, microscopic (2)

More marked pulmonary
congestion with dilated
capillaries and leakage of
blood into alveolar spaces,
leading to appearance of
hemosiderin-laden
macrophages (“heart failure
cells”) containing brown
cytoplasmic hemosiderin
granules ( ) from
breakdown of RBCs
Lecture 4
Case Trigger
A 63-year-old man is hospitalized for a severe case of lobar pneumonia
with sepsis. Within the first 24 hours of his hospitalization, he develops
worsening respiratory failure and requires intubation. A chest x-ray
reveals bilateral patchy opacities. He becomes progressively hypoxemic
even with increased oxygen delivery via the ventilator. You continue to
treat the patient’s pneumonia, but you worry that he will have up to a
40% mortality rate given his current condition.

Lecture 4
Adult Respiratory Distress Syndrome

 ARDS has many synonyms, such as diffuse alveolar damage, adult
respiratory failure, shock lungs, acute alveolar injury, and traumatic
wet lungs
 Clinical features: rapid onset of life-threatening respiratory insufficiency,

cyanosis, and severe arterial hypoxemia that is refractory to oxygen
therapy and sometimes progresses to extrapulmonary multisystem
organ failure
 Almost always associated with evidence of severe pulmonary edema

(often called noncardiogenic, low-pressure, or high-permeability
pulmonary edema)

Lecture 4
ARDS: Causes
Conditions are associated with development of ARDS:
Direct lung injuries
 Diffuse pulmonary infections
 Oxygen toxicity
 Inhalation of toxins and other irritants
 Aspiration of gastric contents
Systemic conditions
 Septic shock
 Shock associated with trauma
 Hemorrhagic pancreatitis
 Burns
 Complicated abdominal surgery
 Narcotic overdose and other drug reactions
Lecture 4
Pathologic features of ARDS

Macroscopic findings: lungs are heavy, filled with fluid, firm, red, and
boggy
Microscopic findings in acute stage: congestion, interstitial and

intraalveolar edema, inflammation, and fibrin deposition along inside of
alveoli in form of hyaline membranes
Healing stage: characterized by organization of fibrin exudate, with

resultant intraalveolar fibrosis and marked thickening of alveolar septa
Fatal cases: These often exhibit superimposed bronchopneumonia
 ARDS carries a 40% mortality rate

Lecture 4
ARDS (Diffuse alveolar damage) gross

Lung is virtually airless, diffusely
firm, and rubbery with a
glistening appearance on cut
section
Diffuse alveolar damage (DAD) is

a form of acute restrictive lung
disease resulting from capillary
wall endothelial
injury from multiple causes (slide
15) Klatt EC. Robbins and Cotran Atlas of Pathology, 3rd Ed. 2015
Lung diffusing capacity for carbon

monoxide (Dlco) is reduced
Diffuse alveolar damage, microscopic
 At low magnification (right panel)
all alveoli are filled with fibrin-rich
edema fluid and inflammatory
cells (noncardiogenic edema from
alveolar injury) from damage to
endothelial and epithelial cells
 At medium magnification (left

panel) alveolar walls are congested
and expanded from inflammation
with acute DAD a form of acute
lung injury (ALI)
20
Lecture 4
Pathogenesis of ARDS (DAD)

ARDS is end result of acute alveolar injury caused by a variety of insults,
whereas respiratory distress syndrome of newborns is caused by
deficiency in pulmonary surfactant
 In ARDS, initial injury affects capillary endothelium (most frequently) or alveolar
epithelium (occasionally), but in end both are clearly affected
Increased capillary permeability is caused by an action of leukocytes on

endothelium followed by interstitial and then intraalveolar edema,
fibrin exudation, and formation of hyaline membranes
Exudates and diffuse tissue destruction not easily resolved result is

organization with scarring in contrast to transudate of cardiogenic
pulmonary edema, which usually resolves
Lecture 4
DAD microscopic, hyaline membranes

In early DAD, hyaline
membranes ( ), as seen here,
line alveoli
 Later in first week after lung
injury, hyaline membranes
resolve, and macrophage
proliferation occurs
 If patient survives more than a
week, interstitial inflammation
and fibrosis become
increasingly prominent, and
lung compliance decreases
N.B. High oxygen tension is needed to treat hypoxia
 There are V˙ /Q˙ mismatches resulting from DAD, and oxygen toxicity from this therapy
exacerbates DAD further
Lecture 4
ARDS: Clinical course

 Initially, patients may have no pulmonary symptoms
 ARDS is heralded by profound dyspnea, tachypnea, but chest radiograph

is initially normal  subsequently, progressive cyanosis and hypoxemia
develop, followed by respiratory failure and appearance of diffuse
bilateral infiltrates on x-ray examination
 Hypoxemia can then become unresponsive to oxygen therapy,

sometimes resulting in respiratory acidosis
 Lab Findings:
 Mismatch on ventilation-perfusion scan
 ABG: Hypoxia PaO2/FIO2 < 200

Lecture 4
ARDS: Clinical course (2)

 Patients’ lungs can be divided into areas that are
 infiltrated, consolidated, or collapsed (and thus poorly aerated
and poorly compliant) and
 regions that have almost normal levels of compliance and
ventilation
 Therapy of ARDS is extremely demanding, and disorder is

frequently fatal (40% or greater)
 Remember: High concentrations of oxygen, required in therapy
for ARDS, can contribute to perpetuation of the damage
(oxygen toxicity)

Lecture 4
Diffuse alveolar damage, CT image

 Chest CT scan with “lung
window” setting reveals
extensive brighter bilateral
ground-glass opacifications
of lung parenchyma
consistent with DAD
Lecture 4
Neonatal Respiratory Distress Syndrome

 Etiology: NRDS predisposed by prematurity, maternal diabetes, and
birth by C-section; caused by deficiency of pulmonary surfactant
 Pathology and Pathophysiology: Surfactant deficiency results in
increased surface tension in lung causing alveolar collapse
 Gross: Heavy, purple lung; engorged pulmonary vessels
 Microscopic: Eosinophilic hyaline membranes within alveoli
 Clinical manifestations: Dyspnea, tachypnea, and cyanosis soon after
birth if nonfatal, complications include:
 bronchopulmonary dysplasia
 PDA
 intraventricular brain hemorrhage, and
 necrotizing enterocolitis
 Treatment: Exogenous surfactant at birth to infants under 28 weeks;
corticosteroids to mother before birth; oxygen therapy
Lecture 4
NRDS, microscopic
 Lung in respiratory distress
syndrome of neonate
 Alveoli are atelectatic, and a
dilated alveolar duct is lined by
a fibrin-rich hyaline membrane
(arrows)
Rubin R and Strayer DS Eds. Rubin’s Pathology: Clinicopathologic

Marc Imhotep Cray, M.D. Foundations of Medicine, 2012 27
Lecture 4
NRDS Intraventricular hemorrhage, gross

 Intraventricular hemorrhage in a
premature infant suffering from
respiratory distress syndrome of
the neonate
Rubin R and Strayer DS Eds. Rubin’s Pathology:

Clinicopathologic Foundations of Medicine, 2012

Lecture 4

Lecture 4
Sources and further study:

Sources:
 Damjanov I, Pathology secrets 3rd ed. Philadelphia: Mosby, 2009
 Kemp WL, Burns DK and Brown TG. The Big Picture: Pathology. New York: McGraw-Hill,
2008
 Klatt EC. Robbins and Cotran Atlas of Pathology, 3rd Ed. Philadelphia: Saunders, 2015
 L. Maximilian Buja LM and Krueger GR. Netter’s Illustrated Human Pathology Updated Ed.
Philadelphia: Saunders, 2014
eLearning:
 IVMS General and Systems Pathology Cloud Folder
 Internet Pathology Laboratory for Medical Education: Pulmonary Pathology
Textbooks:
 Kumar V and Abbas AK. Robbins and Cotran Pathologic Basis of Disease 8th ed.
Philadelphia: Saunders, 2014
 Rubin R and Strayer DS Eds. Rubin’s Pathology: Clinicopathologic Foundations of Medicine,
6th Ed. Baltimore: Lippincott Williams & Wilkins, 2012

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Lecture 4

Prepared and presented by

 Severe atelectasis significantly reduces oxygenation and predisposes

 Acquired atelectasis is generally encountered in adults and may be

 It is a reversible disorder (except that caused by contraction)

Four types of atelectasis

Four types of atelectasis (2)

Modified from: Damjanov I, Pathology Secrets 3rd ed. 2009

Marc Imhotep Cray, M.D. 4

Obstruction (or resorption) atelectasis

 Causes of obstructive atelectasis: Aspirated foreign body, tumor, and

 Mediastinal shift: Toward source of atelectasis

Marc Imhotep Cray, M.D. 5

 Causes of compressive atelectasis: Blood in pleural cavity (i.e.,

 Mediastinal shift: Away from source of atelectasis

Marc Imhotep Cray, M.D. 6

Compressive atelectasis (2)

 Note smaller size of left lung and

Marc Imhotep Cray, M.D. 7

 Causes: Prematurity, interstitial

Rubin R and Strayer DS Eds. Rubin’s Pathology: Clinicopathologic

Pulmonary edema: Causes

 Direct increase in capillary permeability

Pathologic features of pulmonary

Marc Imhotep Cray, M.D. 10

Pulmonary edema, PA chest

 Shows pulmonary congestion and

 Pulmonary veins are distended near

 This patient had mitral stenosis

Pulmonary edema, PA chest (2)

Pulmonary edema, microscopic

 Capillaries within alveolar walls

 Pulmonary congestion with

Pulmonary edema, microscopic (2)

Marc Imhotep Cray, M.D. 15

Adult Respiratory Distress Syndrome

 Clinical features: rapid onset of life-threatening respiratory insufficiency,

 Almost always associated with evidence of severe pulmonary edema

Marc Imhotep Cray, M.D. 16

Pathologic features of ARDS

Microscopic findings in acute stage: congestion, interstitial and

Healing stage: characterized by organization of fibrin exudate, with

Fatal cases: These often exhibit superimposed bronchopneumonia

 ARDS carries a 40% mortality rate

Marc Imhotep Cray, M.D. 18

ARDS (Diffuse alveolar damage) gross

Diffuse alveolar damage (DAD) is

Lung diffusing capacity for carbon

 At medium magnification (left

Pathogenesis of ARDS (DAD)

Increased capillary permeability is caused by an action of leukocytes on

Exudates and diffuse tissue destruction not easily resolved result is

DAD microscopic, hyaline membranes

ARDS: Clinical course

 ARDS is heralded by profound dyspnea, tachypnea, but chest radiograph

 Hypoxemia can then become unresponsive to oxygen therapy,

Marc Imhotep Cray, M.D. 23

ARDS: Clinical course (2)

 Therapy of ARDS is extremely demanding, and disorder is

Marc Imhotep Cray, M.D. 24

Diffuse alveolar damage, CT image

Neonatal Respiratory Distress Syndrome

Rubin R and Strayer DS Eds. Rubin’s Pathology: Clinicopathologic

NRDS Intraventricular hemorrhage, gross

Rubin R and Strayer DS Eds. Rubin’s Pathology:

Marc Imhotep Cray, M.D. 28