Atelectasis, Pulmonary Edema, Acute Lung Injury and Acute - PowerPoint Presentation

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Atelectasis, Pulmonary Edema, Acute Lung Injury and AcuteRespiratory Distress Syndrome

By:

Shefaa

’

Qa’qa

’

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Atelectasis (Collapse)

Atelectasis

refers either to

incomplete expansion of the lungs

(neonatal atelectasis) or to the collapse of previously inflated lung, producing areas of relatively airless pulmonary parenchyma.

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The main types of

acquired atelectasis

, which is encountered principally in

adults

, are the following:

1.

Resorption

atelectasis:

- stems from

complete obstruction of an airway

. Over time, air is resorbed from the dependent alveoli, which collapse.

- Since lung volume is diminished, the

mediastinum shifts toward

the

atelectatic

lung.

- Airway obstruction is most often caused by excessive secretions (e.g.,

mucus plugs

) or exudates within smaller bronchi, as may occur in bronchial

asthma

,

chronic bronchitis

,

bronchiectasis

, and

postoperative states

.

Aspiration

of foreign bodies and, rarely,

fragments of bronchial tumors may also lead to airway obstruction and atelectasis.

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2. Compression atelectasis:

- Results whenever significant volumes of fluid (transudate, exudate or blood), tumor, or air (pneumothorax) accumulate within the pleural cavity.

The mediastinum

shifts away from the affected lung.

3. Contraction atelectasis:

occurs when focal or generalized pulmonary or pleural

fibrosis

prevents full lung expansion.

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Significant atelectasis reduces oxygenation and predisposes to infection.

Except in cases caused by contraction, atelectasis is a reversible disorder.

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Pulmonary Edema

Pulmonary

edema: leakage

of excessive interstitial

fluid which

accumulates in alveolar

spaces.

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Hemodynamic Pulmonary Edema

due to

increased

hydrostatic

pressure

, as occurs most commonly in

left sided congestive

heart failure

.

Fluid accumulates

initially in

the basal regions of the lower lobes because

hydrostatic pressure

is greatest in these sites (

dependent edema

).

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Histologically, the alveolar capillaries

are engorged

,

and an

intra-alveolar transudate appears as finely granular

pale pink

material.

Alveolar

microhemorrhages

and

hemosiderin laden macrophages

(“

heart failure” cells

) may be present.

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In long-standing

pulmonary congestion (e.g., as seen in

mitral stenosis

), hemosiderin-laden macrophages are

abundant, and

fibrosis and thickening of the alveolar walls cause

the soggy

lungs to become firm and brown (

brown induration

).

These changes not only impair normal respiratory

function but

also predispose to infection.

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Edema Caused by Microvascular (Alveolar) Injury

Non-cardiogenic

pulmonary

edema.

Primary

injury to the vascular

endothelium or

damage to alveolar epithelial cells (with

secondary

microvascular

injury) produces an inflammatory

exudate that

leaks into the interstitial space and, in more

severe cases

, into the alveoli

.

Localized

Diffuse ------- acute

respiratory distress syndrome

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Acute Lung Injury and AcuteRespiratory Distress Syndrome(Diffuse Alveolar Damage)

Acute lung injury (

ALI) also

called

noncardiogenic

pulmonary edema

.

characterized

by the abrupt onset

of significant

hypoxemia

and

bilateral pulmonary

infiltrates

in

the absence of cardiac failure.

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Acute respiratory distress syndrome (ARDS) is a manifestation of severe ALI.

The

histologic

manifestation of

these diseases is diffuse alveolar damage (DAD).

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ALI is a well-recognized complication of diverse

conditions, including

both direct injuries to the lungs and

systemic disorders.

In

many cases, a

combination of

predisposing conditions is responsible (e.g.,

shock, oxygen

therapy, and sepsis).

Nonpulmonary

organ

dysfunction may

also be present in severe cases

.

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Pathogenesis:

ALI/ARDS

is initiated by injury of

pneumocytes

and

pulmonary endothelium, setting in motion

a viscous

cycle of increasing inflammation and

pulmonary damage.

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Endothelial activation

is an important early

event:

Directly-

--- circulating

inflammatory mediators (

e.g

, sepsis)

Secondary to

pneumocyte

injury----inflammatory

mediators from resident inflammatory

cells (

alveolar macrophages--- TNF)

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Adhesion and extravasation of neutrophils.

they

degranulate

and

release inflammatory mediators, including

proteases, reactive

oxygen species, and cytokines. causing

more

endothelial

injury

, and local thrombosis.

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Accumulation of

intraalveolar

fluid and formation of

hyaline membranes.

Endothelial activation and injury make

pulmonary

capillaries

leaky

, allowing interstitial

and Intra-alveolar

edema fluid to form.

Damage

and

necrosis of

type II alveolar

pneumocytes

leads to

surfactant abnormalities

, further compromising alveolar

gas exchange

.

Ultimately

, the

inspissated

protein-rich edema

fluid and debris from dead alveolar

epithelial cells

organize into hyaline membranes, a

characteristic feature

of ALI/ARDS.

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Resolution of injury is impeded

in ALI/ARDS due

to epithelial

necrosis and inflammatory damage

that impairs

the ability of remaining cells to assist

with edema

resorption

.

Eventually, however, if the

inflammatory stimulus

lessens,

macrophages

remove

intraalveolar

debris

and release

fibrogenic

cytokines such

as (

TGF-β) and

(

PDGF) leading

to fibrosis

of alveolar walls

.

Bronchiolar stem cells

proliferate to

replace

pneumocytes

.

Endothelial restoration occurs

through proliferation of uninjured

capillary endothelium

.

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Clinical

Course:

Individuals

who develop ALI are

usually hospitalized

for one of the predisposing conditions

listed earlier

. Profound

dyspnea

and

tachypnea

herald ALI,

followed by

increasing

cyanosis

and

hypoxemia

,

respiratory failure

, and the appearance of

diffuse bilateral infiltrates

on radiographic

examination

.

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Hypoxemia may be refractory to oxygen therapy due to

ventilation perfusion

mismatching.

The functional abnormalities in ALI are not evenly

distributed

throughout

the lungs

. The lungs have areas

that are

infiltrated, consolidated, or collapsed (and thus

poorly aerated

and poorly compliant) and regions that have

nearly normal

levels of compliance and ventilation.

Poorly

aerated regions

continue to be perfused, producing

ventilation perfusion mismatch

and hypoxemia.

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There are

no proven specific treatments

; however,

due to

improvements in therapy for sepsis, mechanical

ventilation, and

supportive care, the mortality rate among

the 200,000

ALI/ARDS cases seen yearly in the United

States has

decreased from 60% to about 40%,

with

the majority

of deaths

attributable to sepsis or

multiorgan

failure and,

in some

cases, direct lung injury.

Most

survivors recover

pulmonary function

but many have persistent impairment

in physical

and cognitive functions.

In

a minority of

patients, the

exudate and diffuse tissue destruction result in

scarring, interstitial

fibrosis, and chronic pulmonary disease.