ARDS and Pathology of ARDS

Question 1

Components of ARDS

Answer 1

Low PaO2 (hypoxemia), bilateral infiltrates, low lung compliance. NO left atrial hypertension (problem is ALL pulmonary).

Question 2

Definition of ARDS

Answer 2

PaO2/FIO2 re getting 100% fio2.

Question 3

Definition of ALI

Answer 3

PaO2/FIO2 <300.

Question 4

Causes of ARDS

Answer 4

Sepsis, pneumonia, aspiration, pancreatitis, burns, trauma, transfusions and toxic inhalation.

Question 5

Pathologic state of ARDS and ALI

Answer 5

Diffuse alveolar damage. This is a failure of the alveolar capillary membrane which causes the flooding of alveolar airspaces with proteinaceous material.

Question 6

Makeup of fluid in the alveolar spaces during ARDS

Answer 6

Proteinaceous

Question 7

What happens when there is diffuse alveolar damage?

Answer 7

Proinflammatory cells release proinflammatory cytokines TNF, IL1, IL8. This also causes the production of oxygen derived free radicals.

Question 8

What is the difference between fluid produced in ARDS and left heart failure?

Answer 8

Left heart failure = clean, not proinflammatory like ARDS

Question 9

What happens during ARDS

Answer 9

Depletion of surfactant, disturbance of microcirculation, and fibroblast proliferation in the late stage.

Question 10

What is the consequence of surfactant depletion?

Answer 10

Atalectasis, gas exchange disturbance and decreased pulmonary compliance

Question 11

What is the consequence of microvascular disturbance?

Answer 11

Altered response to NO, cytokine induced activation of the coagulation cascade. This is enhanced by hypoxemia, so theres a high degree of vasoconstriction occurring.

Question 12

Fibroblast proliferation in the late phase

Answer 12

After day 7, fibroblasts enter to help heal and lay down scartissue.

Question 13

VILI

Answer 13

Ventilator induced lung injury. Positive airway pressure delivered to lung can cause barotrauma and volutrauma. This exacerbates the cytokine release and damages the good area of the lung.

Question 14

Distribution of DAD in the lung?

Answer 14

Diffuse!!! Patchy!

Question 15

Phases of ARDS and timing

Answer 15

Exudative phase to start off: Edema from 0-3d. Hyaline membranes from 1-14d. Proliferative phase begins at day 7 with interstitial inflammation and fibrosis.

Question 16

When do type 2 pneumocytes become hypeprlastic

Answer 16

During the proliferative phase.

Question 17

Imaging of ARDS

Answer 17

Bilateral infiltrates and hypoxemia, but normal left heart function. Imaging tells us nothing about the cause. The xray looks whited out. CT scan reveals the patchy nature of ARDS.

Question 18

Management of ARDS

Answer 18

Treat underlying cause first. ARDS is a syndrome, not a disease. Then engage in lung protective strategy of mechanical ventilation with low tidal volume. Also supportive care like pain management and prevention of DVT

Question 19

What happened to other interventions?

Answer 19

Steroids, prone positioning, inhaled NO. DIdn’t work

Question 20

Outcomes of ARDS

Answer 20

about 40% mortality.

Question 21

What determines the degree of mortality from ARDS

Answer 21

Underlying cause

Question 22

Predictors of mortality in ARDS

Answer 22

Advanced age, sepsis, degree of organ dysfunctions

Question 23

After recovering from ARDS what is the problem

Answer 23

Impaired lung function (restrictive) due to fibrosis.

Question 24

Non-pulmonary sequellae of ARDS

Answer 24

Muscle wasting, polyneuropathy, neurocognitive impairment, depression, anxiety. PTSD

Question 25

Neonatal respiratory distress syndrome

Answer 25

Also called hyaline membrane disease. Occurs from premature birth and lack of surfactant. Symptoms occur within minites of birth and include rapid shallow breathing, nostril flairing, retraction breathing, grunting and cyanosis.

Question 26

CXR for neonatal respiratory distress syndrome?

Answer 26

Ground glass appearance

Question 27

Blood gas for neonatal RDS?

Answer 27

Hypoxemia, hypercapnea

Question 28

Risk factors for NRDS?

Answer 28

Maternal diabetes.

Question 29

How to prevent NRDS

Answer 29

Maternal steroids to induce surfactant production.

Question 30

What is idiopathic DAD known as

Answer 30

Acute Interstitial Pneumonia (AIP)

Question 31

What is DAD?

Answer 31

Diffuse alveolar damage -- caused by diffuse alveolar capillary/epithelial damage. Rapid onset of severe life-threatening respiratory insufficiency, cyanosis, and severe arterial hypoxemia. REFRACTORY to oxygen therapy

Question 32

Pathogenesis of DAD

Answer 32

Not well understood, but potential role of PMNs, endotoxins, complement,

Question 33

What does injury to vascular endothelium cause?

Answer 33

Excess vascular fluid and protein leaking out into the alveoli, eventually cellular necrosis, inflammation and fibrosis

Question 34

Key feature of DAD (SUPER IMPORTANT)

Answer 34

Hyaline Membranes, caused by the exudation of protein rich fluid into the alveoli.

Question 35

What does the recovery of DAD look like histologically?

Answer 35

Hyperplasia of type II pneumocytes and fibrosis.

Question 36

Three histologic stages of DAD

Answer 36

Early/acute exudative stage -- characterized by edema and hyaline membranes. Days 1-7 Proliferative/Organizing Stage. Days 7-21 Fibrotic Stage. Day 21+

Question 37

Gross features of early ARDS

Answer 37

Boggy/wet lung. Heavy. Due to exudates.

Question 38

What do hyaline membranes look like?

Answer 38

Pink membrane. Lots of fibrin in the alveolar spaces.

Question 39

Histology of the proliferative phase?

Answer 39

Hyaline membranes disappear then blue fibroblasts proliferate. Type II pneumocyte hyperplasia.

Question 40

Eosinophilic Pneumonia

Answer 40

Usually due to a parasite like ascaris or filiariasis. Most of these are self limited and include simple eosinophilic pneumonia, tropical eosinophilic pneumonia, chronic eosinophilic pneumonia, acute eosinophilic pneumonia. All of these hav eperipheral eosinophilia except for the acute version

Question 41

How is acute eosinophilic pneumonia different from the others?

Answer 41

No peripheral blood eosinophilia

Question 42

How to treat eosinophilic pneumonia?

Answer 42

Steroids

Question 43

Histology of Eosinophilic pneumonia?

Answer 43

LOTS of eosinophils in the alveolar spaces. Looks like regular pneumonia but has eos instead of neutrophils

Question 44

DAD with eosinophilia?

Answer 44

Acute eosinophilic pneumonia. Has hyaline membranes

Question 45

Organizing Pneumonia

Answer 45

Loose connective tissue in alveoli seen as a manifestation of lung injury from a variety of insults. Formally known as bronchiolitis obliterans organizing pneumonia.

Question 46

Clinical features of organizing pneumonia

Answer 46

Subacute cough and SOB.

Question 47

Histology of organizing pneumonia

Answer 47

Fibroblastic plugs in small airways. Intervening lung is more or less normal. NO other findings like granulomas. Usually need to take a wedge biopsy to confirm this.

Question 48

Why does OP happen?

Answer 48

Many etiologies (lupus, drug reaction, others)

Question 49

What is idiopathic organizing pneumonia called?

Answer 49

Cryptogenic organizing pneumonia