This document discusses Acute Respiratory Distress Syndrome (ARDS), a clinical syndrome characterized by severe lung inflammation and injury leading to hypoxemia. It is most commonly caused by pneumonia, sepsis, aspiration, or trauma. The pathogenesis involves an initial exudative inflammatory phase, followed by a proliferative phase and possible fibrotic phase. Diagnostic tests include blood gases, chest X-rays, and CT scans. Treatment focuses on treating the underlying cause, administering oxygen, antibiotics, and corticosteroids. Nursing management centers around pulmonary toilet, monitoring fluid balance, improving breathing and nutrition, and mobilizing the patient.

1. Acute Respiratory Distress
Syndrome
TOPIC

2. Synonyms
 Adult Respiratory Distress Syndrome
 Acute Lung Injury (ALI)
 Shock Lung
 Traumatic Wet Lung
 Diffuse Alveolar Injury

3. ARDS Definition
 Severe, acute lung injury involving diffuse
alveolar damage, increased microvascular
permeability and non cardiogenic pulmonary
edema.
 Acute refractory hypoxemia
 High mortality- 40%-60%
 First described in 1967

4. PATHOGENESIS
EXUDATIVE PROLIFERATIVE
DAY 0-7 14
FIBROTIC
21..
EDEMA
HYALINE
MEMBRANES
INTERSTITIALS
INFLAMMATION
INTERSTITIAL
FIBROSIS
FIBROSIS
4

5. Pathophysiology
3 phases:
1) Exudative (inflamatory): damage to the
alveolar epithelium and vascular endothelium
→ leakage of water, protein, inflammatory
and red blood cells into the interstitium and
alveolar lumen.
 Alveolar Type 1 cell → Hyaline membrane
 Alveolar Type 2 cell → Alveolar collapse

6. Pathophysiology
2) Proliferative :
Type 2 cells proliferate with some epithelial
cell regeneration, fibroblastic reaction, and
remodeling.
3) Irreversible fibrotic phase : occasionally,
collagen deposition in alveolar, vascular
and interstitial beds with development of
microcysts.

7. PATHOGENESIS(con’t)
7

8. NORMAL ALVEOLUS
Type I cell
Endothelial
Cell
RBC’s
Capillary
Alveolar
macrophage
Type II
cell

9. ACUTE PHASE OF ARDS
Type I cell
Endothelial
Cell
RBC’s
Capillary
Alveolar
macrophage
Type II
cell
Neutrophils

10. Most common causes ARDS
Pneumonia (34%)
Sepsis (27%)
Aspiration (15%)
Trauma (11%)
Pulmonary contusion
Multiple fractures
ARDSnet NEJM 2000:342:1301-8.

13. Diagnostic Tests
 An arterial blood gas test. This blood test shows the oxygen
level in your blood. A low level of oxygen in the blood may be a
sign of ARDS.
 Chest x ray. This test is used to take a picture of your lungs. It
can show whether you have extra fluid in your lungs.
 Blood tests, such as a complete blood count, blood chemistries,
and blood cultures. These tests help find the cause of ARDS,
such as an infection.
 Sputum cultures. This test looks at the spit you've coughed up
from your lungs. It can help find the cause of an infection.
 Computed tomography or CT, scan. This test uses a computer
to take detailed pictures of your lungs. It may show lung
problems, such as fluid in the lungs, signs of pneumonia, or a
lung tumor.

15. TREATMENT
 Antiinflammatory therapies : Corticosteroids,
Neutrophil elastase inhibitors, Arachidonic acid
Inhibitors.
 Surfactant.
Nowaday, the new points are based on
clinical evidences, we should give
corticosteroid in the fibroproliferative phase
of ARDS, 7-14 days, without evidence of
infection.
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16. Nursing Management:
1. Administer prescribed medications, such as antibiotics, cardiac
medications, bronchodilators,mucolytics, corticosteroids and
diuretics as ordered.
2. Monitor fluid balance by intake and output measurement, daily
weight.
3. Perform chest physiotherapy and suctioning to remove mucus. Teach
slow, pursed lip breathing to reduce airway obstruction.
4. If the patient becomes increasingly lethargic, can not cough or
expectorate secretions, can not cooperate with therapy, or if PH falls
below 7.30, despite use of the above therapy, report and prepare to
assist with intubation and initiation of mechanical ventilation.

18. 5. Improving breathing pattern
a. Encourage breathing, coughing exercises.
b. Use pursed- lip breathing at intervals and during periods of
dyspnea
6. Improving gas exchange
a. Check ABG’s.
b. Administer oxygen.
c. Inspiratory muscle training.
7. Improving nutrition.
a. Encourage frequent small meals if pt. is dyspneic.
b. Avoid foods producing gas and abdominal discomfort.
c. Monitor body weight.
Nursing Management:

19. Nursing Management:
8. Increasing activity tolerance.
a. Encourage pt. to carry out regular exercise program.
b. Encourage use of portable oxygen system for
ambulation for patient’s with hypoxemia.
9. Instruct the pt. do not do activities that increase venous
stasis such as crossing legs, sitting or standing for long
periods. Instruct pt. to elevate the legs above the level
of heart.

20. Hospitalized the patient.

22. Summary
 ARDS is a clinical syndrome characterized by
severe, acute lung injury, inflammation and
scarring.
 Significant cause of ICU admissions, mortality
and morbidity
 Caused by either direct or indirect lung injury
 Mechanical ventilation with low tidal volumes and
plateau pressures improves outcomes
 So far, no pharmacologic therapies have
demonstrated mortality benefit.
 There is no really specific therapy for ARDS.

23. REFERENCES:
1. Potter PA, Perry AG. Fundamentals of
nursing. 6th ed. St.Louis: Elsevier
Mosby; 2006.
2. New Management strategies in ARDS.
Editor Levy MM. Critical Care Clinics,
January 2002
3. www.worldhealth.org.
4. ww.Answers.com.

24. Thanks for your keen concentration