Management of Patients with ACUTE RESPIRATORY DISTRESS SYNDROME (ARDS)

ARDS
Definitions

Severe form of respiratory failure with mortality rate around 50%. Complex clinical syndrome Characterized by progressive hypoxemia. ARDS
PaO2/FIO2 < 150 200 mmHg

ARDS
Epidemiology
Incidence:
5 71 per 100,000

Caused by direct or indirect pulmonary injury.

a. Direct injury - aspiration, pulmonary infection, near drowning, thoracic trauma or toxic inhalation.
b. Indirect injury shock, sepsis, hypothermia, DIC, multiple transfusion eclampsia, pancreatitis, burns

ARDS
Pathophysiology
Profound inflammatory response: Acute lung injury resulting from an unregulated systemic inflammatory response, which damage the alveolar capillary membrane. Injury to lung causing initiation of inflammatory responses that release mediators (histamine), serotenin. Systemic inflammatory response syndrome that activate neutrophil, macrophages).

Continue..
Increase in capillary membrane permeability, which lead to: diffuse blood out of artery to interstitial space.pulmonary edema, Hypoxemia decrease lung compliance. Increase interstitial pressure & damage to alveolar membrane allow fluid to inter alveoli which dilute & deactivate surfactant. (damage epithelial type I) that lead to hypoxemia.

Pathophysiology continue.
Damage of epithelial type II leads to atelectasis occurs, lungs become less compliant & gas exchange impaired (Alveolar collapse due to V/Q mismatching, hypoventilation, intrapulmonary shunting). Hyaline membrane forms & lungs become fibrotic. Hypoxemia becomes refractory & resistant to improvement even with supplemental O2. Metabolic acidosis occurs leading to multiple organs system dysfunction.

Diffuse alveolar damage

acute exudative phase (1-7days) proliferative phase (3-10 days) chronic/fibrotic phase (> 1-2 weeks)

ARDS
Acute Exudative Phase
Basement membrane disruption
Type I pneumocytes destroyed Type II pneumocytes preserved

Surfactant deficiency
inhibited by fibrin decreased type II production

Microatelectasis/alveolar collapse

Phase I

ARDS
Acute Exudative Phase

ARDS
Proliferative Phase
Type II pneumocyte
proliferate differentiate into Type I cells reline alveolar walls

Fibroblast proliferation
interstitial/alveolar fibrosis

ARDS
Fibrotic Phase
Characterized by:
local fibrosis vascular obliteration

Repair process:
resolution vs fibrosis

Phase II

Phase III

Phase IV

ARDS
Pathophysiology
Interstitial/alveolar edema Severe hypoxemia
due to intra-pulmonary shunt (V/Q = 0) shunt ~ 25% - 50%

Increased airway resistance

ARDS
Pathophysiology
High ventilatory demands
high metabolic state increased VD/VT decreased lung compliance

Pulmonary HTN
neurohumoral factors, hypoxia, edema

ARDS (Etiology)

ARDS
Etiology
Hospital-acquired
infection/sepsis massive blood transfusions gastric aspiration

Community-acquired
trauma pneumonia drugs/aspiration/inhalations

Clinical Manifestations
ARDS develops about 24-72 hrs post initial insult. Manifestations: Stage I (first 12hrs): Dyspnea, Tachypnea, restlessness, normal CXR Respiratory alkalosis. Use of accessory respiratory muscles. Elevated PAP, normal PAWP.

Stage II (24hrs): Client increases respiratory rate & uses accessory muscles. Client becomes cyanotic, dyspnic (severe) and develops crackles. Increase agitation & restlessness. X-ray show alveolar infiltration. Decrease SaO2 despite O2 therapy. Metabolic acidosis. Elevated PAP & Normal PAWP.

Stage III (2-3 days)

Continued resp failure results (worsening hypoxemia),

hemodynamic instability & mental confusion. Systemic Inflammatory Syndrome presentation. Increase interstitial & alveolar inflammatory exudates. X-ray shows diffused alveolar infiltration & decreased lung volume. Decrease GI motility. Generalized edema. Poor skin integrity. Increased WBC, decrease Hb & Platelets. Abnormal clotting factors.

Stage IV (>10 days).

Multiple organ failure or single respiratory system involvement with

gradual improvement over time. Decrease UO, GI motility, impaired coagulation. Difficulty maintaining adequate oxygenation. Worsening hypoxemia & hypercapnia. Sepsis, pneumonia, & multi-system involvement. X-ray shows persistent infiltrates & new pneumonic infiltrates & Pneumothorax. Thickening of interstitial wall with fibrosis, macrophages, & remodling of arterioles.

ARDS
Clinical Features
Acute dyspnea/tachypnea
rales/rhonchi/wheezing

Resistant hypoxemia
PaO2/FIO2 < 150 200 mmHg

CXR
diffuse, bilateral infiltrates

No evidence of LV failure
(PAWP < 18 mmHg)

ARDS
Clinical Features: CXR

Diagnosis of ARDS Physicians diagnose ARDS when: A person suffering from severe infection or injury develops breathing problems. A chest x-ray shows fluid in the air sacs of both lungs. Arterial blood gases show a low level of oxygen in the blood Other conditions that could cause breathing problems have been ruled out. ARDS can be confused with other illnesses that have similar symptoms. The most important is congestive heart failure. In congestive heart failure, fluid backs up into the lungs because the heart is weak and cannot pump well. However, there is no injury to the lungs in congestive heart failure. Since a chest x-ray is abnormal for both ARDS and congestive heart failure, it can be difficult to tell them apart.

Diagnostic procedure
ABGs Hypoxemia PaO2 < 60mmHg. Respiratory acidosis. CXR After 24 hrs of onset shows white out period. PFTs Decrease lung compliance & reduced vital capacity. PAP Differentiates ARDS from pulmonary edema.

managing
Monitoring: Respiratory Hemodynamic Metabolic Infections Fluids/electrolytes

Managements
History to identify contributing factors for ARDS (behavioral, social, medications). Treat cause if possible, for example give antibiotics. Intubation & mechanical ventilation with O2 set to maintain PO2 >60mmHg, & O2Sat is 90% or more. Low tidal volume. High PEEP. Inverse ration of ventilation 2:1or 3:1. Monitor fluid balance (I &O), ABGs level & VS. Nutrition enteral or TPN: 35-45 kcal/day. Risk for aspiration. Prevent complications (DVT, Nosocomial infection, skin breakdown). Positioning (frequent changed, prone), Sedation to promote comfort & reduce respiratory efforts.

Pharmacological Managements
Antibiotics. Bronchodilators & mucolytics. Exogenous surfactant replacement therapy. Nitric oxide (inhaled to cause selective pulmonary

vasodilation & reduce pulmonary hypertension) in the first 24hrs of ARDS. Antioxidant, antilipids, antibodies, anticytokine agent did not show positive effects on the outcome of ARDS treatment.

ARDS
Treatment: Standard
Rx underlying cause Adequate oxygenation/ventilation
PaO2 > 60 mmHg; SaO2 > 90%

PEEP usually needed to meet O2 goals

Prevents/corrects alveolar collapse converts: (V/Q = 0) to V/Q mismatch

PEEP Effects
Increases transpulmonary distending pressure Displaces edema fluid into interstitium Decreases atelectasis Decrease in right to left shunt Improved compliance Improved oxygenation

Prone Positioning
Positioning the patient in the prone position has been shown to improve oxygenation and reduce ventilator induced lung injury.

How does the lung heal? Resorption of alveolar fluid

Removal of alveolar protein

Type II cell proliferation Resolution of inflammation

Complications of ARDS Anyone who stays in the hospital for a long period of time is at greater risk for complications. Common complications in ARDS patients are infections with hospital-acquired infections and pneumothorax. Infections The lungs or other parts of the body may become infected. Infections are treated aggressively to prevent sepsis from developing. Cultures help determine the appropriate antibiotic therapy. Pneumothorax Subcutaneous Emphysem.

Conclusion ARDS is breathing failure that can occur in critically ill persons with underlying illnesses. It is a life-threatening condition that occurs when there is severe fluid build-up in both lungs. Knowledge about its causes, treatments, and complications will help the nurse or other healthcare provider to more effectively manage patient care and provide support to family members.

Thank You