> Table of Contents > Respiratory Distress Syndrome, Acute (ARDS)
Respiratory Distress Syndrome, Acute (ARDS)
Muhammad Imran Khan, MD
Najm Hasan Siddiqui, MD
image BASICS
DESCRIPTION
  • ARDS is an acute, diffuse, inflammatory lung injury that leads to increased pulmonary vascular permeability, increased lung weight, and a loss of aerated tissue (1) with clinical hallmarks of severe hypoxemia and bilateral pulmonary infiltrates.
    • Absence of left atrial hypertension (HTN)
    • By consensus, PaO2/FiO2 <200
    • Most severe form of acute lung injury
  • System(s) affected: pulmonary; cardiovascular
  • Synonym(s): shock lung; wet lung; noncardiac pulmonary edema
EPIDEMIOLOGY
Incidence
ARDS: 10.1 to 86.2 cases/100,000 annually (2)
ETIOLOGY AND PATHOPHYSIOLOGY
Three phases
  • Acute exudative phase: characterized by profound hypoxia and associated with inflammation with infiltration of inflammatory and proinflammatory mediators and diffuse alveolar damage
  • Fibrosing alveolitis phase: coincides with recovery or after ˜1 to 2 weeks; patients continue to be hypoxic and have increased dead space and decreased compliance
  • Resolution may require 6 to 12 months.
  • Several mediators are involved in the initiation and perpetuation of ARDS.
    • Cytokines
    • Complement activation
    • Coagulation activation
    • Platelet-activating factor
    • Oxygen free radicals
    • Lipoxygenase pathways
    • Neutrophil proteases
    • Nitric oxide
    • Endotoxin
    • Cyclooxygenase pathway products
  • Systemic inflammatory response with activation of the previous mediators can occur with direct or indirect injury to the lung.
    • Direct
      • Aspiration
      • Pulmonary infections
      • Air, fat, or amniotic fluid emboli
      • Near-drowning
      • Pulmonary contusion
      • Inhalation of toxic gases and dusts
    • Indirect
      • Sepsis
      • Shock
      • Transfusion
      • Trauma
      • Overdose
      • Pancreatitis, severe
      • Eclampsia
RISK FACTORS
  • Severe infection (localized or systemic) most common
  • Aspiration of gastric contents
  • Shock
  • Infection
  • Trauma with or without lung contusion
  • Pneumonia
  • Toxic inhalation
  • Pancreatitis
  • Fat embolism
  • Near drowning
  • Multiple blood transfusions
GENERAL PREVENTION
No effective measures have been identified.
COMMONLY ASSOCIATED CONDITIONS
  • Severe sepsis
  • Trauma
  • Shock
image DIAGNOSIS
PHYSICAL EXAM
  • Tachypnea and tachycardia during the first 12 to 24 hours; respiratory distress
  • Lethargy, obtundation
  • Flat neck veins
  • Hyperdynamic pulses
  • Physiologic gallop
  • Absence of edema
  • Moist, cyanotic skin
  • Manifestations of underlying disease
DIFFERENTIAL DIAGNOSIS
  • Left ventricular failure
  • Interstitial and airway diseases
  • Hypersensitivity pneumonitis
  • Veno-occlusive disease
  • Mitral stenosis: intravascular volume overload
  • Toxic shock syndrome
DIAGNOSTIC TESTS & INTERPRETATION
Initial Tests (lab, imaging)
  • Arterial blood gases (ABGs) show evidence of severe hypoxemia.
  • PaO2/FiO2 <200
  • ECG: sinus tachycardia; nonspecific ST-T-wave changes
  • Pulmonary artery wedge pressure (PAWP) <15 mm Hg
  • Cardiac index >3.5 L/min/m2
  • Chest x-ray (CXR): normal heart size; fluffy, bilateral infiltrates; air bronchograms common
  • Chest CT scan: diffuse interstitial opacities and bullae
Follow-Up Tests & Special Considerations
  • Serial blood gases
  • Monitor for and treat multisystem organ failure when it occurs.
  • Serial CXRs
Diagnostic Procedures/Other
Invasive monitoring of vital signs, cardiac output, and PAWP has been questioned by large clinical trials.
Test Interpretation
  • Lungs show exudative, early proliferative or late proliferative phases.
  • Interstitial and alveolar edema is present.
  • Inflammatory cells and erythrocytes spill into the interstitium and the alveolus.
  • Type 1 cells are destroyed, leaving a denuded basement membrane.
  • Protein-rich fluid fills the alveoli.
  • Type 2 alveolar cells initially appear unaltered.
  • Type 2 cells begin to proliferate within 72 hours of initial insult and cover the denuded basement membrane.
  • Aggregates of plasma proteins, cellular debris, fibrin, and surfactant remnants form hyaline membranes.
  • Over the next 3 to 10 days, alveolar septum thickens by proliferating fibroblasts, leukocytes, and plasma cells.
  • Capillary injury begins to occur.
  • Hyaline membranes begin to reorganize.
  • Fibrosis becomes apparent in respiratory ducts and bronchioles.
image TREATMENT
GENERAL MEASURES
  • Ensure adequate oxygenation.
  • Ventilatory support generally requires endotracheal intubation and use of positive end-expiratory pressure (PEEP) (3)[A].
  • Provide appropriate cardiorespiratory monitoring.
  • Fluid management
MEDICATION
  • No single drug or combination of drugs prevents or treats full-blown ARDS. Treatment is supportive while addressing the underlying cause.
  • Supplemental oxygen
  • Ventilatory support
    • Most often requires endotracheal intubation with emphasis on lower tidal volumes per weight and optimization of PEEP
    • High-frequency oscillation ventilation seems not to increase the risk of barotrauma or hypotension and reduces the risk of oxygenation failure, it does not improve survival in adult ARDS patients (4)[A].
ISSUES FOR REFERRAL
  • All patients with ARDS should be cared for in an ICU with appropriately trained staff.
  • Pregnant patients with ARDS also should be followed by a high-risk perinatologist or obstetrician.
ADDITIONAL THERAPIES
  • Inotropic agents: dobutamine to maintain adequate cardiac output after appropriate fluid resuscitation fails to restore perfusion
  • Corticosteroids: Short-term use during the acute phase has not been shown to be effective. However, prolonged methylprednisolone treatment accelerates the resolution of ARDS, improving a broad spectrum of interrelated clinical outcomes and decreasing hospital mortality and healthcare utilization (5)[A].
  • Vasodilators: Inhaled nitric oxide (INO) is not recommended for patients with ARDS. INO results in a transient improvement in oxygenation but does not reduce mortality and may be harmful (6)[A].
  • Pulmonary surfactant: successful in neonatal respiratory distress syndrome; investigational outside this age group
  • Inhaled &bgr;2-agonists may be helpful during the resolution phase.
  • P.905

  • There is no current evidence to support or refute the routine use of aerosolized prostacyclin for patients with ARDS (7)[A].
  • There is no effect on mortality with granulocytemacrophage colony-stimulating factor, neutrophil elastase inhibitors, intravenous salbutamol, surfactant, or N-acetylcysteine (8)[A].
  • Early use of neuromuscular-blocking agent treatment of patients with severe sepsis and severe ARDS cannot only improve the severity but also reduce 21-day mortality (9)A].
  • Antioxidants (e.g., Procysteine) have produced conflicting results.
  • Activated protein-C may be helpful in patients with sepsis.
  • Deep vein thrombosis (DVT) prophylaxis
  • Ulcer prophylaxis
Pregnancy Considerations
Supportive care while identifying the underlying cause of ARDS continues to be important in the management of pregnant women with ARDS. However, fetal well-being, possible need for delivery, and physiologic changes associated with pregnancy must be considered.
INPATIENT CONSIDERATIONS
Admission Criteria/Initial Stabilization
All patients with ARDS should be managed in an ICU setting.
  • Consider prone positioning.
  • Identify and treat underlying condition.
  • Circulatory support, adequate fluid volume, and nutritional support
  • Supplemental oxygen
  • Monitoring blood gases, pulse oximetry, bedside pulmonary function test
  • Support ventilation using lung-protective strategies and PEEP.
  • Monitor for systemic hypotension and hypovolemia without fluid overload.
  • BP support, if necessary
  • Vasopressor agents
  • Fluid management with IV crystalloid solutions while monitoring pulmonary status
  • Pulmonary catheter pressure monitoring
  • Treat underlying disease process.
  • Prevent complications.
IV Fluids
  • Maintain the intravascular volume at the lowest level consistent with adequate perfusion (assessed by metabolic acid-base balance and renal function).
  • If perfusion is inadequate after restoration of intravascular volume (e.g., septic shock), vasopressor therapy is indicated.
  • Increase oxygen content with packed erythrocyte transfusions as necessary.
  • Provide appropriate nutritional support with enteral or parenteral nutrition.
  • Steroid therapy
Nursing
May include any or all of the following:
  • Skin, eye, and mouth care
  • DVT prophylaxis
  • GI prophylaxis
  • Suctioning
  • Ensure adequate level of sedation and/or paralysis while on mechanical ventilation.
  • Oxygen supplementation
  • Nebulizer therapy
  • Chest physiotherapy
  • Tracheostomy care
  • Explain all procedures to patient and family; reduce anxiety.
Discharge Criteria
  • Supplemental oxygen
  • Nutrition counseling
  • Family monitoring of signs and symptoms of respiratory distress
image ONGOING CARE
FOLLOW-UP RECOMMENDATIONS
Patient Monitoring
  • Vital capacity and static lung compliance are important measures of lung mechanics.
  • Daily labs are needed until the patient is no longer critical.
  • CXRs to assess endotracheal tube placement, the presence of progressing infiltrates, catheter placement, and complications of mechanical ventilation (e.g., air leaks)
  • A Swan-Ganz catheter to assess oxygen delivery, oxygen consumption, and cardiac output may be helpful but has not been shown to improve survival.
DIET
  • Nutritional support
  • Conservative fluid management shortens ventilator and ICU time but does not affect survival.
PATIENT EDUCATION
ARDS support center and brochure titled “Learn About ARDS”: www.ards.org
PROGNOSIS
  • Mortality rate is 43% (10).
  • Survivors may have pulmonary sequelae with mild abnormalities in oxygenation, diffusion, and lung mechanics, as well as some pulmonary symptoms of cough and dyspnea.
  • The prognosis worsens with elevated cardiac troponin-T levels in ARDS patients (11).
REFERENCES
1. Ranieri VM, Rubenfeld GD, Thompson BT, et al. Acute respiratory distress syndrome: the Berlin definition. JAMA. 2012;307(23):2526-2533.
2. Riviello ED, Kiviri W, Twagirumugabe T, et al. Hospital incidence and outcomes of ARDS using the Kigali modification of the Berlin definition [published online ahead of print September 9, 2015]. Am J Respir Crit Care Med.
3. Petrucci N, Iacovelli W. Ventilation with lower tidal volumes versus traditional tidal volumes in adults for acute lung injury and acute respiratory distress syndrome. Cochrane Database Syst Rev. 2004;(2):CD003844.
4. Gu XL, Wu GN, Yao YW, et al. Is high-frequency oscillatory ventilation more effective and safer than conventional protective ventilation in adult acute respiratory distress syndrome patients? A meta-analysis of randomized controlled trials. Crit Care. 2014;18(3):R111.
5. Meduri GU, Bridges L, Shih MC, et al. Prolonged glucocorticoid treatment is associated with improved ARDS outcomes: analysis of individual patients’ data from four randomized trials and trial-level meta-analysis of the updated literature [published online ahead of print October 27, 2015]. Intensive Care Med.
6. Afshari A, Brok J, Møller AM, et al. Inhaled nitric oxide for acute respiratory distress syndrome (ARDS) and acute lung injury in children and adults. Cochrane Database Syst Rev. 2010;(7):CD002787.
7. Afshari A, Brok J, Møller AM, et al. Aerosolized prostacyclin for acute lung injury (ALI) and acute respiratory distress syndrome (ARDS). Cochrane Database Syst Rev. 2010;(8):CD007733.
8. Duggal A, Ganapathy A, Ratnapalan M, et al. Pharmacological treatments for acute respiratory distress syndrome: systematic review. Minerva Anestesiol. 2015;81(5):567-588.
9. Lyu G, Wang X, Jiang W, et al. Clinical study of early use of neuromuscular blocking agents in patients with severe sepsis and acute respiratory distress syndrome [in Chinese]. Zhonghua Wei Zhong Bing Ji Jiu Yi Xue. 2014;26(5):325-329.
10. Zambon M, Vincent JL. Mortality rates for patients with acute lung injury/ARDS have decreased over time. Chest. 2008;133(5):1120-1127.
11. Rivara MB, Bajwa EK, Januzzi JL, et al. Prognostic significance of elevated cardiac troponin-T levels in acute respiratory distress syndrome patients. PLoS One. 2012;7(7):e40515.
Additional Reading
&NA;
  • Cole DE, Taylor TL, McCullough DM, et al. Acute respiratory distress syndrome in pregnancy. Crit Care Med. 2005;33(10)(Suppl):S269-S278.
  • Wheeler AP, Bernard GR. Acute lung injury and the acute respiratory distress syndrome: a clinical review. Lancet. 2007;369(9572):1553-1564.
Codes
&NA;
ICD10
J80 Acute respiratory distress syndrome
Clinical Pearls
&NA;
  • ARDS is a syndrome characterized by an abrupt onset of diffuse lung injury with severe hypoxemia and bilateral pulmonary infiltrates.
  • Treatment of ARDS requires aggressive supportive care in an ICU setting while also addressing the underlying cause.
  • The benefit of invasive monitoring of vital signs, cardiac output, and PAWP has been questioned by large clinical trials.