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Acute Respiratory Distress Syndrome

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Acute Respiratory Distress Syndrome, Adult Respiratory Distress Syndrome, Acute Lung Injury, ARDS, Traumatic Wet Lung, Shock Lung, Congestive Atelectasis, PaO2/FIO2 Ratio

  • Definition
  1. Acute Respiratory Distress Syndrome (ARDS)
    1. Acute onset of Dyspnea, Tachypnea, Hypoxemia, and bilateral Interstitial Infiltrates
    2. Rapidly progresses to Respiratory Failure
    3. Non-cardiogenic pulmonary edema (contrast with Congestive Heart Failure)
  2. Acute Lung Injury (ALI)
    1. Slightly less severe form of ARDS in hospitalized patients with less severe Hypoxemia than ARDS
  • Epidemiology
  1. Incidence
    1. Acute Lung Injury (ALI)
      1. Adults: Up to 86 cases per 100,000 person years
      2. Children: 9.5 cases per 100,000 person years
    2. Acute Respiratory Distress Syndrome (ARDS)
      1. Adults: Up to 64 cases per 100,000 person years
      2. Children: 12.8 cases per 100,000 person years
  2. References
    1. Rubenfeld (2005) N Engl J Med 353(16): 1685-93 [PubMed]
    2. Zimmerman (2009) Pediatrics 124(1): 87-95 [PubMed]
  • Pathophysiology
  1. Acute, bilateral, complete lung inflammation
    1. Onset 24-48 hours after major Trauma or severe illness
    2. Variant of multi-system organ failure (e.g. Acute Tubular Necrosis, Disseminated Intravascular Coagulation)
  2. Development: Neutrophil mediated endothelial damage
    1. Inflammatory mediator proliferation leads to Neutrophil accumulation within the lung microcirculation
      1. Neutrophils activate and cross the vascular endothelium and the alveolar epithelium
      2. Neutrophils release proteases, cytokines, and reactive oxygen species
    2. Inflammatory mediator cause local destruction
      1. Vascular permeability increases to protein rich fluid
      2. Gaps form at the alveolar epithelial barrier
      3. Alveolar cell (type I and II) necrosis
    3. Local tissue effects ultimately decrease lung compliance and interfere with gas exchange
      1. Low-pressure pulmonary edema
      2. Hyaline membrane formation
      3. Surfactant loss
    4. Fibroblasts infiltrate region of inflammation
      1. Collagen deposition
      2. Fibrosis
      3. Disease progression
  3. Recovery
    1. Neutrophils are deactivated by anti-inflammatory cytokines
      1. Neutrophils undergo apoptosis and later phagocytosis
    2. Alveolar cells proliferate
      1. First Type II, which differentiate into type I
    3. Osmotic gradient reverses
      1. Draws fluid out of alveoli and back into lymphatics and lung microcirculation
    4. Macrophages and alveolar cells activity
      1. Remove protein depositions from the alveoli
  4. Models of pathogenesis
    1. ARDS is analogous to other system failures
      1. Disseminated Intravascular Coagulation (DIC)
      2. Acute Tubular Necrosis (ATN)
    2. Surfactant disorder
      1. Neonatal Respiratory Distress Syndrome
    3. Fibrosis
      1. Idiopathic Pulmonary Fibrosis (chronic)
    4. Granulation
      1. Healing superficial Skin Wound
    5. Microatelectasis
  • Risk factors
  1. Chronic lung disease
  2. Alcoholism
  3. Age over 65 years
  4. ICU admission (7% develop ALI or ARDS)
  5. Mechanical Ventilation (16% develop ALI or ARDS)
  • Causes
  1. Direct lung injury
    1. Pneumonia (highest risk)
    2. Respiratory Syncytial Virus
    3. Gastric acid aspiration
    4. Pulmonary Contusion
    5. Fat embolism
    6. Toxic Inhalation Injury
      1. Smoke Inhalation
      2. Chlorine
      3. Nitrogen dioxide
      4. Phosgene
      5. Ammonia
      6. Cocaine
      7. Clove Cigarettes
    7. Near-drowning (high risk)
    8. Severe Pulmonary Hemorrhage
    9. Oxygen Toxicity
  2. Indirect lung injury
    1. Sepsis (highest risk of ARDS - 79% of cases)
    2. Multiple Trauma (high risk)
    3. Disseminated Intravascular Coagulation
    4. Cardiopulmonary bypass (CABG)
    5. Burn Injury
    6. Acute Pancreatitis
    7. Drug Overdose (Heroin, Cocaine)
    8. Transfusion Reaction
    9. Ingestion
      1. Hydrocarbon Ingestion
      2. Ethchlorvynol (Placidyl)
    10. Non-cardiac pulmonary edema
      1. High Altitude Pulmonary Edema
      2. Neurogenic pulmonary edema
      3. Heroin-induced pulmonary edema
    11. Infection (often in immunocompromised patients)
      1. Miliary Tuberculosis
      2. Diffuse fungal infection
        1. Histoplasmosis
        2. Blastomycosis
        3. Coccidioidomycosis
        4. Cryptococcosis
      3. Parasitic Infections
        1. Babesia species (Babesiosis)
        2. Pneumocystis carinii
        3. Plasmodium species (Malaria)
        4. Strongyloides stercoralis (Threadworm)
  • Symptoms
  1. Onset within 24-72 hours of triggering event
  2. Progressive Dyspnea
  1. Critical for assessment
  2. Most sensitive for identifying ARDS early
  3. Large A-a Gradient
  4. See PaO2/FIO2 under diagnosis below
  • Imaging
  1. Chest XRay
    1. Early: Diffuse, bilateral Interstitial Infiltrates
    2. Later: Diffuse fluffy infiltrates (pulmonary edema)
    3. No cardiomegaly or Pleural Effusions
  2. Chest CT
    1. Acute Phase
      1. Bilateral alveolar opacities
      2. Air Bronchograms
      3. Bullae
      4. Pleural Effusions
    2. Fibroproliferative stage
      1. Bilateral reticular opacities
      2. Decreased Lung Volume
      3. Large bullae
  • Diagnosis
  1. Criteria
    1. Acute onset
    2. Identifiable cause from above list
    3. Not due to Congestive Heart Failure
      1. Pulmonary artery wedge pressure <19 mmHg or
      2. No signs of left atrial Hypertension
    4. Hypoxemia despite Supplemental Oxygen
      1. See PaO2 to FIO2 ratios below
    5. Bilateral Pulmonary Infiltrates on Chest XRay
  2. Spectrum of lung injury based on PaO2/FIO2
    1. Interpretation regardless of PEEP
    2. Normal patient: 500 mmHg
    3. Acute Respiratory Distress Syndrome (ARDS): <300 mmHg
      1. Mild ARDS <300 mmHg (27% mortality)
      2. Moderate ARDS <200 mmHg (32% mortality)
      3. Severe ARDS <100 mmHg (45% mortality)
  3. Resources
    1. Life in the Fast Lane
      1. https://lifeinthefastlane.com/ccc/pao2fio2-ratio/
  4. References
    1. Bernard (1994) Am J Respir Crit Care Med 149:818-24 [PubMed]
    2. (2012) JAMA 307(23):2526-33 +PMID:22797452 [PubMed]
  • Differential Diagnosis
  1. See Hypoxia
  2. Congestive Heart Failure
    1. ARDS is non-cardiogenic pulmonary edema
    2. Critical to distinguish ARDS from CHF, as CHF management is not effective in ARDS
      1. ARDS is managed with supportive care
      2. Avoid Furosemide and ACE Inhibitors in ARDS
    3. ARDS, in contrast to CHF
      1. Heart size is typically normal in ARDS (often difficult to distinguish)
      2. Left atrial Hypertension or volume overload are typically absent in ARDS
    4. CHF is often accompanied by
      1. Edema
      2. Jugular Venous Distention
      3. S3 gallup
      4. Increased ntBNP
  3. Pneumonia
    1. Pneumonia is typically accompanied by a fever, Pleuritic Chest Pain, productive cough and a localized infiltrate
    2. Many of these features can also be present in ARDS, but a constellation of these symptoms suggests Pneumonia
      1. Pneumonia is also the most common cause of ARDS so may be difficult to distinguish from ARDS
      2. Hypoxia that does not improve wtih Supplemental Oxygen suggests ARDS
  4. Atypical infection
    1. Tuberculosis
    2. Fungal Pneumonia (e.g. Blastomycosis or Coccidioidomycosis)
    3. Pneumocystis Pneumonia
  • Management
  • General (Supportive care)
  1. See Ventilatory Support below
  2. Identify and treat underlying cause
    1. Example: Treat site-specific infections (e.g. Pneumonia)
  3. Maximize nutritional status and fluid balance
    1. Conservative fluid therapy titrated down to lower Central Venous Pressures (shortens ICU stay)
    2. Enteral Nutrition started within 24 to 48 hours of ICU admission
    3. Eicosapentaenoic Acid (fish oil extract) effective
  4. Inotropic pressure support may be required
  5. Pulmonary artery catheters (and central venous catheters) are not routinely indicated
    1. Choose selectively in complicated fluid status, and then only by experienced clinicians
    2. Higher risk of complications without significantly improved outcomes
  6. Maintain adequate sedation and analgesia
  7. Stress Ulcer prophylaxis
    1. Sucralfate 1 gram orally or via Nasogastric Tube four times daily or
    2. Ranitidine (e.g. Ranitidine 50 mg IV every 8 hours) or
    3. Proton Pump Inhibitor (e.g. Protonix 40 mg IV)
  8. Deep Vein Thrombosis Prevention
    1. Enoxaparin 40 mg SQ daily or
    2. Daltaeparin 5000 units SQ daily or
    3. Unfractionated Heparin 5000 units SQ twice daily
  9. Prone position reduces dependent consolidation
    1. Prone position requires adequate sedation
    2. Prone position does not alter hemodynamic parameters
  10. Inhaled Beta Agonists appear effective
    1. Reduce Ventilatory pressures and increase oxygenation
  11. Corticosteroids have mixed outcome results
    1. Consult with a medical intensivist about use
    2. Some studies suggest early use of Methylprednisolone decreases days on mechanical Ventilator
    3. Other studies show possible benefit later in course
    4. No consistent benefit shown in terms of reduction in mortality
  12. Measures not proven effective
    1. Inhaled nitric oxide
    2. Aerosolized surfactant replacement
    3. N-Acetylcysteine (Mucomyst)
    4. Vasodilators (e.g. Nitroprusside, Hydralazine)
    5. Prophylactic antibiotics
    6. Prophylactic Chest Tubes
  13. Measures used in Congestive Heart Failure will not be effective in ARDS
    1. Furosemide will not be effective in ARDS
    2. ACE Inhibitors will not be effective for ARDS
    3. Nitroglycerin will not be effective for ARDS
  14. Experimental methods under current evaluation
    1. Liquid ventilation (lung filled with perfluorocarbon)
  1. See Mechanical Ventilation
  2. Overall strategy
    1. Limiting Barotrauma decreases mortality in ARDS
  3. Start with Tidal Volume at 4-6 ml/kg initially
    1. Much lower than Tidal Volume in other conditions (typically 6-8, up to 8-10 ml/kg)
    2. Base Tidal Volume on Ideal Weight for height
  4. Lower FIO2 to avoid alveolar toxicity
    1. Titrate FIO2 down to 0.60 to keep O2 Sat at 88-95%
    2. PaO2 goal 55 to 85 mmHg
  5. Set PEEP for maximal alveolar recruitment
    1. Set PEEP >12 cm H2O
    2. See PEEP Table (adjust in concert with FIO2)
    3. Monitor for reduced Cardiac Output
  6. Allow some hypercapnia to reduce Barotrauma risk (permissive hypercapnia)
    1. Lower minute volumes (lower Tidal Volume and rate)
    2. Titrate to PaCO2 of 50 to 77 mmHg (permissive hypercapnia)
    3. Titrate to pH of 7.20 to 7.30
  7. Maintain plateau pressure (inspiratory pressure) <30 cm H2O
  8. Other settings
    1. Inspiratory to expiratory ratio of 1:2 to 1:3
    2. Respiratory Rate up to 35 breaths per minute
  9. Adjuncts
    1. Consider Tracheostomy for prolonged intubation (anticipated >10 days)
    2. Mobilization therapy reduces days on Ventilator as well as days in ICU
  10. Weaning criteria
    1. Meeting oxygen requirements with non-invasive methods
    2. Hemodynamically stable
    3. Minute ventilation is 15 Liters or less
    4. Positive End-Expiratory Pressure (PEEP) is 5 cm H2O or less
    5. Tolerates 1-2 hour trials of spontaneous breathing
      1. Protects airway
      2. No Agitation
      3. Remains hemodyanmically stable
      4. Oxygen Saturation maintained at 90% or greater
      5. Respiratory frequency to Tidal Volume ratio maintained at 105 or less
      6. Respiratory Rate does not exceed 35 breaths per minute
  • Complications
  1. Nosocomial infection
  2. Pneumothorax (Barotrauma related) in up to 41% of cases
  3. Gastrointestinal Bleeding (Stress Ulcer)
  4. Thromboembolism
  • Course
  1. ARDS presents within 12-24 hours of antecedent event
  2. ARDS patients intubated within 72 hours in 90% cases
  3. High mortality rate
    1. Short-term mortality (ICU: 37%, overall: 42%)
      1. Most deaths are due to multi-organ failure
      2. Refractory Hypoxemia accounts for 16% of deaths
    2. Long-term mortality in the first 3 years following ALI or ARDS
      1. Mechanical Ventilation was required: 57% three year mortality
      2. ICU admission not requiring ventilation: 38% three year mortality
      3. No ICU admission or ventilation: 15% three year mortality
      4. Wunsch (2010) JAMA 303(9): 849-56 [PubMed]
  4. Typical hospital course
    1. ICU stay averages 16 days
    2. Hospital stay averages 26 days
  5. Predictors of better prognosis
    1. Those who survive first 2 weeks have better prognosis
    2. Age under 55 years
      1. Children under age 15 years have an overall mortality rate of 18% (contrast with 42% in adults)
      2. Zimmerman (2009) Pediatrics 124(1): 87-95 [PubMed]
    3. Trauma related ARDS
  6. Predictors of poor prognosis
    1. Elderly (especially over age 70 years)
    2. Immunocompromised patients
    3. Chronic Liver Disease
    4. Increased dead space fraction
  • Management
  • Follow-Up ICU Stay
  1. Applies to over 100,000 survivors of ARDS in United States annually
  2. See Post-ICU Ambulatory Care
  3. See Myopathy Following ICU Admission
  4. Anticipate cognitive Impairment
  5. Anticipate lower quality of life
  6. Anticipate prolonged respiratory recovery period
    1. Even at 5 years, some residual pulmonary function deficit persists
  7. Mortality in first 3 years is very high (see above)
  8. Higher morbidity with prolonged Mechanical Ventilation and ICU stay
  9. Psychiatric illness is common following ARDS episode
    1. Major Depression: Up to 43% of patients
    2. Anxiety Disorder: Up to 48% of patients
    3. Posttraumatic Stress Disorder: Up to 35% of patients