Acute Respiratory Distress Syndrome

First Things First (assess & treat for the following)

  • Definition
    • Acute & persistent syndrome
    • Bilateral radiographic infiltrates
    • PaO2/FiO2 ratio <200 (PaO2 in mmHg, FiO2 expressed as a value between 0.21 & 1.0)
      • For example, FiO2 0.6 and PaO2 90, P/F ratio is 90/0.6 = 150
    • PaO2/FiO2 200-299 defined as acute lung injury (ALI)
    • No evidence of elevated left atrial pressure: pulmonary artery occlusion pressure (PAOP) 18 if measured
  • Treat hypoxemia
    • Initial FiO2 of 1.0 to rapidly correct hypoxemia & gauge need for advanced ventilator strategies
  • Rule out heart failure.
    • Clinical circumstances help differentiate.
    • Radiograph not discriminatory
    • Pulmonary artery catheterization if diagnosis uncertain, but can be misleading
      • “Flash” pulmonary edema with transient LV dysfunction may have normalized PAOP while infiltrates remain.
      • Partially treated cardiogenic pulmonary edema may have PAOP trending downward.
      • ARDS patients can have concomitant LV dysfunction (up to 20%) & elevated PAOP.
  • Evaluate & treat for predisposing condition.
    • Syndrome develops 4-48 hrs after inciting event.
    • >60 identified causes
      • “Primary” or “direct lung injury” if in setting of pulmonary cause, “secondary” or “indirect” if cause is extrapulmonary
    • Consider sepsis first: most common cause.
    • Pneumonia probably most common cause of ARDS acquired as an outpatient
    • Gastric aspiration causes ARDS in approximately one third.
    • Trauma to include fat embolism, lung contusion, pancreatitis, near drowning
    • Transfusion-related ALI (TRALI) associated with massive transfusion but can be seen with single units; increased risk with multiple donors, female/multiparous donors.
  • Pathophysiology
    • Inflammatory injury to the alveoli, particularly vulnerable because lungs receive entire cardiac output & thus are exposed to vast amounts of inflammatory mediators
    • Impaired gas exchange with V/Q mismatch & shunt causing hypoxemia; increased dead space requiring increased minute ventilation to maintain normal pCO2
    • Decreased static & dynamic pulmonary compliance is a hallmark, but disease is anatomically inhomogeneous.
      • Poorly aerated lung units are noncompliant.
      • Disease worse in dependent regions
      • Remaining normally functioning lung has normal compliance but small volume (concept of “baby lungs”).
    • Pulmonary hypertension common
      • Acute cor pulmonale rare
  • Clinical course: 3 typical phases
    • Exudative phase, with diffuse alveolar damage, severe hypoxemia, flooded alveoli
    • Proliferative phase, with resolving edema, proliferation of type II pneumocytes & profibrotic migration into interstitium
      • Oxygenation may improve, but patients remain ventilator-dependent & compliance remains low.
    • Fibrotic phase, with diffuse fibrosis destroying normal architecture
      • Not all patients develop fibrosis.
      • Honeycomb & cyst formation
      • Chronic pulmonary hypertension

History and Physical (assess for the following)

  • History
    • Time course of onset: chronicity excludes ARDS
    • Symptoms of infection
    • Drugs, to include drugs of abuse & over-the-counter
  • Physical
    • Respiratory distress, tachypnea, tachycardia, cyanosis, rales common
    • Hypotension from septic shock
    • In intubated patient, causative condition may be more difficult to ascertain.
    • Search for signs of infection.
    • Abdominal exam for pancreatitis, intra-abdominal infection

Diagnostic Tests

  • CXR: diffuse fluffy bilateral infiltrates with air bronchograms
  • ABG: increased A-a gradient, respiratory alkalosis early, progressing to respiratory acidosis if intubation delayed, metabolic acidosis if prolonged hypoxemia
  • ECG to evaluate for myocardial infarction or ischemia
  • CBC with differential
  • Full chemistry panel to include liver enzymes & amylase
  • Coagulation battery for evidence of DIC
  • Blood cultures
  • Urinalysis with culture
  • CT of chest not needed, but if obtained demonstrates patchy alveolar abnormalities, worse in dependent regions

General Management Principles

  • Determine the cause.
    • If thorough evaluation does not determine a cause, consider bronchoscopy & lavage.
    • Evaluate for overwhelming infection in appropriate clinical setting (aerobic bacteria, mycobacteria, respiratory viruses, atypical bacteria, Pneumocystis, Legionella).
    • Lung biopsy can be safely performed but rarely yields a specific diagnosis. Can be useful in cases of pulmonary vasculitis, disseminated cancer or underlying chronic lung disease with superimposed ARDS.
  • Aggressive supportive care
    • Broad-spectrum antibiotics if sepsis suspected
    • Early attention to nutrition
    • Typical ICU care: VAP prevention, stress gastritis prophylaxis, deep venous thrombosis prophylaxis, prevention & early treatment of decubitus pressure ulcers
    • Avoid volume overload, which will increase quantity of edema fluid.
      • Pulmonary artery catheter may be useful.
      • Diuresis may be beneficial.
      • Furosemide with addition of albumin (25 g q 8 hrs) in hypoproteinemic patients may improve negative fluid balance and oxygenation index.
      • FACTT trial demonstrated decreased ICU days and ventilator days with conservative fluid strategy (CVP maintained <4 mmHg or PAOP <8). No difference in mortality; increased creatinine seen in low CVP group but no increase in dialysis.
  • Adequate oxygenation (oxy-hemoglobin saturation >90%), with nontoxic FiO2 (<0.5-0.6)
  • Avoid further ventilator-associated lung injury by minimizing alveolar overdistention.
    • Ideal level of plateau airway
      • Clearly <35 cm H2O, possibly <20-25 cm H2O
  • Consider deep sedation & possible neuromuscular blockade to decrease oxygen consumption & enhance patient/ventilator synchrony.
  • Apply PEEP in 2-3 cm H2O increments to obtain SaO2 >90% with FiO2 <0.6 & plateau pressure <35 cm H2O.
    • PEEP raises peak & plateau airway pressures, with risk of alveolar overinflation.
    • Increased intrathoracic pressure may diminish venous return.
    • If TV 6 ml/kg and Pplat < 30, clinical outcomes similar whether low or high PEEP (ALVEOLI trial).
    • “Best PEEP” can be estimated as that which demonstrates:
      • Maximal oxygen delivery (DO2) if pulmonary artery catheter in place
      • Highest static compliance: TV/(Pplat – PEEP) in ml/cm H2O
      • Highest PaO2 without decreasing cardiac output or blood pressure
      • Pressure of lower inflection point on static pressure-volume curve
  • Conventional mechanical ventilation
    • Volume-controlled (VC) or pressure-controlled (PC)
    • No studies show improved outcome based on mode of ventilation.
    • VC ventilation risks changes in airway pressures if compliance changes but guarantees set minute ventilation.
    • PC ventilation risks changes in minute ventilation if compliance changes but guarantees preset airway pressures will not be exceeded, minimizing risk of barotrauma & alveolar overdistention.
    • Tidal volume (TV) & respiratory rate (RR) should be set to meet ventilatory requirements.
      • TV of 4-6 mL/kg currently recommended (ARDSnet, 1999)
      • Titrate TV according to plateau airway pressure, with goal not to exceed 35 cmH2O.
      • Titrate RR to allow adequate minute ventilation: normal PaCO2 or mild permissive hypercapnia.
    • Inspiratory flow rate or inspiratory time should ideally be adjusted to maximize patient comfort & minimize air trapping.
      • Typically flow rate 4x minute ventilation
    • Flow pattern: decelerating wave form
  • Sample starting ventilator settings
    • VC
      • Mode: Assist control (AC)
      • TV: 6 mL/kg
      • RR: 15 per min
      • FiO2: 1.0
      • PEEP: 5 cmH2O
      • Decelerating waveform
    • PC
      • Mode: AC
      • RR: 15 per min
      • FiO2: 1.0
      • PEEP: 5 cmH2O
      • Peak inspiratory pressure: 20 cm H2O (PIP)
      • Inspiratory time: 1 second or I:E ratio 1:3
    • MORE IMPORTANT THAN INITIAL VENTILATOR SETTINGS is to observe clinical response to these settings & adjust ventilator accordingly.
      • Patient/ventilator synchrony
      • Oxyhemoglobin saturation
      • Hemodynamic response
      • ABG analysis
  • Advanced ventilator strategies
    • If patient remains hypoxic, requires FiO2 >0.5 or remains with unacceptably high plateau airway pressures with conventional methods above, other ventilatory strategies come into play:
    • Permissive hypercapnia
      • First diminish TV (in VC) or PIP (in PC) incrementally, allowing PaCO2 to rise gradually.
      • Respiratory acidosis develops: minimally acceptable pH is variable, as low as 7.10-7.15 in absence of head injury or catecholamine resistance.
      • Use of IV sodium bicarbonate to buffer pH not recommended
      • Hypercapnia is generally well tolerated as long as oxygenation is ensured.
      • Intracellular pH is maintained due to extensive intracellular buffering mechanisms.
      • Usually requires deep sedation to overcome respiratory drive induced by hypercapnia
      • CONTRAINDICATED in patients with increased ICP, hemodynamic instability, beta blockade (patients require catecholamine response to maintain hemodynamic stability in hypercapnia)
    • Inverse ratio ventilation
      • If oxygenation is inadequate or requires toxic levels of FiO2 to maintain, efforts can be directed at INCREASING MEAN AIRWAY PRESSURE.
      • Prolonging inspiratory time can recruit more diseased lung units; when inspiratory time exceeds expiratory time, inverse ratio ventilation has been instituted.
      • In VC modes, decreasing inspiratory flow rate or adding inspiratory pause will prolong inspiratory time.
      • In PC modes, inspiratory time is directly set in seconds or adjusted as I:E ratio.
      • Inverse ratio ventilation has not been shown to improve survival but does increase mean airway pressure, can decrease peak airway pressure, can decrease FiO2 & can raise SaO2 when other methods have failed.
      • Complications of inverse ratio ventilation: requires deep sedation & neuromuscular blockade, may cause air trapping with consequent barotrauma & hemodynamic effects
      • May be more prone to complications when inspiration prolonged beyond 2:1
    • Other recruitment maneuvers
      • CPAP at 40 cm x 40 sec can be used as a global recruitment measure.
      • Recruitment maneuvers in addition to low TV strategy compared to low TV strategy alone: improved secondary hypoxia related endpoints (refractory hypoxemia, death from hypoxemia) and use of rescue therapies, but did not decrease mortality or barotraumas (“open lung strategy”)
    • Other ventilator modalities shown to improve oxygenation while limiting ventilator toxicity have not been proven of benefit.
      • Airway pressure release ventilation (APRV)
      • High-frequency modes, to include jet ventilation (HFJV) & oscillation (HFO)
  • Prone ventilation
    • Intermittent prone positioning of the patient can improve oxygenation in patients with refractory hypoxemia.
    • Patients who fail to respond to recruitment maneuvers or who require high levels of PEEP or FiO2 (>12 cm, >0.6) are candidates.
    • No mortality benefit demonstrated
    • Multiple mechanisms implicated
    • Benefits to compliance can persist when patient is returned to supine position.
    • >50% are “persistent responders” who maintain improved oxygenation for >1 hr after returning to supine position.
    • >10 mmHg increase in PaO2 over the first 30 min predicts continued improvement over a 2-hr trial.
    • Time limit & cycle length vary from 2 to 20 hrs.
    • Specialty beds facilitate prone positioning, but can be done on regular hospital bed
    • Contraindications to prone positioning
      • Spine instability
      • Hemodynamic instability
      • Open abdomen
      • Immediate postop period for thoracic & abdominal procedures
    • Complications of prone positioning
      • Hemodynamic instability
      • Dysrhythmia
      • Inadvertent extubation
      • Hypoxemia
      • Obstructed endotracheal tube
      • Dislodgement of therapeutic devices
      • Compression of chest tube drainage
      • Ocular injury
  • Novel therapeutic modalities: none of these has been shown to be of consistent benefit
    • Inhaled vasodilators improve V/Q mismatch by preferentially vasodilating in areas that are receiving ventilation.
      • Short half-lives equate to few systemic effects.
      • Nitric oxide (NO) (doses 1.25-40 ppm) yields continuous sustained response, improving hypoxia & decreasing pulmonary hypertension.
      • NO may produce toxic radicals more harmful than high concentrations of FiO2.
      • Inhaled prostacyclin (PGI2) does not require sophisticated equipment to administer.
    • Exogenous surfactant
      • In largest human study, inhaled surfactant did not affect mortality, oxygen indices or length of hospital/ICU stay.
    • Partial liquid ventilation (PLV) with perfluorocarbon uses a liquid capable of gas transport to fill alveolar space.
    • Extracorporeal techniques require expertise; specialized centers report impressive survival rates in moribund patients.
      • Extracorporeal CO2 removal may be useful to minimize ventilator-associated lung injury.

Specific Treatment

  • Care for patients with ARDS is supportive.
    • Treatment of underlying causative process is essential.
    • Methylprednisolone should not be routinely used: early use improved vent-free days, pulmonary dynamics and oxygenation indices without increased infection, but did not improve mortality and did increase neuromuscular weakness. Use of corticosteroids 2 weeks after onset of ARDS may increase mortality.

Ongoing Assessment

  • Daily thorough physical exam & lab studies to evaluate for multiple organ dysfunction & infection
  • Daily CXR
    • Observe for evidence of barotrauma.
    • Note tube placement.
  • ABGs as needed
  • Daily screening for suitability for liberation from ventilator
    • ARDS pts usually require more prolonged ventilatory support.
  • Consider surgical or percutaneous tracheostomy if ventilator course appears likely to be prolonged.
  • Nutritional assessment

Complications

  • Major complications seen in ARDS relate to multiple organ dysfunction syndrome.
  • Mechanical ventilation itself may predispose to development of multiple organ dysfunction syndrome.
  • Mortality typically not primarily due to respiratory failure/ARDS itself
  • Complications of positive-pressure ventilation
    • Barotrauma & volutrauma to include pneumomediastinum, pneumothorax, pneumoperitoneum, subcutaneous emphysema
  • Ventilator-associated pneumonia
    • ARDS patients more likely to develop VAP than other ventilated patients
  • Catheter-related bloodstream infection
  • Deep venous thrombosis
  • GI bleeding
  • Malnutrition
  • Decubitus pressure ulcers

Author

  • Gina Dorlac, MD

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Last updated: April 16, 2010

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TY - ELEC T1 - Acute Respiratory Distress Syndrome ID - 534160 Y1 - 2010/04/16/ BT - Pocket ICU Management UR - https://anesth.unboundmedicine.com/anesthesia/view/Pocket-ICU-Management/534160/all/Acute_Respiratory_Distress_Syndrome PB - PocketMedicine.com, Inc DB - Anesthesia Central DP - Unbound Medicine ER -