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ARDS
Diana May B. Laraya, MD
Acute
Respiratory
Distress
Syndrome
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Definition:
Severe dyspnea of rapid onset
Hypoxemia
Diffuse pulmonary infiltrates
RESPIRATORY FAILURE
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ARDS• Caused by diffuse lung injury
• Medical or surgical disorders
• Direct or Indirect
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18th ed HPIM
• ALI: PaO2/FiO2 ≤ 300mmHg• ARDS: PaO2/FiO2 ≤ 200mmHg
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etiology
• >80% caused by sepsis and Pneumonia• 40-50% : trauma, transfusion-related,
aspiration of gastric contents• Trauma ~ pulmonary contusion, multiple rib
fracture, chest wall trauma/flail chest• Rare causes: head trauma, near-drowning,
toxic inhalation, burns
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ARDS• Clinical course
1. Exudative
2. Proliferative
3. Fibrotic
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ARDS: pathophysiol
ogy
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ARDS: exudative
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ARDS: exudative
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• Early alveolar edema• Neutrophil-rich leukocyte infiltration• Hyaline membrane from diffuse alveolar
damage• ~First 7 days
ARDS: exudative
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• Prominent interstitial inflammation• Early fibrotic changes• ~Day 7-day21
Neutrophillymphocyte ↑type II pneumocytedifferentiate into type I
pneumocyte Synthesis of new pulmonary surfactant
ARDS: proliferative
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• Alveolar type III procollagen peptide ~↑ mortality from ARDS
• Extensive alveolar duct and interstitial fibrosis• Emphysema-like changes with bullae• Intimal fibroproliferation in the pulmonary
microcirculation vascular occlusionpulmonary HPN
ARDS: fibrotic
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• Long-term support on MV and supplemental O2
• INCREASED RISK pneumothorax• REDUCTION in lung compliance• Increased pulmonary dead space
↑↑↑ Morbidity and Mortality
ARDS: fibrotic
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Time course for the development of ARDS
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ARDS: MANAGEMENT
• GENERAL PRINCIPLESRecognition and treatment of the underlying medical and
surgical disorderMinimizing procedures and their complicationsProphylaxis against VTE, GI bleeding, aspiration, excessive
sedation and central venous catheter infectionPrompt recognition of nosocomial infectionsProvision of adequate nutrition
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• Mechanical ventilation management
• VENTILATOR-induced lung injury:• Repeated alveolar lung overdistention• Recurrent alveolar collapse
ARDS: MANAGEMENT
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• National Institute of Health:ARDS Network– RCT comparing low VT (6mL/kg BW) ventilation
vs conventional VT (12mL/kg BW)
- Significantly low mortality rate in the low VT pxs (31%) compare to conventional VT (40%)
ARDS: MANAGEMENT
VT=6mL/kg BW
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• Mechanical ventilation management
• VENTILATOR-induced lung injury:Repeated alveolar lung overdistention• Recurrent alveolar collapse
ARDS: MANAGEMENT
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• Prevention of alveolar collapse• ALVEOLAR COLLAPSE due to– Presence of alveolar and interstitial fluid– Loss of surfactant– Decrease in lung compliance
ARDS: MANAGEMENT
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• Positive end-expiratory pressure (PEEP)– Minimize FiO2
– Maximize PaO2
• “Optimal PEEP” in ARDS: 12-15mmHg
ARDS: MANAGEMENT
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• Inverse-ratio ventilation– Increase mean airway pressure– Longer inspiration time than expiration time
I:E >1:1• ↓ time to exhale => dynamic hyperinflation =>
increased end-expiratory pressure => oxygenation improved
No benefit in ARDS mortality
ARDS: MANAGEMENT
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• PRONE position– Improve arterial oxygenation– Uncertain effect on survival and outcomesHazards:
Accidental endotracheal extubationLoss of central venous cathetersOrthopedic injury
ARDS: MANAGEMENT
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• Other mechanical ventilation strategies:1. High-frequency ventilation (HFV) • High respiratory rates (5-20 cycles per second) and• Low VTS (1-2mLkg)
2. Partial liquid ventilation (PLV) • Perfluorocarbon
No survival benefit from ARDS
ARDS: MANAGEMENT
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• Lung-replacement therapy with extracorporeal membrane oxygenation (ECMO)– Neonates– With survival benefit
ARDS: MANAGEMENT
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adjunctive ventilator therapy (PEEP, HFV, PLV, ECMO, etc)
incomplete efficacy datarescue therapy
ARDS: MANAGEMENT
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ARDS: Fluid Management
• Fluid restriction• Diuretics
reduce left atrial filling pressure↓
Minimizes pulmonary edema prevents further decrements in arterial oxygenation and lung compliance
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NEUROMUSCULAR blockade
• EARLY Neuromuscular blockade for 48H– Cisatracurium besylate
lung-protective ventilation px-ventilator synchrony
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ARDS: Glucocorticoids
• Reduce pulmonary inflammation• Benefit in some studies
• Current evidence does not support the use of glucocorticoids
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OTHER THERAPIES
1. SURFACTANT replacement2. Inhaled nitric oxide3. Inhaled epoprostenol
improve oxygenation-transient***do not improve survival or decrease
time on Mech Vent
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ARDS: Prognosis
• Mortality ~ 26%-44%
Nonpulmonary causes >80% Sepsis Nonpulmonary organ failure
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ARDS: Mortality Risk Factors
• Nonpulmonary cause – major• Advanced age (>75yo)• Preexisting organ failure• Direct lung injury (2x)• Severe hypoxemia (PF ratio <100)
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Functional Recovery in ARDS survivors
• Maximal lung fxn – 6months• 1yr after extubation ~ 1/3 have N spirometry• Most have mild abnormalities in pulmo fxn• 5yr assessment ~ exercise limitation and
decreased physical quality of life
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ARDS
Thank
you…?