Transcript Acute Respiratory Distress Syndrome

Acute Respiratory Distress
Syndrome
Susie Gerik, MD
Children’s Special Services
Objectives
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Describe features of ARDS
List possible inciting conditions
Describe pathophysiology
Discuss treatment strategies
Address morbidity and mortality
History
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Described by William Osler in 1800
Asbaugh et al., Lancet 1967
Observed in adults and children
Definition
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Condition characterized by acute
inflammatory lung injury resulting
in widespread pulmonary edema as
a result of increased alveolar
capillary permeability and epithelial
destruction.
Features
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Acute respiratory distress
Cyanosis refractory to oxygen
Decreased lung compliance
Diffuse infiltrates on CXR
1988 Lung Injury Score
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PEEP
PaO2/FIO2 ratio
Static lung compliance
Degree of infiltrates
1994 Consensus
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Acute onset
PaO2/FIO2 < 200
Bilateral infiltrates
PCWP < 18
1994 Consensus
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Two categories:
Acute lung injury: PaO2/FIO2 ratio
< 300
ARDS: PaO2/FIO2 < 200
Incidence
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Acute Lung Injury: 17.9/100,000
ARDS: 13.5/100,000
~1% of all PICU admissions
Causes
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Shock
Aspiration
Trauma
Infections
Inhaled fumes
Drugs and poisons
Miscellaneous
Ventilator-induced Lung
Injury
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Barotrauma
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Atalectrauma
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large lung volumes
shear forces
Biotrauma
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activation of effector cells to release
mediators
Indirect Injury
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Sepsis syndrome
Severe nonthoracic trauma
Post cardiopulmonary bypass
Post hemodialysis
Disseminated intravascular
coagulation
Pancreatitis
Antiphospholipid syndromes
Pathogenesis
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Inflammatory mediators
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damage to microvascular endothelium
damage to alveolar epithelium
increased alveolar permeability
accumulation of alveolar edema fluid
Pathogenesis
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Neutrophils and macrophages
Complement
Cytokines
Platelet activating factor
Eicosanoids
Free radicals
Pathophysiology
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Abnormalities in gas exchange
Abnormalities in oxygen delivery
and consumption
Abnormalities in cardiopulmonary
interactions
Multiple organ involvement
Gas Exchange - Hypoxemia
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Increased capillary permeability
Interstitial and alveolar exudate
Intrapulmonary shunting
Reduced ventilation-perfusion
matching
Diffusion defect with right to left
shunt
Pulmonary Mechanics
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Reduced lung volume (FRC)
Reduced lung compliance
Impaired function of surfactant
Pathologic Flow
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Uncoupling of oxidative dependency
Oxygen utilization by non-ATP
producing oxidase systems
Increased diffusion distance for O2
between capillary and alveolus
Cardiopulmonary
Interactions
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Pulmonary hypertension ->
increased RV afterload
High PEEP -> decreased preload
Results in decreased cardiac output
Non-pulmonary
Abnormalities
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Multi-organ system failure
Bio-trauma
Pathologic oxygen-supply
dependency
Substrate utilization
Max O2
extraction
VO2
Max O2
extraction
VO2
Critical DO2
DO2
Critical DO2
DO2
Normal
Septic Shock/ARDS
VO2 = DO2 X O2ER
Abnormal Flow Dependency
Acute, Exudative Phase
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Rapid respiratory failure after
trigger
Diffuse alveolar damage with
inflammatory infiltrate
Hyaline membrane formation
Capillary injury
Protein-rich edema fluid in alveoli
Disruption of alveolar epithelium
Subacute, Proliferative
Phase
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Persistent hypoxemia
Development of hypercarbia
Fibrosing alveolitis
Further decrease in pulmonary
compliance
Pulmonary hypertension
Chronic Phase
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Obliteration of alveolar and
bronchiolar spaces and pulmonary
capillaries
Recovery Phase
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Gradual resolution of hypoxemia
Improved lung compliance
Resolution of CXR abnormalities
Goals of Treatment
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Optimize gas exchange and O2
delivery
Minimize ventilator-induced lung
injury
Treat etiology
Avoid multisystem organ failure
Treatment: Respiratory
Support
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Mechanical ventilation
High frequency ventilation
ECMO
Nitric oxide
Liquid ventilation
Exogenous surfactant
Treatment: Monitoring
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Respiratory
Hemodynamic
Metabolic
Infections
Fluid/electrolytes
Optimize VO2/D02
Relationship
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DO2
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hemoglobin
mechanical ventilation
oxygen (PEEP)
VO2
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preload
afterload
contractility
Ventilation Strategies
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Oxygen
PEEP
Inverse I:E ratio
Lower TV
Prone position
PEEP
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Displaces edema fluid into
interstitium
Decreases atalectasis
Decreases right to left shunt
Improves compliance
Improves oxygenation
Nitric Oxide
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Pulmonary vasodilation
Selectively improves perfusion of
ventilated areas
Reduces intrapulmonary shunting
Improves arterial oxygenation
No systemic hemodynamic effects
Prone Position
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Improved gas exchange
Uniform alveolar ventilation
Recruitment of segments in dorsal
region
Improved postural drainage
Redistribution of perfusion away
from edematous, dependent regions
High Frequency Ventilation
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Raises MAP
Recruits lung volume
Small changes in TV
Impedes venous return
Liquid Ventilation
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Perflubron
20x O2 and 30x CO2 solubility
Heavier than water
Higher spreading coefficient
Improved compliance and gas
exchange
Mortality
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40-60%
Multiorgan failure/sepsis
Decreasing because of better
vetilatory strategies and earlier
recognition and treatment
Iatrogenic Contributors to
Morbidity/Mortality
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Inadequate nutrition
Fluid overload
Inappropriate sedation
Neuromuscular blocking agents
Complications from medical
procedures
Medical errors
Prognostic Factors
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Underlying medical condition
Presence of multiorgan failure
Severity of illness
Thank you!