Acute Respiratory Distress Syndrome - ATUDER
Transcript of Acute Respiratory Distress Syndrome - ATUDER
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Acute Respiratory
Distress Syndrome
- challange to Intensive Care
Juliusz Jakubaszko
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COI Disclosure
I have no relevant relationship or
financial/ material support to disclose.
PRESENTER: DR. JULIUSZ JAKUBASZKO
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Wroclaw University
from its history:
• prof. Jan Mikulicz-Radecki (1850-1905), great surgeon
pioneer of modern surgery and antiseptics
• prof. Albert Neisser (1855-1916), dermatologist/bacteriologist
discovered gonococcus ( Neisseria Gonorrhoeae )
• prof. Alois Alzheimer (1864-1915), psychiatrist/neurologist
described neurodegenerative dementia
• prof. Ludwik Hirszfeld (1884-1954) bakteriologist/immunologist
discovered human blood groups
• prof. Max Born (1882-1970) physicist/mathematician
Nobel Prizer in Physics for research on Quantum Mechanics
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Acute Respiratory Distress Syndrome
Definition
(after Berlin Classification Consensus 2012)
1. Timing within 1 week of clinical insult
2. Bilateral chest infiltration
3. Origin of pulmonary edema
4. Hypoxemia a) Mild PaO2/FiO2 200 – 300 mmHg
b) Moderate PaO2/FiO2 100 – 200 mmHg
c) Severe PaO2/FiO2 < 100 mmHg
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Acute Respiratory Distress Syndrome
Etiology
Direct lung injury:
gastric aspiration, pulmonary contusion,
pneumonia, toxic inhalation, …
Indirect lung injury:
sepsis, trauma, burns, pancreatitis,
transfusion related blood products, …
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Acute Respiratory Distress Syndrome
Etiology
Acute lung injury with:
Diffuse alveolar damage (DAD)
Increased capillary permeability
Pulmonary interstitial edema and fibrosis
Ventilation/perfusion mismatch
Refractory hypoxemia
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Acute Respiratory Distress Syndrome
Patophysiology
DAD with interstitial and alveolar edema and
fibrin, hyaline membrane deposition
Extensive right-to-left shunt (25% - 50%
cardiac output)
Reduction of lung compliance
Increase of work of breathing (25% - 50% of
total oxygen consumption)
No characteristic hemodynamic pattern
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Acute Respiratory Distress Syndrome General management
• No specific treatment
• Removing the cause
- infection source, antibiotics, fixation of long bone
fracture,….
• Supportive treatment
- respiratory management
- haemodynamic manipulation
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Acute Respiratory Distress Syndrome
Supportive treatment
Respiratory management
Increased alveolar-capillary permeability:
o Inactivation of lung surfactant
oDecrease lung compliance
oDecreased functional lung size
o Impared O2 intake and CO2 elimination
Life threatening hypoxemia
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Acute Respiratory Distress Syndrome
Supportive treatment
Respiratory management Initially – noninvasive positive pressure ventilation
Lung protection strategy
Adequate sedation
Ventilatory management
o Low tidal volume (VT)
o Minimizing inspiratory pressure ( < 30 cm H2O)
o Higher level of PEEP (up to 20 cm H2O)
o Higher level of FiO2 ( 0,6 – 1,0 )
Patient positioning (prone position)
Extracorporeal membrane oxygenation (ECMO)
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Derceased lung compliance Decreased functional lung size
Driving pressure ∆P = VT / CRS
... Decrease in ∆P owing to changes in
ventilator settings were strongly associated
with increased survival…( NEJM, February, 2015 )
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… In patients with severe ARDS, early application
of prolonged prone – positiong sessions ,
significantly decreased 28-day and 90-day
mortality…
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♂ 50y, viral infection → ARDS, ECMO
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♂ 50y, viral infection → ARDS, ECMO
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♂ 50y, viral infection → ARDS, ECMO
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Acute Respiratory Distress Syndrome
Supportive treatment
Pharmacologic therapies ? No specific medications have been shown
effective in ARDS ( corticosteroids, iNO,…)
Haemodynamic manipulations inotrops, vasoconstrictors, dilators, diuretics,
fluids,…
may improve cardiac output and oxygenation
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Acute Respiratory Distress Syndrome
Supportive treatment
Fluid treatment
ARDS facts :
- increased alveolar-capillary permeability
- extravasation of protein-enriched fluid into
alveoli
- pulmonary exudate in alveoli
- reduced intravascular volume
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Acute Respiratory Distress Syndrome
Supportive treatment
Fluid treatment
Colloids controversies:
- reduce alveolar-capillary permeability,
histological damage, inflamatory cell
infiltration
- faster hemodynamic stabilization
- might increase tissue edema due to
extravasation of colloid molecules
- synthetic colloids ( HAES, gelatins) are
associated with higher risk of AKI and death
Consensus on colloid treatment in ARDS has not
been achieved
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… superiority of combined albumine and
furosemid versus furosemid alone…
… albumin solutions improve the early
oxygenation without affecting mortality…
… there is a need for large RCTs addressing the
potential benefits of albumin or synthetic
colloids as volume expanders in ARDS…
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http://www.medycynaratunkowa.wroc.pl