| What is ARDS? | It is an acute condition of hypoxemic failure with pulmonary edema caused by increased alveolar capillary permeability (opposed to pulmonary congestion due to heart failure)
Onset: 1 week or less, bilateral opacities consistent with edema must be present, PF ratio <300mmHg with min 5cmH2O PEEP/CPAP
Not fully explained by cardiac failure or fluid overload
It is the most serious complication of acute lung injury, part of acute inflammation or injury |
| What is the Berlin Definition of ARDS? | Mild (PaO2/FiO2 200-300, mortality 27%)
Moderate (PaO2/FiO2 100-200, mortality 32%)
Severe (PaO2/FiO2 <100, mortality 45%) |
| When do we consider that we have ARDS/ALI | It may be said in presence of severe acute hypoxemia with diffuse bilateral opacities on CXR with pulmonary occlusive pressures or left ventricular function on Echo are normal
ALI is less severe than ARDS (ALI: 200-300 , ARDS <200)
Consdered as early manifestation of sepsis, where lung injury can develop as soon as 90 min to 24 hours following an insult |
| What are causes of ARDS/ALI? | May directly affect alveoli or not
Direct: Pneumonia, Aspiration, near drowning, toxic inhalation (O2, smoke, chemicals), lung contusion.
Indirect: Sepsis, trauma, upper airway obstruction, cardiopulmonary bypass, anaphylaxis, drugs (chemo, amiodarone...), acute pancreatitis, hematological causes (transfusions/ DIC) |
| How is the epidemiology of ARDS? | 80/100,000, 40-60% mortality, majority of deaths due to MSOF.
Predicitve factors of death: extrapulmo organ dysfunction, sepsis and elderly.
Survivors: restore normal pulmonary function within a year |
| How is the pathophysiology of ARDS? | Endothelial injury increases permeability, leading to protein-rich alveolar edema.
Neutrophils play a role (but it may occur in neutropenic pt)
Proinflammatory cytokines mediate cellular responses lead to microvascular injury
Activation of coagulation system in sepsis can lead to inflammation and tissue ischemia
Due to increased permeability, hydrostatic pressure is unopposed and any increase in pressure will increase the edema (depends on area of lungs affected)
Increase in tissue/gas ratio leads to alveolar collapse and closure, exaggerated by reduction and damage of surfactant |
| How does mechanical ventilation cause ARDS? | It can injure the lungs (only give 4-6 ml/kg - if we give more we may induce ARDS)
It is a result of high inflation pressure (barotrauma)/ overdistention of alveoli (volutrauma)/ cyclic open and closing of alveoli (atelectotrauma)
+ disruption of alveolar endothelia integrity , releasing cytokines (biotrauma) |
| How is the pathology of ARDS? | 3 stages after insult (whatever it was)
Exudative, fibro-proliferative (2-3 days after), and reparative
Lungs are grossly edematous, with area of atelectasis, hemorrhage and consolidation |
| How is the exudative phase of ARDS? | Starts in 1st 3 days, formation of hyaline membranes of fibrin and protein matrix in alveoli and airways.
necrosis of type I pneumocytes and denuded basement membrane
Endothelial injury with edema as well as in situ thrombi formation |
| How is the proliferative phase of ARDS? | Fluid and proteins are resorbed or organized, squamous cells cover the denuded membrane (they are thick so they reduce diffusion)
fibroblast enter hyaline membrane deposits collagen, microcysts and honeycomb changes are manifested, alveoli undergo fibrosis, traction bronchiactasis is exerted with dilation of peripheral bronchi. |
| How is the clinical manifestation of ARDS? | Rapid onset of respiratory failure in phase I, with severe hypoxemia and irresponsive to supplementary O2.
CXR: Pulmonary edema, indistinguishable from CHF, some recover rapidly, others progress to fibrosis as early as 5 days
CT: alveolar filling affecting dependent lung zones in ventral positions |
| How is the mortality of ARDS? how is morbidity? | Varies according to cause of injury.
highest is with sepsis (43%)
Intermediate: pneumonia (36%)
lowest: trauma (11%) [mortality]
significant restrictive physiology and abnormal DLC initially, improve by 3 months and normalize in 1 year
But may have prolonged neuropsychological deficits (result of hypoxemia, medications, cytokines injuring neuromuscles) |
| What is the treatment of ARDS? | Initial evaluation and stabilization, management of underlying cause, oxygenation, ventilation, rescue therapy in case of refractory hypoxemia and supportive care
Outcome depends on dx, adequate nutrition, avoidance of infection, O2, increasing mean alveolar pressure (PEEP) by endotracheal tube |
| What are lung protective strategies used in ARDS? | CT shows small lung portion can be ventilated (baby lung), use small tidal volumes to avoid overinflation which leads to more injury.
Baby lung ventilation is very effective reducing duration of ventilation and decline in proinflammatory cytokines alveolar and plasma (reducing multiorgan failure)
Recruitment maneuvers controversial (high PEEP)_ |
| What is the effect of prone positioning in treatment of ARDS? | Since we see dorsal predominance of opacities on CT scans, prone positioning can be useful improving perfusion to well-ventilated lung zones, oxygenation (reducing FiO2 and PEEP), Introduces hazards of maintaining airway, IV catherters, and monitoring devices |
| What is the role of mechanical ventilation in ARDS? | Volume mode (assist)
Flow rates > pt demands (80L/min)
increase RR 35bpm to maintain pH normal
Can consider bicarb for pH maintenance, FiO2 and PEEP for PaO2 55-80 mmHg / SaO2 88-93%
IBW: Men: 50+ 2.3 (height in inches -60)
Women: 45.5 +2.3 (height in inches -60)
TV: 8ml/kg then go to 6 ml/kg to maintain <30 cmH2O |
| What is the pharmacological treatment of ARDS? | No drug can reduce the injury
Glucocorticoids, PGs, ibuprofin, surfactant, ketoconazole, N-acetylcysteine, NO, anti-TNF and IL1 show no surivial benefit
low dose steroids in fibroproliferative phase may improve injury scores but not effective |
