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acute respiratory distress syndrome; acute lung injury (ARDS, ALI)
ARDS is the most severe form of acute respiratory failure due to acute pulmonary injury. It is a diagnosis of exclusion.
Classification:
1) degree of hypoxemia: [11]
- mild (200 mm Hg < PaO2/FIO2 <= 300 mm Hg)*
- moderate (100 mm Hg < PaO2/FIO2 <= 200 mm Hg)*
- severe (PaO2/FIO2 <= 100 mm Hg)*
2) 4 ancillary variables for severe ARDS: [11]
- radiographic severity
- respiratory system compliance (<=40 mL/cm H2O)
- positive end-expiratory pressure >= 10 cm H2O)
- corrected expired volume per minute (>= 10 L/min)
* with PEEP > 5 cm H2O
Etiology:
1) direct pulmonary injury
a) pneumonia or other pulmonary infection [2] (most important)
b) aspiration of gastric contents
c) major trauma: pulmonary contusion
d) near drowning
e) inhalation injury
- mechanical ventilation
- lower tidal volumes may reduce risk
2) indirect pulmonary injury
a) sepsis, particularly from an abdominal source
b) hemorrhagic shock
c) drug overdose (heroin, methadone, barbiturates)
d) major trauma
- multiple fractures
e) multiple blood transfusions
f) pancreatitis
Epidemiology:
- incidence & mortality increases with age [6]
Pathology:
1) disruption of the alveolar capillary membrane
2) increased vascular permeability
3) accumulation of neutrophils & protein rich edema in the alveolar space
4) up to 70% of alveoli may be non-functional
5) may be component of alveolar dead space [6]
6) a fibroproliferative stage may occur within 2 weeks of onset
a) loss of alveolar structures
b) obliteration of vasculature
c) interstitial infliltration of chronic inflammatory cells
d) deposition of type 1 collagen
e) severity of fibroproliferative reaction correlates with increased mortality
7) varying degrees of multiorgan failure accompany ARDS
Clinical manifestations:
1) rapid onset
a) < 48 hours after precipitating event [2]; < 1 week [2]
b) generally < 24 hours
2) severe dyspnea
3) tachycardia
4) tachypnea
5) diffuse bilateral crackles on chest auscultation
6) hypoxemic respiratory failure
Diagnostic criteria:
- onset within 1 week of ARDS insult (most within 72 hours)
- bilateral lung opacities consistent with pulmonary edema
- acute respiratory failure unrelated to heart failure or volume overload
- PaO2/FiO2 of < 300 mm Hg on at least 5 mm PEEP
- PaO2/FiO2 of 100-200 (moderate); < 100 mm Hg (severe)
Laboratory:
1) arterial blood gas (ABG)
a) hypoxemia, pO2/fiO2 < 200 mm Hg for ARDS
b) pO2/fiO2 < 300 mm Hg for acute lung injury
2) pulse oximetry: SaO2 < 88%
3) sputum for gram stain & culture (essential)
Special laboratory:
1) hemodynamic monitoring
a) distinguish cardiogenic pulmonary edema from ARDS
b) pulmonary artery occlusion pressure < 18 mm Hg
c) not routinely recommended
2) echocardiography
- distinguish cardiogenic pulmonary edema from ARDS
3) fiberoptic bronchoscopy with bronchoalveolar lavage &/or bronchoscopic biopsy is generally performed as indicated after CT [31]
Radiology:
- chest radiograph
a) diffuse bilateral pulmonary infiltrates
b) no pulmonary vascular redistribution (i.e. no heart failure)
c) no cardiomegaly
d) pleural effusions are rare in the absence of another condition predisposing to pleural effusion
- chest CT as indicated [31]
Differential diagnosis:
1) cardiogenic pulmonary edema
- enlarged cardiac silhouette on chest X-ray
- improvement with diuresis &/or afterload reduction
2) diffuse alveolar hemorrhage
- evidence of vasculitis, acute kidney injury, hematuria
- hemosiderin-laden macrophages with bronchoalveolar lavage
- associated with stem cell transplantation
3) acute eosinophilic pneumonia
- cough, fever, pleuritic chest pain, myalgia, precipitated by smoking
- > 15% eosinophils in bronchoalveolar lavage fluid
4) hypersensitivity pneumonitis
- onset generally over weeks, course progressive
- exposure history (farmers, birds, hot tubs)
5) acute interstitial pneumonia
- may be impossible to distinguish for ARDS
- no inciting factors for ARDS
- may responed to glucocorticoids
6) pulmonary embolism unlikely if multifocal pulmonary opacities on chest X-ray [42]
Complications:
1) overall mortality 30-40% worldwide (50 countries) [22]
- mortality is 50% when associated with sepsis
2) multiple organ dysfunction & secondary pulmonary infections may occur if the patient survives the acute phase
3) delirium in the elderly
Management:
1) use high-flow nasal oxygen vs conventional oxygen therapy to reduce risk of intubation [40]
- noninvasive positive-pressure ventilation (NPPV) delivered via helmet may be alternative to mechanical ventilation [23]
2) mechanical ventilation
a) oxygenation
- target partial pressure of oxygen 55-80 mm Hg NEJM [44]
- oxygen saturation levels titrated > 96% SaO2
- no benefit in titration to > 97% SaO2
- oxygen saturation titrated to 88-92% results in higher 90 day mortality (44% vs 30%) [39]
b) PEEP of 5-12 cm H2O
1] 8 vs 13 cm H20 associated with similar outcomes [3]
2] higher PEEP may reduce morbidity but not mortality [3]
- higher PEEP recommended for patients with moderate-to-severe ARDS [43]
3] use lowest PEEP necessary to achieve SaO2 of 88% with FiO2 of < 60% without hypotension [2,13]
4] individualizing PEEP with esophageal balloon-guided PEEP titration does not improve outcomes [35]
c) lung protective ventilation (permissive hypercapnia)
d) peak inspiratory pressure < 30-35 mm Hg
e) end-expiratory pressure (plateau pressure) < 30 cm Hg [14]
f) tidal volume 6 mL/kg IBW [2,15,28] (4-8 mL/kg [40])
- decrease tidal volume by 1 mL/kg as needed to keep plateau pressure < 30 cm Hg
- low tidal volume ventilation is the only intervention shown to reduce mortality in patients with ARDS of any severity [24]
- low tidal-volume ventilation, prone positioning, & early neuromuscular blockade reduce mortality [30,43]
g) recruitment maneuvers (PEEP of 40 cm of water for 40 seconds) of no benefit [30], PEEP of 45 cm of water for 2 minutes harmful [32]
2) prone positioning during mechanical ventilation (4-20 hours/day)
- mortality benefit in patients with moderate-severe ARDS [2,25]
- >= 16 hours/day in prone position [2,16]
- may improve oxgenation decrease 28-day & 90-day mortality [16]
- begin prone positioning early in patients on low tidal-volume ventilation [2]
- prone positioning does not reduce the time to ECMO weaning in patients with severe ARDS [41]
3) recruitment maneuvers (short duration higher inspiratory pressure to open atelectatic alveoli) strongly discouraged. [43]
4) neuromuscular blockade may have a survival benefit in patients with moderate-severe ARDS [26]
- early treatment of patients with severe ARDS [43]
- partial pressure of oxygen [PaO2]:fraction of inspired oxygen [FiO2] <100) -l imit courses to 48 hours or shorter [43]
- cisatricurium besylate for 48 hours [26]
- mortality reduction at 28 days 24% vs 33% [26]
- more important than intravascular volume manangement [30]
- do not routinely use continuous infusion of neuromuscular blocking agent [40]
- no benefit to early neuromuscular blockade [37]
5) intravascular volume management
- maintain lowest possible intravascular volume compatible with adequate tissue perfusion
- limit IV fluid boluses
- use diuretics to keep central venous pressure low [2]
- implement after off vasopressors for 12 hours
- target central venous pressure = 4 mm Hg [2,7]
- conservative fluid management may have short-term benefit [7]
- no mortality benefit [30]
6) glucocorticoids
- may be of benefit for adrenal insufficiency
- hydrocortisone 50 mg IV every 6 hours + fludrocortisone 50 ug PO QD [5]
- glucocorticoids (no adrenal insufficiency)
- may be of benefit in fibroproliferative phase
- methyprednisolone 1 mg/kg IV started early & tapered over 28 days of benefit [9]
- may be of benefit for Covid-19 & community-acquired pneumonia
- early high dose glucocorticoids of no benefit [18]
- number needed to harm = 3 (infection) [18]
- of no benefit for acute treatment of ARDS [2]
7) pulmonary artery catheter of no benefit [8]
8) venovenous extracorporeal membrane oxygenation (ECMO) of no benefit [34]
- recommended for patients with severe ARDS (PaO2:FiO2 <80 or pH <7.25 with PaCO2 >=60 mm Hg), low certainty of evidence [43]
9) unproven therapies [2]
a) inotropic agents (unproven, controversial)
b) nitric oxide:
1] reduces pulmonary artery pressure & improves oxygenation
2] no improvement in mortality [2]
3] not recommended [2]
c) ketoconazole not recommended [2]
d) surfactant not recommended [2]
e) statin of no benefit [17]
f) airway pressure release ventilation
g) IFN-beta-1a of no benefit [38]
10) any red cell transfusion may increase mortality [10]
Prognosis:
1) sepsis is most lethal form [6]
2) most survivors discharged to long-term care facility [6]
3) most survivors regain baseline lung function within 12 months
Notes:
- non-standard care frequent in Europe [22]
Related
neonatal respiratory distress syndrome (hyaline membrane disease, neonatal RDS)
Specific
electronic cigarette vaping-associated lung injury (VALI, EVALI)
transfusion-related acute lung injury (TRALI)
General
respiratory distress syndrome (RDS)
acute respiratory failure
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