Nejm 2005;353:1685; 2000;342:1334

Cause:

Direct injury: multiple agents including pneumonia, aspiration, inhalation injury (30-40% risk), salicylate poisoning (Ann IM 1981;95:405), fat emboli, drowning (Drowning), hantavirus infection in southwestern US (Lassa Fever) (Nejm 1994;330:949)

Indirect injury: bacterial sepsis (30-40% risk) most often from intra-abdominal gi perforation, pancreatitis, neurogenic (head trauma), drug OD, transfusions, bypass

Pathophys:Normal pressure pulmonary edema from capillary leak (Nejm 1982;306:900). Assoc w decreased levels of pulmonary urokinase, which causes increased fibrin deposition and scarring (Nejm 1990;322:890), elevated cytokines and other inflammatory proteins, depressed interleukins and interleukin receptor availability

Incidence increased by risk factors:

Table 16.1 Risk Factors for ARDS

If multiple risk factors, 25% get (Petty-Ann IM 1983;98:593); most develop within 48 h of getting risk factors; hypotension precedes in 90%. Chronic alcohol abuse doubles risk and mortality (Jama 1996;275:50)

Sx:Dyspnea

Si:Hypoxia, tachypnea; PCWP <18 mm Hg

Substantial mortality ~45% (Jama 1995;273:306), usually not respiratory; survivors have significant impairment of exercise capacity and muscle strength even 1 yr out (Nejm 2003;348:683)

Barotrauma, esp if peak pressures >70 cm water for more than a day. Pulmonary fibrosis in 30%

r/o CHF, Pneumocystis cariniiand other overwhelming opportunistic infections

Lab:

ABGs:Hypoxia; P_aO₂/F_iO₂200

Bact:Bronchopulmonary lavage for pathogens

Xray:

Chest shows diffuse bilateral pulmonary infiltrates starting perihilar within 24 h, often looks like CHF; may progress to “white out”

CT shows patchy involvement, the extent of which correlates w ABGs; also can show occult abscesses or barotrauma

Rx:

Treat underlying disease; monitor cardiac output; avoid fluid overload

Ventilator modes: lower volumes and permissive hypercapnia to prevent shear injury; inverse I/E, pressure control; PEEP when on ventilator, 0-30 cm water, can’t use preventively (Nejm 1984;311:281, 323); debate re max and minimal settings parameters (Nejm 1998;338:341, 347, 355, 385); increases in PEEP cause decreases in cardiac output due to left shift of interventricular septum (Nejm 1981;304:387) as well as diminished venous return and elevated pulmonary vascular resistance, which increases R to L shunt in 15% of the population w a potential ASD (Ann IM 1993;119:886)

Nitric oxide inhalation improves V/Q mismatch and arterial pO₂, but unclear if improves survival (Nejm 1993;328:399, 431)

Steroids improve short-term physiology but don’t improve or may worsen long-term outcomes (DBCT—Nejm 2006;354:1671)

Aerosolized surfactant × 24 h does not improve survival (Nejm 2004;351:884)