In an investigation on 19 patients with traumatic (n = 11) and septic (n = 8) shock, at risk of developing adult respiratory distress syndrome (ARDS), various coagulation and fibrinolysis variables and also blood gases and chest x-ray were monitored. Eight patients developed ARDS - two after traumatic shock and six following septic shock.
Laboratory findings: the conventional disseminated intravascular coagulation variables (fibrinogen, platelet counts, activated partial thromboplastin time, ethanol gelation test, thrombotest, normotest and fibrin degradation products) could not discriminate between ARDS and non-ARDS patients, but showed an essentially similar reaction pattern in these two groups. Antithrombin-III and plasminogen levels were significantly lower in patients with ARDS, while factor VIII-related antigen levels were significantly higher in ARDS than in non-ARDS patients.
Clinical data: patients with septic shock run a significantly greater risk of developing ARDS (6 of 8) than those with traumatic shock (2 of 11; P less than 0.02). Furthermore, the onset of ARDS after septic shock seems to occur in a more rapid way, while ARDS following traumatic shock develops more gradually. Early ventilator treatment with positive end expiratory pressure counteracts the classical radiographic picture of ARDS with bilateral alveolar densities.