UNLABELLED: 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.
UNLABELLED: 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.