7 research outputs found
Diagnostic value of prehospital arterial blood gas measurements – a randomised controlled trial
Abstract Background Arterial blood gas analysis is an important diagnostic tool in managing critically ill patients within the hospital. Whether prehospital application of this diagnostic modality contributes to more exact diagnoses and treatments in critically ill prehospital patients is unknown. The aim of this study was to establish whether access to arterial blood gas analysis increased the prehospital diagnostic accuracy of prehospital anaesthesiologists. Furthermore, we investigated whether prehospital blood gas analysis resulted in therapeutic interventions that would not have been carried out if the arterial blood gas analyser had not been available. Methods In a prospective randomised study, two groups of prehospital adult patients with acute critical illness were compared. All patients received standard prehospital care. In the intervention group, an arterial blood gas sample was analysed prehospitally. The primary outcome was the impact of blood gas analysis on the accuracy of prehospital diagnoses. Furthermore, we registered any therapeutic interventions that were carried out as a direct result of the blood gas analysis. Results A total of 310 patients were included in the study. Eighty-eight of these patients were subsequently excluded, primarily due to difficulties in obtaining post hoc consent or venous sampling or other technical difficulties. A total of 102 patients was analysed in the arterial blood gas group (ABG group), while 120 patients were analysed in the standard care group (noABG group). In 78 of the 102 patients in the ABG group, the prehospital physician reported that ABG analysis increased their perceived diagnostic precision. In 81 cases in the noABG group, the lack of arterial blood gas analysis was perceived to have decreased diagnostic accuracy. The claim that ABG analysis increased diagnostic accuracy could, however, not be substantiated as there was no difference in the number of un-specific diagnoses between the groups. Blood gas analysis increased the probability of targeting specific prehospital therapeutic interventions and led to 159 interventions, including intubation, ventilation and/or upgrading the level of urgency, in 71 ABG-group patients (p < 0.001). Conclusion Although prehospital arterial blood gas analysis did not improve the accuracy of the prehospital diagnoses assigned to patients, it significantly increased the quality of treatment provided to patients with acute critical illness. Trial registration ClinicalTrials.gov, NCT03006692, retrospectively registered six months after first patient entry
A comparative study of varying doses of enoxaparin for thromboprophylaxis in critically ill patients:A double-blinded, randomised controlled trial
INTRODUCTION: Critically ill patients are predisposed to venous thromboembolism. We hypothesized that higher doses of enoxaparin would improve thromboprophylaxis without increasing the risk of bleeding. Peak anti-factor Xa (anti-Xa) levels of 0.1 to 0.4 IU/ml reflect adequate thromboprophylaxis for general ward patients. Studies conducted in orthopaedic patients demonstrated a statistically significant relationship between anti-Xa levels and wound haematoma and thrombosis. Corresponding levels for critically ill patients may well be higher, but have never been validated in large studies. METHODS: Eighty critically ill patients weighing 50 to 90 kilograms were randomised in a double-blinded study to receive subcutaneous (sc) enoxaparin: 40 mg once daily (QD), 30 mg twice daily (BID), 40 mg BID, or 1 mg/kg QD, each administered for three days. Anti-Xa activity was measured at baseline, and daily at 4, 12, 16 and 24 hours post administration. Antithrombin, fibrinogen, and platelets were measured at baseline and twice daily thereafter. RESULTS: Two patients were transferred prior to participation. On day 1, doses of 40 mg QD (n = 20) and 40 mg BID (n = 19) yielded mean peak anti-Xa of 0.20 IU/ml and 0.17 IU/ml respectively. A dose of 30 mg BID (n = 20) resulted in much lower levels (0.08 IU/ml). Patients receiving 1 mg/kg QD (n = 19) achieved near steady-state mean peak anti-Xa levels from day 1 (0.34 IU/ml). At steady state (day 3), mean peak anti-Xa levels of 0.13 IU/ml and 0.15 IU/ml were achieved with doses of 40 mg QD and 30 mg BID respectively. This increased significantly to 0.33 IU/ml and 0.40 IU/ml for doses of 40 mg BID and 1 mg/kg QD respectively. Thus anti-Xa response profiles differed significantly over the three days between enoxaparin treatment groups (P <0.0001). Doses of 40 mg BID and1 mg/kg QD enoxaparin yielded target anti-Xa levels for over 80% of the study period. There were no adverse effects. CONCLUSIONS: Doses of 40 mg QD enoxaparin (Europe) or 30 mg BID (North America) yield levels of anti-Xa which may be inadequate for critically ill patients. A weight-based dose yielded the best anti-Xa levels without bioaccumulation, and allowed the establishment of near steady-state levels from the first day of enoxaparin administration. TRIAL REGISTRATION: Current Controlled Trials ISRCTN91570009