Udskriv Udskriv
Switch language
Rigshospitalet - en del af Københavns Universitetshospital

Mild induced hypothermia: Effects on sepsis-related coagulopathy -results from a randomized controlled trial

Publikation: Bidrag til tidsskriftTidsskriftartikelForskningpeer review

  1. Candidate single nucleotide polymorphisms and thromboembolism in acute lymphoblastic leukemia - A NOPHO ALL2008 study

    Publikation: Bidrag til tidsskriftTidsskriftartikelForskningpeer review

  2. Role of spleen and liver for enhanced hemostatic competence following administration of adrenaline to humans

    Publikation: Bidrag til tidsskriftTidsskriftartikelForskningpeer review

  3. Managing antiphospholipid syndrome in pregnancy

    Publikation: Bidrag til tidsskriftReviewForskningpeer review

  4. Prevalence and significance of anti-phosphatidylserine antibodies: A pooled analysis in 5992 patients

    Publikation: Bidrag til tidsskriftTidsskriftartikelForskningpeer review

  5. Tinzaparin for the treatment of foetal growth retardation: An open-labelled randomized clinical trial

    Publikation: Bidrag til tidsskriftTidsskriftartikelForskningpeer review

Vis graf over relationer

INTRODUCTION: Coagulopathy associates with poor outcome in sepsis. Mild induced hypothermia has been proposed as treatment in sepsis but it is not known whether this intervention worsens functional coagulopathy.

MATERIALS AND METHODS: Interim analysis data from an ongoing randomized controlled trial; The Cooling And Surviving Septic shock (CASS) study. Patients suffering severe sepsis/septic shock are allocated to either mild induced hypothermia (cooling to 32-34°C for 24hours) or control (uncontrolled temperature).

TRIAL REGISTRATION: NCT01455116. Thrombelastography (TEG) is performed three times during the first day after study enrollment in all patients. Reaction time (R), maximum amplitude (MA) and patients' characteristics are here reported.

RESULTS: One hundred patients (control n=50 and intervention n=50; male n=59; median age 68years) with complete TEG during follow-up were included. At enrollment, 3%, 38%, and 59% had a hypocoagulable, normocoagulable, and hypercoagulable TEG clot strength (MA), respectively. In the hypothermia group, functional coagulopathy improved during the hypothermia phase, measured by R and MA, in patients with hypercoagulation as well as in patients with hypocoagulation (correlation between ΔR and initial R: rho=-0.60, p<0.0001 and correlation between ΔMA and initial MA: rho=-0.50, p=0.0002). Similar results were not observed in the control group neither for R (rho=-0.03, p=0.8247) nor MA (rho=-0.15, p=0.3115).

CONCLUSION: Mild induced hypothermia did seem to improve functional coagulopathy in septic patients. This improvement of functional coagulopathy parameters during the hypothermia intervention persisted after rewarming. Randomized trials are warranted to determine whether the positive effect on sepsis-related coagulopathy can be transformed to improved survival.

TidsskriftThrombosis Research
Udgave nummer1
Sider (fra-til)175-82
Antal sider8
StatusUdgivet - jan. 2015

ID: 44917029