Critically ill patients with deranged conventional coagulation tests are often perceived to have an increased bleeding risk. Whether anticoagulant prophylaxis for these patients should be withheld is contentious. This study assessed the ability of using in vitro clot strength, as measured by thromboelastography, to predict thromboembolism in patients with abnormal coagulation profiles.
Prospective cohort study.
A tertiary ICU.
Two-hundred and fifteen critically ill coagulopathic patients with thrombocytopenia and/or a derangement in at least one conventional coagulation test (international normalized ratio or activated partial thromboplastin time) within 48 hours of ICU admission.
Thromboelastography was performed for all study patients, and plasma thrombotic biomarkers were measured in a nested cohort (n = 40). Of the 215 patients included, 34 patients (16%) developed subsequent thromboembolism—predominantly among those with a normal (maximum amplitude, 54–72 mm) or increased (maximum amplitude, > 72 mm) in vitro clot strength on thromboelastography (91%; area under the receiver-operating characteristic curve, 0.74; 95% CI, 0.64–0.83). The ability of the maximum amplitude to predict thromboembolism was comparable to plasma P-selectin concentrations (thromboembolism, 78.3 ng/mL vs no thromboembolism, 59.5 ng/mL; p = 0.031; area under the receiver-operating characteristic curve, 0.73; 95% CI, 0.52–0.95). In addition, patients with an increased maximum amplitude were also less likely to receive blood product transfusions within 24 hours of testing compared with those with a subnormal maximum amplitude (12.8% vs 69.2%, respectively; area under the receiver-operating characteristic curve, 0.74; 95% CI, 0.67–0.80).
In patients with abnormal coagulation profiles, an increased in vitro clot strength on thromboelastography was associated with an increased risk of thromboembolism, and a reduced risk of requiring transfusion compared with those with a normal or reduced in vitro clot strength.
1Department of Intensive Care Medicine, Royal Perth Hospital, Perth, WA, Australia.
2Medical School, University of Western Australia, Perth, WA, Australia.
3Department of Intensive Care Medicine, Fiona Stanley Hospital, Perth, WA, Australia.
4School of Veterinary and Life Sciences, Murdoch University, Perth, WA, Australia.
*See also p. 876.
The sponsors/funders of this study are public or nonprofit organizations that support science in general. They had no role in gathering, analyzing, or interpreting the data. The content of this publication does not reflect the views or polices of the Australian and New Zealand College of Anaesthetists, Royal Perth Hospital Medical Research Foundation, Thrombosis and Haemostasis Society of the Australia and New Zealand, or the Western Australia Health and Raine Medical Research Foundation, nor does mention of trade names, commercial products, or organizations imply endorsement by the Australian government or any of the listed funding agencies.
Ms. Harahsheh designed the study; performed the study recruitment; helped with data collection, performed the laboratory analyses, and data analyses; and wrote the article. Dr. Duff designed the study, performed the study recruitment, helped with data collection, and wrote the article. Dr. Ho designed the study, performed the study recruitment, helped with data collection and data analyses, interpreted the results, and wrote the article. All authors agreed with the final version of the article.
Supplemental digital content is available for this article. Direct URL citations appear in the printed text and are provided in the HTML and PDF versions of this article on the journal’s website (http://journals.lww.com/ccmjournal).
Supported, in part, by the Australian and New Zealand College of Anaesthetists (Project Grant 15/010) and the Royal Perth Hospital Medical Research Foundation 2016 Project Grant.
Ms. Harahsheh’s institution received funding from the Australian and New Zealand College of Anaesthetists (ANZCA) - Project Grant 15/010 and Royal Perth Hospital Medical Research Foundation (RPH MRF) - 2016 Project Grant, and was supported by a young investigator travel grant from the Thrombosis and Haemostasis Society of Australia and New Zealand (to present the initial study results at the “Blood” conference; the Australian Annual National Hematology Conference in October 2017). She disclosed that this research was funded by the ANZCA (Project Grant 15/010) and the RPH MRF 2016 Project Grant. Dr. Ho was supported by the Western Australia Health and Raine Medical Research Foundation through the Raine Clinical Research Fellowship. Dr. Duff has disclosed that she does not have any potential conflicts of interest.
For information regarding this article, E-mail: firstname.lastname@example.org