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Association of trauma severity with antibody seroconversion in heparin-induced thrombocytopenia: A multicenter,
Motoo Fujita1, Takuma Maeda, Shigeki Miyata
1From the Division of Emergency and Critical Care Medicine (M.F., S.K.), Tohoku University Graduate School of Medicine, Miyagi; Department of Anesthesiology (T.M.), National Cerebral and Cardiovascular Center; Department of Molecular Pathogenesis (S.M.), National Cerebral and Cardiovascular Center, Osaka; Department of Emergency Medicine (A.M., M.H.), Hokkaido University Hospital, Hokkaido; Emergency and Critical Care Department (N.M.), Sendai City Hospital, Miyagi; Department of Emergency Medicine and Critical Care Medicine (N.U.), Japan Red Cross Maebashi Hospital, Gunma; Emergency and Trauma Center (A.S.), Kameda Medical Center, Chiba; Department of Emergency Medicine and Critical Care Medicine (T.O.), Saiseikai Utsunomiya Hospital, Tochigi; Department of Emergency and Critical Care Medicine (S.I., K.S.), Tokyo Saiseikai Central Hospital, Tokyo; Emergency Medical Center (Y.F., K.K.), Kagawa University Hospital, Kagawa; and Emergency and Critical Care Medicine St. Luke's International Hospital (T.H.), Tokyo, Japan.
Background:
Heparin administration can induce the production of anti-platelet factor 4 (PF4)/heparin antibodies with platelet-activating properties, causing heparin-induced thrombocytopenia (HIT). Previous studies have suggested that trauma severity influences HIT immune responses, but their relationship has not been fully explained. This study aimed to clarify this association by multicenter prospective observational study.
Methods:
Trauma patients who met the criteria of age 18 years or older and Injury Severity Scores (ISSs) of ≥9 from March 2018 to February 2019 were included. Patients who did not receive any heparin and those who received it as flushes or for treatment were also included. Patients were divided into three groups based on trauma severity (to mild [ISS 9-15], moderate [ISS 16-24], and severe injury groups [ISS ≥25]) and were compared by the seroconversion time and rate, as well as the disappearance rate of antibodies on day 30.
Results:
A total of 184 patients were included: 55, 62, and 67 patients were classified into the mild, moderate, and severe injury groups, respectively. Overall, the seroconversion rates of anti-PF4/heparin immunoglobulin G (IgG) and HIT antibodies by washed platelet activation assay were 26.6% and 16.3%, respectively. There was a significant difference in the seroconversion rates of anti-PF4/heparin IgG ( p = 0.016) and HIT antibodies ( p = 0.046) among the groups. Seroconversion rates in both assays increased with increasing trauma severity. The time required to achieve seroconversion was similar (between 5 and 10 days of trauma onset) regardless of heparin administration. Anti-PF4/heparin IgG and HIT antibodies were no longer detected on day 30 in 28.6% and 60.9% of seroconverted patients, respectively.
Conclusion:
Development of HIT antibodies was observed commonly in severely injured trauma patients. Heparin-induced thrombocytopenia antibody development may be related to trauma severity, with a high disappearance frequency on day 30.
Level Of Evidence:
Therapeutic/Care Management; Level III.
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