Platelet Dysfunction after Traumatic Brain Injury: A Review.

Coagulopathy is a known sequela of traumatic brain injury (TBI) and can lead to increased morbidity and mortality. Platelet dysfunction has been identified as one of several etiologies of coagulopathy following TBI and has been associated with poor outcomes. Regardless of whether the platelet dysfunction occurs as a direct consequence of the injury or because of pre-existing medical comorbidities or medication use, accurate detection and monitoring of response to therapy is key to optimal patient care. Platelet transfusion has been proposed as a potential therapeutic intervention to treat platelet dysfunction, with several studies using platelet function assays to monitor response. The development of increasingly precise diagnostic testing is providing enhanced understanding of the specific derangement in the hemostatic process, allowing clinicians to provide patient-specific treatment plans. There is wide variability in the currently available literature on the incidence and clinical significance of platelet dysfunction following TBI, which creates challenges with developing evidence-based management guidelines. The relatively high prevalence of platelet inhibitor therapy serves as an additional confounding factor. In addition, the data are largely retrospective in nature. We performed a literature review to provide clarity on this clinical issue. We reviewed 348 abstracts, and included 97 manuscripts in our final literature review. Based on the currently available research, platelet dysfunction has been consistently demonstrated in patients with moderate-severe TBI. We recommend the use of platelet functional assays to evaluate patients with TBI. Platelet transfusion directed at platelet dysfunction may lead to improved clinical outcome. A randomized trial guided by implementation science could improve the applicability of these practices.

Desmopressin is a transfusion sparing option to reverse platelet dysfunction in patients with severe traumatic brain injury.

BACKGROUND: Platelet dysfunction (PD) is an independent predictor of mortality in patients with severe traumatic brain injury (sTBI). Platelet transfusions (PLTs) have been shown to be an effective treatment strategy to reverse platelet inhibition. Their use is contingent on availability and may be associated with increased cost and transfusion-related complications, making desmopressin (DDAVP) attractive. We hypothesized that DDAVP would correct PD similarly to PLTs in patients with sTBI. METHODS: This retrospective study evaluated all blunt trauma patients admitted to an urban, level 1 trauma center from July 2015 to October 2016 with sTBI (defined as head abbreviated injury scale [AIS] ≥3) and PD (defined as adenosine diphosphate [ADP] inhibition ≥60% on thromboelastography) and subsequently received treatment. Per our institutional practice, patients with sTBI and PD are transfused one unit of apheresis platelets to reverse inhibition. During a platelet shortage, we interchanged DDAVP for the initial treatment. Patients were classified as receiving DDAVP or PLT based on the initial treatment. RESULTS: A total of 57 patients were included (DDAVP, n = 23; PLT, n = 34). Patients who received DDAVP were more severely injured (injury severity score, 29 vs. 23; p = 0.045), but there was no difference in head AIS (4 vs. 4, p = 0.16). There was no difference between the two groups in admission platelet count (244 ± 68 × 10/µL vs. 265 ± 66 × 10/µL, p = 0.24) or other coagulation parameters such as prothrombin time, partial thromboplastin time, or international normalized ratio. Before treatment, both groups had similar ADP inhibition as measured by thromboelastography (ADP, 86% vs. 89%, p = 0.34). After treatment, both the DDAVP and PLT groups had similar correction of platelet ADP inhibition (p = 0.28). CONCLUSION: In patients with severe traumatic brain injury and PD, DDAVP may be an alternative to PLTs to correct PD. LEVEL OF EVIDENCE: Therapeutic, level IV.