Inhibition of platelet function is common following even minor injury

Sirajuddin, Sarah; Valdez, Carrie; DePalma, Louis; Maluso, Patrick; Singhal, R. L.; Schroeder, Mary; Sarani, Babak

doi:10.1097/ta.0000000000001057

Cited by 54 publications

(50 citation statements)

References 19 publications

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“…Finally, Sirajuddin et al recently reported on the apparent ubiquity of platelet dysfunction in a cohort of 459 minimally injured trauma patients (median ISS 5 5). 49 Patients in their study had lower platelet inhibition to ADP and AA stimulation (58% and 30%, respectively) than patients in other studies presenting with hemorrhagic shock (97% and 50%, respectively) 50 or severe TBI (87% and 38%, respectively), 51 but nevertheless had significant platelet inhibition compared with uninjured controls. How should these data be interpreted?…”

Section: Platelet Dysfunctionmentioning

confidence: 66%

“…The specific mechanism is unknown but may involve "platelet exhaustion," where platelets become activated en masse and are refractory to further stimulation for up to 24 hours afterward. 52,53 However, because the minimally injured patients above 49 had little evidence of bleeding (2% mortality and minimal transfusion requirements [Babak Sarani, George Washington University, electronic communication, May 17, 2016]) despite inhibition of platelet function on TEG-PM, the contribution of such platelet dysfunction to TIC is ambiguous. A recent study by Stalker et al investigating location-dependent differential platelet activation and organization may shine some light on this question.…”

Section: Platelet Dysfunctionmentioning

confidence: 99%

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Advances in the understanding of trauma-induced coagulopathy

Chang

Cardenas

Wade

et al. 2016

Blood

246

225

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Ten percent of deaths worldwide are due to trauma, and it is the third most common cause of death in the United States. Despite a profound upregulation in procoagulant mechanisms, one-quarter of trauma patients present with laboratory-based evidence of trauma-induced coagulopathy (TIC), which is associated with poorer outcomes including increased mortality. The most common causes of death after trauma are hemorrhage and traumatic brain injury (TBI). The management of TIC has significant implications in both because many hemorrhagic deaths could be preventable, and TIC is associated with progression of intracranial injury after TBI. This review covers the most recent evidence and advances in our understanding of TIC, including the role of platelet dysfunction, endothelial activation, and fibrinolysis. Trauma induces a plethora of biochemical and physiologic changes, and despite numerous studies reporting differences in coagulation parameters between trauma patients and uninjured controls, it is unclear whether some of these differences may be “normal” after trauma. Comparisons between trauma patients with differing outcomes and use of animal studies have shed some light on this issue, but much of the data continue to be correlative with causative links lacking. In particular, there are little data linking the laboratory-based abnormalities with true clinically evident coagulopathic bleeding. For these reasons, TIC continues to be a significant diagnostic and therapeutic challenge.

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Section: Platelet Dysfunctionmentioning

confidence: 66%

Section: Platelet Dysfunctionmentioning

confidence: 99%

Advances in the understanding of trauma-induced coagulopathy

Chang

Cardenas

Wade

et al. 2016

Blood

246

225

View full text Add to dashboard Cite

show abstract

“…Given their critical roles in hemostasis and inflammation, platelets are a logical cellular target for investigation as a link between the excessive inflammatory response after injury and the regulation of thrombosis. The degree of platelet dysfunction following trauma is profound, with some reports suggesting that up to 45% of patients on admission and 90% of patients in the intensive care unit after trauma have impaired response to platelet agonists (39), with even minimally injured patients manifesting with some dysfunction(40). Importantly, impaired response to platelet agonists has been linked to mortality following trauma(41).…”

Section: Pro: Coagulopathy Should Be a Therapeutic Target In Criticalmentioning

confidence: 99%

Is Coagulopathy an Appropriate Therapeutic Target During Critical Illness Such as Trauma or Sepsis?

Moore

Winfield

Aibiki

et al. 2017

Shock

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Coagulopathy is a common and vexing clinical problem in critically ill patients. Recently, major advances focused on the treatment of coagulopathy in trauma and sepsis have emerged. However, the targeting of coagulopathy with blood product transfusion and drugs directed at attenuating the physiologic response to these conditions have major potential risk to the patient. Therefore, the identification of coagulopathy as a clinical target is an area of uncertainty and controversy. In order to analyze the state of the science regarding coagulopathy in critical illness, a symposium addressing the problem was organized at the 39th annual meeting of the Shock Society in the summer of 2016. This manuscript synthesizes the viewpoints of the four expert panelists at the debate and presents an overview of the potential positive and negative consequences of targeting coagulopathy in trauma and sepsis.

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“…Specifically, trauma patients maintain their dense granules even in the presence of ADP receptor inhibition contradicting the theory of platelet granule exhaustion as the etiology for platelet dysfunction [12]. Furthermore, other studies have documented a significant inhibited response to ADP following minor trauma, suggesting receptor status may be a biomarker of injury rather than a mediator of TIC [13]. Therefore, we propose to assess the role of platelet ADP receptor dysfunction, measured by TEG –PM mapping in predicting mortality, requirement of massive transfusion and platelet transfusion among patients at risk for TIC.…”

Section: Introductionmentioning

confidence: 99%

Platelet adenosine diphosphate receptor inhibition provides no advantage in predicting need for platelet transfusion or massive transfusion

Stettler

Moore

et al. 2017

Surgery

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Introduction Thrombelastography Platelet Mapping (TEG-PM) is a useful assay to assess antiplatelet therapy. Inhibited response to the ADP receptor on platelets occurs early following injury but recent work suggests this alteration occurs even with minor trauma. However, the utility of TEG-PM, specifically the percent of ADP receptor inhibition (%ADP-INH), in predicting outcomes and guiding platelet transfusion in trauma-induced coagulopathy (TIC) remains unknown. We assessed the role of %ADP-INH in predicting survival, requirement for massive transfusion or platelet transfusion in patients at risk for TIC. Methods TEG-PM was assessed in 303 trauma activation patients from 2014–2016 and in 89 healthy volunteers. %ADP-INH is presented as median and interquartile range (IQR). We compared the area under the receiver operating characteristic curve (AUROC) of %ADP-INH, platelet count, and rTEG Maximum amplitude (MA) for in-hospital mortality, massive transfusion (>10 RBC or death/6 hours, and platelet transfusion (>0 platelet units or death/6hrs). Results Overall, 35 (11.5%) patient died, 27 (8.9%) required massive transfusion and 46, platelet transfusions (15.2%). Median %ADP-INH was 42.5% (IQR: 22.4–69.1%), compared to 4.3 % (IQR: 0–13.5%) in healthy volunteers (p<0.0001). Patients that died, had a massive transfusion, or platelet transfusion had higher %ADP-INH than those that did not (p<0.05 for all). However, %ADP-INH did not add significantly to the predictive performance of MA or platelet count for any of the three outcomes, after adjustment for confounders. Subgroup analyses by severe traumatic brain injury, severe injury and requirement of RBCs showed similar results. Conclusion ADP receptor inhibition did not add predictive value to predicting mortality, massive transfusion, or platelet transfusion. Thus, the role of TEG-PM as a solitary tool to guide platelet transfusions in trauma requires continued refinement.

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Inhibition of platelet function is common following even minor injury

Abstract: Prognostic/epidemiogic study, level III.

Cited by 54 publications

References 19 publications

Advances in the understanding of trauma-induced coagulopathy

Advances in the understanding of trauma-induced coagulopathy

Is Coagulopathy an Appropriate Therapeutic Target During Critical Illness Such as Trauma or Sepsis?

Platelet adenosine diphosphate receptor inhibition provides no advantage in predicting need for platelet transfusion or massive transfusion

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