Tissue plasminogen activator challenge thrombelastography is the most accurate assay in predicting the need for massive transfusion in hypotensive trauma patients.

BACKGROUND: Tissue plasminogen activator (tPA) added to thrombelastography (TEG) detects hyperfibrinolysis by measuring clot lysis at 30 min (tPA-challenge-TEG). We hypothesize that tPA-challenge-TEG is a better predictor of massive transfusion (MT) than existing strategies in trauma patients with hypotension. METHODS: Trauma activation patients (TAP, 2014-2020) with 1) systolic blood pressure <90 mmHg (early) or 2) those who arrived normotensive but developed hypotension within 1H postinjury (delayed) were analyzed. MT was defined as >10 RBC U/6H postinjury or death within 6H after ≥1 RBC unit. Area under the receiver operating characteristics curves were used to compare predictive performance. Youden index determined optimal cutoffs. RESULTS: tPA-challenge-TEG was the best predictor of MT in the early hypotension subgroup (N = 212) with positive (PPV) and negative predictive values (NPV) of 75.0%, and 77.6%, respectively. tPA-challenge-TEG was a better predictor of MT than all but TASH (PPV = 65.0%, NPV = 93.3%) in the delayed hypotension group (N = 125). CONCLUSIONS: The tPA-challenge-TEG is the most accurate predictor of MT in trauma patients arriving hypotensive and offers early recognition of MT in patients with delayed hypotension.

Low viscoelastic clot strength, platelet transfusions, and graft dysfunction are associated with persistent postoperative ascites following liver transplantation.

INTRODUCTION: High output, persistent ascites (PA) is a common complication following liver transplant (LT). Recent work has identified that platelets help maintain endothelial integrity and can decrease leakage in pathological states. We sought to assess the association of PA following LT with platelet count and platelet function. METHODS: Clot strength (MA) is a measure of platelet function and was quantified using thrombelastography (TEG). Total drain output following surgery was recorded in 24-h intervals during the same time frame as TEG. PA was considered >1 L on POD7, as that much output prohibits drain removal. RESULTS: 105 LT recipients with moderate or high volume preoperative ascites were prospectively enrolled. PA occurred in 28%. Platelet transfusions before and after surgery were associated with PA, in addition to POD5 TEG MA and POD5 MELD score. Patients with PA had a longer hospital length of stay and an increased rate of intraabdominal infections. CONCLUSION: Persistent ascites following liver transplant is relatively common and associated with platelet transfusions, low clot strength, and graft dysfunction.

Fibrinolysis resistance after liver transplant as a predictor of early infection.

BACKGROUND: Infection is a leading cause of morbidity in liver transplant (LT). Considering that the fibrinolytic system is altered in sepsis, we investigated the relationship between fibrinolysis resistance (FR) and post-transplant infection. METHODS: Fibrinolysis was quantified using thrombelastography (TEG) with the addition of tPA to quantify FR. FR was defined as LY30 = 0% and stratified as transient if present on POD1 or POD5 (tFR), persistent (pFR) if present on both, or no FR (nFR) if absent. RESULTS: 180 LT recipients were prospectively enrolled. 52 (29%) recipients developed infection. 72 had tFR; 37 had pFR; and 71 had nFR. Recipients with pFR had significantly greater incidence of infections (51% vs. 26% tFR vs. 20% nFR, p = 0.002). pFR was independently associated with increased odds of post-transplant infection (adjusted OR 3.39, p = 0.009). CONCLUSIONS: Persistent fibrinolysis resistance is associated with increased risk of post-transplant infection.

GPR37 modulates progenitor cell dynamics in a mouse model of ischemic stroke.

The generation of neural stem and progenitor cells following injury is critical for the function of the central nervous system, but the molecular mechanisms modulating this response remain largely unknown. We have previously identified the G protein-coupled receptor 37 (GPR37) as a modulator of ischemic damage in a mouse model of stroke. Here we demonstrate that GPR37 functions as a critical negative regulator of progenitor cell dynamics and gliosis following ischemic injury. In the central nervous system, GPR37 is enriched in mature oligodendrocytes, but following injury we have found that its expression is dramatically increased within a population of Sox2-positive progenitor cells. Moreover, the genetic deletion of GPR37 did not alter the number of mature oligodendrocytes following injury but did markedly increase the number of both progenitor cells and injury-induced Olig2-expressing glia. Alterations in the glial environment were further evidenced by the decreased activation of oligodendrocyte precursor cells. These data reveal that GPR37 regulates the response of progenitor cells to ischemic injury and provides new perspectives into the potential for manipulating endogenous progenitor cells following stroke.