BACKGROUND: Transfusion of citrated blood products may worsen resuscitation-induced hypocalcemia and trauma outcomes, suggesting the need for protocolized early calcium replacement in major trauma. However, the dynamics of ionized calcium during hemostatic resuscitation of severe injury are not well studied. We determined the frequency of hypocalcemia and quantified the association between the first measured ionized calcium concentration [iCa] and calcium administration early during hemostatic resuscitation and in-hospital mortality. METHODS: We performed a retrospective cohort study of all admissions to our regional level 1 trauma center who (1) were ≥15 years old; (2) presented from scene of injury; (3) were admitted between October 2016 and September 2018; and (4) had a Massive Transfusion Protocol activation. They also (1) received blood products during transport or during the first 3 hours of in-hospital care (1st3h) of trauma center care and (2) had at least one [iCa] recorded in that time. Demographic, injury severity, admission shock and laboratory data, blood product use and timing, and in-hospital mortality were extracted from Trauma Registry and Transfusion Service databases and electronic medical records. Citrate load was calculated on a unit-by-unit basis and used to calculate an administered calcium/citrate molar ratio. Univariate and multivariable logistic regression analyses for the binary outcome of in-hospital death were performed. RESULTS: A total of 11,474 trauma patients were admitted to the emergency department over the study period, of whom 346 (3%; average age: 44 ± 18 years; 75% men) met all study criteria. In total, 288 (83.2%) had hypocalcemia at first [iCa] determination; 296 (85.6%) had hypocalcemia in the last determination in the 1st3h; and 177 (51.2%) received at least 1 calcium replacement dose during that time. Crude risk factors for in-hospital death included age, injury severity score (ISS), new ISS (NISS), Abbreviated Injury Scale (AIS) head, admission systolic blood pressure (SBP), pH, and lactate; all P < .001. Higher in-hospital mortality was significantly associated with older age, higher NISS, AIS head, and admission lactate, and lower admission SBP and pH. There was no relationship between mortality and first [iCa] or calcium dose corrected for citrate load. CONCLUSIONS: In our study, though most patients had hypocalcemia during the 1st3h of trauma center care, neither first [iCa] nor administered calcium dose corrected for citrate load were significantly associated with in-patient mortality. Clinically, hypocalcemia during early hemostatic resuscitation after severe injury is important, but specific treatment protocols must await better understanding of calcium physiology in acute injury.
Purpose of reviewDespite significant advances in trauma management over the last twenty years, uncontrolled hemorrhage remains the leading cause of preventable death in trauma. We review recent changes affecting hemorrhage control resuscitation.Recent findingsEarly blood product usage has become well established as a standard of care in trauma hemorrhage control. To enable this, low titer group A liquid plasma and group O whole blood are increasingly utilized. Single donor apheresis platelets have now replaced pooled donor platelets in the USA and are often pathogen reduced, which has implications for trauma resuscitation. Further work is examining timing and dosing of tranexamic acid and the debate in factor concentrate usage in trauma induced coagulopathy continues to evolve. The ‘Stop the bleed’ campaign has highlighted how important the use of hemostatic dressings are in hemorrhage control, as too is the expanded use of endovascular aortic occlusion. We highlight the ongoing research into desmopressin use and the undetermined significance of ionized calcium levels in trauma. Finally, we discuss our own hospital experience with coagulation testing and the paucity of evidence of improved outcomes with viscoelastic testing.SummaryImproving trauma coagulopathy diagnostics and hemorrhage control are vital if we are to decrease the mortality associated with trauma.
Purpose of reviewFibrin polymerization is essential for stable clot formation in trauma, and hypofibrinogenemia reduces hemostasis in trauma. This review considers fibrinogen biology, the changes that fibrinogen undergoes after major trauma, and current evidence for lab testing and treatment.Recent findingsFibrinogen is a polypeptide that is converted to fibrin by the action of thrombin. During trauma, fibrinogen levels are consumed and reduce within the first few hours because of consumption, dilution, and fibrinolysis. Fibrinogen levels usually rebound within 48 hours of injury and can contribute to thrombotic events. The Clauss fibrinogen assay is the gold standard test for fibrinogen levels, although viscoelastic hemostatic assays are often used when a lab delay is anticipated. An evidence-based threshold for fibrinogen replacement is not well established in the literature, but expert opinion recommends maintaining a level above 150 mg/dl.SummaryHypofibrinogenemia is an important cause of nonanatomic bleeding in trauma. Despite multiple pathologic causes, the cornerstone of treatment remains fibrinogen replacement with cryoprecipitate or fibrinogen concentrates.
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