Ebook Essentials of trauma anesthesia (2/E): Part 2
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Ebook Essentials of trauma anesthesia (2/E): Part 2
Section 1Chapter11Core Principles in Trauma AnesthesiaCoagulation Monitoring of the Bleeding Trauma PatientMarc p. Steurer and Michael T. GanterIntrod Ebook Essentials of trauma anesthesia (2/E): Part 2ductionBlood coagulation is a complex and tightly regulated physiologic network of interacting proteins and cells. If deranged, it may dramatically influence outcome. A comprehensive understanding of normal hemostasis and its pathophysiology is necessary for anesthesiologists working in the perioper Ebook Essentials of trauma anesthesia (2/E): Part 2ative field.Treatment of a massive trauma bleeding requires an interdisciplinary approach for both trauma surgeons and anesthesiologists. Modern transEbook Essentials of trauma anesthesia (2/E): Part 2
fusion strategies and coagulation management are based on a detailed understanding of coagulation physiology and specific coagulation monitoring. BesiSection 1Chapter11Core Principles in Trauma AnesthesiaCoagulation Monitoring of the Bleeding Trauma PatientMarc p. Steurer and Michael T. GanterIntrod Ebook Essentials of trauma anesthesia (2/E): Part 2g used to assess hemostasis. Consequently, specific, individualized, and goal-directed hemostatic interventions are becoming more and more feasible.Abnormal hemostasis is not limited to bleeding. Hypercoagulability and thrombosis are further phenotypes of disturbed hemostasis. The coagulation system Ebook Essentials of trauma anesthesia (2/E): Part 2 represents a delicate balance of forces supporting coagulation (coagulation, antifibrinolysis) and forces inhibiting coagulation (anticoagulation, fiEbook Essentials of trauma anesthesia (2/E): Part 2
brinolysis) (Figure 11.1). The distinctive challenge is to assess and quantify both sides of this balance and to maintain an equilibrium. Specific coaSection 1Chapter11Core Principles in Trauma AnesthesiaCoagulation Monitoring of the Bleeding Trauma PatientMarc p. Steurer and Michael T. GanterIntrod Ebook Essentials of trauma anesthesia (2/E): Part 2rmal blood coagulation exists when procoagulant and anticoagulant forces are in balance.154Chapter 11: CoagulatioiCurrent Concepts of the Coagulation SystemHemostasis is the process that causes bleeding to stop after a vessel injury. It is maintained in the body by three interacting mechanisms: the Ebook Essentials of trauma anesthesia (2/E): Part 2vasculature, primary hemostasis, and secondary' hemostasis. Ill addition, hemostasis initiates sore healing of the injured vessel while preserving theEbook Essentials of trauma anesthesia (2/E): Part 2
general rheologic qualities of the blood.•The vascular part of hemostasis is the first step after a vessel injury. It is mediated in a paracrine way Section 1Chapter11Core Principles in Trauma AnesthesiaCoagulation Monitoring of the Bleeding Trauma PatientMarc p. Steurer and Michael T. GanterIntrod Ebook Essentials of trauma anesthesia (2/E): Part 2ressure temporarily decreases within the vessel.•Primary hemostasis describes the cellular part ofclolling and is primarily mediated by platelets and von Willebrand factor (VWF). Platelet activation (with release of coagulation-active substances), adhesion, aggregation, and finally stabilization res Ebook Essentials of trauma anesthesia (2/E): Part 2ult in a mechanical blockage of the damaged vessel wall by a platelet plug.•Secondary hemostasis illustrates the plasmatic portion of blood clotting aEbook Essentials of trauma anesthesia (2/E): Part 2
nd describes the complex interaction of different clotting factors that finally result in a stable fibrin network.To protect the organism against throSection 1Chapter11Core Principles in Trauma AnesthesiaCoagulation Monitoring of the Bleeding Trauma PatientMarc p. Steurer and Michael T. GanterIntrod Ebook Essentials of trauma anesthesia (2/E): Part 2ive clot formation and promotes lysis of inadvertently formed blood clots.In vivo, the coagulation system becomes primarily activated by tissue factor (TF). Tissue factor exists beyond the blood vessels on smooth muscle cells and fibroblasts. Therefore, the coagulation system is not activated in a h Ebook Essentials of trauma anesthesia (2/E): Part 2ealthy individual. Tissue damage, however, brings TF in contact with blood and activates the clotting system to protect the organism from exsanguinatiEbook Essentials of trauma anesthesia (2/E): Part 2
on. Under certain pathologic circumstances like sepsis, TF can be intravascularly expressed on endothelial cells, monocytes, and circulating micropartSection 1Chapter11Core Principles in Trauma AnesthesiaCoagulation Monitoring of the Bleeding Trauma PatientMarc p. Steurer and Michael T. GanterIntrod Ebook Essentials of trauma anesthesia (2/E): Part 2 (D1C).The key enzyme of secondary hemostasis is thrombin (Flla), a serin-protease similar to trypsin. Besides transformation of fibrinogen to soluble fibrin, thrombin facilitates numerous other biochemical reactions such as coagulation and immune system activation. The net effect of thrombin depend Ebook Essentials of trauma anesthesia (2/E): Part 2s on the context and the molecules that are present locally. Thrombin promotes activation of clotting Factors V, VIII, and XI, thereby activating theEbook Essentials of trauma anesthesia (2/E): Part 2
intrinsic pathway and finally amplifying its own production. Thrombin further activates the thrombin-activated fibrinolysis inhibitor (TAF1), Factor XSection 1Chapter11Core Principles in Trauma AnesthesiaCoagulation Monitoring of the Bleeding Trauma PatientMarc p. Steurer and Michael T. GanterIntrod Ebook Essentials of trauma anesthesia (2/E): Part 2he protection from an overshooting thrombin formation: the antithrombin and protein c system. Antithrombin does so by irreversibly binding and inactivating thrombin. Activated protein c has strong anticoagulatory and pro-fibrinolytic properties that further help balance thrombosis.The historical cas Ebook Essentials of trauma anesthesia (2/E): Part 2cade model of blood coagulation published in 1964 with its intrinsic and extrinsic activation pathways describes the complexity of hemostasis inadequaEbook Essentials of trauma anesthesia (2/E): Part 2
tely, it limits itself to the phenomena of in vitro secondary hemostasis and permits no explanation of certain coagulation disorders in vivo. NevertheSection 1Chapter11Core Principles in Trauma AnesthesiaCoagulation Monitoring of the Bleeding Trauma PatientMarc p. Steurer and Michael T. GanterIntrod Ebook Essentials of trauma anesthesia (2/E): Part 2in lime (PT)/inlernational normalized ratio (INR) and the activated partial thromboplastin lime (aPTT)._________________I156Section 1: Core Principles in Trauma AnesthesiaA more recent and accurate model of blood clotting is the cell-based coagulation model. In contrast to the cascade model, it assu Ebook Essentials of trauma anesthesia (2/E): Part 2mes that coagulation takes place on activated cell surfaces. Besides platelets and endothelial cells, the cell surface of erythrocytes, leukocytes, anEbook Essentials of trauma anesthesia (2/E): Part 2
d microparticles play a central role. Different steps are distinguished:•rhe clotting process is described by the initiation, amplification, and propaSection 1Chapter11Core Principles in Trauma AnesthesiaCoagulation Monitoring of the Bleeding Trauma PatientMarc p. Steurer and Michael T. GanterIntrod Ebook Essentials of trauma anesthesia (2/E): Part 2 termination of coagulation activation (mediated by TF pathway inhibitor, antithrombin and the protein c pathway) and the elimination of overt clot formation (mediated by plasmin).This model illustrates the in vivo coagulation better than the classical cascade model. For example, it can explain the Ebook Essentials of trauma anesthesia (2/E): Part 2bleeding defects observed with Factors XI, IX, and VIII deficiencies, because these proteins are required for generation of Factor Xa (and subsequentlEbook Essentials of trauma anesthesia (2/E): Part 2
y thrombin) on platelet membranes. It further suggests that the extrinsic and intrinsic systems are in fact parallel generators of Factor Xa that occuSection 1Chapter11Core Principles in Trauma AnesthesiaCoagulation Monitoring of the Bleeding Trauma PatientMarc p. Steurer and Michael T. GanterIntrod Ebook Essentials of trauma anesthesia (2/E): Part 2ly represent this model. The cell-based coagulation model can be illustrated much better with whole blood, viscoelastic coagulation analyzers.Assessment of CoagulationTo best assess and quantify the status of a patient’s coagulation system, information on the following four mainstays of perioperativ Ebook Essentials of trauma anesthesia (2/E): Part 2e coagulation monitoring should be collected and combined for clinical interpretation.1Medical HistoryThe patient’s focused medical history is crucialEbook Essentials of trauma anesthesia (2/E): Part 2
for the assessment of the individual bleeding risk and should be carried out with specific questionnaires. This standardized approach has been shown Section 1Chapter11Core Principles in Trauma AnesthesiaCoagulation Monitoring of the Bleeding Trauma PatientMarc p. Steurer and Michael T. GanterIntrod Ebook Essentials of trauma anesthesia (2/E): Part 2preoperative assessment of hemostasis.2Clinical PresentationThe clinical presentation of abnormal hemostasis (c.g., certain phenotypes of bleeding or thrombosis) is critical for the differential diagnosis and gives valuable information on possible etiologies of the underlying coagulation disorder. A Ebook Essentials of trauma anesthesia (2/E): Part 2lso, abnormal laboratorycoagulation studies must always be correlated with the current clinical presentation, before any hemostatic therapy is initiatEbook Essentials of trauma anesthesia (2/E): Part 2
ed. Without clinically relevant bleeding (c.g., “dry” surgical area) no procoagulant therapy should be initiated due to the risk of adverse thromboticSection 1Chapter11Core Principles in Trauma AnesthesiaCoagulation Monitoring of the Bleeding Trauma PatientMarc p. Steurer and Michael T. GanterIntrodGọi ngay
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