Signe Voigt Lauridsen1, Christine Lodberg Hvas2, Emilie Sandgaard3, Tua Gyldenholm3, Ronni Mikkelsen4, Tina Obbekjær5, Niels Sunde5, Else Kirstine Tønnesen2, Anne-Mette Hvas6. 1. Department of Intensive Care, Aarhus University Hospital, Aarhus, Denmark; Department of Clinical Biochemistry, Aarhus University Hospital, Aarhus, Denmark; Department of Anaesthesiology, Aarhus University Hospital, Aarhus, Denmark. Electronic address: sivl@clin.au.dk. 2. Department of Intensive Care, Aarhus University Hospital, Aarhus, Denmark. 3. Department of Clinical Biochemistry, Aarhus University Hospital, Aarhus, Denmark. 4. Department of Neuroradiology, Aarhus University Hospital, Aarhus, Denmark. 5. Department of Neurosurgery, Aarhus University Hospital, Aarhus, Denmark. 6. Department of Clinical Biochemistry, Aarhus University Hospital, Aarhus, Denmark; Department of Clinical Medicine, Aarhus University, Aarhus, Denmark.
Abstract
BACKGROUND: The ability to achieve hemostasis after spontaneous subarachnoid hemorrhage (SAH) plays a pivotal role in outcome. Changes in coagulation in the early hours after SAH have been only sparsely investigated. OBJECTIVE: To investigate changes in coagulation after SAH and illuminate underlying mechanisms. METHODS: We enrolled 46 patients with spontaneous aneurysmal SAH. Blood samples were collected at admission and 24 hours after symptom onset. Thromboelastometry (ROTEM) was performed using the standard assays EXTEM, INTEM, and FIBTEM. Platelet maximum clot elasticity was calculated based on ROTEM results. Thrombin generation, levels of thrombin-antithrombin complex, fibrinogen, and coagulation factor XIII were measured. All data were compared with a gender-matched healthy control group. RESULTS: At admission (median, 3 hours 39 minutes from symptom onset), maximum clot firmness (EXTEM, P < 0.0001; INTEM, P = 0.08; FIBTEM, P < 0.0001) and platelet maximum clot elasticity (P < 0.0001) were higher in patients with SAH than in healthy controls. Thrombin generation showed higher, although nonsignificant, endogenous thrombin potential in patients with SAH than in healthy controls (P = 0.06), and thrombin-antithrombin complex levels were above the reference interval. Median fibrinogen and coagulation factor XIII levels were both within the reference parameters and remained increased 24 hours after symptom onset, whereas endogenous thrombin potential (P = 0.01) and thrombin-antithrombin complex levels decreased (P < 0.0001). CONCLUSIONS: Patients with SAH were in a hypercoagulable state at admission and remained so 24 hours after SAH. Increased clot firmness could be caused by increased platelet function, because platelet maximum clot elasticity was increased despite normal fibrinogen and coagulation factor XIII levels.
BACKGROUND: The ability to achieve hemostasis after spontaneous subarachnoid hemorrhage (SAH) plays a pivotal role in outcome. Changes in coagulation in the early hours after SAH have been only sparsely investigated. OBJECTIVE: To investigate changes in coagulation after SAH and illuminate underlying mechanisms. METHODS: We enrolled 46 patients with spontaneous aneurysmalSAH. Blood samples were collected at admission and 24 hours after symptom onset. Thromboelastometry (ROTEM) was performed using the standard assays EXTEM, INTEM, and FIBTEM. Platelet maximum clot elasticity was calculated based on ROTEM results. Thrombin generation, levels of thrombin-antithrombin complex, fibrinogen, and coagulation factor XIII were measured. All data were compared with a gender-matched healthy control group. RESULTS: At admission (median, 3 hours 39 minutes from symptom onset), maximum clot firmness (EXTEM, P < 0.0001; INTEM, P = 0.08; FIBTEM, P < 0.0001) and platelet maximum clot elasticity (P < 0.0001) were higher in patients with SAH than in healthy controls. Thrombin generation showed higher, although nonsignificant, endogenous thrombin potential in patients with SAH than in healthy controls (P = 0.06), and thrombin-antithrombin complex levels were above the reference interval. Median fibrinogen and coagulation factor XIII levels were both within the reference parameters and remained increased 24 hours after symptom onset, whereas endogenous thrombin potential (P = 0.01) and thrombin-antithrombin complex levels decreased (P < 0.0001). CONCLUSIONS:Patients with SAH were in a hypercoagulable state at admission and remained so 24 hours after SAH. Increased clot firmness could be caused by increased platelet function, because platelet maximum clot elasticity was increased despite normal fibrinogen and coagulation factor XIII levels.
Authors: Sophia Hohenstatt; Christian Ulfert; Christian Herweh; Silvia Schönenberger; Jan C Purrucker; Martin Bendszus; Markus A Möhlenbruch; Dominik F Vollherbst Journal: Clin Neuroradiol Date: 2022-09-06 Impact factor: 3.156