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Hemostasis and fibrinolysis activation after subarachnoid hemorrhage.

作者信息

Peltonen S, Juvela S, Kaste M, Lassila R

机构信息

Wihuri Research Institute and Department of Neurosurgery, Helsinki University Central Hospital, Finland.

出版信息

J Neurosurg. 1997 Aug;87(2):207-14. doi: 10.3171/jns.1997.87.2.0207.

Abstract

The authors assessed hemostasis and fibrinolysis serially: on admission and on the 1st and 7th days after surgery for subarachnoid hemorrhage (SAH), examining the complications of aneurysm rupture and its surgical repair. Of 32 patients, 25 with SAH were compared with seven control patients who underwent surgery for an unruptured intracranial aneurysm. On admission, patients with SAH had higher thrombin-antithrombin III complex (TAT) levels (13.3 +/- 3.8 vs. 3.8 +/- 0.6 ng/ml, p = 0.01), fibrin degradation product, D-dimer levels (1310 +/- 220 vs. 556 +/- 89 ng/ml, p = 0.0001), and leukocyte counts (14.6 +/- 0.7 vs. 10.6 +/- 1.8 x 10(9) cells/L, p < 0.05) than did control patients. Postoperative D-dimer values (p = 0.007) remained higher in the SAH group. Furthermore, admission D-dimer levels were higher in the patients in poor clinical condition than in those in good condition (2017 +/- 377 vs. 934 +/- 208 ng/ml, p = 0.007), and D-dimer levels were associated with the outcome at 3 months after admission. Additionally, thrombin generation and fibrinolytic markers measured on admission were related to clinical grade, amount of subarachnoid blood seen on computerized tomography (CT) scanning, and patient fatality. Patients with hypodense lesions verified on follow-up CT scanning or with persistent neurological deficits at 3 months had higher prothrombin fragments 1 and 2, TAT, D-dimer, and plasminogen activator inhibitor-1 values on the 1st day postoperatively than did patients without such lesions. In short, in patients with SAH, activation of coagulation and fibrinolysis was strongly associated with clinical state, patient fatality, and outcome at 3 months, and postoperatively this activation correlated with the development of brain infarction.

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