Literature DB >> 6537999

Quantitative determination of plasma fibrinolytic activity in patients with ruptured intracranial aneurysms who are receiving epsilon-aminocaproic acid: relationship of possible complications of therapy to the degree of fibrinolytic inhibition.

K J Burchiel, J M Hoffman, R A Bakay.   

Abstract

Fifty-two patients were each given a constant infusion of 1.5 g of epsilon-aminocaproic acid (EACA) per hour after subarachnoid hemorrhage (SAH) from an intracranial aneurysm. Each patient's available plasminogen activity (APA), a measure of plasma fibrinolytic activity, was determined by fluorometric assay before and during EACA treatment. Five categories of potential EACA complications were identified: rebleeding, cerebral vasospasm, hydrocephalus, thrombosis, and miscellaneous (bleeding time prolongation, thrombocytopenia). The APA of the 37 patients with complications was significantly higher than that of the 15 without complications. Four patients suffered rebleeding episodes and had significantly higher APA levels during EACA therapy when compared to all other patients, i.e., those with and without other complications. Patients with vasospasm, hydrocephalus, and thrombotic complications also had significantly higher APA levels during EACA therapy compared to patients without complications. The latter may be simply a reflection of the activation of fibrinolytic activity that occurs after SAH. It is apparent from these studies that, after the initiation of EACA treatment, a maximal steady state inhibition of fibrinolytic activity is not achieved for 2 days and, after the cessation of EACA therapy, normal fibrinolytic activity is not restored for a period of 3 to 4 days. In addition, patients with thrombotic events may show persistently low serum plasminogen activity after discontinuance of EACA therapy, probably due to continuing thrombosis and consumption of plasminogen. These results indicate that patients with recurrent preoperative aneurysmal hemorrhage while on EACA therapy may have inadequate fibrinolytic inactivation, and this may be an important factor contributing to rebleeding episodes.(ABSTRACT TRUNCATED AT 250 WORDS)

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Year:  1984        PMID: 6537999     DOI: 10.1227/00006123-198401000-00012

Source DB:  PubMed          Journal:  Neurosurgery        ISSN: 0148-396X            Impact factor:   4.654


  6 in total

Review 1.  Antifibrinolytic agents in subarachnoid haemorrhage.

Authors:  K W Lindsay
Journal:  J Neurol       Date:  1987-01       Impact factor: 4.849

Review 2.  Management of subarachnoid haemorrhage.

Authors:  T A Kopitnik; D S Samson
Journal:  J Neurol Neurosurg Psychiatry       Date:  1993-09       Impact factor: 10.154

3.  Fibrinolytic activity after subarachnoid haemorrhage and the effect of tranexamic acid.

Authors:  S A Tsementzis; W P Honan; S Nightingale; E R Hitchcock; C H Meyer
Journal:  Acta Neurochir (Wien)       Date:  1990       Impact factor: 2.216

4.  Long-term prognosis of subarachnoid hemorrhages of unknown etiology.

Authors:  A Ruelle; G Lasio; M Boccardo; A Gottlieb; P Severi
Journal:  J Neurol       Date:  1985       Impact factor: 4.849

Review 5.  Antifibrinolytic therapy to prevent early rebleeding after subarachnoid hemorrhage.

Authors:  Mark Chwajol; Robert M Starke; Grace H Kim; Stephan A Mayer; E Sander Connolly
Journal:  Neurocrit Care       Date:  2008       Impact factor: 3.210

6.  D-dimer may predict poor outcomes in patients with aneurysmal subarachnoid hemorrhage: a retrospective study.

Authors:  Jun-Hui Liu; Xiang-Kui Li; Zhi-Biao Chen; Qiang Cai; Long Wang; Ying-Hu Ye; Qian-Xue Chen
Journal:  Neural Regen Res       Date:  2017-12       Impact factor: 5.135

  6 in total

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