Coagulation and fibrinolysis in blood and cerebrospinal fluid after aneurysmal subarachnoid haemorrhage: Effect of tranexamic acid (AMCA)

Fodstad, Harald; Nilsson, Inga Marie

doi:10.1007/bf01400969

Cited by 31 publications

(22 citation statements)

References 49 publications

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“…1 In the past, several studies investigating plasma fibrinolytic activity in patients with SAH did not demonstrate an increase in plasma fibrinolytic activity. [2][3][4] However, in contrast to the results of these older studies, we observed in our study an unexplained 3-week increase in plasma fibrinolytic activity in placebo-treated patients.…”

contrasting

confidence: 56%

Nimodipine Increases Fibrinolytic Activity in Patients With Aneurysmal Subarachnoid Hemorrhage

Roos

Levi

Carroll

et al. 2001

Stroke

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Background and Purpose-The purpose of this study was first, to investigate which factor in the fibrinolytic cascade is responsible for the recently observed increase of fibrinolytic activity in patients with aneurysmal subarachnoid hemorrhage (SAH), and second, the cause of this increase. Methods-Fibrinolytic activity and the main regulators of endogenous fibrinolytic activity, tissue plasminogen activator, and plasminogen activator inhibitor 1 (PAI-1) were measured in patients treated with and without nimodipine. Results-In patients with aneurysmal SAH, fibrinolytic activity significantly increases from 2.7 IU/mL on admission to 4.2 IU/mL in week 3 (PϽ0.01, paired-sample t test), caused by a 1.6-fold decrease in plasma levels of PAI-1. The results also show that increased fibrinolytic activity is seen only in patients treated with nimodipine and that plasminogen activity and PAI-1 returned to baseline levels after treatment with nimodipine had been discontinued. Conclusions-The mechanism of increased fibrinolytic activity in patients with aneurysmal SAH is a decrease in the level of PAI-1, which is most likely caused by treatment with nimodipine. (Stroke. 2001;32:1860-1862.)

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contrasting

confidence: 56%

Nimodipine Increases Fibrinolytic Activity in Patients With Aneurysmal Subarachnoid Hemorrhage

Roos

Levi

Carroll

et al. 2001

Stroke

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“…There is increased local fibrinolytic activity in cerebrospinal fluid (CSF) after aSAH [24,31,32,[34][35][36]. It has been suggested that determination of CSF FDP levels may be beneficial in establishing baseline as well as post-dose CSF fibrinolytic activity, and allow drug regimens to be tailored to individual patients.…”

Section: Pharmacology Of Antifibrinolytic Therapymentioning

confidence: 99%

“…As documented by both the streptokinase clot lysis time [29] and plasminogen activity assay [22], oral or intravenous (IV) EACA administration of 36 g per day produces a maximum steady state inhibition of fibrinolysis in 12-72 h [11,22,29,30]. Maximum inhibitory plasma concentration of TXA is reached within 12 h of IV administration of 1 g of the drug every 4 h without a loading dose [24,25].…”

Section: Pharmacology Of Antifibrinolytic Therapymentioning

confidence: 99%

“…Different doses as well as routes of administration had been used in earlier trials, and effective blood and CSF drug levels might not have been achieved [22][23][24][25]. In addition, studies have shown that calcium channel blocking agents can decrease the incidence of vasospasm and cerebral ischemia among patients treated with antifibrinolytics [26][27][28].…”

Section: Introductionmentioning

confidence: 99%

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Antifibrinolytic Therapy To Prevent Early Rebleeding After Subarachnoid Hemorrhage

et al. 2008

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In the current era of early surgery, there has been little interest in the use of antifibrinolytic therapy to prevent rebleeding after aneurysmal subarachnoid hemorrhage (aSAH). Older studies demonstrated that antifibrinolytics can reduce rebleeding, but long-term therapy results in increased cerebral ischemia from vasospasm, leading to no appreciable effect on mortality. While early surgery would seem to obviate the need for long-term antifibrinolytic use, a subgroup of patients may benefit from early therapy. The rate of pre-operative rebleeding may be as high as 9-17%, causing significant morbidity and mortality. Short-term use of antifibrinolytic agents (less than 3 days) in the presence of calcium channel blocking therapy has shown promising results. A randomized clinical trial of early antifibrinolytic therapy conducted in 2002 showed a significant decrease in rebleeding and a non-significant decrease in overall mortality. In this review, we examine the clinical pharmacology, dosing, monitoring, complications, and side effects of antifibrinolytic treatment. We conclude that early short-term antifibrinolytic therapy might be a reasonable strategy to prevent acute rebleeding and improve long-term outcome in aSAH patients. Additional randomized clinical trials are necessary to determine whether this management strategy is effective.

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“…Takashima et al [81 showed that fibrinolytic activity in brain tissue obtained at autopsy was localised especially to the vascular endothelium. Newborn cerebral vascular endothelium showed less fibrinolytic activity than did adult brain, Following subarachnoid haemorrhage in adults, fibrinolytic activity on fibrin agar plates can be demonstrated in the CSF in some cases [4,9] but no data are available for infants with intracranial haemorrhage. Cross-linked FDPs in the CSF in preterm infants with IVH were raised and were even higher in those going on to develop hydrocephalus [11].…”

Section: Introductionmentioning

confidence: 94%

Endogenous fibrinolysis in neonatal cerebrospinal fluid

Whitelaw

1993

Eur J Pediatr

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Although many infants with intraventricular haemorrhage (IVH) recover without hydrocephalus, little is known about how blood is cleared from the CSF pathways. Fibrinolytic activity was measured by the fibrin plate method in CSF from 11 normal infants and 17 infants with IVH. Normal CSF showed no fibrinolytic activity. All the samples taken less than 17 days from diagnosis of IVH failed to show fibrinolytic activity. All but 1 of the CSF samples taken between 17 and 60 days of IVH showed fibrinolytic activity. In 1 infant where 14 serial samples were taken, there was no detectable fibrinolysis up to 16 days after IVH but from 19 to 52 days there was definite fibrinolytic activity. Delayed endogenous fibrinolysis in the CSF is common after IVH but may, in some cases, be insufficient to prevent hydrocephalus.

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Coagulation and fibrinolysis in blood and cerebrospinal fluid after aneurysmal subarachnoid haemorrhage: Effect of tranexamic acid (AMCA)

Cited by 31 publications

References 49 publications

Nimodipine Increases Fibrinolytic Activity in Patients With Aneurysmal Subarachnoid Hemorrhage

Nimodipine Increases Fibrinolytic Activity in Patients With Aneurysmal Subarachnoid Hemorrhage

Antifibrinolytic Therapy To Prevent Early Rebleeding After Subarachnoid Hemorrhage

Endogenous fibrinolysis in neonatal cerebrospinal fluid

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