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Plasma kinin formation after in vitro activation of factor XII in the coagulation system was examined in 4 patients with hereditary angioneurotic edema. Compared to controls activationcurves showed a steeper increase and higher maximum levels. Administration of tranexamic acid to the patients resulted in partial normalisation of plasma kinin activation.
We studied 99 patients who were undergoing total knee arthroplasty (TKA) to determine the optimum protocol for the administration of tranexamic acid (TNA) in order to reduce blood loss. It decreased by more than 40% after the administration of TNA. The haemostatic effect was greatest when TNA was given preoperatively and on deflation of the tourniquet. There was no increase in the incidence of adverse affects in the patients receiving TNA, compared with a control group. We conclude that two injections of TNA, one given preoperatively and one on deflation of the tourniquet, significantly reduce blood loss without increasing the risk of thromboembolic complications.
Giant hemangiomas occurring in the neonatal period often present a therapeutic challenge, especially when confounded by consumptive coagulopathy (Kasabach-Merritt syndrome). We treated three infants with tranexamic acid after therapy with corticosteroids was ineffective. One patient had a partial response. The remaining two developed progressive disease.
The efficacy of antifibrinolytic therapy in the management of acute upper gastrointestinal haemorrhage has been investigated in a double-blind clinical trial. Two-hundred patients were studied using tranexamic acid, a potent antifibrinolytic agent. Of these, 103 were in the treatment group and 97 in the control group. Patients were analysed to determine severity of initial blood loss, transfusion requirements, together with the incidence of recurrent bleeding, surgical intervention, and death. Final diagnosis as to the site of bleeding was arrived at using endoscopy, barium studies, and the findings at operation and necropsy. The groups were well matched as regards severity of initial haemorrhage, age, sex, aetiological diagnosis, and precipitating factors. A significant difference was observed in the requirement for surgical intervention to control continuing or recurrent haemorrhage. Twenty-three of 97 in the control group and seven of 103 in the treatment group required surgery. There appeared to be a reduction in the transfusion rate after the first three days of hospitalization in the treatment group. There were no significant differences in mortality or in side-effects between the two groups.
The fibrinolytic enzyme system of menstrual and peripheral blood was studied in three groups of women: Group 1, 20 subjects (mean age 37.2 years) with normal menstrual loss; Group 2, 20 patients (mean age 39 years) with dysfunctional uterine bleeding studied before treatment, and Group 3, during treatment with a fibrinolytic inhibitor, tranexamic acid (AMCA) (1 g 8-hourly). The fibrinolytic activity (plasminogen activator and plasmin) of menstrual blood was significantly higher than that of peripheral blood in the three groups (p less than 0.001). Both plasminogen activator and plasmin were higher in the menstrual blood of patients with menorrhagia (Group 2) compared with the control subjects (Group 1) (p less than 0.001 and p less than 0.1 respectively). Treatment with AMCA significantly reduced both plasminogen activator (p less than 0.01) and plasmin (p less than 0.05) in the menstrual blood of patients with menorrhagia (Group 3). No significant differences in fibrinolytic activity were found in peripheral blood between Groups 1 and 2; however, both plasminogen activator and plasmin were significantly lower (p less than 0.01) in Group 3 than in Group 2. Plasmin activity was also significantly lower (p less than 0.05) in Group 3 compared to Group 1. These findings confirm the presence of increased fibrinolytic activity in the uterus in excessive (dysfunctional) bleeding.
One hundred forty patients who underwent laser conization and 220 patients who underwent laser miniconizations were prospectively randomized into two study groups. One treatment group was given antifibrinolytic therapy in the form of tranexamic acid (Cyklokapron, KabiVitrum, Sweden) intraoperatively and for 14 days postoperatively. The other group did not receive antifibrinolytic therapy. In the group of 68 patients with laser conizations who were given antifibrinolytic therapy, no postoperative hemorrhages occurred, whereas there were eight such hemorrhages in 72 conizations (11%) in the untreated patients. This difference is statistically significant (P = .004, Fisher exact test for two proportions). Also, for laser miniconization, the frequency of postoperative hemorrhage was almost halved, from 9.1% in 110 patients not receiving antifibrinolytic therapy to 5.5% in the 110 treated patients. The use of lateral cervical sutures did not reduce the frequency of postoperative hemorrhage at laser conization in the present study.
Four hundred fifteen patients undergoing coronary revascularization over a 12-month period were divided into two groups: 209 controls in the first 6 months received no tranexamic acid (TA) before cardiopulmonary bypass and 206 patients in the second 6 months received TA as a hemostatic agent. The demographics and the surgical techniques used were similar in the two groups. With TA there was a significant decrease in blood loss postoperatively, from 1,114.1 mL in the controls to 803.7 mL in those given TA (p < 0.001); in red blood cell use, from 1.7 units/patient in the controls to 0.69 units/patient in those given TA (p < 0.001); in fresh frozen plasma requirements, from 0.23 units/patient in the controls to 0.024 units/patient in those given TA (p < 0.01); and in platelet transfusion, from 1.06 units/patient in the controls to 0.30 units/patients in those given TA (p < 0.01). The percentages of patients not receiving any blood products were 65% in those given TA versus 49% in the controls (p < 0.01). There was no significant difference between the two groups in the incidence of perioperative myocardial infarction, cerebrovascular accidents, pulmonary embolism, or venous thrombosis to clearly suggest hypercoagulability. In this study, TA profoundly affected the coagulopathy associated with bypass in patients undergoing coronary revascularization. It significantly reduced blood loss and blood product transfusions. Any potential increased thrombotic complications could not be clearly demonstrated in this study, but should not be ignored.
The influence of systemic antifibrinolytic and antiprostaglandin medication on post-operative central corneal thickness was studied. Thirty patients underwent uncomplicated intracapsular cataract extraction with implantation of anterior chamber lens. The patients received either tranexamic acid, naproxen or both. The post-operative oedema did not differ significantly between the three groups studied. Models for studying changes in central corneal thickness are discussed. A review of the influence of drugs on corneal thickness is presented.
The assembly of lipoprotein(a) (Lp(a)) is a two-step process which involves the interaction of kringle-4 (K-IV) domains in apolipoprotein(a) (apo(a)) with Lys groups in apoB-100. Lys analogues such as tranexamic acid (TXA) or delta-aminovaleric acid (delta-AVA) proved to prevent the Lp(a) assembly in vitro. In order to study the in vivo effect of Lys analogues, transgenic apo(a) or Lp(a) mice were treated with TXA or delta-AVA and plasma levels of free and low density lipoprotein bound apo(a) were measured. In parallel experiments, McA-RH 7777 cells, stably transfected with apo(a), were also treated with these substances and apo(a) secretion was followed. Treatment of transgenic mice with Lys analogues caused a doubling of plasma Lp(a) levels, while the ratio of free:apoB-100 bound apo(a) remained unchanged. In transgenic apo(a) mice a 1. 5-fold increase in plasma apo(a) levels was noticed. TXA significantly increased Lp(a) half-life from 6 h to 8 h. Incubation of McA-RH 7777 cells with Lys analogues resulted in an up to 1. 4-fold increase in apo(a) in the medium. The amount of intracellular low molecular weight apo(a) precursor remained unchanged. We hypothesize that Lys analogues increase plasma Lp(a) levels by increasing the dissociation of cell bound apo(a) in combination with reducing Lp(a) catabolism.
INTRODUCTION: Aprotinin (AP) reduces blood loss and transfusions after cardiopulmonary bypass (CPB), but may sensitise patients and is expensive. Tranexamic acid (TA) has less side-effects, but data regarding its efficacy are controversial. The aim of our prospective, randomised, double-blind study was to compare the impact of AP vs. TA on drainage blood loss and transfusion requirements in patients undergoing first time CABG on CPB. MATERIALS AND METHODS: One hundred and twenty adult patients were randomised to receive either high-dose AP according to Hammersmith or a total of 2 g TA. Perioperative blood products were transfused in a standardised fashion. Blood loss was measured up to 24 h. Demographic and clinical patient data were collected until hospital discharge. RESULTS: The data from 118 patients (TA: n = 58, AP: n = 60) who completed the study according to protocol were analysed. Blood loss at 24 h postoperation in TA patients was significantly higher (896 +/- 354 ml) as compared to AP patients (756 +/- 347 ml; p = 0.03). TA patients received 1.5 +/- 1.5 units of red blood cells (AP: 1.5 +/- 1.7, p = 1.0), 1.3 +/- 2.0 units of fresh frozen plasma (AP: 1.0 +/- 2.0, p = 0.38) and 0.5 +/- 1.4 units of platelets (AP: 0.2 +/- 0.7, p = 0.15). Clinical data, including perioperative myocardial infarction rate, acute renal failure, mechanical ventilation, hospital stay and mortality, were not significantly different between either group. CONCLUSION: Our data show a difference in blood loss between TA and high-dose AP. Although statistically significant, it has little clinical relevance, because perioperative transfusion requirements were similar for both groups. Thus, TA appears to be a cost-effective alternative to AP in primary CABG patients.
In the surgical setting, fibrinolysis can be a serious complication of anaphylaxis. We present four cases of anaphylaxis that were associated with fibrinolysis during anaesthesia, and the use of the thrombelastograph to demonstrate this haemostatic defect and its correction using tranexamic acid.
BACKGROUND: Postoperative hematoma and oozing can compromise outcomes after reduction mammoplasty with immediate reconstruction. Intravenous (IV) tranexamic acid (TXA) is antifibrinolytic, but prospective evidence in this setting is limited. OBJECTIVES: The aim of this study was to determine whether a single pre-incision dose of IV TXA reduces perioperative blood loss and fibrinolytic activation vs placebo. METHODS: In this randomized, triple-blinded, placebo-controlled trial, 60 women (American Society of Anesthesiologists I/II, 18-75 years) undergoing bilateral reduction mammoplasty with immediate implant-based reconstruction received TXA 10 mg/kg in 100 mL saline or placebo 10 min before incision. The primary outcome was total blood loss within 24 h (intraoperative suction + swab plus drain output). Secondary outcomes were perioperative changes in hemoglobin, D-dimer and fibrinogen, and complications within 30 days. Intention-to-treat analyses were performed. RESULTS: All patients completed follow-up. Total blood loss was lower with TXA than with placebo (mean ± standard deviation: 221.1 ± 72.4 vs 298.1 ± 90.6 mL; mean difference -77.0 mL; 95% CI, -122.4 to -31.6; P = .001). Intraoperative loss and 24 h drain output were also reduced. Postoperative D-dimer rise was attenuated with TXA (0.31 ± 0.15 vs 0.49 ± 0.22 µg/mL; P = .002); hemoglobin decline was smaller. No thromboembolic, neurologic, or allergic events occurred; no skin-flap necrosis was observed. CONCLUSIONS: Pre-incisional IV TXA safely reduces perioperative bleeding and fibrinolytic activity after reduction mammoplasty. These findings support incorporation of IV TXA into perioperative protocols. LEVEL OF EVIDENCE: 2 (THERAPEUTIC): For image description, please refer to the figure legend and surrounding text.
Bleeding from an induced gastric mucosal wound was monitored for 2 h in a rat model, in which normal hemostasis was disturbed mechanically by perfusing the lesion with saline. The hemorrhage was characterized by continuous bleeding and/or episodes of spontaneous rebleeding, as often seen in patients with gastric hemorrhage. The antifibrinolytic agent, tranexamic acid, significantly reduced total bleeding volume and number of rebleeding episodes, suggesting that plasmin-induced fibrinolysis might aggravate gastric mucosal hemorrhage.
Serial assays of blood coagulation factors as well as of fibrin/fibrinogen degradation products (FDP) and plasminogen activatory activity (PA) on fibrin plates in blood and cerebrospinal fluid (CSF) were performed in 41 consecutive patients with recently ruptured cerebral aneurysms, 21 of whom were randomly treated with tranexamic acid (AMCA). Coagulation factors were unaffected by the drug and plasminogen and FDP decreased in blood after two weeks' treatment. After one week, PA in CSF was increased in control patients and unchanged in AMCA-treated patients, whereas CSF-FDP had decreased among AMCA-treated patients. After two weeks PA as well as FDP in CSF showed the same values in both groups. An increase in CSF-FDP occurred after rebleeding and in patients with cerebral ischaemic symptoms. The results indicate that AMCA inhibits local fibrinolysis in CSF in patients with aneurysm rupture.
The plasminogen activation system is one of the enzyme systems held responsible for bone and cartilage degradation in rheumatoid arthritis (RA). In this study, we evaluated the effect of tranexamic acid (TEA), an inhibitor of plasminogen activation, on urinary collagen cross-link excretion and radiological joint damage in rat adjuvant arthritis (AA) and on urinary collagen cross-link excretion in patients with RA. In the animal study, adjuvant arthritis was induced in male Lewis rats. From day 7 onward, high-dose TEA (500 mg/kg body weight, once daily) or placebo was administered orally. Study groups consisted of TEA-treated normal rats (C + TEA), placebo-treated normal rats (C + plac), AA rats treated with TEA (AA + TEA) or with placebo (AA + plac). To monitor joint destruction, urinary collagen cross-link excretion (pyridinoline, HP; deoxypyridinoline, LP) was measured by high-performance liquid chromatography at days 14 and 21. Radiological evaluation of joints was performed at day 21. In the patient study, TEA was administered to nine patients with RA as adjuvant medication (approximately 20 mg/kg body weight, three times daily) for 12 weeks. Urinary HP and LP excretion levels were measured before and during TEA treatment, and 4 weeks after the cessation of TEA treatment. In AA + TEA rats, a significant reduction of HP and a tendency towards a reduction of LP excretion were found compared with AA + plac rats (P < 0.05), at day 14, whereas the HP/LP ratio did not change. No difference was observed in HP, LP excretion, HP/LP ratio and radiological damage score between the TEA- and placebo-treated AA rats at day 21. In RA patients, a significant reduction of HP and LP excretion was found during the TEA treatment period (P < 0.05). After the cessation of TEA treatment, HP and LP excretion increased towards baseline levels. No effect on disease activity was observed. The plasmin antagonist TEA reduced the excretion of collagen pyridinoline cross-links in both experimental and rheumatoid arthritis. As such, this study not only supports the involvement of the plasminogen activation system in the destructive phase of arthritis, but also suggests a beneficial effect of therapeutic strategies directed against inhibition of matrix proteolysis.
OBJECTIVE: The preservation of ultrafiltration (UF) capacity is crucial to maintaining long-term continuous ambulatory peritoneal dialysis (CAPD).The aim of the present study was to investigate whether the antiplasmin agent tranexamic acid (TNA) increases UF volume in CAPD patients. PATIENTS AND METHODS: Fifteen patients on CAPD, 5 with UF loss and 10 without UF loss, were recruited for the study. The effect of TNA was evaluated with respect to changes in UF volume, peritoneal permeability, peritoneal clearance, bradykinin (BK), and tissue plasminogen activator (tPA) concentration. SETTING: Dialysis unit of the Saiseikai Central Hospital. RESULTS: In patients with UF loss, 2 weeks of treatment with oral TNA produced a significant increase in UF volume in all subjects (5/5).TNA also produced a significant increase in peritoneal clearances of urea and creatinine (Cr). However, the peritoneal equilibration test (PET) revealed that TNA had no effect on dialysate/plasma (D/P) Cr, Kt/V, or the protein catabolic rate (PCR).TNA also had no effect on net glucose reabsorption. In contrast, significant decreases in BK and blood tPA concentrations in response to TNA treatment were noted. BK concentration in drainage fluid was also reduced. In the case of patients without UF loss,TNA produced an increase in UF volume in 70% (7/10). However, no differences were found in blood and drainage BK and tPA concentrations between theTNA treatment and nontreatment periods in these patients. A comparison of basal BK and tPA concentration showed that there were no differences in these parameters between patients with UF loss and those without loss of UF. Furthermore,TNA given intraperitoneally to a patient also produced a marked increase in UF volume. CONCLUSION: The present study suggests thatTNA enhances UF volume in patients both with and without UF loss. SinceTNA did not affect peritoneal permeability and glucose reabsorption, the mechanism by which TNA exerts an enhancing action on UF is largely unknown. We speculate that it may be associated with suppression of the BK and/or tPA system, at least in patients with UF loss.
BACKGROUND: Microvascular bleeding after Cardiopulmonary bypass (CPB) is mainly due to consumption of clotting factors, platelets damage, and hyperfibrinolysis. Aprotinin, the only antifibrinolytic drug effective in preserving platelets, is no longer available; an alternative regimen based on pure antifibrinolytic drugs has been proposed, since hyperfibrinolysis is known to contribute both to clot lysis and platelet dysfunction. In this study the efficacy of two antifibrinolytic drugs, Tranexamic acid (TA) and epsilon-aminocaproic acid (EACA), was tested in patients undergoing cardiopulmonary bypass (CPB), for primary myocardial revascularization. METHODS: Forty-eight consecutive patients were randomized to receive prophylactically equipotent doses of EACA (group A) or TA (Group B). Platelet count, prothrombin time, fibrin digestion products, blood loss and transfusion requirements recorded after 6 and 24 hours from the end of surgery were compared. RESULTS: The two groups were comparable for length of CPB and numbers of grafts; no significant difference was observed in the coagulation parameters considered. Blood losses were less in group B (TA) than in group A (EACA), both at 6 and 24 hours after surgery; homologous blood transfused was also less in group B, but no difference was statistically significant. No adverse effect was observed. CONCLUSIONS: In coronary patients, TA and EACA exhibit the same effects on blood loss and requirements after CPB; either drug can be safely used in cardiac surgery.
The course of a 12-year-old girl with cystic fibrosis (CF) and with recurrent hemoptysis since age 8 years is described. Conservative measures failed to control her bleeding. Hemoptysis was only partially controlled by repeated bronchial arterial embolizations. However, the addition of tranexamic acid (TXA) resulted in complete cessation of bleeding. Attempts to withdraw TXA therapy resulted in recurrence of hemoptysis; this patient has, therefore, been continuously maintained on this therapy for the past 4 years. No side effects of long-term TXA treatment have been noted.