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PubMed2006

The effect of uremia on platelet contractile force, clot elastic modulus and bleeding time in hemodialysis patients.

INTRODUCTION: Uremic bleeding frequently occurs in dialysis patients. Although its mechanism is not well characterized, acquired platelet dysfunction has been implicated in its pathogenesis. Skin bleeding time has been used to characterize platelet dysfunction in this population. However, the bleeding time is prone to error. The goal of this study was to compare the bleeding time to the novel platelet function parameters platelet contractile force and clot elastic modulus as well as platelet aggregation studies in controls and patients receiving maintenance hemodialysis. MATERIALS AND METHODS: Forty-five subjects completed this study (25 controls, 20 dialysis). All subjects had the Ivy skin bleeding time procedure performed, as well as the collection of whole blood samples for the determination of platelet contractile force, clot elastic modulus, % von Willebrand Factor antigen, and platelet aggregation studies. Pearson's correlation determined the relationships between skin bleeding time and platelet function and clot structure parameters and markers of renal dysfunction. RESULTS: Bleeding time was significantly prolonged in the dialysis group relative to controls. The platelet function parameters were not significantly different between groups. There was a significant relationship between bleeding time and creatinine concentration, however, no relationship existed between bleeding time and platelet function parameters. CONCLUSIONS: Skin bleeding time poorly correlates with measurements of platelet function. There were no significant differences noted in platelet function between the groups despite the prolongations in bleeding time in the dialysis group. These data may suggest that the bleeding time reflects perturbations in platelet adhesion or secretion, and not aggregation. Further study is needed to characterize platelet function in dialysis patients.

Adult↗
PubMed1996

Comparative effects of staphylokinase and alteplase in rabbit bleeding time models.

BACKGROUND: The pathogenesis of bleeding associated with thrombolytic therapy remains largely unknown, although spontaneous bleeding appears to correlate with bleeding time prolongation. Here, the comparative effects on cuticle bleeding times (CBT) and ear puncture bleeding times (EBT) of recombinant staphylokinase (Sak) and alteplase (recombinant tissue-type plasminogen activator, rt-PA) at equivalent doses, alone and in combination with aspirin and heparin, were studied in rabbits. METHODS AND RESULTS: Groups of 4 to 9 rabbits were allocated to one of the 8 following intravenous infusions: saline; aspirin 15 mg/kg and heparin - 100 IU/kg bolus and 10 IU/kg infusion over one hour; 1.5 mg/kg rt-PA; 1.5 mg/kg rt-PA plus aspirin and heparin; 4.5 mg/kg rt-PA; 0.5 mg/kg Sak; 0.5 mg/kg Sak plus aspirin and heparin and 1.5 mg/kg Sak. Bleeding times were determined 30 and 15 min before and 5, 15, 30 and 60 min after the administration over one min of saline, rt-PA or Sak, by simultaneously severing a nail cuticle (CBT) and by puncturing the ear (EBT). Bleeding times were unaffected by saline and by both doses of Sak in monotherapy. Heparin-aspirin and low dose rt-PA significantly lengthened EBT but not CBT. Both CBT and EBT were significantly prolonged (to a mean of > 4 times pretreatment at 5 min) after high-dose rt-PA and after the combined administration of heparin and aspirin with either Sak or tr-PA. rt-PA provoked significantly longer bleeding than Sak in the CBT (p = 0.001; mean estimated difference = 23 min), but not in the EBT. rt-PA but not Sak degraded plasma fibrinogen dose-dependently. CBT correlated inversely with fibrinogen (r= -0.66, p=0.001) but EBT did not. CONCLUSION: At equivalent doses Sak displays a significantly higher fibrin specificity and prolongs bleeding time less than rt-PA, particularly in the nail cuticle bleeding time model in which larger vessels are injured that require fibrinogen for hemostasis.

Animals↗
PubMed1986

Clinical trial of a new disposable bleeding-time device.

A new disposable bleeding time device (Hemalet) was tested in 20 normal individuals and 11 patients with various bleeding disorders. The results were compared with those of Simplate II. The mean bleeding time for normal individuals was 5.4 +/- 1.5 (mean +/- 1 SD) minutes by Hemalet and 5.8 +/- 1.4 (mean +/- 1 SD) minutes by Simplate II, with good correlation between the results by the two devices (r = 0.81). The bleeding time in patients with various bleeding disorders were also comparably prolonged between the two devices. The new disposable bleeding time device with a disposable blade has quick release (penetration) into skin and retraction, and offers an alternative means of a bleeding time test.

Bleeding Time↗
PubMed1994

Hematocrit and bleeding time: an update.

The bleeding time is prolonged in anemic patients independent of their platelet count and is shortened by elevating the hematocrit. It is theorized that an increase in circulating red blood cells increases platelet radial movement and interaction with endothelium. Platelet dysfunction in uremia is well known but poorly understood. Anemia is one contributory factor; others may involve storage pool deficiency, increased vessel wall prostaglandin production, and abnormal platelet arachidonic acid metabolism. Ameliorating anemia with red blood cell transfusions has been shown to shorten the bleeding time without affecting other platelet function values. Recently, recombinant human erythropoietin has been shown to shorten the bleeding time, with a parallel rise in hematocrit level to 30%. Clinicians should be aware that a diminished hematocrit may contribute to the bleeding tendency already present in patients with thrombocytopenia.

Anemia↗
PubMed1996

Low-molecular-weight heparin (fragmin) and thrombin active-site inhibitor (argatroban) compared in experimental arterial and venous thrombosis and bleeding time.

The antithrombotic and bleeding effects of a low-molecular-weight heparin (LMWH, fragmin) and a thrombin active-site inhibitor (argatroban) were determined in anesthetized rats. Occlusive thrombi were produced in the vena cava, either by partial stasis of blood flow or transmural vessel injury, and in the carotid artery by transmural vessel injury. Bleeding time was measured by puncturing small mesenteric arteries. Each drug was tested in multiple intravenous (i.v.) doses and inhibited venous and arterial thrombosis when the activated partial thromboplastin time (APTT) was increased as much as or more than twofold, although greater APTT increases were required with fragmin and against arterial thrombosis. Fragmin and argatroban decreased to an equivalent extent the weight of venous thrombi induced by stasis (> or = 99%) or vessel injury (90 and 96%, respectively). The maximum inhibition of arterial thrombosis was less with fragmin (69%) and argatroban (65%) and required higher doses of each drug relative to venous thrombosis. At doses that were just optimal against arterial thrombosis, bleeding time was increased moderately by fragmin (32%) and was unaffected by argatroban. These studies demonstrate that doses of fragmin and argatroban that exert comparable antithrombotic activity in large arteries and veins have only moderate effects on bleeding time in small arteries.

Animals↗
PubMed1988

Platelet function and the bleeding time in progressive renal failure.

Bleeding time and platelet function tests were performed on 31 patients with progressive chronic renal failure (CRF) due to non-immunological (urological) causes, and compared with 22 healthy controls. Patients were classified as mild (plasma creatinine less than 300 mumol/l), moderate (300-600 mumol/l) or severe renal failure (greater than 600 mumol/l). Bleeding time was rarely prolonged in mild and moderate CRF and mean bleeding time significantly elevated only in severe CRF (p less than 0.005). Haematocrit was the only index which correlated with bleeding time (r = -0.40). Platelet counts, collagen stimulated thromboxane generation, and platelet aggregation responses to ADP, collagen and ristocetin were all either normal or increased in all three CRF groups, but thromboxane production in clotting blood was reduced. Plasma fibrinogen, C reactive protein and von Willebrand factor (vWF) were elevated in proportion to CRF. We found no evidence that defects in platelet aggregation or platelet interaction with vWF prolong the bleeding time in patients with progressive CRF.

Bleeding Time↗
PubMed1984

Shortening of bleeding time by 1-deamino-8-D-arginine vasopressin in various bleeding disorders.

To evaluate the effect of 1-deamino-8-D-arginine vasopressin (DDAVP) in various bleeding disorders, 10 micrograms/m2 DDAVP was administered to subjects with von Willebrand disease (13), platelet function defects (12), von Willebrand disease and platelet defects together (8), or isolated prolongation of the bleeding time (5). DDAVP shortened the bleeding time similarly in all patient groups. Shortening of the bleeding time was also observed in 2 patients with aspirin-induced platelet defects and in 2 normal subjects. DDAVP administration was associated with falls in the platelet count, mean platelet volume, and partial thromboplastin time, and rises in platelet adhesion, factor VIII coagulant activity, factor VIII related antigen, and von Willebrand factor activity. The basal bleeding time was the only predictor of the magnitude of the bleeding-time correction. Normal haemostatis was achieved with DDAVP plus epsilon-aminocaproic acid and no blood product support during operations in 18 patients with bleeding disorders.

Adolescent↗
PubMed1983

Cigarette smoking shortens the bleeding time.

The cutaneous bleeding time was shortened after smoking high nicotine cigarettes while not after smoking nicotine free cigarettes. The ADP induced primary platelet aggregation was not enhanced. The number of circulating platelet aggregates did not change due to smoking.

Adult↗
PubMed1991

Synergistic shortening of the bleeding time by desmopressin and ethamsylate in patients with various constitutional bleeding disorders.

Desmopressin and ethamsylate were evaluated for possible synergistic effects on the bleeding time. The drugs were administered individually and together to 12 patients with markedly prolonged bleeding times known to be relatively or absolutely unresponsive to desmopressin alone. The bleeding disorders studied included Glanzmann's thrombasthenia (one), other disorders of platelet function (four), pseudo-von Willebrand disease (one), and von Willebrand disease type I (three), type II (two), and type III (one). Desmopressin alone shortened the bleeding time from 23.9 +/- 1.5 to 19.5 +/- 2.3 min (p = 0.03). Ethamsylate alone was without effect. Desmopressin and ethamsylate together shortened the bleeding time to 11.2 +/- 1.4 min (p less than 0.01 compared to baseline, p = 0.02 compared to desmopressin alone). The combination was ineffective in three patients, with Glanzmann's thrombasthenia (one), and von Willebrand disease type I (one) and type III (one). Toxic effects of the drugs were not observed. Five patients received desmopressin and ethamsylate prior to dental work with mandibular block (one), heart surgery requiring cardiopulmonary bypass (two), and adenotonsillectomy surgery (two). Normal hemostasis was achieved in each case. A synergistic shortening of the bleeding time was observed with the combination of desmopressin and ethamsylate in a wide range of bleeding disorders.

Adolescent↗
PubMed1995

Vampire bat salivary plasminogen activator evokes minimal bleeding relative to tissue-type plasminogen activator as assessed by a rabbit cuticle bleeding time model.

Cuticle bleeding time (CBT) measurements in anesthetized rabbits were performed to assess the potential bleeding risks which may accompany the administration of tissue-type plasminogen activator (tPA) or vampire bat salivary plasminogen activator (BatPA). The dose of BatPA or tPA used in this study, 42 nmol/kg, was previously shown to be efficacious using a rabbit femoral artery thrombosis model (Gardell et al, Circulation 84:244, 1991). CBT was determined by severing the apex of the nail cuticle and monitoring the time to cessation of blood flow. CBT was minimally elevated (1.6-fold, p = NS) following bolus intravenous administration of BatPA; in contrast, bolus intravenous administration of tPA dramatically elevated CBT (6.2-fold, p < 0.05). Rabbits treated with tPA, but not BatPA, displayed profound activation of systemic plasminogen and consequent degradation of Factor VIII and fibrinogen. Elevations in CBT after the administration of tPA were reversed by the replenishment of plasma Factor VIII activity to 40% of control, but were unaffected by complete replenishment of plasma fibrinogen. The results of this study suggest that the administration of BatPA, at a dose that promotes thrombolysis, may evoke a minimal bleeding risk, relative to an equi-efficacious dose of tPA. In addition, the tPA-provoked proteolytic consumption of Factor VIII may be a key contributor to the heightened bleeding risk.

Animals↗
PubMed1991

Heparin, DDAVP and the bleeding time.

The effect on the bleeding time of heparin, followed by an infusion with desmopressin (DDAVP) 0.3 micrograms/kg or placebo in a randomized, double-blind set-up, was investigated in 20 patients treated for acute venous thromboembolism. The bleeding time was on the average prolonged by 90% (95% confidence interval 46%-134%) after at least 1 day of treatment with heparin. At that point DDAVP shortened the bleeding time by 23% with a confidence interval of -35% to -11% whereas the effect of placebo was -2% with a confidence interval of -23% to +20%. There was also a shortening of the APTT after DDAVP but not after placebo. It is concluded that DDAVP induces a partial reversal of the effect of heparin on the bleeding time, and that DDAVP should be tried in case of hemorrhagic problems.

Adult↗
PubMed1983

Nitroglycerin prolongs the bleeding time in healthy males.

Bleeding time was prolonged when measured 6 minutes after the administration of 0.5 mg nitroglycerin (NTG) sublingually in 15 men aged 25-40 years. The prolongation was not caused by a general inhibition of platelet aggregation. 4 g acetylsalicylic acid inhibited the effect of NTG on the bleeding time with a time course similar to the vessel wall cyclooxygenase. This may indicate that the effect of NTG is mediated by prostacyclin.

Adult↗
PubMed2002

Use of the bleeding time in the neonatal intensive care unit.

UNLABELLED: Impairments of primary hemostasis are frequently responsible for serious bleeding in sick infants in the neonatal intensive care unit (NICU). Therefore, a rational approach to these infants with hemorrhagic manifestations, in addition to an accurate medical history, a careful physical examination and routine screening coagulation tests, may include a bleeding time. The bleeding time is the traditional in vivo test for assessing primary hemostasis. It is a useful clinical tool to detect quantitative or qualitative platelet disorders or microvascular defectiveness. Its diagnostic value in neonates is controversial, mainly owing to limited experience in executing the test, which is performed uncommonly in the NICU. Using a template device expressly adapted for neonates (Surgicutt Newborn), a small incision 2.5 mm long and 0.5 mm deep provides a standardized, reproducible and sensitive bleeding time, with minimal scarring and pain. Various hereditary or acquired maternal and neonatal diseases, as well as some antepartum medications given to the mother or drugs commonly used to treat NICU patients, such as indomethacin, ibuprofen, penicillin compounds and theophylline, can impair primary hemostasis and consequently prolong the bleeding time in neonates. Furthermore, other factors distinctive to neonates, including gestational age, the increased von Willebrand factor concentration and function, high hematocrit, the large size of erythrocytes and platelet hyporeactivity in the first 10 d of life, affect platelet-vessel wall interaction and influence the interpretation of bleeding time results in newborn infants. Because the clinical evaluation of primary hemostasis consists of complex laboratory testing, largely reserved for specialized laboratories and currently not routinely performed in newborn infants, automated bleeding time devices specifically generated to make standardized and acceptably small incisions in newborn infants have become a surrogate. CONCLUSION: With awareness of its value and limitations, the bleeding time can be included in the baseline evaluation of neonates in the NICU, for guiding diagnosis and treatment of primary hemostatic disorders.

Bleeding Time↗
PubMed1981

Aspirin-induced prolongation of bleeding time and perioperative blood loss.

One hundred twenty-nine patients undergoing total hip replacement were treated with aspirin at a level of either 300 mg four times a day (1.2 g/day) or 900 mg four times a day (3.6 g/day). Baseline bleeding times before aspirin treatment averaged 4.18 +/- 1.44 minutes. Two hours after 300 mg and 900 mg of aspirin, the bleeding times were 5.83 +/- 1.88 and 5.72 +/- 1.57 minutes, respectively. After three to five days of aspirin therapy at 1.2 g/day and 3.6 g/day, the bleeding times were 6.27 +/- 2.27 and 6.43 +/- 2.11 minutes, respectively. The bleeding times for all the aspirin-treated groups were longer than baseline times. No paradoxical shortening of the bleeding time was noted at the 3.6-g/day dose. Perioperative blood loss for those receiving aspirin was not increased in six of eight subsets by operation and anesthesia when compared with historical control subjects. Neither a bleeding time greater than ten minutes nor a prolongation of the bleeding time by aspirin of more than four minutes over baseline bleeding times was associated with increased perioperative blood loss.

Administration, Oral↗
PubMed1979

Bleeding time in uremia: a useful test to assess clinical bleeding.

Modified Ivy bleeding time (template) and platelet aggregation to ADP, epinephrine, and collagen were studied in 26 uremic patients who had not recently ingested anti-platelet drugs. Regardless of the aggregating agent used, the abnormalities in platelet aggregation were often mild, even with advanced uremia, and frequently less severe than the effects of common anti-platelet drugs. The inhibition of collagen-induced aggregation was significantly correlated with both increased bleeding time and blood urea nitrogen. Platelet aggregation was not discriminative between clinically bleeding and non-bleeding groups of patients, but the bleeding time was helpful in this regard. In certain cases, the aggregometric patterns differed between drug-induced and uremic thrombocytopathies. Platelet aggregometry appears to be of little help clinically in assessing the severity of the uremic bleeding diathesis.

Adenosine Diphosphate↗
PubMed1986

Bleeding time in hemophilia A: potential mechanisms for prolongation.

Prolongation of bleeding time has been previously observed in hemophilia, although no cause has been elucidated. We measured bleeding time, platelet aggregation, nucleotide release, and thromboxane B2 (TXB2), plasma 6-keto-PGF 1 alpha, platelet-associated IgG (PAIgG), and circulating immune complexes in 31 unselected patients with severe hemophilia A and in 17 controls. In 85% of patients with hemophilia A, the bleeding time was greater than 2 SD above the control level (greater than 8 minutes). Sixty-six percent of patients with hemophilia A had circulating immune complexes, and there was a striking relationship between the presence of these complexes and prolonged bleeding time. Plasma 6-keto-PGF 1 alpha levels were significantly elevated in the patient group, and correlated with bleeding time changes. Platelet aggregation and nucleotide release were normal in the patients with hemophilia, although reduced platelet TXB2 biosynthesis was noted in 26%. No correlation was demonstrated between bleeding time and impairment of platelet TXB2 formation. Seventy-two percent of the patients with hemophilia A had elevated levels of PAIgG, and an inverse relationship between PAIgG and platelet count was observed. No relationship was noted between platelet count and bleeding time. This study indicates that the majority of patients with hemophilia A have prolonged bleeding times. The close correlation between bleeding time, plasma 6-keto-PGF 1 alpha levels, and the presence of circulating immune complexes suggests a role for immune complex-mediated defects in vascular function as the basis for bleeding time prolongation.

6-Ketoprostaglandin F1 alpha↗