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At least 793 records · Page 44Linked to original sources
PubMed2002

Effect of desmopressin acetate administration on primary hemostasis in Doberman Pinschers with type-1 von Willebrand disease as assessed by a point-of-care instrument.

OBJECTIVE: To evaluate primary hemostasis following administration of desmopressin acetate (DDAVP) to Doberman Pinschers with type-1 von Willebrand disease (vWD). ANIMALS: 16 nonanemic Doberman Pinschers with type-1 vWD. PROCEDURE: Closure time (CT), defined as time required for occlusion of an aperture by a platelet plug assessed within the point-of-care instrument, plasma von Willebrand factor (vWF) concentration, and buccal mucosal bleeding time (BMBT) were determined before and 1 hour after administration of DDAVP (1 microg/kg, SC). RESULTS: Baseline closure times measured with adenosine diphosphate ([ADP-CT], 108 to > 300 seconds; reference range, 52 to 86 seconds) and epinephrine ([EPI-CT], 285 to > 300 seconds; 97 to 225 seconds) as platelet agonists were prolonged in all dogs. Following DDAVP administration, ADP-CT (59 to 186 seconds) was significantly shortened from baseline, but there was no decrease in EPI-CT. Although mean plasma vWF concentration increased significantly after DDAVP administration, only 1 dog had an increase of > 35 U/dL. There was no correlation between increase in plasma vWF concentration and shortening of the ADP-CT. Baseline BMBT was prolonged in 12 of 14 dogs, with significant shortening of BMBT after DDAVP administration in 6 of 7 dogs. In vitro replacement of vWF-deficient plasma with plasma from an unaffected dog shortened the ADP-CT whereas in vitro addition of DDAVP had no effect. CONCLUSIONS AND CLINICAL RELEVANCE: Administration of DDAVP to Doberman Pinschers with type-1 vWD resulted in improved hemostatic function, as assessed by the point-of-care instrument and shortening of BMBT, despite minimal increase in plasma vWF concentration.

Adenosine Diphosphate↗
PubMed2006

Effects of doxycycline, amoxicillin, cephalexin, and enrofloxacin on hemostasis in healthy dogs.

OBJECTIVE: To determine the effects of enteral administration of doxycycline, amoxicillin, cephalexin, and enrofloxacin at therapeutic dosages for a typical duration on hemostatic variables in healthy dogs. ANIMALS: 14 Beagles. PROCEDURE: Doxycycline (10 mg/kg, PO, q 12 h), amoxicillin (30 mg/kg, PO, q 12 h), cephalexin (30 mg/kg, PO, q 12 h), and enrofloxacin (20 mg/kg, PO, q 24 h) were administered in random order to 10 healthy dogs at standard therapeutic dosages for 7 days, with a 7-day washout period between subsequent antimicrobials. In addition, 4 Beagles served as control dogs. Variables were evaluated before and after antimicrobial administration; they included platelet count, Hct, 1-stage prothrombin time (PT), activated partial thromboplastin time (PTT), fibrinogen concentration, and platelet function. Platelet function was assessed via buccal mucosal bleeding time, aggregation, and a platelet-function analyzer. RESULTS: Administration of all antimicrobials caused a slight prolongation of 1-stage PT and activated PTT and slight decrease in fibrinogen concentration. Cephalexin caused a significant increase in 1-stage PT and activated PTT, amoxicillin caused a significant increase in activated PTT, and enrofloxacin caused a significant decrease in fibrinogen concentration. Platelet count or function did not differ significantly after administration of any antimicrobial. CONCLUSIONS AND CLINICAL RELEVANCE: Oral administration of commonly used antimicrobials in healthy dogs resulted in minor secondary hemostatic abnormalities, with no change in platelet count or function. Although these changes were clinically irrelevant in healthy dogs, additional studies of the effects of antimicrobial administration on hemostasis in animals with underlying disease processes are warranted.

Amoxicillin↗
PubMed2001

Gene targeting in hemostasis. factor XI.

Factor XI (FXI) is the zymogen of a plasma serine protease (FXIa) that contributes to hemostasis by activating factor IX (FIX). This reaction appears to be important for sustaining thrombin production after initial fibrin formation, to consolidate and protect fibrin clots from degradation by fibrinolysis. Humans with congenital FXI deficiency have a variable propensity to bleed after trauma or surgery, but do not experience the "spontaneous" hemorrhage in joints and soft tissue characteristic of hemophilia (FVIII or FIX deficiency). Mice homozygous for a disruption of the FXI gene (FXI-/-) have prolonged activated partial thromboplastin times and no detectable plasma FXI activity. Like their human counterparts, FXI-/- animals are generally healthy, reproduce normally, and do not develop spontaneous hemorrhage. In tail bleeding time assays, FXI-/- animals may have slightly prolonged bleeding compared to FXI+/+ and FXI+/- animals, however, a consistent hemostatic deficit has not been identified. More impressive results are obtained when FXI-/- mice are crossed with protein C deficient mice. Severe FXI deficiency partially ameliorates the devastating hypercoagulable state associated with severe protein C deficiency, indicating that FXI plays a role in certain thrombotic conditions.

Animals↗
PubMed2001

Gene targeting in hemostasis. tissue factor.

Tissue factor (TF) is the primary cellular initiator of blood coagulation. At sites of vascular injury, formation of a TF:FVIIa complex leads to the generation of FXa, thrombin and the deposition of fibrin to limit hemorrhage. In contrast to its beneficial role in hemostasis, TF initiates life-threatening intravascular thrombosis in sepsis, atherosclerosis and cancer. More recently, TF has been proposed to play a role in other biological processes, including tumor-associated angiogenesis, metastasis and inflammation. Indeed, gene targeting of TF resulted in embryonic lethality, which appeared to be due to a defect in the yolk sac vasculature.

Animals↗
PubMed1997

Venocclusive disease of the liver after bone marrow transplantation: the role of hemostasis.

Venocclusive disease of the liver is a relatively frequent early complication of bone marrow transplantation related to pre-transplant toxic injury to the liver. Events that lead to toxicity of the liver in the pre-transplant setting are infection, anti-neoplastic and anti-infectious drug administration and radiation. The histological correlates of venocclusive disease are lesions mainly localized to structures in zone 3 of the liver acinus and in the sublobular central venules. At some point in the pathogenesis of venocclusive disease, blood clotting and inflammation occur. The first is characterized by laboratory signs of coagulation activation, by an increase in several procoagulant proteins and by a decrease in naturally occurring anticoagulants, particularly protein C, the latter being a sensitive index of liver injury. Inflammation is mediated by cytokine production, which maintains procoagulant endothelial responses and liver injury. Severe venocclusive disease is associated with multi-organ failure and elevated mortality. Attempts at finding predictive markers of the disease have succeeded in identifying some coagulation and inflammatory proteins which can be useful in predicting the occurrence of VOD in selected patient groups. The role of hemostasis in venocclusive disease is underscored also by the reports on the successful prophylaxis and management of the disease with heparin and thrombolytic agents.

Alprostadil↗
PubMed1997

[Use of hemostatic clips for endoscopic hemostasis and closure of an esophageal laceration caused by a fish bone].

An 82-year-old woman was admitted to our hospital because of hematemesis. She had had a feeling of a foreign substance in her throat for one week after having eaten fish. On admission she had a fever of 38 degrees C, Hb of 5.8 g/dl, CRP level of 8.8 mg/dl, and bilateral pleural effusions. Endoscopy revealed a deep longitudinal laceration with active bleeding in the esophagus that also caused mediastinitis. Endoscopic hemostasis and closure of the laceration was done with hemostatic clips. The esophageal injury seemed to have been caused by a fish bone. After the treatments described here were carried out, the patient's condition rapidly improved.

Aged↗
PubMed1981

Gelfoam paste in experimental laminectomy and cranial trephination: hemostasis and bone healing.

The hemostatic properties and effect on osteogenesis of gelatin foam paste and bone wax were compared on surgical bone lesions in experimental animals. Thirty rabbits each received four trephine craniotomies and four lumbar laminectomies. Alternate bone incisions in each animal were treated with either gelatin foam paste or bone wax. Blood loss was measured by absorbing the blood into dry surgical cottonoids weighed before and after use. Bone healing sites of three rabbits were examined histologically to assess the effect of each agent on osteogenesis. The trephination sites of eight rabbits were subjected to fracture force testing at 6 weeks postoperatively to compare the effect ot the two agents on bone healing. No significant difference was found between gelatin foam paste and bone wax in either effectiveness of hemostasis or effect on osteogenesis.

Animals↗
PubMed1984

The Nd:YAG laser in neurosurgery. Part 2. Clinical studies: an adjunctive measure for hemostasis in resection of arteriovenous malformations.

The Nd:YAG laser has been used safely to aid in the resection of 10 cases of parenchymal arteriovenous malformations (AVM's). The laser was found helpful for: 1) defining the plane between the AVM and the brain; 2) coagulating any dural component of the AVM; and 3) achieving hemostasis of the bed following resection of the lesion. However, its overall benefit in the resection of AVM's remains to be determined, as it could not arrest active high-flow bleeding from the thin-walled vessels feeding the deep portion of the AVM. This was attributed to the inherent characteristics of these vessels, since the instrument has been effective in non-AVM arteries of similar dimensions containing contractile elements in the vessel walls. Future refinements in focusing instrumentation and operative technique should enhance its capabilities and usefulness. When used within the recommended power range, the Nd:YAG laser is safe and its penetration predictable. The fiberoptic cable light delivery system allows excellent mobility of the handpiece, but the protective eyewear laser-light filters reduce the available light to the surgeon. The instrument appears promising but more work is required.

Adolescent↗
PubMed1990

A new intracranial Silastic encircling clip for hemostasis. Technical note.

A new encircling clip made of a silicone tube has been designed for treating accidentally injured cerebral vessels. No special holders are necessary. This clip can be tailored depending on the shape of the injured vessel. The clip is a simple and effective tool for achieving complete hemostasis.

Cerebral Arteries↗
PubMed1997

Hemostasis and fibrinolysis activation after subarachnoid hemorrhage.

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.

Adult↗
PubMed1997

Hemostasis activation in patients undergoing brain tumor surgery.

Patients undergoing brain tumor surgery are at high risk for the occurrence of a thromboembolic event. To identify a laboratory marker suitable for risk estimation the authors studied the perioperative time pattern of routine coagulation parameters and the specific hemostasis activation marker D-dimer in 28 consecutive patients at high risk (11 patients with glioma and eight patients with meningioma) and low risk (nine patients with metastases) for thromboembolism, as previously reported. As is typical during major surgery, most of the routine parameters declined, probably because of hemodilution, and recovered postoperatively to values higher than baseline, probably because of an acute-phase reaction. On Days 2 and 7 after surgery no difference in the routine parameters was recorded between patients at high (meningioma and glioma) and low risk (metastasis). The level of D-dimer was elevated at baseline in patients with metastasis, indicating a hemostatic hyperactivity that is usual in cancer patients. During surgery a marked increase in D-dimer levels occurred in patients with meningioma and glioma (pre- and postoperative median 90/2000 and 100/1020 ng/ml, respectively), but the increase was less pronounced in patients with metastasis (320/660 ng/ml). Postoperatively, D-dimer declined in patients with metastases to lower than preoperative levels (Day 7, 270 ng/ml); in patients with meningioma or glioma, however, D-dimer levels remained elevated until Day 7 (450 and 200 ng/ml, respectively). These results indicate that levels of D-dimer correlate with the reported high risk for thromboembolism in patients with meningioma and glioma, and D-dimer should be evaluated for its use in estimating individual risk and the efficiency of its use in the control of prophylactic treatment.

Acute-Phase Reaction↗
PubMed1981

Effect of dietary aflatoxin on hemostasis of young turkey poults.

Young turkey poults fed graded levels of aflatoxin (0, 125, 250, and 500 microgram/kg) from hatching for 3 weeks displayed altered hemostasis, manifested in prolonged prothrombin times at 2 and 3 weeks of age. Body weights were only affected in those groups receiving 500 microgram/kg. Total plasma protein, fibrinogen, and plasma calcium were reduced in response to dietary aflatoxin. In comparison with chickens, which exhibit similar hemostatic dysfunction concomitant with reduced body weight, turkeys receiving aflatoxin at lower levels exhibited an altered hemostatic response without exhibiting depressed body weights. Thus, the turkey hemostatic system is a better indicator of aflatoxicosis than is body weight gain.

Aflatoxins↗
PubMed2004

Effect of monthly atorvastatin treatment on hemostasis.

Apart from lowering lipid levels, 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitors (statins) produce many other favorable effects that contribute to their clinical efficacy in the primary and secondary prevention of cardiovascular diseases. The aim of this study was to assess the effect of 30-day atorvastatin treatment on major hemostatic risk factors (fibrinogen, PAI-1 levels, factor VII coagulant activity) in patients with primary hypercholesterolemia. We studied 18 hypercholesterolemic patients and 12 matched control subjects. Compared to the control subjects, hypercholesterolemic patients exhibited increased plasma PAI-1 levels and factor VII activity. Atorvastatin (20 mg/d) not only decreased total cholesterol, LDL cholesterol and oxidized LDL, but also reduced PAI-1 levels and factor VII activity and tended to decrease fibrinogen levels. The hemostatic effects of atorvastatin did not correlate with its lipid-lowering potential. Our study is the first to show that atorvastatin may exhibit a quick, beneficial and multidirectional nonlipid-related effect on hemostasis.

Adult↗
PubMed2004

Monitoring of hemostasis in combat trauma patients.

Bleeding is clearly a major cause of morbidity and death after trauma. When bleeding is attributable to transection of major vessels, surgical repair is appropriate. Posttraumatic microvascular bleeding attributable to coagulopathy secondary to metabolic derangements, hypothermia, and depletion or dysfunction of cellular and protein components requires a different approach. Although transfusion of blood products may be necessary to replace the blood loss, it does not always correct the problem of microvascular bleeding. The type of injury, mode of care, and treatment objectives differ significantly for combat-wounded soldiers versus civilian trauma patients. Although hemorrhage is responsible for 50% of combat deaths, published information about coagulation monitoring among combat patients is very limited. These articles summarize the appropriate monitoring of hemostasis among combat trauma patients, review the unique nature of combat casualties and the medical system used to treat them, and discuss information available from civilian studies. Because the development of coagulopathy is relatively infrequent in the young, otherwise healthy, military population, the routine screening measures currently used are adequate to guide initial blood product administration. However, as new intravenous hemostatic agents are used for these patients, better laboratory measures will be required. Although hemorrhage is the leading cause of death for combat casualties, catastrophic hemorrhage is rarely a prehospital combat medical management problem because, when it occurs, it tends to cause death before medical care can be provided. In civilian environments, most seriously injured victims can be reached and transported by emergency medical services personnel within minutes; in combat, it often takes hours simply to transport casualties off the battlefield. In combat situations, even if the transport distances are small, the hazardous nature of the forward combat areas frequently prevents medical personnel from quickly reaching the wounded. Furthermore, whereas civilian blunt trauma victims may have a "golden hour," casualties with penetrating battlefield trauma often have only a "platinum 5 minutes." Because of the challenges of treating hemorrhage during combat, it is important for military medical personnel to understand their options for treating hemorrhage quickly and efficiently. These articles discuss the causes of posttraumatic microvascular bleeding and the potential treatment options for controlling catastrophic hemorrhage in combat areas.

Hemorrhage↗
PubMed1981

Platelets and their membranes in hemostasis: physiology and pathophysiology.

Platelets form a plug and promote thrombin generation at sites of vascular injury. These processes are initiated by interaction of the platelet plasma membrane with various substances within or accumulating at the injured vessel. Thus, platelet adhesion to exposed subendothelium requires the binding of von Willebrand factor to platelets. Agonists such as thrombin bind to membrane receptors, thereby stimulating the binding of fibrinogen to platelets and resulting in the aggregation of platelets onto those already adherent to the vessel wall. Agonists also stimulate transfer of membrane=bound calcium into the cytoplasm. This triggers the secretion of granule substances and results in the recruitment of additional platelets to the hemostatic plug. Concomitant with secretion, the platelet surface supports several reactions leading to thrombin generation. Thus, hemostasis requires a series of coordinated responses involving platelet membranes. A defect in any of these responses can lead to a bleeding diathesis.

Blood Platelet Disorders↗
PubMed1998

[Some parameters of hemostasis and fibrinolysis in diabetic patients].

The aim of our study was to estimate selected parameters of hemostasis and fibrinolysis in diabetic patients with vascular complications and obesity. The investigation was carried out in 23 type 1 diabetic subjects aged 17-56 ys, in 25 type 2 diabetic patients aged 41-69 ys and in 38 healthy persons: 16 "young"--aged 32.5 +/- 13.2 ys and 22 "old"--aged 56.2 +/- 9.4 ys. The following parameters were determined: glycaemia, HbA1c, blood level fibrinogen, euglobulin clot lysis time, plasminogen activator inhibitor (PAI-1) activity, microalbuminuria, triglyceride, total, HDL- and LDL-cholesterol concentration. Plasma fibrinogen level was elevated in type 2 diabetic subjects, and the highest concentrations were noted in patients with retinopathy or arterial hypertension, in overweight persons and--surprisingly--in type 1 diabetic subjects with nephropathy and coronary vascular disease (CVD). There were also positive correlations between fibrinogen level and systolic blood pressure (r = 0.3413, p < 0.02), diastolic blood pressure (r = 0.3809, p < 0.002) and microalbuminuria (r = 0.3552, p < 0.05). The mean euglobulin clot lysis time was prolonged in type II diabetics in comparison to the control group, especially in obese subjects. The highest activity of PAI-1 was found in overweight controls (28.87 +/- 6.24 Au/ml, p < 0.002). PAI-1 activity was also slightly increased in type 1 diabetic patients, especially with the symptoms of diabetic neuropathy, nephropathy or CHD, in comparison to the other groups. Our results seem to confirm the disturbed balance between coagulation and fibrinolysis--towards and increased risk of a prothrombotic state --in both--obese and diabetic patients--especially with advanced vascular complications.

Adolescent↗
PubMed1991

Perioperative autotransfusion and its correlation to hemostasis and coagulopathies.

The use of autologous blood techniques affords the reduction or elimination of homologous blood transfusions for most patients. In addition, for certain religious faiths such as Jehovah's Witnesses or those patients with rare blood types, intraoperative salvage and return of the patient's own blood is the only source of available blood. Autologous blood salvage in the perioperative period includes: hemodilution; intraoperative salvage of lost blood; postoperative collection of shed blood. Perioperatively, autologous blood is salvaged and returned and the volumes involved do not create any hematological problems for the patient. In those cases involving large volumes of blood being processed and returned to the patient, the autotransfusionist must be aware of the possible alterations that may occur in the patient's coagulation system. The collection and reinfusion of wound drainage fluids from operative sites has the potential to cause severe bleeding problems. This paper will present an overview of autologous blood salvage techniques in the perioperative period along with a review of the clinical effects of autotransfusion on hemostasis. Also discussed will be possible coagulopathies that can be caused by returning collected autologous blood.

Blood Coagulation↗