Hemostatic Disorders
Hemostasis
Blood Coagulation Disorders
Hemostatics
Relationship of fibrinogen levels and hemostatic abnormalities with organ damage in hypertension. (1/16)
Elevated plasma levels of fibrinogen and activated coagulation pathways are risk factors of cardiovascular disease in the general population. In a cross-sectional study of a case series, we investigated the relationship between fibrinogen and hemostatic markers with target-organ damage (TOD) in patients with arterial hypertension. Prothrombin time, partial thromboplastin time, fibrinogen, fibrin D-dimer, prothrombin fragment 1+2 (F1+2), and antithrombin III were measured in 352 untreated patients with mild to moderate essential hypertension and 92 normotensive controls. Staging of TOD was assessed according to W.H.O. guidelines by clinical evaluation and laboratory tests including measurements of creatinine clearance, proteinuria, ophthalmoscopy, electrocardiography, echocardiography, and ultrasound examination of major arteries. F1+2 concentrations were significantly greater in hypertensive patients than normotensive controls and were positively correlated with blood pressure. Age, blood pressure levels, duration of hypertension, smoking, HDL-cholesterol, triglycerides, and plasma fibrinogen, fibrin D-dimer, and F1+2 levels were significantly related to the presence and severity of TOD in univariate analysis. Plasma fibrinogen and D-dimer levels were related to organ damage independent of age, blood pressure, duration of hypertension, and smoking status. Separate analysis indicated significant association of fibrinogen and D-dimer levels with cardiac, cerebrovascular, peripheral vascular, and renal damage. In conclusion, elevated plasma levels of fibrinogen and a prothrombotic state are associated with the presence and severity of TOD in patients with essential hypertension and may contribute to the development of atherosclerotic disease in these patients. (+info)Mouse carotid artery ligation induces platelet-leukocyte-dependent luminal fibrin, required for neointima development. (2/16)
The relationship between platelet and leukocyte activation, coagulation, and neointima development was investigated in noninjured murine blood vessels subjected to blood stasis. The left common carotid artery of C57BL/6J mice was ligated proximal to the bifurcation. Tissue-factor expression in luminal leukocytes progressively increased over 2 weeks. On day 3 after ligation, in addition to infiltrated granulocytes, platelet microthrombi and platelet-covered leukocytes as well as tissue-factor-positive fibrin deposits lined the endothelium. Maximal neointima formation in carotid artery cross sections of control mice equaled 28+/-3.7% (n=11) and 42+/-5.1% (n=8) of the internal elastic lamina cross-sectional area 1 and 2 weeks after ligation. In FVIII(-/-) mice, stenosis was significantly lower 1 (11+/-3.6%, n=8) and 2 (21+/-4.7%, n=7) weeks after ligation (both P:<0.01 versus background-matched controls). In u-PA(-/-) mice, luminal stenosis was significantly higher 1 (38+/-7.0%, n=7) and 2 (77+/-5.6%, n=6) weeks after ligation (P:<0.05 and P:<0.01, respectively, versus matched controls). In alpha(2)-AP(-/-) mice, stenosis was lower at 1 week (14+/-2.6%, n=7, P:<0.01) but not at 2 weeks. Responses in tissue-type plasminogen activator or plasminogen activator inhibitor-1 gene-deficient mice equaled that in controls. Reducing plasma fibrinogen levels in controls with ancrod or inducing partial thrombocytopenia with busulfan resulted in significantly less neointima, but inflammation was inhibited only in busulfan-treated mice. We conclude that stasis induces platelet activation, leading to microthrombosis and platelet-leukocyte conjugate formation, triggering inflammation and tissue-factor accumulation on the carotid artery endothelium. Delayed coagulation then results in formation of a fibrin matrix, which is used by smooth muscle cells to migrate into the lumen. (+info)Aberrations in hemostasis and coagulation in untreated discordant hepatic xenotransplantation: studies in the dog-to-pig model. (3/16)
Discordant liver xenotransplantation is a poorly explored entity. Data from the few large animal studies of hepatic xenotransplantation suggest that severe hemorrhage is encountered. The purpose of the studies described here is to characterize the nature of the hemorrhage that accompanies liver xenotransplantation. Canine livers were transplanted into porcine recipients, and lethal hemorrhage was encountered. Analysis of recipient blood showed that factors V, IX, and X were present in adequate levels until after the hemorrhage appeared, suggesting that coagulation factor loss was the result and not the cause of hemorrhage. Platelet counts decreased dramatically in recipients within minutes of graft reperfusion. There also was no evidence of clotting activity in the blood of recipients of liver xenografts within minutes of graft reperfusion. This loss of clotting activity was specific to liver xenografts, was not seen in renal xenografts with or without venovenous bypass, and also was absent in pig-to-pig liver allografts. In brief, the hemorrhage that accompanies liver xenotransplantation occurs because of a decrease in the number and function of circulating platelets in the recipient. (+info)Plasminogen activator inhibitor 1: physiological and pathophysiological roles. (4/16)
Plasminogen activator inhibitor 1 (PAI-1) inhibits plasminogen activators (u-PA and t-PA) by forming stable complexes endocytosed via a low-density lipoprotein receptor superfamily member-dependent mechanism. PAI-1 circulates actively in plasma and latently in platelets but is also secreted and deposited into the matrix by several cells, where it participates in tissue repair processes. (+info)Clinical studies on coronary revascularization in patients with type 2 diabetes. (5/16)
With the increasing prevalence, diabetes is rapidly growing into a global public health problem. Cardiovascular disease is a major consequence of this chronic condition, and a critical issue facing physicians worldwide today is choice of coronary revascularization procedures in treating these patients. Since the Bypass Angioplasty Revascularization Investigation (BARI) alert in 1995, there have been several reports on subgroup analysis of clinical trials and registries concerning revascularization among patients with diabetes. Although randomized control studies comparing percutaneous and surgical revascularization procedures in this high-risk group of patients are lacking, this article provides the background for the excess risk and reviews the findings of these investigations. Current strategies to improve outcomes in patients with diabetes undergoing coronary revascularization procedures are discussed. (+info)Right thoracic paravertebral analgesia for hepatectomy. (6/16)
Haemostatic deficiencies, common among cirrhotic patients, may deteriorate further after hepatectomy, increasing the bleeding risk associated with the use of thoracic epidural analgesia. We describe two patients who enjoyed immediate post-operative tracheal extubation and satisfactory analgesia using mainly right thoracic paravertebral analgesia after right lobe hepatectomy. (+info)Snake envenomation in a north Indian hospital. (7/16)
OBJECTIVES: To study the clinical profile of snake envenomation in a tertiary referral north Indian hospital. METHODS: Retrospective case note analysis of all cases of snakebite admitted to the medical emergency from January 1997 to December 2001. RESULTS: Of a total of 142 cases of snakebite there were 86 elapid bites presenting with neuroparalytic symptoms and 52 viper bites having haemostatic abnormalities. Some 60.6% of the cases of snakebite occurred when the patient was asleep. Urban to rural ratio was 1:4.7 and male to female ratio was 4.25:1. Median time to arrival at our hospital after the bite was nine hours and mean duration of hospital stay was eight days. Twenty seven cases had acute renal failure and 75% of all elapid bites required assisted ventilation. Seventeen of 119 patients who received antivenom had an adverse event. The average dose of antivenom was 51.2 vials for elapid bites and 31 vials for viper bites. Overall mortality rate was 3.5%. CONCLUSION: Snakebites are common in the rural population of developing countries. There is a need to educate the public about the hazards of snakebite, early hospital referral, and treatment. (+info)Inflammation and hemostasis biomarkers for predicting stroke in postmenopausal women: the Women's Health Initiative Observational Study. (8/16)
(+info)Hemostatic disorders are medical conditions that affect the body's ability to stop bleeding (hemorrhage) after an injury or surgery. The hemostatic system includes blood vessels, platelets, and clotting factors that work together to form a clot and prevent further blood loss.
Disorders of hemostasis can be broadly classified into three categories:
1. Bleeding disorders: These are conditions in which the body is unable to form a clot or forms clots that are too weak, leading to excessive bleeding. Examples include hemophilia, von Willebrand disease, and platelet function disorders.
2. Thrombotic disorders: These are conditions in which the body forms clots that are too large or inappropriately located, leading to obstruction of blood flow. Examples include deep vein thrombosis (DVT), pulmonary embolism (PE), and disseminated intravascular coagulation (DIC).
3. Combined disorders: These are conditions in which both bleeding and thrombotic tendencies may be present, depending on the specific circumstances. Examples include antiphospholipid syndrome and thrombotic microangiopathies.
Hemostatic disorders can be inherited or acquired, and their diagnosis and management require a thorough understanding of the underlying pathophysiology and clinical context.
Hemostasis is the physiological process that occurs to stop bleeding (bleeding control) when a blood vessel is damaged. This involves the interaction of platelets, vasoconstriction, and blood clotting factors leading to the formation of a clot. The ultimate goal of hemostasis is to maintain the integrity of the vascular system while preventing excessive blood loss.
Blood coagulation disorders, also known as bleeding disorders or clotting disorders, refer to a group of medical conditions that affect the body's ability to form blood clots properly. Normally, when a blood vessel is injured, the body's coagulation system works to form a clot to stop the bleeding and promote healing.
In blood coagulation disorders, there can be either an increased tendency to bleed due to problems with the formation of clots (hemorrhagic disorder), or an increased tendency for clots to form inappropriately even without injury, leading to blockages in the blood vessels (thrombotic disorder).
Examples of hemorrhagic disorders include:
1. Hemophilia - a genetic disorder that affects the ability to form clots due to deficiencies in clotting factors VIII or IX.
2. Von Willebrand disease - another genetic disorder caused by a deficiency or abnormality of the von Willebrand factor, which helps platelets stick together to form a clot.
3. Liver diseases - can lead to decreased production of coagulation factors, increasing the risk of bleeding.
4. Disseminated intravascular coagulation (DIC) - a serious condition where clotting and bleeding occur simultaneously due to widespread activation of the coagulation system.
Examples of thrombotic disorders include:
1. Factor V Leiden mutation - a genetic disorder that increases the risk of inappropriate blood clot formation.
2. Antithrombin III deficiency - a genetic disorder that impairs the body's ability to break down clots, increasing the risk of thrombosis.
3. Protein C or S deficiencies - genetic disorders that lead to an increased risk of thrombosis due to impaired regulation of the coagulation system.
4. Antiphospholipid syndrome (APS) - an autoimmune disorder where the body produces antibodies against its own clotting factors, increasing the risk of thrombosis.
Treatment for blood coagulation disorders depends on the specific diagnosis and may include medications to manage bleeding or prevent clots, as well as lifestyle changes and monitoring to reduce the risk of complications.
Hemostatics are substances or agents that promote bleeding cessation or prevent the spread of bleeding. They can act in various ways, such as by stimulating the body's natural clotting mechanisms, constricting blood vessels to reduce blood flow, or forming a physical barrier to block the bleeding site.
Hemostatics are often used in medical settings to manage wounds, injuries, and surgical procedures. They can be applied directly to the wound as a powder, paste, or gauze, or they can be administered systemically through intravenous injection. Examples of hemostatic agents include fibrin sealants, collagen-based products, thrombin, and oxidized regenerated cellulose.
It's important to note that while hemostatics can be effective in controlling bleeding, they should be used with caution and only under the guidance of a healthcare professional. Inappropriate use or overuse of hemostatic agents can lead to complications such as excessive clotting, thrombosis, or tissue damage.
Hemostatic techniques refer to various methods used in medicine to stop bleeding or hemorrhage. The goal of these techniques is to promote the body's natural clotting process and prevent excessive blood loss. Some common hemostatic techniques include:
1. Mechanical compression: Applying pressure directly to the wound to physically compress blood vessels and stop the flow of blood. This can be done manually or with the use of medical devices such as clamps, tourniquets, or compression bandages.
2. Suturing or stapling: Closing a wound with stitches or staples to bring the edges of the wound together and allow the body's natural clotting process to occur.
3. Electrocautery: Using heat generated by an electrical current to seal off blood vessels and stop bleeding.
4. Hemostatic agents: Applying topical substances that promote clotting, such as fibrin glue, collagen, or gelatin sponges, to the wound site.
5. Vascular embolization: Inserting a catheter into a blood vessel and injecting a substance that blocks the flow of blood to a specific area, such as a bleeding tumor or aneurysm.
6. Surgical ligation: Tying off a bleeding blood vessel with suture material during surgery.
7. Arterial or venous repair: Repairing damaged blood vessels through surgical intervention to restore normal blood flow and prevent further bleeding.