Control of bleeding during or after surgery.
Techniques for controlling bleeding.
Agents acting to arrest the flow of blood. Absorbable hemostatics arrest bleeding either by the formation of an artificial clot or by providing a mechanical matrix that facilitates clotting when applied directly to the bleeding surface. These agents function more at the capillary level and are not effective at stemming arterial or venous bleeding under any significant intravascular pressure.
The process which spontaneously arrests the flow of BLOOD from vessels carrying blood under pressure. It is accomplished by contraction of the vessels, adhesion and aggregation of formed blood elements (eg. ERYTHROCYTE AGGREGATION), and the process of BLOOD COAGULATION.
Pathological processes involving the integrity of blood circulation. Hemostasis depends on the integrity of BLOOD VESSELS, blood fluidity, and BLOOD COAGULATION. Majority of the hemostatic disorders are caused by disruption of the normal interaction between the VASCULAR ENDOTHELIUM, the plasma proteins (including BLOOD COAGULATION FACTORS), and PLATELETS.
The process of the interaction of BLOOD COAGULATION FACTORS that results in an insoluble FIBRIN clot.
Endogenous substances, usually proteins, that are involved in the blood coagulation process.
Plasma glycoprotein clotted by thrombin, composed of a dimer of three non-identical pairs of polypeptide chains (alpha, beta, gamma) held together by disulfide bonds. Fibrinogen clotting is a sol-gel change involving complex molecular arrangements: whereas fibrinogen is cleaved by thrombin to form polypeptides A and B, the proteolytic action of other enzymes yields different fibrinogen degradation products.
Heat- and storage-stable plasma protein that is activated by tissue thromboplastin to form factor VIIa in the extrinsic pathway of blood coagulation. The activated form then catalyzes the activation of factor X to factor Xa.
The natural enzymatic dissolution of FIBRIN.
Use of a thrombelastograph, which provides a continuous graphic record of the physical shape of a clot during fibrin formation and subsequent lysis.
A cellulose of varied carboxyl content retaining the fibrous structure. It is commonly used as a local hemostatic and as a matrix for normal blood coagulation.
Soluble protein fragments formed by the proteolytic action of plasmin on fibrin or fibrinogen. FDP and their complexes profoundly impair the hemostatic process and are a major cause of hemorrhage in intravascular coagulation and fibrinolysis.
Sterile, gelatin-base surgical sponge applied topically as an adjunct to hemostasis when the control of bleeding by conventional procedures is ineffective to reduce capillary ooze or is impractical. (From AMA Drug Evaluations Annual, 1994, p797)
Hemorrhagic and thrombotic disorders that occur as a consequence of abnormalities in blood coagulation due to a variety of factors such as COAGULATION PROTEIN DISORDERS; BLOOD PLATELET DISORDERS; BLOOD PROTEIN DISORDERS or nutritional conditions.
Duration of blood flow after skin puncture. This test is used as a measure of capillary and platelet function.
A high-molecular-weight plasma protein, produced by endothelial cells and megakaryocytes, that is part of the factor VIII/von Willebrand factor complex. The von Willebrand factor has receptors for collagen, platelets, and ristocetin activity as well as the immunologically distinct antigenic determinants. It functions in adhesion of platelets to collagen and hemostatic plug formation. The prolonged bleeding time in VON WILLEBRAND DISEASES is due to the deficiency of this factor.
The time required for the appearance of FIBRIN strands following the mixing of PLASMA with phospholipid platelet substitute (e.g., crude cephalins, soybean phosphatides). It is a test of the intrinsic pathway (factors VIII, IX, XI, and XII) and the common pathway (fibrinogen, prothrombin, factors V and X) of BLOOD COAGULATION. It is used as a screening test and to monitor HEPARIN therapy.
Bleeding or escape of blood from a vessel.
A plasma alpha 2 glycoprotein that accounts for the major antithrombin activity of normal plasma and also inhibits several other enzymes. It is a member of the serpin superfamily.
Blood-coagulation factor VIII. Antihemophilic factor that is part of the factor VIII/von Willebrand factor complex. Factor VIII is produced in the liver and acts in the intrinsic pathway of blood coagulation. It serves as a cofactor in factor X activation and this action is markedly enhanced by small amounts of thrombin.
An autologous or commercial tissue adhesive containing FIBRINOGEN and THROMBIN. The commercial product is a two component system from human plasma that contains more than fibrinogen and thrombin. The first component contains highly concentrated fibrinogen, FACTOR VIII, fibronectin, and traces of other plasma proteins. The second component contains thrombin, calcium chloride, and antifibrinolytic agents such as APROTININ. Mixing of the two components promotes BLOOD CLOTTING and the formation and cross-linking of fibrin. The tissue adhesive is used for tissue sealing, HEMOSTASIS, and WOUND HEALING.
Activated form of factor VII. Factor VIIa activates factor X in the extrinsic pathway of blood coagulation.
Laboratory tests for evaluating the individual's clotting mechanism.
Two small peptide chains removed from the N-terminal segment of the alpha chains of fibrinogen by the action of thrombin during the blood coagulation process. Each peptide chain contains 18 amino acid residues. In vivo, fibrinopeptide A is used as a marker to determine the rate of conversion of fibrinogen to fibrin by thrombin.
Clotting time of PLASMA recalcified in the presence of excess TISSUE THROMBOPLASTIN. Factors measured are FIBRINOGEN; PROTHROMBIN; FACTOR V; FACTOR VII; and FACTOR X. It is used for monitoring anticoagulant therapy with COUMARINS.
Formation and development of a thrombus or blood clot in the blood vessel.
A member of the serpin superfamily found in plasma that inhibits the lysis of fibrin clots which are induced by plasminogen activator. It is a glycoprotein, molecular weight approximately 70,000 that migrates in the alpha 2 region in immunoelectrophoresis. It is the principal plasmin inactivator in blood, rapidly forming a very stable complex with plasmin.
Non-nucleated disk-shaped cells formed in the megakaryocyte and found in the blood of all mammals. They are mainly involved in blood coagulation.
A plasma protein that is the inactive precursor of thrombin. It is converted to thrombin by a prothrombin activator complex consisting of factor Xa, factor V, phospholipid, and calcium ions. Deficiency of prothrombin leads to hypoprothrombinemia.
Agents, usually topical, that cause the contraction of tissues for the control of bleeding or secretions.
A member of the serpin family of proteins. It inhibits both the tissue-type and urokinase-type plasminogen activators.
A dry artificial sterile sponge of fibrin prepared by clotting with thrombin a foam or solution of fibrinogen. It is used in conjunction with thrombin as a hemostatic in surgery at sites where bleeding cannot be controlled by more common methods. (From Martindale, The Extra Pharmacopoeia, 30th ed, p648)
Hemorrhage following any surgical procedure. It may be immediate or delayed and is not restricted to the surgical wound.
Loss of blood during a surgical procedure.
An enzyme formed from PROTHROMBIN that converts FIBRINOGEN to FIBRIN.
Spontaneous or near spontaneous bleeding caused by a defect in clotting mechanisms (BLOOD COAGULATION DISORDERS) or another abnormality causing a structural flaw in the blood vessels (HEMOSTATIC DISORDERS).
The internal resistance of the BLOOD to shear forces. The in vitro measure of whole blood viscosity is of limited clinical utility because it bears little relationship to the actual viscosity within the circulation, but an increase in the viscosity of circulating blood can contribute to morbidity in patients suffering from disorders such as SICKLE CELL ANEMIA and POLYCYTHEMIA.
The attachment of PLATELETS to one another. This clumping together can be induced by a number of agents (e.g., THROMBIN; COLLAGEN) and is part of the mechanism leading to the formation of a THROMBUS.
Agents that cause clotting.
The number of PLATELETS per unit volume in a sample of venous BLOOD.
A platelet-specific protein which is released when platelets aggregate. Elevated plasma levels have been reported after deep venous thrombosis, pre-eclampsia, myocardial infarction with mural thrombosis, and myeloproliferative disorders. Measurement of beta-thromboglobulin in biological fluids by radioimmunoassay is used for the diagnosis and assessment of progress of thromboembolic disorders.
A disorder characterized by procoagulant substances entering the general circulation causing a systemic thrombotic process. The activation of the clotting mechanism may arise from any of a number of disorders. A majority of the patients manifest skin lesions, sometimes leading to PURPURA FULMINANS.
Constituent composed of protein and phospholipid that is widely distributed in many tissues. It serves as a cofactor with factor VIIa to activate factor X in the extrinsic pathway of blood coagulation.
Agents that prevent fibrinolysis or lysis of a blood clot or thrombus. Several endogenous antiplasmins are known. The drugs are used to control massive hemorrhage and in other coagulation disorders.
A vitamin-K dependent zymogen present in the blood, which, upon activation by thrombin and thrombomodulin exerts anticoagulant properties by inactivating factors Va and VIIIa at the rate-limiting steps of thrombin formation.
A proteolytic enzyme in the serine protease family found in many tissues which converts PLASMINOGEN to FIBRINOLYSIN. It has fibrin-binding activity and is immunologically different from UROKINASE-TYPE PLASMINOGEN ACTIVATOR. The primary sequence, composed of 527 amino acids, is identical in both the naturally occurring and synthetic proteases.

Primary percutaneous transluminal coronary angioplasty performed for acute myocardial infarction in a patient with idiopathic thrombocytopenic purpura. (1/249)

A 72-year-old female with idiopathic thrombocytopenic purpura (ITP) complained of severe chest pain. Electrocardiography showed ST-segment depression and negative T wave in I, aVL and V4-6. Following a diagnosis of acute myocardial infarction (AMI), urgent coronary angiography revealed 99% organic stenosis with delayed flow in the proximal segment and 50% in the middle segment of the left anterior descending artery (LAD). Subsequently, percutaneous transluminal coronary angioplasty (PTCA) for the stenosis in the proximal LAD was performed. In the coronary care unit, her blood pressure dropped. Hematomas around the puncture sites were observed and the platelet count was 28,000/mm3. After transfusion, electrocardiography revealed ST-segment elevation in I, aVL and V1-6. Urgent recatheterization disclosed total occlusion in the middle segment of the LAD. Subsequently, PTCA was performed successfully. Then, intravenous immunoglobulin increased the platelet count and the bleeding tendency disappeared. A case of AMI with ITP is rare. The present case suggests that primary PTCA can be a useful therapeutic strategy, but careful attention must be paid to hemostasis and to managing the platelet count.  (+info)

Histological changes in the rat common carotid artery induced by aneurysmal wrapping and coating materials. (2/249)

Histological changes in and around the arterial walls of rats were investigated following topical application of aneurysmal wrapping and coating materials, including a fibrin glue, a cyanoacrylate glue (Biobond), and cotton fibers (Bemsheet). Bilateral common carotid arteries were exposed using sterile techniques, and one of the test materials was applied to the right artery. The left artery was used as the control. Changes in arterial histology were evaluated at 2 weeks, 1 month, 2 months, and 3 months after surgery. The fibrin glue was surrounded by intense inflammation at 2 weeks after surgery. Both the fibrin glue and inflammation had disappeared at 2 months, but the glue had induced mild inflammation in the adventitia. Biobond caused chronic inflammation, necrosis of the media, and thickening of the arterial wall due to fibrosis in both the media and adventitia. Bemsheet produced chronic inflammation, progressive fibrosis, and granuloma. Connective tissue increased in the adventitia, but no major changes were observed in the media. The Bemsheet fibers remained unchanged, and adhered to the arterial wall. Although arterial stenoses were not observed in the present study, the results suggest that cyanoacrylate glue can cause the arterial occlusive lesions observed following aneurysm surgery.  (+info)

Thrombin injection versus compression of femoral artery pseudoaneurysms. (3/249)

OBJECTIVE: The compression of femoral artery pseudoaneurysms is a time consuming, painful, and sometimes unsuccessful procedure. Thrombin injection has been advocated as a superior alternative. In this study, we compare our experiences with both techniques. METHODS: All the records of femoral artery false aneurysms that were treated in the vascular laboratory from January 1996 to April 1999 were retrospectively reviewed. Treatment with ultrasound scan-guided compression was compared with treatment with dilute thrombin injection (100 U/mL). RESULTS: Both groups had similar demographics and aneurysm sizes (P >.2). Of the pseudoaneursyms, 88% were caused by cardiac catheterization and the others were the results of femoral artery access for cardiac surgery (6%), arteriography (5%), and renal dialysis (1%). Compression was successful in 25 of 40 patients (63%). Nine persistent aneurysms necessitated operation, and six were treated successfully with thrombin injection. Primary thrombin injection successfully obliterated 21 pseudoaneurysms in 23 patients. Overall, 27 of 29 pseudoaneurysms were treated successfully with thrombin injection (93%). Thrombosis occurred within seconds of the thrombin injection and required, on average, 300 units of thrombin (100 to 600 units). The patients who underwent successful compression required an average of 37 minutes of compression (range, 5 to 70 minutes) and required analgesia on several occasions. No patients in the thrombin group required analgesia or sedation. Neither group had complications. A cost analysis shows that thrombin treatment results in considerable savings in vascular laboratory resource use but not in overall hospital expenditures. CONCLUSION: Ultrasound scan-guided thrombin injection is a safe, fast, and painless procedure that completely obliterates femoral artery pseudoaneurysms. The shift from compressive therapy to thrombin injection reduces vascular laboratory use and is less expensive, although it does not significantly impact hospital costs.  (+info)

Management of massive blood loss: a template guideline. (4/249)

The management of acute massive blood loss is considered and a template guideline is formulated, supported by a review of the key literature and current evidence. It is emphasized that, if avoidable deaths are to be prevented, surgeons, anaesthetists, haematologists and blood-bank staff need to communicate closely in order to achieve the goals of secure haemostasis, restoration of circulating volume, and effective management of blood component replacement.  (+info)

The management of peripheral vascular complications associated with the use of percutaneous suture-mediated closure devices. (5/249)

PURPOSE: The purpose of this study is to identify the peripheral vascular complications associated with the use of percutaneous suture-mediated closure (PSMC) devices and compare them with postcatheterization femoral artery complications not associated with PSMC devices. METHODS: This is a retrospective review of all patients admitted to the vascular surgery service at the Chattanooga Unit of the University of Tennessee Department of Surgery with a peripheral vascular complication after percutaneous femoral arteriotomy between July 1, 1998, and December 1, 1999. The complications followed the use of PSMC devices (group I, n = 11) and traditional compression therapy (group II, n = 14) to achieve arterial hemostasis. Group II was subdivided into patients who required operative intervention (group IIA, n = 8), and those who were treated without operation (group IIB, n = 6). RESULTS: No significant difference was found between groups I and II with regard to age (P =.227), time to vascular surgery consultation (P =.987), or diagnostic versus therapeutic catheterization (P =.897). A significant difference was found with regard to mean pseudoaneurysm size (group I = 5.9 cm, group II 2.9 cm; P =.003). Ultrasound compression was successfully performed in 66.6% of group II patients, but no (0.0%) patient in group I responded to this therapy (P =.016). Groups I and IIA had a significant difference for mean estimated blood loss (group I = 377.2 mL, group II = 121.8 mL; P =.017) and requirement for transfusion (P =.013). More patients in group I required extensive surgical treatment (P =.007), with six of these patients requiring vein patch angioplasty during their treatment. More patients in group I also had infectious complications (n = 3) compared with group IIA (n = 1). CONCLUSION: In comparison with complications that follow percutaneous arteriotomy when PSMC devices are not used for hemostasis: (1) pseudoaneurysms after the use of PSMC devices are larger and do not respond to ultrasound compression, (2) complications associated with PSMC devices result in more blood loss and increased need for transfusion and are more likely to require extensive operative procedures, and (3) arterial infections after the use of PSMC devices are more common and require aggressive surgical management.  (+info)

Iatrogenic vascular injuries from percutaneous vascular suturing devices. (6/249)

OBJECTIVE: The purpose of this study was to examine the patterns of injury and the strategies of surgical repair of iatrogenic vascular injuries from a percutaneous vascular suturing device after arterial cannulation. METHODS: We retrospectively reviewed the clinical experience from an academic vascular surgical practice over a 2-year period. The subjects were patients undergoing vascular repair of iatrogenic vascular injury after deployment of a percutaneous vascular suturing device. Interventions were direct repair of arterial injury (with or without device extraction) or arterial thrombectomy and repair. The main outcome variables included patterns of arterial injury, magnitude of arterial repair, limb salvage, hospital stay, and perioperative mortality and morbidity rates. RESULTS: From August 1998 through August 2000, eight patients (4 men, 4 women; median age, 55 years; range, 44-80 years) required vascular operations for complications of percutaneous suturing devices after diagnostic (2) or therapeutic (6) arteriograms through a transfemoral approach. Complications included four pseudoaneurysms (1 infected) due to arterial tear from suture pull through, two entrapped closure devices due to device malfunction, and two arterial thromboses due to narrowing/severe intimal dissection. All patients required operative intervention. Direct suture repair with or without device removal was performed in five patients, arterial debridement with vein patch angioplasty in one patient, and arterial thrombectomy and vein patch angioplasty in two patients. There were no perioperative deaths. The median hospital stay was 5 days (range, 2-33). Limbs were salvaged in all patients with a mean follow-up of 4.8 months (range, 1-13). CONCLUSIONS: Although abbreviated postangiography recovery periods and early ambulation have motivated the widespread use of percutaneous suturing devices, the infrequent occurrence of vascular injuries produced by these devices can be significantly more challenging than simple acute pseudoaneurysms or hemorrhage. In addition, thrombotic complications have a small but finite risk of limb loss.  (+info)

Vascular complications after percutaneous coronary interventions following hemostasis with manual compression versus arteriotomy closure devices. (7/249)

OBJECTIVES: We evaluated the vascular complications after hemostasis with arteriotomy closure devices (ACD) versus manual compression after percutaneous coronary interventions (PCI). BACKGROUND: Previous clinical studies have indicated that ACD can be used for achievement of hemostasis and early ambulation after PCI. This study investigated the safety of ACD in achieving hemostasis after PCI compared with manual compression in a large cohort of consecutive patients. METHODS: A total of 5,093 patients were followed after PCI was performed with the transfemoral approach. Univariate and multivariate analysis were used to identify the predictors of vascular complications with ACD (n = 516) or with manual compression (n = 5,892) as a hemostasis option after sheath removal. RESULTS: The use of ACD was associated with a more frequent occurrence of hematoma compared with manual compression (9.3 vs. 5.1%, p < 0.001). There was also a higher rate of significant hematocrit drop (>15%) with ACD versus manual compression (5.2% vs. 2.5%, p < 0.001). Similar rates of pseudoaneurysm and arteriovenous fistulae were noted with either hemostasis technique. Vascular surgical repair at the access site was required more often with ACD versus manual compression (2.5 vs. 1.5%, p = 0.03). CONCLUSIONS: In this early experience with ACD after PCI, their use was associated with higher vascular complication rates than hemostasis with manual compression.  (+info)

Traumatic rupture of the thoracic aorta: cohort study and systematic review. (8/249)

PURPOSE: Through a systematic review of the literature, we identified the optimal management of traumatic ruptures of the thoracic aorta (TRTA) and reported the results of a cohort of patients treated with the clamp-and-sew technique (CAS) at a tertiary trauma center. METHODS: Studies were identified through Medline and the Cochrane library and from reference lists and papers from the authors' files. Studies with a single consistent protocol (CAS, Gott shunt [GS], left heart bypass [LHB], or partial cardiopulmonary bypass [PCPB]) that reported mortality and neurologic outcomes were included. Relevance, validity, and data extraction were performed in duplicate. A retrospective review of charts from June 1992 to August 2000 provided the database for our experience. RESULTS: Twenty studies reporting on 618 patients were found to be relevant. Interobserver agreement for relevance and validity decisions was high. Mortality rates for repair with CAS, GS, LHB, and PCPB were 15%, 8%, 17%, and 10%, respectively, and for paraplegia they were 7%, 4%, 0%, and 2%, respectively. The difference in mortality rates was not statistically significant. CAS had a higher incidence of neurologic deficits than GS (odds ratio [OR], 1.8; 95% CI, 0.4-8), LHB (OR, 6.4; 95% CI, 0.8-50), and PCPB (OR, 3.4; 95% CI, 1-10). In our cohort of 25 patients, 21 underwent surgery with CAS. The median abbreviated injury severity score was 20 (range, 4-50). The mean aortic clamp time was 30 +/- 12 minutes. Aortic repair was achieved with graft interposition in 43% of patients, and simple suture was achieved in 57% of patients. Mortality (10%) and neurologic complication (paraplegia, 11%; paraparesis, 5%) rates were not statistically different from those reported in the literature. CONCLUSION: CAS is associated with a similar mortality rate but a higher incidence of neurologic deficits than methods with distal aortic perfusion.  (+info)

Surgical hemostasis refers to the methods and techniques used during surgical procedures to stop bleeding or prevent hemorrhage. This can be achieved through various means, including the use of surgical instruments such as clamps, ligatures, or staples to physically compress blood vessels and stop the flow of blood. Electrosurgical tools like cautery may also be used to coagulate and seal off bleeding vessels using heat. Additionally, topical hemostatic agents can be applied to promote clotting and control bleeding in wounded tissues. Effective surgical hemostasis is crucial for ensuring a successful surgical outcome and minimizing the risk of complications such as excessive blood loss, infection, or delayed healing.

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.

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.

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.

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.

Blood coagulation, also known as blood clotting, is a complex process that occurs in the body to prevent excessive bleeding when a blood vessel is damaged. This process involves several different proteins and chemical reactions that ultimately lead to the formation of a clot.

The coagulation cascade is initiated when blood comes into contact with tissue factor, which is exposed after damage to the blood vessel wall. This triggers a series of enzymatic reactions that activate clotting factors, leading to the formation of a fibrin clot. Fibrin is a protein that forms a mesh-like structure that traps platelets and red blood cells to form a stable clot.

Once the bleeding has stopped, the coagulation process is regulated and inhibited to prevent excessive clotting. The fibrinolytic system degrades the clot over time, allowing for the restoration of normal blood flow.

Abnormalities in the blood coagulation process can lead to bleeding disorders or thrombotic disorders such as deep vein thrombosis and pulmonary embolism.

Blood coagulation factors, also known as clotting factors, are a group of proteins that play a crucial role in the blood coagulation process. They are essential for maintaining hemostasis, which is the body's ability to stop bleeding after injury.

There are 13 known blood coagulation factors, and they are designated by Roman numerals I through XIII. These factors are produced in the liver and are normally present in an inactive form in the blood. When there is an injury to a blood vessel, the coagulation process is initiated, leading to the activation of these factors in a specific order.

The coagulation cascade involves two pathways: the intrinsic and extrinsic pathways. The intrinsic pathway is activated when there is damage to the blood vessel itself, while the extrinsic pathway is activated by tissue factor released from damaged tissues. Both pathways converge at the common pathway, leading to the formation of a fibrin clot.

Blood coagulation factors work together in a complex series of reactions that involve activation, binding, and proteolysis. When one factor is activated, it activates the next factor in the cascade, and so on. This process continues until a stable fibrin clot is formed.

Deficiencies or abnormalities in blood coagulation factors can lead to bleeding disorders such as hemophilia or thrombosis. Hemophilia is a genetic disorder that affects one or more of the coagulation factors, leading to excessive bleeding and difficulty forming clots. Thrombosis, on the other hand, occurs when there is an abnormal formation of blood clots in the blood vessels, which can lead to serious complications such as stroke or pulmonary embolism.

Fibrinogen is a soluble protein present in plasma, synthesized by the liver. It plays an essential role in blood coagulation. When an injury occurs, fibrinogen gets converted into insoluble fibrin by the action of thrombin, forming a fibrin clot that helps to stop bleeding from the injured site. Therefore, fibrinogen is crucial for hemostasis, which is the process of stopping bleeding and starting the healing process after an injury.

Factor VII, also known as proconvertin, is a protein involved in the coagulation cascade, which is a series of chemical reactions that leads to the formation of a blood clot. Factor VII is synthesized in the liver and is activated when it comes into contact with tissue factor, which is exposed when blood vessels are damaged. Activated Factor VII then activates Factor X, leading to the formation of thrombin and ultimately a fibrin clot.

Inherited deficiencies or dysfunctions of Factor VII can lead to an increased risk of bleeding, while elevated levels of Factor VII have been associated with an increased risk of thrombosis (blood clots).

Fibrinolysis is the natural process in the body that leads to the dissolution of blood clots. It is a vital part of hemostasis, the process that regulates bleeding and wound healing. Fibrinolysis occurs when plasminogen activators convert plasminogen to plasmin, an enzyme that breaks down fibrin, the insoluble protein mesh that forms the structure of a blood clot. This process helps to prevent excessive clotting and maintains the fluidity of the blood. In medical settings, fibrinolysis can also refer to the therapeutic use of drugs that stimulate this process to dissolve unwanted or harmful blood clots, such as those that cause deep vein thrombosis or pulmonary embolism.

Thromboelastography (TEG) is a viscoelastic method used to assess the kinetics of clot formation, clot strength, and fibrinolysis in whole blood. It provides a global assessment of hemostasis by measuring the mechanical properties of a clot as it forms and dissolves over time. The TEG graph displays several parameters that reflect the different stages of clotting, including reaction time (R), clot formation time (K), angle of clot formation (α), maximum amplitude (MA), and percentage lysis at 30 minutes (LY30). These parameters can help guide transfusion therapy and inform decisions regarding the management of coagulopathy in various clinical settings, such as trauma, cardiac surgery, liver transplantation, and obstetrics.

Oxidized cellulose is a type of modified cellulose that has undergone oxidation, resulting in the introduction of functional groups such as carboxylic acid or aldehyde groups along the cellulose chain. This process can alter the physical and chemical properties of cellulose, making it more soluble in water and capable of forming gels or films.

Oxidized cellulose is used in a variety of applications, including as a wound dressing material, where it can help to promote healing by providing a moist environment that supports tissue regeneration. It can also be used as a thickening or stabilizing agent in food and cosmetic products, or as a component in the manufacture of specialized papers and textiles.

Fibrin(ogen) degradation products (FDPs) are a group of proteins that result from the breakdown of fibrinogen and fibrin, which are key components of blood clots. This process occurs during the normal physiological process of fibrinolysis, where clots are dissolved to maintain blood flow.

FDPs can be measured in the blood as a marker for the activation of the coagulation and fibrinolytic systems. Elevated levels of FDPs may indicate the presence of a disorder that causes abnormal clotting or bleeding, such as disseminated intravascular coagulation (DIC), deep vein thrombosis (DVT), pulmonary embolism (PE), or certain types of cancer.

It is important to note that FDPs are not specific to any particular disorder and their measurement should be interpreted in conjunction with other clinical and laboratory findings.

A gelatin sponge, absorbable is a surgical implant material that is derived from animal collagen. It is prepared in the form of a sterile, compressed sponge which can be expanded with the addition of fluids. The sponge is designed to absorb and hold surgical drainage, promote healing by providing a framework for the growth of new tissue, and then gradually break down and be absorbed by the body over time. It is often used in neurosurgery, plastic surgery, and other surgical specialties for its hemostatic (bleeding control) and supportive properties.

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.

Bleeding time is a medical test that measures the time it takes for a small blood vessel to stop bleeding after being cut. It's used to evaluate platelet function and the effectiveness of blood clotting. The most common method used to measure bleeding time is the Ivy method, which involves making a standardized incision on the forearm and measuring the time it takes for the bleeding to stop. A normal bleeding time ranges from 2 to 9 minutes, but this can vary depending on the specific method used. Prolonged bleeding time may indicate an impairment in platelet function or clotting factor deficiency.

Von Willebrand factor (vWF) is a large multimeric glycoprotein that plays a crucial role in hemostasis, the process which leads to the cessation of bleeding and the formation of a blood clot. It was named after Erik Adolf von Willebrand, a Finnish physician who first described the disorder associated with its deficiency, known as von Willebrand disease (vWD).

The primary functions of vWF include:

1. Platelet adhesion and aggregation: vWF mediates the initial attachment of platelets to damaged blood vessel walls by binding to exposed collagen fibers and then interacting with glycoprotein Ib (GPIb) receptors on the surface of platelets, facilitating platelet adhesion. Subsequently, vWF also promotes platelet-platelet interactions (aggregation) through its interaction with platelet glycoprotein IIb/IIIa (GPIIb/IIIa) receptors under high shear stress conditions found in areas of turbulent blood flow, such as arterioles and the capillary bed.

2. Transport and stabilization of coagulation factor VIII: vWF serves as a carrier protein for coagulation factor VIII (FVIII), protecting it from proteolytic degradation and maintaining its stability in circulation. This interaction between vWF and FVIII is essential for the proper functioning of the coagulation cascade, particularly in the context of vWD, where impaired FVIII function can lead to bleeding disorders.

3. Wound healing: vWF contributes to wound healing by promoting platelet adhesion and aggregation at the site of injury, which facilitates the formation of a provisional fibrin-based clot that serves as a scaffold for tissue repair and regeneration.

In summary, von Willebrand factor is a vital hemostatic protein involved in platelet adhesion, aggregation, coagulation factor VIII stabilization, and wound healing. Deficiencies or dysfunctions in vWF can lead to bleeding disorders such as von Willebrand disease.

Partial Thromboplastin Time (PTT) is a medical laboratory test that measures the time it takes for blood to clot. It's more specifically a measure of the intrinsic and common pathways of the coagulation cascade, which are the series of chemical reactions that lead to the formation of a clot.

The test involves adding a partial thromboplastin reagent (an activator of the intrinsic pathway) and calcium to plasma, and then measuring the time it takes for a fibrin clot to form. This is compared to a control sample, and the ratio of the two times is calculated.

The PTT test is often used to help diagnose bleeding disorders or abnormal blood clotting, such as hemophilia or disseminated intravascular coagulation (DIC). It can also be used to monitor the effectiveness of anticoagulant therapy, such as heparin. Prolonged PTT results may indicate a bleeding disorder or an increased risk of bleeding, while shortened PTT results may indicate a hypercoagulable state and an increased risk of thrombosis.

Hemorrhage is defined in the medical context as an excessive loss of blood from the circulatory system, which can occur due to various reasons such as injury, surgery, or underlying health conditions that affect blood clotting or the integrity of blood vessels. The bleeding may be internal, external, visible, or concealed, and it can vary in severity from minor to life-threatening, depending on the location and extent of the bleeding. Hemorrhage is a serious medical emergency that requires immediate attention and treatment to prevent further blood loss, organ damage, and potential death.

Antithrombin III is a protein that inhibits the formation of blood clots (thrombi) in the body. It does this by inactivating several enzymes involved in coagulation, including thrombin and factor Xa. Antithrombin III is produced naturally by the liver and is also available as a medication for the prevention and treatment of thromboembolic disorders, such as deep vein thrombosis and pulmonary embolism. It works by binding to and neutralizing excess clotting factors in the bloodstream, thereby reducing the risk of clot formation.

Factor VIII is a protein in the blood that is essential for normal blood clotting. It is also known as antihemophilic factor (AHF). Deficiency or dysfunction of this protein results in hemophilia A, a genetic disorder characterized by prolonged bleeding and easy bruising. Factor VIII works together with other proteins to help form a clot and stop bleeding at the site of an injury. It acts as a cofactor for another clotting factor, IX, in the so-called intrinsic pathway of blood coagulation. Intravenous infusions of Factor VIII concentrate are used to treat and prevent bleeding episodes in people with hemophilia A.

A fibrin tissue adhesive is a type of surgical glue that is used to approximate and secure together cut or wounded tissues in the body during surgical procedures. It is made from fibrin, a protein involved in blood clotting, and is often combined with other substances like thrombin and calcium chloride to promote clot formation and enhance adhesion.

Fibrin tissue adhesives work by mimicking the body's natural clotting process. When applied to the wound site, the fibrinogen component of the adhesive is converted into fibrin by the thrombin component, creating a stable fibrin clot that holds the edges of the wound together. This helps to promote healing and reduce the risk of complications such as bleeding or infection.

Fibrin tissue adhesives are commonly used in various surgical procedures, including dermatologic, ophthalmic, orthopedic, and neurologic surgeries. They offer several advantages over traditional suturing methods, such as reduced operation time, less trauma to the tissues, and improved cosmetic outcomes. However, they may not be suitable for all types of wounds or surgical sites, and their use should be determined by a qualified healthcare professional based on individual patient needs and circumstances.

Factor VIIa is a protein involved in the coagulation cascade, which is a series of chemical reactions that leads to the formation of a blood clot. Factor VIIa is the activated form of factor VII, which is normally activated by tissue factor (TF) when there is damage to the blood vessels. Together, TF and Factor VIIa convert Factor X to its active form, Factor Xa, which then converts prothrombin to thrombin, leading to the formation of a fibrin clot.

In summary, Factor VIIa is an important protein in the coagulation cascade that helps to initiate the formation of a blood clot in response to injury.

Blood coagulation tests, also known as coagulation studies or clotting tests, are a series of medical tests used to evaluate the blood's ability to clot. These tests measure the functioning of various clotting factors and regulatory proteins involved in the coagulation cascade, which is a complex process that leads to the formation of a blood clot to prevent excessive bleeding.

The most commonly performed coagulation tests include:

1. Prothrombin Time (PT): Measures the time it takes for a sample of plasma to clot after the addition of calcium and tissue factor, which activates the extrinsic pathway of coagulation. The PT is reported in seconds and can be converted to an International Normalized Ratio (INR) to monitor anticoagulant therapy.
2. Activated Partial Thromboplastin Time (aPTT): Measures the time it takes for a sample of plasma to clot after the addition of calcium, phospholipid, and a contact activator, which activates the intrinsic pathway of coagulation. The aPTT is reported in seconds and is used to monitor heparin therapy.
3. Thrombin Time (TT): Measures the time it takes for a sample of plasma to clot after the addition of thrombin, which directly converts fibrinogen to fibrin. The TT is reported in seconds and can be used to detect the presence of fibrin degradation products or abnormalities in fibrinogen function.
4. Fibrinogen Level: Measures the amount of fibrinogen, a protein involved in clot formation, present in the blood. The level is reported in grams per liter (g/L) and can be used to assess bleeding risk or the effectiveness of fibrinogen replacement therapy.
5. D-dimer Level: Measures the amount of D-dimer, a protein fragment produced during the breakdown of a blood clot, present in the blood. The level is reported in micrograms per milliliter (µg/mL) and can be used to diagnose or exclude venous thromboembolism (VTE), such as deep vein thrombosis (DVT) or pulmonary embolism (PE).

These tests are important for the diagnosis, management, and monitoring of various bleeding and clotting disorders. They can help identify the underlying cause of abnormal bleeding or clotting, guide appropriate treatment decisions, and monitor the effectiveness of therapy. It is essential to interpret these test results in conjunction with a patient's clinical presentation and medical history.

Fibrinopeptide A is a small protein molecule that is cleaved and released from the larger fibrinogen protein during the blood clotting process. Specifically, it is removed by the enzyme thrombin as part of the conversion of fibrinogen to fibrin, which is the main structural component of a blood clot. The measurement of Fibrinopeptide A in the blood can be used as a marker for ongoing thrombin activation and fibrin formation, which are key events in coagulation and hemostasis. Increased levels of Fibrinopeptide A may indicate abnormal or excessive blood clotting, such as in disseminated intravascular coagulation (DIC) or deep vein thrombosis (DVT).

Prothrombin time (PT) is a medical laboratory test that measures the time it takes for blood to clot. It's often used to evaluate the functioning of the extrinsic and common pathways of the coagulation system, which is responsible for blood clotting. Specifically, PT measures how long it takes for prothrombin (a protein produced by the liver) to be converted into thrombin, an enzyme that converts fibrinogen into fibrin and helps form a clot.

Prolonged PT may indicate a bleeding disorder or a deficiency in coagulation factors, such as vitamin K deficiency or the use of anticoagulant medications like warfarin. It's important to note that PT is often reported with an international normalized ratio (INR), which allows for standardization and comparison of results across different laboratories and reagent types.

Thrombosis is the formation of a blood clot (thrombus) inside a blood vessel, obstructing the flow of blood through the circulatory system. When a clot forms in an artery, it can cut off the supply of oxygen and nutrients to the tissues served by that artery, leading to damage or tissue death. If a thrombus forms in the heart, it can cause a heart attack. If a thrombus breaks off and travels through the bloodstream, it can lodge in a smaller vessel, causing blockage and potentially leading to damage in the organ that the vessel supplies. This is known as an embolism.

Thrombosis can occur due to various factors such as injury to the blood vessel wall, abnormalities in blood flow, or changes in the composition of the blood. Certain medical conditions, medications, and lifestyle factors can increase the risk of thrombosis. Treatment typically involves anticoagulant or thrombolytic therapy to dissolve or prevent further growth of the clot, as well as addressing any underlying causes.

Alpha-2-antiplasmin (α2AP) is a protein found in the blood plasma that inhibits fibrinolysis, the process by which blood clots are broken down. It does this by irreversibly binding to and inhibiting plasmin, an enzyme that degrades fibrin clots.

Alpha-2-antiplasmin is one of the most important regulators of fibrinolysis, helping to maintain a balance between clot formation and breakdown. Deficiencies or dysfunction in alpha-2-antiplasmin can lead to an increased risk of bleeding due to uncontrolled plasmin activity.

Blood platelets, also known as thrombocytes, are small, colorless cell fragments in our blood that play an essential role in normal blood clotting. They are formed in the bone marrow from large cells called megakaryocytes and circulate in the blood in an inactive state until they are needed to help stop bleeding. When a blood vessel is damaged, platelets become activated and change shape, releasing chemicals that attract more platelets to the site of injury. These activated platelets then stick together to form a plug, or clot, that seals the wound and prevents further blood loss. In addition to their role in clotting, platelets also help to promote healing by releasing growth factors that stimulate the growth of new tissue.

Prothrombin is a protein present in blood plasma, and it's also known as coagulation factor II. It plays a crucial role in the coagulation cascade, which is a complex series of reactions that leads to the formation of a blood clot.

When an injury occurs, the coagulation cascade is initiated to prevent excessive blood loss. Prothrombin is converted into its active form, thrombin, by another factor called factor Xa in the presence of calcium ions, phospholipids, and factor Va. Thrombin then catalyzes the conversion of fibrinogen into fibrin, forming a stable clot.

Prothrombin levels can be measured through a blood test, which is often used to diagnose or monitor conditions related to bleeding or coagulation disorders, such as liver disease or vitamin K deficiency.

Astringents are substances that cause the contraction of body tissues, particularly the skin and mucous membranes. They have the ability to shrink or constrict proteins in the skin or mucous membrane, leading to a tightening effect. This is often used in various medical and cosmetic applications.

In a medical context, astringents are often used to:

1. Dry up weeping or oozing wounds or sores.
2. Reduce local inflammation.
3. Control bleeding from minor cuts or wounds by constricting the blood vessels.

Commonly used astringent substances include tannins, found in plants like oak bark and witch hazel, as well as aluminum salts, found in some antiperspirants. Astringents are often applied topically in the form of lotions, gels, or solutions. However, they can also be used systemically, although this is less common.

It's important to note that while astringents have therapeutic uses, they can also cause skin irritation and dryness if not used properly. Therefore, it's recommended to follow the instructions provided by a healthcare professional or as directed on the product label.

Plasminogen Activator Inhibitor 1 (PAI-1) is a protein involved in the regulation of fibrinolysis, which is the body's natural process of breaking down blood clots. PAI-1 inhibits tissue plasminogen activator (tPA) and urokinase-type plasminogen activator (uPA), two enzymes that convert plasminogen to plasmin, which degrades fibrin clots. Therefore, PAI-1 acts as a natural antagonist of the fibrinolytic system, promoting clot formation and stability. Increased levels of PAI-1 have been associated with thrombotic disorders, such as deep vein thrombosis and pulmonary embolism.

Fibrin foam is not a widely recognized medical term, but it does refer to a type of biocompatible material that is used in certain medical and surgical applications.

Fibrin is a protein involved in the clotting of blood, and fibrin foam is created by combining fibrin with a foaming agent to create a porous structure. The resulting material can be used as a scaffold for tissue regeneration or as a filler in surgical procedures.

In some cases, fibrin foam may also be impregnated with various growth factors or other therapeutic agents to promote healing and tissue repair. The use of fibrin foam has been explored in a variety of clinical settings, including wound healing, bone regeneration, and the treatment of soft tissue defects.

Postoperative hemorrhage is a medical term that refers to bleeding that occurs after a surgical procedure. This condition can range from minor oozing to severe, life-threatening bleeding. Postoperative hemorrhage can occur soon after surgery or even several days later, as the surgical site begins to heal.

The causes of postoperative hemorrhage can vary, but some common factors include:

1. Inadequate hemostasis during surgery: This means that all bleeding was not properly controlled during the procedure, leading to bleeding after surgery.
2. Blood vessel injury: During surgery, blood vessels may be accidentally cut or damaged, causing bleeding after the procedure.
3. Coagulopathy: This is a condition in which the body has difficulty forming blood clots, increasing the risk of postoperative hemorrhage.
4. Use of anticoagulant medications: Medications that prevent blood clots can increase the risk of bleeding after surgery.
5. Infection: An infection at the surgical site can cause inflammation and bleeding.

Symptoms of postoperative hemorrhage may include swelling, pain, warmth, or discoloration around the surgical site, as well as signs of shock such as rapid heartbeat, low blood pressure, and confusion. Treatment for postoperative hemorrhage depends on the severity of the bleeding and may include medications to control bleeding, transfusions of blood products, or additional surgery to stop the bleeding.

Surgical blood loss is the amount of blood that is lost during a surgical procedure. It can occur through various routes such as incisions, punctures or during the removal of organs or tissues. The amount of blood loss can vary widely depending on the type and complexity of the surgery being performed.

Surgical blood loss can be classified into three categories:

1. Insensible losses: These are small amounts of blood that are lost through the skin, respiratory tract, or gastrointestinal tract during surgery. They are not usually significant enough to cause any clinical effects.
2. Visible losses: These are larger amounts of blood that can be seen and measured directly during surgery. They may require transfusion or other interventions to prevent hypovolemia (low blood volume) and its complications.
3. Hidden losses: These are internal bleeding that cannot be easily seen or measured during surgery. They can occur in the abdominal cavity, retroperitoneal space, or other areas of the body. They may require further exploration or imaging studies to diagnose and manage.

Surgical blood loss can lead to several complications such as hypovolemia, anemia, coagulopathy (disorders of blood clotting), and organ dysfunction. Therefore, it is essential to monitor and manage surgical blood loss effectively to ensure optimal patient outcomes.

Thrombin is a serine protease enzyme that plays a crucial role in the coagulation cascade, which is a complex series of biochemical reactions that leads to the formation of a blood clot (thrombus) to prevent excessive bleeding during an injury. Thrombin is formed from its precursor protein, prothrombin, through a process called activation, which involves cleavage by another enzyme called factor Xa.

Once activated, thrombin converts fibrinogen, a soluble plasma protein, into fibrin, an insoluble protein that forms the structural framework of a blood clot. Thrombin also activates other components of the coagulation cascade, such as factor XIII, which crosslinks and stabilizes the fibrin network, and platelets, which contribute to the formation and growth of the clot.

Thrombin has several regulatory mechanisms that control its activity, including feedback inhibition by antithrombin III, a plasma protein that inactivates thrombin and other serine proteases, and tissue factor pathway inhibitor (TFPI), which inhibits the activation of factor Xa, thereby preventing further thrombin formation.

Overall, thrombin is an essential enzyme in hemostasis, the process that maintains the balance between bleeding and clotting in the body. However, excessive or uncontrolled thrombin activity can lead to pathological conditions such as thrombosis, atherosclerosis, and disseminated intravascular coagulation (DIC).

Hemorrhagic disorders are medical conditions characterized by abnormal bleeding due to impaired blood clotting. This can result from deficiencies in coagulation factors, platelet dysfunction, or the use of medications that interfere with normal clotting processes. Examples include hemophilia, von Willebrand disease, and disseminated intravascular coagulation (DIC). Treatment often involves replacing the missing clotting factor or administering medications to help control bleeding.

Blood viscosity is a measure of the thickness or flow resistance of blood. It is defined as the ratio of shear stress to shear rate within the flowing blood, which reflects the internal friction or resistance to flow. Blood viscosity is primarily determined by the concentration and size of red blood cells (hematocrit), plasma proteins, and other blood constituents. An increase in any of these components can raise blood viscosity, leading to impaired blood flow, reduced oxygen delivery to tissues, and potential cardiovascular complications if not managed appropriately.

Platelet aggregation is the clumping together of platelets (thrombocytes) in the blood, which is an essential step in the process of hemostasis (the stopping of bleeding) after injury to a blood vessel. When the inner lining of a blood vessel is damaged, exposure of subendothelial collagen and tissue factor triggers platelet activation. Activated platelets change shape, become sticky, and release the contents of their granules, which include ADP (adenosine diphosphate).

ADP then acts as a chemical mediator to attract and bind additional platelets to the site of injury, leading to platelet aggregation. This forms a plug that seals the damaged vessel and prevents further blood loss. Platelet aggregation is also a crucial component in the formation of blood clots (thrombosis) within blood vessels, which can have pathological consequences such as heart attacks and strokes if they obstruct blood flow to vital organs.

Coagulants are substances that promote the process of coagulation or clotting. They are often used in medical settings to help control bleeding and promote healing. Coagulants work by encouraging the formation of a clot, which helps to stop the flow of blood from a wound or cut.

There are several different types of coagulants that may be used in medical treatments. Some coagulants are naturally occurring substances, such as vitamin K, which is essential for the production of certain clotting factors in the body. Other coagulants may be synthetic or semi-synthetic compounds, such as recombinant activated factor VII (rFVIIa), which is used to treat bleeding disorders and prevent excessive bleeding during surgery.

Coagulants are often administered through injection or infusion, but they can also be applied topically to wounds or cuts. In some cases, coagulants may be used in combination with other treatments, such as compression or cauterization, to help control bleeding and promote healing.

It is important to note that while coagulants can be helpful in controlling bleeding and promoting healing, they can also increase the risk of blood clots and other complications. As a result, they should only be used under the guidance and supervision of a qualified healthcare professional.

A platelet count is a laboratory test that measures the number of platelets, also known as thrombocytes, in a sample of blood. Platelets are small, colorless cell fragments that circulate in the blood and play a crucial role in blood clotting. They help to stop bleeding by sticking together to form a plug at the site of an injured blood vessel.

A normal platelet count ranges from 150,000 to 450,000 platelets per microliter (µL) of blood. A lower than normal platelet count is called thrombocytopenia, while a higher than normal platelet count is known as thrombocytosis.

Abnormal platelet counts can be a sign of various medical conditions, including bleeding disorders, infections, certain medications, and some types of cancer. It is important to consult with a healthcare provider if you have any concerns about your platelet count or if you experience symptoms such as easy bruising, prolonged bleeding, or excessive menstrual flow.

Beta-thromboglobulin is a type of protein that is released from platelets (a component of blood) when they are activated. It is often used as a marker for platelet activation, which can occur in various physiological and pathological conditions such as hemostasis, thrombosis, inflammation, and atherosclerosis.

Beta-thromboglobulin is a member of the thromboglobulin family, which also includes platelet factor 4 (PF4) and other proteins that are involved in hemostasis and thrombosis. These proteins play important roles in the regulation of blood clotting and wound healing, but their excessive release or activation can contribute to the development of various cardiovascular diseases, such as myocardial infarction (heart attack) and stroke.

Elevated levels of beta-thromboglobulin have been found in patients with thromboembolic disorders, inflammatory bowel disease, cancer, and other conditions associated with platelet activation. Therefore, the measurement of beta-thromboglobulin can be useful in the diagnosis and monitoring of these diseases.

Disseminated Intravascular Coagulation (DIC) is a complex medical condition characterized by the abnormal activation of the coagulation cascade, leading to the formation of blood clots in small blood vessels throughout the body. This process can result in the consumption of clotting factors and platelets, which can then lead to bleeding complications. DIC can be caused by a variety of underlying conditions, including sepsis, trauma, cancer, and obstetric emergencies.

The term "disseminated" refers to the widespread nature of the clotting activation, while "intravascular" indicates that the clotting is occurring within the blood vessels. The condition can manifest as both bleeding and clotting complications, which can make it challenging to diagnose and manage.

The diagnosis of DIC typically involves laboratory tests that evaluate coagulation factors, platelet count, fibrin degradation products, and other markers of coagulation activation. Treatment is focused on addressing the underlying cause of the condition while also managing any bleeding or clotting complications that may arise.

Thromboplastin is a substance that activates the coagulation cascade, leading to the formation of a clot (thrombus). It's primarily found in damaged or injured tissues and blood vessels, as well as in platelets (thrombocytes). There are two types of thromboplastin:

1. Extrinsic thromboplastin (also known as tissue factor): This is a transmembrane glycoprotein that is primarily found in subendothelial cells and released upon injury to the blood vessels. It initiates the extrinsic pathway of coagulation by binding to and activating Factor VII, ultimately leading to the formation of thrombin and fibrin clots.
2. Intrinsic thromboplastin (also known as plasma thromboplastin or factor III): This term is used less frequently and refers to a labile phospholipid component present in platelet membranes, which plays a role in the intrinsic pathway of coagulation.

In clinical settings, the term "thromboplastin" often refers to reagents used in laboratory tests like the prothrombin time (PT) and activated partial thromboplastin time (aPTT). These reagents contain a source of tissue factor and calcium ions to initiate and monitor the coagulation process.

Antifibrinolytic agents are a class of medications that inhibit the breakdown of blood clots. They work by blocking the action of enzymes called plasminogen activators, which convert plasminogen to plasmin, the main enzyme responsible for breaking down fibrin, a protein that forms the framework of a blood clot.

By preventing the conversion of plasminogen to plasmin, antifibrinolytic agents help to stabilize existing blood clots and prevent their premature dissolution. These medications are often used in clinical settings where excessive bleeding is a concern, such as during or after surgery, childbirth, or trauma.

Examples of antifibrinolytic agents include tranexamic acid, aminocaproic acid, and epsilon-aminocaproic acid. While these medications can be effective in reducing bleeding, they also carry the risk of thromboembolic events, such as deep vein thrombosis or pulmonary embolism, due to their pro-coagulant effects. Therefore, they should be used with caution and only under the close supervision of a healthcare provider.

Protein C is a vitamin K-dependent protease that functions as an important regulator of coagulation and inflammation. It is a plasma protein produced in the liver that, when activated, degrades clotting factors Va and VIIIa to limit thrombus formation and prevent excessive blood clotting. Protein C also has anti-inflammatory properties by inhibiting the release of pro-inflammatory cytokines and reducing endothelial cell activation. Inherited or acquired deficiencies in Protein C can lead to an increased risk of thrombosis, a condition characterized by abnormal blood clot formation within blood vessels.

Tissue Plasminogen Activator (tPA) is a thrombolytic enzyme, which means it dissolves blood clots. It is naturally produced by the endothelial cells that line the interior surface of blood vessels. tPA activates plasminogen, a zymogen, to convert it into plasmin, a protease that breaks down fibrin, the structural protein in blood clots. This enzyme is used medically as a thrombolytic drug under various brand names, such as Activase and Alteplase, to treat conditions like acute ischemic stroke, pulmonary embolism, and deep vein thrombosis by dissolving the clots and restoring blood flow.

Brohi 2008 Lucas, Charles E; Ledgerwood, Anna M (June 1976). "Prospective evaluation of hemostatic techniques for liver ... Pringle described this technique in patients with substantial hepatic trauma in the early twentieth century. The U.S. military ... A number of different techniques can be employed such as using staplers to come across the bowel, or primary suture closure in ... Numerous methods of temporary closure exist, with the most common technique being a negative-vacuum type device. Regardless of ...
Use aggressive hemostatic techniques. Correct coagulopathy immediately. Include a diagnostic workup for hemorrhage, but never ... Various purification techniques are used in plasma-based FIX concentrates to reduce or eliminate the risk of viral transmission ... These techniques inactivate viruses such as hepatitis B virus, hepatitis C virus, and HIV. However, the transmission of ... This technique is well established in acquired hemophilia but not in congenital hemophilia. ...
Hemostatic suturing technique for uterine bleeding during cesarean delivery. Obstet Gynecol. 2000 Jul. 96(1):129-131. [QxMD ... Other than nonconsent, absence of surgical expertise or allergy to specific agents, the techniques used in the management of ... The B-Lynch surgical technique for the control of massive postpartum haemorrhage: an alternative to hysterectomy? Five cases ... An intraumbilical vein saline/oxytocin or saline/misoprostol injection may reduce the need for more invasive removal techniques ...
To the best of our knowledge, this is the first case report showing the “tulip-bundle” technique as a rescue ... Combined use of hemostatic clips and detachable nylon snare (the "tulip-bundle" technique) has been described as an effective ... The technique proved to be highly efficient option for treating primary hemostatic failure with recurrent bleeding [9]. The ... R. E. Pouw, F. J. ten Kate, and J. J. Bergman, "Tulip bundle technique," A Novel Technique for Closing Perforations Caused by ...
Hemostatic surgical techniques are known for reducing the bleeding from incised tissue prior to, during, and subsequent to ... Assignee: Hemostatic Surgery Corporation (Sausalito, CA) Inventor: Philip E. Eggers (Dublin, OH) Primary Examiner: David M. ... One such technique uses a heating element to transfer heat to the severed tissue to thermally reform collagen. Heat transferred ... Justia Patents Bipolar ElectrodesUS Patent for Hemostatic bi-polar electrosurgical cutting apparatus and methods of use Patent ...
... that hemostatic agent training for prehospital personnel include proper wound packing and pressure application techniques. ... We suggest that topical hemostatic agents be delivered in a gauze format that supports wound packing. (Low, Weak) ... We suggest the use of topical hemostatic agents, in combination with direct pressure, for the control of significant hemorrhage ... We advise that tourniquets and topical hemostatic agents be used under clinical practice guidelines and following product ...
Prevention can be achieved by proper puncture technique and site selection, and correct post-procedure hemostatic compression ... Objective: To describe our experience, techniques and results in treating pseudoaneurysms at a large medical center with ...
Hemostatic Technics Hemostatic Technique Technic, Hemostatic Technics, Hemostatic Technique, Hemostatic Techniques, Hemostatic ... Hemostatic Technique. Technic, Hemostatic. Technics, Hemostatic. Technique, Hemostatic. Techniques, Hemostatic. Tree number(s): ... Techniques dhémostase Entry term(s):. Hemostatic Technic. Hemostatic Technics. ... use HEMOSTATIC TECHNIQUES to search HEMOSTATIC TECHNICS 1976-90; search HEMOSTASIS 1966-75 (as Cat E heading). ...
Hemostatic Techniques. -. dc.subject. Horses. -. dc.subject. Male. -. dc.subject. Panax. -. dc.subject. Phytotherapy. - ...
As a result, ligated skin tag removal surgery is an alternative hemostatic technique. The disadvantage of this technique is ... Mukhtar M. Electrotherapeutic technique for treating skin tags and large cutaneous papillomatous growths. Cosmetic Dermatol. ... Bhatia S, Gupta S. Hold firmly, coagulate indirectly, and pull gently: A simple and swift technique for radiofrequency-assisted ... How to cite this article: Mukhtar M. Hemostatic excision of skin tags. CosmoDerma 2022;2:111. ...
Hemostatic Agents.. e) Surgical Techniques and Instruments. The harmonic scalpel, gamma knife; as well as argon beam coagulator ... Surgical and Anesthesia techniques.. The use of electrocautery, laser; as well as new surgical techniques have resulted in a ... d) Hemostatic Drugs. Antifibrinolytics. Careful hemostasis during any surgical procedure; as well as efficient time use, can ... Hemostatic agents; such as collagen pads, thrombin powders, and fibrin glue stop vessel oozing. Both aminocaproic acid and ...
... this dual technique (packing and holding the cervix) was correlated with a 93% hemostatic success rate compared to the previous ... Two-provider technique for bimanual uterine compression to control postpartum hemorrhage. J Midwifery Womens Health 2012;57(4): ... Keogh J, Tsokos N. Aortic compression in massive postpartum haemorrhage an old but lifesaving technique. Aust N Z J Obstet ... Also, these compressive techniques are uncomfortable for the patient and tiring for the provider. Further, it may be difficult ...
Keywords : surgery; oral; hemostatic techniques; organ transplantation. · text in English · pdf in English ... knowledge and skills in the use of local and systemic hemostatic procedures, and a partnership approach between dentists and ...
8 (2): 167-9. Its use has increased with the advent of minimally invasive surgery and compliments other hemostatic techniques ... Hemostatic material was used the Cook Medical website for another region or country and compliments hemostatic! Therefore, ... hemostatic clips mri safety. The material can act as a scaffold to facilitate clot fo… Interventions: The physical deflection ... The two tested hemostatic metal- lic clips proved safe and did not migrate or become U se of metallic clips with ferromagnetic ...
To prevent or minimize surgical blood loss, surgeons may use a variety of techniques, such as:. 1. Applying topical hemostatic ... 4. Failure to control bleeding with proper hemostatic techniques. 5. Pre-existing medical conditions that increase the risk of ... 2. Use of appropriate anesthesia and surgical techniques to minimize tissue trauma. 3. Conservative use of hemostatic agents ... Hemostatics. Agents acting to arrest the flow of blood. Absorbable hemostatics arrest bleeding either by the formation of an ...
Hemostatic Techniques + *Hygiene + *Induced Hyperthermia + *Precision Medicine *Insufflation *Intubation + *Ischemic ... Cosmetic Techniques *Cryotherapy + *Decompression + *Delayed Diagnosis *Directly Observed Therapy *Drainage + *Drug Therapy + * ... Reproductive Techniques + *Respiratory Therapy + *Retreatment + *Rewarming *Salvage Therapy *Secondary Prevention *Self Care + ...
Hemostatic Techniques 1 * Clostridium Infections 1 * Gastrointestinal Hemorrhage 1 Institution. * American Journal of ...
Analytical, Diagnostic and Therapeutic Techniques and Equipment [E]. *Therapeutics [E02]. *Hemostatic Techniques [E02.520] ... Techniques include use of lasers, heater probes, bipolar electrocoagulation, and local injection. Endoscopic hemostasis is ...
Analytical, Diagnostic and Therapeutic Techniques and Equipment [E]. *Therapeutics [E02]. *Hemostatic Techniques [E02.520] ...
Use aggressive hemostatic techniques. Correct coagulopathy immediately. Include a diagnostic workup for hemorrhage, but never ... Various purification techniques are used in plasma-based FIX concentrates to reduce or eliminate the risk of viral transmission ... These techniques inactivate viruses such as hepatitis B virus, hepatitis C virus, and HIV. However, the transmission of ... This technique is well established in acquired hemophilia but not in congenital hemophilia. ...
MATERIALS AND METHODS: A review of Ovid MEDLINE was performed to review the English-language medical literature of hemostatic ... RESULTS: A comprehensive and current list of hemostatic options used in the intraoperative and postoperative period is provided ... The appropriate use and updated knowledge of hemostatic options is provided. ... There are many intraoperative and postoperative techniques to aid hemostasis in dermatologic procedures. An updated ...
... and is associated with a shorter operating time and decreased blood loss compared with conventional haemostatic techniques. ... and is associated with a shorter operating time and decreased blood loss compared with conventional haemostatic techniques.", ... and is associated with a shorter operating time and decreased blood loss compared with conventional haemostatic techniques. ... and is associated with a shorter operating time and decreased blood loss compared with conventional haemostatic techniques. ...
Their technique, which uses an epidural and spinal needle, required a median operation time of 18 minutes (range, 10-30 min) ... A running hemostatic suture around the line of excision is helpful for assuring hemostasis. Plication of the sac (Lord ... Whether an increased use of this technique will reduce the incidence of hydroceles in older children or adults remains to be ... Peng Y, Li C, Lin W, Xu L. Application of a Laparoscopic, Single-port, Double-needle Technique for Pediatric Hydroceles With ...
In this paper, magnetic hemostatic nanoparticles are shown for the first time to assist in minimally invasive treatment of ... 2a-e) (see the synthesis diagram in experimental part). Evaluation of the release profile using the Bradford technique showed ... Hemostatic activity in model blood vessel. The hemostatic effect of the THR@ferria colloid was tested using a model vessel ( ... Scheme of synthesis for the hemostatic THR@ferria colloid. After mixing the Fe2 +/Fe3 + salts, an ammonia solution is added (a ...
Hemostatic Plug: Novel Technique for Closure of Percutaneous Nephrostomy Tract; The Journal of Endourology, Volume 29, Number 3 ... A clever technique for placement of a urinary catheter over a wire; Urology Annals, Jul - Sep 2015 , Vol 7 , Issue 3 ... Davalos and his team are leaders in the tubeless PCNL technique, which is performed as a PCNL surgery but eliminates the need ... Specially trained in the most advanced surgical techniques, including PCNL and Tubeless PCNL, Dr. Davalos is a pioneer in the ...
described a novel technique to divide the CP septum while preserving the mucosa via creation of a short submucosal tunnel. The ... One patientʼs diameter appeared to decrease given measurements were obtained after hemostatic clip placement, which created a ... In contrast, when using the Z-POEM approach, we utilized the same techniques as previously published by Li et al [5]. Prior to ... New and emerging techniques for endoscopic treatment of Zenkerʼs diverticulum: State-of-the-art review. Dig Endosc 2018; 30: ...
Hemostatic Techniques. *Hepatic Veins. *Hospital Design and Construction. *Humans. *Imaging, Three-Dimensional ...
The success rate of interventional techniques was 93.94%, hemostatic rate was 90%. 3 cases died. CONCLUSION: The embolization ... procedural technique details, therapeutic outcomes, the HAIC-related complications and corresponding treatments, and ... therapy is a safe and effective technique, should be as the first-line diagnostic and treatment choice for patients with post- ...

No FAQ available that match "hemostatic techniques"

No images available that match "hemostatic techniques"