Disseminated intravascular coagulation

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Disseminated intravascular coagulation
Other namesDisseminated intravascular coagulopathy, consumptive coagulopathy, defibrination syndrome [1]
Acute thrombotic microangiopathy - pas - very high mag.jpg
Micrograph showing acute thrombotic microangiopathy due to DIC in a kidney biopsy. A clot is present in the hilum of the glomerulus (center of image).
Specialty Haematology
Symptoms Chest pain, shortness of breath, leg pain, problems speaking, problems moving part of the body, bleeding [1]
Complications Organ failure [2]
TypesAcute, chronic [1]
Causes Sepsis, surgery, major trauma, cancer, complications of pregnancy, snake bites, frostbite, burns [1]
Diagnostic method Blood tests [2]
Differential diagnosis Thrombotic thrombocytopenic purpura, hemolytic-uremic syndrome [1]
TreatmentDirected at the underlying condition [3]
Medication Platelets, cryoprecipitate, fresh frozen plasma, heparin [2]
Prognosis20–50% risk of death [4]
Frequency1% of people admitted to hospital [4]

Disseminated intravascular coagulation (DIC) is a condition in which blood clots form throughout the body, blocking small blood vessels. [1] Symptoms may include chest pain, shortness of breath, leg pain, problems speaking, or problems moving parts of the body. [1] As clotting factors and platelets are used up, bleeding may occur. [1] This may include blood in the urine, blood in the stool, or bleeding into the skin. [1] Complications may include organ failure. [2]

Microvessel

Microvessels are the smallest blood vessels in a body, including those responsible for microcirculation. They make up the microvasculature that distributes blood within tissues. Common examples of microvessels include:

Chest pain discomfort or pain felt anywhere along the front of the body between the neck and upper abdomen

Chest pain is pain in any region of the chest. Chest pain may be a symptom of a number of serious disorders and is, in general, considered a medical emergency. Chest pain can be differentiated into heart-related and non heart related chest pain. Cardiac chest pain is called angina pectoris. Some causes of noncardiac chest pain include gastrointestinal, musculoskeletal, or lung issues. Even though chest pain may not be related to a heart problem, noncardiac chest pain can still be due to significant disease. Chest pain can present with different types of pain and associated symptoms which may vary with a person's age, sex, and previous medical conditions. Determining the cause of chest pain is through review of a person's medical history, a physical exam, and other medical tests. Management of chest pain is based on the underlying cause.

Shortness of breath, also known as dyspnea, is the feeling that one cannot breathe well enough. The American Thoracic Society defines it as "a subjective experience of breathing discomfort that consists of qualitatively distinct sensations that vary in intensity", and recommends evaluating dyspnea by assessing the intensity of the distinct sensations, the degree of distress involved, and its burden or impact on activities of daily living. Distinct sensations include effort/work, chest tightness, and air hunger.

Contents

Relatively common causes include sepsis, surgery, major trauma, cancer, and complications of pregnancy. [1] Less common causes include snake bites, frostbite, and burns. [1] There are two main types: acute (rapid onset) and chronic (slow onset). [1] Diagnosis is typically based on blood tests. [2] Findings may include low platelets, low fibrinogen, high INR, or high D-dimer. [2]

Sepsis life-threatening organ dysfunction triggered by infection

Sepsis is a life-threatening condition that arises when the body's response to infection causes injury to its own tissues and organs. Common signs and symptoms include fever, increased heart rate, increased breathing rate, and confusion. There may also be symptoms related to a specific infection, such as a cough with pneumonia, or painful urination with a kidney infection. In the very young, old, and people with a weakened immune system, there may be no symptoms of a specific infection and the body temperature may be low or normal, rather than high. Severe sepsis is sepsis causing poor organ function or insufficient blood flow. Insufficient blood flow may be evident by low blood pressure, high blood lactate, or low urine output. Septic shock is low blood pressure due to sepsis that does not improve after fluid replacement.

Surgery Medical specialty

Surgery is a medical specialty that uses operative manual and instrumental techniques on a patient to investigate or treat a pathological condition such as a disease or injury, to help improve bodily function or appearance or to repair unwanted ruptured areas.

Major trauma injury that could cause prolonged disability or death

Major trauma is any injury that has the potential to cause prolonged disability or death. There are many causes of major trauma, blunt and penetrating, including falls, motor vehicle collisions, stabbing wounds, and gunshot wounds. Depending on the severity of injury, quickness of management and transportation to an appropriate medical facility may be necessary to prevent loss of life or limb. The initial assessment is critical, and involves a physical evaluation and also may include the use of imaging tools to determine the types of injuries accurately and to formulate a course of treatment.

Treatment is mainly directed towards the underlying condition. [2] [3] Other measures may include giving platelets, cryoprecipitate, or fresh frozen plasma. [2] Evidence to support these treatments, however, is poor. Heparin may be useful in the chronic form. [2] About 1% of people admitted to hospital are affected by the condition. [4] In those with sepsis rates are between 20% and 50%. [4] The risk of death among those affected varies from 20 to 50%. [4]

Platelet transfusion

Platelet transfusion, also known as platelet concentrate, is used to prevent or treat bleeding in people with either a low platelet count or poor platelet function. Often this occurs in people receiving cancer chemotherapy. Preventative transfusion is often done in those with platelet levels of less than 10 x 109/L. In those who are bleeding transfusion is usually carried out at less than 50 x 109/L. Blood group matching (ABO, RhD) is typically recommended before platelets are given. Unmatched platelets, however, are often used due to the unavailability of matched platelets. They are given by injection into a vein.

Cryoprecipitate, also called cryo for short, is a frozen blood product prepared from blood plasma. To create cryoprecipitate, fresh frozen plasma thawed at 1-6 °C, is then centrifuged and the precipitate is collected. The precipitate is resuspended in a small amount of residual plasma and is then re-frozen for storage. It is often transfused to adults as two 5-unit pools instead of as a single product. One of the most important constituents is factor VIII, which is why cryoprecipitate is sometimes called cryoprecipitated antihaemophilic factor or cryoprecipitated AHF. In many clinical contexts, use of whole cryoprecipitate has been replaced with use of clotting factor concentrates made therefrom, but the whole form is still routinely stocked by many, if not most, hospital blood banks. Cryo can be stored at -18 °C or colder for 12 months from the original collection date. After thawing, single units of cryo can be stored at 20-24 °C for up to 6 hours. If units of cryo are pooled in an open system, they can only be held at 20-24 °C for up to 4 hours. Presently cryo cannot be re-frozen for storage after it is thawed for use if it is not transfused.

Fresh frozen plasma

Fresh frozen plasma (FFP) is a blood product made from the liquid portion of whole blood. It is used to treat conditions in which there are low blood clotting factors (INR>1.5) or low levels of other blood proteins. It may also be used as the replacement fluid in plasma exchange. Using ABO compatible plasma, while not required, may be recommended. Use as a volume expander is not recommended. It is given by slow injection into a vein.

Signs and symptoms

In DIC, the underlying cause usually leads to symptoms and signs, and DIC is discovered on laboratory testing. The onset of DIC can be sudden, as in endotoxic shock or amniotic fluid embolism, or it may be insidious and chronic, as in cancer. DIC can lead to multiorgan failure and widespread bleeding. [5]

Amniotic fluid embolism

An amniotic fluid embolism (AFE) is a rare childbirth (obstetric) emergency in which amniotic fluid enters the blood stream of the mother to trigger a serious reaction. This reaction then results in cardiorespiratory collapse and massive bleeding (coagulopathy).

Causes

DIC can occur in the following conditions: [5] [6] [7] [8]

Tumors of the hematopoietic and lymphoid tissues tumor that affect the blood, bone marrow, lymph, and lymphatic system

Tumors of the hematopoietic and lymphoid tissues or tumours of the haematopoietic and lymphoid malignancies are tumors that affect the blood, bone marrow, lymph, and lymphatic system. As those elements are all intimately connected through both the circulatory system and the immune system, a disease affecting one will often affect the others as well, making myeloproliferation and lymphoproliferation closely related and often overlapping problems.

Acute promyelocytic leukemia acute myeloid leukemia characterized by accumulation of promyelocytes in the bone marrow and by a translocation between chromosomes 15 and 17

Acute promyelocytic leukemia is a subtype of acute myeloid leukemia (AML), a cancer of the white blood cells. In APL, there is an abnormal accumulation of immature granulocytes called promyelocytes. The disease is characterized by a chromosomal translocation involving the retinoic acid receptor alpha gene and is distinguished from other forms of AML by its responsiveness to all-trans retinoic acid therapy. Acute promyelocytic leukemia was first characterized in 1957 by French and Norwegian physicians as a hyperacute fatal illness, with a median survival time of less than a week. Today, prognoses have drastically improved; 10-year survival rates are estimated to be approximately 80-90% according to one study.

Pre-eclampsia hypertension occurring during pregnancy characterized by large amounts of protein in the urine (proteinuria) and edema, usually by the last trimester of pregnancy.

Pre-eclampsia (PE) is a disorder of pregnancy characterized by the onset of high blood pressure and often a significant amount of protein in the urine. When it arises, the condition begins after 20 weeks of pregnancy. In severe disease there may be red blood cell breakdown, a low blood platelet count, impaired liver function, kidney dysfunction, swelling, shortness of breath due to fluid in the lungs, or visual disturbances. Pre-eclampsia increases the risk of poor outcomes for both the mother and the baby. If left untreated, it may result in seizures at which point it is known as eclampsia.

Liver disease, HELLP syndrome, thrombotic thrombocytopenic purpura/Haemolytic uremic syndrome, and malignant hypertension may mimic DIC but do not occur via the same pathways.[ citation needed ]

Pathophysiology

The coagulation cascade of secondary haemostasis. Coagulation full.svg
The coagulation cascade of secondary haemostasis.

Under homeostatic conditions, the body is maintained in a finely tuned balance of coagulation and fibrinolysis. The activation of the coagulation cascade yields thrombin that converts fibrinogen to fibrin; the stable fibrin clot being the final product of hemostasis. The fibrinolytic system then functions to break down fibrinogen and fibrin. Activation of the fibrinolytic system generates plasmin (in the presence of thrombin), which is responsible for the lysis of fibrin clots. The breakdown of fibrinogen and fibrin results in polypeptides called fibrin degradation products (FDPs) or fibrin split products (FSPs). In a state of homeostasis, the presence of plasmin is critical, as it is the central proteolytic enzyme of coagulation and is also necessary for the breakdown of clots, or fibrinolysis.[ citation needed ]

In DIC, the processes of coagulation and fibrinolysis are dysregulated, and the result is widespread clotting with resultant bleeding. Regardless of the triggering event of DIC, once initiated, the pathophysiology of DIC is similar in all conditions. One critical mediator of DIC is the release of a transmembrane glycoprotein called tissue factor (TF). TF is present on the surface of many cell types (including endothelial cells, macrophages, and monocytes) and is not normally in contact with the general circulation, but is exposed to the circulation after vascular damage. For example, TF is released in response to exposure to cytokines (particularly interleukin 1), tumor necrosis factor, and endotoxin. [9] This plays a major role in the development of DIC in septic conditions. TF is also abundant in tissues of the lungs, brain, and placenta. This helps to explain why DIC readily develops in patients with extensive trauma. Upon exposure to blood and platelets, TF binds with activated factor VIIa (normally present in trace amounts in the blood), forming the extrinsic tenase complex. This complex further activates factor IX and X to IXa and Xa, respectively, leading to the common coagulation pathway and the subsequent formation of thrombin and fibrin. [7]

The release of endotoxin is the mechanism by which Gram-negative sepsis provokes DIC. In acute promyelocytic leukemia, treatment causes the destruction of leukemic granulocyte precursors, resulting in the release of large amounts of proteolytic enzymes from their storage granules, causing microvascular damage. Other malignancies may enhance the expression of various oncogenes that result in the release of TF and plasminogen activator inhibitor-1 (PAI-1), which prevents fibrinolysis. [10]

Excess circulating thrombin results from the excess activation of the coagulation cascade. The excess thrombin cleaves fibrinogen, which ultimately leaves behind multiple fibrin clots in the circulation. These excess clots trap platelets to become larger clots, which leads to microvascular and macrovascular thrombosis. This lodging of clots in the microcirculation, in the large vessels, and in the organs is what leads to the ischemia, impaired organ perfusion, and end-organ damage that occurs with DIC.[ citation needed ]

Coagulation inhibitors are also consumed in this process. Decreased inhibitor levels will permit more clotting so that a positive feedback loop develops in which increased clotting leads to more clotting. At the same time, thrombocytopenia occurs and this has been attributed to the entrapment and consumption of platelets. Clotting factors are consumed in the development of multiple clots, which contributes to the bleeding seen with DIC.[ citation needed ]

Simultaneously, excess circulating thrombin assists in the conversion of plasminogen to plasmin, resulting in fibrinolysis. The breakdown of clots results in an excess of FDPs, which have powerful anticoagulant properties, contributing to hemorrhage. The excess plasmin also activates the complement and kinin systems. Activation of these systems leads to many of the clinical symptoms that patients experiencing DIC exhibit, such as shock, hypotension, and increased vascular permeability. The acute form of DIC is considered an extreme expression of the intravascular coagulation process with a complete breakdown of the normal homeostatic boundaries. DIC is associated with a poor prognosis and a high mortality rate.[ citation needed ]

There has been a recent challenge however to the basic assumptions and interpretations of the pathophysiology of DIC. A study of sepsis and DIC in animal models has shown that a highly expressed receptor on the surface of hepatocytes, termed the Ashwell-Morell receptor, is responsible for thrombocytopenia in bacteremia and sepsis due to Streptococcus pneumoniae (SPN) and possibly other pathogens. The thrombocytopenia observed in SPN sepsis was not due to increased consumption of coagulation factors such as platelets, but instead was the result of this receptor's activity enabling hepatocytes to ingest and rapidly clear platelets from circulation. [11] By removing pro-thrombotic components before they participate in the coagulopathy of DIC, the Ashwell-Morell receptor lessens the severity of DIC, reducing thrombosis and tissue necrosis, and promoting survival. The hemorrhage observed in DIC and among some tissues lacking this receptor may thereby be secondary to increased thrombosis with loss of the mechanical vascular barrier. This discovery has possible significant clinical implications in devising new approaches to reducing the morbidity and mortality of DIC.[ citation needed ]

There is activation of intrinsic as well as extrinsic coagulation pathway, this results in excess thrombus formation in the blood vessels. Due to extensive coagulation there is consumption of coagulation factors which causes bleeding.

Diagnosis

The diagnosis of DIC is not made on a single laboratory value, but rather the constellation of laboratory markers and a consistent history of an illness known to cause DIC. Laboratory markers consistent with DIC include: [3] [7] [12]

A diagnostic algorithm has been proposed by the International Society of Thrombosis and Haemostasis. This algorithm appears to be 91% sensitive and 97% specific for the diagnosis of overt DIC. A score of 5 or higher is compatible with DIC and it is recommended that the score is repeated daily, while a score below 5 is suggestive but not affirmative for DIC and it is recommended that it is repeated only occasionally: [12] [13] It has been recommended that a scoring system be used in the diagnosis and management of DIC in terms of improving outcome. [14]

Treatment

Treatment of DIC is centered around treating the underlying condition. Transfusions of platelets or fresh frozen plasma can be considered in cases of significant bleeding, or those with a planned invasive procedure. The target goal of such transfusion depends on the clinical situation. Cryoprecipitate can be considered in those with a low fibrinogen level.

Treatment of thrombosis with anticoagulants such as heparin is rarely used due to the risk of bleeding.

Recombinant human activated protein C was previously recommended in those with severe sepsis and DIC, but drotrecogin alfa has been shown to confer no benefit and was withdrawn from the market in 2011.

Recombinant factor VII has been proposed as a "last resort" in those with severe hemorrhage due to obstetric or other causes, but conclusions about its use are still insufficient. [16]

Prognosis

Prognosis varies depending on the underlying disorder, and the extent of the intravascular thrombosis (clotting). The prognosis for those with DIC, regardless of cause, is often grim: Between 20% and 50% of patients will die. [17] DIC with sepsis (infection) has a significantly higher rate of death than DIC associated with trauma. [17]

Epidemiology

DIC is observed in approximately 1% of academic hospital admissions. [18] DIC occurs at higher rates in people with bacterial sepsis (83%), [19] severe trauma (31%), [20] and cancer (6.8%). [21]

Related Research Articles

Thrombus blood clot

A thrombus, colloquially called a blood clot, is the final product of the blood coagulation step in hemostasis. There are two components to a thrombus: aggregated platelets and red blood cells that form a plug, and a mesh of cross-linked fibrin protein. The substance making up a thrombus is sometimes called cruor. A thrombus is a healthy response to injury intended to prevent bleeding, but can be harmful in thrombosis, when clots obstruct blood flow through healthy blood vessels.

Coagulation The sequential process in which the multiple coagulation factors of the blood interact, ultimately resulting in the formation of an insoluble fibrin clot; it may be divided into three stages: stage 1, the formation of intrinsic and extrinsic prothrom

Coagulation, also known as clotting, is the process by which blood changes from a liquid to a gel, forming a blood clot. It potentially results in hemostasis, the cessation of blood loss from a damaged vessel, followed by repair. The mechanism of coagulation involves activation, adhesion and aggregation of platelets along with deposition and maturation of fibrin. Disorders of coagulation are disease states which can result in bleeding or obstructive clotting (thrombosis).

Fibrin fibrous, non-globular protein involved in the clotting of blood.

Fibrin is a fibrous, non-globular protein involved in the clotting of blood. It is formed by the action of the protease thrombin on fibrinogen which causes it to polymerize. The polymerized fibrin together with platelets forms a hemostatic plug or clot over a wound site.

Fibrinogen

Fibrinogen is a glycoprotein that circulates in the blood of vertebrates. During tissue and vascular injury it is converted enzymatically by thrombin to fibrin and subsequently to a fibrin-based blood clot. Fibrinogen functions primarily to occlude blood vessels and thereby stop excessive bleeding. However, fibrinogen's product, fibrin, binds and reduces the activity of thrombin. This activity, sometimes referred to as antithrombin I, serves to limit blood clotting. Loss or reduction in this antithrombin 1 activity due to mutations in fibrinogen genes or hypo-fibrinogen conditions can lead to excessive blood clotting and thrombosis. Fibrin also mediates blood platelet and endothelial cell spreading, tissue fibroblast proliferation, capillary tube formation, and angiogenesis and thereby functions to promote tissue revascularization, wound healing, and tissue repair.

Thrombin mammalian protein found in Homo sapiens

Thrombin is a serine protease, an enzyme that, in humans, is encoded by the F2 gene. Prothrombin is proteolytically cleaved to form thrombin in the clotting process. Thrombin in turn acts as a serine protease that converts soluble fibrinogen into insoluble strands of fibrin, as well as catalyzing many other coagulation-related reactions.

Fibrinolysis is a process that prevents blood clots from growing and becoming problematic. This process has two types: primary fibrinolysis and secondary fibrinolysis. The primary type is a normal body process, whereas secondary fibrinolysis is the breakdown of clots due to a medicine, a medical disorder, or some other cause.

D-dimer is a fibrin degradation product, a small protein fragment present in the blood after a blood clot is degraded by fibrinolysis. It is so named because it contains two D fragments of the fibrin protein joined by a cross-link.

Purpura human disease

Purpura is a condition of red or purple discolored spots on the skin that do not blanch on applying pressure. The spots are caused by bleeding underneath the skin secondary to platelet disorders, vascular disorders, coagulation disorders, or other causes. They measure 0.3–1 cm (3–10 mm), whereas petechiae measure less than 3 mm, and ecchymoses greater than 1 cm.

Schistocyte

A schistocyte or schizocyte is a fragmented part of a red blood cell. Schistocytes are typically irregularly shaped, jagged, and have two pointed ends.

Plasminogen activator

Plasminogen activators are serine proteases that catalyze the activation of plasmin via proteolytic cleavage of its zymogen form plasminogen. Plasmin is an important factor in fibrinolysis, the breakdown of fibrin polymers formed during blood clotting. There are two main plasminogen activators: urokinase (uPA) and tissue plasminogen activator (tPA). Tissue plasminogen activators are used to treat medical conditions related to blood clotting including embolic or thrombotic stroke, myocardial infarction, and pulmonary embolism.

Hypoprothrombinemia Human disease

Hypoprothrombinemia is a rare blood disorder in which a deficiency in immunoreactive prothrombin, produced in the liver, results in an impaired blood clotting reaction, leading to an increased physiological risk for spontaneous bleeding. This condition can be observed in the gastrointestinal system, cranial vault, and superficial integumentary system, effecting both the male and female population. Prothrombin is a critical protein that is involved in the process of hemostasis, as well as illustrating procoagulant activities. This condition is characterized as an autosomal recessive inheritance congenital coagulation disorder affecting 1 per 2,000,000 of the population, worldwide, but is also attributed as acquired.

In medicine, glycoprotein IIb/IIIa is an integrin complex found on platelets. It is a receptor for fibrinogen and von Willebrand factor and aids platelet activation. The complex is formed via calcium-dependent association of gpIIb and gpIIIa, a required step in normal platelet aggregation and endothelial adherence. Platelet activation by ADP leads to the aforementioned conformational change in platelet gpIIb/IIIa receptors that induces binding to fibrinogen. The gpIIb/IIIa receptor is a target of several drugs including abciximab, eptifibatide, and tirofiban.

The dysfibrinogenemias consist of three types of fibrinogen disorders in which a critical blood clotting factor, fibrinogen, circulates at normal levels but is dysfunctional. Congenital dysfibrinogenemia is an inherited disorder in which one of the parental genes produces an abnormal fibrinogen. This fibrinogen interferes with normal blood clotting and/or lyses of blood clots. The condition therefore may cause pathological bleeding and/or thrombosis. Acquired dysfibrinogenemia is a non-hereditary disorder in which fibrinogen is dysfunctional due to the presence of liver disease, autoimmune disease, a plasma cell dyscrasias, or certain cancers. It is associated primarily with pathological bleeding. Hereditary fibrinogen Aα-Chain amyloidosis is a sub-category of congenital dysfibrinogenemia in which the dysfunctional fibrinogen does not cause bleeding or thrombosis but rather gradually accumulates in, and disrupts the function of, the kidney.

The fibrinolysis system is responsible for removing blood clots. Hyperfibrinolysis describes a situation with markedly enhanced fibrinolytic activity, resulting in increased, sometimes catastrophic bleeding. Hyperfibrinolysis can be caused by acquired or congenital reasons. Among the congenital conditions for hyperfibrinolysis, deficiency of alpha-2-antiplasmin or plasminogen activator inhibitor type 1 (PAI-1) are very rare. The affected individuals show a hemophilia-like bleeding phenotype. Acquired hyperfibrinolysis is found in liver disease, in patients with severe trauma, during major surgical procedures, and other conditions. A special situation with temporarily enhanced fibrinolysis is thrombolytic therapy with drugs which activate plasminogen, e.g. for use in acute ischemic events or in patients with stroke. In patients with severe trauma, hyperfibrinolysis is associated with poor outcome. Moreover, hyperfibrinolysis may be associated with blood brain barrier impairment, a plasmin-dependent effect due to an increased generation of bradykinin.

Thromboelastometry (TEM), previously named rotational thromboelastography (ROTEG) or rotational thromboelastometry (ROTEM), is an established viscoelastic method for hemostasis testing in whole blood. It is a modification of traditional thromboelastography (TEG). TEM investigates the interaction of coagulation factors, their inhibitors, anticoagulant drugs, blood cells, specifically platelets, during clotting and subsequent fibrinolysis. The rheological conditions mimic the sluggish flow of blood in veins. TEM is performed with the ROTEM whole blood analyzer and is an enhancement of thrombelastography, originally described by H. Hartert in 1948.

Intravascular immunity describes the immune response in the bloodstream, and its role is to fight and prevent the spread of pathogens. Components of intravascular immunity include the cellular immune response and the macromolecules secreted by these cells. It can result in responses such as inflammation and immunothrombosis. Dysregulated intravascular immune response or pathogen evasion can create conditions like thrombosis, sepsis, or disseminated intravascular coagulation.

Thrombodynamics is a method for blood coagulation monitoring and anticoagulant control. This test is based on imitation of coagulation processes occurring in vivo, is sensitive both to pro- and anticoagulant changes in the hemostatic balance. Highly sensitive to thrombosis.

The platelet plug, also known as the hemostatic plug or platelet thrombus, is an aggregation of platelets formed during the earlier stage of hemostasis in response to blood vessel wall injury. After platelets are recruited and begin to accumulate around the breakage, their “sticky” nature allows them to adhere to each other. This forms a platelet plug, which prevents more blood from leaving the body as well as any outside contaminants from getting in. The plug provides a temporary blockage of the break in the vasculature. As such, platelet plug formation occurs after vasoconstriction of the blood vessels but before the creation of the fibrin mesh clot, which is the more permanent solution to the injury. The result of the platelet plug formation is the coagulation of blood. It can also be referred to as primary hemostasis.

References

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