Medication
What is a supportive treatment for a client with disseminated intravascular coagulation? Transfuse fresh frozen plasma. Which statements are correct regarding platelets? -Platelet formation is stimulated by the hormone thrombopoietin. -Platelets spend one-third of their lives in the spleen.
Procedures
Acute Disseminated Intravascular Coagulation. Treatment may include blood transfusions, medicines, and oxygen therapy. (Oxygen is given through nasal prongs, a mask, or a breathing tube.) A blood transfusion is a safe, common procedure. You receive blood through an intravenous (IV) line in one of your blood vessels.
Nutrition
The cornerstone of supportive treatment of this coagulopathy is management of the underlying condition. Additionally, administration of heparin may be useful, and restoration of physiological anticoagulants has been suggested, but has not been proven successful in improving clinically relevant outcomes so far.
What is a supportive treatment for a client with disseminated intravascular coagulation?
In patients with major bleeding or at risk for hemorrhagic complications, administration of platelet concentrates, plasma, or coagulation factor concentrates should be considered. A variety of disorders, including severe sepsis, systemic inflammatory conditions, trauma, and malignant disease, will lead to activation of the coagulation system.
What is acute disseminated intravascular coagulation?
What are the supportive treatments for coagulopathy?
When are coagulation factor concentrates indicated in the treatment of sepsis?
What is global coagulation test?
What are the abnormalities of the hemostatic system in patients with DIC?
What are the laboratory parameters used to diagnose DIC?
What is DIC in a patient?
What is DIC in a hospital?
What is reduced fibrinogen level?
What is the name of the DIC that is caused by a large amount of blood?
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Which treatment is most appropriate for patients with DIC?
Treatment of underlying conditions is recommended in three types of DIC, with the exception of massive bleeding. Blood transfusions are recommended in patients with the bleeding and massive bleeding types of DIC. Meanwhile, treatment with heparin is recommended in those with the non-symptomatic type of DIC.
What do you give a patient with DIC?
In critically ill, non-bleeding patients with DIC, prophylaxis for venous thromboembolism with prophylactic doses of heparin or low molecular weight heparin is recommended. Consider treating patients with severe sepsis and DIC with recombinant human activated protein C (continuous infusion, 24 microg/kg/h for 4 d).
Which therapy is appropriate for chronic disseminated intravascular coagulation DIC?
Enoxaparin has been used for treatment and prophylaxis of chronic DIC in specific clinical situations. In a multicenter, cooperative, double-blinded trial from Japan that compared dalteparin with unfractionated heparin, the former was associated with a decreased bleeding tendency and reduced organ failure.
What does the nursing management of a patient with DIC include?
The following are the common nursing care planning and goals for clients with DIC: maintenance of hemodynamic status, maintenance of intact skin and oral mucosa, maintenance of fluid balance, maintenance of tissue perfusion, prevention of complications.
What is DIC and how is it treated?
There is no specific treatment for DIC. The goal is to determine and treat the underlying cause of DIC. Supportive treatments may include: Plasma transfusions to replace blood clotting factors if a large amount of bleeding is occurring.
How is coagulation treated?
Specific deficiencies in coagulation factors, such as fibrinogen, may be corrected by administration of purified coagulation factor concentrates. Vitamin K must be remembered as a useful non–blood product alternative to correcting vitamin K–dependent factors and will work within 4 to 6 hours after a dose.
Is heparin used for DIC?
Heparin, as an anticoagulant, which, not only inhibits the activation of the coagulation system, but is also an anti-inflammatory and immunomodulatory agent, has been widely used during DIC treatment and in the prevention and treatment of thrombotic diseases. It is easy to obtain and inexpensive.
Why is FFP given in DIC?
In conjunction with other options based on prompt and rigorous treatment of the underlying cause of DIC, fresh frozen plasma plays an important role in therapeutic management when overt bleeding is present or anticipated in DIC patients with disturbed coagulation or when an invasive procedure is being planned.
Why is cryoprecipitate given in DIC?
Patients with DIC and low fibrinogen are probably best treated with a combination of FFP and cryoprecipitate, to minimize the risk of inducing thrombosis with transfusion of cryoprecipitate alone. Adequate transfusion should be given to maintain the fibrinogen level above 100 mg/dL.
Do you give whole blood in DIC?
Some blood transfusions involve whole blood (blood with all of its parts). More often though, only some parts of blood are transfused. If you have DIC, you may be given platelets and clotting factors, red blood cells, and plasma (the liquid part of blood).
Which of the following conditions is most likely to be associated with disseminated intravascular coagulation?
People who have one or more of the following conditions are most likely to develop DIC: Sepsis (an infection in the bloodstream) Surgery and trauma. Cancer.
How I treat disseminated intravascular coagulation
A variety of organs in patients with DIC show intravascular fibrin deposition at pathological examination related to the clinical dysfunction of the organs. 15 Experimental DIC in animals causes intra- and extravascular fibrin deposition in the kidneys, lungs, liver, and brain, and amelioration of the hemostatic defect improves organ failure and, in some cases, mortality. 15,16 In addition ...
How is Disseminated Intravascular Coagulation Treated?
Treatment for disseminated intravascular coagulation (DIC) depends on its severity and cause. The main goals of treating DIC are to control bleeding and clotting problems and treat the underlying cause.
DIC: which laboratory tests are most useful - PubMed
In patients with disseminated intravascular coagulation (DIC) a variety of altered coagulation parameters may be detectable, such as thrombocytopenia, prolonged global coagulation times, reduced levels of coagulation inhibitors, or high levels of fibrin split products. In addition, more sophisticate …
Disseminated intravascular coagulation - Treatment algorithm | BMJ Best ...
Treatment recommended for ALL patients in selected patient group. A platelet transfusion should be considered when the platelet count is <20 x 10⁹/L (<20 x 10³/microlitre) or <50 x 10⁹/L (<50 x 10³/microlitre) with active bleeding. Levi M, Toh CH, Thachil J, et al. Guidelines for the diagnosis and management of disseminated intravascular coagulation.
Disseminated Intravascular Coagulation (DIC) Treatment & Management
Disseminated intravascular coagulation (DIC) is characterized by systemic activation of blood coagulation, which results in generation and deposition of fibrin, leading to microvascular thrombi in various organs and contributing to multiple organ dysfunction syndrome (MODS). Consumption and subsequent exhaustion of coagulation proteins and pl...
What are the mechanisms of coagulation in DIC?
The initiation and propagation of procoagulant pathways with simultaneous impairment of natural anticoagulant systems and suppression of endogenous fibrinolysis as a result of systemic inflammatory activation are leading to platelet activation and fibrin deposition. 15, 29 Important mediators that regulate these processes are cytokines, such as interleukin-1 (IL-1) and IL-6 and tumor necrosis factor-α (TNF-α). In addition, recent studies point to a prominent role of intravascular webs (neutrophil extracellular traps) consisting of denatured DNA from damaged cells and entangling neutrophils, platelets, fibrin, and cationic proteins, such as histones, in the development of thrombus deposition. 30
What are the causes of coagulation activation?
A variety of disorders, including severe sepsis, systemic inflammatory conditions, trauma, and malignant disease, will lead to activation of the coagulation system. In many cases, this coagulation will not result in clinical complications and will not even be identified by routine laboratory tests, but can only be detected when sensitive molecular markers for activation of coagulation pathways are used. 1 However, if the activation of coagulation is sufficiently strong, consumption of platelets and coagulation proteins may become visible through prolongation of routine clotting tests and increasing thrombocytopenia. Systemic activation of coagulation in its most extreme form is known as disseminated intravascular coagulation (DIC). DIC is classically characterized by the simultaneous occurrence of widespread vascular clot deposition, compromising an adequate blood supply to various organs, and thereby contributing to organ failure. 2-5 Due to ongoing activation of the coagulation system and other factors, such as impaired synthesis and increased degradation of coagulation proteins and protease inhibitors, exhaustion of factors and platelets may occur, potentially resulting in profuse bleeding from various sites. In addition, high levels of fibrin degradation products may affect platelet function and fibrin cross-linking and thereby further contribute to the bleeding tendency. 6, 7
What is the role of mononuclear cells in clot formation?
Mononuclear cells express tissue factor resulting in thrombin generation and subsequent fibrinogen to fibrin conversion, which, in combination with increased platelet vessel wall interaction and activation of platelets, contribute to microvascular clot formation. P-selectin released from activated platelets further upregulates tissue factor expression. Binding of fibrin to Toll-like receptor 4 and activated coagulation proteases to specific protease activated receptors (PARs) on inflammatory cells (dotted lines) modulates inflammation through the additional release of proinflammatory cytokines. Cytokines also play a key role in the suppression of endogenous fibrinolysis and impairment of physiological anticoagulant pathways, such as the APC pathway.
What is the pathway that initiates thrombin generation in DIC?
Thrombin generation in DIC is initiated through the tissue factor/factor VII (a) pathway that activates downstream coagulation factors. 31 Tissue factor may be expressed by activated monocytes, but also by vascular endothelial cells or cancer cells. Besides inflammation causing procoagulant effects, the activation of coagulation also modulates inflammation ( Figure 1 ).
What is DIC in coagulopathy?
Disseminated intravascular coagulation (DIC) is a condition characterized by systemic activation of coagulation, potentially leading to thrombotic obstruction of small and midsize vessels, thereby contributing to organ dysfunction. At the same time, ongoing consumption of platelets and coagulation proteins results in thrombocytopenia and low concentrations of clotting factors, which may cause profuse hemorrhagic complications. DIC is always secondary to an underlying condition, such as severe infections, solid or hematologic malignancies, trauma, or obstetric calamities. A reliable diagnosis of DIC can be made through simple scoring algorithms based on readily available routine hemostatic parameters. The cornerstone of supportive treatment of this coagulopathy is management of the underlying condition. Additionally, administration of heparin may be useful, and restoration of physiological anticoagulants has been suggested, but has not been proven successful in improving clinically relevant outcomes so far. In patients with major bleeding or at risk for hemorrhagic complications, administration of platelet concentrates, plasma, or coagulation factor concentrates should be considered.
What are the symptoms of liver cirrhosis?
At physical examination, the most prominent signs were hepatic encephalopathy, jaundice, splenomegaly, and ascites. Laboratory test results showed a hemoglobin concentration of 7.0 mmol/L (11.3 g/dL), a leukocyte count of 7.9.2 × 10 9 /L, a platelet count of 88 × 10 9 /L (1 week before admission, 84 × 10 9 /L), a bilirubin concentration of 84 μmol/L (1.2 mg/dL), and an albumin concentration of 28 g/L. Coagulation tests reveal a PT of 17 seconds (normal, <12 seconds), an aPTT of 52 seconds (normal, <28 seconds), a D-dimer concentration of 1.0 μg/mL (normal, <0.5 μg/mL), and a fibrinogen concentration of 2.1 g/L (normal, 1-3 g/L). The question is whether these coagulation abnormalities are due to liver failure-related coagulopathy or DIC, secondary to an infection.
What organs are affected by intravascular fibrin deposition?
15 Experimental DIC in animals causes intra- and extravascular fibrin deposition in the kidneys, lungs, liver, and brain, and amelioration of the hemostatic defect improves organ failure and, in some cases, mortality. 15, 16 In addition, DIC has been shown to be an independent and relatively strong predictor of organ dysfunction and mortality in critically ill patients. 9, 17 In patients with sepsis and DIC, mortality is almost 2 times higher as compared with patients who do not have DIC.
What is disseminated intravascular coagulation?
Disseminated intravascular coagulation is a rare and serious condition that can disrupt your blood flow. It is a blood clotting disorder that can turn into uncontrollable bleeding. DIC affects about 10% of all people who are very ill with sepsis, diseases such as cancer or pancreatitis, as well as people recovering from traumatic injuries such as burns or serious complications from pregnancy and delivery.
What is DIC in medical terms?
Disseminated intravascular coagulation (DIC) is a rare and serious condition that disrupts your blood flow. It is a blood clotting disorder that can turn into uncontrollable bleeding. DIC can affect people who have cancer or sepsis. It can also affect people recovering from complications from pregnancy and delivery or who have been injured.
What does it mean when you have DIC?
Most people who have DIC are already coping with illness or a medical condition. Being diagnosed with disseminated intravascular coagulation means you have another medical concern to manage as you continue the treatment and testing for the medical condition that caused your DIC. Here are some suggestions that might help:
What happens when you have DIC?
Then, having used up the proteins and platelets that make your blood clot, DIC might cause uncontrollable internal or external bleeding.
What is the most common cause of DIC?
Sepsis, which is wide-spread inflammation or swelling in your body. Sepsis is the most common cause of DIC.
What is a D-dimer?
D-dimer. This is a blood test to check for blood clots.
What is PT test?
Prothrombin time (PT) test. This test measures the time it takes for your blood to clot.
What is the treatment for disseminated intravascular coagulation?
The main goals of treating DIC are to control bleeding and clotting problems and treat the underlying cause.
What are the parts of blood that are given to you with DIC?
If you have DIC, you may be given platelets and clotting factors, red blood cells, and plasma (the liquid part of blood).
What is the best way to prevent blood clots?
Blood thinners help prevent blood clots from forming. They also keep existing blood clots from getting larger.
What is the treatment for DIC?
Treatment may include blood transfusions, medicines, and oxygen therapy. (Oxygen is given through nasal prongs, a mask, or a breathing tube.)
Why do we need blood transfusions?
Blood transfusions are done to replace blood loss due to an injury, surgery, or illness. Blood is made up of various parts, including red blood cells, white blood cells, platelets, and plasma. Some blood transfusions involve whole blood (blood with all of its parts). More often though, only some parts of blood are transfused.
What is global coagulation test?
Global coagulation tests provide important evidence regarding the degree of coagulation factor activation and consumption. Although the PT is prolonged in approximately 50% of patients with DIC at some point during their clinical course [21], abnormalities are often observed in patients with liver disease or vitamin K deficiency. A reduction in the platelet count or clear downward trend in subsequent measurements is a sensitive sign of DIC [3], although this pattern is also observed in patients with bone marrow disorders. A reduced fibrinogen level is a valuable indicator regarding a diagnosis of DIC due to leukemia or obstetric diseases; however, it is not observed in most septic DIC patients [3]. Elevated fibrin-related markers (FRMs), such as FDP [26], D-dimer [27], or soluble fibrin (SF), reflect fibrin formation. SF [28] assays offer theoretical advantages in detecting DIC, more closely reflecting the effects of thrombin on fibrinogen, although the half-life is short. It is important to consider that many conditions, such as trauma, recent surgery, bleeding, or venous thromboembolism (VTE), are associated with elevated FRMs. Reductions in the levels of natural anticoagulants, such as antithrombin (AT) and protein C, are common in patients with DIC. Although measuring the AT activity is useful for achieving the full efficacy of heparin [29], this parameter cannot be quickly and easily measured in all hospitals. These activities are correlated with the liver function and/or concentration of albumin. A reduced ADAMTS13 (a disintegrin-like and metalloproteinase with thrombospondin type 1 motifs 13) activity and elevated soluble thrombomodulin (TM), PAI-I, and von Willebrand factor propeptide levels are often observed in patients with DIC and have been shown to have prognostic significance [30–32]. The biphasic waveform of the activated partial thromboplastin time (APTT) has been shown to be associated with DIC and appears to have a positive predictive value for the disease [33, 34]. Although many attractive markers for DIC have been reported, no single marker can be used to diagnose DIC alone (Table 2). Therefore, the above four guidelines [3–6] recommend that DIC could not be diagnosed according to the level of a single marker but rather based on the combination of laboratory markers. Among the four types of DIC, PT, fibrinogen, and platelets are important parameters for diagnosing the massive bleeding type of DIC, while fibrinogen, FDP, and plasmin-plasmin inhibitor complex (PPIC) are important for detecting the bleeding type of DIC. Meanwhile, platelets, PT, and AT are important for diagnosing the organ failure type of DICand hemostatic molecular markers, such as SF and the thrombin-AT complex, are important for diagnosing the non-symptomatic type of DIC.
What are the abnormalities of the hemostatic system in patients with DIC?
Abnormalities of the hemostatic system in patients with DIC result from the sum of vectors for hypercoagulation and hyperfibrinolysis (Figure 1). When the vector for hyperfibrinolysis is remarkable and dominant, bleeding is the primary symptom; this type is called the bleeding type or hyperfibrinolysis predominance type of DIC. This form of DIC is often seen in patients with leukemia, such as acute promyelocytic leukemia (APL), obstetric diseases, or aortic aneurysms [2, 7]. On the other hand, when the vector for hypercoagulation is remarkable and dominant, organ failure is the main symptom; this type of DIC is called the organ failure type, hypercoagulation predominance type or hypofibrinolysis type of DIC. This form of DIC is often observed in patients with infection, particularly sepsis. An increase in the level of plasminogen activator inhibitor I (PAI-I) induced by markedly increased levels of cytokines [8, 9] and lipopolysaccharide (LPS) [2, 7] in the blood has been reported to a cause of hypofibrinolysis. Moreover, neutrophil extracellular traps (NETs) [10], which release DNA with histone, neutrophil elastase, and cathepsin G in order to trap and kill pathogens, are present in patients with sepsis. Histones promote the apoptosis of vascular endothelial cells and platelet aggregation [11], while neutrophil elastase and cathepsin G decompose tissue factor pathway inhibitor (TFPI) in order to promote thrombus formation [12]. Moreover, high mobility group box 1 (HMGB-1) [13] is emitted from injured and dead cells in order to enhance the inflammatory reaction.
What are the laboratory parameters used to diagnose DIC?
Various underlying clinical conditions can have an effect on the laboratory parameters that are usually obtained to diagnose DIC, such as global coagulation tests, the platelet count, prothrombin time (PT), and the fibrinogen, fibrinogen, and fibrin degradation products (FDPs). In order to facilitate the diagnostic process for detecting DIC, the use of a scoring system is recommended by each of the four different guidelines [3–6]. Three different diagnostic criteria incorporating similar global coagulation tests have been established by the ISTH/SSC [1], Japanese Ministry Health, Labour and Welfare (JMHLW) [17], and Japanese Association of Acute Medicine (JAAM) [18]. The JMHLW score is well correlated with the severity of DIC and can be used to predict the outcome of the disease [14]. The ISTH overt DIC score is useful and specific for diagnosing DIC due to infective and non-infective etiologies [13, 19]. The JAAM score is sensitive for detecting septic DIC and is correlated with the ISTH and JMHLW scores and disease outcome [13, 18]. A prospective study in Japan reported no significant differences in the odds ratio for predicting DIC outcomes among these three diagnostic criteria [20], suggesting that the identification of molecular hemostatic markers and changes of global coagulation tests is required in addition to the application of scoring systems. The use of a combination of tests repeated over time in patients with suspected DIC can be used to diagnose the disorder with reasonable certainty in most cases [21–23]. A template for a non-overt-DIC scoring system, including global coagulation tests, changes in global coagulation tests as well as hemostatic molecular markers, has been proposed [1, 24, 25].
What is DIC in a patient?
Disseminated intravascular coagulation (DIC) is a syndrome characterized by the systemic activation of blood coagulation, which generates intravascular thrombin and fibrin, resulting in the thrombosis of small- to medium-sized vessels and ultimately organ dysfunction and severe bleeding [1, 2]. DIC may result as a complication of infection, solid cancers, hematological malignancies, obstetric diseases, trauma, aneurysms, and liver diseases, etc., each of which presents characteristic features related to the underlying disorder. The diagnosis and treatment of DIC must therefore consider these underlying etiological features. The type of DIC is related to the underlying disorder. Three guidelines for diagnosis and treatment of DIC [3–5] have been published in the literature by the British Committee for Standards in Haematology (BCSH), Japanese Society of Thrombosis and Hemostasis (JSTH), and Italian Society for Thrombosis and Haemostasis (SISET). Although these three guidelines are broadly similar, there are variations in several recommendations regarding DIC treatment. Therefore, the subcommittee for DIC of the Scientific and Standardization Committee (SSC)/International Society of Thrombosis and Haemostasis (ISTH) harmonized these three guidelines in a report entitled, Guidance for the diagnosis and treatment of DIC from harmonization of the recommendations from three guidelines[6] (Table 1). The present review describes several recommendations for the diagnosis and treatment of DIC related to the type of DIC.
What is DIC in a hospital?
Disseminated intravascular coagulation (DIC) is categorized into bleeding, organ failure, massive bleeding, and non-symptomatic types according to the sum of vectors for hypercoagulation and hyperfibrinolysis. The British Committee for Standards in Haematology, Japanese Society of Thrombosis and Hemostasis, and the Italian Society for Thrombosis and Haemostasis published separate guidelines for DIC; however, there are several differences between these three sets of guidelines. Therefore, the International Society of Thrombosis and Haemostasis (ISTH) recently harmonized these differences and published the guidance of diagnosis and treatment for DIC. There are three different diagnostic criteria according to the Japanese Ministry Health, Labour and Welfare, ISTH, and Japanese Association of Acute Medicine. The first and second criteria can be used to diagnose the bleeding or massive bleeding types of DIC, while the third criteria cover organ failure and the massive bleeding type of DIC. Treatment of underlying conditions is recommended in three types of DIC, with the exception of massive bleeding. Blood transfusions are recommended in patients with the bleeding and massive bleeding types of DIC. Meanwhile, treatment with heparin is recommended in those with the non-symptomatic type of DIC. The administration of synthetic protease inhibitors and antifibrinolytic therapy is recommended in patients with the bleeding and massive bleeding types of DIC. Furthermore, the administration of natural protease inhibitors is recommended in patients with the organ failure type of DIC, while antifibrinolytic treatment is not. The diagnosis and treatment of DIC should be carried out in accordance with the type of DIC.
What is reduced fibrinogen level?
A reduced fibrinogen level is a valuable indicator regarding a diagnosis of DIC due to leukemia or obstetric diseases; however, it is not observed in most septic DIC patients [3]. Elevated fibrin-related markers (FRMs), such as FDP [26], D-dimer [27], or soluble fibrin (SF), reflect fibrin formation.
What is the name of the DIC that is caused by a large amount of blood?
When both vectors for hypercoagulation and hyperfibrinolysis are remarkable and strong, major bleeding occurs, followed by death, if a sufficient amount of blood is not transfused; this type of DIC is called the massive bleeding or consumptive type of DIC.