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    - DIC results from dysregulation of coagulation and fibrinolysis pathways, leading to widespread clotting and bleeding. It is triggered by the release of tissue factor and thrombin generation, causing microvascular thrombosis. - Signs and symptoms include bleeding, organ dysfunction, and thrombocytopenia. Causes include sepsis, trauma, pregnancy complications, cancer, and liver disease. - Diagnosis is based on clinical history, lab findings of coagulopathy, thrombocytopenia, and elevated fibrin degradation products. Treatment focuses on managing the underlying condition, replacing clotting factors, and providing organ support.

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    - DIC results from dysregulation of coagulation and fibrinolysis pathways, leading to widespread clotting and bleeding. It is triggered by the release of tissue factor and thrombin generation, causing microvascular thrombosis. - Signs and symptoms include bleeding, organ dysfunction, and thrombocytopenia. Causes include sepsis, trauma, pregnancy complications, cancer, and liver disease. - Diagnosis is based on clinical history, lab findings of coagulopathy, thrombocytopenia, and elevated fibrin degradation products. Treatment focuses on managing the underlying condition, replacing clotting factors, and providing organ support.

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    - DIC results from dysregulation of coagulation and fibrinolysis pathways, leading to widespread clotting and bleeding. It is triggered by the release of tissue factor and thrombin generation, causing microvascular thrombosis. - Signs and symptoms include bleeding, organ dysfunction, and thrombocytopenia. Causes include sepsis, trauma, pregnancy complications, cancer, and liver disease. - Diagnosis is based on clinical history, lab findings of coagulopathy, thrombocytopenia, and elevated fibrin degradation products. Treatment focuses on managing the underlying condition, replacing clotting factors, and providing organ support.

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    11 views11 pages

    Assignment

    Uploaded by

    rehamoh1997
    - DIC results from dysregulation of coagulation and fibrinolysis pathways, leading to widespread clotting and bleeding. It is triggered by the release of tissue factor and thrombin generation, causing microvascular thrombosis. - Signs and symptoms include bleeding, organ dysfunction, and thrombocytopenia. Causes include sepsis, trauma, pregnancy complications, cancer, and liver disease. - Diagnosis is based on clinical history, lab findings of coagulopathy, thrombocytopenia, and elevated fibrin degradation products. Treatment focuses on managing the underlying condition, replacing clotting factors, and providing organ support.

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    of 11

    Assessment and management of Disseminated

    Intravascular Coagulation

    Name: Ali Ayman Alarady


    ID:2180002603
    Contents
    Subject Page

    physiology 1

    Pathophysiology 2

    Pathophysiology 3

    -Sign and symptoms 4


    -Causes

    Diagnosis 5

    Pre-hospital Assessment and 6


    managemnet
    Hospital management 7

    summery 8

    References 9
    :physiology
    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

    :Pathophysiology
    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. 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
    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
    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

    2
    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

    :Signs and symptoms


    Chest pain -
    - shortness of breath
    - leg pain
    - problems speaking
    -problems moving part of the body
    -bleeding

    :Causes
    :DIC can occur in the following conditions
    - Solid tumors and blood cancers (particularly acute promyelocytic leukemia)
    Obstetric complications: abruptio placentae, pre-eclampsia or eclampsia, -
    amniotic fluid embolism, retained intrauterine fetal demise, septic abortion, post
    partum haemorrhage
    Massive tissue injury: severe trauma, burns, hyperthermia, rhabdomyolysis, -
    extensive surgery
    Sepsis or severe infection of any kind (infections by nearly all microorganisms -
    can cause DIC, though bacterial infections are the most common): bacterial
    (Gram-negative and Gram-positive sepsis), viral, fungal, or protozoan infections
    Transfusion reactions (i.e., ABO incompatibility haemolytic reactions) -
    - Severe allergic or toxic reactions (i.e. snake venom)
    - Giant haemangiomas (Kasabach–Merritt syndrome)
    - Large aortic aneurysms
    Liver disease, HELLP syndrome, thrombotic thrombocytopenic -
    purpura/Haemolytic uremic syndrome, and malignant hypertension may mimic
    .DIC but do not occur via the same pathways

    4
    :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
    Characteristic history (this is important because severe liver disease can -
    essentially have the same laboratory findings as DIC)
    Prolongation of the prothrombin time (PT) and the activated partial -
    thromboplastin time (aPTT) reflect the underlying consumption and impaired
    .synthesis of the coagulation cascade
    Fibrinogen level has initially thought to be useful in the diagnosis of DIC but -
    because it is an acute phase reactant, it will be elevated due to the underlying
    inflammatory condition. Therefore, a normal (or even elevated) level can occur in
    over 57% of cases. A low level, however, is more consistent with the consumptive
    .process of DIC
    -.A rapidly declining platelet count
    High levels of fibrin degradation products, including D-dimer, are found owing to -
    the intense fibrinolytic activity stimulated by the presence of fibrin in the
    .circulation
    The peripheral blood smear may show fragmented red blood cells (known as -
    schistocytes) due to shear stress from thrombi. However, this finding is neither
    sensitive nor specific for DIC
    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: It has been recommended that a scoring system be
    .used in the diagnosis and management of DIC in terms of improving outcome

    Presence of an underlying disorder known to be associated with DIC (no=0,


    yes=2)
    :Global coagulation results
    .Platelet count (> 100k = 0, < 100 = 1, < 50 = 2)
    Fibrin degradation products such as D-Dimer (no
    increase = 0, moderate increase = 2, strong increase =
    .3)
    Prolonged prothrombin time (< 3 sec = 0, > 3 sec = 1, > 6
    .sec = 2)
    .Fibrinogen level (> 1.0g/L = 0; < 1.0g/L = 1)
    cell fragments (schistocytes)

    :Pre- hospital assessment


    When evaluating your patient in the prehospital environment, be alert for abrupt
    bleeding that quickly became severe, with blood oozing from venipuncture sites,
    surgical incisions, drainage tubes and partially healed wounds. Patients may also
    experience a GI bleed, genitourinary bleed, CNS bleed and have fingers, nose,
    toes and ears that may become cyanotic.2 When assessing the skin, look for
    bruises and hemorrhages that do not blanche when pressed. Be alert for
    respiratory insufficiency, abdominal pain, confusion and seizures indicating poor
    .perfusion

    :Pre-hospital Management Goals


    Management of DIC in the field involves finding and treating your patient for the
    underlying disease or trauma and providing supportive care. DIC can
    spontaneously resolve when the underlying disorder is properly managed.
    Monitor pulse oximetry and provide ventilator assistance and oxygen as needed.
    Remove the triggering mechanism if possible. This may be intravenous fluids if
    the patient is hypovolemic or hypotensive, treating for hypoxemia, acidosis, or a
    .transfusion reaction
    Avoid unnecessary needle sticks, use of manual and automatic BP cuffs, and
    other procedures that could cause bleeding, bruising or hematomas. Consider
    using low suction for tracheal or oral suctioning, and comfort measures with pain
    management. For blood pressure control, Dopamine and other vasopressors are
    effective and the administration of low molecular weight heparin helps to block
    the formation of new clots if the patient has not had recent surgery, or a CNS or
    .GI bleed
    If blood products are available, packed red blood cells help to restore oxygen
    carrying capacity, fresh frozen plasma replaces clotting factors, cryoprecipitate
    can be given to replenish depleted fibrinogen, and platelet concentrate helps to
    .correct thrombocytopenia
    Be aware that if you are doing a critical care transport of a patient with DIC your
    patient has a high risk for venous thromboembolic events (VTEs) if they are older,
    have had recent surgery, have been immobilized, have an in-dwelling vascular
    .catheter or have had previous VTEs
    :Hospital management
    -.Clotting factor replacement such as fibrinogen. This is used to stop bleeding
    Oxygen therapy to allow more oxygen to reach the lungs, the heart, and the rest -
    .of the body if blood clots are preventing oxygen from reaching your organs
    -Plasma transfusion, which provides clotting factors, to stop or prevent bleeding
    - .Platelet transfusion to quickly raise platelet levels to stop or prevent bleeding
    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

    :Summery
    Disseminated intravascular coagulation (DIC) is a condition in which
    blood clots form throughout the body, blocking small blood vessels.
    Symptoms may include chest pain, shortness of breath, leg pain,
    problems speaking, or problems moving parts of the body. As clotting
    factors and platelets are used up, bleeding may occur. This may
    include blood in the urine, blood in the stool, or bleeding into the
    skin. Complications may include organ failure. Pre-hospital care is
    mainly supportive. Monitor pulse oximetry and provide ventilator
    .assistance as needed. And IV fluids resuscitation

    8
    :References

    Disseminated Intravascular Coagulation | NHLBI, NIH". www.nhlbi.nih.gov. "


    Retrieved 20 December 2017
    Disseminated Intravascular Coagulation (DIC) - Hematology and Oncology". "
    Merck Manuals Professional Edition. September 2016. Retrieved 20 December
    2017
    Robbins, Stanley L.; Cotran, Ramzi S.; Kumar, Vinay; Collins, Tucker (1999).
    Robbins' Pathologic Basis of Disease (6 ed.). Philadelphia: Saunders. ISBN 0-
    7216-7335-X
    Haematology: Basic Principles and Practice (6 ed.). Elsevier Saunders. 2012.
    ISBN 978-1437729283
    Taylor, F; Toh, C-h; et al. (2001). "Towards Definition, Clinical and Laboratory
    Criteria, and a Scoring System for Disseminated Intravascular Coagulation".
    Thrombosis and Haemostasis. 86 (5): 1327–30. doi:10.1055/s-0037-1616068. PMID
    11816725
    Levi, M; Toh, C-H; et al. (2009). "Guidelines for the diagnosis and management of
    disseminated intravascular coagulation". British Journal of Haematology. 145 (5):
    24–33. doi:10.1111/j.1365-2141.2009.07600.x. PMID 19222477
    Dressler DK. Coping with a coagulation crisis. Nursing, 2004; 34

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