Which factors put a patient at risk for developing acute disseminated intravascular coagulation DIC )? Select all that apply?

Disseminated intravascular coagulation (DIC) involves abnormal, excessive generation of thrombin and fibrin in the circulating blood. During the process, increased platelet aggregation and coagulation factor consumption occur. DIC that evolves slowly (over weeks or months) causes primarily venous thrombotic and embolic manifestations; DIC that evolves rapidly (over hours or days) causes primarily bleeding. Severe, rapidly evolving DIC is diagnosed by demonstrating thrombocytopenia, an elevated partial thromboplastin time and prothrombin time, increased levels of plasma D-dimers (or serum fibrin degradation products), and a decreasing plasma fibrinogen level. Treatment includes correction of the cause and replacement of platelets, coagulation factors (in fresh frozen plasma), and fibrinogen (in cryoprecipitate) to control severe bleeding. Heparin is used as therapy (or prophylaxis) in patients with slowly evolving DIC who have (or are at risk of) venous thromboembolism.

Disseminated intravascular coagulation usually results from exposure of tissue factor to blood, initiating the extrinsic coagulation cascade. In addition, the fibrinolytic pathway is activated in DIC (see figure Fibrinolytic pathway Fibrinolytic pathway

Which factors put a patient at risk for developing acute disseminated intravascular coagulation DIC )? Select all that apply?
). Stimulation of endothelial cells by cytokines and perturbed microvascular blood flow causes the release of tissue plasminogen activator (tPA) from endothelial cells. Both tPA and plasminogen attach to fibrin polymers, and plasmin (generated by tPA cleavage of plasminogen) cleaves fibrin into D-dimers and other fibrin degradation products. DIC can, therefore, cause both thrombosis and bleeding (if the consumption of platelets and/or coagulation factors is excessive).

Fibrinolytic pathway

DIC occurs most often in the following clinical circumstances:

  • Infection, particularly with gram-negative organisms: Gram-negative endotoxin causes generation or exposure of tissue factor activity in phagocytic, endothelial, and tissue cells.

  • Cancer, particularly mucin-secreting adenocarcinomas of the pancreas Pancreatic Cancer Pancreatic cancer, primarily ductal adenocarcinoma, accounts for an estimated 57,600 cases and 47,050 deaths in the US annually ( 1). Symptoms include weight loss, abdominal pain, and jaundice... read more , adenocarcinomas of the prostate Prostate Cancer Prostate cancer is usually adenocarcinoma. Symptoms are typically absent until tumor growth causes hematuria and/or obstruction with pain. Diagnosis is suggested by digital rectal examination... read more , and acute promyelocytic leukemia Acute Myeloid Leukemia (AML) In acute myeloid leukemia (AML), malignant transformation and uncontrolled proliferation of an abnormally differentiated, long-lived myeloid progenitor cell results in high circulating numbers... read more

    Which factors put a patient at risk for developing acute disseminated intravascular coagulation DIC )? Select all that apply?
    : Tumor cells express and expose (or release) tissue factor.

Less common causes of DIC include

  • Severe tissue damage due to head trauma, burns, frostbite, or gunshot wounds

  • Complications of prostate surgery that allow prostatic material with tissue factor activity (along with plasminogen activators) to enter the circulation

  • Profound intravascular hemolysis

Slowly-evolving disseminated intravascular coagulation typically results mainly from cancer, aneurysms, or cavernous hemangiomas.

Severe, rapidly evolving DIC, in contrast, causes thrombocytopenia, depletion of plasma coagulation factors and fibrinogen, and bleeding. Bleeding into organs, along with microvascular thromboses, may cause dysfunction and failure in multiple organs. Delayed dissolution of fibrin polymers by fibrinolysis may result in the mechanical disruption of red blood cells, producing schistocytes and mild intravascular hemolysis.

Symptoms and Signs of DIC

In severe, rapidly evolving DIC, skin puncture sites (eg, IV or arterial punctures) bleed persistently, ecchymoses form at sites of parenteral injections, and serious gastrointestinal bleeding may occur.

  • Platelet count, prothrombin time (PT), partial thromboplastin time (PTT), plasma fibrinogen, plasma D-dimer

Disseminated intravascular coagulation is suspected in patients with unexplained bleeding or venous thromboembolism, especially if a predisposing condition exists. If DIC is suspected, platelet count, PT, PTT, plasma fibrinogen level, and plasma D-dimer levels (an indication of in vivo fibrin polymer generation and degradation) are obtained.

Slowly evolving DIC produces

  • Mild thrombocytopenia

  • Normal to minimally prolonged PT (results are typically reported as international normalized ratio [INR]) and PTT

  • Normal or moderately reduced fibrinogen level

  • Increased plasma D-dimer level

Because various disorders stimulate increased synthesis of fibrinogen as an acute-phase reactant, a declining fibrinogen level on 2 consecutive measurements can help make the diagnosis of DIC. Initial PTT values in slowly evolving DIC may actually be shorter than normal, probably because of the presence of activated coagulation factors in the plasma.

Rapidly evolving DIC results in

  • More severe thrombocytopenia

  • More prolonged PT and PTT

  • Rapidly declining plasma fibrinogen level

  • High plasma D-dimer level

A factor VIII level can sometimes be helpful if severe, acute DIC must be differentiated from massive hepatic necrosis, which can cause similar abnormalities in coagulation studies. The factor VIII level is elevated in hepatic necrosis because factor VIII is made in hepatic sinusoidal endothelial cells, and released as they are destroyed; factor VIII may be reduced in DIC because of the thrombin-induced generation of activated protein C, which proteolyses the activated form of factor VIII.

  • Treatment of cause

  • Possibly replacement therapy (eg, platelets, cryoprecipitate, fresh frozen plasma))

  • Sometimes heparin

Immediate correction of the cause is the priority (eg, broad-spectrum antibiotic treatment of suspected gram-negative sepsis, evacuation of the uterus in abruptio placentae, blood volume repletion). If treatment is effective, disseminated intravascular coagulation should subside quickly.

If bleeding is severe or involves a critical location (eg, brain, gastrointestinal tract), or if there is an urgent need for surgery, then adjunctive replacement therapy is indicated. Replacement may consist of

  • Platelet concentrates to correct thrombocytopenia (in case of rapidly declining platelet count or platelets < 10,000 to 20,000/microL [< 10 to 20 ×109/L])

  • Cryoprecipitate to replace fibrinogen (and factor VIII) if the fibrinogen level is declining rapidly or is < 100 mg/dL (< 2.9 micromol/L).

  • Fresh frozen plasma to increase levels of other clotting factors and natural anticoagulants (antithrombin, proteins C, S, and Z)

Heparin is useful in the treatment of slowly evolving disseminated intravascular coagulation with venous thrombosis or pulmonary embolism. Heparin usually is not indicated in rapidly evolving DIC with bleeding or bleeding risk. An exception is in women with a retained dead fetus and evolving DIC with a progressive decrease in platelets, fibrinogen, and coagulation factors. In these latter patients, heparin is given for several days to control DIC, increase fibrinogen and platelet levels, and decrease excessive coagulation factor consumption. Heparin is then stopped and the uterus evacuated.

  • In disseminated intravascular coagulation (DIC), coagulation is usually activated when blood is exposed to tissue factor. In association with coagulation, the fibrinolytic pathway is also activated.

  • DIC usually begins rapidly and causes bleeding and microvascular occlusion, leading to organ failure.

  • DIC sometimes begins slowly and causes thromboembolic phenomena rather than bleeding.

  • Severe, rapid-onset DIC causes severe thrombocytopenia, prolonged prothrombin time and partial thromboplastin time, a rapidly declining plasma fibrinogen level, and a high plasma D-dimer level.

  • Immediate correction of the cause is the priority; severe bleeding may also require replacement therapy with platelets, cryoprecipitate (containing fibrinogen), and fresh frozen plasma (containing other coagulation factors).

  • Heparin is useful in slow-onset DIC, but rarely in DIC of rapid onset (except in women with a retained dead fetus).

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Which factors put a patient at risk for developing acute disseminated intravascular coagulation DIC?

Risk factors for DIC include:.
Blood transfusion reaction..
Cancer, especially certain types of leukemia..
Inflammation of the pancreas (pancreatitis).
Infection in the blood, especially by bacteria or fungus..
Liver disease..
Pregnancy complications (such as placenta that is left behind after delivery).

What are risk factors for DIC?

Risk factors include: Sepsis, which is wide-spread inflammation or swelling in your body. Sepsis is the most common cause of DIC. Major damage to organs or tissues through illnesses such as pancreatitis, severe trauma, burns or major surgery.

What causes disseminated intravascular coagulation DIC?

DIC is usually caused by inflammation from an infection, injury, or illness. Some common causes include: Sepsis: This is a body-wide response to infection that causes inflammation. Sepsis is the most common risk factor for DIC.

Which client would be most at risk for developing disseminated intravascular coagulation DIC )?

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.