Wednesday, May 10, 2017

Disseminated Intravascular Coagulation

Also called consumption coagulopathy and defibrination syndrome, disseminated intravascular coagulation (DIC) occurs as a complication of diseases and conditions that accelerate clotting. This accelerated clotting process causes small blood vessel occlusion, organ necrosis, depletion of circulating clotting factors and platelets, and activation of the fibrinolytic system—which, in turn, can provoke severe hemorrhage.
Clotting in the microcirculation usually affects the kidneys and extremities but may occur in the brain, lungs, pituitary and adrenal glands, and GI mucosa. Other conditions, such as vitamin K deficiency, hepatic disease, and anticoagulant therapy, may cause a similar hemorrhage.
DIC is generally an acute condition but may be chronic in cancer patients. The prognosis depends on early detection and treatment, the severity of the hemorrhage, and treatment of the underlying disease or condition.


DIC may result from:
  • infection (the most common cause of DIC), including gram-negative or gram-positive septicemia; viral, fungal, or rickettsial infection; and protozoal infection (falciparum malaria)
  • obstetric complications, such as abruptio placentae, amniotic fluid embolism, and retained dead fetus
  • neoplastic disease, including acute leukemia and metastatic carcinoma
  • disorders that produce necrosis, such as extensive burns and trauma, brain tissue destruction, transplant rejection, and hepatic necrosis.
Other causes include heatstroke, shock, poisonous snakebite, cirrhosis, fat embolism, incompatible blood transfusion, cardiac arrest, surgery necessitating cardiopulmonary bypass, giant hemangioma, severe venous thrombosis, and purpura fulminans.
It isn’t clear why such disorders lead to DIC; nor is it certain that they lead to it through a common mechanism. In many patients, the triggering mechanisms may be the entrance of foreign protein into the circulation and vascular endothelial injury.


Regardless of how DIC begins, the typical accelerated clotting results in generalized activation of prothrombin and a consequent excess of thrombin. Excess thrombin converts fibrinogen to fibrin, producing fibrin clots in the microcirculation.
This process consumes exorbitant amounts of coagulation factors (especially fibrinogen, prothrombin, platelets, and factor V and factor VIII), causing hypofibrinogenemia, hypoprothrombinemia, thrombocytopenia, and deficiencies in factor V and factor VIII. Circulating thrombin activates the fibrinolytic system, which lyses fibrin clots into fibrin degradation products.

The hemorrhage that occurs may largely be the result of the anticoagulant activity of fibrin degradation products as well as depletion of plasma coagulation factors.

Clinical Manifestations
The most significant sign of DIC is abnormal bleeding, without an accompanying history of a serious hemorrhagic disorder.
Principal signs of such bleeding include cutaneous oozing, petechiae, ecchymoses, and hematomas caused by bleeding into the skin. Bleeding from sites of surgical or invasive procedures (such as incisions or I.V. sites) and from the GI tract are equally significant indications, as are acrocyanosis and signs of acute tubular necrosis.
Related symptoms and other possible effects include nausea, vomiting, dyspnea, oliguria, seizures, coma, shock, failure of major organ systems, and severe muscle, back, and abdominal pain.

Abnormal bleeding in the absence of a known hematologic disorder suggests DIC. Initial laboratory findings supporting a tentative diagnosis of DIC include:
  • prolonged prothrombin time (PT): greater than 15 seconds
  • prolonged partial thromboplastin time (PTT): greater than 60 to 80 seconds
  • decreased fibrinogen levels: less than 150 mg/dl
  • decreased platelet count: less than 100,000/µl
  • increased fibrin degradation products: commonly greater than 100 µg/ml.
  • positive D-dimer test: specific for DIC; test is positive at less than 1/8 dilution
Other supportive data include positive fibrin monomers, diminished levels of factors V and VIII, fragmentation of red blood cells (RBCs), and decreased hemoglobin (less than 10 g/dl). Assessment of renal status demonstrates a reduction in urine output (less than 30 ml/hour) and elevated blood urea nitrogen (greater than 25 mg/dl) and serum creatinine (greater than 1.3 mg/dl) levels.
Final confirmation of the diagnosis may be difficult because many of these test results also occur in other disorders (primary fibrinolysis, for example). Additional diagnostic measures determine the underlying disorder.

Successful management of DIC necessitates prompt recognition and adequate treatment of the underlying cause. Treatment may be supportive (when the underlying disorder is self-limiting, for example) or highly specific.
If the patient isn’t actively bleeding, supportive care alone may reverse DIC. However, active bleeding may require I.V. heparin and administration of blood, fresh frozen plasma, platelets, or packed RBCs to support hemostasis.

Special considerations
  • To prevent clots from dislodging and causing fresh bleeding, don’t scrub bleeding areas. Use pressure, cold compresses, and topical hemostatic agents to control bleeding.
  • Protect the patient from injury. Enforce complete bed rest during bleeding episodes. If the patient is agitated, pad the side rails.
  • Check all I.V. and venipuncture sites frequently for bleeding. Apply pressure to injection sites for at least 10 minutes. Alert other personnel to the patient’s tendency to hemorrhage.
  • Monitor intake and output hourly in acute DIC, especially when administering blood products.
  • Watch for transfusion reactions and signs of fluid overload. Weigh the patient daily, particularly in renal involvement.
  • To measure the amount of blood lost, weigh dressings and linen and record drainage.
  • Watch for bleeding from the GI and genitourinary tracts. If you suspect intra-abdominal bleeding, measure the patient’s abdominal girth at least every 4 hours, and monitor closely for signs of shock.
  • Monitor the results of serial blood studies (particularly hematocrit, hemoglobin, and coagulation times).
  • Inform the family of the patient’s progress. Prepare them for his appearance (I.V. lines, nasogastric tubes, bruises, dried blood). Provide emotional support for the patient and his family. As needed, enlist the aid of a social worker, chaplain, and other members of the health care team in providing such support.

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