coagulation
(kō-ag‵yŭ-lā'shŏn 
)
[L. coagulatio, clotting]
The thickening of a liquid into a gel or solid.
ABBR: APC
The destruction of tissues with heat generated by applying an electrical current to an argon plasma. The plasma distributes heat to a minimal depth so that only superficial structures are coagulated while deeper ones remain undisturbed. APC is used in several applications, e.g., in the destruction of some superficial cancers and in the treatment of some stenoses that have formed within normally hollow organs, such as the trachea.blood c.The clumping together of blood cells to form a clot. This may occur in vitro, intravascularly, or when a laceration of the skin allows the escape of blood from an artery, vein, or capillary. Coagulation of blood may occur in two pathways, depending on the beginning of the process.
Extrinsic: The extrinsic pathway requires the blood to be exposed to a subendothelial tissue factor originating outside the blood. This factor begins a complex series of chemical reactions involving thromboplastin, factor VII, and calcium; binding to factor X, causing its conversion to factor Xa; and the resulting conversion of prothrombin to thrombin to fibrinogen and eventually fibrin.
Intrinsic: The intrinsic pathway occurs when blood is drawn without contamination by tissue factor. This clotting pathway does not require an additive. It is triggered when the blood is exposed to a foreign surface and factor XII is activated. Factor XII may also be activated through limited cleavage by kallikrein. This process is accelerated by high-molecular-weight kininogen (HMWK). This leads to formation of factor XII, a process that produces more HMWK to accelerate kallikrein production. The process continues, and factors XI and IX, and HMWK, together with calcium, generate factor Xa. The clotting cascade then continues as in the extrinsic pathway, and prothrombin is converted to thrombin, which acts on fibrinogen to produce fibrin.
SEE: coagulation factor.
ABBR: DIC
A life-threatening disease occurring as a complication of other conditions in which the coagulation pathways are hyperstimulated, resulting in diffuse rather than localized activation of coagulation factors. The accelerated clotting occludes small blood vessels (usually in the kidneys and extremities, but sometimes in the brain, lungs, pituitary and adrenal gland s, and gastrointestinal [GI] mucosa), resulting in organ necrosis. Clotting factors are consumed to such an extent that generalized bleeding may occur.SEE: acute respiratory distress syndrome; hypofibrinogenemia; sepsis; serine protease inhibitor; systemic inflammatory response syndrome; .
SEE: Nursing Diagnoses Appendix.
DIC is usually an acute condition but may be chronic in cancer patients. Various conditions have been associated with DIC, including sepsis; extensive burns or other trauma; pancreatitis; acute intravascular hemolysis; gram-negative or gram-positive septicemia; acute viral, rickettsial, or protozoal infection; abruptio placentae, septic abortion, and other obstetric complications; surgical procedures; heatstroke; certain poisonous snake bites; severe head injury; malignancy; retained dead fetus; liver disease; incompatible blood transfusion; and systemic lupus erythematosus.
Symptoms of DIC include bleeding from surgical or invasive procedure sites and from the GI tract, oral cavity, nose, or urinary tract. The patient may also experience nausea and vomiting; dyspnea; severe muscle, back, and abdominal pain; chest pain; hemoptysis; epistaxis; seizures; and oliguria. Peripheral pulses and blood pressure may be decreased, and the patient may demonstrate confusion or other changes in mental status.
The underlying illness must be recognized and treated promptly. In some cases, depending on the cause, heparins or antithrombin III may be administered; patients may receive transfusional support (blood, cryoprecipitate, fresh frozen plasma, packed red blood cells, or platelets).
In acute DIC, intake and output are monitored hourly, esp. when blood products are given, and the patient is observed for transfusion reactions and fluid overload. The blood pressure cuff is used infrequently to avoid triggering subcutaneous bleeding. Any emesis, drainage, urine, or stool should undergo a test for occult blood, and dressings and linens should be weighed to measure the amount of blood lost. Daily weights are obtained, particularly in cases of renal involvement. The patient is observed closely for signs of shock, and the abdominal girth measured every 2 to 4 hr if intra-abdominal bleeding is suspected.
The results of serial blood studies (such as hemoglobin, hematocrit, and coagulation studies) are monitored. All venipuncture sites are checked frequently for bleeding. Analgesics are given as prescribed, as well as heparin therapy, if prescribed (the latter is controversial). The patient is repositioned every 2 hr, and meticulous skin care is provided. Prescribed oxygen therapy is administered. Areas at risk can be washed gently with hydrogen peroxide and water to remove crusted blood. Pressure, cold compresses, and topical hemostatic agents are applied to control bleeding. Parenteral injections are avoided and venipunctures limited whenever possible; pressure should be applied to an injection site for at least 20 min after removal of a needle or intravenous catheter. The patient is protected from injury by enforcement of complete bedrest during bleeding episodes and by padding the bed rails if the patient is at risk for agitation. Frequent rest periods are provided.
The disorder, the patient's progress, and treatment options and posttreatment appearance are explained, and the patient and family are encouraged to express their feelings and concerns and are referred for further counseling or support as needed.