Excessive Bleeding

Various clinical signs and symptoms point to unusual or excessive bleeding. Patients may present with unexplained nosebleeds (epistaxis), reinforced or prolonged menstrual bleeding (menorrhagia), prolonged bleeding after a small cut, by brushing or flossing or after trauma. Other patients have unexplained skin lesions, including petechiae (minor bleeding into the skin or mucosa), purpura (mucosal or Hauteinblutungen that are larger than petechiae), ecchymosis (bruising) and telangiectasia (enhanced small vessels in the skin or mucous membrane). Some seriously ill patients can suddenly bleed after vascular punctures or injuries of the skin and develop severe bleeding at these sites or from the gastrointestinal or genitourinary tract. In other patients, an abnormal laboratory finding is the first indication of the susceptibility to severe bleeding that is found by chance. Etiology Various causes may be responsible for excessive bleeding (see table: causes of excessive bleeding), including the following: platelet disorders clotting disorders damage to blood vessels platelet disorders can be caused by abnormal platelet count (usually too few platelets, although a significant increase in platelet count with thrombosis or with strong may be associated bleeding), platelet dysfunction or view both. Coagulation disorders may be acquired or congenital. The most common causes of excessive bleeding Severe thrombocytopenia Excessive anticoagulation as warfarin or heparin liver disease (insufficient production of coagulation factors) causes of excessive bleeding cause examples platelet disorders (quantitative disorder) some Decreased platelet count Inadequate platelet formation (z. B. in leukemia, aplastic anemia and myelodysplastic syndromes) sequestration in the spleen (z. B. in cirrhosis with congestive splenomegaly) Increased platelet degradation or consumption (eg. B. Increased in immune thrombocytopenia [ITP], DIC, thrombotic thrombocytopenic purpura, haemolytic uraemic syndrome, septicemia, and HIV infection) Drug-induced degradation (eg., By heparin, quinidine, quinine, sulphonamides, sulphonylureas or rifampicin) platelet count (quantitative disorder) Essential thrombocythemia (thrombosis may be more common than bleeding) inadequate platelet function (qualitative disorder) Arneimittelinduzierte von Willebrand syndrome (insufficient vWF-mediated platelet adhesion) dysfunction (eg., by aspirin or NSAIDs) Systemic disorders (uremia, occasionally myeloproliferative or myelodysplastic syndromes, multiple myeloma) Coagulation disorders Acquired vitamin K deficiency liver disease anticoagulation with warfarin, heparin, or the direct oral inhibitors of thrombin or Factor Xa DIC Hereditary hemophilia A (factor VIII deficiency), hemophilia B (factor IX deficiency) Vascular Acquired vitamin C deficiency IImmunglobulin-A-associated vasculitis Hereditary connective tissue diseases (eg. B. Ehlers-Danlos syndrome, osteogenesis imperfecta, Marfan syndrome), hereditary hemorrhagic telangiectasia DIC disseminated intravascular coagulation; vWF = von Willebrand factor. Clarification history Clarification of the current disease, the bleeding sites, the strength and duration of bleeding and other bleeding should cover triggering events. In the investigation of organ systems should be specifically wanted by bleeding in places through which the patient does not report itself (eg. As should patients who complain of a tendency to bruise, after frequent nosebleeds, bleeding gums during brushing, melena, hemoptysis, asks blood in the stool or urine). Even symptoms of possible causes should be interrogated, including abdominal pain and diarrhea (gastrointestinal disease), joint pain (connective tissue), amenorrhea and morning sickness (pregnancy). The history is aimed at detecting systemic diseases from which are associated with a defect in platelets, or blood clotting, particularly Severe infections, malignant tumors, liver cirrhosis, HIV infection, pregnancy, SLE or uremia Past strong or unusual bleeding or transfusions family history of excessive bleeding The ingested drugs (especially heparin, warfarin, newer oral thrombin inhibitors or factor Xa inhibitors, aspirin and NSAIDs) should be reviewed. (N. D. Übers .: In Germany will take warfarin usually warfarin, such. As warfarin, used). In patients taking warfarin who are taking drugs and foods (including herbal supplements) should be asked that affect the Warfarinabbau and thereby the anticoagulant effect verstärken.Körperliche investigation vital signs and general appearance are evidence of hypovolemia (tachycardia, hypotension, pallor give, sweating) or infection (fever, tachycardia, hypotension with sepsis). The skin and mucous membranes (nose, mouth, vagina) are examined for petechiae, purpura and telangiectasia. By a digital rectal examination of the gastrointestinal tract bleeding can be detected. Pain in motion and local swelling, muscular hematoma and intracranial bleeding confusion, neck stiffness and focal neurological abnormalities may be signs of bleeding in deeper tissues alone or in combination. Characteristic findings for alcohol abuse or liver disease are ascites, splenomegaly (secondary as a result of portal hypertension) and Gelbsucht.Warnzeichen The following findings are of particular importance: a sign of hypovolemia or hemorrhagic shock pregnancy or recent past birth sign of infection or sepsis interpretation of the findings bleeding in patients on warfarin occur most frequently when the dose was increased or another drug or food has been taken, which may affect warfarin inactivation. Telangiectasias of the face, lips, oral or nasal mucosa, and fingers and toes in a patient with a positive family history of major bleeding probably speak for hereditary haemorrhagic telangiectasia. On a quantitative or qualitative platelet disorder or a defect in the blood vessels (eg. As amyloidosis) indicate bleeding from superficial bodies, including skin and mucous membranes, out. Bleeding into deep tissue (eg. As haemarthrosis, muscle hematomas, retroperitoneal bleeding) are an indication of a clotting disorder (coagulopathy). For a hereditary coagulation (z. B. Hemophilia), a qualitative platelet disorder, a type of von Willebrand syndrome, or hereditary hemorrhagic telangiectasia speak excessive bleeding in the family history. If bleeding family history are not known, but a hereditary disorder of hemostasis can not be excluded. Bleeding in pregnant or Patienen who recently had a birth that are in shock or have a severe infection, indicate a disseminated intravascular coagulation (DIC). Bloody diarrhea and thrombocytopenia in a patient with fever and gastrointestinal symptoms, one evidence of hemolytic uremic syndrome (HUS) be, often with infection by Escherichia coli O157: H7 associated (or other other Shiga-like toinproduzierende types of E. coli. a palpable purpura on the extensor surfaces of the extremities in favor of an immunoglobulin-a-associated vasculitis, particularly if fever, polyarthralgia or gastrointestinal symptoms are also present. coagulopathy, splenomegaly or thrombocytopenia can occur with a known alcohol abuse or liver disease in patients. in patients with intravenous drug abuse or possible sexual contact history of HIV infection should be taken into consideration werden.Tests in most patients the laboratory values ??are determined (see Table: laboratory studies on the blood clotting after coagulation phase). the first Tests are blood count with platelet count Peripheral blood smear prothrombin time (PT) and partial thromboplastin time (PTT) The screening tests detect the different components of hemostasis, including the number of circulating platelets and the plasma coagulation factors. The usually carried out screening tests for the investigation of coagulation disorders are the platelet count and the determination of prothrombin time (PT) and partial thromboplastin time (PTT). If this show abnormal results, a specific test can determine the defect usually accurate. The determination of fibrin degradation products gives information about the activation of fibrinolysis in the body (usually by an excessive coagulation in DIC). The examination of the prothrombin time (PT) shows changes of the extrinsic coagulation system and the common components of the extrinsic and intrinsic systems (plasma factors VII, X, V, prothrombin and fibrinogen). The prothrombin time is expressed by the INR (International Normalized Ratio), which represents the value of the PT of the patient relative to the control values ??of the laboratory. By calculating the INR PT values ??between different laboratories are comparable. Typical normal values ??for PT are between 10 and 13 seconds. Since reagents and technical equipment of individual laboratories may vary, each laboratory establish normal values ??for the PT and PTT. An INR> 1.5 or an extension of the PT ? 3 seconds normally be regarded as pathological and requires further investigation. The INR is a valuable screening test for the determination of coagulation disorders under various conditions acquired (z. B. Vitamin K deficiency, liver disease, disseminated intravascular coagulation). In addition, the therapy with oral vitamin K antagonists (eg. As warfarin) (translator’s note. D. .: In Germany, instead usually warfarin, phenprocoumon, such as. For example, warfarin, used) by means of INR monitored. The partial thromboplastin time (PTT) is a screening test for coagulation factors in the intrinsic system and the common components of the intrinsic and extrinsic system (prekallikrein, high molecular weight kininogen, factor XII, XI, IX, VIII, X and V, prothrombin, fibrinogen). Means PTT – with the exception of the factor VII, which is determined by the PT, and the factor XIII – detects all coagulation factors. The normal range is between 28 and 34 seconds. A normal result indicates that at least 30% of the coagulation factors in the plasma of the cascade are provided. The PTT is extended under administration of heparin and is often used to monitor heparin therapy. To the PTT elongating inhibitors autoantibodies to factor VIII (hemophilia, hemophilia, coagulation disorders by circulating anticoagulants, coagulation disorders by circulating anticoagulants) belong., As well as antibodies to the protein-phospholipid complex (lupus anticoagulant s coagulation disorders by circulating anticoagulants, Thrombotic diseases in overview; thrombotic diseases, coagulation disorders by circulating anticoagulants). Reasons for a prolonged PT or PTT can be coagulation factor deficiency presence of an inhibitor (including the presence of Throbin or factor Xa) for a component of the coagulation cascade, the PT and PTT are prolonged only when one or more of the tested clotting factors are reduced by at least 70% , In order to determine if the extension is due to a lack of one or more of the tested clotting factors or the presence of an inhibitor, the test is repeated. Here, patients with plasma is normal plasma in the ratio 1: 1. Since all coagulation factors are present in this mixture in about 50% of the amount of the normal value, indicated a further extension of the existing tests indicate the presence of an inhibitor in the patient’s plasma. The tests previously used to determine the bleeding time are of dubious reliability. Laboratory tests for blood coagulation according coagulation phase test importance formation of the primary platelet thrombus platelet count determines the number of platelets Platelet aggregation examined the response of platelets to physiological stimuli that lead to platelet activation (eg. As collagen, ADP, arachidonic acid) identifies abnormal values ??with congenital or acquired platelet dysfunctionvWF antigen measures the total concentration of the vWF in plasma vWF multimer composition Analyzes distribution of vWF multimers in the plasma (eg. As large multimers (often part of routine testing for the vWD) ristocetin cofactor activity serves the quantitative determination of large VWF multimers absent in vWD type II) ristocetin agglutination screening test that examines the presence of large vWF multimers in patients with platelet-rich plasma plasma in patients with formalin-fixed “test platelets” fibrin PT screening test that measures the coagulation factors of the extrinsic and common components of the extrinsic and intrins European System examined (factor VII, X, V, prothrombin and fibrinogen) Partial thromboplastin time (PTT) screening test that the factors of the intrinsic and common components of the extrinsic and intrinsic system studied (prekallikrein, high molecular weight kininogen, factor XII, XI, IX, VIII, X and V, prothrombin and fibrinogen) specific functional tests for coagulation factors determining the activity of a specific coagulation factor as a percentage of normal thrombin time (TT) the analysis is the last phase of coagulation, cleaves at the thrombin of fibrinogen to fibrin extended with heparin-induced Antithrombinaktivierung and qualitative change of fibrinogen or hypofibrinogenemia reptilase In normal value and simultaneously the present prolonged thrombin time the plasma sample likely contains heparin (eg. B. Heparin residues after extracorporeal bypass or heparin used to hold open i.v. Access to blood sampling); is not affected by heparin-induced Antithrombinaktivierung fibrinogen Measures the fibrinogen in the plasma; increases in acute phase reactions and decreases in severe liver diseases and severe DIC fibrinolysis clot stability after 24 h incubation in saline and 5M urea The dissolution of the clot in saline at excessive fibrinolytic activity or in 5M urea at Factor XIII deficiency If in delayed wound healing or multiple miscarriages performed are plasminogen Measures the plasminogen in the plasma; reduces thrombosis events in young adulthood (congenital, rare) alpha2-antiplasmin Measures the plasma levels of this Fibrinolyseinhibitors; reduced in excessive bleeding due to increased fibrinolysis (rare) Serumfibrinogen and fibrin screening tests on DIC increased when plasmin acting in vivo on fibrinogen or fibrin has (z. B. at DIC) been replaced by a plasma D-dimer assay plasma D dimer is measured either with monoclonal antibodies and latex agglutination test or ELISA High values ??indicate that has arisen in vivo thrombin, resulting in fibrin deposition and activation of the crosslinking enzyme factor XIII and secondary fibrinolysis has the practical advantage that it with citrated can be carried out and therefore, unlike the test for fibrin, no gore in ei nem special tubes for the recovery of serum fibrinogenfreiem is necessary particular, the sensitive ELISA determination is in the diagnosis of DIC and thrombosis (eg. As deep vein thrombosis or pulmonary embolism) helpful ADP = adenosine diphosphate; DIC disseminated intravascular coagulation; ELISA = enzyme-linked immunosorbent assay; vWD = von Willebrand’s syndrome; vWF = von Willebrand factor. Main results of the first tests exclude many poor circulation. Among the main exceptions include the von Willebrand disease and hereditary hemorrhagic telangiectasia. When von Willebrand syndrome, a common disease, the factor VIII deficiency is often very pronounced in order to prolong the PTT. Patients with normal test results, but with symptoms or signs of bleeding, and a positive family history should be tested for the von Willebrand disease; to this, the von Willebrand-factor (vWF) antigen, ristocetin cofactor activity are determined (indirect test on large vWF multimers), the vWF multimer and the factor VIII levels. In thrombocytopenia, the peripheral blood smear often provides clues to the cause (see Table: Findings in blood count in platelet diseases). If the smear normal, should be tested for HIV infection. If the HIV test is negative, not pregnant, and no drugs have been ingested, the cause platelet degradation, idiopathic thrombocytopenia is likely. If signs of hemolysis (fragmented erythrocytes in the smear, falling hemoglobin) is suspected thrombotic thrombocytopenia (TTP) or hemolytic uremic syndrome (HUS); However, other hemolytic diseases can show the same results. HUS occurs with hemorrhagic colitis in patients. In TTP and HUS the Coombs test is negative. When the blood and the peripheral blood smear show other cytopenias or abnormal leukocytes, a hematological abnormality of several cell types may be present; in this case, a bone marrow aspiration aspiration and biopsy for diagnosis are necessary. For hemophilia A or B a prolonged thromboplastin time (PTT) speaks (PT) in normal platelets and normal prothrombin time. Factor VIII and Factor IX tests are displayed. Among the PTT prolonging inhibitors include an autoantibody against factor VIII and antibodies to the protein-phospholipid complex. If after mixing with normal plasma in the ratio 1: further a prolonged PTT is 1, one of these inhibitors is believed to be the cause. Prolonged PT with normal platelets and normal PTT indicates a factor VII deficiency. The congenital Factor VII deficiency is rare; However, the short half-life of Factor VII results in plasma that the Factor VII values ??decrease more quickly than those of other vitamin K-dependent coagulation factors in patients that start with Warfarinantikoagulation or Patienen with early liver disease). Prolonged PT and PTT with thrombocytopenia indicate a disseminated intravascular coagulation, especially in connection with pregnancy complications, sepsis, malignant tumors or shock. Using multiple tests can be suspected by elevated D-dimer levels (or fibrin) and decreasing plasma fibrinogen levels are confirmed. To a prolonged PT or PTT at normal platelet count occurs in liver disease, vitamin K deficiency, or during the anticoagulation with warfarin, unfractionated heparin or the newer orally taken or thrombin inhibitors. Factor Xa. A suspected diagnosis of liver diseases is provided on the basis of medical history and confirmed by increases in serum transaminases and bilirubin; a test for hepatitis is recommended. To detect occult bleeding in patients with coagulation disorders, often imaging techniques must be used. For example, a CT scan of the head should be performed in patients with severe headache, head injury or loss of consciousness. A CT scan of the abdomen is indicated in patients with abdominal pain or other indications of intraperitoneal or retroperitoneal bleeding. Treatment Treat the underlying disease. Treatment depends on the underlying disease and after hypovolemia. For the immediate treatment of bleeding due to coagulopathy, which has not yet been diagnosed, should until the diagnosis fresh frozen plasma (FFP, fresh frozen plasma) are used, which contains all coagulation factors. Summary Disseminated intravascular coagulation should be adopted in patients with sepsis, shock or complications during pregnancy or childbirth. Aspirin or NSAIDs often cause mild platelet dysfunction. A slight tendency to bruise with no other clinical signs and normal laboratory values ??are probably benign.

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