Disseminated intravascular coagulation (disseminated or diffuse intravascular coagulation, DIC) is due to various reasons, coagulation factors and platelet activation, thrombin increased micro-thrombosis and extensive pathological features of acquired clinical syndrome.
In the occurrence of DIC, the development process, the initiating part is due to some large number of procoagulant substances into the blood, the blood coagulation system is activated, thereby causing blood coagulation - anticoagulation balance disorders. Widely in microvascular fibrin formed mainly by the (fibrin, Fbn) and aggregation of platelet microthrombi composed of the process, consuming a large number of coagulation factors and platelets, together with secondary fibrinolysis increased, resulting in significant bleeding in patients , shock, organ dysfunction and anemia.
DIC patients with varying severity of disease, and some very mild symptoms, or even hidden (occult), the patient body symptoms were not evident, only with more sensitive laboratory methods can be found; but can also be more serious, such as acute DIC patients with acute onset, poor prognosis, the mortality rate as high as 50% to 60%.
Section disseminated intravascular coagulation in pathogenesis
First, disseminated intravascular coagulation causes
Cause of DIC DIC is likely to cause some of the basic disease. The following table shows some common causes of DIC, DIC caused by infection factors which account for about 30% of the incidence of DIC, such as bacterial sepsis is a common cause of acute DIC; cancer, acute promyelocytic leukemia about the incidence of DIC 20% ~ 28.3%; surgical procedures and extensive tissue damage due to DIC about 12.7% to 15%; In addition, acute obstetric DIC accident about 8% to 20%. Therefore, there is encountered in the clinical basis for disease susceptibility in patients with DIC, and the emergence of available clinical evidence can not explain the bleeding, you should think of the possible occurrence of DIC.
Classification of the cause of DIC
Gram-negative or-positive bacterial infections, viral hepatitis, epidemic hemorrhagic fever, viral myocarditis, etc.
Metastatic carcinoma, sarcoma, malignant lymphoma
Acute and chronic leukemia, hemolytic disease, hyperlipidemia and other abnormal protein
Gynecological and obstetrical diseases
Infected abortion, stillbirth retention, toxemia of pregnancy, amniotic fluid embolism, placental abruption, etc.
Trauma and surgery
Severe soft tissue injury, crush injury syndrome, extensive burns, major surgery, etc.
In addition, certain factors in the disease process can also trigger the coagulation system and the promotion of DIC occurred, development, for example: hypoxia, acidosis, and antigen - antibody complex, free fatty acids and lipid substances and have been activated, triggering fibrinolysis system, kinin system, complement system, such as the triggering factor of DIC.
Second, DIC in the pathogenesis of
DIC occurrence and development of the mechanism is very complicated.
(A), coagulation system activation
On the coagulation system activation mechanism, in the past has been that there is blood to activated as part of initiating the intrinsic coagulation system startup process play a key role in blood clotting. But over the past decade studies have shown that tissue factor (tissue factor, TF; thromboplastin, CD142) expression, the release of the boot process in the coagulation play an important role. So on the pathogenesis of tissue factor in the role of DIC, more and more attention.
DIC caused when the main mechanism for activation of the coagulation system can be summarized the following four areas:
1. Tissue serious injury
Clinically, severe trauma and burns, surgery, obstetrics accident, a large number of necrotic lesions of organs, tissue necrosis or extensive cancer and other causes of bloody transfer, can promote massive release of TF into the blood, leading to DIC occurred. (TF is a 263 amino acid residues of the transmembrane glycoprotein, mainly in the endoplasmic reticulum in cells, the outer layer of the vascular smooth muscle cells, fibroblasts and pericytes, astrocytes, cells can be enough to condyle constant to express TF). When the body when blood vessels are damaged, TF released from damaged cells into the blood, TF containing negatively charged - carboxylic acid (-carboxyglutamate, GLA) combined with Ca2. Factor by Ca2 with TF to form complexes ( a-TF), a-TF to a large number of factor activation (the traditional pathway, classical pathway), to form factor a- a-Ca2-PL complex; also available through factor Activation (select pathway, alternative pathway) form factor a- a-Ca2-PL complex. Both then produce prothrombin activator, leading to thrombin generation. Positive feedback of thrombin and can accelerate factor , factor , factor activation, which also accelerated the thrombin generation, and accelerate the coagulation and platelet activation, aggregation process, a large number of micro-thrombus formation in microvessels.
2. Vascular endothelial cell injury
Bacteria, viruses, endotoxins, antigen - antibody complex, sustained hypoxia, acidosis, particles or colloidal material into the body, they all can damage the VEC, in particular microvascular VEC. the expression of VEC injury, the release of a large number of TF and activated coagulation system, leading to the occurrence of DIC; injury exposed subendothelial collagen and other organizations can directly activate factor or factors endogenous coagulation system startup; trigger platelet activation, resulting in sticky attachment, aggregation and release reaction, increased micro-thrombosis.
In addition, a variety of inflammatory cells to release TNF, IL-1, IFN, platelet activating factor (platelet-activating factor, PAF), complement components C3a, C5a, and humoral factors such as oxygen free radical damage and stimulate VEC exacerbated TF expression, further to promote and accelerate the coagulation process.
3. Extensive damage to blood cells, platelets are activated
platelets and red blood cell damage that exists in the inner membrane exposed to acidic phospholipids, thereby triggering the DIC. Of platelets in the pathogenesis of the role of DIC in two different understanding. One view is that platelet injury may result and not DIC DIC production mechanism, because studies have shown that lack of platelets can still place the animal hyperlipidemia caused by toxins from within DIC. Another view was that the occurrence of platelets in the development of DIC play an important role.
When trauma causes VEC injury, exposed collagen, the platelet membrane glycoprotein GP b through the vascular von Willebrand factor Von Will-ebrand factor (Von Will-ebrand factor, vWF) and collagen binding, resulting in adhesion. At the same time collagen, thrombin, ADP, TXA2, PAF, respectively, such as the activator of platelet adhesion to the surface with the corresponding receptors, through G protein-mediated effect in that the platelets to produce a second messenger (cAMP, IP3, d G, etc. ) play a series of physiological effects and changes. These changes in platelet, signal transduction through biological transmission system from the inside out, so that platelet membrane glycoprotein GP b / a complex ( b) activation. Activated GP b / a is the platelet membrane receptor fibrin, fibrinogen as a dimer with two adjacent platelet membrane GP b / a combination, resulting in bridging role, so that platelet aggregation. Aggregation of platelets lead to further structural changes, and induced the expression of ligand binding sites (ligand-induced binding sites, LIBS) to produce some of the signal transduction from outside to inside, causing platelet cytoskeleton re-build, lead to platelet flat and stretch, etc. deformation changes.
The surface of activated platelets, or inositol phospholipid phosphatidylserine and other negatively charged phospholipids (phospholipid, PL) to a variety of clotting factors in platelet phospholipid surface is concentrated, limited, resulting in a large number of prothrombin activator, the prothrombin is activation. Thus the formation of fibrin network, recruit other blood cells to form blood clots. Platelets pseudopodia stretching fibrin network, due to contraction of actin in platelets that clot retraction occurs, and gradually form a more solid thrombus.
extensive damage to white blood cells, can release a large number of high procoagulant activity (TF expression and release of lysosomal enzymes). For example, activation of neutrophils causes the release of various cytokines and vascular wall damage VEC; release of trypsin can degrade and inactivate factor , factor , AT- , TFPI, PAI, etc., causing blood clotting - anticoagulant balance disorder, resulting in DIC occurred.
shaped blood transfusion, malaria, blood and other factors enter the excess inventory resulting massive destruction of red blood cells, can release large amounts of ADP and red blood cell factors. ADP has a role in activating platelets, resulting in blood clotting; red pigment with a TF-like effect, activation of coagulation system.
4. Other ways to activate the coagulation system
acute hemorrhagic pancreatitis a large number of trypsin into the blood, as trypsin has a direct role in activating prothrombin, leading to a large number of micro-thrombosis.
bee venom, snake venom is an exogenous procoagulant substances, they can directly activate factor , prothrombin or directly to fibrinogen (fibrinogen, Fbg) into fibrin monomer (FM).
some tumor cells can secrete specific procoagulant protein (CP), can directly activate factor , activation of coagulation system.
(B), fibrinolytic dysfunction
Fibrinolysis (fibrinolytic function) is the body's important anti-coagulation, it is clear the blood vessels and glands in the excretion duct formation and deposition of Fbn, to prevent thrombosis play an important role.
In the fibrinolytic system, plasminogen (plasmingen, Plg) activation of three ways:
The activation pathway: tissue-type plasminogen activator (t-PA) and urokinase-type plasminogen activator (u-PA). t-PA is secreted by the VEC release; u-PA by the urinary and reproductive system synthesis and secretion of epithelial cells. u-PA primarily in the urine, blood concentration is very low.
the activation pathway: the endogenous coagulation system activator a, a, a, KK.
exogenous activator ways: drugs (SK, UK, recombinant t-PA, etc.) on the activation of Plg.
Plg activation in the activator produced under Pln (plasmin, plasminogen), Pln can be hydrolyzed Fbg (fibrinogen) or Fbn (fibrous protein) fibrin degradation products (FgDP / FDP). Similarly, in the fibrinolytic system in the negative feedback regulation of plasminogen activator inhibitor (PAI) can inhibit the t-PA and u-PA activity; a2 - antiplasmin (a2-AP) can be combined with Pln the formation of plasmin-a2 antiplasmin complex (PAP), the Pln loss of activity.
1. Decreased fibrinolysis
DIC VEC damage is occurring, the key to development. VEC injury anticoagulant loss of the normal function of the local benefit Fbn deposition and micro-thrombosis. For example, the surface negative charge decreased VEC to produce TFPI and AT- adsorption of anticoagulant substances such as reduced local anticoagulant function to reduce microvascular; Similarly, damaged VEC membrane thrombomodulin (TM) expression decreased to promote protein C (protein, PC) reduced ability to activate, but also lead to local anticoagulant and fibrinolytic function (referred to as: fibrinolytic function) decreased. VEC have affected plasminogen activator inhibitor (PAI-1) increased and the secretion of tissue-type plasminogen activator (t-PA) reduced, and thus reduce fibrinolysis, which are conducive to the local deposition Fbn and micro-thrombosis. In addition, the microvascular sites may not be significantly reduced fibrinolytic activity, but a large number of microvascular coagulation Fbn hyperthyroidism and the formation of plasmin timely removal of more than ability, making Fbn precipitation and the formation of microthrombi. Therefore, reduced anticoagulant activity of the local capillaries and reduced fibrinolytic activity in absolute or relative, is transparent to micro-thrombosis and retained another important condition.
2. Enhancement of secondary fibrinolysis
Secondary fibrinolysis (secondary fibrinolysis) is the activation of the coagulation system have been caused after the activation of fibrinolytic system and play the role of dissolved Fbn and Fbg process. DIC secondary fibrinolysis is an important pathological process of acute DIC is one of the important pathological features.
Enhanced fibrinolysis secondary hyperparathyroidism in the coagulation occurs at the same time; also be seen in the blood coagulation in hyperthyroidism was followed one after another.
The mechanisms are:
coagulation system is activated, produce large amounts of thrombin, factor a, kallikrein (KK) and by thrombin activated a, these factors can promote the activation of Plg into Pln. Pln with the degradation of Fbg, Fbn and other coagulation factors (complement, , , , , ), lower the blood coagulation status in secondary.
relatively normal microvascular VEC in Fbn, BK stimulated the release of such t-PA; PK and VEC membrane HMK-K with the HMK-K under the action of PK is converted to KK. KK can single-chain u-PA into the double-stranded highly active u-PA (tcu-PA). t-PA and u-PA can act on the Plg generated Pln.
TM is a thrombin receptor membrane of VEC. Combined with thrombin, reducing the clotting activity, but significantly enhanced the activation of PC role. APC by blocking factor and factor a a composition of the formation of factor activator, factor a stop and factor a composition of the formation of prothrombin activator, prevents platelet factor a combination, and to stimulate and promote the release of PA The role of fibrinolysis.
Therefore, the secondary fibrinolysis in hyperthyroidism in the promotion of micro-capillary thrombolysis, but also increase the body only, blood coagulation disorder caused by bleeding.
Section III of disseminated intravascular coagulation factor in the development of
DIC clinical impact of the occurrence and development of factors, for example, in the same clotting factor into the blood, some occur DIC, there was no DIC, suggesting that the state of the body on the occurrence of DIC plays a big role.
A single core - macrophage system dysfunction
Monocyte - macrophage phagocytosis and clearance system has, you can eat a certain amount of blood removed procoagulant coagulation and anticoagulation to maintain the dynamic balance between. Monocyte - macrophage phagocytic clearance to bacterial endotoxin, cell fragments, immune complexes, cytokines, and procoagulant substances such as ADP. In addition, the process of blood coagulation system is activated, monocytes - macrophages were also able to thrombin, Fbg, Fbn, FM, FDP, Pln, complement the formation of complexes such as phagocytosis, clearance. Therefore, when a single core - macrophage system with severe dysfunction (such as: large quantities of glucocorticoids, severe liver disease) or due to excessive swallowing (such as: bacteria, endotoxin, lipid, necrotic tissue) causes cell function by the closed When monocyte - macrophage procoagulant on blood clearance reduced accumulation of a large number of procoagulant, easily induced DIC occurred.
Generalized Shwartzman reaction (general Shwartzman reaction, GSR) is the interval of 24h to the animal a small dose of the intravenous injection of endotoxin non-lethal, then after the second injection animals received a second shock or bleeding tendency occurred, that kind of pathology caused by DIC change. Currently considered, GSR the mechanism is due after the first injection of endotoxin monocyte - macrophage system and Fbn endotoxin phagocytosis was closed, so when the second injection, monocyte - macrophage phagocytic activation of coagulation system reduced ability factor and not the inactivation of endotoxin. Endotoxin activation of coagulation factors and injury with VEC role to promote the role of platelet aggregation and contraction of blood vessels, it can cause pathological changes of DIC samples.
Second, severe hepatic dysfunction
synthetic anticoagulant to reduce the liver: anti-clotting substances PC, AT- and Flg are synthesized by the liver, so the migration of chronic hepatitis and cirrhosis, decreased liver synthetic anticoagulant, the blood is hypercoagulable state, easy to induce DIC .
inactivation of activated coagulation factor reduces the liver: the blood coagulation system activation, activation of coagulation factor a, factor a, factor a, TAT, PAP were cleared in the liver and inactivated, in severe acute hepatitis, liver inactivation of activated coagulation factors when hardening to reduce the blood is hypercoagulable state, easy to induce DIC.
acute hepatic necrosis can be a lot of free TF.
some causes of liver dysfunction (virus, some drugs) to activate coagulation factors.
The occurrence of these factors in DIC, the development of a role in both.
Third, blood hypercoagulability
Hypercoagulability of the blood is in some physiological or pathological conditions, increased blood coagulation, thrombosis in favor of a state.
1. Primary hypercoagulable state
Primary hypercoagulable state seen in hereditary AT- , PC, PS deficiency and structural abnormalities induced factor PC against disease.
2. Secondary hypercoagulable state
Secondary hypercoagulable state found in a variety of blood and non-blood diseases, such as nephrotic syndrome, cancer, leukemia, pregnancy poisoning. Pregnancy can be Yousheng rational hypercoagulable state, three weeks from the beginning of pregnancy in maternal blood platelets and coagulation factors ( , , , , , , , etc.) gradually increased, while AT- , t-PA, u-PA reduced; placenta plasminogen activator inhibitor (plasminogen activator inhibitor, PAI) increased gradually so that the blood hypercoagulable state, to the end of pregnancy the most obvious.
When the mechanism of obstetric accidents caused by DIC are: amniotic fluid embolism, placental abruption, the amniotic fluid with a class of thromboplastin, TF and platelet factor type role, with a strong procoagulant effect, can cause activation of blood coagulation factor . post-abortion infection, postpartum infection, which is mainly due to the clotting activity of the uterus with TF into the blood result in DIC. intrauterine fetal death, fetal death can release tissue factor into the blood start the extrinsic coagulation system.
Blood coagulation factors have gradually increased with increased age, the trend may go further physiological hypercoagulable state appears.
Acidosis can induce the occurrence of DIC, its mechanisms are: cause VEC injury, activation of the clotting system, the incidence of induced DIC; lower blood pH that increased activity of coagulation factors, reduced anticoagulant activity of heparin; make enhanced platelet aggregation, platelet aggregation can be released after a series of procoagulant factors in the blood hypercoagulability.
Shock caused by severe microcirculatory disturbances, slow blood flow in the microcirculation, there swirl or stasis of blood, blood cell aggregation, promote DIC formation.
Fifth, inhibition of fibrinolysis
Inappropriate application of clinical fibrinolysis inhibitor such as 6 - aminocaproic acid (6-aminocaproic acid, EACA) or carboxy benzylamine (p-aminomethyl benzoic acid, PAMBA), etc., in the over-inhibition of fibrinolysis in the body circumstances, if in the event of infection, trauma and other events can trigger DIC.
In addition, DIC is also with the occurrence and development of procoagulant substances into the blood volume, speed and pathway. Procoagulant substances into the blood less and slower, as the body compensatory function (phagocytosis) sound, does not occur or only showed obvious symptoms of the chronic type of DIC; procoagulant substances into the blood too much too fast, more than compensatory ability of the body When can cause acute DIC. In addition, procoagulant way into the blood and micro site of thrombosis has an important relationship between the blood into the venous system, DIC-based distribution of the lung; the main artery into the blood to kidney.
Disseminated intravascular coagulation in the fourth quarter of the main clinical manifestations
The main clinical symptoms of DIC can be summarized as hemorrhage, multiple organ dysfunction, microcirculation (shock), and anemia. Symptoms of acute DIC is more common when the previous three.
First, the bleeding
DIC is mainly due to bleeding caused by excessive generation of thrombin and plasmin's.
(1) consume a lot of blood clotting substances (consumptive coagulopathy): DIC occurred in the development process, because a large number of platelets and coagulation factors are consumed, and consumed more than compensatory increase in the blood Fbg, factor , factor , factor , and platelet factor sharp decline, it is also known as consumptive coagulopathy DIC patients (consumptive coagulopathy).
(2) activation of secondary fibrinolysis: fibrinolytic system enhancements produce a large number Pln, Pln is a strong activity of the protease, in addition to degradation of Fbg / Fbn, but also of the hydrolysis of various coagulation factors, the blood clotting substances dropped sharply, and increased coagulation disorders and cause bleeding.
(3) fibrin (ogen) degradation products formed: Pln hydrolysis of Fbg / Fbn cracking a variety of FgDP, FDP components, such as X, Y, D, E and other fragments. FDP is caused by the formation of blood only, coagulation disorders and bleeding caused by DIC important mechanism. X, Y form a soluble fragment of FM with FM complex (SFMC), FM with each other to prevent the formation of soluble fibrin cross-linking; fragment Y, E has anti-thrombin; D fragment inhibited the FM cross-linked together; FDP inhibit platelet adhesion and aggregation. DIC, through FgDP / FDP various components have a strong anti-clotting and anti-platelet aggregation, so that the body was significantly reduced hemostatic function, resulting in a severe bleeding tendency.
(4) vascular injury: DIC during the development of a variety of factors can lead to capillary wall damage, hemorrhage DIC is one of the mechanisms.
Second, the shock
Occurrence of acute DIC is often accompanied by shock; chronic, subacute DIC may have shock can also be no shock. Between DIC and shock, reinforce each other, can form a vicious cycle. DIC is often caused by shock following characteristics: suddenly appear or does not match with the disease; with severe extensive bleeding and distal limbs, cyanosis; multiple organ dysfunction syndrome appeared; comprehensive treatment of the lack of response to shock high mortality.
The mechanism of shock caused by acute DIC are: micro-thrombosis, so change thy blood less; bleeding can affect the blood volume; coagulation system, kinin system and activation of the complement system produce large amounts of bradykinin, histamine, etc., which have enhanced microvascular permeability and a strong vasodilator. FDP small fragments ingredients A, B, C, and various complement components are vasodilators or enhance the role of microvascular permeability; micro-thrombosis in myocardial capillaries, affecting myocardial contractility, reduced cardiac function caused. Because of these factors reduce the effective circulating blood volume, blood vessel expansion, change thy blood volume and cardiac output decreased and decreased, resulting in significantly lower blood pressure and severe dysfunction of the microcirculation.
Third, the multi-system organ dysfunction
DIC when the multi-system organ dysfunction mainly due to a wide range of micro microvascular thrombosis, microvascular obstruction, give rise to different organ tissues in different parts of ischemia and hypoxia, which occurred in metabolism, dysfunction or necrosis, severe can lead to organ dysfunction or failure. Clinical organ dysfunction in patients with the scope and degree of diversity, the light is only part of the performance of individual organ dysfunction, but severe cases often occur simultaneously or in succession two or more organ dysfunction, the formation of multiple organ failure (MODS), MODS is caused by DIC in patients with major cause of death.
For example: extensive pulmonary micro-thrombosis, can cause alveolar - capillary membrane injury, adult respiratory distress syndrome occurs (ARDS) a class of clinical symptoms of acute respiratory failure; wide range of micro-thrombosis, such as kidney, can cause two side of the renal cortical necrosis and acute renal failure, clinical manifestations of oliguria, hematuria and proteinuria; digestive system DIC can cause nausea, vomiting, diarrhea, gastrointestinal bleeding; can cause liver micro-thrombosis and portal hypertension liver dysfunction, there digestive tract congestion, edema, jaundice and other symptoms; involvement of the heart led to decreased myocardial contractility, reduced cardiac output, cardiac index reduced creatine kinase and lactate dehydrogenase increased significantly; involving the adrenal gland can cause hemorrhagic cortical necrosis and acute adrenal failure, with the obvious shock syndrome and skin ecchymosis and other large body of disease, known as China - Buddha syndrome; pituitary necrosis, Sheehan syndrome can cause (sheehan syndrome); nervous system lesions appeared confusion, drowsiness, coma, convulsions and other non-specific symptoms.
Fourth, microangiopathic hemolytic anemia (microangiopathic hemolytic anemia)
DIC patients may be associated with a special type of anemia, that is, microangiopathic hemolytic anemia. Its features are: number of peripheral blood smear shows the contraction of barbed red blood cells, visible crescent, helmet-shaped red blood cells of various shapes such as debris, known as split cells (schistocyte). Since brittle fracture of high somatic cell, is prone to hemolysis.
DIC cells generated when the crack is in the coagulation mechanism of the early fibrin strands formed in the fine capillary network, when the cycle of RBC flow mesh too small, you can stick, stuck, or hung on the fibrin strands, in the blood constantly under the impact of the RBC rupture, the formation of split cells; hypoxia, acidosis reduced the RBC deformability, RBC forced through such fibrin network more vulnerable to injury; split cells and secondary polycythemia because of spherical cells area / volume ratio becomes smaller and less deformation, brittle significantly improved, it is easy to rupture hemolysis. DIC light of early hemolysis, difficult to detect, easy to find later in the peripheral blood cells have a special crack. Broken red blood cells in peripheral blood is greater than 2% of a secondary diagnosis of DIC. Some sub-acute DIC and chronic DIC can often be symptoms of hemolytic anemia. This debris not only in RBC DIC, also seen in malignant hypertension, thrombotic thrombocytopenic purpura and so on.
V disseminated intravascular coagulation stage and type
A, DIC staging
According to DIC in the pathogenesis and clinical features, the typical course of the disease can be divided into the following three DIC.
1. Coagulation of
2. Low consumption of coagulation
3. Hyperactivity of secondary fibrinolysis
The Principles】 【3P
Protamine added to the plasma was seized after protamine with the plasma X-FM combination of fragments in X so that separation of FM and X fragments, separation of the FM self-aggregation in plasma and coagulation. The role of the enzyme without, and the phenomenon of the formation of fibrin coagulation test called the deputy. However, when too strong fibrinolytic activity, X fragment was completely broken down into small molecular substances, X-FM to significantly reduce, 3P test of anti-can be negative.
Fbg plasminogen decomposition, the resulting degradation products without D-dimer, because there is no fibrin D, connected to each other. Similarly, decomposition of the soluble plasminogen FM, D-dimer does not exist. Stable only in the decomposition of the fibrin fibers (micro-thrombosis), it can produce D-dimer, because the two ends of soluble FM adjacent D, D, FM, participation in the E site, interconnected to form a stable fiber protein filaments. DD test is by detecting the plasma D-dimer levels, to determine the presence of thrombus. D-dimer is a micro-thrombosis (DIC) to form an important marker of secondary fibrinolysis is also reflected in an important indicator of hyperthyroidism.
Second, DIC type
1. DIC occurs at the speed of typing
(1) acute type: common in severe infection and shock, severe trauma, amniotic fluid embolism, blood group incompatibility in blood transfusions, acute graft rejection reactions. DIC can be characterized in a few hours or 1 to 2 days sick. The clinical manifestations of the main shock and bleeding, his condition deteriorated rapidly. Phases is not obvious. DIC can occur in patients with acute markedly abnormal laboratory tests, platelet count decreased, FDPs increased, PT prolonged, TT prolonged, PTT extension and Fbg concentration was decreased. Because patients with acute DIC, in the absence of severe hepatitis cases, often appear Fbg factor and the lack of post-nature, so when Fbg <100mg/dl should be associated with bleeding symptoms, consider the presence of acute DIC.
(2) Chronic type: common in cancer, collagen disease, chronic hemolytic anemia, characterized by slow onset, longer course, the body can increase clotting factor synthesis by the liver to compensate. Therefore, chronic DIC, the coagulation factor depletion is often disguised, the results of experiments in the screening test, only a few indicators of abnormal, such as the platelet count decreased, but Fbg to normal. Thus, if thrombin was significantly higher in patients should be based on clinical symptoms, patients can be diagnosed with chronic DIC; If the patient mononuclear phagocyte system function more robust, less or no obvious clinical manifestations, this diagnosis with a to be difficult, patients often an organ dysfunction as the main performance. Under certain conditions, chronic DIC, may be turned into acute type.
(3) subacute type: common in cancer metastasis, such as patients with intrauterine fetal death. Its characteristics are gradually formed within a few days DIC. The clinical manifestations: between between acute and chronic.
2. DIC's compensation case by typing
DIC occurs in the development process, according to the situation clotting material consumption and compensation, DIC can be divided into three types.
(1) decompensated type (overt DIC): mainly observed in acute DIC. This type is characterized by the consumption of coagulation factors and platelets more than generation, the body time to compensate. Laboratory examination: visible platelet and coagulation factor fibrinogen was significantly reduced. Patients often have significant bleeding and shock.
(2) compensatory type (non-overt DIC): mainly seen in mild DIC, which is characterized by the consumption of coagulation factors and platelets and their compensation largely to maintain balance. Patients with subclinical or only mild symptoms of bleeding and thrombosis, easily overlooked, can also be converted to type decompensated DIC. Laboratory tests often without obvious abnormalities, but also only mild symptoms of bleeding or thrombosis. Diagnosis more difficult.
(3) over-compensatory type: mainly seen in the recovery of chronic DIC or DIC. Characterized by the body's compensatory function in patients with good blood coagulation factor by the compensation (Fbg, F , F , F , F ) and thrombopoietin increases, even more than consumption. Fbg clotting factors such as laboratory tests have a temporary increase; platelet counts decreased but sometimes it is not obvious. Clinical symptoms of bleeding and thrombosis is not obvious. DIC is seen locally based rejection after organ transplantation, vascular tumors and cardiac aneurysm and so on.