Disseminated intravascular coagulation in the elderly
Introduction
Introduction to disseminated intravascular coagulation in the elderly Disseminated intravascular coagulation (DIC) is not an independent disease, but an important intermediate process in the development of many diseases, characterized by activation of intravascular coagulation, microcirculation thrombosis, massive consumption of coagulation factors and Platelets, resulting in the massive production of secondary plasmin, clinical bleeding, organ dysfunction, microvascular hemolysis and shock and other symptoms. basic knowledge Sickness ratio: 0.0012% Susceptible people: the elderly Mode of infection: non-infectious Complications: shock, coma
Cause
Disseminated intravascular coagulopathy in the elderly
Causes
Many diseases can cause DIC, and most importantly, due to the triggering of these disease processes, the internal and external coagulation pathways are activated, leading to DIC, a common cause. Although many diseases can be complicated by DIC, the most common clinical complications are obstetric complications, severe systemic infections, severe trauma, and metastatic tumors.
Many diseases destroy the normal blood coagulation, anticoagulation, and the balance of fibrinolytic system. Hemostasis, coagulation and fibrinolysis abnormalities can occur in the body. Due to the excessive formation of pathological thrombin and plasmin, DIC is caused. The mechanism has the following aspects.
Severe bacterial infection (endotoxin production), viral infection, antigen-antibody complex, surgical trauma, etc. cause extensive damage to vascular endothelial cells, exposure of vascular basement membrane and collagen fibers, activation of factor XIII, thereby activating endogenous coagulation pathways; At the same time, surgery, tissue factor (TF) released during severe trauma, pathological procoagulants enter the blood circulation, with the participation of calcium ions, TF and VII form a TF/VII complex, which in turn activates exogenous coagulation Pathways, both internal and external coagulation pathways can activate X to Xa, which together with Va, Ca2+, and phospholipids form a prothrombin complex that converts prothrombin to thrombin; followed by conversion of fibrinogen to fibrin , forms a thrombus in the microvascular.
Stimulated by endotoxin, inflammatory cytokines and complement activation, mononuclear macrophages can express activated TF on the surface and secrete TNF, IL-1 and platelet activating factor (PAF). TNF and IL-1 can increase fiber. Expression of lysogen activator (tPA) and plasminogen activator inhibitor-1 (PAI-1), and reduction of protein C (PC) activation by inhibiting the production of thrombomodulin (TM) in endothelial cells; In addition, due to the production of thrombin, the elimination of activated coagulation factors by the mononuclear-phagocytic system is inhibited, and blood coagulation is also promoted.
During normal coagulation, the body has a complex anticoagulant system that acts through both body fluids and cells to ensure blood circulation in the blood vessels: endothelial cells secrete TM to bind to thrombin, eliminating thrombin to XII, fibrinogen and platelets. The procoagulant effect, endothelial cells also secrete a tissue factor pathway inhibitor (TFPI), which inactivates the TF/VIIa complex and inhibits Xa activation, which plays a role in maintaining microcirculation perfusion. Under pathological conditions, endothelial cells are damaged. The action of TM is weakened, so that the procoagulant activity of thrombin is enhanced and the blood coagulation is accelerated. At the same time, the decrease of TM also reduces the activation of protein C, and the inactivation of VIIIa and Va is inhibited; the procoagulant enters the blood circulation and excessively consumes TFPI. One of the mechanisms by which DIC occurs.
With the extensive formation of microthrombus in the body, a large number of coagulation factors and platelets are consumed. Thrombin activates the XIII factor and activates the plasmin while changing fibrinogen to fibrin; and removes Xa and XIIa during coagulation. The fragments can also activate plasmin; release of tPA when the vascular endothelium is damaged, activate plasmin and enhance fibrinolysis, and plasminogen can digest fibrinogen and fibrin to form corresponding degradation products. That is, FDP has anticoagulant and anti-platelet aggregation effects, thereby aggravating bleeding caused by depleted coagulation factors and platelet deficiency.
Prevention
Disseminated intravascular coagulation prevention in the elderly
Active treatment of the primary disease is essential, and the elimination of the cause and cause is the most important measure to stop intravascular coagulation, such as active and effective control of infection and early removal of abscess.
Complication
Disseminated intravascular coagulation complications in the elderly Complications, shock, coma
Commonly, hemorrhage is the main, followed by thrombosis, renal dysfunction, pulmonary dysfunction, central nervous system and liver dysfunction, shock, coma and so on.
Symptom
Disseminated intravascular coagulation symptoms in the elderly Common symptoms Hemorrhagic tendency nausea dyspnea coagulopathy bloody proteinuria convulsions sputum hypotension coma
The main symptoms and signs after DIC are related to the primary disease. It should be emphasized that DIC is a dynamic development process. At different stages of disease development, the clinical manifestations are very different. According to the different states of the body's coagulation and fibrinolysis system, it can be divided into different states. Phase 3.
1. High coagulation period:
Blood coagulation is often found only in laboratory tests, acute type is difficult to find, and chronic type is more obvious.
2. Consumable low condensation period:
(1) Bleeding: Due to the massive consumption of plasma coagulation factors and platelets, clinically obvious bleeding symptoms are characterized by the extensive extent and severity of bleeding that cannot be explained by the primary disease. The common sites of bleeding are the skin, kidney, and gastrointestinal tract. , puncture, surgical site and extensive oozing after surgery, early bleeding spots, ecchymosis, a large number of ecchymoses in the late stage.
(2) Microvascular embolism: Symptoms vary depending on the affected blood vessels, hemorrhagic necrosis or finger toe gangrene can be seen in the skin; renal involvement can cause hematuria, oliguria, urinary closure, tubular necrosis, acute renal failure; pulmonary microvascular involvement Respiratory insufficiency may occur, acute type I respiratory failure is more common; brain involvement may cause cerebral hypoxia, edema, clinical manifestations of lethargy, convulsions and even coma.
(3) Shock: It is a symptom that occurs earlier in DIC. It is difficult to explain with the primary disease, and the effect of anti-shock therapy is poor. The main reasons are:
1 microthrombus formation reduces the amount of blood returning to the heart, and the blood output of the heart decreases;
At 2DIC, the factor XII is activated to produce kallikrein, which relaxes the arterioles, exudes plasma, and decreases circulating blood volume;
3 hypocoagulable state causes bleeding to further reduce blood volume;
4 blood concentration, increased plasma viscosity;
5 fibrin peptides A (FPA) and B (FPB) cleavage during fibrinolysis can cause small blood vessels to sputum and aggravate shock.
(4) Microangiopathic hemolysis: Fibrin filaments appear in microvessels during DIC, resulting in mechanical damage of red blood cells, red blood cell deformation, debris, and microvascular hemolytic anemia in severe cases.
3. Secondary fibrinolysis period:
Clinical bleeding is extensive and serious. The main cause is the consumption of a large number of clotting factors, the blood is in a hypocoagulable state, and secondary fibrinolysis, FDP inhibits platelet aggregation and has anticoagulant effect, aggravating bleeding, and shock, acidosis also causes the disease to continue to deteriorate.
4. Clinical classification:
According to the length of the disease, it is divided into:
(1) acute type: rapid onset, several hours or 1-2 days, hemorrhagic symptoms are heavy, the condition is dangerous.
(2) Chronic type: The course of disease can reach several months, and there are few clinical symptoms. Most of them are abnormal in laboratory tests, such as decreased platelet count, increased FDP, and positive 3P test.
Should have the basic diseases causing DIC; meet the clinical manifestations of DIC; have laboratory diagnosis basis, the DIC diagnostic criteria developed by the Fifth National Society of Hemorrhage and Hemostasis in 1994.
Examine
Examination of disseminated intravascular coagulation in the elderly
It is divided into screening test and confirmatory test. The screening test is mainly evidence of platelet, clotting factor consumption and fibrinolysis abnormalities, such as platelet count, PT, APTT, 3P test, Fbg and FDP determination; confirmation test is to find out the key Evidence for thrombin and plasmin formation.
In the early stage of pulmonary embolism, X-rays may have abnormal changes.
Diagnosis
Diagnostic differential diagnosis of disseminated intravascular coagulation in the elderly
Diagnostic criteria
Clinical manifestation
(1) There are basic diseases that cause DIC.
(2) There are two or more clinical manifestations:
1 multiple bleeding tendency.
2 should not use the primary disease to explain microcirculation failure or shock.
3 symptoms and signs of multiple microvascular embolism, such as: skin, subcutaneous, mucosal embolism, necrosis and early emergence of kidney, lung, brain and other organ dysfunction.
2. Laboratory examination
(1) The following three or more exceptions:
1 platelet count <100 × 109 / L or progressive decline (liver disease, leukemia patients platelet count can be <50 × 109 / L); or more than two of the following plasma platelet activation products: beta platelet globulin ( -TG), platelet factor IV (PF4), thromboxane B2 (TXB2) or granule membrane protein-140 (GMP-140).
2 plasma fibrinogen content <1.5g / L or progressive decline or more than 4g / L (leukemia or other malignant tumor patients <1.8g / L, liver disease <1.0g / L).
The 33P test was positive or the plasma FDP was >20 mg/L (liver disease >60 mg/L) or the D-dimer level was elevated (positive).
4 prothrombin time shortened or prolonged more than 3s or showed a dynamic change (patients with liver disease extended PT for more than 5s).
5 plasminogen content and activity decreased.
6 antithrombin III content and activity decreased (not suitable for liver disease).
7 plasma VIII: C activity <50% (necessary for liver disease).
(2) The following cases should have more than one abnormality in difficult cases:
1VIII: C activity decreased, vWF: Ag increased, and VIII: C and vWF: Ag ratio decreased.
2 elevated plasma thrombin-antithrombin complex (TAT) concentration or elevated prothrombin fragment 1+2 (F1+2) levels.
3 Plasma plasmin and plasmin inhibitor complex (PIC) concentrations increased.
4 blood (urine) FPA levels increased.
Differential diagnosis
Acute DIC should be differentiated from thrombotic thrombocytopenic purpura (TTP), primary fibrinolysis, and severe liver disease.
