DIC syndrome: treatment and diagnosis. Laboratory diagnosis of disseminated intravascular coagulation syndrome

DIC syndrome is also called disseminated intravascular coagulation syndrome. It is not a separate pathology or nosological entity. It is a complex process consisting of several stages, during which increased thrombus formation is observed in the lumen of blood vessels. This is a fairly common situation. Most often, surgical doctors and pediatricians encounter it. Treatment of DIC syndrome is extremely complex, requiring early diagnosis of the process.

The causes of DIC syndrome are determined by the diseases that provoked it. The most common triggers are.

1. Severe infectious pathologies - sepsis, accompanied by a state of shock, viral processes.
2. Other types of shock, which is inherently the main cause of DIC. These include traumatic, hypovolemic, infectious-toxic and even painful.
3. Any terminal condition can provoke disseminated intravascular coagulation.
4. Surgical operations, especially massive ones, in which artificial blood circulation machines are used.
5. Cancer diseases.
6. Hemodialysis.
7. Excessive blood loss.
8. Against the background of massive blood transfusion, this pathology also occurs.
9. In obstetric practice, DIC syndrome occurs with placental abruption, complications of labor with amniotic fluid embolism, toxicosis, and Rh conflict.
10. Pathologies of cardio-vascular system.

Based on the above, we can conclude that disseminated intravascular coagulation is caused by severe pathological processes or terminal conditions. At the same time, pathology practically does not occur in healthy newborn babies. Here it is important to correctly differentiate it from other coagulopathies, such as hemophilia or von Willebrand disease.

Stages of development and forms of DIC syndrome

Doctors classify this condition in different ways. All these divisions are based on etiological, pathogenetic features, as well as variants clinical course. Taking into account the mechanisms of pathology triggering, the following stages of DIC syndrome are distinguished.

1. First, hypercoagulation occurs.
2. It gives way to the so-called consumption coagulopathy, which gradually gives way to the third stage.
3. Hypocoagulation – terminal stage shock, if you do not provide assistance to the patient at this stage, the mortality rate will be very high.
4. Restorative, includes the process of restoring the body after correction of the shock state.

Pathogenesis

The pathogenesis of DIC syndrome is based on mechanisms that occur during all its stages. The failure of the body's hemostatic system is due to increased stimulation of blood coagulation, as well as depletion of anticoagulant and fibrinolytic mechanisms.

The pathophysiology of DIC depends on many factors that serve as activators of the coagulation process. They act independently or act as mediators of effects on the endothelium vascular wall. Activators of all stages of DIC include toxins, bacterial waste products, immune complexes, decreased circulating blood volume, and many others. It is they who determine the flow options of the internal combustion engine.

The pathological component is based on the stages of the process.

1. The first phase of DIC is hypercoagulation, during which cells inside the vessels begin to stick together. It is triggered by thromboplastin entering the bloodstream. Its duration is several minutes.
2. The pathophysiology of DIC syndrome includes consumption coagulopathy, in which there is a pronounced deficiency of fibrinogen and other coagulation factors due to rapid consumption, and the body does not have time to replace them.
3. Secondary fibrinolysis is accompanied by hypocoagulation, the blood clots very slowly or does not clot at all.
4. Recovery is characterized by residual effects or complications.

Clinical manifestations

The symptoms of DIC syndrome are not questioned when they occur skin manifestations(they may be called hemorrhagic manifestations), decreased diuresis, lung damage. These are the main signs of pathology.

Symptoms are determined by the main link of pathogenesis, this increased coagulability blood. Parenchymal organs and skin are the first to suffer. The severity of the condition depends on the severity of thrombus formation.

1. When skin is involved, it is noted hemorrhagic rash, it resembles minor hemorrhages and areas of tissue necrosis.
2. The lungs react by developing acute respiratory failure. Shortness of breath occurs, severe cases are accompanied by pulmonary edema or respiratory arrest.
3. An excess of fibrin in the blood plasma triggers kidney problems - renal failure, the terminal stage will manifest itself as anuria and electrolyte imbalance.
4. Brain damage is determined by the presence of neurological symptoms.

In addition to the changes described above, the patient may develop massive external or internal hemorrhages and hematomas.

Diagnosis of DIC syndrome

To determine the presence of disseminated intravascular coagulation in a patient, it is necessary to carefully collect anamnestic data and establish a diagnosis that provoked this condition. DIC syndrome requires laboratory diagnostics, which includes a coagulogram, a general blood test, and a study of blood coagulation factors. A very important point is to determine the severity of the patient in order to prescribe adequate correction.

It is necessary to take into account that the patient may bleed from several places at once. Moreover, if a chronic process has developed or it is not very aggressive, then hypercoagulation can only be detected through laboratory diagnostics.

The doctor must prescribe:

• blood test to determine platelets;
• coagulogram, which will display the amount of fibrinogen, blood clotting time, thrombin level, prothrombin level, APTT.

There are specific tests - RFMC, D-dimer. They are performed by enzyme immunoassay.

Doctors consider the main criteria for DIC syndrome to be the identification of fragmented red blood cells, an insufficient number of platelets, and a decrease in fibrinogen concentration. Also noted low activity antithrombin-III, increased duration of aPTT and thrombin time. Weak clot formation or instability indirectly indicate a violation of hemostasis.

The doctor is obliged to check the functional performance of the organs that are first exposed to shock - the kidneys, liver, lungs.

Chronic DIC syndrome

The main characteristics of chronic DIC are:

1. Constantly increased entry into the systemic bloodstream of substances that act as activators of the hemostasis system.
2. Increased rate of fibrin formation inside blood vessels.
3. Decreased platelet consumption.
4. There is no secondary activation of fibrinolysis, as well as generalized intravascular fibrinolysis.
5. Fibrin blocks the microcirculation of parenchymal organs, causing their severe dysfunction.

The acute process is activated by thromboplastin, which enters the blood from tissues that have undergone decay due to various triggering factors. These could be injuries, burns, surgical manipulations on target organs, destructive processes, obstetric diseases. Much less often, phospholipids of the endothelium of the vascular wall or blood cells become triggers of DIC syndrome. This mechanism is more typical for bacterial processes and shock conditions. Chronic disseminated intravascular coagulation is caused by less aggression of the above activation factors, which contributes to its slow onset and a better prognosis for the patient’s life.

Treatment

Successful treatment of DIC syndrome is only possible if the condition is diagnosed in the early stages of its development. Active actions medical personnel necessary for severe manifestations - bleeding, development of multiple organ failure. Emergency care for DIC is provided in an intensive care unit. The chronic process requires hemodynamic correction, electrolyte disturbances, symptomatic therapy.

In acute cases, it is necessary to quickly determine the cause and then eliminate it. This could be an emergency delivery, the appointment of powerful antibacterial drugs. Hypercoagulation is corrected with fibrinolytics, anticoagulants, and antiplatelet agents. Patients with such pathologies are under constant supervision medical workers, they monitor the hemostatic system every 15-30 minutes.

DIC syndrome- a severe catastrophe of the body, putting it on the brink between life and death, characterized by severe phase disturbances in the hemostasis system, thrombosis and hemorrhages, impaired microcirculation and severe metabolic disorders in organs with severe dysfunction, proteolysis, intoxication, development or deepening of shock.

ETIOPATHOGENESIS and CLINICAL PICTURE

DIC syndrome develops in many diseases and in almost all terminal states as a result of the appearance of tissue thromboplastin in the bloodstream. DIC syndrome is nonspecific and universal, therefore, it is currently considered as a general biological process intended by nature both to stop bleeding when the integrity of the vessel is violated, and to delimit the affected tissues from the entire body.

Microthrombosis and blockade of microcirculation may develop:
throughout the entire circulatory system with a predominance of the process in target organs (or shock organs) - lungs, kidneys, liver, brain, stomach and intestines, adrenal glands, etc.
in individual organs and parts of the body(regional forms).

The process may be:
acute (often lightning fast)- accompanies severe infectious and septic diseases (including during abortion, during childbirth, in newborns, all types of shock, destructive processes in organs, severe injuries and traumatic surgical interventions, acute intravascular hemolysis (including incompatible blood transfusions), obstetric pathologies (previa and early abruption of the placenta, embolism with amniotic fluid, especially infected, manual release placenta, hypotonic bleeding, massage of the uterus during its atony), massive blood transfusions (the danger increases when using blood for more than 5 days of storage), acute poisoning (acids, alkalis, snake venoms etc.), sometimes acute allergic reactions and all terminal conditions;
subacute - observed with a milder course of all the above diseases, as well as with late toxicosis of pregnancy, intrauterine death fetus, leukemia, immune complex diseases (subacute forms hemorrhagic vasculitis), hemolytic-uremic syndrome (acute DIC syndrome may also occur);
chronic - often complicates malignant neoplasms, chronic leukemia, all forms of blood thickening (erythremia, erythrocytosis), hyperthrombocytosis, chronic cardiac and pulmonary heart failure, chroniosepsis, vasculitis, giant hemangiomas (Kasabach-Merritt syndrome), massive contact of blood (especially repeated) with a foreign surface (hemodialysis with chronic renal failure, use of extracorporeal circulation devices);
recurrent with periods of exacerbation and subsidence.

Depending on the initial mechanism of hemostasis activation, the following forms of DIC syndrome can be distinguished::
with predominant activation of the procoagulant component of hemostasis due to tissue thromboplastin entering the bloodstream from outside, causing blood clotting via an external mechanism ( obstetric complications, crash syndrome, etc.);
with predominant activity of vascular-platelet hemostasis as a result of generalized damage vascular endothelium and/or primary activation of platelets (systemic lupus erythematosus, systemic vasculitis, allergic reactions, infections);
with the same activity of procoagulant and vascular-platelet hemostasis as a result of contact and phospholipid activation of the internal coagulation mechanism through factor XII and phospholipids cell membranes(extracorporeal circulation, prosthetics of blood vessels and heart valves, intravascular hemolysis, acute transplant rejection).

The aggregation of blood cells (sludge syndrome) in the microcirculation zone, leading to its disruption, is of great importance in the development of DIC syndrome. At the same time, the release of substances with procoagulant activity from cells aggravates the activation of the hemostatic system, contributes to the development of multiple microthrombosis and the progression of DIC syndrome. This mechanism plays a significant role in all types of shock, including hypovolemic shock, which in some cases complicates nephrotic syndrome with a critically low level of blood albumin (below 15 g/l), diseases occurring with erythrocytosis and thrombocytosis.

Stages of DIC syndrome (M.S. Machabeli):
Stage I – hypercoagulation stage - generalized activation of the process of coagulation and cell aggregation (in the chronic course of the process, it persists for a long time due to the compensatory mechanisms of the anticoagulant system, the failure of the latter causes its transition to the second stage);
Stage II – increasing consumptive coagulopathy - there is a decrease in the number of platelets and fibrinogen due to their loss (consumption) for the formation of blood clots, consumption of plasma coagulation factors;
Stage III – stage of severe hypocoagulation - formation of soluble fibrin-monomer complexes that are resistant to thrombin occurs; The pathogenesis of this stage is associated with several factors:
- consumption coagulopathy,
- activation of fibrinolysis (during which fibrin degradation products are formed, which have anticoagulant and antiplatelet properties);
- blocking the polymerization of fibrin monomers formed under conditions of excess thrombin in the circulation, and fibrinogen by accumulating fibrin degradation products;
IV stage - reverse development DIC syndrome.

!!! in acute DIC, the first short-term phase is often visible; To identify it, you should pay attention to slight thrombosis of punctured veins and needles when taking blood for tests, very rapid blood clotting in test tubes (despite mixing it with citrate), the appearance of unmotivated thrombosis and signs of organ failure (for example, decreased diuresis due to impaired microcirculation in kidneys as an early sign of developing renal failure)

!!! Stage III of DIC syndrome is critical; it is the stage that often ends in death even with intensive therapy that corrects the hemostatic system

Schematically, the pathogenesis of DIC syndrome can be represented by the following sequence pathological disorders: activation of the hemostasis system with alternating phases of hyper- and hypocoagulation - intravascular coagulation, aggregation of platelets and erythrocytes - microthrombi of blood vessels and blockade of microcirculation in organs with their dysfunction and dystrophy - depletion of components of the blood coagulation system and fibrinolysis, physiological anticoagulants (antithrombin III, proteins C and S), a decrease in platelet levels in the blood (consumptive thrombocytopenia). The toxic effect of protein breakdown products, which accumulate in large quantities both in the blood and in the organs as a result of a sharp activation of proteolytic systems (coagulation, kallikreinin, fibrinolytic, complement, etc.), impaired blood supply, hypoxia and necrotic changes in tissues, has a significant effect. frequent weakening detoxification and excretory functions of the liver and kidneys.

Clinical picture of DIC syndrome varies from oligosymptomatic and even asymptomatic forms with a latent course of the process to clinically manifest ones, manifested by a clear multi-organ pathology. Clinical polymorphism DIC symptoms-syndrome is caused by ischemic (thrombotic) and hemorrhagic damage, primarily to organs that have a well-defined microcirculatory network (lungs, kidneys, adrenal glands, liver, gastrointestinal tract, skin), the blockade of which due to generalized thrombus formation leads to their dysfunction. In this case, the symptoms of DIC syndrome are superimposed on the symptoms of the underlying disease that caused this complication.

Complications of DIC syndrome:
blockade of microcirculation in organs, leads to disruption of their functions (the most common target organs are the lungs and (or) kidneys due to the characteristics of microcirculation in them) in the form of acute pulmonary failure and acute renal failure; possible development of liver necrosis; the presence of thrombosis of small vessels in gastrointestinal tract can lead to the development of acute ulcers, mesenteric thrombosis with the development of intestinal infarction, the presence of thrombosis of small vessels in the brain can cause the development of ischemic stroke; due to thrombosis of adrenal vessels, acute adrenal insufficiency may develop
hemocoagulative shock is the most severe complication of DIC and is associated with a poor prognosis;
hemorrhagic syndrome- characterized by hemorrhages in the skin and mucous membranes, nasal, uterine, gastrointestinal bleeding, less often - renal and pulmonary bleeding;
posthemorrhagic anemia(almost always aggravated by the addition of a hemolytic component, unless DIC syndrome develops in diseases characteristic feature which is intravascular hemolysis);

!!! characteristic of acute disseminated intravascular coagulation syndrome is a combined lesion of two or more organs

DIAGNOSTICS

Early diagnosis DIC syndrome is situational in nature and is based on identifying diseases and conditions in which DIC syndrome develops naturally. In all these cases, it is necessary to start early preventive therapy until pronounced clinical and laboratory signs of DIC syndrome appear.

Diagnosis should be based on the following measures:
critical analysis clinics;
a thorough examination of the hemostatic system to determine the form and stage of the syndrome;
assessing the response of hemostasis to therapy with antithrombotic drugs.

Laboratory manifestations of DIC syndrome include:
thrombocytopenia;
red blood cell fragmentation(schizocytosis) due to their damage by fibrin threads;
prolongation of PT (prothrombin time; serves as an indicator of the state of the external coagulation mechanism), APTT (activated partial thromboplastin time; reflects the activity of the internal coagulation mechanism and the level of factor XII, factor XI, factor IX, factor VIII, high molecular weight kininogen and prekallikrein) and thrombin time;
decreased fibrinogen levels as a result of consumption of clotting factors;
level up fibrin degradation products(PDF) due to intense secondary fibrinolysis (for the latter, the immunological determination of D-dimers, reflecting the breakdown of stabilized fibrin, is most specific).

The tendency to bleed is most correlated with a decrease in fibrinogen levels.

PRINCIPLES OF THERAPY OF DIC SYNDROME

Due to the pronounced heterogeneity of the causes leading to the development of DIC, it is not possible to give comprehensive recommendations for its treatment for each specific case.

When treating DIC syndrome, it is necessary to adhere to following principles :
complexity;
pathogeneticity;
differentiation depending on the stage of the process.

!!! The purpose of therapeutic measures is to stop intravascular thrombus formation

First of all, the doctor’s actions should be aimed at elimination or active therapy of the main cause of DIC syndrome. These should include measures such as the use of antibiotics (broad-spectrum with the inclusion of targeted immunoglobulins), cytostatics; active antishock therapy, normalization of bcc; delivery, hysterectomy, etc. Without early successful etiotropic therapy, one cannot count on saving the patient’s life. Patients need urgent referral or transfer to the intensive care unit, and the mandatory involvement of transfusiologists and specialists in the pathology of the hemostatic system in the treatment process.

Infusion-transfusion therapy for DIC syndrome. High effectiveness of treatment is achieved by early use of jet transfusions of fresh frozen plasma (up to 800–1600 ml/day in 2–4 doses). The initial dose is 600–800 ml, then 300–400 ml every 3–6 hours. Such transfusions are indicated at all stages of DIC because they: compensate for the deficiency of all components of the coagulation and anticoagulation systems, including antithrombin III and proteins C and S (the decrease in the content of which in DIC syndrome is especially intense - several times faster than all procoagulants); allow it to enter the bloodstream full set natural antiproteases and factors that restore the antiaggregation activity of the blood and thromboresistance of the endothelium. Before each transfusion of fresh frozen plasma, 5,000–10,000 units of heparin are administered intravenously to activate the antithrombin III administered with the plasma. This also prevents plasma clotting by circulating thrombin. In DIC syndrome of an infectious-toxic nature and the development of pulmonary distress syndrome, plasmacytapheresis is indicated, since leukocytes play a significant role in the pathogenesis of these forms, some of which begin to produce tissue thromboplastin (mononuclear cells), and others - esterases that cause interstitial pulmonary edema (neutrophils) . Methods of plasma therapy and plasma exchange increase the effectiveness of treatment of DIC and the diseases that cause it, reduce mortality several times, which allows them to be considered one of the main methods of treating patients with this disorder of hemostasis.

With significant anemia and decreased hematocrit it is necessary to carry out transfusions of fresh canned blood (daily or up to 3 days of storage), red blood cells. The requirement for transfusion of fresh hemopreparations is due to the fact that microclots form in canned blood for more than 3 days of storage, the entry of which into the blood only leads to potentiation of DIC syndrome. Hematocrit must be maintained at least 22%, hemoglobin level - more than 80 g/l, red blood cells - 2.5 x 1012 / l and above). Rapid and complete normalization of red blood counts should not be an end in itself, because moderate hemodilution helps restore normal microcirculation in the organs. We must not forget that excessively abundant blood transfusions lead to aggravation of disseminated intravascular coagulation syndrome, and therefore caution is necessary when carrying out infusion-transfusion therapy - the amount of blood transfused must be strictly taken into account, as well as blood loss, loss of body fluid, and diuresis. It should be remembered that acute DIC is easily complicated by pulmonary edema, so significant circulatory overload of the cardiovascular system is highly undesirable. Excessive intensity of infusion-transfusion therapy can not only complicate the treatment of DIC syndrome, but also lead to its irreversibility.

In stage III of DIC syndrome and with pronounced proteolysis in tissues(lung gangrene, necrotizing pancreatitis, acute liver dystrophy, etc.) plasmapheresis and jet transfusions of fresh frozen plasma are indicated (under the cover of small doses of heparin - 2,500 units per infusion) combined with repeated intravenous administration large doses of contrical (up to 300,000–500,000 units or more) or other antiproteases.

In the later stages of development of DIC syndrome and its varieties occurring against the background of bone marrow hypoplasia and dysplasia (radiation, cytotoxic diseases, leukemia, aplastic anemia), to stop bleeding it is necessary to carry out transfusions of erythrocyte concentrates or erythrocyte mass and platelet concentrates (4– 6 doses per day).

Use of heparin in the treatment of DIC syndrome justified at any stage due to the fact that it counteracts the development of intravascular thrombus formation. Heparin has antithromboplastin and antithrombin effects, inhibits the transition of fibrinogen to fibrin, reduces the aggregation of erythrocytes and, to a lesser extent, platelets. The main method of administering heparin is intravenous drip (in isotonic solution sodium chloride, with plasma, etc.). In some cases it can be supplemented subcutaneous injections into the anterior tissue abdominal wall below the umbilical line. Intramuscular injections are not recommended due to the different rates of resorption of the drug (which makes dosing difficult), and the easy formation of large, infectious hematomas in conditions of DIC syndrome. The tactics of heparin therapy depend on the course of DIC and the presence or absence of a wound surface in the patient. Thus, in the acute course of the syndrome, you can get by with a single use of a minimal dose of heparin. This may be enough to break vicious circle: intravascular coagulation - bleeding. In subacute DIC, on the contrary, repeated administration of heparin is required. The presence of a fresh wound in a patient requires great caution when prescribing heparin therapy or refusing it altogether. The dose of heparin varies depending on the form and phase of DIC syndrome: in stage I (hypercoagulation) and at the beginning of the initial period (with blood clotting still sufficiently preserved), heparin has preventive value and him daily dose in the absence of heavy initial bleeding, it can reach up to 40,000–60,000 units (500–800 units/kg). An initial dose of 5,000–10,000 units is administered intravenously as a bolus, and then switched to drip administration. In stage II of DIC, heparin has a therapeutic value: it neutralizes the effect of tissue thromboplastin that continues to enter the bloodstream and the formation of thrombin from it. If the onset of DIC is accompanied by profuse bleeding (uterine, from an ulcer or disintegrating tumor, etc.) or there is high risk its occurrence (for example, in early postoperative period) the daily dose of heparin should be reduced by 2–3 times, or its use should be discontinued altogether. In such situations, as in the phase of deep hypocoagulation (stage III of DIC), heparin is used mainly to cover plasma and blood transfusions (for example, at the beginning of each transfusion, 2,500–5,000 units of heparin are administered dropwise along with a hemotherapy). If there are “acute phase” proteins in the patient’s blood (for example, in acute infectious and septic processes, massive tissue destruction, burns), the dose of heparin should be maximum, because in this case heparin is inactivated, which prevents its anticoagulant effect. The insufficient effect of heparin may be associated with a blockade and decrease in the content of its plasma cofactor, antithrombin III, in the patient’s plasma.

An important link complex therapy DIC syndrome is the use of antiplatelet agents and drugs that improve blood microcirculation in organs (curantil, dipyridamole in combination with trental; dopamine - for renal failure, a-blockers - sermion, ticlopedine, defibrotide, etc.).

An important component of therapy– early connection artificial ventilation lungs.

Removing the patient from shock The use of anti-opioid drugs (naloxone, etc.) contributes to this.

The basis of therapy for subacute forms of DIC syndrome lies the treatment of the underlying disease that led to the development of the syndrome. Along with this, drip intravenous or subcutaneous injections of heparin (daily dose from 20,000 to 60,000 units), antiplatelet agents (dipyridamole, trental, etc.) are added. Rapid relief or weakening of the process is often achieved only by performing plasmapheresis (removal of 600–1200 ml of plasma daily) with partial replacement with fresh, native or fresh frozen plasma, and partially with blood replacement solutions and albumin. The procedure is carried out under the cover of small doses of heparin.

The chronic form of DIC is treated in the same way.. If the patient has polyglobulia and blood thickening, he is indicated for blood exfusion, leeching, cytapheresis (removal of red blood cells, platelets and their aggregates), hemodilution (reopolyglucin intravenously up to 500 ml daily or every other day). For hyperthrombocytosis - disaggregants (acetylsalicylic acid 0.3–0.5 g daily, trental, etc.).

DIC syndrome often has a latent, chronic course during pregnancy, and during childbirth and postpartum period its implementation and manifestation occur. Chronic syndrome accompanies a number of diseases of internal organs and complications of pregnancy (such as cardiovascular diseases, anemia, kidney disease, diabetes, chronic infections, gestosis in the second half of pregnancy, threat of miscarriage, etc.).

Symptoms and stages of development of DIC syndrome

Thrombotic phenomena. The occurrence of thrombosis in vessels, primarily damaged by the underlying pathological process. First of all, I would like to note the most common thrombosis of the mesenteric arteries, which subsequently leads to necrosis of intestinal loops.

Hemorrhagic phenomena are not always a manifestation of this syndrome. There are widespread hemorrhagic syndrome (pronounced both internal and external bleeding) and local bleeding. Symptoms of the disease are manifested by spontaneous bruises and bruises around the injection sites, hemorrhages in the subcutaneous and retroperitoneal tissue, nasal, gastrointestinal, pulmonary bleeding, as well as hemorrhages in various organs (brain, heart, adrenal glands, etc.). Local bleeding includes bleeding from wounds caused by injuries or surgical interventions.

Impaired microcirculation in the vessels of various organs as a symptom of DIC syndrome. These disorders occur due to the formation of microthrombi in the bloodstream and the sedimentation of these clots in small blood vessels of tissues and organs. The organs most dependent on the timely supply of oxygen are the lungs, kidneys, liver, stomach and intestines. As a result of insufficient oxygen supply, the function of these organs suffers, and zones of necrosis appear in them. Muscles and skin are the least susceptible to microcirculatory disorders.

Anemic manifestations of the disease are often characteristic - a decrease in the number of red blood cells and hemoglobin. This condition occurs due to intravascular destruction of red blood cells and bleeding.

Stages of DIC syndrome

The following stages of the disease are distinguished:

lightning fast,

I'll make it more acute

and chronic.

The presence of a particular syndrome and its severity vary significantly at different stages of DIC syndrome. With each form of DIC, one or another manifestation prevails. For example, during the fulminant stage of this syndrome, severe bleeding prevails. Only after they have been successfully stopped (which cannot always be achieved) are pronounced microcirculatory disorders, accompanied by acute renal, hepatic, pulmonary insufficiency, ulceration of the gastrointestinal mucosa.

Acute stage of DIC syndrome develops with sepsis, massive blood transfusions, premature abruption of a normally located placenta, severe forms gestosis and other reasons not related to obstetric pathology. In the acute stages of DIC, bleeding also prevails in the clinic, but its severity is not so significant. Acute forms are manifested initially by nosebleeds, gum bleeding, bleeding from injection sites, and later gastrointestinal bleeding appears. In acute forms, a pronounced anemic syndrome and impaired tissue repair are also observed.

Subacute stage of the syndrome can be observed in all of the above conditions, the severity of which is less pronounced, as well as in other diseases of a woman’s internal organs (systemic lupus erythematosus, subacute glomerulonephritis and many others). In turn, subacute forms occur with significantly less pronounced clinical manifestations.

Chronic course of DIC syndrome found in clinical practice more often. Its course is asymptomatic for a long time and does not manifest itself hemorrhagic syndrome(small or large hemorrhages on the skin) or thrombosis. However, with the progression of the disease, which was the root cause of the development of DIC, the symptoms of DIC become more pronounced. The following diseases can lead to the chronic course of DIC syndrome: long-term gestosis in the second half of pregnancy, heart failure, chronic glomerulonephritis, chronic renal failure, ischemic disease hearts, etc.

Symptoms of the fulminant stage of DIC syndrome

Fulminant stage of DIC syndrome develops due to amniotic fluid embolism. Vascular embolism with amniotic fluid is a fairly rare situation. But there are also severe embolisms, characterized by blockage of the pulmonary artery.

The cause of amniotic fluid embolism is damage to the vessels of the placenta, body and cervix and, as a consequence, the penetration of amniotic fluid into these vessels. Then a complex cascade of pathological processes is launched, which determines the pathophysiology and clinical picture of the type of DIC syndrome. Symptoms of the development of amniotic embolism are varied. Firstly, embolism can be lightning fast and acute, which is most often observed. Secondly, the obstetric pathology that provoked the embolism or accompanies it is important.

A typical picture of the fulminant stage of DIC and amniotic fluid embolism begins with sudden deterioration the state of a woman in labor or postpartum, sometimes it even seems that this is happening against the background of complete well-being. The woman complains of a feeling of suffocation, shortness of breath, coughing, intense pain in the chest, weakness, and a feeling of fear of death.

The patient's condition in the fulminant stage of DIC syndrome is deteriorating alarmingly every minute; sometimes a woman does not have time to say what is bothering her before loss of consciousness occurs, severe cyanosis of the face (cyanosis), and a pronounced increase in heart rate. With slower development, which is associated with the rate of entry of amniotic fluid into the vascular bed and the state of the maternal body at the time of the disaster, other symptoms appear due to the development of a type of disseminated intravascular coagulation syndrome.

Forms of DIC syndrome

There are also four forms of the disease:

blood hypercoagulation;

blood hypocoagulation without generalized fibrinolysis activity;

blood hypocoagulation;

complete non-coagulation of blood.

Diagnosis of DIC syndrome

Diagnosis of DIC syndrome is often difficult because clinical symptoms are not strictly specific to of this disease. The chronic form of DIC syndrome, due to the absence of any symptoms at all for a long time, is determined after a long period of time.

In a laboratory blood test, the acute form of DIC syndrome is characterized by:

prolongation of blood clotting time (more than 10 minutes),

drop in platelet count and fibrinogen level,

the time of plasma recalcification, prothrombin and thrombin time increases,

the concentration of fibrin dehydration products and soluble complexes of fibrin/fibrinogen monomers increases.

Diagnostic methods DIC syndrome

Currently, it is possible to establish the stage of DIC using a test. Thanks to it, blood clotting time, spontaneous clot lysis, thrombin test, PDF (ethanol test and immunoprecipitation), platelet count, thrombin time, erythrocyte fragmentation test are assessed. Diagnostic results are assessed as follows:

The first stage is characterized by a shortening of blood clotting time and thrombin time, and a positive ethanol test.

In the second stage of DIC, there is a moderate decrease in the number of platelets, an extension of the thrombin time to 60 s or more, and PDF and damaged erythrocytes are detected.

The third stage is characterized by prolongation of blood clotting time, test thrombin and thrombin time, the number of platelets decreases, and rapid lysis of the formed blood clot occurs.

And in the fourth stage, a clot does not form, the thrombin test takes more than 60 seconds, and the number of platelets decreases even more.

Features of the treatment of DIC syndrome

Therapy of the disease comes down to reducing the blood coagulation system, i.e. reducing the amount of blood clotting activators, and removing pathological products formed during blood coagulation. At the same time, a complex of necessary therapy is certainly carried out to treat the underlying disease or complications of pregnancy that caused the development of DIC syndrome. Integral components of the treatment of DIC syndrome are the effects on various parts of its pathological manifestations:

dealing with shock

elimination of septic infection,

improvement of microcirculation,

restoration of circulating blood volume,

elimination of influences that may maintain or aggravate DIC syndrome.

Infusion-transfusion therapy for DIC syndrome

When bleeding develops, replenishment of circulating blood volume is paramount. Because of acute form DIC syndrome is often combined with hemorrhagic shock, this pathology First of all, it needs restoration of central and peripheral hemodynamics. For infusion-transfusion treatment of DIC syndrome in such cases, preference is given to erythromass and plasma. Gelatinol, albumins, Hemofusin and crystalloids (Ringer's solution, sodium lactate, lactosol) are also administered.

It should be noted that the main difficulty of this type of treatment for DIC lies in ways to normalize the coagulation properties of the blood, for which it is necessary to stop the process of intravascular coagulation, reduce fibrinolytic activity and restore the coagulation potential of the blood. This problem should be solved by a hematologist together with an obstetrician-gynecologist under the control of a coagulogram.

In order to inhibit the utilization of fibrinogen as the initial link in the development of thrombohemorrhagic syndrome, Heparin is used in the treatment of DIC syndrome. The dose of Heparin is determined by the stage of DIC syndrome: in the first stage, 50 IU/kg is administered, in the second stage up to 30 IU/kg, and in the third and fourth stages of the disease, Heparin is strictly prohibited, as well as in the presence of an extensive wound surface. In turn, if an overdose of Heparin occurs, Protamine sulfate is used; 100 units of heparin neutralizes 0.1 ml of 1% solution of protamine sulfate.

Inhibition of fibrinolytic activity in the treatment of DIC syndrome is also carried out with the help of Contrical, Trasylol, Gordox. It is not recommended to use intravenously synthetic proteolysis inhibitors (Epsilon-aminocaproic acid), because they cause changes in the microcirculation system and lead to severe circulatory disorders in the kidneys, liver and brain. The use of these drugs in the treatment of DIC syndrome is possible only locally.

It should be noted that fibrinolysis inhibitors are used only when indicated, since a sharp decline fibrinolytic activity can lead to increased intravascular fibrin deposition with subsequent necrosis of tissue of the kidneys, liver and other organs. The best effect is observed from the administration of these drugs in the third and fourth phases of DIC syndrome.

Treatment of chronic DIC syndrome in pregnant women

Treatment of chronic disease in pregnant women with preeclampsia or other somatic diseases includes the use of low-molecular blood substitutes (Reopoliglyukin, Hemodez, Polideza) in combination with antispasmodic therapy. Therapy is aimed at improving the rheological properties of blood, preventing microthrombosis and helping to optimize tissue perfusion.

With this form of DIC syndrome good effect is also achieved after the use of Heparin or low molecular weight Fraxiparine. Heparin is administered subcutaneously at 5,000–10,000 units every 12 hours until the platelet count and fibrinogen level normalize. Since Heparin is an anticoagulant direct action, it reduces platelet adhesion and has antithromboplastin activity. The latter helps to normalize blood circulation in the parenchymal organs and the uteroplacental complex.

Causes of DIC syndrome and its prevention

The onset of the disease is associated with the activation of blood and tissue thromboplastin due to hypoxia and metabolic acidosis of any origin (injury, toxins entering the blood, etc.). From this moment, the first and longest phase of hemostasis begins, in which many blood coagulation factors take part.

The next phase of DIC syndrome is thrombin formation, followed by fibrin formation. It should be noted that, in addition to changes in the procoagulant component of hemostasis, activation of the platelet component occurs, leading to adhesion and aggregation of platelets with biological release active substances: kinins, prostaglandins, histamine, catecholamines and many others. Subsequently, a change in vascular permeability occurs under the influence of these substances. This leads to vascular spasm, opening of arteriovenous shunts, slowing down blood flow in the microcirculation system, which contributes to blood stasis, the development of sludge syndrome, deposition and redistribution of blood, and ultimately the formation of blood clots.

Because of this, with the symptoms of DIC syndrome, a disruption of the blood supply to tissues and organs occurs, including vital ones: the liver, kidneys, lungs and some parts of the brain. In turn, the body develops response protective mechanisms to normalize hemodynamics and microcirculation in organs and tissues. The result of this is that, against the background of disseminated intravascular coagulation, increased bleeding develops and thrombohemorrhagic syndrome is formed.

Causes of acute DIC syndrome

Lead to the occurrence of acute disseminated intravascular coagulation syndrome following states

embolism (blockage) of arterial vessels with amniotic fluid,

uterine rupture,

massive hypotonic bleeding,

state of shock.

The most important condition, allowing you to avoid the development of DIC syndrome in advance is the correct and full treatment underlying disease, less traumatic operation caesarean section, combating the onset of shock and microcirculation disorders.

DIC syndrome is a disease affecting the blood, its qualitative and quantitative composition. Since blood is a natural fluid of the body, and only thanks to it is the normal functioning of organs and systems of the whole body, this pathology has a very unpleasant consequences for humans, even to the point of death.

DIC syndrome, or (thrombohemorrhagic syndrome) is a significant increase in blood clotting, which leads to the formation of blood clots in the capillaries, and subsequently in other blood vessels. Naturally, such changes lead to serious disruption of blood flow. The blood formula changes, the number of platelets decreases, and the blood’s ability to naturally clot is lost. In fact, the normal functioning of the human body is blocked.

DIC syndrome is a disease affecting the blood, its qualitative and quantitative composition

Why does DIC occur?

The causes of disseminated intravascular coagulation syndrome are quite extensive, let's consider the most common of them:

• Blood transfusion. The group and Rh affiliation are not always correctly established, therefore, with such procedures, if the recipient receives blood that is not his group or with a different Rh, such manifestations are possible.
• Pregnancy and childbirth. With these conditions, women may experience various deviations from the norm at any stage of pregnancy. In this case, the body of the mother and fetus suffers. The same applies to gynecological operations, forced termination of pregnancy or spontaneous miscarriages. The survival rate for DIC syndrome caused by these factors is very low.
• Any surgical interventions. The body is very weakened after such effects, so one of the complications during operations may be disseminated intravascular coagulation syndrome.
• Shock states of different nature: from anaphylactic shock caused by an allergic reaction to any substance to nervous breakdown caused by shock due to some tragic event.
• Blood poisoning (sepsis) and severe infections (AIDS, HIV). The diseases are severe in themselves, so DIC will be a peculiar reaction of the body.
• Inflammatory processes in the digestive tract and urinary system.
• Various malignant and benign neoplasms.
• Organ transplantation.

There are quite a large number of factors that provoke this pathology. These are just the most common ones.

Any surgical intervention can cause this disease

Symptoms of DIC syndrome

Let's find out what external signs suggest the presence of such a disease. You need to understand that this depends on the pathology that caused such a reaction in the body, the general condition of the patient, and the stage of development of the syndrome. The clinic of DIC syndrome is a combination pathological process from the blood (formation of blood clots, bleeding disorders, bleeding), organs, systems of the whole body. Consider these symptoms depending on severity:

• Acute internal combustion engine. With this course of the disease, there is a massive appearance of foci of hemorrhage, pathological bleeding from internal organs, and accordingly, sharp drop blood pressure, deterioration of cardiac activity and respiratory depression. The prognosis for this type of DIC syndrome is very sad. In most cases, the process ends in death.
• Moderate pathology. Sluggish DIC syndrome is identified by small bruises on the skin for no apparent reason. Unusual discharge such as tears or saliva may appear Pink colour. The blood mixes with the lymph and comes out. Unusual allergic reactions appear: diathesis, urticaria and other rashes on the skin, its folds and mucous membranes. Swelling of the internal organs is possible. The skin is usually pale.
• Chronic internal combustion engine. This stage of the disease manifests itself in the presence hemorrhagic diathesis, vegetative asthenic syndrome, general weakness, lethargy, impaired recovery rate skin, suppuration of small wounds and abrasions.

Diagnosis of DIC syndrome

Since this syndrome is a disease affecting circulatory system, then diagnosis is impossible without several special blood tests. The patient is prescribed general and biochemical analysis blood. The doctor needs to identify the degree of blood clotting disorder, its thickness, viscosity, and tendency to form blood clots.

Blood clotting test

Mandatory diagnostic items are:

• screening;
• blood clotting marker tests;
• identification of prothrombin index indicators.

A hematologist evaluates the frequency and amount of bleeding. With this pathology, they are observed from several organs. Blood loss from the intestines, nose, and genitals is often diagnosed.

In addition to laboratory diagnostics, when clarifying the diagnosis, it also becomes clear general state person. It is important for the doctor to know how the patient’s organs and systems (heart, lungs, liver) function.

Treatment

After clarification of the diagnosis, treatment of thrombohemorrhagic syndrome begins. Scheme therapeutic actions directly depends on the stage of the process and the reasons that caused it. At acute pathology the patient is hospitalized and undergoes active treatment. With timely assistance, recovery occurs in most cases.

Active anti-shock measures are carried out, drugs are introduced that improve blood composition - Heparin, Dipyridamole, Pentoxifylline. Patients are treated with constant monitoring of laboratory studies of the effectiveness of drug administration. If necessary, one medicine is replaced with another.

Heparin-Biolic solution for injection, 5000 units/ml in 5 ml bottles

The following is administered intravenously to the patient:

• donated blood plasma;
• "Cryoprecipitate";
• "Sodium chloride" (saline solution);
• “Glucose” solution at a concentration of 5 or 10%;
• "Aminocaproic acid";
• donor blood.

If necessary, procedures such as plasmapheresis, oxygen treatment, hormone therapy. In addition, it is necessary to carry out therapeutic measures to restore the functioning of the brain, heart, blood vessels.

Patients often ask: “Is it worth treating sudden, sluggish DIC during pregnancy? Is it dangerous for the mother and baby?” Therapy for this pathology is mandatory, because this is the only way to preserve the life and health of the woman and the fetus.

First aid for DIC syndrome

To help a patient with such a pathology before entering the hospital, it is necessary, first of all, to eliminate the causes of this process, of course, if this is possible. It is necessary to make every effort to stop bleeding and normalize the body’s main indicators - breathing, cardiac activity, blood pressure.

Emergency personnel administer alpha-blockers (Phenolamine) and other drugs to restore blood volume (Reopoliglucin) intravenously to the patient.

The disease is quite serious, so therapy must be carried out immediately. Treatment of pathology is carried out only in a hospital setting.

To diagnose DIC syndrome there is no one simple test; it is necessary to use a complex laboratory methods to identify this pathology. Diagnosis of disseminated intravascular coagulation syndrome should be urgent, informative, based on a system of simple and easily performed tests. In addition, the diagnostic value of the techniques used is determined by regular monitoring.

I. The first group of diagnostic tests is based on detection of destruction, consumption and aggregation of blood cells— platelets and erythrocytes:

• progressive decrease in the number of platelets in peripheral blood;
• a simultaneous increase in the plasma content of platelet factor 4 (antiheparin factor), which indicates the intravascular aggregation of these cells and the intensive release of dense granule components from them;
• intensive destruction of erythrocytes in the microcirculation zone leads to an increase in indirect bilirubin, and in blood smears to the appearance of fragments of destroyed, divided into parts erythrocytes;
• increased spontaneous platelet aggregation.

II. Determination of fibrin-monomer complexes(paracoagulation products):

• ethanol test;
• protamine sulfate test (with DIC syndrome, the test is less likely to give positive result than ethanol, but is often determined to be positive when the latter becomes negative);
• determination of fibrinogen B. The method is based on the precipitation of fibrinogen B alcohol solution beta-naphthol. This test is less specific than the ethanol test, since beta-naphthol precipitates not only blocked fibrin-monomer complexes, but also other proteins not related to the blood coagulation system;
• determination of fibrinogen degradation products (FDP). Normally, 0.05 g/l of PDF is released in plasma. With disseminated intravascular coagulation and massive thrombosis, accompanied by activation of fibrinolysis, the level of PDP rises significantly;
• The most specific test is currently considered to be the detection of D-dimers.

III. Change (shortening or lengthening) of general chronometric coagulation tests:

• Lee-White total clotting time;
• Autocoagulation test;
• Activated partial thromboplastin time;
• Prothrombin time;
• Thrombin time.

IV. Increase or decrease in fibrinogen concentration.

V. Inhibition or activation of the fibrinolytic system:

• XIIa-dependent fibrinolysis;
• Spontaneous fibrinolysis;
• Content of plasminogen, its activators and inhibitors.

VI. Decreased activity of antithrombin III.

If there is an appropriate clinical situation and symptoms of DIC, the detection of at least 4-5 of the above tests should be considered as confirmation of the diagnosis.

In the first phase of DIC syndrome (hypercoagulable) hypercoagulation is detected, combined with increased platelet aggregation and a decrease in their content in the peripheral blood. Hyperfibrinogenemia often appears in the first phase. PDFs may still be normal.

In the 2nd phase of DIC syndrome (normocoagulation or transitional) Some tests still reveal hypercoagulation, while others show hypo- or normocoagulation. Thus, multidirectional coagulogram indicators appear. Paracoagulation tests that appeared in phase 1 remain positive. Plasma PDP levels increase. There is severe thrombocytopenia. The aggregation function of platelets is reduced. AT-III deficiency is increasing.

In the 3rd phase (hypocoagulative) the prolongation of clotting time is determined in all tests. The concentration of fibrinogen decreases down to afibrinogenemia. Thrombocytopenia worsens and platelet function is severely impaired. Ethanol and protamine sulfate tests become negative. The content of soluble fibrin-monomer complexes and fibrinogen degradation products increases. Activation of fibrinolysis is detected (Table 1).

Table 1

Laboratory diagnostics DIC syndrome (A. A. Ragimov, L. A Alekseeva, 1999)