Criteria for DIC syndrome. Causes of acute DIC syndrome. The patient is given intravenously

The frequency of DIC syndrome in different types of pathology is heterogeneous. In some diseases and influences it occurs without fail and becomes an integral part of the pathological process, in others it occurs less frequently.
More often, DIC syndrome is caused by the following pathological processes and influences.

Generalized infections and septic conditions (bacteremia, viremia - the presence of viruses in the blood), including during abortion, childbirth, and long-term vascular catheterization. In septic shock, acute disseminated intravascular coagulation syndrome always occurs. Most cases of DIC in newborns are associated with infections.
All types of shock, such as hemorrhagic, traumatic, burn, anaphylactic (occurring from allergies), septic and cardiogenic. DIC syndrome is a mandatory accompaniment of shock of any origin. Moreover, the severity of the syndrome in question is directly proportional to the severity and duration state of shock.
Surgical interventions that are particularly traumatic for the patient (especially with malignant neoplasms, operations on parenchymal organs, the use of APCs and intravascular interventions). Bleeding, collapse, and massive blood transfusions increase the incidence of DIC.
DIC syndrome is accompanied by any terminal conditions.
DIC syndrome always develops if a patient experiences acute intravascular hemolysis (destruction of cells inside blood vessels), including incompatible transfusions (blood transfusions that are not suitable for the patient according to group affiliation).
Obstetric pathology, in particular placenta previa, premature placental abruption or manual separation, blockage of uterine vessels with amniotic fluid, intrauterine fetal death. In all of the above conditions, severe disseminated intravascular coagulation syndrome is registered in 20-35% of cases. Its manifestations are much more common when
Pathogenesis (what happens?) during DIC syndrome
There are currently a huge number of reasons that can cause the development of DIC syndrome in a patient. Despite this, the basis for the formation of disseminated intravascular coagulation syndrome is the activation of the blood coagulation system and platelet hemostasis by various factors of endogenous origin, i.e., factors formed directly in the human body. These factors primarily include: tissue thromboplastin, decay products of tissues and blood cells, fragments of damaged vascular endothelium (their inner lining). The last condition for the development of this pathology can occur in the event of exposure to an infectious agent, immune complexes, components of the complement system and other factors. In addition, the following exogenous factors (entering the human body from outside) play an important role in the mechanism of DIC syndrome, the presence of which also activates the blood coagulation system: various bacteria and viruses, rickettsia, drugs, substances used as blood substitutes, amniotic fluid, venoms of various snakes, deep violations blood circulation (including heavy blood loss), hypoxia (reduced oxygen supply) to tissues, acidosis (impaired acid-base balance in the body), microcirculation disorders, primary or secondary depression of anticoagulant mechanisms (deficiency of antithrombin III) and components of the fibrinolytic system (deficiency of plasminogen and its activators, a sharp increase in antiplasmin activity ), insufficient functional ability or generalized damage to the vascular endothelium, a decrease in its antithrombotic activity. The combined participation of several of these mechanisms is possible.
The central place in the development of disseminated intravascular coagulation syndrome is given to excessive synthesis of thrombin in the vascular bed, which leads to thrombinemia, as well as depletion of the blood anticoagulant system. The appearance of thrombin in the circulation is a necessary condition for both the transformation of fibrinogen into fibrin and the “gluing” of blood cells (platelets and erythrocytes).
In most cases of disseminated intravascular coagulation, the initiator of the pathological process is tissue thromboplastin (blood coagulation factor III). In combination with blood coagulation factor VII, it promotes the activation of factor X. Tissue thromboplastin enters the bloodstream from damaged and decaying tissues, which occurs during injuries, operations, necrosis and tissue destruction bacterial origin, during childbirth along with amniotic fluid. With the participation of activated platelets, tissue thromboplastin can also be produced by damaged vascular endothelium during immune and immune complex lesions, damage to the endothelium by toxins, and hemolysis products. From blood cells, as is known for late toxicosis of pregnancy, infection of amniotic fluid, cesarean section, heavy bleeding, intense massage of the uterus. Occasionally, DIC syndrome develops during normal childbirth.
Tumors, especially hematological malignancies, leukemia or hyperviscosity syndrome, lung cancer, liver, pancreas, prostate, kidney. In acute leukemia, DIC syndrome is different stages The disease is detected in 33-45% of patients, with acute promyelocytic leukemia - in the majority of patients.
Various diseases leading to destruction of the liver, kidneys, pancreas and other organs and their systems.
Burns of various origins, such as thermal, chemical burns esophagus and stomach, especially with severe hemolysis.
Immune and immunocomplex diseases, including systemic lupus erythematosus, rheumatism, rheumatoid arthritis with visceral lesions, Senlein-Henoch hemorrhagic vasculitis, glomerulonephritis.
Hemolytic-uremic syndrome.
Allergic reactions of medicinal and any other origin.
Heavy bleeding.
Thrombotic thrombocytopenic purpura.
Poisoning with snake venoms.
Transfusion of large volumes of blood; administration of hemo-preparations containing activated factors coagulation.
Treatment with drugs that cause platelet aggregation, increase blood clotting and reduce its anticoagulant and fibrinolytic potentials, especially when used in combination (a-adrenergic stimulants, synthetic progestins, aminocaproic acid and other fibrinolysis inhibitors).
Incorrect use of fibrinolytics and anticoagulants in doses that cause depletion of the antithrombin III reserve and the fibrinolytic system.
Treatment with defibrinating drugs - Arvin, Ancrod, defibrase, reptilase (therapeutic disseminated intravascular coagulation syndrome).
Multiple and giant angiomas (Kasabach-Merritt type).

Currently, the first place among the causes of the development of DIC (disseminated intravascular coagulation syndrome) is occupied by generalized infections, both bacterial and viral, as well as septicemia. They account for 30-40% of all cases of this pathology, and in the neonatal period - more than 70%. IN the latter case The pathology in question is called “malignant purpura of newborns.” Bacteremia is often the cause of obstetric thrombohemorrhagic syndrome. The sudden spread of infection from the genital tract, either alone or with infected amniotic fluid, forms the most severe forms of postpartum DIC. One should always think about such an infection if there is an early rupture or tear of the amniotic membrane, the appearance of unmotivated tachycardia in the woman in labor and the fetus, an increase in temperature above 38°C after the discharge of amniotic fluid, their unpleasant smell, increased content of leukocytes in amniotic fluid, increased leukocytosis in the mother’s blood. At the same time, it should be remembered that with the early development of septic shock, the woman in labor may not have an increase in temperature and leukocytosis. Early on, only macrophages (monocytes) are capable of producing tissue thromboplastin, and this process plays an important role in the mechanism of DIC syndrome in bacteremia, endotoxemia, immune and immune complex diseases and some other forms of pathology. Preliminary removal of these cells from the bloodstream in such cases prevents the development of DIC syndrome or sharply weakens it.

DIC syndrome in malignant tumors is associated with activation of coagulation by special enzymes associated with tumor cells, with contact activation of platelets by them, and with the production of tissue thromboplastin by many tumors. However, in many types of cancer, the bulk of tissue thromboplastin is also produced by monocytes. This activation process is attenuated by warfarin and enhanced by the presence of heparin.

Less commonly, DIC is associated with alternative blood clotting pathways, which are activated under the influence of intracellular and tissue enzymes, as well as enzymes produced by bacteria and included in snake venoms.

In the development of some types of disseminated intravascular coagulation syndrome, the main role does not belong to tissue thromboplastin, but to the activation of the coagulation process of a contact nature, which occurs during hemodialysis, extracorporeal circulation, and artificial heart valves.

As DIC progresses, the blood level of the main physiological anticoagulant, which is antithrombin III, decreases. This substance is used to inactivate coagulation factors. The components of the fibrinolysis system are consumed in a similar way.

Bleeding in DIC syndrome is caused by impaired blood clotting, aggregation and intense loss of the most complete platelets from the bloodstream, and blockade of the remaining platelets. Heavy bleeding in DIC syndrome is often stopped or stopped by transfusion of platelet concentrates.

The mechanism of development and severity of DIC syndrome depend on the disturbance of microcirculation in organs and the degree of their dysfunction. Constant companions of DIC syndrome are shock lung, acute renal failure and other organ disorders. Their development is associated with massive blockade of the microcirculatory bed by clots formed by blood clots, stasis of blood cells due to shifts in the rheological properties of blood and hemodynamics, and swelling of red blood cells.

Symptoms of DIC syndrome

DIC syndrome can be acute, exacerbating, protracted and hidden. With all these options, especially in acute cases, repeated transitions from thrombotic complications to hemorrhagic ones, and vice versa, are possible.

Classification

Stage I - hypercoagulation and platelet aggregation.

Stage II is transitional. At this stage, increasing coagulopathy with thrombocytopenia and multidirectional changes in general coagulation tests are noted.

Stage III - stage of deep hypocoagulation. At this stage, the blood's ability to clot may be completely lost.

Stage IV - recovery. In the case of an unfavorable course of DIC, various complications develop at this stage, leading in most cases to death.

In practice, it is more convenient to use the following most important indicators:

1) the state of the hemostatic system, which is determined by:

a) according to general coagulation tests;

d) by the level of antithrombin III;

e) according to the reserve of plasminogen and its activators;

f) to identify coagulation deficiency when recording a thromboelastogram (anomalies in the structure, fixation and mechanical properties of the clot);

g) according to the ability of the patient’s plasma to accelerate or inhibit coagulation and clot formation in the thromboelastogram of normal blood or plasma;

2) presence, severity and localization:

a) thrombosis;

b) bleeding;

3) the severity and duration of hemodynamic disorders (decrease in arterial and central venous pressure, circulating blood volume, etc.), taking into account the leading mechanisms of their origin:

a) the causative factor that caused DIC syndrome (trauma, intoxication,
anaphylaxis);

b) hemocoagulation;

c) hemorrhagic;

4) the presence and severity of respiratory failure and hypoxia, indicating their form and stage;

5) the presence and severity of damage to other target organs that suffer the most in DIC syndrome:

a) kidneys (acute renal failure);

b) liver;

d) hearts;

e) adrenal glands and pituitary gland;

f) stomach and intestines (acute ulcers, bleeding due to increased permeability of the vascular wall);

6) severity of anemia;

7) imbalance of blood electrolytes (sodium, potassium, chlorine, calcium) and acid-base balance.

The clinical picture of DIC syndrome consists of symptoms of the underlying disease that caused it, signs of developed shock (in acute forms), deep disturbances in all parts of the hemostatic system, thrombosis and bleeding, hypovolemia (decreased filling of the vascular bed) and anemia, dysfunction and dystrophic changes in organs, metabolic disorders.

The more acute the DIC syndrome, the shorter the hypercoagulation phase (increased blood clotting) and the more severe the phase of severe hypocoagulation (reduced blood clotting) and bleeding. Such acute forms are characteristic mainly of infectious-septic, obstetric, post-traumatic (crash syndrome, burns, bone fractures), surgical (traumatic operations), toxic (snake bites) and all types of shockogenic (including cardiogenic shock) DIC syndrome. The severity of DIC in such cases depends not only on the severity of the underlying pathology and the general initial state of the patient’s body, but also on the timeliness and sufficiency of first aid, the completeness of pain relief and further anesthetic care, the timeliness and maximum atraumaticity of surgical interventions, control over the hemostatic system and completeness preventing and eliminating its violations, maintaining the rheological properties of blood, combating microcirculation and general hemodynamics disorders.

The emergence and progression of DIC syndrome is facilitated by insufficiently rapid and complete recovery of the patient from shock and hypotension ( decreased tone), increased traumaticity of surgical interventions (removal of organs from adhesions by blunt means with their kneading and tearing, intense massage of the uterus after childbirth), insufficient correction of hypovolemia and non-indicated transfusions of canned blood containing a huge number of microclots and aggravating DIC syndrome, instead of plasma, albumin, rheopolyglucin and other solutions.

Acute DIC syndrome is also observed during destructive processes in organs, during destruction of the lungs of staphylococcal and other origins, acute liver dystrophy of toxic or viral origin (hepatorenal syndrome), acute necrotizing or hemorrhagic pancreatitis. These forms of pathology are very often combined with septicemia (the appearance of a pathological agent in the blood) and various forms of difficult-to-treat superinfection. With all these types of pathology, a wave-like course of DIC syndrome is possible - periods of severe hemostatic impairment are temporarily replaced by a completely satisfactory condition of the patients, after which catastrophic deterioration occurs again.

In addition to the symptoms of the underlying disease, the clinical picture of acute DIC consists of the following main components.

Hemocoagulative shock. It occurs as a result of impaired blood circulation in the microvessels of various organs, tissue hypoxia, with the formation in the blood and the entry into it from the outside of toxic products, including those formed during the process of blood coagulation (hemocoagulation) and fibrinolysis (melting of formed blood clots). It is quite difficult to follow the transformation of the shock that appeared cause of internal combustion engine-syndrome, into hemocoagulation, since they merge into a general acute breakdown of hemodynamics with a catastrophic drop in arterial and central venous pressure, microcirculation disorders in organs with the development of their acute functional failure. As a result, acute renal or hepatorenal (hepatic-renal) failure, shock lung and other complications may develop. DIC syndrome, starting with shock, is always more catastrophic than non-shock forms, and the more severe and prolonged the shock, the worse the prognosis for the patient’s life.

When bleeding occurs, hemocoagulative shock transforms into hemorrhagic shock immediately or after temporary improvement.

Disorders of hemostasis go through different phases - from hypercoagulation to more or less deep hypocoagulation up to the complete loss of the blood's ability to clot. Detecting hypercoagulation does not require much effort - it is detected already when blood is extracted from a vein: the blood immediately coagulates in a needle or in a test tube. In such cases, the laboratory receives a response that it is impossible to examine the blood coagulation system, since the sent blood has clotted. If there was no technical error when taking blood, then such an answer in itself has diagnostic value, indicating pronounced hypercoagulation.

In the second phase, some coagulation tests detect hypercoagulation, while others detect hypocoagulation. The multidirectionality of these shifts, which confuses doctors when assessing a coagulogram, is also a typical laboratory sign of DIC syndrome. There is moderate thrombocytopenia (decreased platelet count), platelet aggregation function is significantly reduced.

In the hypocoagulation phase, the thrombin time is sharply increased and other parameters of the coagulogram are disturbed to one degree or another - clots are small, loose or not formed at all. A “transfer” effect is observed: the patient’s plasma either accelerates the coagulation of normal plasma or slows it down. In the third phase, thrombocytopenia deepens, platelet function is severely impaired. When coagulated with epha poison, a large amount of blocked (soluble) fibrin is detected. Part of the soluble fibrin is coagulated by strong thrombin (causing coagulation of normal plasma in 3-4 s).

True afibrinogenemia (lack of fibrin in the blood plasma) almost never occurs in DIC syndrome, but there is more or less pronounced hypofibrinogenemia (decreased amount of fibrin in the blood plasma) and binding of a significant part of fibrinogen to soluble fibrin. The epha venom test reveals both this blocked fibrinogen/fibrin and the ability of the blood to clot during heparin therapy (fibrin therapy). Only in the terminal phase of DIC does coagulation sharply prolong in the test with epha poison, which is a poor prognostic sign.

A decrease in the level of fibrinogen in plasma compared to the initial level is always observed in acute DIC syndrome, but in protracted and chronic forms it is rare. However, in acute forms that developed against the background of initial hyperfibrinogenemia (increased amount of fibrin), this decrease only leads to the fact that the concentration of fibrinogen in plasma reaches a normal level. Such forms occur frequently, since hyperfibrinogenemia is observed in all septic and acute inflammatory diseases, myocardial infarction and other organs, pregnancy, especially with toxicosis, and immune diseases. Taken together, all these forms account for about 50% of cases of acute DIC.

Early and steadily in DIC, the level of plasma antithrombin III, which is a physiological antiplatelet agent, decreases. It is used to inactivate all blood clotting factors. The assessment of this disorder is of great clinical importance, since depression of antithrombin III to 75% and below reflects the severity of DIC syndrome.

Relatively early in the plasma, the content of plasminogen and some of its activators decreases, which is detected by rapid tests. The level of endothelial activators of thrombus melting is significantly increased in most cases. The content of von Willebrand factor in the plasma of patients also naturally increases, which indicates deep damage to the inner lining of the blood vessels.

Hemorrhagic syndrome - a frequent and dangerous, but far from obligatory manifestation of disseminated intravascular coagulation. In most cases, it occurs in acute disseminated intravascular coagulation syndrome, often in the hypocoagulation phase, although often multiple and heavy bleeding are also recorded in the second phase against the background of normal or slightly reduced fibrinogen content in plasma. The most severe bleeding occurs, naturally, with complete or almost complete incoagulability of the blood. From a clinical point of view, it is important to clearly distinguish between local bleeding associated with damage or destructive changes in organs, and widespread hemorrhagic syndrome caused by general changes in the hemostatic system.

Local type bleeding includes bleeding from injuries and surgical interventions, postpartum and post-abortion uterine bleeding, bleeding from acutely formed stomach ulcers or duodenum, hematuria (the appearance of blood in the urine) due to renal infarction. These bleedings are associated not only with general disorders of hemostasis, but also with local (organ) pathology, which must be identified in time, correctly assessed by a doctor and taken into account when carrying out complex therapy. For example, the frequent combination of disseminated intravascular coagulation syndrome with uterine atony requires, in addition to hemostatic therapy, a set of actions that restore the normal tone of this organ; in case of bleeding from acute gastric ulcers - local stoppage of bleeding (through a fibrogastroscope) and changes in the general treatment tactics.

General bleeding is characterized by the appearance of bruises, bruises and hematomas in the skin, subcutaneous and retroperitoneal tissue, nasal, gastrointestinal, pulmonary and renal bleeding, hemorrhages in various organs (the brain and its membranes, heart, adrenal glands, lungs, uterus), diffuse blood sweating into the pleural and abdominal cavities, sometimes into the pericardial sac. In each patient, one or another form of bleeding predominates.

Bleeding leads to acute posthemorrhagic anemia, in severe cases- to hemorrhagic shock. A decrease in hematocrit below 15-17% and the inability to increase it by replacement therapy red blood cell mass are prognostically unfavorable and indicate ongoing blood loss, although it is not always easily detected.

Violation of microcirculation in organs with their dysfunction and dystrophy - another group of the most important disorders that determine the clinical picture, severity, outcome and complications of DIC syndrome. In different patients and with different pathogenetic forms of this syndrome, first one or other organs are affected, referred to in the literature as target organs.

Very often, such an organ is the lungs, into the vessels of which a huge amount of fibrin microclots, blood cell aggregates and proteolysis products are introduced from the venous system. As a result, acute pulmonary circulatory failure develops - shortness of breath, cyanosis, decreased blood oxygen saturation, and then increased carbon dioxide V arterial blood; interstitial edema appears, pulmonary infarctions and other signs of “shock lung”, often with the development respiratory distress syndrome. Intensive transfusion therapy used for DIC often aggravates these disorders by increasing the accumulation of water, sodium and albumin in the lung tissue.

Patients often show a special sensitivity to intravenous fluid administration and massive blood transfusions; sometimes an extra 200-300 ml of fluid sharply increases hypoxia and provokes pulmonary edema. In the case of the pulmonary variant of the lesion, special care should be taken to compare the amount of fluid administered with diuresis and blood loss, and to promptly add diuretics and Lasix to the complex therapy. It is also necessary to promptly transfer the patient to artificial ventilation with the creation of positive expiratory pressure.

Acute renal failure - the second most common organ damage in DIC syndrome. It manifests itself in the form of a decrease in the amount of urine excreted, up to complete anuria (lack of urination), and the release of protein and red blood cells in the urine. In this case, the water-electrolyte balance, as well as the acid-base balance in the body, is disturbed; an increase in the level of creatinine is noted in the blood serum, and subsequently -residual nitrogen and urea. In general, this syndrome does not differ from other types of acute renal failure.

Combined forms are more severe - "shock lung" with acute kidney injuryinsufficiency or hepatorenal syndrome ( hepatic-renal failure). In these cases, metabolic disorders are more severe and varied, which creates additional difficulties in treating patients.

Typical renal forms of DIC include hemolytic-uremic Gasser syndrome and all types of acute intravascular hemolysis, but hemolysis is also common in many other forms of DIC.

Less commonly, liver damage occurs with the development of parenchymal jaundice, and sometimes acute pain in the right hypochondrium. More often, the opposite phenomenon is observed - the development of DIC syndrome against the background of acute or severe chronic liver damage (acute toxic and viral hepatitis, terminal phase of liver cirrhosis).

Target organs include the stomach and intestines. These lesions are accompanied by deep focal degeneration of the mucous membrane of the duodenum and stomach, the formation of microthrombi and stasis in their vessels, the appearance of multiple bleedings, which in severe cases turn into continuous hemorrhagic impregnation of organs, the formation of acute erosive and ulcerative defects, which are a source of repeated bleeding, giving high mortality . Large doses of glucocorticosteroids (in order to bring the patient out of shock), drugs that cause erosion of the gastric mucosa (acetylsalicylic acid), as well as adrenergic stimulants (adrenaline, norepinephrine) increase the frequency and aggravate these dangerous manifestations of disseminated intravascular coagulation syndrome.

With DIC, the rest of the intestine is also severely affected, which can become a source of not only severe bleeding, but also additional intoxication due to paresis, villi rejection and massive autolysis.

Cerebral circulation disorders, thrombosis and bleeding in this area give rise to a wide variety of symptoms - from headaches, dizziness, confusion and fainting states to typical thrombotic or hemorrhagic strokes, meningism phenomena.

Lesions of the adrenal glands and pituitary gland, leading to a typical picture of acute adrenal insufficiency (prolonged collapse, diarrhea, electrolyte disturbances, dehydration) and diabetes insipidus, are observed mainly in DIC syndrome of septic and shockogenic origin. They are associated either with thrombosis of the vessels feeding these glands, or with hemorrhages in them.

Diagnosis of DIC syndrome

Diagnosis of acute disseminated intravascular coagulation syndrome is greatly facilitated by the fact that in some types of pathology it is the only form of hemostatic impairment. In shock and terminal conditions, severe forms of sepsis, massive injuries and burns, acute intravascular hemolysis and viper bites, disseminated intravascular coagulation is a constant component of the disease, its integral part. For all these types of pathology, DIC syndrome is diagnosed simultaneously with recognition of the underlying disease and its therapy is immediately started.

More serious difficulties are associated with the recognition of several hemostasis disorders, especially in cases where they are successively layered on top of each other. Such polysyndromy is observed in liver diseases, leukemia, systemic lupus erythematosus, bleeding in newborns and in a number of other situations. Differential diagnosis is necessary using a set of tests that reflect the state of different parts of the hemostatic system. Various pathological abnormalities in general coagulation tests in combination with thrombocytopenia and an increase in plasma levels of fibrinogen degradation products together provide the basis for the diagnosis of DIC syndrome.

Initial laboratory diagnosis of DIC is carried out using the simplest laboratory and instrumental techniques at the patient's bedside - total blood clotting time, prothrombin and thrombin time (with assessment of the quality of the resulting clot), changes in the shape and parameters of the thromboelastogram, indications of paracoagulation tests, dynamics of the number of platelets in the blood . This primary information can be supplemented by more accurate standardized tests - an autocoagulation test, determination of fibrinogen degradation products, quick tests with snake venoms, especially a test with sand ephas venom. For early diagnosis and the correct treatment of patients, the determination of antithrombin III and the sensitivity of the patient’s plasma to heparin is important. The diagnostic value of different tests for DIC syndrome is not the same, and each of them in a greater or lesser number of cases may not detect abnormalities (which depends on the form and stage of DIC syndrome). In addition, the readings of each test separately may be impaired not due to DIC syndrome, but for other reasons, since all of them are nonspecific. For example, the frequency of thrombocytopenia in DIC syndrome is very high (on average, it is detected in 95% of patients), but it can also be caused by other reasons (immune thrombocytopenia in systemic lupus erythematosus or in newborns, as well as those associated with heparin therapy) .

For all these reasons, diagnosis should not be based on the indications of individual laboratory research, but on the aggregate assessment of the results of a group of the most informative tests.

In general, experience shows that in the appropriate clinical situation and with the symptoms characteristic of DIC syndrome, the identification of at least 4-5 of the above basic and additional laboratory signs confirms the diagnosis and requires appropriate pathogenetic therapy. A dynamic study of antithrombin III and plasminogen has not only diagnostic significance (especially for the early diagnosis of DIC syndrome), but also for reasonable treatment of patients.

Laboratory examination of patients should in no case be limited to the hemostasis system. Other definitions are also extremely important: changes in hematocrit, levels of hemoglobin and red blood cells in the blood, arterial and venous pressure, respiratory efficiency and degree of hypoxemia, acid-base status, electrolyte balance, diuresis and urinary symptoms, dynamics of creatinine and urea in the blood.

In subacute and protracted (chronic) DIC, the process often begins with long period hypercoagulation, phlebothrombosis - venous thrombi occur (Trousseau syndrome) with thromboembolism and ischemic phenomena in organs. Without control of the hemostatic system, these initial disorders, characterized by hypercoagulation (increased intensity of blood coagulation), high spontaneous platelet aggregation, increased levels of fibrinolysis products, are often overlooked or associated with local thrombosis. In such cases, the fight against DIC syndrome often begins late - in the terminal period, with massive and multiple thromboses of organ and main veins, often with multiple emboli in the pulmonary artery basin (pulmonary infarctions), or with the transformation of the thrombotic process into the terminal phase of acute hypocoagulation and bleeding (mainly gastrointestinal).

Prolonged DIC is observed in most oncological, immunocomplex and myeloproliferative diseases, in heart failure, in destructive sclerotic processes in organs (cirrhosis of the liver), as well as in chronic hemodialysis, prosthetics of blood vessels and heart valves.

Many of these protracted forms of DIC have very significant qualitative features associated with the initial (background) pathology and treatment methods. Thus, DIC syndrome with erythremia and other myeloproliferative diseases and symptomatic polyglobules is characterized by high hematocrit, increased blood viscosity, microcirculation disorders in organs, a tendency to thrombosis and heart attacks, and cerebral circulatory disorders. With these forms, chronic, often asymptomatic gastroduodenal ulcers often develop, producing heavy bleeding during heparin therapy or transformation of DIC syndrome into the final phase. Hyperthrombocytosis (increased platelet content) characteristic of myeloproliferative diseases supports the tendency to thrombosis and DIC syndrome. These forms of pathology are accompanied by hemostasis disorders associated with thrombocythemia (when the platelet content in the blood is more than 1000 H 109 / l), in which thrombohemorrhagic phenomena are mainly caused by increased aggregation of blood platelets and a weakening of the antithrombotic properties of the endothelium.

In contrast, in chronic renal failure, activation of the coagulation component of hemostasis predominates, developing against the background of thrombocytopathy and often thrombocytopenia and anemia. Chronic hemodialysis steadily worsens all these disorders, stimulates the deposition of fibrin in the pulmonary circulation, increases the content of soluble fibrin and fibrinolysis products in the circulation. The use of plasmapheresis in complex therapy of such patients significantly reduces intoxication and microcirculation disorders.

The undulating course of DIC syndrome is often observed during destructive processes in organs, especially those associated with pathogenic microflora (staphylococci, Proteus, Pseudomonas aeruginosa) or with toxic influences. In these forms, temporary remissions are replaced by repeated acute disturbances of hemostasis, leading patients to death.

Treatment of DIC syndrome

Treatment of DIC syndrome is very difficult and is not always successful. Mortality in acute forms is 30%. The inconsistency and insufficient reliability of data on mortality are associated, on the one hand, with the fact that statistical reports include patients with background diseases of different severity and with of varying severity DIC syndrome.

First of all, in the treatment of disseminated intravascular coagulation syndrome, an intensive fight is being carried out against the pathological processes that cause and aggravate DIC syndrome. Such therapy should be aimed at eliminating the purulent-septic processes that often underlie DIC syndrome. In this situation, the earliest possible, based on clinical indications, and not on lagging ones bacteriological research antimicrobial therapy.

The basis for starting the above therapy is data on the connection of DIC syndrome with infection, abortion, early discharge of amniotic fluid (especially turbid), increased body temperature, signs of destructive inflammatory process in the lungs, abdominal cavity, urinary tract, genitals, signs of intestinal toxic infection, meningeal signs.

A rapid increase in body temperature, as well as changes laboratory parameters blood tests, such as leukocytosis, shift of the leukocyte formula to the left, are an additional reason for prescribing antibacterial therapy. As a rule, this therapy is carried out with broad-spectrum antibiotics, often including γ-globulins in therapy.

For staphylococcal and other bacterial destruction in organs, therapy is often effective only when large doses of antiproteases are added to antibiotics (for example, Contrical 100,000-300,000 units/day or more). These drugs are included in therapy to stop tissue breakdown, as well as intoxication and the entry of tissue thromboplastin into the bloodstream due to tissue destruction.

Also, the leading point in the treatment of DIC syndrome is the relief of the developing state of shock, the rapid elimination of which can interrupt the onset of DIC syndrome or sufficiently soften it. Such therapy is used intravenous injections saline solutions, jet-drop plasma transfusions, rheopolyglucin (up to 500 ml/day), glucocorticosteroids (prednisolone intravenously 80 mg). When using plasma for intravenous infusions, it is necessary to add 5000 units of heparin.

At the very first stages of development of disseminated intravascular coagulation syndrome, α-blockers have a fairly good effect. Their action is based on improving microcirculation in organs, preventing thrombosis of blood vessels, and reducing platelet aggregation. Trioproperazine, dibenamine, mazeptyl, phentolamine, which are used in a 1% solution of 5 mg intravenously, have such properties.

The high effectiveness of α-blockers in DIC syndrome is also noted if they are used early. It should be noted that adrenaline and norepinephrine very significantly aggravate DIC syndrome, increasing both blood coagulation and platelet aggregation, as well as increasing fibrin deposition in the capillaries of the kidneys, lungs and other organs.

Microcirculation and the preservation of active platelets in the bloodstream are favorably influenced by the combined use of trental and chimes, 100-200 mg intravenously, repeatedly. The above drugs should be used both in the early stages of the process and in the development of acute renal and respiratory failure, as well as during hemodialysis, plasmapheresis and other situations when blood comes into contact with a foreign surface.

It should be noted that heparin can increase the loss of functionally active platelets from the bloodstream and deepen thrombocytopenia, creating a threat of bleeding in this way, and not just by its anticoagulant effect.

Dynamic control over the content of platelets in the blood becomes extremely important during DIC syndrome, including during its treatment with heparin.

Heparin is often ineffective due to its late administration during the period when the formation of fibrin and platelet aggregation with their deposition in the microvasculature has largely been completed, as well as due to a significant deficiency of antithrombin III and a high content of acute phase proteins in the blood that block heparin, or because -for education abnormal forms thrombin.

When heparin therapy, the following basic rules should be followed. It is necessary to use heparin as early as possible - in the hypercoagulation phase in doses of 20,000-40,000 IU/day, and in the second (transitional) phase - in doses not exceeding 20,000 IU/day.

During these periods, heparin is used to “cover” the basic therapy with fresh frozen plasma.

In the stage of hypocoagulation and bleeding, heparin is used only in small doses to “cover” transfusion therapy (2500 units before blood and plasma transfusions). In slightly larger doses it can be used in combination with contrical and other antiproteases.

If DIC is caused by severe bleeding, antienzymes (contrical, gordox) are included in the treatment.

In case of bleeding, rheopolyglucin should not be used for blood replacement, since it further disrupts hemostasis.

With the development of the third stage of disseminated intravascular coagulation syndrome, when this pathological condition is accompanied by heavy bleeding, blood incoagulability, severe hypocoagulation, and also if the clinical picture is complicated by bleeding from ulcers of the gastrointestinal tract (bloody vomiting, tarry stools), severe uterine bleeding, heparin is strictly contraindicated.

It should also be noted that blood loss is not always detected on time, therefore indications for discontinuation of heparin are signs of rapidly progressing hemorrhagic collapse and anemia (decrease in blood pressure and tachycardia with a simultaneous drop in hematocrit, lack of their correction during transfusions of red blood cells, albumin, plasma).

Another contraindication is rapidly progressing thrombocytopenia, since heparin can sharply worsen this disorder.

In the phase of deep hypocoagulation, bleeding and thrombocytopenia, the most relevant is the administration not of heparin, but of large doses of protease inhibitors (contrical 50,000-100,000 units intravenously). If bleeding resumes, this dose can be repeated several times a day.

In case of disseminated intravascular coagulation syndrome, which has developed against the background of bleeding or is associated with destructive processes in organs, such as staphylococcal destruction of the lungs, large doses of Contrical should be included in therapy from the very beginning. This therapy not only relieves DIC, but also suppresses tissue breakdown, eliminates intoxication and the flow of thromboplastin from tissues into the blood.

Antiproteases also inhibit the production of tissue thromboplastin and the activation of coagulation by proteases associated with cancer cells and blasts. This effect explains the possibility of stopping DIC syndrome in acute promyelocytic leukemia with Contrical and other antiproteases. In some cases of disseminated intravascular coagulation, a good therapeutic effect is achieved by the combined use of Contrical and heparin.

Transfusion therapy forms the basis for the treatment of disseminated intravascular coagulation syndrome, which ensures the correction of hemostasis disorders; replacement of the volume of fluid in the circulation and restoration of central venous pressure impaired due to shock and (or) blood loss; replacement of blood cells - red blood cells and platelets.

Some of the above goals are achieved by massive transfusions of plasma containing all the components of the blood coagulation system and other plasma enzyme systems and having antiprotease activity, including large amounts of antithrombin III.

Treatment with fresh frozen plasma should begin as early as possible at the stage of hypercoagulation and continue until all manifestations of disseminated intravascular coagulation syndrome are eliminated. It has been proven that plasma helps to relieve not only DIC syndrome, but also destructive processes in organs, intoxication, and immune disorders.

In the absence of fresh frozen plasma, treatment can be carried out using antihemophilic or native plasma, although these drugs are less effective.

Also in infusion therapy, in addition to plasma, saline solutions, polyglucin, and albumin solution are used. It is possible to use rheopolyglucin; it is used mainly in the hypercoagulation phase in a volume of no more than 400 ml/day. In this phase, rheopolyglucin functions not only as a blood substitute, but also as an agent that inhibits platelet and erythrocyte aggregation and improves microcirculation in organs.

During the period of hypocoagulation and bleeding, as well as severe thrombocytopenia, it should not be prescribed, since, according to the experience of many authors, in such a situation, reopolyglucin can increase bleeding and weaken the therapeutic effect of other drugs.

Anemization, decreased hematocrit, and heavy bleeding are indications for red blood cell replacement. To achieve this goal, transfusions of red blood cells and red blood cell suspension are prescribed.

To summarize, it should be noted that when transfusion therapy for disseminated intravascular coagulation syndrome, the physician must strive to achieve the following main goals.

Rapid restoration of circulating blood volume and hemodynamics (by cryoplasma, albumin, saline solutions, polyglucin and rheopolyglucin) and maintaining the mass of erythrocytes in the blood above the critical level (for hematocrit - above 22%, for erythrocytes - above 2.5 H 1012 / l).
If the specified level cannot be achieved, attention should be paid to any possible ongoing bleeding, visible or invisible.
Often joint use Fresh frozen plasma and platelet concentrates (4-8 doses each) can stop many of these bleedings.
Even at the most late stages disseminated intravascular coagulation syndrome, effective stopping of bleeding, especially uterine, occurs due to simultaneous intravenous administration of large doses of contrical (50,000-100,000 units or more; daily dose- up to 500,000 units or more).
Local influences should also be used, such as irrigating bleeding areas, erosions, wounds with adroxon, a 6% solution of aminocaproic acid, and applying biological glue to these areas.

The use of plasma and cytapheresis in the treatment of DIC syndrome

The successful use of plasmapheresis in the treatment of DIC syndrome, especially in its protracted and recurrent forms, has also been proven. 600-800 ml of plasma are removed, replacing it with fresh frozen plasma. With this procedure, which can be repeated as necessary, immune and protein complexes, activated coagulation factors are removed from the patient’s blood, and with partial cytapheresis (removal of the buffy coat), activated monocytes and platelet aggregates are removed.

The most relevant is the use of therapeutic plasmapheresis for protracted forms of DIC associated with renal and liver failure, purulent-destructive processes, as well as chronic hemodialysis.

For chronic DIC syndromes, erythrothrombocytapheresis in combination with the following drugs gives a rapid therapeutic effect: trental, dipyridamole, ticlopidine, a-blockers.

Acetylsalicylic acid is dangerous in acute disseminated intravascular coagulation syndrome: aggravating thrombocytopathy and forming acute erosions in the stomach, it creates the preconditions for severe massive bleeding.

Thus, the main components of complex therapy for DIC syndrome are:

1) treatment aimed at eliminating the causative factor; antishock therapy and maintaining the required volume of circulating blood: transfusion of fresh frozen plasma with heparin; administration of protease inhibitors and antibradykinin drugs (especially during destructive processes and during bleeding);

2) perhaps more early application adrenergic blockers and drugs that improve microcirculation and reduce the loss of platelets from the bloodstream (trental, chimes, ticlodipine);

3) replacing the loss of red blood cells and maintaining the hematocrit above 22%; in case of severe hypocoagulation and bleeding - transfusion of platelet concentrates, administration of contrical in large doses;

4) use of plasmacytapheresis as indicated.

The next therapeutic effect is the direction to eliminate “shock lung” and acute renal failure using drugs such as Lasix, osmotic diuretics, heparin, with controlled artificial ventilation, influencing the acid-base state and electrolyte balance.

In case of disseminated intravascular coagulation syndrome, the use of fibrinogen should be avoided, which easily coagulates in the bloodstream, increasing the blockade of microcirculation.

In most cases of DIC syndrome, both fibrinolysis inhibitors such as aminocaproic acid and activators of this system (streptokinase, urokinase) are contraindicated. Their use is fraught with dangerous complications.

For gastroduodenal bleeding, local effects are used whenever possible through a gastrofibroscope - covering bleeding erosions with local hemostatic drugs.

Patients with disseminated intravascular coagulation syndrome require intensive round-the-clock monitoring and treatment with monitoring of the effectiveness of breathing and circulation, and frequent repetition of laboratory tests. Based on all of the above, such patients should be in intensive care units or in wards intensive care.

Prevention of DIC syndrome

Timely elimination of the causes of DIC syndrome, proper treatment of the underlying disease, possibly less traumatic surgical interventions, combating the onset of shock and microcirculation disorders - the most important conditions warnings of DIC syndrome. Particular attention should be paid to the need to combat septic complications after abortion, often leading to acute disseminated intravascular coagulation syndrome.

In case of thrombogenic danger (old age, pathology of pregnancy, tumor diseases) you should not prescribe drugs that increase the coagulation potential of the blood (synthetic hormonal contraception, fibrinolysis inhibitors, including aminocaproic acid).

It should be remembered that blood loss in adults, not exceeding 1 liter, must be replaced not with blood, but with albumin, plasma or blood substitutes.

In the treatment of purulent-destructive processes, which are a common cause of disseminated intravascular coagulation syndrome, along with antibiotics and other antibacterial drugs protease inhibitors and drugs that improve rheological properties blood, and antithrombotic agents.

Which doctors should you contact if you have DIC syndrome?

Hematologist

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Clinical picture consists of signs of the underlying (background) disease that caused the development of intravascular coagulation, and the DIC syndrome itself. The latter goes through the following stages in its development:

I - hypercoagulation and thrombosis;
II - transition from hyper- to hypocoagulation with multidirectional shifts in different blood clotting parameters;
III - deep hypocoagulation (up to complete blood incoagulability and severe thrombocytopenia);
IV - reverse development of 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). More often, acute DIC syndrome is first detected at the time of the appearance of multiple hemorrhages at injection sites, palpation, below the site of application of the cuff for measuring blood pressure, in sloping parts of the body; with prolonged and often repeated bleeding from skin puncture sites on the fingers or in the elbow area, a sharp increase in bleeding diffuse type from surgical wounds; with bleeding from the uterus (during childbirth, after an abortion, etc.) without visible local causes, bleeding serous membranes, poor coagulability of escaping blood (small, rapidly lysing clots, complete incoagulability). Often, nasal and gastrointestinal bleeding occur simultaneously, signs of microcirculation disorders appear in the organs - lungs (suddenly developing frequent ineffective breathing, cyanosis, wheezing), kidneys (decrease in diuresis, protein and red blood cells in the urine), brain (lethargy, congestion), adrenal gland (repeated drops in blood pressure), liver (pain in the right precostal area, hyperbilirubinemia, jaundice). One or the other organ disorders may predominate.

Laboratory signs - multidirectional shifts in the blood coagulation system, turning into deep hypocoagulation (deceleration of blood and plasma coagulation in the partial thromboplastin test, autocoagulation test, thromboelastogram, prolongation of thrombin and prothrombin time, decrease in the level of plasma coagulation factors (including fibrinogen); increased spontaneous platelet aggregation (flakes in plasma) in combination with thrombocytopenia; increased content of destroyed (fragmented) red blood cells in the blood; positive results of one or more paracoagulation tests that reveal the circulation in the blood of active thrombin and soluble fibrin-monomer complexes (SFMC) - ethanol, protamine sulfate, beta-naphthol, orthophenanthroline. Due to intense fibrinolysis, the content of fibrin enzymatic degradation products (PDF) in the plasma increases, determined immunologically or by the staphylococcal adhesion test (TSA). As a result of intense intravascular coagulation and fibrinolysis in the circulation, the content of not only coagulation factors decreases blood and platelets, but also the most important anticoagulants - antithrombin III (heparin cofactor), proteins C and S, as well as plasminogen (profibrinolysin) and its activators (plasma prekallikrein, high molecular weight kininogen, etc.).

Due to the blockade of microcirculation and hypoxia of organs, disturbances in the gas composition of the blood are detected, acid-base balance, later the plasma levels of creatinine, urea (acute renal failure), and bilirubin (hemolysis, liver damage) increase.

Thus, acute DIC syndrome is a severe catastrophe of the body, putting it on the line 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 phenomena (hemocoagulation-hypopemic nature).

Subacute DIC syndrome is characterized by a longer period than in acute DIC syndrome, the initial period of hypercoagulation is asymptomatic or manifested by thrombosis and microcirculation disorders in organs (congestion, anxiety, a feeling of unaccountable fear, decreased diuresis, edema, protein and casts in the urine).
In chronic disseminated intravascular coagulation syndrome, against the background of signs of the underlying disease, there is pronounced hypercoagulation of the blood (rapid coagulation in the veins - spontaneous and when punctured by needles, test tubes), hyperfibrinogenemia, a tendency to thrombosis, positive paracoagulation tests (ethanol, protamine sulfate, etc.). The bleeding time according to Duke and Borchgrevink is often shortened, and the platelet content in the blood is normal or increased. Their spontaneous hyperaggregation is often detected - small flakes in the plasma. In a number of forms, there is an increase in hematocrit, a high level of hemoglobin and red blood cells, and a slowdown in ESR. In some cases, unmotivated multiple venous thromboses manifest, including with unrecognized cancer of different localization (Trousseau syndrome), with immune vasculitis, collagenosis, etc. In other cases, hemorrhages, petechiae, bruises, bleeding from the nose and gums, etc. easily appear. (in combination with and without thrombosis).

Description

Acute DIC is accompanied by severe infectious and septic diseases (including during abortion, during childbirth, in newborns - more than 50% of all cases), all types of shock, destructive processes in organs, severe injuries and traumatic surgical interventions, acute intravascular hemolysis (including incompatible blood transfusions), obstetric pathology (placenta previa and early abruption, amniotic fluid embolism, especially infected, manual separation of the placenta, hypotonic bleeding, massage of the uterus with its atony), massive blood transfusions (the danger increases when using blood for more than 5 days storage), acute poisoning (acids, alkalis, snake venoms, etc.), sometimes acute allergic reactions and all terminal conditions. The pathogenesis of the syndrome in most cases is associated with a massive intake of blood coagulation stimulants (tissue thromboplastin, etc.) and platelet aggregation activators from tissues into the blood, damage to a large area of the vascular endothelium (bacterial endotoxins, immune complexes, complement components, cellular and protein breakdown products) . During infectious and septic processes, blood clotting stimulants and enzymes that damage the walls of microvessels are also intensively produced by macrophages (monocytes) and neutrophils; elastase secreted by the latter plays an important role in the formation of pulmonary distress syndrome (shock lung).

Subacute DIC syndrome, giving way to an acute one in the terminal phase, is observed with a milder course of all the diseases listed above, as well as with late toxicosis of pregnancy, intrauterine fetal death, leukemia, immune complex diseases (subacute forms hemorrhagic vasculitis), temolyticouremic syndrome (acute disseminated intravascular coagulation syndrome may also occur).

Chronic DIC often complicates malignant neoplasms (cancer of the lung, kidney, prostate, liver, etc.), chronic leukemia, all forms of blood thickening (erythremia, erythrocytosis), hyperthrombocytosis, chronic cardiac and pulmonary-heart failure, chroniosepsis, vasculitis, giant hemangiomas (Kasabach-Merritt syndrome). Chronic DIC also leads to massive contact of blood (especially repeated) with a foreign surface - hemodialysis in chronic renal failure, the use of extracorporeal circulation devices.

A pathogenetically special form associated with a decrease in the antiaggregation potential of the vascular wall and blood is thrombotic thrombocytopenic purpura (Moshkovich disease).

Schematically, the pathogenesis of DIC syndrome can be represented by the following sequence pathological disorders: activation of the system, hemostasis 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), decreased platelet content 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, frequent weakening of the detoxification and excretory functions of the liver and kidneys. This proteolytic explosion with the accumulation of toxic protein breakdown products in the blood and extravascular space served as the basis for the development and use of a number of new effective methods for treating DIC syndrome - plasmapheresis and transfusions of fresh native or fresh frozen plasma, administration of high doses of antiproteases, the use of extracorporeal blood purification methods and etc.

Diagnostics

Early diagnosis is situational in nature and is based on identifying those diseases and influences under which DIC syndrome naturally develops (infectious and septic processes, all types of shock and severe hypovolemia, acute intravascular hemolysis, a number of types of obstetric pathology, etc.). In all these cases, early preventive therapy of DIC syndrome is necessary before the development of pronounced clinical and laboratory signs. In the presence of causal factors, causing DIC syndrome, the development of the latter becomes undoubted with the appearance of hemorrhage of different localization, signs of acute respiratory failure (tachypnea, suffocation, cyanosis), acute renal or hepatorenal failure, intensification and recurrence of the phenomena of shock, multidirectional disturbances of various parameters of blood coagulation, the transition of hypercoagulation to deep hypocoagulation in combination with aggregation of blood cells in the plasma (turbidity, flakes) and thrombocytopenia. The type of bleeding is mixed. Additionally, DIC syndrome is documented by positive paracoagulation tests (ethanol, protamine sulfate, beta-naphthol, ortho-phenanthroline), detection high content in plasma PDF (express method - staphylococcal adhesion test), detection of blocked fibrinogen in the serum after coagulation when adding the venom of the sand epha snake to it (formation of a second clot in the serum). All of these tests can be performed quickly, but therapy should not be delayed until they are completed.

Diagnosis of subacute disseminated intravascular coagulation syndrome is based on identifying a combination of symptoms of the underlying disease with thrombosis and (or) hemorrhages of various locations (bruises, especially at injection sites, thrombosis at venipuncture sites) and signs of impaired microcirculation in organs. Blood tests reveal changes in the phases of hyper- and hypocoagulation, multidirectional shifts in coagulation tests, hyper- or moderate hypofibrinogenemia, and often hyperthrombocytosis. Paracoagulation tests (ethanol, protamine sulfate, etc.) are consistently positive; PDPs in plasma are increased.

Treatment

Treatment of acute DIC should be aimed primarily at quickly eliminating its cause. Without early successful etiotropic therapy, one cannot count on saving the patient’s life. Patients need immediate referral or transfer to the intensive care unit, mandatory involvement in healing process resuscitators-transfusiologists and specialists in the pathology of the hemostatic system. The main pathogenetic methods of treatment are anti-shock measures, intravenous drip administration of heparin, jet transfusions of fresh native or fresh frozen plasma, if necessary, with plasma replacement, the fight against blood loss and deep anemia (blood substitutes, freshly citrated blood, erythroplasty suspension), acute respiratory disorders (early connection to artificial ventilation) and acid-base balance, acute renal or hepatorenal failure.

Heparin should be administered intravenously, in some cases in combination with subcutaneous injections into the anterior tissue. abdominal wall below the umbilical line. Intramuscular injections are not recommended due to the different rates of drug resorption (which makes dosing difficult), easy education in conditions of development of DIC syndrome of large, infected hematomas. The dose of heparin varies depending on the form and phase of DIC syndrome.

If there are acute phase proteins in the patient’s blood (for example, during acute infectious and septic processes, massive tissue destruction, burns), the dose of heparin, on the contrary, should be the highest, since these proteins bind heparin and prevent 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. Therefore, often a significant increase in the effectiveness of treatment is achieved not by increasing doses of heparin, but by early connection of jet transfusions of fresh native or fresh frozen plasma. Such transfusions are indicated in all stages of DIC; they compensate for the deficiency of all components of the coagulation and fibrinolytic systems, including antithrombin III and proteins C and S (the depletion of which in DIC is especially intense - several times faster than all procoagulants) , allow you to introduce into the bloodstream a full set of natural antiproteases and factors that restore the antiaggregation activity of the blood and thromboresistance of the endothelium.

In some cases (especially in infectious-toxic forms of DIC), transfusions of fresh frozen or fresh native plasma are carried out after plasmapheresis sessions (only after stabilization of hemodynamics!). In DIC syndrome of an infectious-septic 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) . These methods of plasma therapy and plasma exchange significantly increase the effectiveness of treatment of DIC and the diseases that cause it, reduce mortality several times, which allows them to be considered the main method of treating patients with this hemostasis disorder. With significant anemia, transfusions of fresh canned blood (daily or up to 3 days of storage), red blood cell mass and red blood cell suspension are added to this therapy. One should not strive for a quick and complete normalization of red blood parameters, since moderate hemodilution is necessary to restore normal microcirculation in the organs. It should be remembered that excessively abundant blood transfusions (especially canned blood for more than 3 days of storage) aggravate DIC syndrome (massive transfusion syndrome), and therefore during transfusion therapy a certain restraint is required, strict accounting of the amount of blood transfused, its components and blood substitutes, as well as blood loss, loss of body fluid, diuresis. It should be remembered that acute DIC syndrome is easily complicated by pulmonary edema, so significant overload of the circulatory system during the syndrome is dangerous.

IN Stage III DIC syndrome and with pronounced proteolysis in tissues ( gangrene of the lung, necrotizing pancreatitis, acute liver dystrophy, etc.) plasmapheresis and jet transfusions of fresh frozen plasma or other antiproteases. In the later stages of development of DIC syndrome and its varieties occurring against the background of hypoplasia and dysplasia bone marrow(radiation, cytotoxic diseases, leukemia, aplastic anemia) to stop bleeding, it is also necessary to perform transfusions of platelet concentrates.

An important part of complex therapy is the use of disaggregants and drugs that improve microcirculation in organs. An important component of therapy is the early connection of artificial ventilation. The use of antiopioids helps bring the patient out of shock.

The transition to the hypocoagulable and hemorrhagic phase occurs either gradually or suddenly (often with transformation into acute disseminated intravascular coagulation syndrome). Repeated changes in the phases of hyper- and hypocoagulation are common (especially in infectious-septic, neoplastic forms).

Treatment of subacute disseminated intravascular coagulation syndrome by adding intravenous and subcutaneous drips of heparin and antiplatelet agents to the treatment of the underlying disease. Rapid relief or weakening of the process is often achieved only by performing plasmapheresis, replacing partly with fresh, native or fresh frozen plasma, and partly with blood replacement solutions and albumin. The procedure is carried out under the cover of small doses of heparin.

Treatment of chronic DIC syndrome is the same as for the subacute form. For polyglobulia and blood thickening - bloodletting, leeches, cytapheresis (removal of red blood cells, platelets and their aggregates), hemodilution. For hyperthrombocytosis - disaggregants.

Great Medical Encyclopedia

Disseminated intravascular coagulation- a violation of hemostasis, which is characterized by diffuse coagulation of blood in the circulation with the formation of microclots and aggregates of blood cells, which cause blockade of microcirculation and deep degenerative changes in organs with the subsequent development of hypocoagulation and thrombocytopenia of consumption and often bleeding.

Causes of DIC syndrome

DIC syndrome often occurs as a complication of infectious and inflammatory processes of various localizations. The development of DIC is most typical in gram-negative infections - with meningococcal sepsis, DIC develops in 100% of cases. Gram-positive infections can also cause the development of DIC, including:

typhoid fever;
staphylococcal sepsis with lung destruction;
viral infection - herpes, rubella, smallpox, viral hepatitis, hemorrhagic fevers, etc.;
mycoses - histoplasmosis, aspergillosis;
rickettsial infection;
protozoal infections - malaria, trypanosomiasis.

Infections can cause disseminated intravascular coagulation in patients with a removed spleen. In these cases, a generalized, most often pneumococcal, infection often develops, which in almost all cases leads to the development of DIC syndrome. The cause of disseminated intravascular coagulation can be all types of shock - anaphylactic, traumatic, burn, septic shock, as well as shock that occurs during prolonged crush syndrome.

Acute intravascular hemolysis can lead to the development of DIC in case of incompatible blood transfusion, during a crisis in patients with hemolytic anemia, in case of poisoning with hemolytic poisons, in microangiopathic hemolytic anemia, paroxysmal nocturnal hemoglobinuria.

DIC syndrome can develop with malignant neoplasms various localizations- stomach cancer, prostate cancer, pancreas cancer, ovarian cancer, lung cancer, etc. Another cause may be malignant diseases blood systems - acute leukemia, especially the promyelocytic variant, blast crisis in chronic leukemia, essential thrombocythemia, etc.

A common cause of disseminated intravascular coagulation is massive tissue damage. The causes of such damage may be burns, severe injuries, long-term compression syndrome, fractures of long bones with fat embolism, electrical trauma. DIC syndrome can also occur during extensive traumatic surgical interventions. The risk of developing disseminated intravascular coagulation during major surgical operations increases significantly in the presence of concomitant pathology ( cardiovascular diseases, malignant tumors), the use of vascular prostheses. Disseminated intravascular coagulation syndrome can also develop during operations using artificial blood circulation machines.

DIC often develops in obstetric and gynecological pathologies: premature abruption, placenta previa, amniotic fluid embolism, septic abortion and chorioamnionitis, hydatidiform mole, intrauterine fetal death, fetal destructive operations, cesarean section, severe late toxicosis of pregnancy, etc.

DIC can develop due to pathologies of cardio-vascular system: congenital heart defects, large-focal myocardial infarction, atherosclerotic artery disease, cavernous and giant hemangiomas, congestive heart failure, coarctation of the aorta, pulmonary embolism, myocardial diseases (diffuse myocarditis, cardiomyopathies).

DIC can be caused by: systemic diseases connective tissue and systemic vasculitis, systemic lupus erythematosus, rheumatoid arthritis, periarteritis nodosa, etc.; acute and chronic inflammatory kidney diseases of immunoinflammatory origin; severe drug-induced allergic reactions; Transplantation of organs and tissues. DIC syndrome is detected in all cases of severe traumatic brain injury.

Other causes of DIC: diabetes mellitus, acute iron intoxication, frostbite, radiation sickness, epilepsy (status epilepticus), hyperthermic and hypothermic conditions.

Clinical picture of DIC syndrome

The clinical picture of DIC is characterized, on the one hand, by thrombotic and ischemic damage to organs and tissues, and on the other, by hemorrhagic syndrome, with organs and tissues that have an intensively functioning microcirculatory system (liver, kidneys, lungs, etc.) being primarily affected. .).

There are several types of DIC syndrome:

fulminant - DIC syndrome develops within an hour;
acute - pathology develops within several hours;
subacute - the syndrome develops over several days;
chronic - the syndrome develops over months and years;
recurrent - characterized by periodic exacerbation of DIC with intervals of remission;
latent.

During DIC syndrome there are several stages (phases):

phase of hypercoagulation and platelet hyperaggregation;
transition phase - there is a tendency towards hypocoagulation according to some tests and hypercoagulation - according to others;
phase of hypocoagulation and activation of fibrinolysis (hemorrhagic phase);
recovery phase (if the course is unfavorable - the phase of severe complications and death).

Symptoms of acute DIC syndrome
The acute course of DIC is characterized, as mentioned above, by the development of symptoms within several hours. An acute form of pathology is observed in sepsis, severe combined injuries, extensive burns, frostbite, long-term compartment syndrome and other conditions.

In the hypercoagulable phase a picture of hemocoagulative shock develops, which is characterized by confusion, lethargy of the patient, strong fall blood pressure (BP). The patient is pale, the skin is covered with cold sweat, acrocyanosis is noted, the hands and feet are cold to the touch. The pulse is thread-like, often arrhythmic, muffled heart sounds and tachycardia are noted. A clinical picture of thromboembolism of the pulmonary, renal and other arteries may be observed. Venous thrombosis is possible.

Most patients experience damage to the respiratory system, which is manifested by the development of acute respiratory failure and acute respiratory distress syndrome. Shortness of breath and cough mixed with blood appear. Auscultation of the lungs reveals crepitus and fine rales, mainly in lower sections, in some cases - scattered dry wheezing. X-ray of the lungs shows an increase in the pulmonary pattern.

Kidney damage is diagnosed in 66-70% of patients and manifests itself as symptoms of acute renal failure. Patients are bothered by severe pain in the lower back, the amount of urine excreted decreases. Casts, red blood cells, and protein in the urine are determined. The level of urea and creatinine in the blood increases, which is a reflection of renal failure.

Liver damage is observed in approximately half of patients. It manifests itself as pain in the right hypochondrium, a feeling of bitterness and a metallic taste in the mouth, loss of appetite, pale icteric coloration of the skin, darkening of the urine, and an increase in the size of the liver. When the liver is damaged, severe liver failure develops, hepatic odor from the mouth and symptoms of hepatic encephalopathy appear - confusion, delirium, hallucinations, etc. Severe liver damage can lead to the development of complete hepatic coma. Acute thrombosis of the hepatic or portal vein may occur. With portal vein thrombosis, severe abdominal pain, bloody vomiting appears, ascites quickly develops, but the size of the liver remains normal. Acute thrombosis of the hepatic veins is manifested by intense pain in the epigastrium and right hypochondrium, vomiting (sometimes bloody), the liver quickly enlarges, ascites develops, and jaundice appears in about half of the patients.

Damage to the microvasculature of the myocardium is manifested by shortness of breath, arrhythmias, expansion of the borders of the heart, dullness of heart sounds, etc. Severe damage to the microvasculature of the myocardium leads to left ventricular failure.

The occurrence of microthrombosis in the bloodstream of the adrenal glands leads to the development of acute adrenal insufficiency. Weakness, adynamia, nausea, vomiting (sometimes with blood), abdominal pain, frequent loose stools, sharp drop BP, thready pulse. The skin is pale, covered with cold sweat; facial features are pointed, eyes are sunken, tongue and lips are dry. Particularly severe damage to the adrenal glands is observed in patients with DIC against the background of meningococcal sepsis. Acute adrenal insufficiency significantly aggravates the course of hemocoagulative shock and can lead to death.

In DIC syndrome, damage to the gastrointestinal tract (GIT) is often observed. Characteristic are dystrophic changes in the mucous membrane of the stomach and duodenum, microthrombosis and stasis in their vessels. Multiple erosions and hemorrhages are noted. Pain in the epigastrium appears, intensifying after eating, vomiting (often bloody), heartburn, and sour belching. In some cases, mesenteric thrombosis develops, leading to intestinal infarction.

Damage to the central nervous system (CNS) in the hypercoagulable stage of DIC syndrome is caused by thrombosis in the microvasculature. Lesions of the central nervous system are characterized by such general symptoms as: dizziness, headache, confusion, etc. Clinical symptoms of cerebral vascular thrombosis may develop. In this case, psychomotor agitation may be observed, followed by loss of consciousness, convulsions, paresis and paralysis due to ischemic stroke.

In the intermediate phase symptoms characteristic of the hypercoagulable stage of DIC remain. At the same time, in laboratory tests of the state of the hemostatic system and in the clinical picture, signs of hypocoagulation appear. The intermediate stage of DIC syndrome, as a rule, quickly passes into the phase of hypocoagulation and activation of fibrinolysis.

In the phase of hypocoagulation and activation of fibrinolysis Coagulopathy and consumption thrombocytopenia develop, fibrinolysis is significantly activated, which ultimately leads to the development of severe hemorrhagic syndrome. Petechiae, sometimes extensive hemorrhages, hematomas, and ecchymoses appear on the skin. Bleeding at the sites of subcutaneous injections and venipuncture is typical. Local bleeding occurs in tissues and organs that have undergone trauma or surgery. Severe violations hemostasis lead to bleeding - gastrointestinal, renal, uterine. Bleeding gums and nosebleeds are noted. May develop intracerebral hemorrhages, hemorrhages in the pericardium, pleural cavity, peritoneum.

In the recovery phase, with successful treatment of DIC, relief of symptoms and gradual restoration of the functional state of the affected organs is observed. However, sometimes a severe course of DIC syndrome is observed, in which profound dysfunction of the affected organs is possible, which ends in incomplete or insignificant recovery or even death.

It should be noted that this staged development of DIC syndrome is not always clearly expressed. Often the hypercoagulable phase quickly turns into a hypocoagulable phase, when severe hemorrhagic manifestations come to the fore. The intermediate phase is recognized mainly by laboratory methods.

Symptoms of subacute DIC syndrome
The subacute course of DIC is characterized by the development of clinical symptoms over several days (up to three weeks). Clinical picture when subacute course DIC is generally similar to that in the acute type of course. At the same time, it is less pronounced and leads to fewer negative consequences for the body. Microcirculation disorders and dysfunction predominate internal organs.

Symptoms of chronic DIC syndrome
The chronic course of DIC continues for months and years. Characteristic feature The chronic form of DIC syndrome is that with an exacerbation of the underlying disease, as well as with an increase in its severity, the symptoms of DIC intensify. Hemorrhagic syndrome develops, thrombotic phenomena and microcirculatory disorders occur. Exacerbation of DIC symptoms, in turn, significantly worsens the course of the underlying disease. Sclerotic changes develop in the affected organs, due to which their functional ability is subsequently significantly reduced. The clinical picture of the chronic form of DIC often occurs under the guise of nonspecific inflammatory diseases individual organs ( chronic nephritis, hepatitis, pancreatitis, pneumonia). Exacerbations of DIC syndrome can also cause exacerbation of coronary heart disease.

Symptoms of recurrent DIC syndrome
Recurrent DIC has a long, multi-year course, characterized by frequent exacerbations, relapses, followed by remission. During the period of exacerbation of the underlying disease, an exacerbation of the symptoms of disseminated intravascular coagulation is also observed. This is manifested by hypercoagulability, thrombotic symptoms, microcirculatory disorders and organ dysfunction. Quite often, during the period of exacerbation of the disease, hemorrhagic syndrome dominates, which disappears during the period of remission. With frequent relapses of DIC, significant degenerative changes gradually develop in organs and tissues, which ultimately leads to disruption of their functions.

Latent course of DIC syndrome
Clinically, the latent course of DIC does not manifest itself in any way. Only symptoms of the underlying disease are observed. DIC can be detected only during a laboratory examination of the patient.

Treatment of DIC syndrome

Treatment of DIC syndrome presents significant difficulties and is not always successful. The frequency of deaths in acute forms of DIC reaches 30%.

Treatment is aimed primarily at combating pathological processes that cause and aggravate the course of DIC syndrome. The basis for starting such therapy may be data on the connection of DIC with infection, abortion, signs of meningeal syndrome, inflammatory process in the lungs, abdominal cavity, urinary tract, etc. A sharp increase in body temperature, changes in blood parameters (leukocytosis, shift of the leukocyte formula to the left) are additional indication for prescribing antibacterial therapy.

Another leading direction in the treatment of DIC is the relief of shock. Rapid elimination of the growing phenomena of shock can, if not stop the developing DIC syndrome, then significantly mitigate its complications. To relieve shock, intravenous injections of saline solutions, jet-drip infusions of plasma, rheopolyglucin, glucocorticoids, and narcotic analgesics are used.

In the early stages of development of DIC, alpha-blockers (phentolamine, etc.) are prescribed. The effectiveness of their use is due to improved microcirculation in organs, reduced platelet aggregation and prevention of vascular thrombosis.

To improve microcirculation and preserve active platelets in the bloodstream, the combined use of trental and chimes is prescribed. These drugs should be used both in the early stages of the pathological process and in the development of acute renal and respiratory failure.

Intravenous administration of heparin is used - in the hypercoagulation stage in doses of 20,000-40,000 units/day, in the transition stage - in doses not exceeding 20,000 units/day. In the hypocoagulation phase, it is used in small doses - 2500 units before blood and plasma transfusions. When combined with Contrical and other antiproteases, heparin may be prescribed in higher doses. In the hypocoagulation phase, with the addition of heavy bleeding, blood incoagulation, severe hypocoagulation, the use of heparin is strictly contraindicated. Another contraindication is progressive thrombocytopenia, since heparin can sharply worsen this phenomenon.

In the stage of deep hypocoagulation, bleeding and thrombocytopenia, they resort to the introduction of large doses of protease inhibitors (contrical). In case of DIC that occurs against the background of bleeding or is associated with damage to internal organs, such as staphylococcal destruction of the lungs, high doses of Contrical are prescribed from the very beginning of treatment.

The basis of treatment of DIC syndrome is transfusion therapy, which provides correction of hemostasis disorders; replacement of the volume of circulating fluid and restoration of central venous pressure. This is achieved by transfusion of plasma containing all the components of the blood coagulation system and other enzyme systems. Transfusion of fresh frozen plasma begins immediately, at the hypercoagulation stage, and continues until all signs of disseminated intravascular coagulation disappear. In addition to plasma, saline solutions, albumin solution, and polyglucin can be used.

Anemization, decreased hematocrit, and heavy bleeding are indications for red blood cell replacement. For this purpose, transfusions of red blood cells and red blood cell suspension are prescribed.

Some studies have noted a positive effect of plasmapheresis in the treatment of DIC syndrome. Its use is most justified in protracted and recurrent forms of the disease.

DIC syndrome (disseminated intravascular coagulation) is considered one of the most severe complications of gynecological diseases in obstetrics. It promotes the development of thrombosis and bleeding, which can cause death.

The causes of this pathology mainly lie in problems that arise during pregnancy and childbirth. DIC syndrome can also develop in postpartum period both in the mother and in the newborn.

Diagnosis and treatment of DIC syndrome is very complex. According to statistics, the mortality rate from this pathology in its acute form is 30%. It is important to remember that thanks to the vigilance of doctors and professional diagnostics, it is possible to stop the disease at the first stage of its development or to significantly reduce the risk of the pathology transitioning to subsequent phases.

What is DIC syndrome?

Disseminated intravascular coagulation (DIC) is a disorder of hemostasis (the body's inability to cope with bleeding), which is characterized by blood clotting with the formation of microclots and aggregates of blood cells that block blood circulation. As a result of such changes, profound dystrophic changes develop in organs, which are accompanied by a decrease in the ability of blood to clot (hypocoagulation), a decrease in the amount per unit volume of blood (thrombocytopenia) and bleeding (hemorrhage).

The severity and speed of development of DIC syndrome are very diverse. There are several forms of its development: fulminant (over an hour), acute (over several hours), subacute (over several days), chronic (over months and years), recurrent (the condition periodically worsens with intervals of remission), latent ( hidden).

DIC syndrome during pregnancy, as a rule, has a chronic or acute form. Chronic form DIC syndrome occurs as a result of extragenital pathology in pregnant women (cardiovascular diseases, glomerulonephritis, blood diseases and other diseases), the acute form is as a result of significant blood loss (hypotonic bleeding, embolism).

Causes of DIC syndrome in pregnant women

DIC syndrome in pregnant women often occurs as a complication of infectious and inflammatory processes. Among the main reasons for the development of pathology are the following:

Amniotic fluid embolism― develops during complicated childbirth and is characterized by the entry of amniotic fluid into the bloodstream, which can occur after rupture of the uterus or its cervix, cesarean section, pathological development shells. The entry of amniotic fluid into the bloodstream is facilitated by placenta previa, premature abruption of a normally located placenta, and increased hydrostatic pressure in the uterine cavity.
Premature placental abruption― detachment of a normally located placenta before the birth of a child. In most cases it is accompanied by bleeding from the genital tract. After abruption, a hematoma can sometimes form behind the placenta.
Preeclampsia― severe late toxicosis of pregnancy, which usually develops in the third trimester. Characterized by the appearance of protein in the urine, edema, increased blood pressure and leads to disruption of the uteroplacental circulation.
Hemorrhagic shock― very strong stress on the body, which can occur due to hemorrhages.
Sepsis― a generalized purulent blood infection, which can be triggered by intrauterine fetal death, septic abortion and inflammation of the membranes, transfusion of incompatible blood.
Endometritis- inflammation of the inner lining of the uterus, which develops after childbirth and can be complicated by the fulminant form of DIC syndrome.

DIC syndrome can also occur in pregnant women who have diseases of the cardiovascular system, kidneys, liver, Rh conflict, etc.

Stages of development of DIC syndrome

Hypercoagulation (increased blood clotting)

Lasts from several minutes (acute DIC) to several days (chronic DIC). Without laboratory diagnostics, this stage may be latent. External signs: increased blood supply (hyperemia) of the skin and its bluish coloration (cyanosis), often a marbled pattern on the upper and lower extremities, sometimes chills.

Hypocoagulation (reduced blood clotting) without active dissolution of blood clots and blood clots

External signs: increased bleeding from birth canal or areas of the surgical wound, nosebleeds, hemorrhages on the skin, bloody rashes on the sides of the chest, thighs, and upper eyelid. Blood from the uterus contains loose clots that quickly break down.

Hypocoagulation with active dissolution of blood clots and blood clots

External signs: liquid non-coagulating blood is released, sometimes single small clots are formed that are quickly destroyed, bleeding occurs from the uterus or the area of the surgical wound, as well as from injection sites, blood appears in the urine, hemorrhages occur in the chest and abdominal cavities, and pericardium.

Complete non-clotting of blood (afibrinogenemia)

The duration of clinical manifestations is 7-9 hours or more.

Prevention and treatment of DIC syndrome in pregnant women

All pregnant women need to undergo a hemostasis study to identify any disorders. The first sign of concern may be the results of a pregnant woman’s blood test for hemostasis.

The study of the blood coagulation system is called a coagulogram. This analysis allows us to identify the characteristics of coagulation disorders in a pregnant woman and some complications of pregnancy. It is advisable to take a coagulogram once every trimester, and if there are deviations in hemostasis indicators, as prescribed by a doctor, even more often.

Blood for analysis is taken from a vein in the morning on an empty stomach. Diagnosis of the severity of hemostasis disorders will help timely treatment.

Treatment of DIC syndrome during pregnancy

Treatment of DIC syndrome is prescribed by a hematologist in accordance with the characteristics of the stage of development of the disease. IN effective treatment Not only the doctor’s recommendations are important, but also the assistance of the midwife.

The main keys to successful treatment are the elimination of pathological processes in the body and the elimination of the patient’s shock state. Pathological processes aggravate the development of DIC syndrome, therefore, to begin therapy, laboratory diagnosis of all phases of DIC syndrome, establishing its connection with inflammatory and infectious processes, surgical interventions.

Eliminating the resulting shock can help stop the further development of DIC or significantly mitigate its complications.

To combat these phenomena, the doctor prescribes complex transfusion therapy, which consists of intravenous administration of various medications in the form of solutions in order to correct disturbances of homeostasis.

Especially for Love is simple

Criteria for DIC syndrome. Causes of acute DIC syndrome. The patient is given intravenously

Pathogenesis (what happens?) during DIC syndrome

Symptoms of DIC syndrome

Diagnosis of DIC syndrome

Treatment of DIC syndrome

Prevention of DIC syndrome

Which doctors should you contact if you have DIC syndrome?

Description

Diagnostics

Treatment

Causes of DIC syndrome

Clinical picture of DIC syndrome

Treatment of DIC syndrome

What is DIC syndrome?

Causes of DIC syndrome in pregnant women

Stages of development of DIC syndrome

Hypercoagulation (increased blood clotting)

Hypocoagulation (reduced blood clotting) without active dissolution of blood clots and blood clots

Hypocoagulation with active dissolution of blood clots and blood clots

Complete non-clotting of blood (afibrinogenemia)

Prevention and treatment of DIC syndrome in pregnant women

Treatment of DIC syndrome during pregnancy