Definition of DIC syndrome. DIC syndrome: treatment and diagnosis. What can you do

The development of the syndrome in a newborn is possible due to intrauterine development factors or pathologies after birth or during childbirth.

In puberty, the following factors contribute to the development of the disease:

• placenta previa,
• fetoplacental insufficiency,
• death of one child during multiple pregnancy,
• malignant neoplasms of the uterus with damage to its soft tissues,
• severe preeclampsia in late pregnancy,
• unreasonably prolonged stimulation of labor activity.

Reasons for the development of DIC in the perinatal and neonatal period:

• conflicting Rh factor,
• oxygen deprivation,
• premature birth,
• infection during childbirth
• respiratory disorders,
• birth trauma resulting in disorders of the central nervous system.

Symptoms

In the presence of DIC in a pregnant woman, with a probability of 90%, we can say that this problem of blood flow will also be in her baby.

Immediately after birth, it is impossible to visually detect the manifestations of the disease in the newborn. An operational blood test is needed, which will report data on the composition of the blood, plasma and the concentration of thromboplastin in it.

The newborn also goes through all stages of the development of the syndrome.

• hypercoagulation - agglutination of blood cells,
• hypocoagulation - excessive thinning of the blood,
• fibrinolysis is the most critical stage with pronounced thrombocytopenia,
• recovery - normalization of the level of platelets in the blood.

Diagnosis of DIC in a newborn

In an infant, these stages develop rapidly. In the absence of timely diagnosis, the onset of the third stage for most infants becomes fatal, since the body itself cannot cope with the anomaly and multiple internal hemorrhages occur.

The immediate response of specialists to deviations in the hemostasis of a newborn can save a small person from serious complications and tragic consequences.

Complications

Intrauterine development of DIC syndrome threatens with fading of pregnancy, premature birth.

If the disease is detected immediately after birth and prompt treatment, the prognosis is quite favorable.

If the diagnosis is made late, then the probability of death of the baby is 30-50%.

Treatment

What can you do

A young mother needs to be extremely attentive, clearly follow all medical recommendations, agree with the doctor's treatment tactics and take the necessary medications. Only in agreement with specialists, it is possible to restore the baby's blood clotting as quickly as possible and without side effects.

In no case should you resort to the help of alternative therapy. Her methods can only make matters worse.

A young mother needs to remain calm in order to avoid difficulties with lactation. After all, it is breast milk that is the best immunomodulator during infancy, as well as an excellent sedative, but only in the case of a good mental state of the mother.

What does a doctor do

A group of specialists is working on the treatment of DIC in a newborn. They make up an individual treatment regimen in each case. Therapeutic tactics depend on the stage of the disease, its causes and the general condition of the newborn. In any case, doctors adhere to the following principles.

• Immediate initiation of treatment after receiving the results of a blood test.
• Surgical removal of the causes of DIC syndrome. First of all, therapy is aimed at removing the intoxication of the child's body and at the withdrawal from the state of shock.
• Calculation of possible risks, on the basis of which methods of treatment and elimination of symptoms are selected.

In any case, the treatment is complex. As a rule, therapy goes in several directions at once, which allow you to achieve a quick and good effect.

• anti-shock measures
• maintaining the composition and volume of blood and plasma,
• treatment of the underlying disease
• elimination of pathological abnormalities,
• heparin therapy,
• administration of drugs,
• rehabilitation therapy with drugs, vitamins and physiotherapy.

Prevention

Syndromic disturbance of homeostasis is easier to prevent than to treat. In order to avoid childhood pathology, the expectant mother should begin to take care of her child even before conception. Of course, care should continue after birth. For the prevention of DIC in a newborn, it is necessary:

• before pregnancy, identify pathological abnormalities in your body and eliminate them,
• during pregnancy, visit a gynecologist, lead a healthy lifestyle, eat right, protect yourself from negative impacts. All this is done for the purpose of the normal course of pregnancy and fetal development.
• with the onset of labor, call an ambulance or get to the maternity hospital on your own, do not give birth at home,
• if necessary, immediately after childbirth, consent to the treatment of the infant.

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

ETIOPATOGENESIS and CLINICAL PICTURE

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

Microthrombosis and blockade of microcirculation may develop:
throughout the 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 abortions, 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 pathology (previa and early placental abruption, amniotic fluid embolism, especially infected, manual separation of the placenta, hypotonic bleeding, massage of the uterus with its atony), massive blood transfusions (the risk increases when blood is used 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 of the fetus, leukemia, immunocomplex diseases (subacute forms of hemorrhagic vasculitis), hemolytic-uremic syndrome (acute DIC may also occur);
chronic - often complicates malignant neoplasms, chronic leukemia, all forms of blood clotting (erythremia, erythrocytosis), hyperthrombocytosis, chronic heart and pulmonary heart failure, chronic sepsis, vasculitis, giant hemangiomas (Kazabakh-Merritt syndrome), massive blood contact (especially repetitive) with a foreign surface (hemodialysis in chronic renal failure, the use of extracorporeal circulation devices);
recurrent with periods of exacerbation and subsidence.

Depending on the initial mechanism of activation of hemostasis, the following forms of DIC can be distinguished:
with a predominance of activation of the procoagulant link of hemostasis due to tissue thromboplastin entering the bloodstream from outside, causing blood clotting by an external mechanism (obstetric complications, crush syndrome, etc.);
with predominant activity of vascular-platelet hemostasis as a result of a generalized lesion of the 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 of cell membranes (extracorporeal circulation, prosthetics of blood vessels and heart valves, intravascular hemolysis, acute graft rejection).

Of great importance in the development of DIC is the aggregation of blood cells (sludge syndrome) in the microcirculation zone, leading to its disruption. At the same time, the release of substances with procoagulant activity from cells exacerbates the activation of the hemostasis system, contributes to the development of multiple microthromboses and the progression of DIC. 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 (M.S. Machabeli):
I stage - hypercoagulation stage - generalized activation of the process of coagulation and aggregation of cells (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);
II stage - increasing consumption coagulopathy - there is a decrease in the number of platelets and fibrinogen due to their loss (consumption) for the formation of blood clots, the consumption of plasma coagulation factors;
III stage - stage of severe hypocoagulation - there is a formation of soluble fibrin-monomer complexes with resistance to thrombin; The pathogenesis of this stage is associated with several factors:
- consumption coagulopathy,
- activation of fibrinolysis (during which fibrin degradation products are formed that have anticoagulant and antiplatelet properties);
- blocking the polymerization of fibrin monomers, which are formed under conditions of excess thrombin in 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 detect it, attention should be paid to slight thrombosis of punctured veins and needles during blood sampling 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, a decrease in diuresis due to impaired microcirculation in kidneys as an early sign of developing renal failure)

!!! Stage III of DIC is critical, it is it that often ends in death even with intensive therapy that corrects the hemostasis system.

Schematically, the pathogenesis of DIC can be represented by the following sequence of pathological disorders: activation of the hemostasis system with a change in phases of hyper- and hypocoagulation - intravascular coagulation, aggregation of platelets and erythrocytes - microthrombosis of blood vessels and blockade of microcirculation in organs with their dysfunction and dystrophy - depletion of the components of the coagulation system blood and fibrinolysis, physiological anticoagulants (antithrombin III, proteins C and S), a decrease in the content of platelets in the blood (consumption thrombocytopenia). The toxic effect of protein decay products, which accumulate in large quantities both in the blood and in organs as a result of a sharp activation of proteopic systems (coagulation, kallikreinkinin, fibrinolytic, complement, etc.), circulatory disorders, hypoxia and necrotic changes in tissues, frequent weakening of the detoxification and excretory functions of the liver and kidneys.

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

Complications of DIC syndrome:
blockade of microcirculation in organs, leads to a violation of their functions (the most common target organs in this case are the lungs and (or) kidneys due to the peculiarities of microcirculation in them) in the form of acute pulmonary insufficiency and acute renal failure; possible development of liver necrosis; the presence of thrombosis of small vessels in the 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 ischemic stroke; due to thrombosis of the vessels of the adrenal glands, the development of acute adrenal insufficiency is possible
hemocoagulative shock is the most severe complication of DIC and is associated with 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 develops in diseases characterized by intravascular hemolysis);

!!! characteristic of acute DIC is a combined lesion of two or more organs

DIAGNOSTICS

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

Diagnosis should be based on the following activities:
critical analysis of the clinic;
a thorough study of the hemostasis system to determine the form and stage of the syndrome;
assessment of the response of hemostasis to ongoing therapy with antithrombotic drugs.

Laboratory manifestations of DIC include:
thrombocytopenia;
fragmentation of erythrocytes(schizocytosis) due to their damage by fibrin strands;
prolongation of PT (prothrombin time; serves as an indicator of the state of the external clotting mechanism), APTT (activated partial thromboplastin time; reflects the activity of the internal clotting mechanism and the level of factor XII, factor XI, factor IX, factor VIII, high molecular weight kininogen and prekallikrein), and thrombin time;
a decrease in fibrinogen levels as a result of the consumption of coagulation 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 DIC THERAPY

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

In the treatment of DIC, the following principles should be followed::
complexity;
pathogeneticity;
differentiation depending on the stage of the process.

!!! the meaning of therapeutic measures is to stop intravascular thrombosis

First of all, the actions of the doctor should be aimed at elimination or active therapy of the underlying cause of DIC. These include measures such as the use of antibiotics (broad-spectrum with the connection of directed 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 an urgent referral or transfer to the intensive care unit, the mandatory involvement of transfusiologists and specialists in the pathology of the hemostasis system in the treatment process.

Infusion-transfusion therapy for DIC. High efficiency of treatment is achieved by early connection 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 lack 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 is especially intense - several times faster than all procoagulants); allow you to enter into the bloodstream a complete set of 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 antithrombin III administered with plasma. It also prevents clotting of plasma by circulating thrombin. With DIC of an infectious-toxic nature and the development of pulmonary distress syndrome, plasmacytapheresis is indicated, since leukocytes play an important 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 the treatment of DIC and the diseases that cause it, reduce mortality by several times, which allows us to consider them one of the main methods of treating patients with this disorder of hemostasis.

With significant anemization and a decrease in hematocrit it is necessary to carry out transfusions of fresh canned blood (daily or up to 3 days of storage), erythrocyte mass. The requirement for transfusion of fresh blood preparations is due to the fact that microclots are formed in preserved blood for more than 3 days of storage, the entry of which into the blood leads only to the potentiation of DIC. Hematocrit must be maintained within at least 22%, hemoglobin level - more than 80 g / l, erythrocytes - 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 organs. We must not forget that excessively abundant blood transfusions lead to aggravation of DIC, and therefore, when carrying out infusion-transfusion therapy, caution is necessary - one must strictly take into account the amount of transfused blood, as well as blood loss, loss of body fluid, 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, but also lead to its irreversibility.

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

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

The use of heparin in the treatment of DIC justified at any stage due to the fact that it counteracts the development of intravascular thrombosis. 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 way to administer heparin is intravenous drip (in isotonic sodium chloride solution, with plasma, etc.). In some cases, it can be supplemented with subcutaneous injections into the tissue of the anterior abdominal wall below the umbilical line. Intramuscular injections are not recommended because of the different rate of resorption of the drug (which makes it difficult to dose), the easy formation of extensive, infected hematomas in the conditions of DIC. The tactics of heparin therapy depend on the course of DIC and the presence or absence of a wound surface in the patient. So, in the acute course of the syndrome, a single application of the minimum dose of heparin can be dispensed with. This may be enough to break the vicious circle: intravascular coagulation - bleeding. In the subacute course of 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 even refusing to carry it out. The dose of heparin varies depending on the form and phase of DIC: in stage I (hypercoagulation) and at the beginning of the initial period (with still sufficiently preserved blood clotting), heparin has a prophylactic value and its daily dose in the absence of heavy initial bleeding can reach up to 40,000 -60,000 IU (500-800 IU / kg). An initial dose of 5,000–10,000 IU is given as an intravenous bolus followed by a drip. In stage II of DIC, heparin has a therapeutic value: it neutralizes the action 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 bleeding, from an ulcer or decaying tumor, etc.) or there is a high risk of its occurrence (for example, in the early postoperative period), the daily dose of heparin should be reduced by 2-3 times or it use should be abolished altogether. In such situations, as in the phase of deep hypocoagulation (stage III DIC), the introduction of heparin is used mainly to cover transfusions of plasma and blood (for example, at the beginning of each transfusion, 2,500–5,000 IU of heparin are administered drip together with a hemodrug). In the presence of "acute phase" proteins in the patient's blood (for example, in acute infectious-septic processes, massive tissue destruction, burns), the doses of heparin should be maximum, because this inactivates heparin, which prevents its anticoagulant effect. The insufficient effect of the action of heparin may be associated with blockade and a decrease in the content of its plasma cofactor, antithrombin III, in the patient's plasma.

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

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

Getting the patient out of shock promotes the use of anti-opioid drugs (naloxone, etc.).

The basis of therapy for subacute form of DIC is 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 with plasmapheresis (removal of 600-1200 ml of plasma daily) with partial replacement with fresh, native or fresh frozen plasma, partially with blood-substituting solutions and albumin. The procedure is carried out under the cover of small doses of heparin.

The chronic form of DIC is treated similarly.. If the patient has polyglobulia and blood clotting, he is shown blood exfusion, staging of leeches, cytopheresis (removal of red blood cells, platelets and their aggregates), hemodilution (reopoliglyukin intravenously up to 500 ml daily or every other day). With hyperthrombocytosis - antiplatelet agents (acetylsalicylic acid 0.3–0.5 g daily, trental, etc.).

Disseminated intravascular coagulation occurs with the accelerated formation of blood clots in response to shock, massive trauma, severe infection, obstetric pathology. It is characterized by bleeding due to the massive consumption of factors responsible for stopping them.

May be asymptomatic or lead to acute respiratory and renal failure. To make a diagnosis, you need to take into account the symptoms, conduct blood tests. Treatment involves the introduction of anticoagulants, antiplatelet agents, transfusion of blood or its components, plasmapheresis. Read more in this article.

📌 Read this article

What is DIC syndrome

Due to the influence of pathological factors, loose thrombotic masses, microthrombi, and accumulations of platelets are formed in small vessels. They disrupt blood circulation, microcirculation, lead to oxygen starvation, dysfunction of internal organs. Most of all, dystrophy and cell destruction cover the parenchyma of the kidneys, lungs, liver and adrenal glands. This is due to the developed microcirculatory vascular network in them.

The danger of thrombohemorrhagic syndrome also lies in the fact that the main supply of coagulation factors, platelets, is usually spent on the formation of clots inside the vessels. Therefore, the risk of heavy bleeding, which is very difficult to stop, increases. The development of DIC can be caused by various pathologies in which blood flow and its movement in the capillaries are disturbed.

According to clinical manifestations, the disease can have a latent, protracted course, as well as lightning-fast reactions leading to death. Damage to the internal organs are local and minor, or there is widespread blood clotting in all small vessels with an extremely severe course.

Causes in adults and children

DIC is provoked by conditions in which there is a destruction of the inner layer of blood vessels, blood cells, and tissue damage. This causes activation of blood coagulation, impaired blood flow in small capillaries, venules and arterioles. The reasons for this condition may be:

• infections of a viral or bacterial nature, complicated by sepsis;
• shock state;
• toxicosis of the second half of pregnancy (gestosis);
• earlier detachment of the placenta;
• fetal death;
• atony of the uterus with profuse bleeding;
• C-section;
• metastases in malignant neoplasms;
• embolism with amniotic fluid;
• prolonged compression of the limbs;
• extensive trauma, burns or surgery, especially in conditions of cardiopulmonary bypass;
• blood transfusion, organ transplant;
• bleeding;
• or ;
• abortions, childbirth;
• long stay of the catheter in the vessel;
• intravascular destruction of red blood cells in case of poisoning with hemolytic poisons (lead, mercury, acetic acid, snake bite);
• leukemia;
• radiation sickness;
• intensive anticancer therapy.

Forms of manifestation

According to the rate of increase in microcirculation disorders and their complications, DIC is divided into acute, subacute and chronic.

Spicy

It occurs in patients with a massive intake of substances into the blood that increase the formation of blood clots. It happens in severe, critical conditions (polytrauma, difficult childbirth, operations, tissue compression). A feature of this form is the rapid change in the phases of the disease, the absence of protective reactions of the body that prevent massive coagulation.

Subacute

It takes weeks (up to 1 month) to develop. The course is more favorable than in the acute form, the insufficiency of the function of the internal organs is less pronounced or moderate, bleeding is weak or moderate. Diagnosed with tumors of the blood, lungs, kidneys, rejection of transplanted tissues, the use of hormonal contraceptives.

If they are joined by blood loss, blood transfusion, the introduction of hemostatic agents, stress, then it can turn into an acute process.

Chronic

Lasts several months. Disorders of the organs grow slowly, usually characterized by chewed lesions. It is caused by chronic inflammation of the lungs, liver, tumors, autoimmune diseases, leukemia, and widespread atherosclerosis. To identify clinical signs, as a rule, is not enough. It is necessary to confirm DIC with laboratory diagnostics.

Classification

Several types of the disease are known. Clinical variants of the course can manifest themselves depending on:

• prevalence of lesions - limited (one organ) and generalized (several systems or the entire body);
• degree of compensation - compensated (no symptoms, blood clots are destroyed by activation of fibrinolysis, coagulation factors are synthesized or out of reserves), subcompensated (there is bleeding of moderate severity), decompensated (a cascade of reactions of resorption of blood clots is triggered, coagulation is impaired, severe bleeding).

Stages of progression

The peculiarity of the disease is the successive change of symptoms. In the classic version, DIC has the following stages of progression:

1. Increased blood clotting and cell aggregation. Caused by the release of thromboplastin from destroyed tissues or similar substances. They activate the processes of thrombosis. Lasts from ten minutes to several months.
2. A coagulation disorder due to a lack of fibrinogen, platelets, coagulation factors, since they were intensively consumed in the first phase, and new ones have not yet formed.
3. Critical phase of low clotting ability. There is no fibrinogen in the blood, erythrocytes are destroyed, coagulation properties may be completely absent.
4. Recovery or development of complications. There are either residual signs of dystrophy and destruction, followed by recovery, or acute organ failure is growing.

Symptoms in the pathology of blood coagulation

Clinical manifestations of thrombohemorrhagic syndrome consist of signs of the underlying disease, of which it is a complication, and the symptom complex of DIC.

state of shock

Associated with blood clotting, microcirculation stop, oxygen starvation of tissues. In the process of formation of blood clots and their destruction, many toxic compounds enter the blood, they lead to a violation of the systemic circulation. Most often it is difficult to determine which changes arose due to microthrombosis, and which were its cause. The symptoms of shock are:

• a sharp drop in blood pressure and a decrease in central venous pressure;
• acute disorders of microcirculation;
• low functional activity of internal organs.

Complications may be renal, hepatic, respiratory failure, or combinations thereof. DIC against the background of shock always has a severe course, and with a long period - catastrophic.

In the first phase, excessive blood clotting is obvious, it can even be visual, when a blood clot forms even before analysis, immediately after sampling. In the second phase, against the background of excess, insufficient coagulation also appears. At this time, some tests show an increased, and others a sharply reduced ability to clot formation.

Hemorrhagic syndrome

Increased bleeding most often occurs in the acute course of the disease. Abundant blood loss can also occur against the background of a normal concentration of fibrinogen or a slightly reduced one. Local bleeding can be both a manifestation of DIC and diseases of the organs themselves (gastric ulcer, kidney infarction, uterine atony). Common signs of hemorrhage are:

• hemorrhages in the skin, hematomas;
• nasal, pulmonary, renal blood loss;
• hemorrhage in the brain tissue, adrenal glands, pericardial sac;
• impregnation of plasma and erythrocytes into the chest and abdominal cavity.

Acute renal failure

Decreased urination up to its absence. Protein and erythrocytes are found in the urine. In the blood, the balance of salts, acids and alkalis is disturbed, urea, creatinine and residual nitrogen increase. The most severe violation of the kidneys occurs when combined with hepatic or pulmonary insufficiency,.

Target organ damage

The progression of DIC leads to a generalized disorder - multiple organ failure. Her symptoms:

• destruction of liver cells with jaundice and pain in the right hypochondrium;
• erosion, ulcers and bleeding on the gastric mucosa;
• ulcerative defects in the intestine;
• stopping the movements of the intestinal wall, the penetration of toxins into the blood (weakening of intestinal motility or obstruction;
• -, headache, impaired consciousness, there may be;
• pituitary and adrenal insufficiency - severe, diarrhea, dehydration.

Diagnosis of DIC syndrome

To make a diagnosis, the presence of bruising on the skin, bleeding from several organs and such laboratory signs (according to a blood test) are taken into account:

• destroyed red blood cells;
• decrease in platelets and fibrinogen;
• an increase in the level of fibrin destruction products;
• low activity of antithrombin 3;
• prolongation of thrombin time and activated thromboplastin;
• clots do not form or quickly disintegrate.

In case of doubt, a determination is prescribed, paracoagulation tests, soluble fibrin complexes.

Treatment of the disease

If there are no clinical manifestations of DIC, then its laboratory signs are corrected by influencing the underlying condition. In the acute course of the disease, it is necessary to urgently eliminate the cause of its appearance, including by surgery. For drug therapy used:

Many famous people have had Marfan syndrome, the signs of which are pronounced. The reasons lie in the improper development of connective tissue. Diagnosis in adults and children is no different. What is the treatment and prognosis?

The syndrome of disseminated intravascular coagulation is a complex process that often accompanies many pathologies. It is characterized by the occurrence of widespread blood coagulation in the circulation and blockade of microcirculation, hypoxia in tissues and disruption of organs.

DIC in children due to the increase in the properties of blood viscosity slows down normal blood flow. When passing through small capillaries, the blood stratifies, plasma and red blood cells are released. In a child, this process is manifested by staining the skin with a marble pattern. Subsequently, peripheral blood becomes depleted, anemia and intoxication develop.

Causes of pathology

The main factors contributing to the development of DIC correlate with factors in the process of fetal development. With a high probability, the doctor can predict the occurrence of the syndrome in newborns when fixing premature detachment of the placenta or intrauterine gestational lesion.

As DIC grows older, the syndrome in a child is formed when the body is affected by inflammatory and infectious diseases. Provoking factors include Rh conflict with the mother, improper functioning of the liver and kidneys, blood transfusion of the wrong group.

Symptoms of the disease

DIC in newborns or older children is a serious complication of various maternal diseases in the perinatal period. In newborns, the pathology often takes a fulminant or acute form and has four stages of development:

• Stage of hypercoagulability.
• stage of hypocoagulation.
• fibrinolytic stage.
• Recovery stage.

In the fetus or newborn, DIC often develops when there is fetal injury or tissue necrosis that releases tissue thromboplastin into the maternal and fetal circulation. Violation of tissue integrity occurs in the case of detachment of a normally located placenta or the death of one of the two fetuses.

The acute course of the pathology is characterized by the fact that the signs of DIC syndrome have been occurring for several hours. The acute form manifests itself with sepsis, with extensive burns or frostbite, with prolonged compression syndrome, etc.

In most patients, there is a violation of the respiratory system, which is manifested by severe shortness of breath. In 60 - 70% of cases, kidney failure develops, pain in the lower back, the volume of urine decreases, the presence of erythrocytes, protein, and cylinders is detected in it.

Diagnostics

The methods of conducting and the volume of laboratory studies in the development of DIC depend on the conditions in which the treatment is carried out.

Clinical data are determined according to two factors:

1. The severity of the violation of blood flow in the microcirculation of various organs, which explains their dysfunction.
2. The degree of spread and intensity of development of hemorrhage. In addition, bleeding affects the functioning of internal organs, changing the symptoms of the disease.

Violations of microcirculation can provoke insufficiency of the functioning of systems and organs, depending on the location of the lesion and prevalence. Such a process manifests itself as follows:

• Signs of abnormal peripheral blood flow - blanching of the skin, marble pattern on the skin, pastosity of the hands and feet.
• The occurrence of an acute form of kidney failure.
• Acute form of insufficiency of respiratory processes.
• Acute deviations of blood flow in the brain.
• hepatorenal syndrome.
• Acute adrenal insufficiency.

Pathology treatment process

The organization of the treatment of DIC syndrome involves the elimination of the cause of its development. Subsequently, experts base therapy on ridding the body of intoxication, normalizing blood flow and eliminating complications in the development of such. Much attention must be paid to the rheological characteristics of the blood when the body is affected by influenza and catarrhal pathologies, which are complemented by a strong increase in body temperature. This can lead to massive DIC in infants or toddlers.

The process of treating this pathology is a complex clinical problem that needs an integrated approach. It is important to adhere to the following rules and principles of therapy:

• Treatment of an acute form of pathology should begin immediately after taking blood for analysis. And only in chronic forms, a preliminary study is allowed.
• The doctor should immediately take measures to eliminate the etiological factors of DIC and influences that can aggravate its course. First of all, the elimination of shock and intoxication is organized.
• In the course of treatment, it is mandatory to evaluate the clinical picture, taking into account the potential danger of treatment, which can only exacerbate the manifestations of DIC.

The main components of complex treatment include:

1. Elimination of the causes of the disease and pathogenetic therapy of primary pathology.
2. Anti-shock treatment and maintenance of the required composition and volume of blood circulating in the vessels.
3. Jet infusions.
4. Heparin therapy.
5. The introduction of inhibitors depending on the indications.
6. Previously, the use of drugs that help improve microcirculation and reduce the loss of platelets from the blood stream.
7. Replacement of lost red blood cells.
8. In severe hypocoagulation, severe bleeding and pronounced thrombocytopenia, transfusion of platelet concentrates is performed, as well as the introduction of large doses of counterkal.
9. Organization of local hemostasis using a fibrogastroscope.

term DIC denotes a nonspecific general pathological process, which is based on diffuse diffuse blood clotting in the vessels with the formation of many microclots and aggregates of blood cells, blocking blood circulation in the organs and the development of deep dystrophic changes in them.

Major pathological conditions in which DIC of the blood develops:

Infections - sepsis, bacterial dysentery, viral hepatitis, salmonellosis, HFRS, food poisoning, tropical fevers, etc.

shock - anaphylactic, septic, traumatic, cardiogenic, hemorrhagic, burns, - with prolonged crushing syndrome and others.

Acute intravascular hemolysis - transfusions of incompatible blood, crises of hemolytic anemia, poisoning with hemolytic poisons, hemolytic-uremic syndrome, etc.

Tumors- disseminated forms of cancer III-IV stage, Trousseau's syndrome, acute leukemia, blast crises of chronic leukemia, etc.

Injuries- fractures of tubular bones, polytrauma, burns, frostbite, electrical trauma, crash syndrome, etc.

Traumatic surgical interventions - major abdominal and orthopedic operations, operations on the lungs, liver, pancreas, operations for polytrauma, etc.

Obstetric and gynecological pathology - detachment, presentation and rupture of the placenta; embolism with amniotic fluid; atonic uterine bleeding; antenatal fetal death; stimulation of labor activity and fruit-destroying operations; postpartum sepsis; cystic skid; criminal abortion; severe late preeclampsia; eclampsia.

Immune and immunocomplex diseases- SLE, systemic scleroderma, hemorrhagic vasculitis, acute diffuse glomerulonephritis, etc.

Cardiovascular pathology - macrofocal myocardial infarction, congestive heart failure, cardiac asthma, congenital "blue" malformations, deep vein thrombosis of the lower leg, pulmonary embolism, etc.

Acute and subacute inflammatory-necrotic and destructive processes and diseaseslevaniya - acute pancreatitis, systemic vascular lesions, nonspecific lung diseases, bronchial asthma, liver disease, kidney disease and acute renal failure, diabetes mellitus, radiation sickness.

Hyperviscosity Syndrome - polyglobulinemia (polyglobulia) of various origins, paraproteinemia and cryoglobulinemia, erythrocytosis and erythremia.

Transplantation organs and tissues, prosthetics of valves and vessels, extracorporeal procedures, etc.

Massive blood transfusions and reinfusions of blood.

Thrombotic thrombocytopenic purpura.

Poisoning by snake hemocoagulating venoms.

Medicinal forms iatrogenic - large doses of antibiotics, corticosteroids, cytostatics, α-agonists, ε-ACC, misuse of anticoagulants and fibrinolytics, oral contraceptives, etc.

The basis of the internal combustion engine in all cases is excessive (pathological) activation of hemostasis, leading to massive blood coagulation, blockade of microcirculation in vital organs (lungs, kidneys, liver, adrenal glands, etc.) by loose fibrin masses and cell aggregates, and the development of multiple organ dysfunction. DIC is characterized by a significant consumption of coagulation factors and platelets during the formation of numerous thrombi and blood clots, activation of fibrinolysis, accumulation in the bloodstream of fibrin/fibrinogen breakdown products (PF/f) and other proteins that exhibit anticoagulant properties and have a damaging effect on the walls of blood vessels. This leads to the development hypocoagulation state , which may be accompanied by severe hemorrhagic syndrome in the form of bleeding of various localization.

DIC-syndrome - pathogenesis. ICE - is such variant of coagulopathy, in which especiallyclearly there is an imbalance between the coagulation, anticoagulationand fibrinolytic systems of the body. A feature of the "tragedy" of DIC is disseminated, scattered, multiple formation of blood clots and fibrin clots, in fact, where hemostasis is not required.

Etiological factors lead to hypercoagulation, the formation of small loose fibrin clots or microthrombi in almost the entire microcirculatory system. They are immediately dissolved by the fibrinolytic system. New blood clots and new clots are formed and all the main factors of the coagulation system - platelets, prothrombin, fibrinogen - are gradually depleted. Hypocoagulation develops due to consumption coagulopathy. If the integrity of the vascular wall is disturbed somewhere, a thrombus cannot form. At the same time, there are anticoagulant substances in excess, due to which the bleeding cannot be stopped either. Fibrin clots and microthrombi formed in microvessels block tissue blood flow, cause tissue ischemia, disrupt the function of such vital organs as the heart, lungs, and kidneys.

The mechanism of development of DIC

I phase. Formation of active thromboplastin- the longest phase of hemostasis. Plasma factors take part in it. (XII, XI, IX, VIII, X, IV, V) and platelet factors (3, 1).

II phase. The transition of prothrombin to thrombin. Occurs under the action of active thromboplastin and the participation of calcium ions (factor IV).

III phase. Formation of fibrin polymer. Thrombin (with the participation of calcium ions - factor IV and platelet factor - 4) converts fibrinogen into fibrin monomer, which, under the action of plasma factor VIII and platelet factor 2, turns into insoluble fibrin-polymer filaments.

Changes in procoagulants in the hemostasis system, activation of the platelet link lead to platelet aggregation with the release of biologically active substances: kinins, prostaglandins, catecholamines and others that affect the vascular system.

With a slow flow of blood through the branching of small vessels, it is stratified into plasma and red blood cells that fill different capillaries. Losing plasma, erythrocytes lose their ability to move and accumulate in the form of slowly circulating, and then non-circulating formations. Stasis, aggregation, and then lysis occur, and blood thromboplastin associated with the stroma of erythrocytes is released. The introduction of thromboplastin into the bloodstream causes the process of intravascular coagulation. The fibrin strands that fall out at the same time entangle clumps of erythrocytes, forming "sludges" - lumps that settle in the capillaries and further violate the homogeneity of the blood structure. An important role in the development of the "sludge" phenomenon is played by two interrelated phenomena - a decrease in blood flow and an increase in blood viscosity (MA Repina, 1986). There is a violation of the blood supply to tissues and organs. In response to the activation of the coagulation system, protective mechanisms are activated - the fibrinolytic system and cells of the reticuloendothelial system. Against the background of disseminated intravascular coagulation due to increased consumption of procoagulants and increased fibrinolysis, increased bleeding develops.

DIC-syndrome - classification.

Clinical classification.

The clinical picture of DIC syndrome consists of the signs of the underlying disease that caused intravascular coagulation, and the DIC itself. According to the clinical course, it happens:

sharp (up to lightning fast);

subacute;

chronic;

recurrent.

Stages of DIC:

Hypercoagulability and platelet aggregation.

Transient, with increasing consumption coagulopathy, thrombocytopenia, multidirectional shifts in general coagulation tests.

Deep hypocoagulation up to complete blood incoagulability.

Poor outcome or recovery stage.

1. hypercoagulation stage- at this stage, there is a sharp increase in the adhesiveness of platelets, and in connection with this, the activation of the first phase of coagulation, an increase in the concentration of fibrinogen. These indicators can be determined using a coagulogram, which allows you to determine the state of the coagulation and anticoagulation system.

Blood clots form in the peripheral vessels: platelets stick together, the formation of fibrin globules begins, and blood clots form in small vessels. This thrombosis of small vessels, as a rule, does not lead to necrosis, however, it causes significant ischemia of the tissues of various organs.

Thrombosing occurs throughout the body, so the syndrome is called disseminated (disseminated). The period of hypercoagulation is characterized by activation of plasma systems of blood coagulation, intravascular aggregation of platelets and other blood cells, microcirculation disorders in various organs as a result of blockade of the vascular bed by fibrin masses and cell aggregates. The hypercoagulable phase can develop gradually, with a slow intake of small doses of prothrombinase. However, a slow flow can end in an explosion with the rapid development of DIC.

In addition to disseminated intravascular coagulation, in some cases only local limited intravascular coagulation and thrombus formation are noted.

2. Consumption coagulopathy. As a result of disseminated intravascular coagulation, the main resources of the factors of the blood coagulation system (fibrinogen, prothrombin) leave, they become scarce. Such a depletion of blood clotting factors leads to the fact that bleeding develops, if it is not stopped then from the main source, and bleeding from other vessels is also possible, even with minor injuries.

Intravascular coagulation also causes activation of the fibrinolytic system, leading to the dissolution of blood clots and creating prerequisites for the development of hemorrhagic syndrome. Naturally, the inclusion of mechanisms that cause hypocoagulation has a certain sequence and significance throughout the entire process: exhaustion of blood coagulation mechanisms - accumulation of fibrin degradation products - activation of the fibrinolytic system. Based on this position, some authors detail the phase of hypocoagulation, highlighting a number of stages in it. So, M. S. Machabeli (1981) and V. P. Balud (1979) distinguish between the phases of hypocoagulation and hypocoagulation with secondary fibrinolysis, A. V. Papayan (1982) - stages of consumption coagulopathy and afibrinogenemia, or pathological fibrinolysis, 3. C Barkagan (1980) - stages of hypocoagulation and deep hypocoagulation. As already noted, for practical purposes, it is possible to isolate the general phase of hypocoagulation.

In the coagulogram, there are signs of hypo- or afibrinogenemia, but the concentration of fibrinogen S increases even more, it already turns into fibrin, which contributes to the formation of peptidases, resulting in vasospasm, which further increases the ischemia of various organs. Characterized by hypoprothrombinemia, the number of platelets decreases further. As a result, the blood loses its ability to clot. At the same stage, the fibrinolytic system is activated. This leads to the fact that the formed blood clots begin to dissolve, melt, including melting of the clots that clog the bleeding vessels.

3. Third stage - fibrinolysis. It begins as a defensive reaction, but as a result of the melting of clots of bleeding vessels, bleeding intensifies, which becomes profuse.

The indicators of the coagulogram at the stage of fibrinolysis differ slightly from those at the stage of consumption coagulopathy, therefore this stage is recognized by clinical manifestations: all tissues, like a sponge, begin to bleed.

If therapeutic measures are effective, then this process can be stopped at any of the stages, including sometimes at the stage of fibrinolysis. Then develops - 4 phase.

4. Phase recovery. Here, signs of multiple organ failure begin to come to the fore. As a result of prolonged ischemia, cardiovascular insufficiency occurs. Possible cerebrovascular accident.

The onset of this stage is recorded in the coagulogram: the indicators may improve or normalize. Depending on the phase of DIC in which treatment is started, mortality is about 5% at the stage of hypercoagulability, 10-20% at the stage of consumption coagulopathy, 20-50% at the fibrinolysis stage, and up to 90% at the recovery stage.

In the fourth stage, with its favorable outcome, to one degree or another, the function of the organs is restored, which depends on the degree of their damage (dystrophic changes, sclerosis, etc.). The stage can end with a complete recovery. It is possible to develop severe complications already in the absence of DIC as such - renal, hepatic failure, neurological, cardiac and other complications.

V. P. Baluda (1979) identifies several main causes of death in the acute course of DIC):

1. The death of the body can occur instantly when the main vessels of vital organs are blocked.

2. If the body does not die in the first minutes from blockage of blood vessels by blood clots, then death can be determined by the development of severe hemorrhagic syndrome in the form of local bleeding at the site of vascular damage (surgery, trauma), or generalized bleeding and hemorrhage into internal organs.

3. In a later period, a lethal outcome is possible due to severe dysfunction of individual organs (kidneys, liver, lungs, spleen, myocardium, brain, pituitary gland, adrenal glands, digestive tract).

DIC-syndrome - clinic. The course of DIC can be acute, subacute, protracted and undulating. At the same time, "their own" etiological factors are characteristic for various variants of the course. Acute DIC develops in shock conditions, severe forms of sepsis, massive injuries and burns, acute intravascular hemolysis, bites of some snake species. Protracted DIC is observed in oncological diseases, immunocomplex and myeloproliferative processes, circulatory failure in patients with cardiomyopathies, liver cirrhosis, severe active hepatitis, chronic hemodialysis. An undulating, relapsing course is observed during destructive processes in organs caused by virulent microflora or toxic influences.

Hemorrhagic manifestations in DIC have their own characteristics. Can be bleeding local type or widespread hemorrhage. In the first case, there are hemorrhages from wounds with injuries, postpartum and post-abortion uterine bleeding, hematuria. These bleeding is prolonged and torpid to routine hemostatic therapy. In the case of widespread hemorrhages, a mixed "bruising-hematoma" type of bleeding is noted in combination with nasal, gastrointestinal, pulmonary, uterine bleeding, diffuse bleeding of blood into the pleural and abdominal cavities, and the pericardium.

DIC is characterized by a combination of hemorrhagic disorders with a number of syndromes caused by microcirculation disorders in organs, their degeneration and dysfunction. A "shock" lung and acute respiratory failure, acute renal failure, dyscirculatory encephalopathy, adrenal insufficiency, acute erosions and ulcers in the stomach and intestines develop.

The duration of clinical manifestations of DIC can reach 7-9 hours or more. Changes in the hemocoagulation system, determined using laboratory methods, persist longer than clinical ones. Therefore, laboratory diagnosis of DIC is of paramount importance: it allows you to more accurately determine the degree or phase of the syndrome and choose the right treatment.

Clinical manifestations of DIC of blood can be diverse depending on the involvement of various organs and systems. Yes, there are signs dysfunction:

of cardio-vascular system(tachycardia, hypotension, collapse, shock);

lungs(shortness of breath, wheezing, pulmonary edema, respiratory failure);

brain(lethargy, drowsiness, sensory disturbances and motorfunctions, stroke, stupor, coma);

kidney(decreased diuresis, proteinuria, hematuria, anuria, acute renal failure);

adrenal glands(acute insufficiency with a drop in blood pressure and hypoglycemia);

liver(hyperbilirubinemia, hepatosis, liver failure);

gastrointestinal tract(dysmotility, erosion and ulcers), etc.

Clinically I ICE phase proceeds very variably: from asymptomatic forms ("laboratory DIC") to manifestations of thrombosis of any localization (myocardial infarction, transient cerebrovascular accident, ischemic stroke, pulmonary embolism, thrombosis of mesenteric vessels, etc.). Possible tachycardia, muffled heart tones, shortness of breath, drop in blood pressure, in severe cases - the development of multiple organ failure.

InIIICE phase may be observed: tachycardia, shortness of breath, hypotension, collapse, pallor or marbling of the skin, decreased diuresis due to impaired renal function, impaired intestinal motility, depression of consciousness, etc. In severe cases, multiple organ failure syndrome (MOS) develops. In this phase, thrombosis and bleeding of any localization are possible; however, in some patients, the disease may be asymptomatic ("DIC of the blood without DIC").

IIIDIC phase often critical, mortality from acute DIC reaches 40-50%. A pronounced hemorrhagic syndrome with a mixed type of bleeding is characteristic: nasal, gingival, uterine, gastrointestinal and hemorrhoidal bleeding, hemorrhages in the sclera and at injection sites, numerous petechiae and "bruises" on the skin, bleeding from surgical wounds, micro- and macrohematuria, hemoptysis, etc. The phenomena of cardiovascular, respiratory, renal, hepatic insufficiency are expressed; often there is a picture of shock with pallor or marbling of the skin, acrocyanosis and cold extremities, shortness of breath, hypotension and confusion. Death can occur as a result of hemorrhages in the brain, pituitary gland, adrenal glands; acute gastrointestinal bleeding; acute renal or cardiopulmonary failure, etc.

Early diagnosis of DIC is facilitated by the identification of underlying diseases and conditions (infectious-septic processes, all types of shock and severe hypovolemia, acute intravascular hemolysis, obstetric pathology, etc.). It is important to note that DIC of blood is necessaryto detect at an early stage, i.e. to DIC, there are no pronounced clinical manifestations yet, but there are already laboratory symptoms. The main task of the doctor is to interrupt DIC during the I-II phases of the process (before the development of irreversible disorders), while preserving the functions of the organs and systems of the patient's body.

The most important help for a clinician in recognizing DIC in the early stages, before the appearance of a detailed clinical picture, is laboratory diagnostics.

The diagnosis of chronic DIC is made on the basis of laboratory studies of the hemostasis system.

DIC-syndrome - diagnostic methods.

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

Diagnostics should be based on the following activities:

critical analysis of the clinic;

a thorough study of the hemostasis system to determine the form and stage of the syndrome;

assessment of the response of hemostasis to ongoing therapy with antithrombotic drugs.

Diagnosis of DIC is based on a set of studies that characterize the hemostasis system. They should be appointed as early as possible, repeated in dynamics. This is due to the fact that with DIC, almost all links of hemostasis are disturbed, often these violations are in different directions.

The general trend of changes in hemocoagulation tests is as follows: the number of platelets decreases, the clotting time lengthens, the content of fibrinogen decreases, the prothrombin index decreases, fibrinogen degradation products increase, and clot retraction decreases.

AT hypercoagulation phase noted shortening of blood clotting time, plasma recalcification, increased consumption of prothrombin, shortening of prothrombin and thrombin time. The same information is provided by standardized samples - kaolin-cephalin time, autocoagulation test, etc. Also increased adhesion of platelets.

At the end of the hypercoagulation phase, in the initial period of hypocoagulation, the following typical shifts are found (3. S. Barkagan, 1980):

a) the presence of fragments of erythrocytes in a peripheral blood smear (fragmentation phenomenon);

b) progressive thrombocytopenia;

c) prolongation of prothrombin time;

d) prolongation of thrombin time;

e) decrease in the level of fibrinogen in plasma;

e) increase in plasma levels of degradation products of fibrinogen and fibrin (PDF);

g) an increase in the content of antiheparin factor (factor 4) in platelet-free plasma;

h) in some cases, the preservation of positive paracoagulation tests (ethanol, protamine sulfate), which are usually noted in the early stages.

Hypocoagulation phase characterized a pronounced violation of blood coagulation, which is reflected by all low- and high-sensitivity coagulation tests. It is necessary to determine antithrombin III, as well as plasminogen.

The table shows the indicators of hemostasis at various stages of DIC (according to E.P. Ivanov)

DIC-syndrome - treatment.

The general scheme for the treatment of DIC is shown in the figure. Heparin, antiplatelet agents (aspirin), reopoliglyukin are usually administered in the early stages of the syndrome. Reopoliglyukin improves the rheological properties of blood, prevents adhesion and aggregation of platelets. Aspirin works in the same direction. Heparin stops the action of plasma coagulation factors, prevents the conversion of fibrinogen into fibrin. With an increase in the phenomena of hypocoagulation, the most effective is the introduction of fresh frozen plasma, which eliminates the deficiency of coagulation factors - antithrombin III, fibrinogen, plasminogen. If the amount of antithrombin III is sufficient, fibrinolysis inhibitors e-aminocaproic acid, trasilol, contrykal can be administered.

There are recommendations for differentiated treatment of DIC, depending on the clinical variant of the course (A.A. Martynov). Option I - violations of the functions of the shock organs, moderate hemorrhages. Shown transfusion of fresh frozen plasma, the introduction of heparin and antiplatelet agents.

Option II - severe hemorrhagic syndrome. It is advisable to administer high doses of antiproteases, low doses of heparin, fresh frozen plasma and antiplatelet agents.

Option III - massive local thrombosis and / or thromboembolism. It is necessary to administer thrombolytic agents, intermittent administration of fresh frozen plasma and the appointment of antiplatelet agents.

High efficiency of treatment is achieved by early (!) connection 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 lack 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 is especially intense - several times faster than all procoagulants); allow you to enter into the bloodstream a complete set of 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 in order to activate antithrombin III administered with plasma. It also prevents clotting of plasma by circulating thrombin.

With DIC of an infectious-toxic nature and the development of pulmonary distress syndrome, plasmacytopheresis is indicated, since leukocytes play an important role in the pathogenesis of these forms. Some of them begin to produce tissue thromboplastin (mononuclear cells), while others - esterases that cause interstitial pulmonary edema (neutrophils).

Methods of plasma therapy and plasma exchange increase the effectiveness of the treatment of DIC and the diseases that cause it, reduce mortality by several times, which allows us to consider them one of the main methods of treating patients with this disorder of hemostasis.

With significant anemia and a decrease in hematocrit, it is necessary to carry out transfusions of fresh canned blood (daily or up to 3 days of storage), erythrocyte mass. The requirement for transfusion of fresh blood preparations is due to the fact that microclots are formed in preserved blood for more than 3 days of storage, the entry of which into the blood leads only to the potentiation of DIC. Hematocrit must be maintained at a level not lower than 22%, hemoglobin index - more than 80 g / l, erythrocytes - 2.5 * 10¹² / l and above.

It should be remembered that acute DIC is easily complicated by pulmonary edema, therefore, significant circulatory overloads of the cardiovascular system are highly undesirable, and therefore, caution and strict accounting of the amount of transfused blood, as well as blood loss, loss of body fluid, diuresis are necessary.

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

ANEMIA

Anemia- clinical and hematological syndrome, characterized by a decrease in hemoglobin content per unit volume of blood, which leads to the development of oxygen starvation of tissues.

Anemia classification. There are various classifications. Of greatest interest is pathogenetic classification, the basic principles of which were developed by M.P. Konchalovsky and further improved by I.A. Kassirsky (1970), L.I. Idelson (1979), P.A. Vorobyov (1994) :

I. Anemia due to blood loss (posthemorrhagic).

Acute posthemorrhagic anemia.

Chronic posthemorrhagic anemia.

II. Anemia due to impaired formation of red blood cells and hemoglobin.

Iron-deficiency anemia.

Iron redistributive anemia.

Iron-saturated (sideroahrestic) anemia associated with impaired heme synthesis.

Megaloblastic anemia associated with impaired DNA synthesis.

6.1. B12 and folate deficiency anemia.

hypoproliferative anemia.

Anemia associated with bone marrow failure.

1. Hypoplastic (aplastic) anemia

   Refractory anemia in myelodysplastic syndrome.

metaplastic anemia.

1. Anemia in hemoblastoses.

   Anemia in cancer metastases to the bone marrow.

Dyserythropoietic anemia.

III . Anemia due to increased blood destruction (hemolytic).

Hereditary.

1. Associated with a violation of the structure of the erythrocyte membrane (Minkowski-Chaffard microspherocytic anemia, ovalocytosis, acanthocytosis).

   Associated with deficiency of enzymes in red blood cells

   Associated with impaired hemoglobin synthesis (sickle cell anemia, hemoglobinosis, thalassemia).

Acquired.

1. Autoimmune.

   Paroxysmal nocturnal hemoglobinuria.

   Medicinal

   Traumatic and microangiopathic

   Due to poisoning with hemolytic poisons and bacterial toxins.

IV. Mixed anemia.