The main cause of DIC syndrome is. What is DIC syndrome?

Description:

DIC syndrome is the most common type of hemostasis pathology. Its basis is generalized blood coagulation in the vessels of the microvasculature with the formation large quantity microthrombi and blood cell aggregates. In this case, normal blood circulation is blocked in most organs and systems, leading to the development of deep dystrophic changes in them. Following intense blood clotting, hypocoagulation (decreased blood clotting ability), (decrease in the number of platelets per unit volume of blood) and hemorrhage (bleeding) develop. The syndrome occurs in a wide variety of diseases, always leading to a loss of fluid properties of the blood and disruption of its circulation in the capillaries, which is incompatible with the normal functioning of the body. At the same time, the severity, prevalence and rate of development of DIC syndrome are very diverse - from fulminant fatal forms to latent (hidden) and protracted, from generalized blood coagulation to regional and organ thrombohemorrhages.

Symptoms:

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, there is an increase in thrombocytopenia and multidirectional changes in general clotting tests.

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

IV   stage - 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)   state of the hemostasis 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 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,
anaphylaxis);

b) hemocoagulation;

c) hemorrhagic;

4)         presence and severity 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:

b) liver;

c) brain;

d) hearts;

e) adrenal glands and pituitary gland;

e) stomach and intestines (acute ulcers, with increased permeability vascular wall);

6)         expressiveness;

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, bone fractures), surgical (traumatic operations), toxic (snake bites) and all types of shockogenic (including) DIC syndrome. The severity of DIC syndrome in similar 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 management, the timeliness and maximum atraumaticity of surgical interventions, control over the hemostatic system and the completeness of the prevention and elimination of its violations, maintenance rheological properties blood, combating microcirculation disorders and general hemodynamics.

The emergence and progression of disseminated intravascular coagulation syndrome is facilitated by insufficiently rapid and complete recovery of the patient from shock and hypotension (decreased tone), increased trauma of surgical interventions (removal of organs from adhesions by blunt means with kneading and tearing, intensive massage of the uterus after childbirth), insufficient correction of hypovolemia and non-indicated transfusions of canned blood, which contains a huge number of microclots and aggravates DIC, 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 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 monitor the transformation of shock, which was the cause of DIC, into hemocoagulation, since they merge into a general acute disruption 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.

Hemostasis disorders go through different phases - from hypercoagulation to more or less deep hypocoagulation up to total loss blood clotting ability. Detection of hypercoagulability does not require special 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 a response in itself has diagnostic value, indicating severe 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 typical laboratory sign 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) with DIC almost never occurs, but there is more or less pronounced (decrease in the 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 violation is of great importance clinical significance, since antithrombin III up 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.
- a frequent and dangerous, but far from obligatory manifestation of disseminated intravascular coagulation. In most cases, it occurs in acute disseminated intravascular coagulation syndrome, more often in the hypocoagulable phase, although multiple and heavy bleeding is often 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 hemostasis system.

Local bleeding includes bleeding from injuries and surgical interventions, postpartum and post-abortion uterine bleeding, bleeding from acutely formed stomach ulcers or duodenum, (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 DIC syndrome with uterine atony requires, in addition to hemostatic therapy, a set of effects 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 general tactics treatment.

General bleeding is characterized by the appearance of 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 sweating of blood in pleural and abdominal cavities, sometimes into the pericardial sac. In each patient, one or another form of bleeding predominates.

Bleeding leads to acute, and 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.

Disruption of microcirculation in organs with their dysfunction and dystrophy is 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 - cyanosis, decreased blood oxygen saturation, and then increased carbon dioxide in arterial blood; interstitial edema, pulmonary infarctions and other signs of “shock lung” appear, often with the development. 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 exhibit a special sensitivity to intravenous fluid administration and massive blood transfusions; sometimes an extra 200-300 ml of fluid sharply increases hypoxia and provokes. 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.
- 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 (no urine output), 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 disrupted; an increase in the level of creatinine, and subsequently residual nitrogen and urea, is noted in the blood serum. In general, this syndrome does not differ from other types of acute renal failure.

Combined forms are more severe - “shock lung” with acute renal failure 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 Gasser and all types of acute intravascular hemolysis, but hemolysis is also common in many other forms of DIC.

Liver damage occurs less frequently with the development parenchymal jaundice, and sometimes with 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 s, terminal phase).

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, causing 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.

Disturbances of cerebral circulation, thrombosis and bleeding in this area give a wide variety of symptoms - from confusion and fainting to typical thrombotic or hemorrhagic strokes, the phenomena of meningism.

Lesions of the adrenal glands and pituitary gland, leading to a typical picture of acute (protracted 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.

Causes:

Frequency of DIC syndrome in different types pathology is heterogeneous. With some diseases and influences, it necessarily occurs and becomes an integral part of the pathological process, with others it is less common.
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 of the shock state.
Surgical interventions that are particularly traumatic for the patient (especially when malignant neoplasms, operations on parenchymal organs, the use of APCs and intravascular interventions). Bleeding and massive collapse 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, or its manual separation, blockage of uterine vessels amniotic fluid, . In all of the above conditions, severe disseminated intravascular coagulation syndrome is registered in 20-35% of cases.

Treatment:

For treatment the following is prescribed:

Treatment of DIC syndrome is very difficult and is not always successful. Mortality in acute forms is 30%. The inconsistency and lack of reliability of data on mortality are associated, on the one hand, with the fact that statistical reports include patients with different severity background diseases and with different severity of 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 antimicrobial therapy is needed, based on clinical indications, and not on delayed bacteriological studies.

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 a 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 in laboratory parameters of blood tests, such as, shift 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.

Also noted high efficiencyα-blockers for DIC syndrome if 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 preservation of active platelets in the bloodstream have a beneficial effect complex application 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 medical treatment, and in 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 only through 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 fibrin formation and platelet aggregation with their deposition in the microvasculature have largely been completed, as well as due to a significant deficiency of antithrombin III and high levels of proteins in the blood acute phase blocking heparin, or due to the formation of abnormal forms of 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" basic therapy 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, with the addition of heavy bleeding, blood incoagulability, severe hypocoagulation to this pathological condition, and also if the clinical picture is complicated by bleeding from ulcers gastrointestinal tract(bloody, 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 a simultaneous drop in hematocrit, lack of 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, good therapeutic effect provides complex 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, are used saline solutions, polyglucin, albumin solution. 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 stop bleeding, especially uterine bleeding, 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 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) earlier use of 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 hematocrit above 22%; in case of severe hypocoagulation and bleeding - transfusion of platelet concentrates, administration of contrical in large doses;

4)         use according to indications of plasmacytapheresis.

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, affecting 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, frequent repetition laboratory research. Based on all of the above, such patients should be in intensive care units or intensive care wards.

is a disorder of the hemostasis process, which contributes to the formation of blood clots, as well as the development of various hemorrhagic and microcirculatory disorders. The full name of the disease is disseminated intravascular coagulation; you can also find such a designation of the syndrome as thrombohemorrhagic syndrome.

DIC syndrome is characterized by hemorrhagic diathesis with increased blood coagulation inside the vessels, which leads to the formation of blood clots that stop them. This, in turn, entails the development of pathological changes in organs of a dystrophic-necrotic and hypoxic nature.

DIC syndrome poses a threat to the patient's life, as there is a risk of bleeding. They can be extensive and difficult to stop. Also, internal organs may be involved in the pathological process, the functioning of which will be completely disrupted. The kidneys, liver, spleen, lungs and adrenal glands are primarily at risk.

The syndrome can occur with the most various pathologies, but it always leads to thickening of the blood, disruption of its circulation through the capillaries, and this process is not compatible with normal life activity human body.

DIC syndrome can lead to both immediate death of the patient and protracted latent fatal forms of disorders.

The statistics of DIC syndrome cannot be calculated, since in different diseases the syndrome occurs with different frequencies. Some pathologies are always accompanied by DIC syndrome, while with other diseases it occurs somewhat less frequently. This syndrome can be regarded as an abnormal protective reaction of the body, which it produces in order to suppress bleeding that occurs when blood vessels are damaged. In this way, the body seeks to protect itself from affected tissues. Thrombohemorrhagic syndrome is often encountered in the practice of doctors of various specialties. Gynecologists, surgeons, resuscitators, traumatologists, hematologists, etc. are familiar with it.

Causes of DIC syndrome

The causes of DIC syndrome are various diseases which are accompanied by damage to tissues, blood vessels and blood cells. In this case, a failure of hemostasis occurs in the body with an increase in blood clotting.

The following pathological processes can lead to the development of thrombohemorrhagic syndrome:

Septic conditions that are a complication of a viral or bacterial infection. Septic shock always provokes the development of this syndrome.

Generalized infections. In this case, the syndrome most often occurs in newborns.

Obstetric pathologies – severe gestosis, premature detachment placenta or its presentation, death of the fetus inside the womb, manual separation of the placenta, uterine bleeding, C-section, embolism with anatomical fluid.

Surgical interventions accompanied by an increased risk of trauma to the patient. Most often, these are operations that are performed to remove malignant tumors, interventions performed on organs that primarily consist of parenchyma, and operations on blood vessels. If at the same time the patient requires a massive blood transfusion, or he develops collapse or, then the risk of developing thrombohemorrhagic syndrome increases.

Any terminal conditions of the human body lead to the development of DIC of varying severity.

With 100% probability, DIC syndrome will develop in people against the background of intravascular hemolysis. Destruction of blood cells most often occurs when a person is transfused with blood of a different type (incompatible transfusion).

Risk factors for the development of DIC include surgical procedures such as organ transplantation, implantation of a prosthetic heart valve or blood vessels, and the need to artificially start blood circulation.

Taking some medicines increases the risk of developing the syndrome. These are diuretics oral contraceptives, drugs from the group of fibrinolysis inhibitors and Ristomycin (an antibacterial drug).

Giant angiomas with their multiple appearance.

Bites from poisonous snakes and other acute poisonings of the human body can provoke the development of DIC syndrome.

In some cases, allergic reactions become the cause of the development of a dangerous condition.

Immune diseases, such as: glomerulonephritis, etc.

Vascular pathologies, including congenital heart defects, myocardial infarction, heart failure, etc.

However, the main reason for the development of DIC is sepsis (virological and bacteriological) and shock of any etiology. These pathologies account for up to 40% of cases of all registered DIC syndromes. If we are talking about newborn children, then this figure rises to 70%. But instead of the term DIC syndrome, doctors use the designation “malignant purpura of newborns.”

With DIC syndrome, there is a failure of the complex of body reactions that are triggered in order to prevent bleeding. This process is called hemostasis. In this case, the function responsible for blood clotting is excessively stimulated, and the anticoagulant (anticoagulant) and fibrinolytic systems that balance it, on the contrary, are quickly depleted.

Enzymes produced by bacteria that enter the body, toxins, immune complexes, amniotic fluid, phospholipids, low cardiac effusion into the bloodstream, acidosis and other factors pathogenic to the body can influence the manifestation of DIC syndrome. At the same time, they will circulate either in the bloodstream or act on the vascular endothelium through mediators.

DIC always develops according to certain patterns and goes through several successive stages:

At the first stage the process of excessive blood clotting, as well as cell aggregation inside the vessels, starts. An excess amount of thromboplastin or a substance with a similar effect is released into the blood. This starts the coagulation processes. The time of the initial stage can vary widely and take from a minute to several hours if the syndrome develops acutely. The pathological process will take place from several days to several months if the syndrome is chronic.

The second stage is characterized by the launch of the process of consumption coagulopathy. At the same time, there is an increasing lack of fibrogen, platelets and other plasma factors responsible for the blood clotting process in the body.

The third stage is critical. At this time, secondary fibrinolysis occurs, blood coagulation reaches a maximum, until this process completely stops. In this case, hemostasis appears to be significantly unbalanced.

Recovery stage characterized by normalization of hemostasis. Residual dystrophic-necrotic changes are observed on organs and tissues. Another end of DIC syndrome may be acute failure of one or another organ.

The full development of DIC syndrome (its severity and mechanism of development) depends on the degree of disturbance of blood microcirculation and on the degree of damage to organs or their systems.

Symptoms of DIC syndrome

Symptoms of DIC syndrome will be determined clinical manifestations the disorder that provoked its development. They also depend on how quickly the pathological process develops, in what state the mechanisms responsible for compensating hemostasis are, and also at what stage of DIC the patient is.

Symptoms of acute DIC syndrome.

In the acute form of DIC, the pathological process quickly spreads throughout the body. Most often this happens within a few hours.

The person is in a state of shock, his blood pressure drops to 100/60 or below.

The patient loses consciousness, symptoms of acute respiratory failure and pulmonary edema are observed.

Bleeding increases, profuse and massive bleeding develops. This process involves systems and organs of the human body such as the uterus, lungs, and gastrointestinal tract organs. Development is possible.

Against the background of acute DIC, destructive destruction of pancreatic tissue is observed with the development of functional failure of the organ. Possible addition of gastroenteritis of an erosive-ulcerative nature.

Foci of ischemic dystrophy appear in the myocardium.

With amniotic fluid embolism, disseminated intravascular coagulation syndrome develops at lightning speed. In a few minutes, the pathology goes through all three stages, making the condition of the mother and fetus critical. Patients undergo hemorrhagic and cardiopulmonary shock, which are difficult to stop. In this regard, the prognosis for life is unfavorable and death occurs in 80% of cases.

Symptoms of subacute DIC syndrome

The course of the syndrome in this case is more favorable.

Hemosyndrome is expressed in the occurrence of hemorrhagic rashes.

Bruises and large hematomas may appear on the skin.

Injured areas and injection sites are characterized by increased bleeding.

Mucous membranes are also susceptible to bleeding. Blood may be present in sweat and tears.

Skin characterized by excessive pallor, even marbling. When you touch the skin, you feel an unnatural coldness.

The internal organs swell, fill with blood, necrotic areas and hemorrhages appear on them. Susceptible pathological changes gastrointestinal organs, liver and kidneys, as well as adrenal glands and lungs.

As for the chronic form of DIC, it not only occurs more often than others, but in most cases it occurs hidden. The patient, due to the absence of symptoms, may not even be aware of the development of pathologies in the hemostatic system. However, as the disease that provoked DIC progresses, its symptoms will become more pronounced.

Other symptoms

Other symptoms that may indicate the development of chronic DIC syndrome:

Deterioration and prolongation of the regeneration process of any wounds.

An increase in asthenic syndrome with a corresponding symptom complex.

Attachment of a secondary purulent infection.

Formation of scars on the skin in places where there was damage.

Complications of DIC syndrome are usually very severe and threaten not only the health, but also the life of the patient.

More often than others, the following conditions develop:

Hemocoagulative shock. Organs and tissues begin to experience oxygen deficiency, since blood microcirculation is disrupted in the small vessels responsible for their nutrition. In addition, the amount of toxins in the blood itself increases. As a result, the patient’s pressure drops sharply, both arterial and venous, and organ failure, shock, etc. occur.

Acute respiratory failure. Is borderline state posing a direct threat to the patient’s life. As hypoxia intensifies, loss of consciousness occurs, and hypoxic coma develops and occurs.

Acute renal failure is another most common complication of DIC syndrome. The patient stops urinating until complete absence urine discharge. Water-salt balance is disrupted, the level of urea, nitrogen, and creatinine in the blood increases. This condition refers to potentially reversible.

Liver necrosis.

From the gastrointestinal tract: stomach ulcer, intestinal infarction, pancronecrosis.

From the cardiovascular system -.

From the hematopoietic system – acute hemorrhagic anemia.

Diagnosis of DIC syndrome

Diagnosis of DIC syndrome is based on examining the patient, taking an anamnesis and conducting laboratory tests.

The patient needs to undergo the following tests:

Blood smear;

Blood for coagulogram, as the main method for diagnosing hemostasis (platelets, fibrogens and other important indicators are counted);

ELISA (determination of PDF, RFMC, D-dimer as the main markers of blood coagulation inside blood vessels):

Blood for paracoagulation tests (allows you to confirm or refute the diagnosis).

The doctor finds out the reason that led to the development of DIC syndrome, determines its stage and nature.

If the course of the syndrome is hidden, then hypercoagulation can be determined solely by laboratory tests. In this case, fragmented red blood cells will be present in the blood smear, thrombosed time and aPTT will increase, and the concentration of PDP will increase. A blood test will indicate a lack of fibrinogen and platelets.

If the syndrome is confirmed, then the most vulnerable organs must be examined: kidneys, liver, heart, brain, lungs, adrenal glands.

Treatment of DIC syndrome is a rather complex process, and the patient’s recovery does not occur in every case. If an acute form of the syndrome is diagnosed, then death occurs in 30% of cases, which is a fairly high rate. However, it is not always possible to accurately establish the reason why the patient died. Has DIC become a critical condition, or has the patient died as a result? negative impact underlying disease.

Doctors observing DIC syndrome first of all make efforts to eliminate or minimize the factor that led to the development of the syndrome and stimulates its progression. It is important to eliminate purulent-septic conditions, which most often provoke impaired hemostasis. At the same time, there is no point in waiting for the results of bacteriological studies; therapy is carried out in accordance with the clinical signs of the disease.

Antibacterial therapy against the background of DIC syndrome is indicated in the following cases:

Previous abortion;

Premature discharge of amniotic fluid, especially when it is not clear and contains turbidity;

Increase in body temperature;

Symptoms indicating inflammation of the lungs, urinary tract, abdominal organs;

Signs of meningitis.

Used for treatment antibacterial drugs broad spectrum of action, with the inclusion of γ-globulins in the treatment regimen.

To relieve shock conditions, injections of saline solutions, plasma transfusions with Heparin, Prednisolone (intravenously), and Reopoliglucin are used. If shock syndrome is eliminated in a timely manner, it is possible to stop the development of disseminated intravascular coagulation syndrome, or to significantly mitigate its manifestations.

As for Heparin, when administered there is a risk of bleeding. It has no positive effect if used late. It should be administered as early as possible, strictly following the recommended dosage. If the patient is at the third stage of development of DIC syndrome, then the administration of Heparin is a direct contraindication. Signs indicating a prohibition on the use of this drug are: drop in pressure, bleeding (it may be hidden), hemorrhagic collapse.

If the syndrome has just begun to develop, then the administration of a-blockers is indicated: Dibenamine, Phentolamine, Thioproperazine, Mazeptil. The drugs are administered intravenously in the required concentration. They help normalize microcirculation in organs and resist the formation of blood clots inside blood vessels. You should not use adrenaline and norepinephrine drugs, as they can worsen the situation.

When renal and liver failure develops, in the early stages of development of DIC syndrome, it is also possible to use drugs such as Trental and Curantil. They are administered intravenously.

At the third stage of development of DIC syndrome, it is necessary to administer protease inhibitor drugs. The drug of choice is Contrikal, the method of administration is intravenous, the dose is no more than 100,000 units at a time. If such a need arises, the infusion can be repeated.

Local effects are reduced to treating bleeding erosions, wounds and other areas with Androxon at a 6% concentration.

To summarize, it can be noted that complex treatment DIC syndrome comes down to the following points:

Elimination of the root cause that provoked the development of the syndrome.

Carrying out antishock therapy.

Replenishment of blood volumes with transfusion of plasma enriched with Heparin, if there are no contraindications to this.

Early use of adrenergic blockers and drugs that help reduce the number of platelets in the blood: Curantil, Trental, Ticlodipine.

Administration of Contrikal, platelet transfusion to normalize hematocrit against the background of severe bleeding.

Prescribing plasmacytapheresis, if indicated.

To normalize microcirculation in the affected organs, nootropics, angioprotectors and other syndromic drugs are used.

With the development of acute renal failure, hemodiafiltration and hemodialysis are performed.

Patients with DIC syndrome are required to be hospitalized and are under 24-hour medical supervision. They are located either in the intensive care unit or in intensive care wards.

As for the prognosis, it is very variable. To a greater extent, it depends on what caused the development of DIC syndrome, on the degree of hemostasis impairment, on how quickly first aid was provided and how adequate it was.

It is impossible to exclude a lethal outcome, since it can occur against the background of heavy blood loss, shock, or organ failure.

Doctors should pay special attention to patients belonging to risk groups - elderly people, pregnant women, newborns, people with underlying diseases.

About the doctor: From 2010 to 2016 practicing physician at the therapeutic hospital of the central medical unit No. 21, the city of Elektrostal. Since 2016 he has been working at diagnostic center No. 3.

Disseminated intravascular coagulation or disseminated intravascular coagulation (DIC) is a disorder of the ability of blood to clot, which develops against the background of excessive influence of pathological factors. The disease entails the formation of blood clots and damage to internal organs and tissues. This disorder cannot be independent; moreover, the more severe the underlying illness, the more pronounced this syndrome is. In addition, even if the underlying disease affects only one organ, then with the development of thrombohemorrhagic syndrome, the involvement of other organs and systems in the pathological process is inevitable.

A disease such as DIC syndrome belongs to a group of severe disorders that require immediate medical intervention. This is due to the fact that death occurs in more than half of the registered cases. The syndrome is accompanied by increased bleeding, the appearance of a characteristic rash, and impaired functioning of the affected organs. In severe cases of the disease, shock and severe hemorrhages may occur. Extensive bleeding that is difficult to eliminate is life-threatening.

Diagnosis of DIC syndrome is carried out using the presence of characteristic features illness, as well as thanks to a coagulogram and other laboratory tests. Treatment of DIC syndrome is aimed at restoring the blood's ability to clot through the use of medications. In many ways, the success of therapy depends on the time of the patient’s admission to the clinic, the stage of the disease and compliance with the doctor’s recommendations.

Etiology

DIC syndrome is quite rare and independent disorder- often it occurs against the background of other diseases. Predisposing causes of the disease are:

• severe inflammatory and infectious processes of different nature– bacterial, viral, fungal;
• complications after surgery;
• autoimmune diseases;
• malignant neoplasms on internal organs;
• pathological reaction to transfusion of blood components;
• acute organisms from ingestion chemical substances or snake venom;
• a sharp decrease in blood pressure;
• long-term use of medications that interfere with clotting or increase the risk of blood clots.

DIC syndrome is widespread in obstetrics, since such a disorder is often observed in newborns. Predisposing factors may be:

• complicated pregnancy;
• oxygen deficiency;
• hypothermia of the expectant mother's body;
• injuries.

In junior and adolescence The main reasons for the expression of this syndrome are:

• severe course after infections;
• complication of inflammatory processes that impair the functioning of the liver and kidneys;
• wide range of injuries.

In pregnant women, the main prerequisites for the appearance of thrombohemorrhagic syndrome are:

• extensive blood loss - during childbirth or injury;
• premature separation of the placenta from the uterus;
• severe pregnancy with the manifestation of gestosis, eclampsia and preeclampsia;
• incompatibility of blood type and Rh factor between mother and child;
• the presence of a dead fetus in the uterus for a long time;
• birth canal injuries;
• uterine rupture;
• transfusion of red blood cells incompatible with the woman’s blood;
• prolonged stimulation of labor.

Any changes in blood clotting can be detected by performing a coagulogram.

Varieties

There is a classification of the disease depending on the stage of its progression:

• hypercoagulation – increased ability of blood to clot;
• transitional – the simultaneous presence of blood clots and extensive bleeding in the patient;
• hypocoagulation – reduced coagulability;
• outcome stage. There are several options for ending the disease - death or recovery.

In some situations, phases may reappear.

According to the clinical course, this disorder is divided into:

• acute DIC syndrome – characterized by lightning-fast development of the disease. Time ranges from several hours to days;
• subacute – development occurs over the course of a week;
• chronic disseminated intravascular coagulation syndrome – a protracted course that can last for months or years;
• wavy - periods of increased hemorrhage alternate with periods of blood clot formation.

In addition, the syndrome can be localized - affecting only one organ, or local - several organs and systems, or the entire body, are exposed to the pathological process. Any changes in blood clotting can be detected using a coagulogram.

Symptoms

The degree to which symptoms of the disease are expressed directly depends on the stage of the disease. In the acute course, within a few hours, signs such as a significant decrease in blood pressure, periods of loss of consciousness, swelling of the lungs, as well as extensive bleeding - uterine, nasal, and pulmonary - appear. At this stage of DIC during pregnancy, there is a high probability of death for both the mother and the newborn.

The subacute stage is often local in nature and has a more favorable pathogenesis. It is expressed by a hemorrhagic rash, bruises and hematomas, increased bleeding from wounds or mucous membranes. The skin is pale and cold. Edema of the tissues of the kidneys, liver, and gastrointestinal tract develops sharply. As thrombohemorrhagic syndrome progresses, dysfunction of the affected organs and systems is observed.

Other symptoms of the disease in adults and children are:

• the skin acquires a bluish tint on the tips of the fingers and nose;
• rapid breathing indicates lung damage;
• impaired coordination of movements;
• is a sign;
• reducing the volume of urine excreted;
• convulsions;
• bouts of vomiting;
• diarrhea;
• ulceration of the gastric mucosa;
• body;
• extensive hemorrhages.

When the first symptoms occur, especially in newborns and small children, you should immediately contact a medical facility. In the early stages, it is possible to identify the syndrome using a coagulogram.

Complications

Since DIC syndrome is an acute condition that requires immediate medical care, untimely contact with specialists entails complications in adults and children such as:

• disruption of the normal functioning of the affected internal organs due to the cessation of blood flow in them and the formation of blood clots;
• state of shock - due to a sharp decrease in blood pressure;
• decreased hemoglobin levels as a result of extensive hemorrhages;
• coma.

Without proper and, most importantly, timely treatment, almost every patient with this syndrome dies. To prevent this from happening, it is necessary to immediately consult a doctor when the first symptoms appear, who will prescribe a coagulogram - a test of the blood's ability to clot. With effective therapy, four out of five patients can survive.

Diagnostics

Diagnosis of DIC syndrome involves carefully collecting information about the pathogenesis, possible causes of the disease, the presence and severity of symptoms. A physical examination of the patient plays an important role in confirming the diagnosis - detection of a yellowish tint of the skin and mucous membranes, rapid pulse, and decreased blood pressure.

To know more information and laboratory blood tests will help determine the stage of the disease, in particular a coagulogram - an assessment of the blood’s ability to clot. Carrying out biochemical analysis will help determine the level of components such as cholesterol, uric acid, glucose, creatinine, and electrolytes in the bloodstream. The duration of blood clotting is assessed. In addition, several special tests are performed to detect subcutaneous hemorrhages.

Hardware examination of patients includes:

• Ultrasound – makes it possible to detect changes in the structure of organs and large blood clots;

In some cases, additional consultations with a therapist may be necessary - if the patients are adults, a hematologist - for newborns, children younger age and adolescents, obstetrician-gynecologist - for pregnant women.

After receiving all test results, in particular coagulograms, and examinations, the specialist prescribes the most effective tactics for treating the syndrome and guidelines that must be followed during therapy.

Treatment

Patients who have been diagnosed with this disease require immediate resuscitation. The basis of treatment for DIC syndrome is:

• eliminating the main cause of the disease - taking antibiotics, antifungal and antiviral drugs, as well as substances to normalize blood pressure;
• restoration of normal blood flow - by introducing plasma substitutes;
• normalization of blood clotting - transfusion or intravenous administration plasma and platelets. It is necessary to use hardware blood purification and take medications to help stop the formation of blood clots. The effectiveness of treatment is observed through regular coagulation tests.

Depending on the damage to the internal organs, these disorders are eliminated. In pregnant women with premature labor, urgent stimulation of labor is necessary.

Prevention

Preventive measures for thrombohemorrhagic syndrome include compliance with the following rules:

• timely elimination of predisposing factors that can lead to the occurrence of the syndrome in newborns, young children, adolescents and adults;
• when treating infections, take anticoagulants;
• limit contact with toxic substances.

The prognosis of the disease directly depends on the pathogenesis, the causes of the formation of the disease, timely treatment and compliance with the guidelines established by the attending physician. For a greater likelihood of a favorable prognosis, when the first signs of the disease appear, you need to contact specialists who will prescribe a coagulogram, with which you can diagnose DIC in the early stages.

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Disseminated intravascular coagulation syndrome (DIC) is one of the most severe complications of many diseases. This is a real headache for any resuscitator, since a patient in this condition can die at any moment. It develops quite quickly, is not very easy to treat, and the prognosis for life when it appears becomes quite unfavorable.

Definition

ICE is pathological condition, developing as a result of depletion of factors that promote and counteract blood clotting. The basis of this process is blockade small vessels loose blood clots resulting from the release of a large number of clotting factors into the blood (hypercoagulation). The blood remaining in the vascular bed loses its ability to clot due to a decrease in the amount of coagulation factors, activation of substances that dissolve clots, and accumulation of breakdown products of proteins that have anticoagulant activity.

Causes of DIC syndrome

Many severe and critical conditions can cause DIC syndrome. Almost any pathology in which there is damage to the vascular wall, a change in the properties of blood, and the speed of its flow through the vessels, can trigger a cascade of reactions leading to intravascular coagulation. The main causes of the disease are as follows:

1. Any form of shock. In this condition, there is a serious deterioration in the rheological properties of the blood (increased viscosity), as well as damage to the walls of small vessels.
2. Severe septic infections. In this case, the mechanism of intravascular coagulation can be triggered directly by bacterial toxins or indirectly through the destruction of the endothelium (inner lining) of blood vessels by microorganisms and their metabolic products.
3. Hemolysis(massive destruction of red blood cells). It occurs as a result of transfusion of incompatible or expired blood, in severe physical activity, severe hypothermia, extremes atmospheric pressure, as well as taking certain medications (quinidine, nitrofuran and sulfonamide chemotherapy drugs).
4. Massive transfusion syndrome. A transfusion volume of more than 5 liters can become a trigger factor for DIC syndrome.
5. Necrosis in various organs. Myocardial infarction, acute disorder cerebral circulation(stroke), some forms of pancreatitis, acute liver dystrophy, burns of the skin and mucous membranes, massive surgical interventions and injuries, crash syndrome (or syndrome prolonged compression) - all this leads to a powerful release into the blood of the so-called tissue factor - the main substance that triggers a cascade of hypercoagulation reactions.
6. Immune and immune complex diseases.
7. Tumor process, especially with multiple metastases.
8. Hemodialysis, hemosorption, extracorporeal circulation(for example, during heart surgery).
9. Acute poisoning with hemolytic poisons.
10. Obstetric pathology. This includes many situations that arise during pregnancy and childbirth - gestosis, placenta previa, early rupture of amniotic fluid, early placental abruption, intrauterine fetal death).

Symptoms of DIC syndrome

The symptoms of this pathology depend on the stage of development of the disease, as well as the form of the syndrome - acute or chronic. By stage, the clinical picture of acute DIC syndrome may be as follows:

1. Hypercoagulation stage, during which massive formation of blood clots is observed in blood vessels of small diameter. The duration of this stage is very short, and the clinical picture is usually masked by the symptoms of a severe underlying disease.
2. Hypocoagulation stage This is the period when the first bleeding appears. In this phase, factors that prevent coagulation are activated and, at the same time, factors that enhance coagulation are depleted. As a result, the main clinical sign of DIC syndrome is a variety of bleeding. There are:
   • Early bleeding, occurring mainly in the place where the tissues were destroyed: during abortion or childbirth - uterine, during surgical interventions - in the incision areas, during destructive processes in the lungs - respectively, pulmonary. In parallel, the appearance of hemorrhages and other localizations is noted - subcutaneous, submucosal, intradermal at injection sites.
   • Late bleeding is a manifestation of the deterioration of the patient's condition. This may include nasal and gastrointestinal bleeding, the appearance of hematomas in the subcutaneous fat, in the buttocks, lower back, etc.
3. In subsequent stages, along with bleeding, the symptoms of functional and then organic failure affected organs, and the organs penetrated by a rich capillary network are the first to suffer: adrenal glands, kidneys, lungs, liver, gastrointestinal tract, spleen, skin, mucous membranes.

Chronic DIC usually manifests itself as thrombosis and thromboembolism localized in various organs. This form of pathology most often occurs in people suffering from malignant cancers. Deep vein thrombosis, which develops into pulmonary embolism, is one of the most common causes of death in patients with tumors.

Diagnosis of DIC syndrome

Clinical diagnosis of DIC at an early stage is very difficult: the symptoms are scanty, there is no bleeding, and its duration is very short. When blood coagulation factors are depleted and hemorrhages appear, the diagnosis of the pathology can be made with fairly high confidence. Moreover, the more time has passed since the first bleeding, the easier it is to identify DIC syndrome. The downside of watchful waiting is the rapid deterioration in the prognosis of the disease. That is why patients are urgently given a series of tests showing the state of the coagulation system:

• blood clotting time, which, being normal or even shortened in the hypercoagulation stage, progressively lengthens as the disease develops (up to 30 minutes or more);
• the number of platelets in peripheral blood, which gradually decreases relative to normal;
• thrombin time, increasing depending on the stage from normal 5-11 seconds to 60 or more;
• analysis for D-dimers, which are normally absent, but with intravascular coagulation they are sharply increased.

Other tests are also used in practice, but do not provide additional information important for diagnosis.

The specialist treating the patient must clearly know all the methods for diagnosing DIC syndrome and their results, since correct definition The stage of the process also depends on the tactics of medical measures.

Treatment of DIC syndrome

Treatment of the underlying disease is the main thing that needs to be done when fighting intravascular coagulation. If the cause of the complication is not eliminated, it will be impossible to get rid of it. That's why rational antibiotic therapy in case of infections, adequate hemostasis in case of injuries of any nature, detoxification in case of poisoning can even lead to the spontaneous disappearance of DIC syndrome.

If spontaneous regression does not occur, you should immediately begin to fight the pathology. Treatment of the disease is carried out taking into account its stage:

• Stage 1. Hypercoagulation should be prevented by using heparin, intravenous infusions of rheopolyglucin in combination with antiplatelet agents, and the administration of corticosteroids.
• Stage 2. To the drugs listed above, an intravenous infusion of albumin, fresh frozen plasma, whole blood or red blood cells is added.
• Stage 3. In this phase, the approach to treatment changes dramatically, since here the activity of the system that prevents blood clotting comes first. Drugs that suppress the activity of anticoagulation factors (Gordox, Contrical) and enhance platelet function (etamzilate) are used. In parallel with this, they strive to activate the coagulation system by infusing plasma. If hemoglobin is low, whole blood is also infused in small quantities. Heparin administration is stopped.
• Stage 4. At this stage, the activities are the same as in the third stage with the addition of solutions based on albumin and gelatin.

In parallel with these actions, they correct disturbances in water-electrolyte and acid-base conditions, normalize kidney function, and support respiratory functions, compensate for blood loss.

Prevention

Knowledge of the causes of DIC syndrome makes possible measures to prevent it. Of course, it is impossible to foresee everything, but following several rules can seriously reduce the risk of developing this serious pathology:

• if necessary surgical treatment– selection of the most gentle surgical technique;
• the use of anticoagulants for any pathology that can be complicated by DIC syndrome;
• avoiding snake bites and chemical intoxication;
• refusal or minimal use of whole blood in favor of its derivatives (erythrocyte mass, plasma) and plasma substitutes;
• early detection and treatment of cancer.

DIC syndrome is an extremely severe complication clinical pathology, characterized by a very high mortality rate - depending on the cause, up to 50% of patients die. That is why preventive measures can be considered even more important than therapeutic measures. The British have a proverb: “An ounce of prevention is better than a pound of cure,” and it applies perfectly to disseminated intravascular coagulation syndrome.

Bozbey Gennady Andreevich, emergency physician

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 that cause blockade of microcirculation and deep dystrophic changes in organs with the subsequent development of hypocoagulation and thrombocytopenia 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 and 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 the case of transfusion of incompatible blood, 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 injuries can be burns, severe injuries, prolonged compartment syndrome, fractures of long bones with fat embolism, and electrical trauma. DIC syndrome can also occur during extensive traumatic surgical interventions. The risk of developing DIC with extensive surgical operations increases significantly in the presence of concomitant pathology ( cardiovascular diseases, malignant tumors), 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 with pathologies of the cardiovascular system: birth defects heart, 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).

ICE may be caused by: systemic diseases connective tissue and systemic vasculitis, systemic lupus erythematosus, rheumatoid arthritis, periarteritis nodosa and 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 intoxication iron, 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, while organs and tissues that have an intensively functioning microcirculatory system (liver, kidneys, lungs, etc.) are 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):

1. phase of hypercoagulation and platelet hyperaggregation;
2. transition phase - there is a tendency towards hypocoagulation according to some tests and hypercoagulation - according to others;
3. phase of hypocoagulation and activation of fibrinolysis (hemorrhagic phase);
4. 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 hemocoagulation shock develops, which is characterized by confusion, lethargy of the patient, and a strong drop in 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 bubbling rales, mainly in the lower parts, and in some cases scattered dry rales. 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. If the liver is damaged, severe liver failure develops, liver odor and symptoms appear hepatic encephalopathy- confusion, delirium, hallucinations, etc. Severe liver damage can lead to the development of complete hepatic coma. Possible occurrence of acute thrombosis of the liver or portal vein. With portal vein thrombosis, severe abdominal pain, bloody vomiting appears, ascites quickly develops, but the size of the liver remains normal. Acute hepatic vein thrombosis manifests itself 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 stool, sharp drop in blood pressure, thready pulse. The skin is pale, covered with cold sweat; facial features are pointed, eyes are sunken, tongue and lips are dry. Especially severe lesions adrenal glands are 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 the following general symptoms, such 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 been injured, surgical interventions. Severe hemostasis disorders lead to bleeding - gastrointestinal, renal, uterine. Bleeding gums and nosebleeds are noted. Intracerebral hemorrhages, hemorrhages in the pericardium, pleural cavity, and peritoneum may develop.

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 less negative consequences for the body. Microcirculation disorders and dysfunction of internal organs predominate.

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 of 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. ICE can be detected only when laboratory examination sick.

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 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.