Severe hypercoagulability. The causes of hypercoagulation are related to. How to determine the presence of pathology

Blood is the main living medium that performs very important function V human body, which involves transporting oxygen, nutrients and other elements. The functioning of the cardiovascular system and all internal organs.

If a person’s blood begins to thicken, this will negatively affect the processes of oxidation, as well as tissue regeneration (liver, kidneys, brain, etc.). Hypercoagulation of blood modern medicine is regarded as an independent form of pathology, which should not be confused with thrombohemorrhagic syndrome.

What causes blood to thicken?

Hypercoagulation of blood in most cases is not accompanied by the formation of blood clots in the vascular bed. Despite the fact that laboratory tests will show the patient's tendency to rapidly clot, he should not panic and thoughtlessly take blood thinning medications. If he does form a blood clot, then its structure will be loose, which is why it will lack elasticity.

The causes of hypercoagulability can be varied. Some patients developed blood problems due to cancer. In other people, a hereditary factor caused hypercoagulability. It is also worth noting the following factors that can change the composition of the blood:

• vascular injury, including atherosclerosis;
• thrombophilia (hematogenous);
• overweight (any stage of obesity);
• sedentary lifestyle;
• bad habits;
• erythremia, hemangioma or antiphospholipid syndrome;
• previous heart surgeries during which an artificial valve was installed;
• autoimmune diseases;
• pregnancy or taking contraceptives, etc.

How to identify pathology?

The difficulty of diagnosing this pathology lies in the fact that hypercoagulation does not have a pronounced clinical picture. Some patients who have this syndrome complain of lethargy, general weakness, painful sensations in my head. To identify this disease, it is necessary to undergo a laboratory examination, which consists of taking venous blood. The laboratory technician will immediately notice that the biological material taken from the patient has signs of hypercoagulation, since the blood will almost instantly clot in the needle.

The study of venous blood allows you to confidently determine blood hypercoagulation

A coagulogram can easily identify hypercoagulability syndrome, since laboratory tests will reveal changes in the following indicators:

Treatment of hypercoagulability

Patients who have been diagnosed with this disease should not self-medicate, as this can lead to unpleasant consequences. They need to go to a medical institution where qualified assistance will be provided. Highly specialized specialists will select therapy for such patients on an individual basis, taking into account all the characteristics of their body.

In most cases, doctors prescribe medicines(For example, unique drug Thrombo ACC, made on the basis of aspirin), dilutes platelets, in parallel with which traditional medicine recipes can be used. An example is meadowsweet. Not only tinctures are made from this plant, but also various drugs. Its unique components can become a substitute for aspirin. Many doctors prescribe meadowsweet for diseases of the blood vessels and blood system.

If a pregnant patient is to be treated, then specialists select the course of therapy with special care. Most often, this category of patients is prescribed heparins (low molecular weight). When treating hypercoagulability, you can take the following drugs (after consultation with your doctor):

• Aspirin,
• Pentoxifylline,
• Kurantin,
• Clopidogrel.

If hypercoagulation is detected in a pregnant patient, then drug treatment is prescribed with caution.

When treating patients who have other diseases in addition to the syndrome, doctors prescribe Warfarin or Syncumar (they are anticoagulants). In cases where hypercoagulation is accompanied by major bleeding, patients are transfused with donor blood. The use of colloidal or saline solutions is also allowed.

In order for the therapy to bring the desired results, patients must strictly follow all the instructions of the attending physician and follow the following recommendations:

• lead a healthy lifestyle;
• give up bad habits (smoking, for example, contributes to the development of hypercoagulation;
• Healthy food;
• exclude strong physical activity;
• spend more time outdoors, etc.

Is it necessary to follow a diet for hypercoagulability?

For patients who have been diagnosed with hypercoagulation syndrome in the laboratory, doctors strongly recommend that, in addition to drug treatment, they review their diet. IN mandatory The following products should be excluded:

• any canned food;
• smoked meats;
• fatty and fried foods;
• marinades;
• sweets;
• flour;
• buckwheat;
• bananas;
• potato;
• spicy and highly salted foods;
• alcohol;
• carbonated drinks, etc.

A person who has been diagnosed with blood hypercoagulation should eat properly and give up bad habits

Those patients whose hypercoagulation was caused by an incorrect or sedentary lifestyle need to urgently pay attention to their health. This is due to the fact that this category of patients is more at risk of stroke.

Hypercoagulability and pregnancy

Pregnant women are also at risk, as they often develop mild hypercoagulability. This is due to the fact that during gestation the coagulation systems of such patients are in a state of increased activity. Thanks to hypercoagulation syndrome, they are protected from large blood losses during labor.

During pregnancy, rapid pregnancy can be triggered by various factors, sometimes independent of the state of the woman’s body or her lifestyle:

• kidney and liver diseases;
• problems with the cardiovascular system;
• gene mutation;
• stress conditions, depression, nervous disorders;
• mature age (problems most often arise in women who are over 40 years old), etc.

Coagulogram is a mandatory examination for monitoring a patient with hypercoagulability

To eliminate unpleasant consequences, every pregnant woman must monitor hemostasis. To do this, it is enough to take a coagulogram once a month (if the diagnosis is confirmed, then the test should be taken once every 2 weeks) for blood clotting. If any pathologies are identified, such patients will be given safe therapy that will not harm the developing fetus. Being under the supervision of attending physicians and taking prescribed medications, pregnant women can safely survive this difficult period and give birth to healthy babies.

The process of blood clotting is very important for the human body. It allows you to avoid unnecessary blood loss even with serious injuries. Only in laboratory conditions can the level of blood clotting be determined.

During pregnancy, the body undergoes major changes. Preparing for upcoming birth sometimes accompanied by increased blood clotting. This process is necessary because the body thus reduces the risk of developing heavy bleeding from vessels on the placenta.

What is hypercoagulation during pregnancy?
Your gynecologist will always advise you on what hypercoagulation is during pregnancy. An additional blood circulation circulates through the placenta, which separates the baby’s and mother’s bodies. In the placenta, interaction between two organisms occurs, so this environment is quite active. If additional thrombosis of the spiral arteries is observed, then a pregnant woman may experience quite serious complications.

Hypercoagulability syndrome during pregnancy
Hypercoagulation during pregnancy can be quite dangerous. This occurs in cases where the hemostatic system changes quite strongly.
Hypercoagulation syndrome during pregnancy can cause some consequences that are undesirable for the woman and the fetus. For example, the fetus may be significantly delayed in development, and the placenta may wear out too quickly. The consequence of such deviations may be antenatal death of the fetus, or the fetus may develop abnormally, with abnormalities.

Treatment of hypercoagulability during pregnancy
Treatment of hypercoagulability during pregnancy is necessary. Only with the help of properly selected medications, approved by the pregnant woman by her attending physician, can the development of complications be prevented. Most often, for treatment, the doctor prescribes anticoagulants that block disorders and prevent them from developing. You should not use them independently, without the consent of your doctor. But there is no need to be afraid - all these drugs are approved for use by pregnant women.

Chronometric hypercoagulation during pregnancy
Chronometric hypercoagulation during pregnancy is a fairly common occurrence. The blood will thicken as the baby grows and the period increases. The body’s natural defense against blood loss may not work for the good, disrupting microcirculation in the placenta. Such a deviation can be dangerous at any stage of pregnancy.

Hypercoagulation during pregnancy can have serious consequences in women who have cardiovascular diseases and gestosis. If in previous pregnancies there were problems with premature placental abruption, this can lead to hypercoagulation during the current pregnancy.

Typically, the doctor conducts a series of tests to identify genes responsible for microcirculation disorders. Then a study of the hemostasis system is carried out if the woman has variant genes that cause deviations. After a series of tests, the doctor selects hemostatic drugs and a regimen for taking them. In this case, once a month the condition and coagulability of the patient’s blood is checked.

Any discomfort during pregnancy - most often indicate various malfunctions in the body, and therefore deliver to the expectant mother...

Hypercoagulation (hypercoagulation syndrome): causes, forms, symptoms, tests, treatment

Hypercoagulation is a medical term meaning a state of increased activity of the blood coagulation system. This pathology can be an independent disease or a manifestation of concomitant ailments. Hypercoagulation syndrome in most cases is accompanied by an increased tendency to. The resulting blood clot is loose in structure and lacks elasticity.

Blood is the vital medium of the body, performing a transport function and ensuring the delivery of oxygen and nutrients to all internal organs. It consists of plasma - the liquid part in which cellular elements are located. The number of blood cells and plasma is in the ratio of 4:6. When this balance is disrupted and the number of cellular elements begins to predominate, the blood thickens.

Blood thickening is a serious problem that must be actively combated. When the blood begins to thicken, its viscosity increases, and the processes of oxidation and tissue regeneration are disrupted.

Hypercoagulation is primary. Its cause is a hereditary predisposition. Secondary hypercoagulation develops against the background of pathologies existing in the body.

Causes

Causes of hypercoagulability very diverse. Pathology never occurs spontaneously. This pathological process provoked by the following factors:

• During pregnancy, additional stress occurs on the fragile female body, as a result of which the functioning of the blood coagulation system is disrupted.
• Intoxication with signs of dyspepsia - vomiting and diarrhea, as well as polyuria caused by diabetes mellitus, kidney disease, pulmonary edema, burns and injuries, are common causes of hypercoagulation. Excessive loss of fluid makes the blood highly concentrated. When dehydrated, brain function and health are impaired. blood vessels. After the diseased body is restored, the volume and viscosity of the blood are normalized.
• Taking many medications also leads to dehydration. Long-term treatment In women, hormonal contraceptives impair blood flow. Its concentration becomes normal after the end of therapy.
• develops as a result of excessive consumption of fatty foods. In this case, the blood becomes very viscous. To push it through the blood vessels, the heart begins to work harder.
• Viral or bacterial infection of the body and helminthic infestations are accompanied by toxic damage to target organs, damage to blood vessels, and blood thickening.
• Acquired and congenital enzymopathies slow down blood flow and lead to hypercoagulation.
• Liver diseases - hepatitis and cirrhosis disrupt microcirculation and oxygen imbalance.
• Oncopathologies - hemangioma, fibroids, lipoma, some forms of leukemia, myeloma.
• Hereditary predisposition.
• Diseases of the blood and blood vessels - erythemia, and disseminated intravascular coagulation syndrome.
• Lifestyle features - smoking, and overweight bodies.
• Surgical interventions on the heart, replacement of its valves.
• Systemic diseases connective tissue- vasculitis, scleroderma.
• Adrenal dysfunction, amyloidosis.

Hypercoagulation is a problem from which no one is immune. When faced with it, you should not panic and self-medicate. You need to pull yourself together and see a doctor. Thoughtless use of blood-thinning medications can lead to dire consequences.

diagram - distribution of causes of congenital hypercoagulable states

Mechanistically, hypercoagulation occurs as a result of:

1. Increased concentration of procoagulants in the blood and their excessive activation, which occurs with severe hyperprothrombinemia, hyperfibrinogenemia or;
2. Suppression of the activity of anticoagulants in shock, burns,;
3. Deficiency and inhibition of fibrinolytic coagulation factors in severe thrombotic syndrome, damage to vascular walls, atherosclerosis.

Hypercoagulation in advanced cases leads to the formation of multiple blood clots in main vessels and microvasculature.

Hypercoagulability and pregnancy

Chronometric hypercoagulation is often diagnosed in women carrying a child. This is due increased activity blood coagulation system of mother and fetus. In turn, hypercoagulation syndrome protects the woman’s body from large blood loss during childbirth. Hypercoagulation during pregnancy occurs in the second trimester and is a normal variant.

The pathological increase in coagulation in pregnant women is caused by various factors:

• Diseases of internal organs,
• Gene mutations
• Stress, conflicts, depression,
• Mature age - over 40 years old.

To monitor hemostasis, all pregnant women need to donate blood once a month for a coagulogram and coagulation test. If signs of hypercoagulation are detected, they are given safe therapy that does not harm the fetus. Otherwise, thrombosis of the spiral arteries occurs in a pregnant woman, which leads to serious complications: delayed fetal development, rapid wear of the placenta, antenatal death.

Clinical picture and diagnosis

Hypercoagulation is most often a symptom various diseases, but it can also be an independent illness that does not have a clearly defined clinical picture. The slowing down of blood flow, its formation, and the formation of microclots are clinically manifested by headache, paresthesia, and general asthenia of the body. Patients complain about deterioration general well-being, lethargy, lethargy, apathy, drowsiness, absent-mindedness, hypertension, dry mouth, Bad mood, cold extremities.

Clinical signs of the disease may be absent. In such cases, determine increased clotting blood can only be based on the results of laboratory tests, without which specialists will not be able to give objective assessment situations.

In the absence of timely and adequate therapy, hypercoagulation leads to the development of thrombotic and hemorrhagic complications.

To detect hypercoagulability syndrome, it is necessary to undergo a complete laboratory examination. To do this, patients are tested by taking blood from the antecubital vein.

In the laboratory, indicators are determined and blood is examined for clotting. , measurement and indicators of acid-base status complement the data obtained.

Diagnosis is made by characteristic features and laboratory tests of the hemostatic system.

Treatment

To restore normal blood flow and get rid of hypercoagulation, you need to visit a specialist who will conduct a diagnostic examination and provide qualified assistance. Doctors on an individual basis They will select a treatment regimen taking into account all the characteristics of the body.

Treatment of hypercoagulation is aimed at eliminating causative factors, conducting anti-shock therapy, restoring circulating blood volume, improving microcirculation, maintaining hematocrit at an optimal level, correcting hemodynamics and coagulation system disorders:

1. Medicines: aspirin-based medicines that prevent thrombus formation: - “Thrombo ACC”, “Cardiomagnyl”, “ Acetylsalicylic acid"; - “Warfarin”, “Heparin”, “Fragmin”; fibrinolytics - Thromboflux, Fortelysin, Streptase.
2. Symptomatic therapy - antispasmodics “No-shpa”, “Papaverine”, “Spazmalgon”; anti-inflammatory drugs - "Ibuklin", "Indomethacin", vascular drugs - "Pentoxifylline", "Curantil".
3. If present in the body bacterial infection carry out antibacterial therapy with the addition of antiproteases, for example, Cefazolin and Contrical, Azithromycin and Gordox.
4. To mitigate the developing shock state, it is administered intravenously saline solutions, plasma with heparin, "Reopoliglucin", albumin solution.
5. When hematocrit develops and decreases, transfusions of red blood cells or suspension are performed.
6. At autoimmune diseases plasmapheresis is performed and prescribed steroid hormones- Prednisolone, Dexamethasone.

In severe cases, patients are given intravenous drips of colloidal and crystalloid solutions and transfused with donor blood. Transfusions donated blood save the lives of patients after injuries accompanied by blood loss.

In parallel with traditional drug therapy apply traditional medicine recipes. Meadowsweet tincture, according to herbalists, is a substitute for aspirin. This plant is used to treat not only blood diseases, but also the cardiovascular system. A decoction prepared from the fruits of hawthorn, meadow clover, valerian root, lemon balm, and yellow clover improves the condition of blood vessels and has a beneficial effect on the blood circulation process.

Diet therapy requires eating natural foods prepared by boiling, stewing or steaming. Products enriched with vitamin E restore blood fluidity. It is good to eat a tablespoon of sprouted wheat grains a day. The diet of patients must include dairy products, vegetables, fruits, meat and fish dishes, seafood. The most useful berries and fruits are: cranberries, currants, cherries, grapes, apples, citrus fruits, peaches. You should definitely exclude canned, smoked, fatty, fried and pickled foods, sweets, baked goods, buckwheat, potatoes, alcohol, and soda.

Patients suffering from hypercoagulability should follow the basic recommendations of specialists:

• Quit smoking
• Eat properly,
• Walk a lot in the fresh air
• Exercise,
• Optimize your daily routine
• Get enough sleep
• Avoid stressful situations and conflicts,
• Lead a healthy lifestyle,
• Get blood tests periodically.

The prognosis of hypercoagulation syndrome is ambiguous and depends on the severity of the underlying disease, the general condition of the body, and existing changes in hemostasis.

Prevention of hypercoagulation involves identifying patients at risk - pregnant women, the elderly and people with cancer, as well as treating the underlying disease.

The functioning of the cardiovascular system and all internal organs directly depends on its condition.

What causes blood to thicken?

Hypercoagulation of blood in most cases is not accompanied by the formation of blood clots in the vascular bed. Despite the fact that laboratory tests will show the patient's tendency to rapidly clot, he should not panic and thoughtlessly take blood thinning medications. If he does form a blood clot, then its structure will be loose, which is why it will lack elasticity.

The causes of hypercoagulability can be varied. Some patients developed blood problems due to cancer. In other people, a hereditary factor caused hypercoagulability. It is also worth noting the following factors that can change the composition of the blood:

• vascular injury, including atherosclerosis;
• thrombophilia (hematogenous);
• overweight (any stage of obesity);
• sedentary lifestyle;
• bad habits;
• erythremia, hemangioma or antiphospholipid syndrome;
• previous heart surgeries during which an artificial valve was installed;
• autoimmune diseases;
• pregnancy or taking contraceptives, etc.

How to identify pathology?

The difficulty of diagnosing this pathology lies in the fact that hypercoagulation does not have a pronounced clinical picture. Some patients who have this syndrome complain of lethargy, general weakness, and pain in the head. To identify this disease, it is necessary to undergo a laboratory examination, which consists of collecting venous blood. The laboratory technician will immediately notice that the biological material taken from the patient has signs of hypercoagulation, since the blood will almost instantly clot in the needle.

The study of venous blood allows you to confidently determine blood hypercoagulation

A coagulogram can easily identify hypercoagulability syndrome, since laboratory tests will reveal changes in the following indicators:

What is a hemostasiogram?

CJSC Laboratories TsIR What is a hemostasiogram?

Blood coagulation system. Laboratory diagnosis of hemostasis disorders. Interpretation of results. Features of hemostasis during pregnancy. Molecular genetic analyses. Platelet function.

Blood clotting tests are important for identifying possible disorders in the hemostatic system, as well as for assessing the effectiveness of therapy, selecting the dose and monitoring therapy to prevent complications. Only with the help of laboratory diagnostics can an accurate diagnosis be made and the effect of medications adequately assessed.

High quality laboratory diagnostics very important to accept the right decision attending physician. We use high-quality foreign-made reagents, conduct internal quality control and participate in external quality control programs. Comprehensive tests are developed jointly with clinicians who are our strict experts. We provide not only the results, but also a detailed report from the laboratory doctor on the hemostasiogram, determination of lupus anticoagulant, and platelet aggregation.

The need for hemostasis studies may arise in a person of any age and gender! Our laboratory examines women preparing for pregnancy and pregnant women; women taking contraceptives; patients receiving therapy with aspirin and heparin. Therefore, we provide excellent research quality, which is highly valued by clinicians.

Our laboratory offers different kinds hemostasis studies. Both screening tests, such as a basic coagulation test, and complex studies, such as induced platelet aggregation, are performed.

Tests are taken at all three CIR clinics, which is convenient for our patients. Test results can be obtained from e-mail or by courier.

The hemostasis system performs two main functions: maintaining blood in liquid form inside the vessels on the one hand, and on the other hand fast reaction for vascular damage (formation of blood clots to stop bleeding). The following are involved in blood clotting: the vascular wall, blood cells, and blood plasma proteins. The plasma hemostasis system consists of three interconnected systems - the coagulation system (coagulation), the anticoagulation system (anticoagulant) and the fibrinolysis system (thromt dissolution).

Coagulation parameters characterize the cascade leading to the formation of fibrin, the protein that forms the basis of the blood clot. Triggering of coagulation can occur as a result of activation of the intrinsic and extrinsic pathways.

Blood clotting disorders: hypocoagulation- decreased blood clotting, manifested by bleeding, hypercoagulability- increased blood clotting, manifested by thrombosis, thrombophilia- tendency to form blood clots.

Assessment of blood coagulation: hemostasiogram (coagulogram). Contents of blood cellular elements. Cellular elements (platelets, erythrocytes, leukocytes) ensure the formation of a primary plug in the damaged area. Activation of cellular elements is an important factor in launching the plasma component of hemostasis. Enabling Individual Metrics general analysis blood in the hemostasiogram helps to correctly interpret deviations in the analysis and the clinical picture.

Screening tests for studying the plasma component of hemostasis - APTT, prothrombin time, prothrombin index, prothrombin according to Quick, INR, thrombin time, fibrinogen, soluble complexes of fibrin monomers (SCFM).

APTT or APTT (activated partial or partial thromboplastin time) is an assessment of the internal pathway of blood coagulation, the activator is phospholipids. The aPTT is the time required for plasma to clot when intrinsic pathway factors (calcium, phospholipids, and kaolin) are added.

Prolongation of aPTT is observed with a deficiency of coagulation factors XII, XI, IX, VIII, kininogen, prekallikrein, factors V, X, prothrombin and fibrinogen, antiphospholipid syndrome, DIC syndrome.

A shortened APTT is observed during hypercoagulation, including during pregnancy. Phase 1 of DIC syndrome.

The property of aPTT to lengthen with an excess of heparin makes it possible to monitor therapy with heparin-type drugs. Adequate prolongation of APTT - up to 2.5 times. When APTT changes important has APTT control when corrected with normal plasma. Thus, correction of an increased aPTT with normal plasma indicates that the concentration of blood coagulation factors in the plasma is reduced. Lack of correction may indicate the presence of blood clotting inhibitors (for example, lupus anticoagulant).

Prothrombin time is the time required for plasma to clot when calcium and tissue factor are added. The method reproduces the external pathway of blood coagulation with the assessment of the so-called prothrombin complex - factors VII, X, prothrombin. The extrinsic pathway involves vitamin K-dependent coagulation factors, so PT is used to evaluate therapy indirect anticoagulants.

There are three standard ways of presenting the results of this test: prothrombin index - the ratio of the PT result to the PT of normal plasma. Prothrombin according to Quick reflects the content of coagulation factors as a percentage and serves to assess the external coagulation pathway. INR (International Normalized Ratio) A comparison is made of the patient's blood clotting with special plasma normalized by international standard, which makes it possible to assess the state of the patient’s external pathway of plasma hemostasis with a greater degree of reliability. This is important for assessing the effect of drugs and selecting the dose.

Prolongation of PT (PI decreases, PC and INR increase) may indicate a congenital deficiency of factors II, V, VII, X, liver diseases with impaired liver function, vitamin K deficiency (malabsorption, cholestasis, dietary habits, intestinal dysbiosis), treatment with indirect anticoagulants , decrease or change in the structure of fibrinogen.

A shortening of PT (PI increases, PC and INR decrease) indicates hypercoagulation, including during pregnancy and after childbirth, as well as when taking certain contraceptives.

Ways to express prothrombin test:

MICH - International Sensitivity Index

Fibrinogen- a blood protein that is synthesized in the liver. When blood clotting begins, fibrinogen polymerizes to form fibrin.

An increase in fibrinogen concentration indicates a state of thrombophilia, observed with burns, in recent months pregnancy, after childbirth, with myocardial infarction, after surgical interventions. In addition, the level of fibrinogen is increased during inflammatory processes and stress. A decrease in the amount of fibrinogen can be hereditary or acquired (liver dysfunction).

Thrombin time (TT) is the time during which fibrin is formed from fibrinogen. This indicator evaluates the rate of blood clotting when thrombin is added. The rate of fibrin formation depends on the quantity and quality of fibrinogen and the presence of anticoagulants in the blood.

TV increases with a decrease in fibrinogen concentration and changes in its molecule, the presence of inhibitors of fibrin formation, autoantibodies to thrombin, paraproteinemia, increased content fibrinogen/fibrin degradation products, the presence of heparin and other conditions. A decrease in TV is observed in the first stage of DIC syndrome and a significant increase in fibrinogen in the blood.

Thus, competent comprehensive assessment APTT results, prothrombin time, thrombin time and fibrinogen indicators allow us to identify the presence of certain disorders, assess the effectiveness of therapy, suspect the risk of thrombosis or bleeding, and allow us to prescribe necessary medications and prevent drug overdose.

Anticoagulant system< p>Accidental activation of the coagulation mechanism is prevented by a special system, which includes several important proteins: antithrombin III, protein C and protein S. Adequate operation of the anticoagulation system is an important condition maintaining the liquid state of blood inside the vessels. A decrease in the activity of anticoagulant factors can cause severe thrombotic complications. Our laboratory carries out the determination of antithrombin III and protein C.

Even in in good condition polymerization of fibrinogen can occur in the body. But as soon as this process begins, the fibrinolysis system is activated to prevent blockage of blood vessels. Then fibrin breakdown products - RKMF and D-dimers - are formed in the blood. An increase in the level of these factors indicates that the fibrin content is increased. During pregnancy, fibrin is deposited on the surface of the placenta. If it is deposited excessively, the permeability of the placenta is impaired, which can cause intrauterine fetal hypoxia and other pregnancy complications. Determination of performance indicators of the fibrinolysis system is used to diagnose the risk of pregnancy complications, as well as to diagnose DIC syndrome. Assessment of changes in fibrinolysis indicators should be carried out only with the participation of other hemostasis indicators, since it does not reflect the site of initiation molecular mechanism fibrinolysis. Thus, an increase in fibrinolysis rates can be observed with bruises and nosebleeds.

RKMF (soluble complexes of fibrin monomers)- a test to diagnose the activation of blood clotting inside blood vessels. The basis blood clot makes up fibrin, which is formed from fibrinogen. This process goes through the formation of fibrin monomers. Therefore, the determination of RKMF is used to diagnose the activation of blood coagulation inside blood vessels.

RKMP increases with hypercoagulation, increased fibrinolysis, and increased fibrinogen concentrations. During pregnancy, there is a physiological increase in fibrinogen levels, therefore RKMF are also often elevated. For more accurate and full diagnostics intravascular coagulation is used to determine the level of D-dimers.

Features of blood clotting during pregnancy During pregnancy, a third circle of blood circulation appears - the placental. The placenta is an organ that separates the mother and fetus. A special feature is that the placenta does not have a capillary link on the maternal side. Directly from the spiral arteries, the mother's blood enters the intervillous space and the chorion villi are washed with maternal blood. Through the veins of the deciduous membrane, blood returns back to the mother's bloodstream. That is, the placenta represents the boundary of interaction between two organisms, an aggressive phase that leads to the activation of thrombotic mechanisms. Hidden tendencies of impaired hemostasis appear in the arteries of the placenta with a greater degree of probability and lead to additional excessive blood clotting. Many pregnancy complications arise from thrombosis of the spiral arteries. During pregnancy, the activity of factors in the internal blood coagulation pathway increases, which is manifested by a shortening of the aPTT. During pregnancy, the amount of fibrinogen increases, the level of RCMP and D-dimers increases. Despite these changes, when normal pregnancy There is no pathological activation of hemostasis; these changes are considered adaptive. It is advisable to assess blood coagulation at different stages of pregnancy. It is very important that the first blood coagulation test is carried out on early stages pregnancy. Then the likelihood of risks when prescribing medications in a timely manner will be minimal.

Excessive blood clotting leads to increased fibrin deposition in the placenta and premature aging of the placenta. Purpose specific therapy allows you to slow down this process and prevent premature aging of the placenta.

A hemostasiogram is a screening test and reflects the state of blood coagulation at the time of blood donation. Therefore, a hemostasiogram may not show those risks whose mechanisms have not yet been activated. To assess the risks of thrombophilia, which is the cause of miscarriage, severe gestosis, myocardial infarction, stroke and other thrombosis, other studies are required. Hidden hereditary risk factors for blood clotting disorders pose a particular danger in obstetric and gynecological practice. At the moment of conception, each of us receives genetic material from our parents. This genetic material may contain genes whose presence is associated with increased risk one state or another. If both parents pass on such a gene, this condition is called homozygosity, if only one - heterozygosity. For some genes, a heterozygous state is sufficient; for others, a homozygous state is sufficient. In order to find out whether there are pathological genes and in what state they are (hetero- or homozygous), molecular genetic studies are carried out.

To assess the risks of developing pathology in the hemostasis system, the following molecular genetic studies are carried out at CJSC Laboratories TsIR:

• Polymorphism of genes of the hemostasis system - 11 factors, including the common Leiden mutation (f.V), prothrombin gene mutation, MTHFR mutation.

You need to take these tests if you answer “yes” to at least one of these points:

• If there have been two or more fetal growth arrests in the past in early pregnancy
• with several unsuccessful attempts IVF
• if you have had severe pregnancy complications in the past ( severe forms late toxicosis of intrauterine fetal death, fetal growth retardation)
• when an increase in the level of antiphospholipid antibodies and/or an increase in the level of homocysteine ​​is detected
• in the presence of a history of blood clotting disorders (thrombosis) in the presence of relatives with thrombotic complications under the age of 50 years (deep vein thrombosis, thromboembopia) pulmonary artery, stroke, myocardial infarction, sudden death)

Hypercoagulation (hypercoagulation syndrome): causes, forms, symptoms, tests, treatment

Hypercoagulation is a medical term meaning a state of increased activity of the blood coagulation system. This pathology can be an independent disease or a manifestation of concomitant ailments. Hypercoagulability syndrome in most cases is accompanied by an increased tendency to thrombus formation. The resulting blood clot is loose in structure and lacks elasticity.

Blood is the vital medium of the body, performing a transport function and ensuring the delivery of oxygen and nutrients to all internal organs. It consists of plasma - the liquid part in which cellular elements are located. The number of blood cells and plasma is in the ratio of 4:6. When this balance is disrupted and the number of cellular elements begins to predominate, the blood thickens.

Blood thickening is a serious problem that must be actively combated. When the blood begins to thicken, its viscosity increases, and the processes of oxidation and tissue regeneration are disrupted.

Hypercoagulation is primary. Its cause is a hereditary predisposition. Secondary hypercoagulation develops against the background of pathologies existing in the body.

Causes

The causes of hypercoagulation are very diverse. Pathology never occurs spontaneously. This pathological process is provoked by the following factors:

• During pregnancy, additional stress occurs on the fragile female body, as a result of which the functioning of the blood coagulation system is disrupted.
• Intoxication with signs of dyspepsia - vomiting and diarrhea, as well as polyuria caused by diabetes mellitus, kidney disease, pulmonary edema, burns and injuries, are common causes of hypercoagulation. Excessive loss of fluid makes the blood highly concentrated. When dehydrated, brain function and the condition of blood vessels are disrupted. After the diseased body is restored, the volume and viscosity of the blood are normalized.
• Taking many medications also leads to dehydration. Long-term treatment of women with hormonal contraceptives worsens blood flow. Its concentration becomes normal after the end of therapy.
• Hypercholesterolemia develops as a result of excessive consumption of fatty foods. In this case, the blood becomes very viscous. To push it through the blood vessels, the heart begins to work harder.
• Viral or bacterial infection of the body and helminthic infestations are accompanied by toxic damage to target organs, damage to blood vessels, and blood thickening.
• Acquired and congenital enzymopathies slow down blood flow and lead to hypercoagulation.
• Liver diseases - hepatitis and cirrhosis disrupt microcirculation and oxygen imbalance.
• Oncopathologies - hemangioma, fibroids, lipoma, some forms of leukemia, myeloma.
• Hereditary predisposition.
• Blood and vascular diseases - atherosclerosis, thrombophilia, erythemia, varicose veins veins and venous stasis, DIC syndrome.
• Features of lifestyle - smoking, physical inactivity and excess body weight.
• Surgical interventions on the heart, replacement of its valves.
• Systemic connective tissue diseases - vasculitis, systemic lupus erythematosus, scleroderma.
• Adrenal dysfunction, amyloidosis.

Hypercoagulation is a problem from which no one is immune. When faced with it, you should not panic and self-medicate. You need to pull yourself together and see a doctor. Thoughtless use of blood-thinning medications can lead to dire consequences.

diagram - distribution of causes of congenital hypercoagulable states

Mechanistically, hypercoagulation occurs as a result of:

1. Increased concentration of procoagulants in the blood and their excessive activation, which occurs with severe hyperprothrombinemia, hyperfibrinogenemia or thrombocytosis;
2. Suppression of the activity of anticoagulants in shock, sepsis, burns, DIC syndrome;
3. Deficiency and inhibition of fibrinolytic coagulation factors in severe thrombotic syndrome, damage to vascular walls, vasculitis, atherosclerosis.

Hypercoagulation in advanced cases leads to the formation of multiple blood clots in the great vessels and microvasculature.

Hypercoagulability and pregnancy

Chronometric hypercoagulation is often diagnosed in women carrying a child. This is due to the increased activity of the blood coagulation system of the mother and fetus. In turn, hypercoagulation syndrome protects the woman’s body from large blood loss during childbirth. Hypercoagulation during pregnancy occurs in the second trimester and is a normal variant.

The pathological increase in coagulation in pregnant women is caused by various factors:

• Diseases of internal organs,
• Gene mutations
• Stress, conflicts, depression,
• Mature age - over 40 years old.

To monitor hemostasis, all pregnant women need to donate blood once a month for a coagulogram and coagulation test. If signs of hypercoagulation are detected, they are given safe therapy that does not harm the fetus. Otherwise, thrombosis of the spiral arteries occurs in a pregnant woman, which leads to serious complications: delayed fetal development, rapid wear of the placenta, and antenatal death.

Clinical picture and diagnosis

Hypercoagulation most often acts as a symptom of various diseases, but it can also be an independent disease that does not have a pronounced clinical picture. The slowing down of blood flow, its thickening, and the formation of microclots are clinically manifested by headache, paresthesia, and general asthenia of the body. Patients complain of a deterioration in general health, lethargy, lethargy, apathy, drowsiness, absent-mindedness, hypertension, dry mouth, bad mood, cold extremities.

Clinical signs of the disease may be absent. In such cases, increased blood clotting can be determined only by the results of laboratory tests, without which specialists will not be able to give an objective assessment of the situation.

In the absence of timely and adequate therapy, hypercoagulation leads to the development of thrombotic and hemorrhagic complications.

To detect hypercoagulability syndrome, it is necessary to undergo a complete laboratory examination. To do this, patients are tested by taking blood from the antecubital vein.

In the laboratory, coagulogram parameters are determined and blood is examined for clotting. CBC, hematocrit measurements and acid-base parameters complement the data obtained.

The diagnosis is established by characteristic signs and laboratory tests of the hemostatic system.

Treatment

To restore normal blood flow and get rid of hypercoagulation, you need to visit a specialist who will conduct a diagnostic examination and provide qualified assistance. Doctors will individually select a treatment regimen taking into account all the characteristics of the body.

Treatment of hypercoagulation is aimed at eliminating causative factors, conducting anti-shock therapy, restoring circulating blood volume, improving microcirculation, maintaining hematocrit at an optimal level, correcting hemodynamics and coagulation system disorders:

1. Medicines that thin the blood: medicines based on aspirin that prevent blood clots: antiplatelet agents - Thrombo ACC, Cardiomagnyl, Acetylsalicylic acid; anticoagulants - “Warfarin”, “Heparin”, “Fragmin”; fibrinolytics - “Thromboflux”, “Fortelysin”, “Streptase”.
2. Symptomatic therapy - antispasmodics “No-shpa”, “Papaverine”, “Spazmalgon”; anti-inflammatory drugs - “Ibuklin”, “Indomethacin”, vascular drugs - “Pentoxifylline”, “Curantil”.
3. If there is a bacterial infection in the body, antibacterial therapy is carried out with the addition of antiproteases, for example, Cefazolin and Contrikal, Azithromycin and Gordox.
4. To mitigate the developing state of shock, saline solutions, plasma with heparin, Reopoliglucin, and albumin solution are administered intravenously.
5. With the development of anemia and a decrease in hematocrit, transfusions of red blood cells or suspension are performed.
6. For autoimmune diseases, plasmapheresis is performed and steroid hormones are prescribed - Prednisolone, Dexamethasone.

In severe cases, patients are given intravenous drips of colloidal and crystalloid solutions and transfused with donor blood. Donor blood transfusions save the lives of patients after injuries accompanied by blood loss.

In parallel with traditional drug therapy, traditional medicine recipes are used. Meadowsweet tincture, according to herbalists, is a substitute for aspirin. This plant is used to treat not only blood diseases, but also the cardiovascular system. A decoction prepared from the fruits of hawthorn, meadow clover, valerian root, lemon balm, and yellow clover improves the condition of blood vessels and has a beneficial effect on the blood circulation process.

Diet therapy requires eating natural foods prepared by boiling, stewing or steaming. Products enriched with vitamin E restore blood fluidity. It is good to eat a tablespoon of sprouted wheat grains a day. The diet of patients must include fermented milk products, vegetables, fruits, meat and fish dishes, and seafood. The most useful berries and fruits are: cranberries, currants, cherries, grapes, apples, citrus fruits, peaches. You should definitely exclude canned, smoked, fatty, fried and pickled foods, sweets, baked goods, buckwheat, potatoes, alcohol, and soda.

Patients suffering from hypercoagulability should follow the basic recommendations of specialists:

• Quit smoking
• Eat properly,
• Walk a lot in the fresh air
• Exercise,
• Optimize your daily routine
• Get enough sleep
• Avoid stressful situations and conflicts,
• Lead a healthy lifestyle,
• Get blood tests periodically.

The prognosis of hypercoagulation syndrome is ambiguous and depends on the severity of the underlying disease, the general condition of the body, and existing changes in hemostasis.

Prevention of hypercoagulation involves identifying patients at risk - pregnant women, the elderly and people with cancer, as well as treating the underlying disease.

Hypercoagulation: what it is, causes and treatment

Blood is the main living medium, which plays a very significant role in the human body, which consists in transporting various kinds of nutrients, oxygen and other components. Its condition directly determines the activity of the internal organs as a whole and the cardiovascular system.

Description

The medical term “hypercoagulation” (we’ll look at what it is in this article) is a condition in which the activity of the blood coagulation system is increased. Pathology of this type can be either an independent disease or a manifestation of ailments that accompany it. Hypercoagulation syndrome is predominantly accompanied by an increased susceptibility to thrombosis. The blood clot formed in this case is not elastic and has a loose structure.

Serious problem

Blood thickening is quite serious problem, and we need to actively fight it. If the blood begins to thicken, then its property such as viscosity increases, the processes of tissue regeneration and oxidation are disrupted.

Hypercoagulation may be primary. In this case, its cause is a hereditary predisposition. The secondary type occurs against the background of pathologies that exist in the body.

What is chronometric hypercoagulation? More on this below.

Causes

Pathology can arise from various reasons. The disease never appears spontaneously. This pathological process can be triggered by the following factors:

• During pregnancy, an additional load is placed on the female body, as a result of which the activity of the blood coagulation system is disrupted.
• Intoxication with signs characteristic of dyspepsia, that is, diarrhea and vomiting, and polyuria caused by kidney disease, diabetes mellitus, pulmonary edema, burns and injuries, often provoke hypercoagulation of the blood (what is this is interesting to many). Due to large volumes of fluid loss, the blood becomes highly concentrated. Dehydration causes problems brain activity and the condition of blood vessels. When the patient’s body recovers, the viscosity and volume of the blood return to normal.
• The use of various types of medications also causes dehydration. During long-term therapy of women with contraceptives hormonal type blood flow deteriorates. After completion of treatment, its concentration becomes normal.
• Due to excessive consumption of fatty foods, hypercholesterolemia develops. The blood is highly viscous. To push it through the blood vessels, the heart has to work harder.

• Bacterial or viral infection of the body, as well as helminthic infestations, are simultaneously accompanied by toxic damage to certain organs, blood vessels and blood thickening.
• Both congenital and acquired enzymopathies slow down blood flow and cause hypercoagulation.
• Liver diseases such as cirrhosis and hepatitis disrupt oxygen balance and microcirculation.
• Pathologies of an oncological nature - fibroids, hemangioma, myeloma, lipoma, certain types of leukemia.
• Vascular and blood diseases - thrombophilia, varicose veins, atherosclerosis, erythremia, disseminated intravascular coagulation syndrome, venous stagnation.
• Specific lifestyle features are physical inactivity, smoking, excess body weight.
• Systemic connective tissue diseases - scleroderma, systemic lupus erythematosus, vasculitis.
• Surgical interventions performed on the heart, as well as prosthetic valves of this organ.
• Amyloidosis, adrenal dysfunction.

Hypercoagulation syndrome is a problem from which no one can be immune. When faced with it, there is no need to panic and try to heal on your own. You need to calm down, pull yourself together and go to see a specialist. If you thoughtlessly take blood-thinning medications, everything can end very sadly.

The mechanism of development of hypercoagulation

If we consider the occurrence of hypercoagulation (we explained what it is) from the point of view of the mechanism, then it appears as a result of a number of reasons. This:

• increased concentration of procoagulants in the blood and their excessive activation, which is characteristic of thrombocytosis, as well as severe hyperfibrinogenemia and hyperprothrombinemia;
• inhibition of the activity of anticoagulants in conditions such as sepsis, shock, disseminated intravascular coagulation syndrome, burns;
• deficiency and suppression of fibrinolytic coagulation factors in the presence of thrombotic syndrome in severe form, damage to vascular walls, atherosclerosis, vasculitis.

In advanced cases, structural hypercoagulation becomes the cause of the formation large quantity blood clots in the microvasculature and great vessels.

How to determine the presence of pathology?

The difficulty in diagnosing a pathology of this kind lies in the fact that hypercoagulation does not have any clearly defined clinical picture. Some patients with this syndrome complain of general weakness, lethargy, and pain in the head. To identify this disease, a laboratory test is required, which involves collecting venous blood. In this case, the laboratory technician will immediately see that the biological material taken from the patient has signs of hypercoagulation, since the blood in this case will almost immediately clot in the needle.

Hypercoagulability therapy

If the patient has been diagnosed with a disease such as hypercoagulability inner path blood clotting, you should not self-medicate, as its consequences can be unpleasant. He needs to go to any medical institution where they can provide qualified assistance. Specialists of a narrow profile will select individual therapy for such patients, taking into account all characteristic features specific organism.

Drugs

Most often, specialists prescribe in this case medications (for example, Thrombo ACC, which has aspirin as the main component) that dilute platelets. Along with them, it is also possible to use traditional medicine techniques. For example, meadowsweet, from which not only tinctures are made, but also various kinds of preparations. Its components are unique and can replace aspirin. Meadowsweet is prescribed by many doctors for diseases of the blood system and blood vessels, including hypercoagulation along the internal pathway of blood coagulation. If a pregnant patient is undergoing treatment, then the therapeutic course should be selected especially carefully. Low molecular weight heparins are prescribed for this category of patients. When treating hypercoagulation, it is allowed to take drugs such as Aspirin, Curantil, Pentoxifylline, Clopidogrel. They are prescribed after consultation with a specialist.

When treating patients who have other diseases along with this syndrome, Syncumar or Warfarin, which are anticoagulants, are often prescribed. If significant bleeding occurs during hypercoagulation (what it is is now known), then patients require blood transfusions from donors. In addition, it is possible to use saline or colloidal solutions.

To achieve the desired results from treatment, patients are required to follow the instructions of their physician with precision and adhere to recommendations such as:

• conducting healthy image life;
• giving up various kinds of bad habits (for example, smoking can be one of the factors contributing to the development of hypercoagulation along the internal route);
• exclusion of significant physical activity;
• proper nutrition.

It is important to spend as much time as possible outside, in the fresh air.

Is it necessary to follow a diet for hypercoagulability?

If patients have been diagnosed with hypercoagulation syndrome in the laboratory, then experts recommend not only drug treatment, but also changes in their diet. It is necessary to exclude such products as:

• smoked meats;
• fried and fatty foods;
• various canned foods;
• marinades;
• flour;
• buckwheat;
• sweets;
• potato;
• bananas;
• too salty and spicy food;
• carbonated drinks;
• alcohol, etc.

It will also be useful to enter into your daily diet fermented milk products that contain fat in minimal quantities, as well as vegetables, fruits, dark chocolate, cocoa, ginger root, garlic, artichokes, lemons, etc.

If the patient's hypercoagulation was provoked by sedentary or in the wrong way life, it is urgent to pay attention to your own health. The fact is that this category of patients is especially at risk of having a stroke.

Specifics of hypercoagulation during pregnancy

Hypercoagulation chronic type often found in women who are pregnant. This condition is normal, since the body of the expectant mother forms protective properties before childbirth, which means there is an increase in blood clotting. In a pregnant woman, the level of fibrinogen can increase by one and a half to two times. However, there are cases of multiple increases in coagulation rates. This phenomenon cannot be ignored, since the fetus may die in the early stages, or placental abruption may occur prematurely in the last trimester. The so-called hypercoagulation syndrome is known in medicine.

Hemostasis must be carefully monitored during pregnancy, and for this it is recommended to undergo a coagulogram. If a pathology is detected, it is imperative to be treated in accordance with the doctor’s instructions. If this disease is detected in a timely manner, possible complications can be avoided.

We looked at what it is - hypercoagulation.

Hypocoagulation. Hemorrhagic syndrome

The following mechanisms underlie the decrease in blood clotting: 1) decrease in the concentration of procoagulants in the blood; 2) insufficient activation of procoagulants; 3) increased concentration or excessive activation of anticoagulants; 4) increased concentration or excessive increase in the activity of fibrinolytic factors.

Procoagulant deficiency (the first mechanism) is very common. It may be caused by thrombocytopenia, thrombocytopathy, insufficient or impaired synthesis of various plasma coagulation factors, excessive increased consumption these factors in the coagulation process.

I. Thrombocytopenia. According to pathogenesis they are divided into the following types:

1) associated with increased destruction of platelets as a result of: a) immune conflicts; b) mechanical destruction (splenomegaly);

2) associated with a lack of platelet formation due to: a) decreased proliferation of unipotent cells bone marrow- platelet precursors (aplastic anemia); b) replacement of bone marrow with tumor tissue; c) lack of vitamin B 12 and folic acid;

3) associated with increased consumption (usually with multiple thrombosis). Most common cause thrombocytopenia is increased cell destruction. In this case, an inherited defect in the structure of platelet membranes or a decrease in the activity of glycolytic enzymes or the Krebs cycle is usually detected. As a consequence, there is a significant shortening of the lifespan of platelets (several hours, instead of 7–10 days) and an increase in their destruction in the spleen. At the same time, there is an increase in platelet formation per unit time. The reason is an increase in the level of thrombocytopoietins due to thrombocytopenia.

IN clinical practice most common:

A) drug-induced thrombocytopenia. Diagnosed based on the coincidence in time of taking the drug and the development of thrombocytopenia (can be caused by taking estrogens, thiazide diuretics, antitumor drugs, ethanol, etc.);

b) autoimmune thrombocytopenia - the result of increased destruction of platelets under the influence of antiplatelet antibodies (usually develops in previously healthy people);

c) thrombocytopenia in pregnant women. Occurs in 5–10% of pregnant women and usually does not cause serious complications in the woman and fetus;

d) thrombocytopenia caused by HIV infection. Thrombocytopenia is often found in HIV carriers and may be the first manifestation of infection;

e) thrombocytopenia caused by transfusions. It can develop after massive blood transfusions or the use of artificial circulation, which is due to the dilution of platelets in the blood or their mechanical removal. This thrombocytopenia persists for 3–5 days and can be corrected by platelet transfusion. Signs of the disease usually appear approximately 7 days after the blood transfusion. Thrombocytopenia of this type is usually severe and may be accompanied by intracranial hemorrhages;

f) thrombotic thrombocytopenic purpura - more rare syndrome, characterized by thrombocytopenia, microangiopathic hemolytic anemia, transitory neurological disorders, often combined with fever and kidney damage. The diagnosis is made based on the symptoms of microangiopathy - fragmentation of red blood cells in smears peripheral blood, increased reticulocyte levels and serum lactate dehydrogenase activity - in the absence of signs of DIC according to laboratory data.

However, it must be remembered that usually when the platelet content in the blood is more than 1 μl, significant bleeding is not observed; If the platelet count is greater than 1 μl and there are no abnormalities associated with coagulation factors or platelet function, then severe spontaneous bleeding rarely occurs.

II. Thrombocytopathies. Thrombocytopathies (TP), unlike thrombocytopenias, are characterized by stable, long-lasting functional, biochemical and morphological changes in platelets, which are observed even with their normal quantity and do not disappear when thrombocytopenia is eliminated, if it was combined with dysfunction blood platelets.

By origin, thrombocytopathies are divided into: 1) hereditary and congenital (primary); 2) acquired (secondary).

Causes- factors of physical, chemical and biological nature. Types of TP: 1) with predominant violation“contact” activity: aggregation and/or adhesion of platelets (disaggregation TP); 2) with a predominant violation of the “clotting” (procoagulant) activity of platelets (“discoagulant” TP).

Pathogenesis: 1) violation of synthesis and accumulation in platelets and their granules biologically active substances: procoagulants, factors of coagulation and fibrinolytic systems; 2) disruption of the reactions of “degranulation” and “release” of platelet factors into the blood plasma; 3) violation physical and chemical properties and the structure of platelet membranes (changes in surface charge, disruption of the conformation of membrane glycoproteins, proteins, etc.).

An example of hereditary disaggregation thrombocytopathy is Glanzmann's thrombasthenia. This pathology was first described in 1918 as a hereditary hemorrhagic diathesis, transmitted by a recessive autosomal type, characterized by an increase in the time of capillary bleeding (according to Duke) and the absence or sharp weakening of blood clot retraction with normal or almost normal normal content platelets in the blood. The type of bleeding is microcirculatory: slight appearance of pitechia and ecchymoses on the skin, decreased vascular resistance (positive pinch test, cupping test), possible recurring nasal and gingival bleeding, menorrhagia, bleeding during tooth extraction, etc.

A fundamental role in the origin of Glanzmann’s thromboasthenia is played by the absence in the membranes of blood plates of a complex of glycoproteins (IIb and IIIa), necessary for the interaction of these cells with aggregation stimulants and fibrinogen. The prognosis for thrombosthenia is favorable in most cases, but worsens with hemorrhage in the brain and retina. Hemorrhagic syndrome with this pathology is noticeably more pronounced in childhood and adolescence and in females.

In the clinic, some patients show signs of simultaneous disturbances in both “contact” and “procoagulant” platelet activity. Thus, with Wiskott-Aldrich syndrome (a hereditary disease that occurs in boys, transmitted recessively, linked to the X chromosome), there is a violation of the synthesis and storage of granule components various types, as well as releasing their contents. This is accompanied by a disorder of the adhesive, aggregative and procoagulant activity of platelets.

Clinical manifestations of thrombocytopathies are not pathognomonic and usually consist of hemorrhagic syndrome.

Violation of the synthesis of plasma factors. A number of procoagulants are formed in the liver. Therefore, the pathology of this organ is accompanied by a decrease in the synthesis of factors I (fibrinogen), II (prothrombin), V (proaccelerin), VII (proconvertin), etc. It follows that with liver damage, hypofibrinogenemia, hypoprothrombinemia, etc. are observed. Sometimes there is a disruption in the synthesis of these factors. In such cases they talk about dysfibrinogenemia, dysprothrombinemia, etc.

Many of the coagulation factors are synthesized in the liver with the participation of vitamin K (factors II, VII, IX, etc.) - these are the so-called “vitamin-dependent procoagulants.” Their synthesis becomes sharply reduced when the level of this vitamin in the body is insufficient, which happens: 1) with insufficient formation of vitamin K in the intestines; 2) with liver pathology (lack of bile, impaired absorption in the intestine); 3) when long-term use or overdose of vitamin K antagonists (anticoagulants with an indirect mechanism of action).

Reductions or abnormalities in the synthesis of procoagulants can be genetically determined. Example: hemophilia A - hereditary disease, which is based on a deficiency of antihemophilic globulin (f.VIII). Other types of hemophilia are possible. Their characteristics are given in detail in textbooks.

There is a known mechanism for reducing the concentration of procoagulants in the blood, due to their binding by autoantibodies (these are factors V, VIII, IX). In this case, severe diseases (tumors, sepsis, etc.) play a provoking role.

The second mechanism for the development of hypocoagulation - insufficient activation of procoagulants (at their normal concentration) is largely associated with a decrease in the activating role of platelets (factor 3 deficiency, ADP). As a rule, it is observed with severe thrombocytopenia or thrombocytopathy. Impaired activation of procoagulants can also be caused by disorders of the kallikrein-kinin system (in liver disease, sepsis, extensive inflammation or hereditary deficiency of components of this system).

The third mechanism of hypocoagulation is associated with disturbances in the system of anticoagulation factors. For example, when anaphylactic shock, others allergic reactions, some leukemias, radiation sickness, hyperheparinemia may occur. In liver pathology, the activity of antithromboplastins may increase. Finally, in autoimmune diseases, the appearance in the blood of pathological proteins that have anticoagulant activity has been described.

The fourth way of development of hypocoagulation is excessive activation of fibrinolytic mechanisms. Massive release of tissue plasminogen activators into the blood can occur during extensive injuries, burns, tissue necrosis, and various toxic conditions. Microbial kinases may play a similar role in severe infectious diseases. Hypocoagulation under conditions of excess plasmin is explained by the fact that it breaks down not only fibrin and fibrinogen, but also coagulation factors V, VIII, etc.

To the reasons for the development of hypocoagulation (we have already touched on this), we should add the effect of the group medicines, used for the prevention and treatment of hypercoagulable conditions and thrombosis. These are anticoagulants (heparin, vitamin K antagonists, etc.) and fibrinolytic drugs (fibrinolysin, streptokinase, etc.). Their overdose or incorrect prescription is dangerous for the development of hypocoagulation and hemorrhagic syndrome. In addition, cytostatics can cause thrombocytopenia and disruption of the synthesis of procoagulants in the liver, and antibiotics can lead to the development of intestinal dysbiosis and, in connection with this, disruption of the endogenous synthesis of vitamin K and corresponding hypovitaminosis. Finally, many drugs can cause the formation autoimmune pathology platelets.

Hemorrhagic syndrome is manifested by a tendency to repeated hemorrhages and bleeding that occurs after a minor injury or even “spontaneously”, without a reason sufficiently noticeable to the patient. Under conditions of hypocoagulation, even small surgical operations(tooth extraction, etc.) can become deadly if preventive correction of impaired blood clotting is not carried out and vigorous measures are not taken to stop the onset of blood loss.

If hemorrhagic manifestations in a patient exist constantly or are repeated quite often, they speak of hemorrhagic diathesis (Greek diathesis - predisposition, tendency). Hemorrhagic diathesis characteristic of hereditary forms of hypocoagulation (hemophilia, etc.), hereditary thrombocytopathies, prolonged thrombocytopenic conditions, chronic liver diseases, etc. Spicy hemorrhagic syndrome occurs as a complication of many forms of pathology - post-traumatic conditions, radiation sickness, leukemia, infectious diseases, drug disease.

It is necessary to pay attention to the fact that hemorrhagic syndrome accompanies not only hypocoagulation conditions, but also some forms of pathology vascular wall(vasopathies), for example, hemorrhagic vasculitis. The basis of this disease is inflammatory process, affecting capillaries and other small vessels and raising their permeability (for red blood cells and platelets) and impaired elasticity (increased fragility). Causes of vasopathy: 1) infectious-toxic; 2) hypovitaminosis (C, PP); 3) medications.

The study of coagulation hemostasis is carried out using tests that record the time of clot formation in citrated plasma after the addition of calcium, phospholipids and the appropriate activating agent. Staging accurate diagnosis one or another form of coagulopathy, monitoring the therapy is helped by studying the patient’s coagulogram - a complex laboratory analysis blood coagulation system, including up to 20 different tests. As an example, I will dwell on just a few of them.

1) Duke capillary bleeding time. Shortening of time means increased platelet aggregation or an increase in their number. Elongation - a decrease in the ability of platelets to aggregate or a decrease in the number of platelets. Normally it is 2–5 minutes.

2) Prothrombin time- this is the time of formation of a blood clot after the addition of tissue thromboplastin (tissue factor and phospholipids) to recalcified plasma. Normal PT is approximately 10–18 s, but can fluctuate significantly. With the help of PT, the activity of the external and general blood coagulation mechanisms is assessed; this is the most sensitive method for diagnosing deficiency of factors VII and X. An increase in PT is also observed with deficiency of factor V, prothrombin and fibrinogen.

3) Activated partial thromboplastin time(APTT) is normally 30–40 s. It is measured as the time of blood clot formation after the addition of a phospholipid to recalcified plasma that has been preincubated with inert particles causing contact activation of the intrinsic coagulation mechanism. An increase in APTT indicates a decrease in the concentration of factors VIII, IX, XI or XII by 30% or more compared to normal.

4) Thrombin time is the time it takes for a clot to form after thrombin is added to the plasma. Normally, it is 14–16 s and can increase with disseminated intravascular coagulation syndrome, hypo- and dysfibrinogenemia. Heparin also causes its increase, but the effect of heparin can be neutralized by adding protamine sulfate to the plasma. Reflects the state of the final stage of hemocoagulation - fibrin formation. Shortening of time - hypercoagulability.

5) Fibrin degradation products(PDF) in serum is determined by agglutination of latex particles carrying antibodies to PDF or fibrinogen. Increased level PDF (>8 μg/ml) occurs in DIC syndrome, thromboembolic complications and during fibrinolytic therapy. Serious illnesses liver can cause a moderate increase in PDP; False-positive results may occur in the presence of rheumatoid factor.

6) Ethanol test. It consists of the formation of a clot after 10 minutes at a temperature not exceeding 26 °C - a qualitative indicator of latent hypercoagulation, indicating the presence of activated thrombin in the plasma.

7) Determination of deficiency of individual blood coagulation factors is based on changes in the time of clot formation in plasma with a known deficiency of hemostasis factor after adding the patient’s plasma to it. The results of the study are expressed as a percentage of the activity of mixed plasma from healthy donors. In healthy individuals, the activity of coagulation factors ranges from 60–160%, but these limits must be determined independently in each laboratory.

8) The content of von Willebrand factor (VWF) is determined in cases where the bleeding time is increased, the platelet count is within normal limits and not obvious reasons platelet dysfunction. VWF is synthesized by endothelial cells and megakaryocytes; it forms aggregates containing from 2 to 40 or more subunits. VWF is required for normal platelet adhesion. Determination of the cofactor activity of ristocetin is based on the ability of this antibiotic to stimulate in vitro the interaction of VWF with platelet glycoprotein. In most cases of von Willebrand disease, this indicator is reduced.

But it happens that the degree of blood thickening exceeds the maximum permissible values ​​for pregnancy (hypercoagulation) and such “defense” begins to work as an “attack”, disrupting microcirculation in the area of ​​implantation - attachment ovum(If we're talking about about early stages) or in the uteroplacental system (in terms of more than 14 weeks), causing malnutrition of the baby, which, if progressed, can lead to the most unfavorable pregnancy outcomes.

To the group increased risk hypercoagulation during pregnancy includes women who have cardiovascular diseases, have previously experienced a stop in the development of pregnancy at any stage, complications of past pregnancies such as gestosis, feto-placental insufficiency, premature detachment placenta. During examination at the stage of preparation for pregnancy, such women are often found to carry special gene variants that lead to a tendency to microcirculation disorders (,). When such mutations are detected, a mandatory examination of the hemostatic system is carried out outside of provoking factors (outside pregnancy, taking hormonal drugs etc.).

Based on the results, an appropriate regimen for taking “blood-thinning” drugs is selected at the stage of pregnancy planning and an action plan is developed when pregnancy occurs.

During pregnancy, such patients are monitored for the functioning of the blood coagulation system once every 4 weeks, even if “everything is normal.”

Very often, hypercoagulation is an incidental finding during pregnancy and is detected only during a routine examination. (It is worth knowing that you should check your pregnancy at least 3 times - upon registration, then at 22-24 weeks, then at 32-34 weeks).

And, sometimes, timely treatment can prevent a lot of problems with the baby’s development.