Hypercoagulability syndrome. Late hemorrhagic disease of the newborn (clinical analysis) Coagulopathy code according to ICD 10 in children

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1 Federal State Budgetary Educational Institution of Further Professional Education “Russian Medical Academy of Continuing Professional Education” of the Ministry of Health of the Russian Federation, Moscow; GBUZ "Children's City Clinical Hospital named after. FOR. Bashlyaeva" DZ Moscow
2 Federal State Budgetary Educational Institution of Further Professional Education RMANPO of the Ministry of Health of Russia, Moscow; GBUZ "DGKB im. FOR. Bashlyaeva DZM"
3 GBUZ "DGKB im. FOR. Bashlyaeva DZM", Moscow, Russia

For quotation: Zaplatnikov, Dmitrieva Yu.A., Shishkina S.V., Kataeva L.A., Brazhnikova O.V., Gavelya N.V. Late hemorrhagic disease of the newborn (clinical analysis) // Breast cancer. 2014. No. 21. S. 1547

Among all pathological conditions in children, hemorrhagic disorders occupy a special place, which is due to a potentially high risk of developing serious complications. The reasons for this, as a rule, are late diagnosis and inadequate therapy.

Untimely nosological verification of hemorrhagic syndrome is often due to underestimation of anamnestic data, incorrect interpretation of clinical manifestations, as well as errors in the interpretation of laboratory examination results. In addition, in some cases, the reason for a late diagnosis is terminological confusion, as a result of which a practicing pediatrician may have an erroneous idea about the age limits for certain types of hemorrhagic disorders.
Thus, the generally accepted term “hemorrhagic disease of the fetus and newborn” (code P53 according to ICD-10), from a formal point of view, should be used only in cases where vitamin K-deficient coagulopathy is detected in the perinatal period. At the same time, it has been proven that vitamin K deficiency in a child’s body can clinically manifest itself not only during the newborn period, but also in subsequent weeks and even months of life. In these cases they speak of “late hemorrhagic disease of the newborn.” However, the correctness of this term raises reasonable doubts, since it is used to refer to hemorrhagic syndrome that manifests itself in the postneonatal period. The erroneous association of vitamin K deficiency only with the neonatal period creates the prerequisites for ignoring these conditions when searching for the causes of hemorrhagic disorders in children over 1 month of age. Underestimation of the role of vitamin K deficiency in the genesis of hemorrhagic syndrome in the postneonatal period can cause late diagnosis and the risk of developing serious complications. As an example of late verification of vitamin K-dependent coagulopathy, we present our own clinical observation.

Girl aged 1 month. 11 days with a diagnosis of “Gastroduodenal reflux? Esophagitis? was referred by a local pediatrician for hospitalization due to frequent regurgitation and the appearance of brownish streaks in the vomit.
From the anamnesis we know: a girl from a somatically healthy woman, 26 years old. From the first pregnancy, which occurred with toxicosis in the first trimester. 1st birth, spontaneous at 38 weeks, physiological. Body weight at birth - 3100 g, height - 51 cm. Apgar score - 8-9 points. Attached to the breast immediately after birth. She took the breast actively. From the 3rd day of life, icterus of the skin was noted, which was regarded as a manifestation of physiological jaundice. In the maternity hospital, she was vaccinated against tuberculosis and hepatitis B. She was discharged from the maternity hospital on the 4th day in satisfactory condition.
The girl has been breastfed freely since birth. Body weight gain during the first month of life was 1100 g. While breastfeeding, from the first days of life, slight regurgitation after feeding was noted, which was regarded as a manifestation of infant regurgitation; no therapy was carried out. Within 3 weeks. The child retained yellowness of the skin with gradual fading. In 1 week Before hospitalization, regurgitation became more frequent.
Upon admission to the department, the child’s condition was of moderate severity. Moderate lethargy. The skin is pale. On the left shoulder and in the area of ​​the left breast there are dense subcutaneous nodules up to 1.0 and 0.5 cm in diameter, respectively (according to the mother - “due to the clip-on closures on the undershirt”). Mucous membranes are moist and clean. Heart sounds are sonorous, rhythmic, gentle systolic murmur at the apex. Breathing in the lungs is puerile. The abdomen is soft and accessible to deep palpation. Liver +1.0 cm. Stool is independent, mushy, with a small admixture of mucus. Urination is free. There are no focal or meningeal symptoms. Reflux contains scanty streaks of blood.
Upon admission, clinical and biochemical blood tests, a general urine test, and ultrasound of internal organs were performed with an additional assessment of the functional state of the gastroesophageal area (water-siphon test). In this case, mild normochromic, normocytic anemia was detected: HGB 106 g/l, RBC 3.4x1012, MCV 81 fl, MCH 26.1 pg, CP 0.93, moderate thrombocytosis: 612x109. A biochemical blood test revealed slight hyperbilirubinemia (total bilirubin - 30 µmol/l, direct bilirubin - 7 µmol/l) and a moderate increase in LDH (1020 units/l). Ultrasound data of internal organs indicated the absence of gastroesophageal reflux, chalasia and pyloric stenosis.
During the 1st day of the child's stay in the department, attention was paid to continued bleeding from the sites where blood was collected for research. Taking into account the persistent hemorrhagic syndrome (bleeding from injection sites, streaks of blood in the vomit), the child underwent (cito!) a clinical blood test with reticulocytes, neurosonography and a coagulogram. At the same time, the anamnesis and clinical data were analyzed in detail, which further revealed the following:
- absence of hemorrhagic diseases in the family;
- during pregnancy and after childbirth (this time period was studied, taking into account the feeding of the child exclusively with breast milk), the mother did not receive medications that could affect hemostasis;
- menadione sodium bisulfite was not administered to the child in the maternity hospital;
- streaks of blood in the refluxate appeared within 1 week. before hospitalization;
- clearly limited change in skin color (like “bruises”) up to 0.5 and 1.0 cm in diameter above the “nodules” in the area of ​​the nipple of the mammary gland on the left and left shoulder. Palpation of the indicated tumor-like formation in the area of ​​the left mammary gland revealed hemorrhagic discharge from the nipple. After the outflow of hemorrhagic discharge, the “nodule” ceased to be palpable, but limited blueness of the skin in this place remained. All this made it possible to consider the identified “nodules” as subcutaneous hematomas, which the mother interpreted as a manifestation of skin traumatized by the clips on children’s clothing.
Taking into account the ongoing bleeding and the emerging clinical signs of anemia, immediately after blood sampling, emergency syndromic therapy was started: intravenous administration of menadione sodium bisulfite (1 mg/kg), fresh frozen plasma (FFP) (20 ml/kg), a pressure bandage was applied to the area injections with a hemostatic sponge.
Analysis of the results of the conducted (sito!) examination revealed changes in the clinical blood test in the form of the appearance of hypochromic hyperregenerative anemia of moderate severity (Hb - 88 g/l, red blood cells - 3.2x1012, color index - 0.83, reticulocytes - 5.3% ), persistent thrombocytosis (621x109) and a normal level of bleeding duration (according to Duque - 2 minutes). At the same time, according to the coagulogram data, attention was drawn to the absence of coagulation along the internal (activated partial thromboplastin time (APTT) - no clot) and external (prothrombin index - no clot) coagulation pathways with normal fibrinogen levels (3.81 g/l) and final stage of coagulation (thrombin time (TV) - 15.1 s) (Table 1). Neurosonography data allowed us to exclude intracranial hemorrhagic changes.
The results of the laboratory examination made it possible to diagnose a violation of plasma hemostasis as a vitamin K-dependent coagulopathy. This was supported by:
- absence of disorders of primary hemostasis (neither thrombocytopenia nor prolongation of bleeding according to Duque was detected);
- the presence of disturbances only in those links of secondary hemostasis, the functional activity of which is determined by vitamin K. Thus, there was pronounced hypocoagulation along the internal and external coagulation pathways, while fibrinogen and TB remained within normal limits.
Thus, the anamnesis data, clinical picture and examination results made it possible to verify late hemorrhagic disease of the newborn, which determined the need to continue therapy with menadione sodium bisulfite for another 3 days. It should be emphasized that the hemorrhagic syndrome in the child was relieved after the administration of FFP, while complete normalization of coagulogram parameters occurred only after completion of the course of treatment with menadione with sodium bisulfite (Table 1).
Taking into account the fact that vitamin K deficiency in the child’s body could be caused not only by a nutritional factor (exclusive breastfeeding, characterized by a low vitamin K content), but also by its insufficient synthesis by endogenous intestinal microflora, as well as by a violation of its utilization in the intestine, research was carried out additional examinations. There were no clinical or laboratory signs of cholestasis or malabsorption. This made it possible to consider the lack of prophylactic administration of menadione sodium bisulfite in the early neonatal period and exclusive breastfeeding as the main provoking factors for the development of vitamin K-dependent coagulopathy in this patient.
Final diagnosis: main - “Late hemorrhagic disease of the newborn”; complications - “Posthemorrhagic anemia of moderate severity”; accompanying - “Infantile regurgitation”. On an outpatient basis, it is recommended to continue breastfeeding if the mother follows a rational diet for nursing women and takes daily multivitamins. To correct anemia, a polymaltose complex of ferric iron (5 mg/kg/day for elemental iron) was prescribed for 1 month. with subsequent monitoring of clinical blood test parameters.

The presented clinical case demonstrates the need for a pediatrician to be alert to any, even the most minimal, hemorrhagic manifestations, especially in young children. At the same time, replacing the widely used term “late hemorrhagic disease of the newborn” with “vitamin K-dependent coagulopathy” will avoid the erroneous association of vitamin K deficiency conditions exclusively with the neonatal period. Inclusion of this pathological condition in the list of possible causes of hemorrhagic syndrome in children, regardless of their age, will allow timely verification of the diagnosis and prescribing adequate therapy.

Literature
1. Barkagan L.Z. Hemostasis disorders in children. M., 1993.
2. Nelson Textbook of Pediatrics, 19th Edition /R.M. Kliegman, B.M. Stanton, J. St. Geme, N. Schor, R.E. Behrman. New York, London: Elsevier Inc., 2014.
3. Childhood diseases / ed. N.P. Shabalova / 6th ed. St. Petersburg: Peter, 2009.
4. Dolgov V.V., Svirin P.V. Laboratory diagnosis of hemostasis disorders. M.: Triad, 2005.
5. Shabalov N.P. Hemorrhagic disorders in newborns / In the book: Neonatology.
In 2 vols. / 3rd ed., rev. and additional M.: MEDpress-inform, 2004. T. 2. P. 208-223.
6. Neonatology. National leadership. Krat. ed. / ed. N.N. Volodina. M.: GEOTAR-media, 2013.
7. Takahashi D., Takahashi Y., Itoh S. et al. Late vitamin K deficiency bleeding in an infant born at a maternity hospital // Pediatr Int. 2014 Jun. Vol. 56(3). R. 436.
8. Van Winckel M., De Bruyne R., van de Velde S., van Biervliet S. Vitamin K an update for the pediatrician // Eur J Pediatr. 2009 Feb. Vol. 168(2). R. 127-134.
9. Hubbard D., Tobias J.D. Intracerebral hemorrhage due to hemorrhagic disease of the newborn and failure to administer vitamin K at birth // South. Med. J. 2006. Vol. 99(11). R. 1216-1220.

Increased blood clotting is a hypercoagulability syndrome. Let's consider the main causes of this condition, types, stages, methods of treatment and prevention.

Bleeding disorders or coagulopathy can be either physiological or pathological. Human blood consists of formed elements (platelets, erythrocytes, leukocytes) and a liquid part (plasma). Normally, the composition of the biological fluid is balanced and has a hematocrit ratio of 4:6 in favor of the liquid part. If this balance shifts towards the formed elements, then blood thickening occurs. Increased thickness may be associated with an increase in the amount of prothrombin and fibrinogen.

Blood clotting is an indicator of the body's protective reaction to bleeding. At the slightest damage to blood vessels, blood elements form blood clots that stop blood loss. Coagulability is not constant and largely depends on the state of the body, that is, it can change throughout life.

In the normal state of the body, bleeding stops after 3-4 minutes, and after 10-15 minutes a blood clot appears. If this happens much faster, it indicates hypercoagulation. This condition is dangerous, as it can cause the development of thrombosis, varicose veins, heart attacks, strokes and damage to internal organs (gastrointestinal tract, kidneys). Due to thick blood, the body suffers from oxygen deficiency, and overall health and performance deteriorate. In addition, the risk of blood clots increases.

ICD-10 code

D65 Disseminated intravascular coagulation [defibration syndrome]

Epidemiology

According to medical statistics, the epidemiology of hypercoagulation syndrome is 5-10 cases per 100 thousand population. The pattern of development of the disease is associated with the prevalence of risk factors for the pathology.

The disorder occurs due to congenital and acquired disorders. Most often due to external factors: various diseases, improper use of medications, vitamin deficiency, insufficient water consumption and much more.

Causes of hypercoagulability syndrome

Hypercoagulation does not have pronounced clinical symptoms. Sometimes patients complain of headaches, lethargy and general weakness. The causes of hypercoagulability syndrome are usually divided into genetic and acquired.

• Congenital – family history of thrombophilia, unexplained miscarriages, repeated blood clots before the age of 40 years.
• Acquired – bad habits (smoking, alcoholism), overweight and obesity, high cholesterol, aging, pregnancy, use of birth control pills or hormone replacement therapy, prolonged bed rest due to surgery or any illness, lack of physical activity, dehydration body, hypothermia, heavy metal poisoning, microbial invasions, deficiency of Omega-3 polyunsaturated fatty acids, thermal and chemical burns.

Increased blood clotting is most often congenital, but can occur due to external factors. There are conditions in which pathology can develop:

• Long-term stressful experiences and neuroses.
• Vascular injuries.
• Erythremia.
• Contact of blood with foreign surfaces.
• Oncological diseases.
• Autoimmune diseases: aplastic anemia, systemic lupus erythematosus, thrombotic thrombocytopenic purpura.
• Hematogenous thrombophilias.
• Prolonged bleeding from the gastrointestinal tract.
• Antiphospholipid syndrome.
• An artificial heart valve or use of a heart-lung machine.
• Large hemangiomas.
• Atherosclerosis of the coronary arteries.
• Taking contraceptives.
• The use of estrogens during menopause.
• Pregnancy and postpartum period.
• Von Willebrand's disease.

Risk factors

There are certain risk factors that provoke bleeding disorders, that is, hypercoagulation. The pathological condition may be associated with the following conditions:

• Water deficiency - blood is 85% water, and plasma is 90%. A decrease in these indicators leads to thickening of the biological fluid. Particular attention should be paid to water balance in the summer due to the heat and in winter when the indoor air is dry. Fluid reserves need to be replenished when playing sports, as the body increases heat transfer to cool itself.
• Enzymopathy is a pathological condition in which there is a deficiency of food enzymes or disturbances in their activity. This leads to incomplete breakdown of food components, which is why under-oxidized breakdown products enter the blood, acidifying and thickening it.
• Poor nutrition – a number of foods (eggs, legumes and cereals) contain heat-stable protein inhibitors that form stable complexes with gastrointestinal proteinases. This leads to disruption of protein digestion and absorption. Undigested amino acids enter the blood and interfere with its clotting. The pathological condition may be associated with overeating carbohydrates, fructose and sugar.
• Deficiency of vitamins and minerals - water-soluble vitamins (group B, C) are required for the biosynthesis of enzymes. Their deficiency leads to incomplete digestion of food and, as a result, hypercoagulation. It is also possible to develop certain diseases and deteriorate the protective properties of the immune system.
• Impaired liver function - every day the organ synthesizes 15-20 g of blood proteins, which are responsible for regulatory and transport functions. Violation of biosynthesis provokes pathological changes in the chemical composition of the blood.

Pathogenesis

The mechanism of development of increased blood clotting depends on the pathological factors causing the disorder. Pathogenesis is associated with depletion of plasma factors, activation of fibrinolysis and fibrin formation, a decrease in the number of platelets, their adhesion and aggregation.

Hypercoagulability syndrome is characterized by the release of proaggregants and procoagulants and damage to endothelial cells. As the pathological condition progresses, the formation of blood clots of loose consistency is observed. The consumption of factors from the coagulation, anticoagulation and fibrinolytic systems of the body is gradually increasing.

Symptoms of hypercoagulability syndrome

Increased blood viscosity has no characteristic manifestations. But there are a number of disorders that may indicate a disease. The following symptoms of hypercoagulability syndrome are distinguished:

• Fatigue due to poor oxygen supply to the brain due to excessive blood thickness.
• Aching headaches.
• Dizziness with brief loss of coordination.
• Muscle weakness.
• Fainting and nausea.
• Impaired sensitivity in the arms and legs: paresthesia, numbness, burning.
• Increased dryness, bluish discoloration of the skin and mucous membranes.
• Increased sensitivity to cold.
• Sleep disorders, insomnia.
• Painful sensations in the heart area: tingling, shortness of breath, rapid heartbeat.
• Depressive state, increased anxiety and absent-mindedness.
• Decreased hearing and vision, tinnitus.
• Increased tearing and burning in the eyes.
• High hemoglobin levels.
• Slow bleeding from cuts and wounds.
• Miscarriage, repeated miscarriages.
• Presence of chronic diseases.
• Frequent yawning due to lack of oxygen to the brain.
• Cold feet, heaviness and pain in the legs, protruding veins.

The above symptoms require careful differential diagnosis. After a set of instrumental and laboratory tests, the doctor can identify blood thickening syndrome.

First signs

Like any disease, a bleeding disorder has certain early signs. Symptoms of pathology can manifest themselves as follows:

• Circulating immune complexes in the blood as a response to foreign bodies: activated complement components C1-C3, fetal organ-specific antigens, maternal antibodies.
• Erythrocytosis and hyperthrombocytosis.
• Unstable blood pressure.
• Increased prothrombin index and platelet aggregation.

Sometimes the clinical picture of the disease is completely absent. In these cases, the disease is determined by taking blood from a vein, when the biological fluid coagulates in the needle.

Hypercoagulability syndrome in liver cirrhosis

Many diseases lead to changes in the chemical composition of the blood. Hypercoagulation syndrome in liver cirrhosis is associated with the destruction and death of organ cells. The pathological process is accompanied by chronic inflammation and disruption of many body functions.

The procoagulant imbalance and the severity of thrombotic complications depend entirely on the stage of cirrhosis. But even the early stages of the disease lead to the fact that the hemostatic system remains unstable for a long time, causing disruptions in the blood composition and significant deviations from the norm.

Treatment of increased viscosity of biological fluid in liver cirrhosis is very difficult. This is associated with the risk of thrombotic and hemorrhagic complications, that is, the patient may suffer from thrombosis or blood loss.

Hypercoagulability syndrome during pregnancy

Blood thickening in the expectant mother may be associated with hereditary pathologies or develop due to a number of negative factors. Hypercoagulation syndrome during pregnancy occurs due to the carriage of thrombophilia genes, dehydration, obesity, stress, impaired vascular tone, overheating or physical inactivity.

The presence of such conditions does not necessarily indicate a difficult pregnancy. The younger the female body, the higher its resistance to various pathologies and the lower the chances of developing the syndrome. If a woman has a predisposition to thrombophilia, then very often the first pregnancy proceeds absolutely normally, but it can become an activator of hypercoagulation syndrome. Then the second pregnancy becomes more risky.

Complications of increased blood viscosity during pregnancy:

• Termination of pregnancy at any stage.
• Regressive pregnancy.
• Intrauterine fetal death.
• Bleeding and placental abruption.
• Placental insufficiency.
• Delays in fetal development.
• Deterioration of uteroplacental blood flow.
• Bleeding during delivery.
• Preeclampsia.

To minimize the complications described above, it is necessary to properly plan your pregnancy. If there are signs of hypercoagulation, then the disease should be prevented even before conception. Even with minimal changes in the hemostatic system, normal pregnancy and birth of a healthy baby are possible. In case of severe disorders detected in the early stages, the expectant mother will receive special treatment that normalizes blood clotting.

Stages

Increased blood clotting has certain stages of development, which are based on the symptoms of the disease. Based on the pathogenesis, hypercoagulability syndrome has the following stages:

• Hypercoagulation - thromboplastin enters the blood, which triggers coagulation processes and the formation of blood clots.
• Consumptive coagulopathy - at this stage there is an intensive consumption of coagulation factors and an increase in fibrinolytic activity.
• Due to the consumption of components of the blood coagulation system, incoagulability and thrombocytopenia occur.

When damaged with bleeding, a protective mechanism is activated. The blood clots quickly and blood clots form in the wound. Its treatment depends on the stage of the disease.

Forms

Hypercoagulation can be primary, that is, caused by hereditary factors, and secondary, which develops due to external stimuli. Let's take a closer look at the main types of the disease:

• Congenital – caused by a decrease in the qualitative and/or quantitative composition of the blood. There are several forms of the pathological condition. The most common hemophilias are A, B, C, which can occur in both men and women, regardless of their age.
• Acquired – the disorder is associated with complications of a disease. In many patients, increased blood viscosity develops due to infectious diseases, liver pathologies, or tumor processes.

Types of hypercoagulation are distinguished by their characteristic symptoms. During diagnosis, the stage and type of disease are taken into account, since the treatment method depends on this.

Complications and consequences

High blood viscosity syndrome can cause serious consequences and complications. Most often, elderly people and men encounter pathology. According to medical statistics, the disorder can lead to problems such as:

• Hypertension.
• Atherosclerosis.
• Frozen pregnancy in the early stages.
• Spontaneous late-term abortions and miscarriages.
• Infertility of unknown etiology.
• Varicose veins.
• Stroke, heart attack.
• Headaches and migraines.
• Retinal vascular thrombosis.
• Thrombocytopenia.

The most dangerous consequence is the tendency to thrombosis and thrombus formation. As a rule, small vessels are thrombosed. This creates the risk that a blood clot will block a cerebral vessel or coronary artery. Such thromboses are called acute tissue necrosis of the affected organ and lead to the development of ischemic stroke or myocardial infarction.

The risk of developing complications in hypercoagulability syndrome largely depends on the underlying cause of its occurrence. The main goal of therapy is to eliminate the underlying disease and prevent its complications.

Miscarriage and hypercoagulability syndrome

Sudden termination of pregnancy due to a blood clotting disorder occurs in every third woman with this problem. The state of the blood is very important, as it supports the vital functions of two or more organisms at once. More viscous blood flows slowly and heavily through the vessels and does not cope with the functions assigned to it. The body suffers due to increased stress on all organs and systems.

During pregnancy, hypercoagulation provokes poor circulation of biological fluid, because of this, oxygen and nutrients reach the baby in a smaller amount, and waste products of the fetus are retained in the placenta. Miscarriage and hypercoagulability syndrome are based on the risk of developing the following complications:

• Intrauterine fetal hypoxia
• Intrauterine growth restriction
• Impaired blood flow in the mother-placenta-fetus system
• Fading pregnancy and miscarriage.

To prevent this condition during the planning period of conception, it is very important to undergo a comprehensive examination of the body. A coagulogram, that is, a test for blood clotting, is mandatory. Signs of increased blood viscosity during pregnancy are elevated values ​​of a number of indicators:

• High level of fibrinogen: normally 2-4 g/l, by the end of gestation the value can reach 6 g/l.
• Acceleration of thrombin time.
• Presence of lupus anticoagulant.
• Decreased activated partial thromboplastin time.

Such deviations indicate a dysfunction of the blood. Ignoring this condition threatens termination of pregnancy and a number of other complications for both the mother and the fetus.

Diagnosis of hypercoagulability syndrome

Clinical signs of increased blood clotting do not appear in all patients. Diagnosis of hypercoagulability syndrome in most cases is associated with the development of complications of the pathological condition. That is, based on any deviations or violations, a number of clarifying studies are carried out.

The doctor collects anamnesis: assesses the nature of the complaints, the presence of hereditary factors or interrupted pregnancies. To detect hypercoagulability, a comprehensive laboratory study is indicated. In severe stages of the disease, when all the signs of thrombophilia are present, instrumental diagnostic methods are used that allow one to assess the overall picture of the disease. Hypercoagulability is also differentiated from various disorders with similar symptoms.

Analyzes

To detect increased blood clotting, the patient is prescribed laboratory tests:

• General blood test, hematocrit - establishes the number of formed elements of biological fluid, the level of hemoglobin and their proportions with the total volume of blood.
• Coagulogram - allows you to obtain information about the state of the hemostatic system, the integrity of blood vessels, the level of coagulation, and the duration of bleeding.
• Activated partial thromboplastin time (aPTT) – assesses the efficiency of the coagulation pathway (intrinsic, general). Determines the level of plasma factors, anticoagulants and inhibitors in the blood.

Particular attention is paid to the behavior of blood when it is taken from a vein. If hypercoagulability is present, it may coagulate in the needle. The disease is confirmed by the following test results: shortened clotting time and prothrombin time, high fibrinogen, prolonged fibrinolysis, shortened APTT, increased platelet aggregation with agonists, increased prothrombin index, increased amount of D-dimer. A test to study platelet receptor genes may also be ordered. That is, genetic markers of hypercoagulation.

Instrumental diagnostics

A comprehensive examination of the body if hypercoagulation syndrome is suspected involves instrumental diagnostics. This study is necessary to determine the condition of internal organs (liver, spleen, brain, intestines), as well as the condition of veins, lumens, valves and the presence of thrombotic masses.

• Ultrasound Dopplerography - determines the speed and direction of blood flow in the vessels. Provides information about the anatomy and structure of veins.
• Phlebography is an X-ray examination with an iodine-containing contrast agent to detect blood clots.
• Magnetic resonance imaging, ultrasound examination - examine the general condition of the body, identify various abnormalities.

Based on the test results, treatment or a set of additional studies may be prescribed.

Differential diagnosis

A blood clotting defect can be caused by various factors; to establish the true cause of the pathology, differential diagnosis is necessary. Increased viscosity of biological fluid is differentiated from Werlhof's disease, autoimmune disorders, thrombocytopenia and impaired coagulation factors, which require vitamin K, and pathologies of internal organs, especially the liver.

Hemostasis disorder is compared with disseminated intravascular coagulation, that is, DIC syndrome, as well as with malignant neoplasms and hemolytic-uremic syndrome. Based on the results of a set of studies, the doctor draws up a treatment plan or gives preventive recommendations.

Treatment of hypercoagulability syndrome

To restore normal blood flow and eliminate increased blood viscosity, you need to visit a doctor who will prescribe a set of diagnostic examinations and tests. Treatment of hypercoagulability syndrome during pregnancy is individual for each woman. Taking into account all the characteristics of the body, the doctor draws up a treatment regimen.

In case of pronounced changes in the hemostatic system, the expectant mother is prescribed anticoagulants, that is, drugs that reduce the risk of thrombosis: Warfarin, Heparin, Fragmin. Medicines are administered subcutaneously, the course takes about 10 days. After treatment, a hemostasiogram is performed to evaluate the therapy performed. Antiplatelet agents can also be prescribed that slow down the process of platelet aggregation, reducing blood viscosity: Acetylsalicylic acid, Cardiomagnyl, Thrombo ACC.

Particular attention is paid to diet therapy. To correct blood viscosity during pregnancy, it is recommended to consume foods rich in vitamin E. Food should be boiled, stewed or steamed. The diet should include fermented milk products, vegetables, fruits, meat and fish. At the same time, the consumption of canned, pickled, fatty and fried foods, as well as sweets, baked goods, potatoes, alcohol and carbonated drinks is prohibited.

Medicines

Treatment of hypercoagulation syndrome is aimed at eliminating the causes that provoked the pathology, restoring circulating blood volume, correcting hemodynamics and hemostasis disorders, improving microcirculation and maintaining hematocrit at an optimal level. The doctor selects medications based on test results and the general condition of the patient.

Medicines for hypercoagulability are necessary to thin the blood and prevent blood clots. Patients may be prescribed the following medications:

1. Antiplatelet agents are a group of medications that prevent the formation of blood clots. They act at the stage of blood coagulation, when platelet aggregation occurs. The active components inhibit the process of gluing blood platelets, preventing an increase in the level of coagulation.

• Thrombo ACC is a medicine with the active ingredient acetylsalicylic acid. Reduces the level of thromboxane in platelets, reduces their aggregation, and inhibits the formation of fibrin. Used to prevent disorders of the hemostasis system. Tablets are taken 1-2 times a day, the duration of therapy is determined by the attending physician. Side effects manifest themselves in the form of attacks of nausea and vomiting, possible pain in the epigastric region, ulcerative lesions of the gastrointestinal tract, anemia, increased tendency to bleeding, various allergic reactions, headaches and dizziness. The medicine is contraindicated in case of intolerance to its components, erosive lesions of the gastrointestinal tract and in the first trimester of pregnancy.
• Cardiomagnyl - tablets containing acetylsalicylic acid and magnesium hydroxide. The drug is used for the primary prevention of thrombosis and diseases of the cardiovascular system, as well as for chronic and acute coronary heart disease. The medicine is taken 1-2 tablets per day, the course of treatment is individual for each patient. Side effects: decreased platelet aggregation, aplastic anemia, hypoglycemia, thrombocytopenia. The drug is contraindicated in cases of intolerance to its components, various allergic reactions, kidney diseases, and gastrointestinal tract diseases. Overdose results in increased adverse reactions.
• Acetylsalicylic acid is an NSAID with a pronounced antiplatelet effect. The mechanism of action of the drug is based on the blockade of enzymes responsible for regulating the synthesis and metabolism of prostaglandins in platelets and vascular walls. The medicine is used to prevent the formation of blood clots, reduce fever and pain. The dosage depends entirely on the severity of the pathological condition.

1. Anticoagulants are a group of drugs that suppress the activity of the hemostatic system. They reduce the risk of blood clotting by reducing the formation of fibrin. They affect the biosynthesis of substances that inhibit clotting processes and change the viscosity of biological fluid.

• Warfarin is a medicine that contains substances that prevent blood from clotting. Inhibits the effect of vitamin K, reduces the risk of blood clots. It is used for hypercoagulation, venous thrombosis and pulmonary embolism, acute myocardial infarction and other conditions associated with disruption of the hemostatic system. The medicine is taken for 6-12 months, the dosage is determined by the attending physician. Side effects include disorders of the digestive system, possible increased activity of liver enzymes, the appearance of pigmentation on the body, hair loss, heavy and prolonged menstruation. The medicine is contraindicated in acute bleeding, during pregnancy, acute arterial hypertension, severe renal and liver dysfunction.
• Heparin is a direct anticoagulant that inhibits the blood clotting process. It is used for the treatment and prevention of thromboembolic diseases and their complications, for thrombosis, acute myocardial infarction, embolic conditions and to prevent blood clotting during laboratory diagnostics. The dosage and duration of treatment are individual for each patient. Side effects include the risk of bleeding. Heparin is contraindicated in hemorrhagic diathesis and other conditions of blood hypocoagulation.
• Fragmin - has a direct effect on the blood coagulation/anti-coagulation system. It is used for thrombosis, thrombophlebitis, for the prevention of high blood viscosity, for myocardial infarction and unstable angina. The medicine is administered subcutaneously, the dosage is determined by the attending physician. Symptoms of overdose occur in 1% of patients; these can be various disorders of the gastrointestinal tract and blood system. The drug is contraindicated in case of intolerance to its components, coagulopathy, septic endocarditis, recent operations on the central nervous system, visual or hearing organs.

1. Fibrinolytics - destroy fibrin threads that form the structure of blood clots, dissolve blood clots and thin the blood. Such drugs are used only in extreme cases, as they can cause increased platelet aggregation and increase the risk of thrombophilia.

• Thromboflux is a fibrinolytic agent that dissolves fibrin in blood clots and thrombi. It is used for high blood viscosity, as a prophylactic against thrombosis, and acute myocardial infarction. The dosage is determined by the doctor. Side effects and symptoms of overdose are manifested by hemostasis disorders, allergic reactions and adverse gastrointestinal symptoms.
• Fortelysin – activates plasminogen, reduces the level of fibrinogen in the blood. It is used for acute myocardial infarction and for the prevention of hypercoagulation syndrome. The medicine is administered intravenously, the dosage and duration of therapy is determined by the doctor, individually for each patient. Side effects: bleeding of varying severity, allergic reactions. The medication is contraindicated in diseases with increased bleeding, recent injuries and extensive surgical interventions, liver and central nervous system diseases.

In especially severe cases, patients are prescribed intravenous drip administration of colloid and crystalloid solutions, and donor blood transfusion. All blood thinners are used only as prescribed by a doctor. Independent use of such drugs can lead to bleeding and a number of other equally serious complications.

Vitamins

Treatment of high blood viscosity consists not only of drug therapy, but also the use of vitamins and minerals beneficial to the body that restore the hemostasis system. Vitamins are prescribed depending on the stage of the disease.

Let's consider what vitamins need to be taken for blood thickening and for its prevention:

• Vitamin E is an antioxidant, rejuvenates the body and slows down the aging process. Contained in whole cereal grains, sprouted wheat grains, chestnuts, bran, broccoli, olive oil, animal liver, avocado, sunflower seeds.
• Vitamin C – has antioxidant properties, takes part in the synthesis of structural elements of venous walls. Contained in citrus fruits, bell peppers, watermelons, pears, apples, grapes, potatoes, rose hips, black currants, garlic.
• Vitamin P - strengthens the walls of blood vessels, inhibits enzymes that destroy hyaluronic acid and disrupt the composition of hemostasis. Contained in citrus fruits, apricots, raspberries, walnuts, cabbage, grapes, peppers.

In addition to the vitamins described above, for the prevention and treatment of hypercoagulation, it is necessary to take products with hesperidin (increases vascular tone, found in lemons, tangerines, oranges), quercetin (reduces the risk of thrombophlebia, found in cherries, garlic, green tea, apples, onions). It is recommended to avoid foods rich in vitamin K, as it contributes to blood thickening.

Physiotherapeutic treatment

To eliminate hypercoagulation syndrome and normalize the hemostatic system, combination therapy is used. Physiotherapeutic treatment is necessary to consolidate the achieved results. For increased blood viscosity, hirudotherapy is recommended, as this is one of the most effective ways to thin thick blood. The action of this method is based on the composition of leech saliva, which contains hirudin and a number of other enzymes that dilute biological fluid and prevent the formation of blood clots.

Hirudotherapy is carried out in sanatorium-resort complexes or hydropathic clinics. Despite the positive effect on the body, the physiotherapy procedure has a number of contraindications: severe forms of anemia, thrombocytopenia, hypotension, the presence of malignant tumors, cachexia, hemorrhagic diathesis, pregnancy and recent cesarean section, patient age under 7 years and individual intolerance. In all other cases, hirudotherapy is used in combination with drug treatment.

Traditional treatment

Thick blood syndrome can be eliminated not only with the help of medications, but also by using unconventional methods. Traditional treatment is based on the use of medicinal plants that thin the blood.

• Take 100 g of Sophora japonica seeds and pour 500 ml of vodka over them. The product should be infused for 14 days in a dark, cool place. The medicine is taken 3 times a day before meals, 10 drops per ¼ glass of water.
• Take 20 g of meadowsweet, pour 250 ml of boiling water and test in a water bath. As soon as the product has cooled, it should be strained and taken before meals, 1/3 cup.
• Mix 20 g of string with 10 g of coriander fruits, licorice root, chamomile, sweet clover, toadflax and marsh grass. Pour 500 ml of boiling water over the herbal mixture and let it brew in a sealed container for 2-3 hours. After cooling, the infusion should be filtered and taken 2-3 times a day, 200 ml. If desired, you can add honey to the medicine; it is better to consume it after meals.
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Herbal treatment

Another option for non-traditional treatment of hypercoagulability syndrome is herbal treatment. Let's look at the most effective recipes for blood thinning:

• Take dandelion grass and thorn flowers in equal proportions. Pour 500 ml of boiling water over the herbal mixture and let it brew for 3-4 hours. The product should be strained and taken ½ cup 3-4 times a day. It is not recommended to eat meat and eggs during treatment.
• Pour 250 ml of boiling water over a teaspoon of sweet clover and take 2 glasses 2-3 times a day. The infusion has antispasmodic properties and reduces blood viscosity. The course of treatment is 30 days.
• Wash 200 g of fresh mulberry roots well and chop. Place the raw materials in a saucepan and pour 3 liters of cold water. The product should sit for 1-2 hours, after which it should be put on low heat, and after boiling, remove and cool. Strain the finished broth and take 200 ml 2-3 times a day before meals. The course of treatment is 5 days with a break of 2-3 days; to restore normal hemostasis, 2-3 courses are needed.
• Take a liter glass jar and fill it with chopped porcini mushrooms. Pour vodka over everything and leave for 14 days in a dark, cool place. After 2 weeks, strain and squeeze out the raw materials. Take 1 teaspoon of infusion, diluting it in 50 ml of water 1-2 times a day.
• Ginkgo biloba has blood thinning properties. Pour 50 g of dry leaves of the plant with 500 ml of vodka and let it brew for 14 days. After this, the tincture should be strained and taken 1 teaspoon 2-3 times a day before meals. The course of treatment is a month with breaks of 5-7 days.

When treating hypercoagulation with herbs, it is strictly contraindicated to use plants with blood-clotting properties (nettle, water pepper). Before using folk remedies, medical consultation is necessary, since many recipes have contraindications.

Homeopathy

Thick blood negatively affects the condition of the entire body. To treat this problem, both traditional and non-traditional methods are used. Homeopathy is an alternative method, but when used correctly it can help with hypercoagulability.

Popular homeopathic remedies for increased blood clotting:

• Aesculus 3, 6
• Apis mellifica 3, 6
• Belladonna 3, 6
• Hamamelis virginica 3
• Aorta suis-Injee
• Vena suis-Injeel

The above medications can only be used as prescribed by a homeopathic doctor who has familiarized himself with the medical history and conducted a series of examinations of the patient. Using such remedies on your own is life-threatening.

Surgical treatment

Surgical methods for eliminating bleeding disorders are used extremely rarely. Surgical treatment is possible if hypercoagulation syndrome has led to abscess formation of venous thrombophlebitis. In this case, the patient is indicated for surgery to install a titanium vena cava filter. If the syndrome causes arterial thrombosis of the vessels of the extremities or parenchymal organs, then surgical thrombectomy is performed.

Surgical treatment of hemostasis is ineffective without adequate drug therapy with components of the blood coagulation system. Surgery can be performed to treat the underlying disease that caused the blood clotting. But even in this case, the treatment plan includes a course of medications to thin the blood.

Prevention

Patients with hypercoagulability syndrome or those at increased risk of developing it should follow the preventive recommendations of specialists to prevent the disease. Prevention of hypercoagulation is based on identifying patients at risk, that is, pregnant women, the elderly, people with cancer pathologies and diseases with disorders of the blood coagulation system.

To prevent hypercoagulation and thrombophilia, it is necessary to give up bad habits (smoking, alcoholism), eat right and drink properly, play sports and spend a lot of time in the fresh air. It is also recommended to optimize your daily routine, get enough sleep, avoid conflicts and stressful situations if possible, promptly treat any diseases and periodically take blood tests.

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Coagulopathy is a process in which abnormalities occur in the blood clotting system. It is characterized by extensive nasal hemorrhages, lack of iron in the blood, as well as the formation of large hematomas on the skin.

Pathology can be transmitted from mother to child and develop throughout a person’s life. In the latter case, there is a sufficient amount of formed components in the blood, but their quality suffers.

In a normal state, a sufficient amount of hemoglobin protein, platelets and red blood cells circulate in the body in dynamic equilibrium. When there is open bleeding, the body initiates a process called coagulation., so that the blood coagulates and is delivered to the site of injury, stopping the bleeding.

Clogging of the wound occurs with the help of adhesive platelets, which replace the damaged walls of blood vessels and arteries.

ICD-10

According to the classification of coagulopathy according to the International Classification of Diseases, coagulopathy belongs to the class “Bleeding disorders, purpura and others,” with coding D65.

Types of coagulopathy

The occurrence of blood clotting abnormalities has many different causes, but is divided into types solely according to the method of occurrence. There are two main types of coagulopathy:

Progressive throughout life. Pathology is acquired during the development of diseases, and is a complication against the background of another disease, being one of the symptoms.

Coagulopathy is mainly observed in infections caused by bacteria and malignant tumors. Some medications can also cause clotting disorders.

Transmitted from mother to child. In this case, the pathology is congenital, and the disorder occurs at the level of homeostasis. The qualitative composition of formed elements is affected by a decrease in the saturation of biologically active substances in the blood.

There is a failure in the platelet formation system. Hereditary coagulopathies are divided into forms, depending on the absence of one or another component during the formation of a blood clot.

With extensive blood loss, the body cannot quickly restore the normal quantitative concentration of formed elements, which leads to a decrease in blood clotting and leads to coagulopathy.

Hereditary pathologies contain all forms of increased bleeding.

Blood loss and cardiac arrest lead to death in patients, without taking effective therapy.

The general name for all forms of congenital coagulopathy is hemophilia.

And they are characterized by insufficient thromboplastin saturation.

The congenital form is divided into three more types, based on blood clotting factors:

• Group A. This subtype is characterized by insufficient saturation with antihemophilic globulin;
• Group B. Characterized by abnormalities in the balance of the Christmas factor (blood coagulation factor IX, alpha globulin protein);
• Group C. Progresses due to insufficient amount of factor IX, which precedes thrombolastin.

Symptoms during the development of various forms of congenital pathology do not differ significantly. The first two forms affect only the male sex, a consequence of transmission of the disease from a woman, this is influenced by the X chromosome.

The last form (group C) can affect both men and women; this coagulopathy is not associated with chromosomal inheritance.

Developing throughout life include a large number of different conditions that manifest themselves in the form of coagulation disorders and bleeding. Gender does not play a role; it is mainly related to genetics.

In some cases, coagulopathy may be a consequence of the production of low amounts of prothrombin.

Its formation occurs in the intestines, with the help of vitamin K, bile and gastric juice.

With intestinal pathologies, infectious lesions, lack of vitamins in the liver, all this leads to a reduced formation of prothrombin, or the process of its absorption by the body is disrupted.

In many cases, coagulopathy associated with a high concentration of fibrin in the blood is recorded, which leads to a decline in fibrinogen. All this leads to thrombocytopenia (decreased platelet count), which in turn provokes increased bleeding.

What causes low blood clotting?

All types of low coagulability progress rapidly in the body.

The following factors can provoke coagulopathy:

An aggravation of less blood clotting occurs when bacteria and viruses are present in the body.

One of the sharp exacerbations occurs with kidney failure. Since at this moment the blood is filtered less, and there is a greater accumulation of toxins and wastes that stagnate in the blood.

During periods of bearing a child, when the increasing size of the uterus puts pressure on the urethra and there is a load on the kidneys, reduced blood filtration in the kidneys and stagnation of waste are often recorded. Bed rest helps restore healthy blood circulation.

How to identify symptoms?

Symptoms are the same for both types of coagulopathy. An accurate diagnosis is made by a qualified doctor.

If you notice the following symptoms, you should go to the hospital for examination:

Prolonged blood loss leads to the loss of large amounts of vitamin B and iron.

In childhood, coagulopathy is very dangerous, since at the stage of formation of the body a large amount of vitamins and iron is needed.

What happens during pregnancy?

Predominantly coagulopathy develops in pregnant women with the occurrence of some pathologies presented below:

• Disease of the circulatory system and formation of blood cells;
• Diseases caused by a lack of vitamins in the body;
• Varicose veins;
• Thrombophlebitis of a chronic nature (is an inflammation of the venous walls, with the formation of blood clots in them).

Women who have had significant blood losses in the past, with complications of thromboembolism, are at greater risk. People suffering from diabetes are also prone to developing coagulopathy.

Such women should be monitored by a doctor throughout the entire period of pregnancy., regularly undergoing tests and examinations, as well as taking prescribed courses of therapy. In most cases, such expectant mothers are hospitalized for the entire duration of pregnancy.

Making a diagnosis

Initially, you need to come for an examination to a doctor. At the first meeting, he listens to the patient’s complaints and performs an initial examination, studying the medical history. After which, if coagulopathy is suspected, the doctor will order blood tests (clinical and biochemical), as well as a urine test.

If the results of a urine test contain a large amount of calcium, suspicions arise about the presence of malignant tumor formations in the body, which lead to bleeding.

If a large amount of proteins is found in the urine, then perform an ultrasound of the kidneys to determine their performance and activity.

Among blood tests, the main stages that doctors pay attention to are:

Due to the fact that coagulopathy can be only one of the symptoms of the disease, examinations of the body are carried out to identify pathologies of organs, blood and vessels.

Among them:

The choice of the study is at the discretion of the doctor, taking into account additional symptoms and complaints of the patient.

How is low coagulation treated?

For an effective course of treatment, it is necessary not only to constantly take medications, but also to lead a healthy lifestyle and diet. The main goal of therapy is to eliminate the cause that caused the disease.

In case of severe injury, a patient with coagulopathy requires urgent hospitalization. In intensive care replenish lost blood using special solutions in the form of droppers. In case of large blood losses, a transfusion of compatible donor blood is given.

To normalize coagulation to the desired level, certain medications are mainly used:

• Iron-containing preparations (Fenuls, Sorbifer);
• Antibiotics (Clarithromycin, Amoxiclav, Amoxicillin);
• Chemotherapeutic agents;
• Plasma substitutes;
• Consumption of complexes of vitamins and minerals;
• Antispasmodics (Drotaverine, Spazgan);
• Glucocorticosteroids (Dexamethasone, Prednisolone).

To stop open bleeding in a patient with coagulopathy, a homeostatic collagen sponge or powder is used. In case if they do not bring any effect, then the spleen is removed, by surgery.

Preventive actions

There are no special measures to prevent coagulopathy.

• Regular examinations;
• Avoiding traumatic situations. It is necessary to prevent possible injuries, since bleeding stops slowly. And large injuries, with coagulopathy, can lead to disastrous consequences;
• Proper nutrition. Another key to preventing many diseases is a balanced, healthy diet. You should consume more foods rich in vitamin K (spinach, soy, strawberries, potatoes, veal, tomatoes, cod, cauliflower, rose hips).

The key to preventing most diseases is maintaining a healthy lifestyle and a balance between work and proper rest.

What's the forecast?

With timely access to the hospital, proper examination and taking an effective course of complex therapy, the outcome is favorable. The level of coagulation is successfully maintained with medications.

If coagulopathy is a symptom of another disease, then the course of treatment is aimed at eliminating the root cause. A healthy lifestyle, proper diet and giving up bad habits, will help not only normalize coagulation, but also prevent coagulopathy.

If you do not pay attention to the symptoms and ignore visiting a doctor, this can lead to disastrous consequences. With medium-sized wounds, heavy bleeding occurs, which are very difficult to stop, which can lead to large blood losses and cardiac arrest.

If you notice any symptoms, consult a doctor! Do not self-medicate and be healthy!

Class III. Diseases of the blood, hematopoietic organs and certain disorders involving the immune mechanism (D50-D89)

Excluded: autoimmune disease (systemic) NOS (M35.9), certain conditions arising in the perinatal period (P00-P96), complications of pregnancy, childbirth and the puerperium (O00-O99), congenital anomalies, deformities and chromosomal disorders (Q00- Q99), endocrine diseases, nutritional and metabolic disorders (E00-E90), disease caused by human immunodeficiency virus [HIV] (B20-B24), trauma, poisoning and certain other consequences of external causes (S00-T98), neoplasms (C00-D48), symptoms, signs and abnormalities identified by clinical and laboratory tests, not classified elsewhere (R00-R99)

This class contains the following blocks:
D50-D53 Anemia associated with nutrition
D55-D59 Hemolytic anemias
D60-D64 Aplastic and other anemias
D65-D69 Bleeding disorders, purpura and other hemorrhagic conditions
D70-D77 Other diseases of the blood and hematopoietic organs
D80-D89 Selected disorders involving the immune mechanism

The following categories are marked with an asterisk:
D77 Other disorders of the blood and hematopoietic organs in diseases classified elsewhere

NUTRITION-RELATED ANEMIA (D50-D53)

D50 Iron deficiency anemia

Included: anemia:
. sideropenic
. hypochromic
D50.0 Iron deficiency anemia secondary to blood loss (chronic). Posthemorrhagic (chronic) anemia.
Excludes: acute posthemorrhagic anemia (D62) congenital anemia due to fetal blood loss (P61.3)
D50.1 Sideropenic dysphagia. Kelly-Paterson syndrome. Plummer-Vinson syndrome
D50.8 Other iron deficiency anemias
D50.9 Iron deficiency anemia, unspecified

D51 Vitamin B12 deficiency anemia

Excludes: vitamin B12 deficiency (E53.8)

D51.0 Vitamin B12 deficiency anemia due to intrinsic factor deficiency.
Anemia:
. Addison
. Birmera
. pernicious (congenital)
Congenital intrinsic factor deficiency
D51.1 Vitamin B12 deficiency anemia due to selective malabsorption of vitamin B12 with proteinuria.
Imerslund(-Gresbeck) syndrome. Megaloblastic hereditary anemia
D51.2 Transcobalamin II deficiency
D51.3 Other vitamin B12 deficiency anemias associated with diet. Anemia of vegetarians
D51.8 Other vitamin B12 deficiency anemias
D51.9 Vitamin B12 deficiency anemia, unspecified

D52 Folate deficiency anemia

D52.0 Diet-related folate deficiency anemia. Megaloblastic nutritional anemia
D52.1 Folate deficiency anemia is drug-induced. If necessary, identify the drug
use an additional external cause code (class XX)
D52.8 Other folate deficiency anemias
D52.9 Folate deficiency anemia, unspecified. Anemia due to insufficient intake of folic acid, NOS

D53 Other diet-related anemias

Includes: megaloblastic anemia not responding to vitamin therapy
nom B12 or folate

D53.0 Anemia due to protein deficiency. Anemia due to amino acid deficiency.
Orotaciduric anemia
Excludes: Lesch-Nychen syndrome (E79.1)
D53.1 Other megaloblastic anemias, not elsewhere classified. Megaloblastic anemia NOS.
Excludes: DiGuglielmo disease (C94.0)
D53.2 Anemia due to scurvy.
Excludes: scurvy (E54)
D53.8 Other specified diet-related anemias.
Anemia associated with deficiency:
. copper
. molybdenum
. zinc
Excludes: malnutrition without mention of
anemia, such as:
. copper deficiency (E61.0)
. molybdenum deficiency (E61.5)
. zinc deficiency (E60)
D53.9 Diet-related anemia, unspecified. Simple chronic anemia.
Excludes: anemia NOS (D64.9)

HEMOLYTIC ANEMIA (D55-D59)

D55 Anemia due to enzyme disorders

Excludes: drug-induced enzyme deficiency anemia (D59.2)

D55.0 Anemia due to glucose-6-phosphate dehydrogenase [G-6-PD] deficiency. Favism. G-6PD deficiency anemia
D55.1 Anemia due to other disorders of glutathione metabolism.
Anemia due to deficiency of enzymes (except G-6-PD) associated with hexose monophosphate [HMP]
bypass of the metabolic pathway. Hemolytic nonspherocytic anemia (hereditary) type 1
D55.2 Anemia due to disorders of glycolytic enzymes.
Anemia:
. hemolytic non-spherocytic (hereditary) type II
. due to hexokinase deficiency
. due to pyruvate kinase deficiency
. due to triosephosphate isomerase deficiency
D55.3 Anemia due to disorders of nucleotide metabolism
D55.8 Other anemias due to enzyme disorders
D55.9 Anemia due to enzyme disorder, unspecified

D56 Thalassemia

D56.0 Alpha thalassemia.
Excludes: hydrops fetalis due to hemolytic disease (P56.-)
D56.1 Beta thalassemia. Cooley's anemia. Severe beta thalassemia. Sickle cell beta thalassemia.
Thalassemia:
. intermediate
. big
D56.2 Delta beta thalassemia
D56.3 Carriage of thalassemia trait
D56.4 Hereditary persistence of fetal hemoglobin [HFH]
D56.8 Other thalassemias
D56.9 Thalassemia unspecified. Mediterranean anemia (with other hemoglobinopathy)
Thalassemia minor (mixed) (with other hemoglobinopathy)

D57 Sickle cell disorders

Excludes: other hemoglobinopathies (D58. -)
sickle cell beta thalassemia (D56.1)

D57.0 Sickle cell anemia with crisis. Hb-SS disease with crisis
D57.1 Sickle cell anemia without crisis.
Sickle cell(s):
. anemia)
. disease) NOS
. violation )
D57.2 Double heterozygous sickle cell disorders
Disease:
. Hb-SC
. Hb-SD
. Hb-SE
D57.3 Carriage of the sickle cell trait. Carriage of hemoglobin S. Heterozygous hemoglobin S
D57.8 Other sickle cell disorders

D58 Other hereditary hemolytic anemias

D58.0 Hereditary spherocytosis. Acholuric (familial) jaundice.
Congenital (spherocytic) hemolytic jaundice. Minkowski-Choffard syndrome
D58.1 Hereditary elliptocytosis. Ellitocytosis (congenital). Ovalocytosis (congenital) (hereditary)
D58.2 Other hemoglobinopathies. Abnormal hemoglobin NOS. Congenital anemia with Heinz bodies.
Disease:
. Hb-C
. Hb-D
. Hb-E
Hemolytic disease caused by unstable hemoglobin. Hemoglobinopathy NOS.
Excludes: familial polycythemia (D75.0)
Hb-M disease (D74.0)
hereditary persistence of fetal hemoglobin (D56.4)
altitude-related polycythemia (D75.1)
methemoglobinemia (D74. -)
D58.8 Other specified hereditary hemolytic anemias. Stomatocytosis
D58.9 Hereditary hemolytic anemia, unspecified

D59 Acquired hemolytic anemia

D59.0 Drug-induced autoimmune hemolytic anemia.
If it is necessary to identify the drug, use an additional code for external causes (class XX).
D59.1 Other autoimmune hemolytic anemias. Autoimmune hemolytic disease (cold type) (warm type). Chronic disease caused by cold hemagglutinins.
"Cold agglutinin":
. disease
. hemoglobinuria
Hemolytic anemia:
. cold type (secondary) (symptomatic)
. thermal type (secondary) (symptomatic)
Excludes: Evans syndrome (D69.3)
hemolytic disease of the fetus and newborn (P55. -)
paroxysmal cold hemoglobinuria (D59.6)
D59.2 Drug-induced non-autoimmune hemolytic anemia. Drug-induced enzyme deficiency anemia.
If it is necessary to identify the drug, use an additional code for external causes (class XX).
D59.3 Hemolytic-uremic syndrome
D59.4 Other non-autoimmune hemolytic anemias.
Hemolytic anemia:
. mechanical
. microangiopathic
. toxic
If it is necessary to identify the cause, use an additional external cause code (class XX).
D59.5 Paroxysmal nocturnal hemoglobinuria [Marchiafava-Micheli].
D59.6 Hemoglobinuria due to hemolysis caused by other external causes.
Hemoglobinuria:
. from load
. marching
. paroxysmal cold
Excludes: hemoglobinuria NOS (R82.3)
D59.8 Other acquired hemolytic anemias
D59.9 Acquired hemolytic anemia, unspecified. Chronic idiopathic hemolytic anemia

APLASTIC AND OTHER ANEMIA (D60-D64)

D60 Acquired pure red cell aplasia (erythroblastopenia)

Includes: red cell aplasia (acquired) (adults) (with thymoma)

D60.0 Chronic acquired pure red cell aplasia
D60.1 Transient acquired pure red cell aplasia
D60.8 Other acquired pure red cell aplasias
D60.9 Acquired pure red cell aplasia, unspecified

D61 Other aplastic anemias

Excluded: agranulocytosis (D70)

D61.0 Constitutional aplastic anemia.
Aplasia (pure) red cell:
. congenital
. children's
. primary
Blackfan-Diamond syndrome. Familial hypoplastic anemia. Fanconi anemia. Pancytopenia with developmental defects
D61.1 Drug-induced aplastic anemia. If necessary, identify the drug
use an additional code for external causes (class XX).
D61.2 Aplastic anemia caused by other external agents.
If it is necessary to identify the cause, use an additional code of external causes (class XX).
D61.3 Idiopathic aplastic anemia
D61.8 Other specified aplastic anemias
D61.9 Aplastic anemia, unspecified. Hypoplastic anemia NOS. Bone marrow hypoplasia. Panmyelophthisis

D62 Acute posthemorrhagic anemia

Excludes: congenital anemia due to fetal blood loss (P61.3)

D63 Anemia in chronic diseases classified elsewhere

D63.0 Anemia due to neoplasms (C00-D48+)
D63.8 Anemia in other chronic diseases classified elsewhere

D64 Other anemias

Excluded: refractory anemia:
. NOS (D46.4)
. with excess blasts (D46.2)
. with transformation (D46.3)
. with sideroblasts (D46.1)
. without sideroblasts (D46.0)

D64.0 Hereditary sideroblastic anemia. Sex-linked hypochromic sideroblastic anemia
D64.1 Secondary sideroblastic anemia due to other diseases.
If necessary, an additional code is used to identify the disease.
D64.2 Secondary sideroblastic anemia caused by drugs or toxins.
If it is necessary to identify the cause, use an additional code of external causes (class XX).
D64.3 Other sideroblastic anemias.
Sideroblastic anemia:
. NOS
. pyridoxine-reactive, not elsewhere classified
D64.4 Congenital dyserythropoietic anemia. Dyshematopoietic anemia (congenital).
Excludes: Blackfan-Diamond syndrome (D61.0)
DiGuglielmo disease (C94.0)
D64.8 Other specified anemias. Childhood pseudoleukemia. Leukoerythroblastic anemia
D64.9 Anemia, unspecified

BLOOD CLOTTING DISORDERS, PURPURA AND OTHERS

HEMORRHAGIC CONDITIONS (D65-D69)

D65 Disseminated intravascular coagulation [defibration syndrome]

Afibrinogenemia acquired. Consumptive coagulopathy
Diffuse or disseminated intravascular coagulation
Acquired fibrinolytic bleeding
Purpura:
. fibrinolytic
. lightning fast
Excluded: defibration syndrome (complicating):
. in a newborn (P60)

D66 Hereditary factor VIII deficiency

Factor VIII deficiency (with functional impairment)
Hemophilia:
. NOS
. A
. classical
Excludes: factor VIII deficiency with vascular disorder (D68.0)

D67 Hereditary factor IX deficiency

Christmas disease
Deficit:
. factor IX (with functional impairment)
. thromboplastic plasma component
Hemophilia B

D68 Other bleeding disorders

Excluded: complicating:
. abortion, ectopic or molar pregnancy (O00-O07, O08.1)
. pregnancy, childbirth and the puerperium (O45.0, O46.0, O67.0, O72.3)

D68.0 Von Willebrand's disease. Angiohemophilia. Factor VIII deficiency with vascular impairment. Vascular hemophilia.
Excludes: hereditary capillary fragility (D69.8)
factor VIII deficiency:
. NOS (D66)
. with functional impairment (D66)
D68.1 Hereditary factor XI deficiency. Hemophilia C. Plasma thromboplastin precursor deficiency
D68.2 Hereditary deficiency of other coagulation factors. Congenital afibrinogenemia.
Deficit:
. AC globulin
. proaccelerin
Factor deficiency:
. I [fibrinogen]
. II [prothrombin]
. V [labile]
. VII [stable]
. X [Stuart-Prower]
. XII [Hageman]
. XIII [fibrin stabilizing agent]
Dysfibrinogenemia (congenital). Hypoproconvertinemia. Ovren's disease
D68.3 Hemorrhagic disorders caused by anticoagulants circulating in the blood. Hyperheparinemia.
Content enhancement:
. antithrombin
. anti-VIIIa
. anti-IXa
. anti-Xa
. anti-XIa
If necessary, identify the anticoagulant used, use an additional external cause code.
(Class XX).
D68.4 Acquired coagulation factor deficiency.
Coagulation factor deficiency due to:
. liver diseases
. vitamin K deficiency
Excludes: vitamin K deficiency in the newborn (P53)
D68.8 Other specified bleeding disorders. Presence of systemic lupus erythematosus inhibitor
D68.9 Bleeding disorder, unspecified

D69 Purpura and other hemorrhagic conditions

Excludes: benign hypergammaglobulinemic purpura (D89.0)
cryoglobulinemic purpura (D89.1)
idiopathic (hemorrhagic) thrombocythemia (D47.3)
lightning purpura (D65)
thrombotic thrombocytopenic purpura (M31.1)

D69.0 Allergic purpura.
Purpura:
. anaphylactoid
. Henoch(-Schönlein)
. non-thrombocytopenic:
. hemorrhagic
. idiopathic
. vascular
Allergic vasculitis
D69.1 Qualitative platelet defects. Bernard-Soulier syndrome [giant platelets].
Glanzmann's disease. Gray platelet syndrome. Thrombasthenia (hemorrhagic) (hereditary). Thrombocytopathy.
Excludes: von Willebrand disease (D68.0)
D69.2 Other non-thrombocytopenic purpura.
Purpura:
. NOS
. senile
. simple
D69.3 Idiopathic thrombocytopenic purpura. Evans syndrome
D69.4 Other primary thrombocytopenias.
Excludes: thrombocytopenia with absent radius (Q87.2)
transient neonatal thrombocytopenia (P61.0)
Wiskott-Aldrich syndrome (D82.0)
D69.5 Secondary thrombocytopenia. If it is necessary to identify the cause, use an additional external cause code (class XX).
D69.6 Thrombocytopenia, unspecified
D69.8 Other specified hemorrhagic conditions. Capillary fragility (hereditary). Vascular pseudohemophilia
D69.9 Hemorrhagic condition, unspecified

OTHER DISEASES OF THE BLOOD AND BLOOD FORMING ORGANS (D70-D77)

D70 Agranulocytosis

Agranulocytic tonsillitis. Children's genetic agranulocytosis. Kostmann's disease
Neutropenia:
. NOS
. congenital
. cyclic
. medicinal
. periodic
. splenic (primary)
. toxic
Neutropenic splenomegaly
If it is necessary to identify the drug causing the neutropenia, use an additional external cause code (class XX).
Excludes: transient neonatal neutropenia (P61.5)

D71 Functional disorders of polymorphonuclear neutrophils

Defect of the cell membrane receptor complex. Chronic (childhood) granulomatosis. Congenital dysphagocytosis
Progressive septic granulomatosis

D72 Other white blood cell disorders

Excludes: basophilia (D75.8)
immune disorders (D80-D89)
Neutropenia (D70)
preleukemia (syndrome) (D46.9)

D72.0 Genetic abnormalities of leukocytes.
Anomaly (granulation) (granulocyte) or syndrome:
. Aldera
. May-Hegglina
. Pelguera-Huet
Hereditary:
. leukocyte
. hypersegmentation
. hyposegmentation
. leukomelanopathy
Excluded: Chediak-Higashi (-Steinbrink) syndrome (E70.3)
D72.1 Eosinophilia.
Eosinophilia:
. allergic
. hereditary
D72.8 Other specified white blood cell disorders.
Leukemoid reaction:
. lymphocytic
. monocytic
. myelocytic
Leukocytosis. Lymphocytosis (symptomatic). Lymphopenia. Monocytosis (symptomatic). Plasmacytosis
D72.9 White blood cell disorder, unspecified

D73 Diseases of the spleen

D73.0 Hyposplenism. Postoperative asplenia. Atrophy of the spleen.
Excludes: asplenia (congenital) (Q89.0)
D73.1 Hypersplenism
Excluded: splenomegaly:
. NOS (R16.1)
.congenital (Q89.0)
D73.2 Chronic congestive splenomegaly
D73.3 Spleen abscess
D73.4 Spleen cyst
D73.5 Splenic infarction. Splenic rupture is non-traumatic. Torsion of the spleen.
Excludes: traumatic splenic rupture (S36.0)
D73.8 Other diseases of the spleen. Splenic fibrosis NOS. Perisplenitis. Splenitis NOS
D73.9 Disease of the spleen, unspecified

D74 Methemoglobinemia

D74.0 Congenital methemoglobinemia. Congenital deficiency of NADH-methemoglobin reductase.
Hemoglobinosis M [Hb-M disease]. Hereditary methemoglobinemia
D74.8 Other methemoglobinemias. Acquired methemoglobinemia (with sulfhemoglobinemia).
Toxic methemoglobinemia. If it is necessary to identify the cause, use an additional external cause code (class XX).
D74.9 Methemoglobinemia, unspecified

D75 Other diseases of the blood and hematopoietic organs

Excludes: swollen lymph nodes (R59. -)
hypergammaglobulinemia NOS (D89.2)
lymphadenitis:
. NOS (I88.9)
. spicy (L04. -)
. chronic (I88.1)
. mesenteric (acute) (chronic) (I88.0)

D75.0 Familial erythrocytosis.
Polycythemia:
. benign
. family
Excludes: hereditary ovalocytosis (D58.1)
D75.1 Secondary polycythemia.
Polycythemia:
. acquired
. related to:
. erythropoietins
. decreased plasma volume
. height
. stress
. emotional
. hypoxemic
. nephrogenic
. relative
Excluded: polycythemia:
. newborn (P61.1)
. true (D45)
D75.2 Essential thrombocytosis.
Excludes: essential (hemorrhagic) thrombocythemia (D47.3)
D75.8 Other specified diseases of the blood and hematopoietic organs. Basophilia
D75.9 Disease of the blood and hematopoietic organs, unspecified

D76 Selected diseases involving lymphoreticular tissue and the reticulohistiocytic system

Excludes: Letterer-Sieve disease (C96.0)
malignant histiocytosis (C96.1)
reticuloendotheliosis or reticulosis:
. histiocytic medullary (C96.1)
. leukemic (C91.4)
. lipomelanotic (I89.8)
. malignant (C85.7)
. non-lipidic (C96.0)

D76.0 Langerhans cell histiocytosis, not elsewhere classified. Eosinophilic granuloma.
Hand-Schueller-Crisgen disease. Histiocytosis X (chronic)
D76.1 Hemophagocytic lymphohistiocytosis. Familial hemophagocytic reticulosis.
Histiocytoses from mononuclear phagocytes other than Langerhans cells, NOS
D76.2 Hemophagocytic syndrome associated with infection.
If it is necessary to identify an infectious pathogen or disease, an additional code is used.
D76.3 Other histiocytosis syndromes. Reticulohistiocytoma (giant cell).
Sinus histiocytosis with massive lymphadenopathy. Xanthogranuloma

D77 Other disorders of the blood and hematopoietic organs in diseases classified elsewhere.

Splenic fibrosis in schistosomiasis [bilharzia] (B65. -)

SELECTED DISORDERS INVOLVING THE IMMUNE MECHANISM (D80-D89)

Includes: defects in the complement system, immunodeficiency disorders other than disease,
caused by human immunodeficiency virus [HIV] sarcoidosis
Excludes: autoimmune diseases (systemic) NOS (M35.9)
functional disorders of polymorphonuclear neutrophils (D71)
human immunodeficiency virus [HIV] disease (B20-B24)

D80 Immunodeficiencies with predominant antibody deficiency

D80.0 Hereditary hypogammaglobulinemia.
Autosomal recessive agammaglobulinemia (Swiss type).
X-linked agammaglobulinemia [Bruton] (with growth hormone deficiency)
D80.1 Nonfamilial hypogammaglobulinemia. Agammaglobulinemia with the presence of B-lymphocytes carrying immunoglobulins. General agammaglobulinemia. Hypogammaglobulinemia NOS
D80.2 Selective immunoglobulin A deficiency
D80.3 Selective deficiency of immunoglobulin G subclasses
D80.4 Selective immunoglobulin M deficiency
D80.5 Immunodeficiency with elevated levels of immunoglobulin M
D80.6 Insufficiency of antibodies with close to normal levels of immunoglobulins or with hyperimmunoglobulinemia.
Antibody deficiency with hyperimmunoglobulinemia
D80.7 Transient hypogammaglobulinemia in children
D80.8 Other immunodeficiencies with a predominant antibody defect. Kappa light chain deficiency
D80.9 Immunodeficiency with predominant antibody defect, unspecified

D81 Combined immunodeficiencies

Excludes: autosomal recessive agammaglobulinemia (Swiss type) (D80.0)

D81.0 Severe combined immunodeficiency with reticular dysgenesis
D81.1 Severe combined immunodeficiency with low T- and B-cell counts
D81.2 Severe combined immunodeficiency with low or normal B-cell counts
D81.3 Adenosine deaminase deficiency
D81.4 Nezelof syndrome
D81.5 Purine nucleoside phosphorylase deficiency
D81.6 Deficiency of class I molecules of the major histocompatibility complex. Naked lymphocyte syndrome
D81.7 Deficiency of class II molecules of the major histocompatibility complex
D81.8 Other combined immunodeficiencies. Biotin-dependent carboxylase deficiency
D81.9 Combined immunodeficiency, unspecified. Severe combined immunodeficiency disorder NOS

D82 Immunodeficiencies associated with other significant defects

Excludes: ataxic telangiectasia [Louis-Bart] (G11.3)

D82.0 Wiskott-Aldrich syndrome. Immunodeficiency with thrombocytopenia and eczema
D82.1 DiGeorge syndrome. Pharyngeal diverticulum syndrome.
Thymus gland:
. alymphoplasia
. aplasia or hypoplasia with immune deficiency
D82.2 Immunodeficiency with dwarfism due to short limbs
D82.3 Immunodeficiency due to a hereditary defect caused by the Epstein-Barr virus.
X-linked lymphoproliferative disease
D82.4 Hyperimmunoglobulin E syndrome
D82.8 Immunodeficiency associated with other specified significant defects
D 82.9 Immunodeficiency associated with significant defect, unspecified

D83 Common variable immunodeficiency

D83.0 General variable immunodeficiency with predominant abnormalities in the number and functional activity of B cells
D83.1 General variable immunodeficiency with a predominance of disorders of immunoregulatory T cells
D83.2 Common variable immunodeficiency with autoantibodies to B or T cells
D83.8 Other common variable immunodeficiencies
D83.9 Common variable immunodeficiency, unspecified

D84 Other immunodeficiencies

D84.0 Lymphocyte functional antigen-1 defect
D84.1 Defect in the complement system. C1 esterase inhibitor deficiency
D84.8 Other specified immunodeficiency disorders
D84.9 Immunodeficiency, unspecified

D86 Sarcoidosis

D86.0 Pulmonary sarcoidosis
D86.1 Sarcoidosis of the lymph nodes
D86.2 Sarcoidosis of the lungs with sarcoidosis of the lymph nodes
D86.3 Sarcoidosis of the skin
D86.8 Sarcoidosis of other specified and combined localizations. Iridocyclitis in sarcoidosis (H22.1).
Multiple cranial nerve palsies in sarcoidosis (G53.2)
Sarcoid:
. arthropathy (M14.8)
. myocarditis (I41.8)
. myositis(M63.3)
Uveoparotitic fever [Herfordt's disease]
D86.9 Sarcoidosis, unspecified

D89 Other disorders involving the immune mechanism, not elsewhere classified

Excludes: hyperglobulinemia NOS (R77.1)
monoclonal gammopathy (D47.2)
non-engraftment and graft rejection (T86. -)

D89.0 Polyclonal hypergammaglobulinemia. Hypergammaglobulinemic purpura. Polyclonal gammopathy NOS
D89.1 Cryoglobulinemia.
Cryoglobulinemia:
. essential
. idiopathic
. mixed
. primary
. secondary
Cryoglobulinemic(s):
. purpura
. vasculitis
D89.2 Hypergammaglobulinemia, unspecified
D89.8 Other specified disorders involving the immune mechanism, not elsewhere classified
D89.9 Disorder involving the immune mechanism, unspecified. Immune disease NOS

Normal pregnancy occurs with a slight increase in blood clotting ability, which occurs due to an increase in the number of coagulation factors (VII, VIII, X and fibrinogen). This process is important because these changes may cause some forms of bleeding disorders to go undiagnosed.

Types of blood clotting disorders

The main diseases of the blood coagulation system that occur during pregnancy are diseases associated with a decrease in platelet levels (thrombocytopenia) and congenital coagulopathies.

Thrombocytopenia in pregnant women includes:

• Gestational thrombocytopenia.
• Idiopathic thrombocytopenic purpura.
• HELLP syndrome.
• Thrombotic thrombocytopenic purpura.
• Hemolytic-uremic syndrome.

The main hereditary bleeding disorders that can occur during pregnancy are von Willebrand disease and hemophilia A and B.

A separate dangerous condition that occurs during childbirth or in the postpartum period is disseminated blood coagulation syndrome (DIC).

Causes of coagulopathy in pregnancy

The main causes of coagulation disorders during pregnancy are:

• The influence of hormonal changes in the mother’s body on the lifespan of platelets.
• Due to an increase in the amount of circulating blood, the number of platelets in relation to the total blood volume decreases.
• Poor nutrition in pregnant women, which leads to a deficiency of vitamin B12, which inhibits the process of platelet formation.
• Complication of pregnancy in the form of kidney disease.
• Acute viral infections during pregnancy.
• If pathological activation of the immune system occurs, antibodies to one’s own platelets are produced.
• Allergic reactions.
• Taking medications that affect platelet levels.
• Intrauterine fetal death.

Symptoms

All blood coagulation disorders in pregnant women occur with similar clinical manifestations. The main ones are:

• The appearance of bruises on the body after a minor injury or touch. Sometimes bruises appear for no reason.
• Nosebleeds and bleeding from the gums (more often when brushing teeth) are common.

The most dangerous disorder of blood coagulation is the development of disseminated intravascular coagulation syndrome, which can occur during or after childbirth and lead to the death of a woman in labor from massive bleeding caused by a critical decrease in platelet levels.

Treatment

Treatment of blood clotting disorders is carried out if the platelet count decreases to 40 thousand per μl or lower. The main thing in treatment is to eliminate the factor that caused the decrease in platelet levels.

In addition to treating the underlying disease, it is necessary to maintain adequate functioning of the blood system by prescribing steroid hormones (prednisolone, dexamethasone). If these drugs are administered late in pregnancy, they help accelerate the maturation of the child’s lungs.

If the administration of corticosteroids does not give the desired effect, the patient is prescribed immunoglobulin. During the gestation period, it can be administered 3-4 times; in addition, it is recommended to give one more injection immediately before and after childbirth.

Platelet transfusions are quite rare in the treatment of blood clotting disorders in pregnant women. This procedure is carried out only in very severe cases, if there is a risk to the life of the mother in labor.

If a pregnant woman experiences a significant decrease in platelet levels during the first trimester of pregnancy, which cannot be raised with diet, traditional medicines or traditional medicine, then removal of the spleen is recommended. This operation is performed no later than the second trimester of pregnancy to eliminate the risk of harm to the baby.

Herbal treatment

Treatment of bleeding disorders in pregnant women using medicinal herbs is an effective and safe method. Herbs stimulate the formation of platelets and basic blood clotting factors without harming the fetus. It must be remembered that traditional medicine is a complementary method of treating coagulopathy and should not be used as the only method of treatment. Before taking any medications during pregnancy, be sure to consult your doctor!

One of the most common plants that can increase platelet levels in the blood is nettle. For oral administration, use freshly squeezed nettle juice, which is mixed with fresh milk in a 1:1 ratio and taken half an hour before meals three times a day, 100 ml. The mixture must be constantly fresh; it cannot be stored, as it loses its medicinal properties. The course of treatment is two weeks, but if the desired effect is not observed, it can be extended until the desired platelet level is achieved.

Another folk remedy for improving blood clotting is a decoction made from viburnum bark. Boil two tablespoons of crushed bark in 300 ml of water for 30 minutes, then strain and cool. This decoction should be taken 5 times a day, 2 tablespoons each, if bleeding occurs.

Forecast

Serious blood clotting disorders are dangerous for a pregnant woman, as they can cause uterine bleeding during childbirth, which is difficult to stop. The delivery tactics are chosen by the doctor, and they are individual for each patient.

Minor thrombocytopenia (with a decrease in platelet levels to 80 thousand per μl) does not require correction and does not pose a particular threat to the life of the fetus and mother. Such patients are closely monitored with platelet levels monitored. If thrombocytopenia worsens, then treatment should be carried out immediately, because there is a risk of bleeding, which poses a significant risk to the life of both the fetus and the mother.

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Pathogenesis

When an artery, vein or capillary is damaged, hemorrhage occurs in areas of soft tissue located next to the vessel.

To restore the integrity of the hollow organ, platelets begin to attract each other, forming a large conglomerate. Such a blood clot quickly seals the deformed vessel, restoring blood circulation.

The causes of coagulopathy are different, but they all provoke a failure of the blood clotting mechanism at one of the following stages:

1. After damage to the vessel, a thrombus forms within a few minutes, which is called primary.
2. Soon the blood clots enlarge. The process involves specific plasma proteins - fibrinogens. The result of aggregation is a secondary thrombus.
3. After the integrity of the capillaries is restored, the thrombus resolves, and the products of its metabolism leave the bloodstream.

Types of pathological process

Despite the multiple causes of coagulopathy, the pathology is classified only by the mode of occurrence. Experts divide the disease into the following types:

• Congenital. In this case, the failure occurs already at the stage of homeostasis. The concentration of biologically active substances in the bloodstream decreases, which certainly affects its qualitative composition. The balance of the system responsible for thrombus formation is disrupted. Congenital coagulopathies, in turn, are divided into various forms, each of which is characterized by the absence of a specific component during the formation of a blood clot.
• Purchased. The anomaly is formed against the background of a developed acute or chronic disease. Coagulopathy is a complication of pathology, and it can also be classified as specific symptoms. This is exactly what the clinical picture of malignant neoplasms and severe bacterial infections looks like. Pharmacological drugs for the treatment of systemic diseases have similar side effects.

Poor blood clotting is almost always diagnosed in patients who have suffered heavy blood loss and is transient in nature. The body is simply unable to quickly replenish the supply of red blood cells and platelets, and fibrinogen production decreases.

Congenital pathologies include all forms of hemophilia. Without medical intervention, a person may die from blood loss and cardiac arrest.

All hemophilias are types of primary coagulopathies caused by gene mutations. Hemorrhages can be found in muscles, fatty tissue, the gastrointestinal tract and pulmonary parenchyma.

Causes of the disease

The main types of coagulopathy, regardless of whether they belong to acquired or congenital pathologies, develop rapidly in the human body. The trigger for bleeding disorders are provoking factors:

• autoimmune diseases occurring against the background of increased blood clot formation;
• systemic pathologies characterized by thinning of the walls of small vessels;
• malignant and benign tumors;
• long-term anticoagulant therapy;
• fatty liver, hepatitis, cirrhosis;
• lack of fat-soluble vitamin K in the body;
• intoxication with poisons of plant and animal origin, caustic alkalis and acids, heavy metals;
• hormonal imbalance;
• sensitization reactions;
• impaired absorption of biologically active substances in the small and large intestines.

Hereditary coagulopathies are caused by various types of thrombocytopenia. Pathologies worsen as the body's resistance to viral and bacterial infections decreases.

Homeostasis is disrupted especially sharply in acute renal failure. The ability of paired organs to filter blood decreases, and a significant concentration of waste and toxins accumulates in it.

This condition is often diagnosed during pregnancy, when the growing uterus puts pressure on the kidneys and urethra. Therefore, during the period of bearing a child, gynecologists and urologists recommend bed rest for some patients with a predisposition to coagulopathy.

In this way, normal blood circulation in a woman’s urinary system can be restored. Coagulopathy in pregnant women is often treated in a hospital setting under the supervision of medical personnel.

Symptoms of the pathological condition

The classification of coagulopathies does not depend on the symptoms shown, however, there are signs of pathology that are characteristic of a particular type. Only an experienced doctor can accurately diagnose the homeostasis abnormality, but you should immediately contact a medical facility if the following symptoms appear:

• pale skin, cyanosis of the nasolabial folds and hands;
• swelling of the joints due to hemorrhage in the cavity;
• blood does not clot for a very long time even after using hydrogen peroxide, alcohol solutions of iodine or brilliant green;
• the occurrence of extensive hematomas against the background of minor bruises;
• increased bleeding of the skin and mucous membranes.

With prolonged bleeding, a significant loss of B vitamins and iron occurs. A person’s teeth crumble, nails peel, and hair loss occurs. Coagulopathy is especially dangerous in children: during the formation of joints, muscles, bones and tendons, the lack of iron and vitamins leads to negative consequences.

Diagnostics

At the first stage of diagnosis, the doctor listens to the patient’s complaints and assesses his state of health. A history of diseases will help to suspect the presence of coagulopathy. But blood and urine tests are the most informative.

The detection of large amounts of calcium in urine often becomes a signal of the presence of malignant tumors that provoke bleeding. If the urine contains a lot of proteins, then an ultrasound examination of the kidneys is performed to assess their functional activity.

Since coagulopathy may be a symptom or complication of a more severe disease, further diagnosis becomes necessary. Patients are required to undergo the following examination procedures:

• computed tomography;
• X-ray examination;
• magnetic resonance imaging;
• ultrasound examination.

Using a blood test, the disturbance of homeostasis and the stage of development of coagulopathy are determined. Laboratory signs of poor blood clotting are low concentrations of hemoglobin, red blood cells, platelets in a biological sample.

This also indicates low immunity and developing iron deficiency anemia. Patients undergo tests (coagulation tests) to determine the ability of platelets to aggregate.

Treatment of the pathological condition

Congenital coagulopathies imply a certain lifestyle - constant use of pharmacological drugs and adherence to a special diet. Therapy for acquired pathologies is complex and aimed at eliminating the cause of the disease.

When the provoking factor is severe injury, the patient must be urgently hospitalized. In the intensive care unit, lost blood is replaced with solutions for parenteral administration. If necessary, donor blood transfusions are performed.

To maintain coagulation at the proper level, the following drugs are used for treatment:

• glucocorticosteroids - Dexamethasone, Prednisolone;
• antibiotics - Amoxiclav, Clarithromycin, Amoxicillin;
• chemotherapy drugs;
• antispasmodics - Drotaverine, Spazgan;
• complexes of vitamins and microelements;
• iron preparations - Fenyuls, Sorbifer.

Plasma substitutes and (or) platelet mass help restore normal blood clotting. To stop external bleeding, a collagen homeostatic sponge or powder is used. If there is no effect from treating coagulopathy with pharmacological agents, surgeons remove the spleen.

Timely treatment of diseases, undergoing an annual medical examination and a correct lifestyle are the most effective prevention of acquired coagulopathy. If you are diagnosed with a predisposition to bleeding, you should make changes to your diet. Nutritionists advise completely eliminating spicy, salty, fried foods from the menu, and limiting the consumption of alcoholic beverages.

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coagulopathy during pregnancy what is it

coagulopathy during pregnancy is

Hypercoagulability syndrome during pregnancy

It is very rare in our age of stress, bad genetics and poor nutrition that women get pregnant without problems. Sometimes, while carrying a baby, existing illnesses can worsen. Diseases of the circulatory system are no exception. So, what is hypercoagulability syndrome? How does it combine with pregnancy?

Medical research has proven that entire families and dynasties can be susceptible to thrombosis. A high-risk condition for this pathology is called hypercoagulation syndrome. Statistics say that about 5% of people suffer from it. If we talk about pregnant women, then every third of them experiences hypercoagulation syndrome. In people over 60 years of age, its manifestations are very frequent. This is 3/4 men and women.

In the presence of this syndrome, even minor factors can provoke the development of thrombosis. That is why diagnosis and neutralization of such factors is a measure of disease prevention.

There are increased and high risks of thrombosis. In the first case, preventive measures should be carried out only during periods of intense physical work, travel with long flights, during surgical operations, injuries, childbearing, during and after childbirth.

Phlebologists say that if there is a genetic predisposition to thrombosis, it may not occur if a person follows these recommendations:

When working sedentarily and staying in a static position for a long time, take breaks after 40 minutes, getting up and moving for 2-3 minutes.

This condition can significantly complicate the course of pregnancy. We are talking about its fading at an early stage; development of retrochorial hematomas; chorion presentation; spontaneous self-abortions in late pregnancy; development of eclampsia and preeclampsia. Also

What is coagulopathy?

Coagulopathy is a process in which abnormalities occur in the blood clotting system. It is characterized by extensive nasal hemorrhages, a lack of iron in the blood, and the formation of large hematomas on the skin.

Pathology can be transmitted from mother to child and develop throughout a person’s life. In the latter case, there is a sufficient amount of formed components in the blood, but their quality suffers.

In a normal state, a sufficient amount of hemoglobin protein, platelets and red blood cells circulate in the body in dynamic equilibrium. When there is open bleeding, the body initiates a process called coagulation to allow blood to clot and be delivered to the site of injury, stopping the bleeding.

Clogging of the wound occurs with the help of adhesive platelets, which replace the damaged walls of blood vessels and arteries.

ICD-10

According to the classification of coagulopathy according to the International Classification of Diseases, coagulopathy belongs to the class “Bleeding disorders, purpura and others,” with coding D65.

Types of coagulopathy

The occurrence of blood clotting abnormalities has many different causes, but is divided into types solely according to the method of occurrence. There are two main types of coagulopathy:

Progressive throughout life. Pathology is acquired during the development of diseases, and is a complication against the background of another disease, being one of the symptoms.

Coagulopathy is mainly observed in infections caused by bacteria and malignant tumors. Some medications can also cause clotting disorders.

Transmitted from mother to child. In this case, the pathology is in

Symptoms of coagulopathy and its treatment

Coagulopathy is a set of diseases that cause bleeding due to complex disorders in the coagulation and anticoagulation mechanisms of the blood. The type of bleeding in this disease is hematomatic in nature.

Depending on whether the disease is hereditary or acquired, it is caused either by insufficient quantities of plasma components or by their poor quality. In both cases, this is due to a genetic factor.

Symptoms, causes, diagnosis

Patients with coagulopathy experience pallor of the skin and hemorrhagic syndrome, in which blood flows from the walls of blood vessels into adjacent tissues or comes out. These are the main symptoms of the disease caused by a malfunction of hemostasis or changes in the structure of its components (damage to the vessel wall, changes in the number of platelets, etc.)

Sometimes hemostasis is impaired due to the use of certain medications that cause disruption of platelet adhesion and the blood clotting mechanism.

secondary, its duration is minutes, after which fibrin is formed (the end product of the blood clotting process), which holds the blood clot together;

Coagulopathies can be diagnosed only with a comprehensive examination using clinical and laboratory methods and differential diagnosis. It is necessary to do a detailed blood test.

Classification of coagulopathies

Hereditary coagulopathy occurs from a decrease in the components of hemostasis (the body system that works to prevent and stop bleeding) or from their disruption. The most common forms of the disease are hemophilia types A, B, C and afibrinogenemia.

As for acquired coagulopathy, it occurs against the background of infectious diseases, liver damage, severe enteropathies, as well as

Coagulopathy: causes and treatment

Coagulopathy is a set of negative processes characterized by disorders of blood clotting mechanisms. The pathology can be either acquired (renal failure) or congenital (hemophilia). The disease is manifested by dangerous prolonged bleeding, the development of iron deficiency anemia, and the formation of extensive hematomas on the skin.

Diagnosis of coagulopathy involves conducting laboratory and instrumental studies. After studying the results, patients are given comprehensive treatment aimed at eliminating the cause of the pathology, as well as its symptoms. Antibiotics, hormonal drugs, vitamins and microelements are used in the treatment of the disease.

Pathogenesis

Coagulopathy - what is it, why do nosebleeds become more frequent in a previously completely healthy person? The pathogenesis of the disease is based on a violation of the blood clotting process under the influence of external or internal provoking factors.

The normal circulation of platelets, red blood cells and hemoglobin is determined by special homeostasis mechanisms to maintain dynamic equilibrium. In order for the blood to clot when life-threatening situations arise, the body starts the coagulation process.

When factors that provoke coagulopathy occur, complete blood clotting does not occur. Therefore, when diagnosing, it is extremely important to establish at what stage of thrombus formation and its disposal disturbances occur.

Types of pathological process

Congenital. In this case, the failure occurs already at the stage of homeostasis. The concentration of biologically active substances in the bloodstream decreases, which certainly affects its qualitative composition. The balance of the system responsible for thrombus formation is disrupted. Congenital

Collapse during pregnancy

In pregnant women, usually young and healthy, with the exception of simple fainting, collapse with cardiac arrest occurs very rarely.

Collapse during pregnancy usually indicates a severe, life-threatening condition. The typical sequence of events during the development of collapse is agitation, shallow breathing, then confusion, loss of consciousness and collapse. Even if the diagnosis is unclear, resuscitation measures must be started immediately. During an emergency examination, the presence of consciousness, breathing and significant blood loss is determined. Resuscitation measures are carried out in accordance with standard protocols for intensive life support, and the diagnosis is clarified only after emergency measures are carried out.

Causes of collapse during pregnancy

Bleeding as a result of: blood loss - disrupted ectopic pregnancy, placental abruption, uterine rupture; coagulopathies - sepsis, placental abruption, amniotic fluid embolism

Normally, due to reduced peripheral resistance in the second trimester of pregnancy, blood pressure usually decreases. Blood pools in the lower extremities and requires greater muscle effort in pregnant women than in non-pregnant women to ensure adequate venous return. Therefore, pregnant women are more susceptible to the development of syncope for all reasons that enhance these normal physiological changes. Standing for long periods of time, such as on public transport, and getting up quickly from a supine position in late pregnancy are more likely to cause fainting than in non-pregnant people. Hot weather increases peripheral vasodilation and syncope is more likely.

How to cancel DIVIGEL? Can there be a breakdown after withdrawal?

The diagnosis is usually confirmed by anamnesis (according to the woman or eyewitnesses) and the situation of occurrence, for example, standing in a crowded, stuffy train. Losing consciousness does not happen suddenly, it

How to eliminate coagulopathy during pregnancy

Coagulopathy is a pathology that occurs during gestation. A distinctive feature is a blood clotting disorder, which can cause numerous bleeding. Coagulopathy during pregnancy is a very serious disease that requires special attention from doctors and the expectant mother.

Normal blood changes

In a woman carrying a child, the body undergoes serious changes, which increases the amount of blood involved in circulation. In the case when the pregnancy itself goes well, the ability of blood to clot increases, since a large number of factors appear that ensure this process. Thanks to such changes, you may not find out about any pathological disorders of blood clotting, which is why fibrinogen levels in the blood are studied.

Types of violations

Basically, if the blood circulation is exposed to any diseases, it signals a low platelet count. In some cases, doctors discover congenital coagulopathy in a woman.

Inherited bleeding disorders are divided into hemophilia A and B, as well as von Willebrand disease. Sometimes, during childbirth, or some time after it, DIC syndrome occurs.

Reasons

Poor nutrition, which causes insufficient production of vitamin B12, which affects the formation of platelets.

Symptoms

Most of all, you should be wary of DIC syndrome that occurs during childbirth or after it. In case of complications and severe bleeding, the woman in labor may die.

Treatment

An insufficiently balanced diet and other reasons lead to a lack of vitamins and microelements in the body, which is why a pregnant woman feels lethargic, weak, metabolism is disrupted, and functions appear.

It is necessary to take action when the platelet level drops to 40 tons per μl. The main goal of treating coagulopathy is to eliminate the factor that interferes with the production of the necessary particles. In addition to getting rid of this pro

Coagulopathy

Blood is an important component of the human body, which ensures the delivery of oxygen and nutrients to the internal organs and their cells. Sometimes the operation of this mechanism fails and a number of diseases develop. When considering blood diseases, special attention should be paid to coagulopathy - this is the general concept of a number of pathological disorders of blood clotting that can arise during life or be inherited. There are many varieties of the disease that differ in course, symptoms, and, accordingly, treatment. If the slightest alarming signs appear (for example, bleeding does not stop for a long time after a cut or tooth extraction), you should definitely consult a doctor, establish the cause of this phenomenon and choose the most effective ways to eliminate it.

What is coagulopathy?

In medicine, the concept of “coagulopathy” has a broad meaning and includes a number of pathological disorders of blood clotting. Hemostasis is a set of body reactions that are aimed at stopping bleeding and blood clotting. With the development of a number of diseases, this process is disrupted, which leads to large blood loss and other negative consequences. Pathological changes can occur at any stage of hemostasis; therefore, different types of coagulopathies are distinguished, which differ in clinical manifestations, causes of development and treatment.

Causes of the disease

Hereditary - develops as a result of the presence of genetic pathologies, in particular, insufficient content of plasma components of homeostasis, their low quality. The most common form of the disease is hemophilia.

Acquired - in this case, coagulopathy occurs due to a serious infectious disease, as a result of liver disease, kidney disease, or the presence of malignancy