Homemade cereal bars with persimmons
Nutritionists say that for good health and a slim figure, you must include snacks in your diet....
Topic: “HAEMOSTASIS AND BLOOD GROUPS.”
Lecture No. 4.
Plan:
1. Hemolysis and its types.
2. Erythrocyte sedimentation rate and its determination.
3. Hemostasis and its mechanisms.
4. Blood groups.
5. Rh factor.
GOAL: Know physiological mechanisms hemolysis, erythrocyte sedimentation rate, hemostasis (vascular-platelet and coagulation).
Be able to distinguish between blood groups, understand the essence of Rh conflict.
This knowledge and skills are necessary in the clinic to monitor the course of the disease and recovery, when stopping bleeding, transfusion of donor blood, and carrying out measures to prevent miscarriage during repeat pregnancy in Rh-negative women.
Hemolysis(Greek haima - blood, lusis - decay, dissolution), or hematolysis, erythrolysis, is the process of intravascular breakdown of red blood cells and the release of hemoglobin into the blood plasma, which turns red and becomes transparent ("varnish blood") .
1) Osmotic hemolysis occurs when osmotic pressure decreases, which first leads to swelling and then destruction of red blood cells. A measure of the osmotic stability (resistance) of erythrocytes is the MaCl concentration at which hemolysis begins. In humans, this occurs in a 0.4% solution, and in a 0.34% solution all red blood cells are destroyed. In some diseases, the osmotic stability of erythrocytes decreases, and hemolysis can occur at high concentrations of NaCl in plasma.
2) Chemical hemolysis occurs under the influence chemical substances, destroying the protein-lipid membrane of erythrocytes (ether, chloroform, alcohol, benzene, bile acids, etc.).
3) Mechanical hemolysis is observed under strong mechanical influences on the blood, for example, when transporting ampoule blood on a bad road, vigorously shaking the ampoule with blood, etc.
4) Thermal hemolysis occurs when ampoule blood is frozen and thawed, as well as when it is heated to a temperature of 65-68°C.
5) Biological hemolysis develops when transfusion of incompatible or poor quality blood, from the bites of poisonous snakes, scorpions, under the influence of immune hemolysins, etc.
6) In-hardware hemolysis can occur in the heart-lung machine during blood perfusion (pumping).
Erythrocyte sedimentation rate (reaction)(abbreviated ESR, or ROE) is an indicator reflecting changes in the physicochemical properties of blood and the measured value of the plasma column released from red blood cells when they settle from a citrate mixture (5% sodium citrate solution) for 1 hour in a special pipette of the T.P. device. Panchenkova.
IN normal ESR is equal to:
for men - 1-10 mm/hour;
for women - 2-15 mm/hour;
in newborns - 0.5 mm/hour;
in pregnant women before childbirth - 40-50 mm/hour.
An increase in ESR greater than the specified values is, as a rule, a sign of pathology. The value of ESR depends on the properties of plasma, primarily on the content of large molecular proteins in it - globulins and especially fibrinogen. The concentration of these proteins increases during all inflammatory processes. During pregnancy, the fibrinogen content before childbirth is almost 2 times higher than normal, and ESR reaches 40-50 mm/hour. The influence of plasma properties on the ESR value is indicated by the experimental results. (For example, male red blood cells placed in male blood plasma settle at a rate of 5-9 mm/hour, and in the plasma of a pregnant woman - up to 50 mm/hour. Likewise, female red blood cells settle in male blood plasma at a rate of about 9 mm /hour, and in the plasma of a pregnant woman - up to 60 mm/hour. It is believed that large molecular proteins (globulins, fibrinogen) reduce the electrical charge of blood cells and the phenomenon of electrical repulsion, which contributes to a higher ESR (the formation of longer coin columns from red blood cells). with an ESR of 1 mm/hour, coin columns are formed from approximately 11 erythrocytes, and with an ESR of 75 mm/hour, clusters of erythrocytes have a diameter of 100 μm or more and consist of a large number (up to 60,000) of erythrocytes.)
To determine ESR, a T.P. Panchenkov device is used, consisting of a stand and graduated glass pipettes (capillaries).
Hemostasis(Greek haime - blood, stasis - motionless state) - this is a stop in the movement of blood through a blood vessel, i.e. stop bleeding. There are 2 mechanisms to stop bleeding:
1) vascular-platelet (microcirculatory) hemostasis;
2) coagulation hemostasis (blood clotting).
The first mechanism is capable of independently stopping bleeding from the most frequently injured small vessels in a few minutes with a fairly low blood pressure. It consists of two processes:
1) vascular spasm,
2) formation, compaction and contraction of the platelet plug.
The second mechanism for stopping bleeding is blood clotting (hemocoagulation) ensures cessation of blood loss in case of damage to large vessels, mainly muscular type. It is carried out in three phases: Phase I - formation of prothrombinase;
Phase II - thrombin formation;
Phase III - conversion of fibrinogen to fibrin.
In the blood coagulation mechanism, in addition to the wall blood vessels And shaped elements, 15 plasma factors are involved: fibrinogen, prothrombin, tissue thromboplastin, calcium, proaccelerin, convertin, antihemophilic globulins A and B, fibrin-stabilizing factor, etc. Most of these factors are formed in the liver with the participation of vitamin K and are proenzymes related to the globulin fraction of proteins plasma. Trigger Blood clotting is caused by the release of thromboplastin by damaged tissue and disintegrating platelets. Calcium ions are required to carry out all phases of the coagulation process.
A network of insoluble fibrin fibers and the red blood cells, leukocytes and platelets entangled in it form a blood clot.
Blood plasma devoid of fibrinogen and some other substances involved in coagulation is called serum. And blood from which fibrin has been removed is called defibrinated.
The normal time for complete coagulation of capillary blood is 3-5 minutes, for venous blood - 5-10 minutes.
In addition to the coagulation system, the body simultaneously has two more systems: anticoagulant and fibrinolytic.
Anticoagulant system interferes with the processes of intravascular coagulation or slows down hemocoagulation. The main anticoagulant of this system is heparin, secreted from lung and liver tissue and produced by basophilic leukocytes and tissue basophils ( mast cells connective tissue). Heparin inhibits all phases of the blood coagulation process, suppresses the activity of many plasma factors and the dynamic transformations of platelets.
Allocable salivary glands medicinal leeches hirudin acts depressingly on the third stage of the blood coagulation process, i.e. prevents the formation of fibrin.
Fibrinolytic the system is capable of dissolving formed fibrin and blood clots and is the antipode of the coagulation system. Main function fibrinolysis- splitting fibrin and restoring the lumen of a vessel clogged with a clot. Disruption of the functional relationships between the coagulation, anticoagulation and fibrinolytic systems can lead to serious diseases: increased bleeding, intravascular thrombus formation and even embolism.
Blood groups- a set of characteristics characterizing the antigenic structure of erythrocytes and the specificity of anti-erythrocyte antibodies, which are taken into account when selecting blood for transfusions (Latin transfusio - transfusion).
In 1901, the Austrian K. Landsteiner and in 1903 the Czech J. Jansky discovered that when mixing blood different people erythrocytes sticking to each other is often observed - a phenomenon agglutination(Latin agglutinatio - gluing) followed by their destruction (hemolysis). It was found that erythrocytes contain agglutinogens A and B, adhesive substances of glycolipid structure, antigens. Found in plasma agglutinins a and b, modified proteins of the globulin fraction, antibodies that glue erythrocytes. Agglutinogens A and B in erythrocytes, like agglutinins a and b in plasma, may be present one at a time, together, or absent in different people. Agglutinogen A and agglutinin a, as well as B and b are called the same name. The adhesion of red blood cells occurs when the red blood cells of the donor (the person giving blood) meet the same agglutinins of the recipient (the person receiving blood), i.e. A + a, B + b or AB + ab. From this it is clear that in the blood of every person there are opposite agglutinogen and agglutinin.
According to the classification of J. Jansky and K. Landsteiner, people have 4 combinations of agglutinogens and agglutinins, which are designated as follows:
People of group I can only receive blood transfusions from this group. Group I blood can be transfused to people of all groups. Therefore, people with blood type I are called universal donors. People with group IV can be transfused with blood of all groups, so these people are called universal recipients. Group IV blood can be transfused to people with group IV blood. The blood of people of groups II and III can be transfused to people with the same, as well as with IV blood group.
However, currently in clinical practice only blood of the same group is transfused, and in small quantities (no more than 500 ml), or the missing blood components are transfused (component therapy). This is due to the fact that:
firstly, with large massive transfusions, dilution of the donor’s agglutinins does not occur, and they glue the recipient’s red blood cells together;
secondly, with a careful study of people with blood type I, immune agglutinins anti-A and anti-B were discovered (in 10-20% of people); transfusion of such blood to people with other blood groups causes serious complications. Therefore, people with blood type I, containing anti-A and anti-B agglutinins, are now called dangerous universal donors;
thirdly, many variants of each agglutinogen have been identified in the ABO system. Thus, agglutinogen A exists in more than 10 variants
In 1930, K. Landsteiner, speaking at the award ceremony Nobel Prize for the discovery of blood groups, suggested that in the future new agglutinogens will be discovered, and the number of blood groups will grow until it reaches the number of people living on earth. This scientist’s assumption turned out to be correct. To date, more than 500 different agglutinogens have been discovered in human erythrocytes.
To determine blood groups, you need to have standard sera containing known agglutinins, or anti-A and anti-B coliclones containing diagnostic monoclonal antibodies. If you mix a drop of blood from a person whose group needs to be determined with serum of groups I, II, III or with anti-A and anti-B coliclones, then by the agglutination that occurs, his group can be determined.
Transfused blood always has a multilateral effect. In clinical practice there are:
1) replacement effect - replacement of lost blood;
2) immunostimulating effect - to stimulate the defenses;
3) hemostatic (hemostatic) effect - to stop bleeding, especially internal;
4) neutralizing (detoxification) effect - in order to reduce intoxication;
5) nutritional effect - introduction of proteins, fats, carbohydrates in an easily digestible form.
As we just noted! In addition to the main agglutinogens A and B, erythrocytes may contain other additional ones, in particular, the so-called Rh agglutinogen (Rh factor). It was first found in 1940 by K. Landsteiner and I. Wiener in the blood of a rhesus monkey. 85% of people have the same Rh agglutinogen in their blood. This blood is called Rh positive. Blood that lacks Rh agglutinogen is called Rh negative (in 15% of people). The Rh system has more than 40 varieties of agglutin genes - D, C, E, of which D is the most active . A special feature of the Rh factor is that people do not have anti-Rhesus agglutinins. However, if a person with Rh-negative blood is repeatedly transfused with Rh-positive blood, then under the influence of the administered Rh agglutinogen, specific anti-Rh agglutinins and hemolysins are produced in the blood. In this case, transfusion of Rh-positive blood to this person can cause agglutination and hemolysis of red blood cells - transfusion shock will occur.
The Rh factor is inherited and is of particular importance for the course of pregnancy. For example, if the mother does not have the Rh factor, but the father has it (the probability of such a marriage is 50%), then the fetus may inherit the Rh factor from the father and turn out to be Rh positive. The fetal blood enters the mother's body, causing the formation of anti-Rhesus agglutinins in her blood. If these antibodies cross the placenta back into the fetal blood, agglutination will occur. With a high concentration of anti-Rhesus agglutinins, fetal death and miscarriage may occur. In mild forms of Rh incompatibility, the fetus is born alive, but with hemolytic jaundice.
Rh conflict occurs only with a high concentration of anti-Rhesus agglutinins. Most often, the first child is born normal, since the titer of these antibodies in the mother’s blood increases relatively slowly (over several months). But when a Rh-negative woman becomes pregnant again with a Rh-positive fetus, the threat of Rh-conflict increases due to the formation of new portions of anti-Rhesus agglutinins. Rh incompatibility during pregnancy is not very common: approximately one case in 700 births.
To prevent Rh-conflict, pregnant Rh-negative women are prescribed anti-Rh-gammaglobulin, which neutralizes Rh-positive fetal antigens.
Hemolysis is the process of destruction of the membranes of red blood cells - erythrocytes, with further release of hemoglobin into the plasma. provoked by the release of a substance - hemolysin. The membranes of red blood cells are destroyed under the influence of specific toxins of a bacterial nature or produced by enzymes.
The class and types of hemolysis depend on the location of the processes and on the reasons that contributed to the disintegration of the erythrocyte membranes:
The reasons that trigger the process of destruction of hemolysis can be either external (damage to cells during or transportation of material) or internal (takes place inside the red blood cell itself).
Internal factors of cell damage include a number of diseases:
During internal damage red cells are destroyed in the liver, spleen and bone marrow. This occurs due to the development of microspherocytosis congenital form, and autoimmune nature, .
Considering a number of factors that destroy the membranes of red blood cells, it becomes clear that hemolysis poses a danger to the entire body, as it often causes an enlargement of the spleen and liver, leading to the development of very serious diseases.
During pregnancy, the destruction of the walls of red blood cells is due to the presence. In this case, hemolysis during pregnancy is not a severe pathology, but only a physiological process. To normalize a woman’s condition, it is necessary to compensate for the lack of iron in the body. To do this, just stick to and use pomegranates regularly.
The main symptoms of the process of destruction of red blood cells, which patients primarily note:
It also happens that a person does not even suspect that he has such severe pathological processes as hemolysis in his body. The presence of blood hemolysis is detected during donation.
During an exacerbation, the patient experiences following signs hemolysis:
The process of breakdown of red blood cells in many cases leads to the development of anemia, quite dangerous disease, which, in turn, can lead to the formation of stones in the bile ducts (cholelithiasis).
What are the consequences of hemolysis and should I worry? In many patients, when pathology is detected, a psychosomatic illness begins to form. They find signs of non-existent diseases in themselves only because they know what is happening inside their body.
As a rule, if hemolysis is detected as a result, a repeat blood donation is prescribed. This is explained by the fact that they could be destroyed under the influence of a mechanical factor - due to careless work with the test tube material.
Damage to blood cells may be caused by the nurse pushing the blood too quickly or by using a needle that is too thin during the test.
Damage to red cells is often observed when the material is incorrectly transferred from a test tube into a special flask. Breaking against the glass walls, red blood cells stain the plasma pink, which makes it impossible to separate it in a centrifuge. Such cases of red blood cell damage are called partial hemolysis. This phenomenon is not a disease, but only an error in collecting material and incorrect analysis.
Before repeating hemolysis, the patient needs to drink a small amount of plain water. If a repeated analysis again shows the presence of destroyed red blood cells, a diagnosis of acute hemolysis is made.
This is a very serious pathological process, acute hemolysis can lead to serious consequences.
If the patient is conscious at the time the disease is diagnosed, he may complain of a number of symptoms of acute hemolysis:
The cause of acute hemolysis of blood is the erroneous infusion of incorrectly selected donor blood and the alienation of its red blood cells by the recipient’s body.
With the development of acute hemolysis, during surgery using general anesthesia, symptoms pathological process will be sharp, and if there is a catheter with a urinal, it will be visible that the urine has become red. Sometimes black urine is discharged.
In order to confirm the presence of a pathological process of destruction of red blood cells in the body, it is necessary to analyze the patient’s blood and urine. With hemolysis, the processes of bilirubinemia, fibrinolysis, hemoglobinemia, and reduced coagulant potential will be identified. The presence of hyperkalemia and hemoglobinuria is noted in the urine. As red blood cells break down, the patient's daily urine output decreases, and in some cases, urine may be completely absent.
The uncontrolled destruction of red blood cells must be treated immediately. If the cause of the pathology is an error during blood transfusion, therapeutic methods are used aimed at stopping the infusion of red blood cells from incompatible blood.
To prevent the occurrence of hyperfusion in the kidneys and hypovolemia, special solutions are administered. A procedure is carried out with intravenous administration of Heparin. The procedure is aimed at removing free hemoglobin from the blood. Prednisolone is also used in the treatment of acute hemolysis.
Drug treatment acute hemolysis is prescribed by the attending physician, based on the clinical picture and symptoms of each individual case. It is important to know exactly when the pathological process began to develop in the patient’s body.
In particular severe cases for treatment it is necessary to urgently prescribe hemodialysis, especially if there is renal failure.
One of the reasons for the rapid destruction of red blood cells is long-term use certain medications. These are mainly anti-tuberculosis drugs, drugs from the sulfonamide group and hypoglycemic antibiotics.
With this clinical picture, hemolysis of the destruction of blood cells is not a pathology, and does not indicate the presence of serious diseases - it is just a natural reaction of the body to taking certain medications, the patient’s condition normalizes after completing the course of taking them.
Hemolysis of red blood cells, or destruction, occurs constantly in the body, and completes their life cycle, which lasts 4 months. The process by which this happens as planned goes unnoticed by humans. But if the destruction of oxygen carriers is carried out under the influence of external or internal factors, hemolysis becomes hazardous to health. To prevent it, it is important to follow preventive measures, and to successful treatment– quickly recognize characteristic symptoms and find out the reasons why the pathology develops.
Hemolysis of red blood cells is their damage, in which hemoglobin is released into the blood plasma, and the blood itself becomes transparent and acquires a red color, like a dissolved dye in distilled water, and is called “lacquer blood.”
The process occurs under the influence of a substance - hemolysin, in the form of an antibody or bacterial toxin. Red blood cells survive destruction in the following way:
The video shows the process clearly
Hemolysis of erythrocytes occurs against the background of impaired hemoglobin production, excess erythromycin blood cells, physiological jaundice, genetic inferiority of red blood cells, in which they are prone to destruction, as well as autoimmune disorders, when antibodies show aggression towards own cells blood. This happens when acute leukemia, myeloma and systemic lupus erythematosus.
Similar signs appear after the administration of certain medications and vaccines.Based on the site of red blood cell breakdown, hemolysis happens:
The mechanism of hemolysis in the body happens as follows:
Exists several reasons why it develops hemolysis, but the most common are the following:
An experienced specialist must know not only the reasons why hemolysis of red blood cells develops, but also the characteristic signs, since in the first stages the pathology is asymptomatic and appears only during acute stage, which is developing quickly. Clinically this manifests itself in the following:
In a severe form of hemolysis, a person experiences convulsions, consciousness is depressed, and anemia is always present, externally manifesting itself in the form of malaise, pale skin and shortness of breath. An objective feature is listening to a systolic murmur in the heart. Both forms of hemolysis are characterized by an enlargement of the spleen and liver. Intravascular destruction of red blood cells changes the color of urine.
In the case of subcompensation, the symptoms become less, anemia is absent or insufficiently expressed.An acute condition that occurs with pronounced hemolysis is called acute hemolysis. Develops with hemolytic anemia, pathologies or transfusions of incompatible blood, under the influence of poisons or certain medications. It is characterized by rapidly increasing anemia, an increase in the concentration of free bilirubin, neutrophilic leukocytosis, reticulocytosis, etc. As a result, a large number of red blood cells disintegrate with the release of hemoglobin.
The crisis begins with the appearance of weakness, fever, nausea with vomiting, pain in the form of contractions in the lower back and abdomen, increasing shortness of breath, tachycardia, and rising temperature. A severe degree of pathology is typical sharp decline Blood pressure, development of collapse and anuria.
The spleen almost always enlarges, less often the liver.Very often hemolysis is associated with hemolytic anemia. In this state, the breakdown of red blood cells occurs at a faster rate, after which the indirect fraction is released. With anemia, the life of red blood cells is shortened and the time of their destruction is reduced. This type of anemia divided into 2 types:
After this, the child feels much worse, which manifests itself in lack of appetite, weakness, and limb cramps. In severe forms of jaundice, significant skin and subcutaneous swelling, anemia, and an increase in the size of the spleen and liver occur. Light form characterized by a fairly easy course without any significant deviations.
Timely therapy minimizes probable complications jaundice and prevents its consequence – the child’s developmental delay.See a doctor if you suspect pathological hemolysis contact if a person has the following symptoms:
Doctor begins the examination after the following questions:
Testing to identify the disease will require:
Treatment of hemolysis consists of eliminating the cause of the disease and accompanying unpleasant symptoms. It is possible to use immunosuppressive drugs that depress the immune system, glucocorticosteroids (for the autoimmune variety), as well as replacement therapy(transfusion of red blood cells and blood components). When hemoglobin drops to critical limits, the most effective therapy- This is a transfusion of red blood cells. If conservative treatment is ineffective, the spleen is removed.
Vitamin therapy and physiotherapy provide additional protection, especially if work or living are associated with harmful conditions. At the slightest characteristic symptoms And unknown reason, why hemolysis occurred, it is important to bring the body back to normal as quickly as possible.
The content of the article:
Today there are many diseases that affect the human body. People can get sick from some of them several times a year (viral), others have a chronic form, and there are also diseases that are acquired in nature or selectively affect the human body.
No matter what, no one wants to get sick, be it common cold, or more serious problems with health. Unfortunately, no one asks us or warns us about the appearance of this or that disease, blood hemolysis is no exception.
On the one hand, it is a vital physiological process, but this is only when red blood cells, as expected, live 120-130 days, then die of natural causes. Sometimes things don’t happen the way we would like them to, and we are faced with another problem.
Hemolysis - (destruction or decay), as a result of this process, the destruction of red blood cells (red blood cells) occurs, which causes hemoglobin to enter the environment. Under natural and normal conditions, the lifespan of a blood cell inside the vessels is 125 days, and then “death” occurs - hemolysis (blood clotting).
A very interesting fact is that hemolysis can sometimes happen outside human body, for example when taking a blood test. In such cases, the analysis will not be accurate and reliable, or it will not work at all. Basically, the blame for blood clotting falls on the people who work with blood in the future, after the collection.
Regardless of whether you suffer from pathological hemolysis or not, always be attentive to yourself and listen to the “internal signals” that your body gives you. Never ignore these “signals”, because it can be not only about your health, but also about your life.
Learn more about the structure and function of red blood cells from this video:
Hemolysis- this is the physiological destruction of blood cells, namely cells of the erythrocyte series, reflecting natural process their aging. Direct destruction of erythrocyte blood cells occurs under the influence of hemolysin, which most often plays the role of bacterial toxins.
Depending on the origin, all variants of the course of the hemolytic reaction can be attributed to one of two main options: natural or pathological. Natural hemolysis is a continuous chain of chemical processes, as a result of which a “physiological renewal” of the composition of red blood cells occurs, provided normal functioning structures of the reticuloendothelial system.
Variants of hemolytic reactions that are observed in laboratory conditions include temperature and osmotic hemolysis. In the first type of hemolysis, a chain of hemolytic reactions is triggered as a result of exposure to critical low temperatures on blood components. In osmotic hemolysis, red blood cells are destroyed when blood enters a hypotonic environment. For healthy people characterized by minimal osmotic resistance of erythrocytes, which is within 0.48% NaCl, while complete destruction The bulk of red blood cells is observed at a NaCl concentration of 0.30%.
In a situation where the patient has endotoxemia caused by the action of infectious microorganisms, conditions are created for the development of biological hemolysis. A similar hemolytic reaction is also observed during transfusion of incompatible whole blood or its components.
Another variant of the hemolytic reaction is the mechanical type of hemolysis, the appearance of signs of which is facilitated by the provision of a mechanical effect on the blood (for example, shaking a test tube containing blood). This type of hemolytic reaction is typical for patients who have undergone cardiac valve replacement.
There is a whole range of substances with active hemolyzing properties, among which the most active are: snake venoms and insect poison. The development of hemolysis is facilitated by exposure to a number of chemicals from the group of chloroform, gasoline and even alcohol.
A rare and at the same time the most severe etiopathogenetic form of hemolytic reaction for the patient is autoimmune hemolysis, the occurrence of which is possible if the patient’s body produces antibodies to its own red blood cells. This pathology is accompanied by severe anemia of the body and the release of hemoglobin in the urine in a critically high concentration.
In a situation where a person does not show signs of pathological hemolysis, and the destruction of red blood cells occurs as planned with the participation of the structures of the reticuloendothelial system according to the intracellular type, no external manifestations a person will not feel hemolysis.
The clinical picture of hemolysis is observed only in the case of pathological course and includes several periods: hemolytic crisis or acute hemolysis, a subcompensated phase of hemolysis and a period of remission.
The development of acute hemolysis, which is characterized by a lightning-fast course that significantly worsens the patient’s health, is most often observed with transfusion of incompatible blood components, severe infectious lesion body and toxic effects, for example, taking medications. Danger this state is that the hemolytic reaction is so intense that the body lacks compensatory capabilities to produce a sufficient number of red blood cells. Due to this, clinical symptoms hemolytic crisis consists of manifestations of bilirubin intoxication and a severe form of anemic syndrome. Specific signs of an acute hemolytic crisis that occurs intraoperatively are the appearance of unmotivated excessive bleeding of the wound surface, as well as the release of dark urine through the catheter.
Manifestations of bilirubin intoxication are changes in the color of the skin in the form of icterus, which is diffuse and intense. In addition, the patient experiences severe nausea and repeated vomiting unrelated to food intake, severe pain in the area abdominal cavity, which does not have a clear localization. At severe course hemolytic crisis develops at lightning speed in the patient convulsive syndrome and varying degrees of impairment of consciousness.
Symptoms that are a reflection of anemic syndrome are severe weakness and the inability to perform normal physical activity, visual pallor of the skin, respiratory distress in the form of increasing shortness of breath, and an objective examination of the patient often reveals a systolic murmur in the projection of auscultation of the apex of the heart. A pathognomonic symptom of intracellular pathological hemolysis is an increase in the size of the spleen and liver, and intravascular hemolysis is characterized by a change in urine in the form of darkening.
A specific reflection of acute hemolysis is the appearance of specific changes in blood and urine tests in the form of severe bilirubinemia and hemoglobinemia, and a decrease in fibrinolysis factors, hemoglobinuria and a significant increase in creatinine and urea.
The danger of hemolysis occurring in an acute form is the possible development of complications in the form of regenerative crisis and acute renal failure.
In the subcompensatory phase of hemolysis, the processes of production of blood cells by the erythroid sprout are activated bone marrow, therefore the severity of clinical manifestations decreases, but remains skin manifestations and hepatosplenomegaly. Anemic syndrome in this stage of hemolysis is practically not observed, and with clinical trial blood is noted increased number reticulocytes, reflecting the regenerative process in the blood.
A special form of hemolytic reaction is hemolytic disease, which is observed in children during the neonatal period. Even in the prenatal period, the fetus experiences hemolytic manifestations caused by incompatibility blood counts mother and fetus. The intensity of the development of the hemolysis reaction has a clear correlation with the magnitude of the increase in antibody titer in the blood of a pregnant woman.
The clinical manifestation of hemolysis in newborns can occur in three ways: classic options. The most unfavorable option for the child’s recovery is the edematous variant, which significantly increases the risk of stillbirth. In addition to pronounced swelling of the soft tissues, there is an excessive accumulation of fluid in the natural cavities (pleural, pericardial, abdominal cavity).
Jaundice syndrome manifests itself in changes in the color of the skin, amniotic fluid and vernix lubrication. The child exhibits signs of toxic damage to the structures of the central nervous system in the form of increased convulsive readiness, rigidity and opisthotonus, oculomotor disorders and the “setting sun” symptom. The appearance of these symptoms can be fatal.
Anemic syndrome in a newborn child, as a rule, is not accompanied by pronounced clinical manifestations and consists only of changes laboratory analysis. The duration of anemic syndrome with a favorable course of hemolysis in a newborn child, as a rule, does not exceed three months.
Provided the normal functioning of all organs and systems of the human body, the processes of formation of red blood cells and their destruction are in balance. The predominant localization of the process of destruction of erythrocyte blood cells is the structures of the reticuloendothelial system, the main representatives of which are the spleen and liver, in which fragmentation of the erythrocyte and its subsequent lysis are observed. As red blood cells age, they lose their elasticity and ability to change their shape, making it difficult for them to pass through the splenic sinuses. The result of this process is the retention of red blood cells in the spleen and their further sequestration.
In fact, not all red blood cells circulating in the blood stream undergo passage through the splenic sinuses, but only 10% of their total mass. Due to the fact that the fenestrae of the vascular sinuses have a significantly smaller lumen than the diameter of a standard red blood cell, old cells, characterized by rigidity of the membrane, are retained in the sinusoids. Subsequently, red blood cells are subject to metabolic disorders caused by low acidity and low glucose concentrations in the splenic sinuses. Elimination of red blood cells retained in the sinuses occurs with the help of macrophage cells that are constantly present in the spleen. Thus, intracellular hemolysis is the direct destruction of the blood cells of the erythrocyte series by macrophages of the reticuloendothelial system.
Depending on the predominant localization of the process of destruction of red blood cells, two main forms are distinguished: intracellular and intravascular hemolysis.
Extravascular hemolysis destroys up to 90% of red blood cells, provided that the structures of the reticuloendothelial system are functioning normally. The destruction of hemoglobin consists of the primary cleavage of iron and globin molecules and the formation of biliverdin under the influence of heme oxygenase. Subsequently, a chain of enzymatic reactions is launched, the end product of which is the formation of bilirubin and its entry into the general bloodstream. At this stage, hepatocytes are activated, the function of which is aimed at absorbing bilirubin from the blood plasma. In a situation where a patient experiences a significant increase in the concentration of bilirubin in the blood, part of it does not bind to albumin and is filtered in the kidneys.
Adsorption of bilirubin from plasma occurs in the liver parenchyma by activating the structures of the transport system, after which it is conjugated with glucuronic acid. This chemical transformation occurs with the participation of a large number of enzymatic catalysts, the activity of which directly depends on the state of the hepatocytes. A newborn child has low enzymatic activity liver, and therefore, excessive hemolysis in children is caused precisely by the inability of the liver to conjugate bilirubin quickly enough.
Further transformation of conjugated hemoglobin involves its release by hepatocytes together with bile, which also contains other complexes (phospholipids, cholesterol, bile salts). In the lumen biliary tract bilirubin undergoes a chain of changes under the influence of the enzyme dehydrogenase and the formation of urobilinogen, which is absorbed by the structures duodenum and undergoes further oxidation in the liver. Part of the bilirubin that is not absorbed in the small intestine enters the thin section intestines, where a new form of it is formed - stercobilinogen.
Most of the stercobilinogen is excreted in the feces, and the rest is excreted in the urine as urobilin. Thus, intensive hemolysis of erythrocytes can be monitored by determining the concentration of stercolibin. At the same time, to assess the intensity of hemolysis, one should not consider an increase in the concentration of urobilinogen, which increases not only in a situation where increased hemolysis occurs, but also with morphological and functional damage to the mass of hepatocytes.
Main diagnostic criteria, reflecting the process of increased intracellular hemolysis, is an increase in the concentration of the conjugated fraction of bilirubin, as well as a sharp increase in the release of stercobilin and urobilin from natural biological fluids. The development of pathological intracellular hemolysis is facilitated by the patient’s hereditary deficiency of the erythrocyte membrane, impaired hemoglobin production, as well as an excess number of erythrocyte blood cells, which occurs with physiological jaundice.
In physiological intravascular hemolysis, the destruction of erythrocyte blood cells occurs directly in the circulating blood stream, and the component of this type of hemolytic reaction does not exceed 10% of the total mass of destroyed erythrocytes. The normal intravascular hemolysis reaction is accompanied by the release of hemoglobin and the binding of the latter to plasma globulins. The resulting complex enters the structures of the reticuloendothelial system and undergoes further transformations.
Massive intravascular hemolysis is accompanied by a reduced hemoglobin-binding capacity of plasma globulins, which is reflected in the release of large amounts of hemoglobin through the structures of the urinary tract. Entering the kidneys, hemoglobin causes changes in its structures in the form of hemosiderin deposition on the surface of the epithelium of the renal tubules, which causes a decrease in tubular reabsorption and the release of free hemoglobin along with the urine.
It should be borne in mind that there is no clear correlation between the degree of hemoglobinemia and the intensity of free hemoglobin excretion in the urine. Thus, a reduced hemoglobin-binding capacity of plasma is accompanied by the development of hemoglobinuria, even with a slight increase in the concentration of hemoglobin in the blood. Thus, the main markers of increased intravascular hemolysis are an increase in the concentration of free bilirubin in the urine and blood, as well as concomitant hemosiderinuria.
Due to the fact that acute hemolytic crisis belongs to the category emergency conditions, specialists have developed a unified algorithm for providing emergency care to this category of patients, including medicinal and non-medicinal components. Relief of signs of hemolytic crisis in acute period must be carried out only in a hematology hospital on intensive care unit beds.
In a situation where hemolysis is accompanied by a critical decrease in hemoglobin levels, the only effective method treatment is a transfusion of red blood cells in a calculated daily volume of 10 ml per 1 kg of the patient’s body weight. In case of existing signs of an aregenerative crisis, transfusion therapy is recommended to be supplemented with anabolic steroids (Retabolil at a dose of 25 mg once every 2 weeks).
The presence of signs of acute autoimmune hemolysis in a patient is the basis for the use of glucocorticosteroid drugs. The initial daily dose of Prednisolone is 60 mg, but in some situations the dose may be increased to 150 mg. After stopping the crisis, it is advisable to gradually reduce the dosage (no more than 5 mg per day) to a level of 30 mg. Further reduction in dosage involves taking the drug with a 2.5 mg lower dose every fifth day until complete withdrawal.
In a situation where therapy with glucocorticosteroid drugs does not have the desired effect in the form of periods of remission of 7 months or more, it is recommended that the patient undergo surgical removal of the spleen.
Refractory forms of autoimmune hemolysis involve the simultaneous use of glucocorticosteroid drugs and immunosuppressive drugs (Imuran in the calculated daily dose 1.5 mg per 1 kg of patient weight).
The deep stage of the hemolytic crisis should be stopped by transfusion of red blood cells after performing the Coombs test. In order to relieve hemodynamic disturbances that often accompany the course of acute hemolysis, it is recommended intravenous administration Reogluman at an estimated dose of 15 ml per 1 kg of patient weight.
The presence of signs of an increase in urea and creatinine in a patient is the basis for hemodialysis. It should be taken into account that a violation of the technique and a change in the composition of the dialysate fluid may in itself provoke the development of an enhanced hemolytic reaction.
In order to prevent the development of renal failure, patients with hemolysis should be prescribed sodium bicarbonate at a dose of 5 g with simultaneous oral administration of Diacarb at a dose of 0.25 g.
Drug treatment of hemolysis in newborn children consists of a primary replacement transfusion of Rh-negative blood. The calculation of the required amount of administered blood is 150 ml/kg of body weight. Blood transfusion should be combined with adequate glucocorticosteroid therapy ( intramuscular injection Cortisone at a dose of 8 mg short course). Signs of damage to the structures of the central nervous system are leveled out after the use of Glutamic acid at a dose of 0.1 g orally.
K not medicinal methods Prevention of recurrence of hemolysis in newborns is to avoid breastfeeding.
Hemolysis - which doctor should you contact?
? If you have or suspect the development of hemolysis, you should immediately seek advice from doctors such as a hematologist or transfusiologist.