Thrombocytopenia – hemorrhagic diathesis of various etiologies, pathogenesis and course, characterized by a tendency to increased bleeding due to a decrease in the number of blood platelets. The threshold criterion for thrombocytopenia in hematology is considered to be a platelet level below 150×109/L. However, the expanded clinical picture of thrombocytopenia usually develops with a decrease in platelets to 50×109/L, and a level of 30×109/L and below is critical. The physiological thrombocytopenia that occurs in women during menstruation or pregnancy (gestational thrombocytopenia) usually does not reach a pronounced degree. Pathological thrombocytopenia, due to various reasons, occurs in 50-100 of 1 million people.
Platelets (Bizzozero plaques) are small blood plates 1-4 microns in size. They are formed from bone marrow megakaryocytes with the direct stimulating effect of the polypeptide hormone thrombopoietin. The normal level of platelets is 150-400×109/l; approximately 70% of platelets circulate continuously in the peripheral blood, and 1/3 of the part is in the splenic depot. The average lifespan of platelets is 7-10 days, after which they are destroyed in the spleen.
Thrombocytopathy is an extensive group to which hemorrhagic problems of a person of a congenital nature or acquired through an improper lifestyle belong.
Diseases are mainly characterized by changes in the proper functioning of platelets. In this case, the number of red blood cells in plasma is fixed at a sufficient or almost ideal level.
In 35% of cases, congenital thrombocytopathy is detected. The occurrence of the remaining 65% involves external or internal negative factors.
In most cases, preschool patients and adolescents suffer from bleeding. Often poor-quality diagnosis leads to the fact that the child is being treated for another disease.
Thrombocytopathy has quite eloquent signs of manifestation – incessant bleeding and fixation of a specific hemorrhagic rash on the skin. If the symptoms of the disease are not discerned in time, serious complications with the health of the child may follow.
For example, hemorrhage in the lining of the brain negatively affects the entire condition of the patient. If treatment is started in a timely manner with effective drugs, the disease is quickly neutralized and the patient’s quality of life improves.
Thrombocytopenia is usually classified on the basis of a number of signs: causes, nature of the syndrome, pathogenetic factor, severity of hemorrhagic manifestations. According to the etiological criterion, primary (idiopathic) and secondary (acquired) thrombocytopenia are distinguished. In the first case, the syndrome is an independent disease; in the second, it develops a second time, with a number of other pathological processes.
Thrombocytopenia can have an acute course (lasting up to 6 months, with a sudden onset and a rapid decrease in platelet count) and chronic (lasting more than 6 months, with a gradual increase in manifestations and a decrease in platelet count).
Given the leading pathogenetic factor, there are:
- dilution thrombocytopenia
- thrombocytopenia distribution
- thrombocytopenia consumption
- thrombocytopenia due to insufficient platelet formation
- thrombocytopenia due to increased platelet destruction: non-immune and immune (alloimmune, autoimmune, transimmune, heteroimmune)
The criterion for the severity of thrombocytopenia is the level of blood platelets and the degree of violation of hemostasis:
- I – platelet count 150-50×109/l – satisfactory hemostasis
- II – platelet count 50-20 x 109/l – with minor trauma, intradermal hemorrhages, petechiae, prolonged bleeding from wounds occur
- III – platelet count 20×109/L and below – spontaneous internal bleeding develops.
Thrombocytopathy is divided into two large groups of a heterogeneous type. The following variants of the disease are distinguished: congenital (hereditary) type and acquired disease, with symptomatic manifestation.
Congenital thrombocytopathy is divided into the following types:
- With a change in platelet adhesion.
- With abnormal disturbances in the release reaction.
- With a violation of the aggregation function in platelets – thrombocytopathy of an aggregation-free nature, in which low blood coagulation is recorded.
- With problems of preservation of granules and their components.
- A disease of thrombocytopathy combined with various abnormalities diagnosed at birth.
In most cases (60% of emerging diseases) are recorded in the first years of a child’s life. This pathology is due to a hereditary predisposition.
Complications and consequences
If treatment is not done on time, the symptoms will only increase. The likelihood of serious complications increases sharply. Bonding and platelet destruction process are fixed.
It should be clearly understood the consequences of ignoring the urgent recommendations of the attending doctor:
- Intensive uterine bleeding
- Hemorrhage in the human pulmonary system, as well as in the digestive organs
- Hemorrhagic stroke
- low hemoglobin due to the small amount of iron in the blood;
- decreased protection of the immune system;
- bleeding from the nose;
- anemic coma.
The consequences and complications can be avoided with timely medical attention.
Maintaining a healthy lifestyle is one of the preventive measures that you must follow regardless of whether you have a disease or not.
At the first symptoms, it is important to consult a doctor who will decide which treatment method is best for the patient.
Prognosis and prevention
Detection of the disease in the early stages of manifestation in both a child and an adult patient can affect the conduct of effective symptomatic therapy. Such treatment will improve the patient’s life and provoke a long period of remission.
In the event that multiple hemorrhages in the lining of the brain are detected at a later date, the prognosis for the patient has no comforting information.
Prevention measures for patients are consulted by the doctor with the patient’s family, who are told all possible complications and problems during the course of the disease. When fixing the disease, you should lead only a healthy lifestyle and adhere to a specific diet. Uncontrolled medication and self-treatment of any disease are prohibited.
Thus, when a dangerous disease is detected, treatment should be started in a short time. Lack of therapy leads to serious complications and death. Therefore, preventive measures and symptomatic elimination of symptoms during the acute course should be followed.
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Congenital thrombocytopenia, for the most part, is part of hereditary syndromes, such as Viskot-Aldrich syndrome, Fanconi anemia, Bernard-Soulier syndrome, May-Hegglin anomaly, etc. Since hereditary thrombocytopenia, as a rule, qualitative changes in platelets are also observed, they are usually referred to thrombocytopathy.
The causes of acquired thrombocytopenia are extremely diverse. So, compensation for blood loss with infusion media, plasma, red blood cell mass can lead to a decrease in platelet concentration by 20-25% and the emergence of the so-called dilution thrombocytopenia. The basis of thrombocytopenia distribution is sequestration of platelets in the spleen or vascular tumors – hemangiomas, with a significant amount of platelet mass turned off from the general bloodstream. Thrombocytopenia distribution can develop in diseases accompanied by massive splenomegaly: lymphomas, sarcoidosis, portal hypertension, spleen tuberculosis, alcoholism, Gaucher disease, Felty syndrome, etc.
The most numerous group is thrombocytopenia, due to increased destruction of platelets. They can develop both in connection with the mechanical destruction of platelets (for example, with prosthetic heart valves, cardiopulmonary bypass, paroxysmal nocturnal hemoglobinuria), and in the presence of an immune component.
Alloimmune thrombocytopenia may result from transfusion of heterogeneous blood; transimmune – penetration of maternal antibodies to platelets through the placenta to the fetus. Autoimmune thrombocytopenia is associated with the production of antibodies to their own unchanged platelet antigens, which occurs with idiopathic thrombocytopenic purpura, systemic lupus erythematosus, autoimmune thyroiditis, myeloma, chronic hepatitis, HIV infection, etc.
Heteroimmune thrombocytopenia is caused by the formation of antibodies against foreign antigens that are fixed on the surface of platelets (drug, viral, etc.). Drug-induced pathology occurs when taking sedatives, antibacterials, sulfonamides, alkaloids, gold compounds, bismuth, heparin injections, etc. A moderate reversible decrease in platelet count is observed after viral infections (adenovirus infection, influenza, chickenpox, rubella, measles, infectious mononucleosis), vaccination.
Thrombocytopenia due to insufficient platelet formation (productive) develops with a deficiency of hematopoietic stem cells. This condition is characteristic of aplastic anemia, acute leukemia, myelofibrosis and myelosclerosis, tumor metastases in the bone marrow, iron deficiency, folic acid and vitamin B12, the effects of radiation therapy and cytostatic chemotherapy.
Finally, thrombocytopenia of consumption occurs in connection with an increased need for platelets to ensure blood coagulation, for example, with DIC, thrombosis, etc.
Usually, the first signal for a decrease in platelet count is the appearance of skin hemorrhages with minor trauma (shock, compression) of soft tissues. Patients note the frequent occurrence of bruises, a specific small-pointed rash (petechiae) on the body and extremities, hemorrhages in the mucous membranes, increased bleeding of the gums, etc. During this period, thrombocytopenia is detected only on the basis of changes in the hemogram, often studied for another reason.
At the next stage, an increase in bleeding time with minor cuts, prolonged and heavy menstrual bleeding in women (menorrhagia), and the appearance of ecchymoses at injection sites are noted. Bleeding caused by trauma or medical manipulation (for example, tooth extraction) can last from several hours to several days. Splenomegaly with thrombocytopenia usually develops only against the background of concomitant pathology (autoimmune hemolytic anemia, chronic hepatitis, lymphocytic leukemia, etc.); enlarged liver is not characteristic. In the case of arthralgia, you should think about the presence of collagenosis in the patient and the secondary nature of thrombocytopenia; with a tendency to form deep visceral hematomas or hemarthrosis – about hemophilia.
With a significant decrease in platelet count, spontaneous bleeding occurs (nose, uterine, pulmonary, renal, gastrointestinal), severe hemorrhagic syndrome after surgery. Profuse, non-stopping bleeding and brain hemorrhage can be fatal.
When establishing the secondary nature of thrombocytopenia, the main treatment is to treat the underlying disease. At the same time, the presence of severe hemorrhagic syndrome requires hospitalization of the patient and the provision of emergency medical care. With active bleeding, platelet transfusions, the appointment of angioprotectors (etamsyla), fibrinolysis inhibitors (aminocaproic acid) are indicated. Acceptance of acetylsalicylic acid, anticoagulants, NSAIDs is excluded.
Patients with idiopathic thrombocytopenic purpura undergo glucocorticoid therapy, intravenous administration of immunoglobulin, plasmapheresis, chemotherapy with cytostatics. In some cases (with the ineffectiveness of drug therapy, repeated bleeding), splenectomy is indicated. With non-immune thrombocytopenia, symptomatic hemostatic therapy is performed.
Thrombocytopenia is a condition characterized by a decrease in the number of platelets (red blood cells) to 140/μl and below and accompanied by increased bleeding.
Platelets are involved in the process of stopping local inflammatory phenomena, and also play a major role in stopping bleeding. With a decrease in the number of such cells in the blood, a large number of point hemorrhages occurs in the body.
The main cause of the pathological process is metaplasia of the megakaryocytic branch in the bone marrow producing platelets. Metaplasia is caused by several pathological conditions:
- Metastatic neoplasms in the bone marrow,
- Oncology of the hematopoietic system (leukemia, lymphoma, myeloma),
In cancerous tumors, the causes of platelet lowering are as follows:
- Inhibition of bone marrow function by toxic substances,
- Spleen enlargement,
- Severe iron deficiency anemia,
- Ejection by abnormal cells of a megakaryocytic process,
- With immune thrombocytopenia, autoantibodies are produced that destroy platelets.
As a rule, pathological changes caused by thrombocytopenia are characterized by vivid symptoms, therefore, for experienced doctors, the diagnosis is not difficult. After a physical examination and questioning of the patient, the doctor prescribes a series of diagnostic procedures to confirm or refute the diagnosis.
Additional studies include the following procedures:
- Bone marrow puncture
- Blood test – allows you to determine the number of constituent blood elements,
- Immunological research.
In children with thrombocytopenia, the prognosis is favorable – recovery occurs independently within six months. Therefore, if there is no threat of severe internal hemorrhage, monitoring the condition of the child is recommended.
With hemorrhagic syndrome, rashes on the mucous membranes or face, bleeding, or a rapid decrease in the number of red blood cells, steroid therapy, such as prednisone, is prescribed. A positive therapeutic effect is usually noticeable in the early days of treatment; after 7-10 days, the rashes completely disappear.
Self-healing of adults with thrombocytopenia is very rare. With platelet counts in excess of 50/μl, treatment is usually not performed. At lower rates (000 – 30/μl) and a high probability of bleeding caused, for example, by a stomach ulcer and 000 duodenal ulcer, as well as high hypertension, drug therapy is prescribed.
With a red cell volume of less than 30/μl, immediate treatment is required. In the case of a decrease in platelets to 000/μl and below, hospitalization of the patient is necessary.
Treatment includes the administration of prednisone for a month. The success criteria for therapy are as follows:
- Full recovery – the number of red blood cells after the end of the course of treatment is about 150/μl,
- Partial recovery – the number of red cells increases to 50/μl,
- No effect – signs of pathology persist, while the number of red blood cells increases by no more than 15/μl.
In the absence of the desired results of therapy, immunotherapeutic treatment is prescribed, which involves the introduction of immunoglobulins and high doses of steroid drugs into the body, the action of which is aimed at inhibiting the production of antibodies. In the absence of a therapeutic effect, a splenectomy is performed within six months, as a result of which the number of blood cells rises to a normal level.
Therapy of secondary thrombocytopenia is aimed at eliminating the primary disease and eliminating possible complications. With a critical decrease in platelet count, a blood transfusion is performed and prednisone is prescribed.
Platelets are cells that are responsible for blood coagulation. Strictly speaking, they are not literally cells, since they lack a nucleus that stores genetic information.
Platelets are “fragments” of megakaryocytes – large bone marrow cells.
If the wall of the blood vessel is damaged, the first – cellular – immunity link is launched, which is carried out precisely thanks to platelets.
They perform the following functions:
- Attach to the vascular wall (adhesion phase).
- “Stick together” with each other (aggregation phase).
- Substances that attract fibrinogen to the site of the vascular defect (phase of secretion and secondary aggregation) are secreted into the bloodstream.
Violation of any of these phases leads to the development of thrombocytopathy – a pathology of platelets without reducing their number in the blood (as opposed to thrombocytopenia).
Hereditary and acquired thrombocytopathies are distinguished.
- Hereditary thrombocytopathies are caused by genetic defects in the structure and function of platelets. This group of diseases includes Bernard-Soulier disease, Glanzmann thrombasthenia, and thrombocytopathy release.
- Acquired, or symptomatic, thrombocytopathies that occur against the background of prolonged use of certain drugs, exposure to industrial poisons and radioactive radiation.
Despite the difference in the development mechanisms and the genetic disorders that underlie them, all hereditary thrombocytopathies have the same clinical picture.
The first signs of the disease appear at an early age and proceed the same way:
- Point hemorrhages (petechiae) and bruises appear on the skin. They can occur both after skin damage and spontaneously.
- Spontaneous bleeding from the mucous membranes (gingival, nasal, uterine, sometimes gastrointestinal).
- Gingival bleeding – the appearance of blood during and after brushing your teeth. Often they imitate periodontal disease and periodontitis.
- Uterine bleeding can manifest itself as a blood discharge outside the cycle, as well as longer and more plentiful menstruation.
- Bleeding during injuries, operations, childbirth and so on.
Often, bleeding becomes more frequent and more severe in other diseases (including colds), as well as when taking medications that worsen blood coagulation (anticoagulants, antiplatelet agents, and others).
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