Secondary thrombocytopenia according to ICD 10. Thrombocytopenia ICD. Choosing the timing and method of delivery

Congenital thrombocytopenias are mostly part of hereditary syndromes, such as Wiskot-Aldrich syndrome, Fanconi anemia, Bernard-Soulier syndrome, May-Hegglin anomaly, etc. Since with hereditary thrombocytopenias, as a rule, qualitative changes in platelets are also observed, they are usually classified as thrombocytopathies .
The causes of acquired thrombocytopenia are extremely varied. Thus, replacement of blood loss with infusion media, plasma, and red blood cells can lead to a decrease in platelet concentration by 20-25% and the occurrence of so-called dilution thrombocytopenia. Thrombocytopenia of distribution is based on the sequestration of platelets in the spleen or vascular tumors - hemangiomas with the exclusion of a significant amount of platelet mass from the general bloodstream. Thrombocytopenia of distribution can develop in diseases accompanied by massive splenomegaly: lymphomas, sarcoidosis, portal hypertension, splenic tuberculosis, alcoholism, Gaucher disease, Felty syndrome, etc.
The most numerous group consists of thrombocytopenia, caused by increased destruction of platelets. They can develop both in connection with mechanical destruction of platelets (for example, during prosthetic heart valves, artificial circulation, paroxysmal nocturnal hemoglobinuria), and in the presence of an immune component.
Alloimmune thrombocytopenia may result from transfusion of foreign blood; transimmune - penetration of maternal antibodies to platelets through the placenta to the fetus. Autoimmune thrombocytopenia is associated with the production of antibodies to one's own unchanged platelet antigens, which occurs in idiopathic thrombocytopenic purpura, systemic lupus erythematosus, autoimmune thyroiditis, multiple 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 (drugs, viruses, etc.). Drug-induced pathology occurs when taking sedatives, antibacterials, sulfa drugs, alkaloids, gold compounds, bismuth, heparin injections, etc. A reversible moderate decrease in the number of platelets is observed after viral infections ( adenovirus infection, influenza, chicken pox, rubella, measles, infectious mononucleosis), vaccinations.
Thrombocytopenia, caused by insufficient platelet formation (productive), develops with a deficiency of hematopoietic stem cells. This condition is typical for aplastic anemia, acute leukemia, myelofibrosis and myelosclerosis, tumor metastases in the bone marrow, iron deficiency, folic acid and vitamin B12 effects radiation therapy and cytostatic chemotherapy.
Finally, consumption thrombocytopenia occurs due to an increased need for platelets to ensure blood clotting, for example, in DIC syndrome and thrombosis.

The code must contain an additional digit after the period, which will clarify the diagnosis:

• 0 – purpura caused by an allergic reaction;
• 1 – defects in the structure of platelets with a normal number;
• 2 – purpura of another, non-thrombocytopenic origin (in case of poisoning);
• 3 – idiopathic thrombocytopenic purpura;
• 4 – other primary platelet deficiencies;
• 5 – secondary lesions;
• 6 – unspecified variants of pathologies;
• 7 – other types of hemorrhages (pseudogemophilia, increased fragility of blood vessels, and so on);
• 8 – unspecified hemorrhagic conditions.

This group of diseases is located under the heading of blood pathologies, hematopoietic organs and immune disorders of cellular origin.

Danger of thrombocytopenia

Because of the gravity clinical manifestations, thrombocytopenia in international classification diseases contains protocols emergency care with severe hemorrhagic syndromes.

A danger to life with a strong decrease in the number of platelets appears even when scratches appear, since the wound is not healed by primary blood clots and continues to bleed.

People with a lack of white blood cells can die from spontaneous internal hemorrhages, so the disease requires timely diagnosis and adequate treatment.

Secondary thrombocytopenia

Definition and general information [edit]

Drug-induced immune thrombocytopenia is most often caused by antibodies to the drug that cross-react with platelet antigens. Less commonly, the drug is fixed on platelets to form a complete antigen, where it serves as a hapten and platelets serve as a carrier.

The drugs that most often cause thrombocytopenia are listed in Table. 16.5.

Heparin-induced thrombocytopenia is a heparin-induced, immune-mediated prothrombotic disorder accompanied by thrombocytopenia and venous and/or arterial thrombosis.

Approximately 1% of patients develop heparin-induced thrombocytopenia for at least one week after heparin use, and approximately 50% of these experience thrombosis. Heparin-induced thrombocytopenia is slightly more common in women.

Etiology and pathogenesis[edit]

Heparin-induced thrombocytopenia results from a humoral immune reaction directed against a complex involving endogenous platelet factor 4 and exogenous heparin; autoantibodies recognize endogenous platelet factor 4 only when it is combined with heparin. This immune complex activates circulating platelets through their surface FcγRIIA receptors, leading to thrombocytopenia and hypercoagulability. The characteristics of heparin (bovine > porcine), its composition (unfractionated > low molecular weight > fondaparinux), dose (prophylactic > therapeutic > single), route of administration (subcutaneous > intravenous) and duration of administration (more than 4 days > less than 4 days) are all factors determining the development and severity of thrombocytopenia.

Clinical manifestations[edit]

With drug-induced thrombocytopenia petechiae, gastrointestinal bleeding and hematuria usually appear several hours after administration of the drug. The duration of thrombocytopenia depends on the rate of drug elimination. Usually 7 days after its discontinuation, the platelet count returns to normal.

Heparin-induced thrombocytopenia can occur at any age (> 3 months), but cases are rare in children. Moderate thrombocytopenia usually begins 5-10 days after heparin administration. If the patient has already been exposed to heparin within the last 100 days, a rapid reaction may occur, with a drop in platelet count occurring within minutes to hours of heparin administration. Delayed heparin-induced thrombocytopenia is also possible; thrombocytopenia develops after discontinuation of the drug. Thrombocytopenia is usually asymptomatic and bleeding is rare. Heparin-induced thrombocytopenia is accompanied by high risk thrombotic complications (eg, pulmonary embolism, myocardial infarction, thrombotic stroke) with a strong tendency to arterial thrombosis of the arteries of the extremities and deep vein thrombosis. Additional microvascular thrombosis can lead to the development of venous gangrene/limb amputation. Other complications include skin necrosis at heparin injection sites and anaphylactoid reactions (eg, fever, hypotension, joint pain, dyspnea, cardiopulmonary failure) following intravenous bolus administration.

Secondary thrombocytopenia: Diagnosis[edit]

The diagnosis of heparin-induced thrombocytopenia can be suspected based on the clinical picture - thrombocytopenia, thrombosis, the absence of another cause of thrombocytopenia. The diagnosis is confirmed by the detection of antibodies to the endogenous platelet factor 4/heparin complex and is confirmed by the detection of pathological platelet-activating antibodies using a serotonin release assay or a heparin-induced platelet activation test.

Differential diagnosis[edit]

Differential diagnoses include non-immune heparin-associated thrombocytopenia (due to the direct interaction of heparin with circulating platelets occurring in the first days after heparin administration), as well as postoperative hemodilution, sepsis, non-heparin-induced thrombocytopenia, disseminated intravascular coagulation, and multiple organ failure.

Secondary thrombocytopenia: Treatment[edit]

For some patients receiving heparin, regular monitoring of platelet counts is recommended. If heparin-induced thrombocytopenia is suspected or confirmed, treatment is to discontinue heparin and use an alternative anticoagulant, either non-heparin anti-factor Xa (danaparoid, fondaparinux) or direct thrombin inhibitors (eg, argatroban, bivalirudin). Warfarin is contraindicated during the acute thrombocytopenic phase because it can cause microvascular thrombosis, with the potential for necrosis of the ischemic limb (venous gangrene syndrome). Thrombocytopenia usually resolves after an average of 4 days, with values ​​greater than 150 x 109/L, although in some cases it may take 1 week to 1 month.

The prognosis for platelet count recovery is good, but postthrombotic complications may occur (eg, limb amputation in 5-10% of patients, stroke, bilateral hemorrhagic adrenal necrosis with adrenal insufficiency). Mortality from heparin-induced thrombocytopenia (eg, fatal pulmonary embolism) is observed in 5-10% of cases.

Prevention[edit]

Other [edit]

Thrombocytopenic purpura caused by red blood cell transfusion

1. Clinical picture. Thrombocytopenic purpura is a rare complication of red blood cell transfusion. It is manifested by sudden thrombocytopenia, bleeding from the mucous membranes and petechiae, which occur 7-10 days after transfusion. The diagnosis is based on medical history. This form of thrombocytopenic purpura most often occurs in multiparous women and people who have undergone multiple red blood cell transfusions. According to the mechanism of development, it is similar to thrombocytopenia of newborns caused by maternal antibodies. Thrombocytopenic purpura, caused by red blood cell transfusion, occurs in individuals who lack the Zw a antigen. It has been shown that this antigen is part of glycoprotein IIb/IIIa. Transfusion of red blood cells mixed with platelets carrying the Zw a antigen leads to the appearance of antibodies to this antigen. It is believed that they cross-react with glycoprotein IIb/IIIa of the patient’s own platelets.

A. Platelet transfusions are not performed because they are usually ineffective. In addition, platelet donors in this disease can only be 2% of people whose platelets do not carry the Zw a antigen.

b. Prednisone, 1-2 mg/kg/day orally, reduces hemorrhagic syndrome and increases the platelet count.

V. The disease goes away on its own after the patient’s blood is freed from the donor’s platelets.

d. Subsequently, red blood cells from donors who lack the Zw a antigen should be used for transfusion.

Purpura and other hemorrhagic conditions (D69)

Excluded:

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

In Russia, the International Classification of Diseases, 10th revision (ICD-10) has been adopted as a single normative document to take into account morbidity, reasons for the population’s appeals to medical institutions all departments, causes of death.

ICD-10 was introduced into healthcare practice throughout the Russian Federation in 1999 by order of the Russian Ministry of Health dated May 27, 1997. No. 170

The release of a new revision (ICD-11) is planned by WHO in 2017-2018.

With changes and additions from WHO.

Processing and translation of changes © mkb-10.com

Thrombocytopenia and platelet dysfunction

A disorder of the blood system, in which an insufficient number of platelets circulates in it - cells that provide hemostasis and play a key role in the process of blood clotting, is defined as thrombocytopenia (ICD-10 code - D69.6).

Why is thrombocytopenia dangerous? A reduced concentration of platelets (less than 150 thousand/μl) impairs blood clotting so much that there is a threat of spontaneous bleeding with significant blood loss at the slightest damage to blood vessels.

Platelet diseases include abnormally elevated platelet levels (thrombocythemia in myeloproliferative disorders, thrombocytosis as a reactive phenomenon), decreased platelet levels - thrombocytopenia, and platelet dysfunction. Any of these conditions, including a condition with an increase in platelet levels, can cause impaired hemostatic clot formation and bleeding.

Platelets are fragments of megakaryocytes that provide hemostasis to circulating blood. Thrombopoietin is synthesized by the liver in response to a decrease in the number of bone marrow megakaryocytes and circulating platelets and stimulates the bone marrow to synthesize platelets from megakaryocytes. Platelets circulate in the bloodstream for 7-10 days. About 1/3 of platelets are temporarily deposited in the spleen. The normal platelet count is 40,000/µl. However, the platelet count may vary slightly depending on the phase menstrual cycle, decrease in later pregnancy (gestational thrombocytopenia) and increase in response to inflammatory cytokines inflammatory process(secondary or reactive thrombocytosis). The platelets are ultimately destroyed in the spleen.

ICD-10 code

Causes of thrombocytopenia

Causes of thrombocytopenia include impaired platelet production, increased platelet sequestration in the spleen with normal platelet survival, increased platelet destruction or consumption, platelet dilution, and a combination of the above. Increased platelet sequestration in the spleen suggests the presence of splenomegaly.

The risk of bleeding is inversely proportional to the platelet count. A platelet count of less than/µL easily causes minor bleeding and increases the risk of major bleeding. With platelet levels between i/µl, bleeding may occur even with minor trauma; when the platelet level is less than / µl, spontaneous bleeding is possible; when the platelet level is less than 5000/μl, severe spontaneous bleeding is likely to develop.

Platelet dysfunction can occur when there is an intracellular defect of platelet abnormality or when external influence, damaging the function of normal platelets. Dysfunction can be congenital or acquired. Of the congenital disorders, von Willebrand disease is the most common and intracellular platelet defects are less common. Acquired platelet dysfunction is often caused by various diseases, taking aspirin or other medications.

Other causes of thrombocytopenia

Platelet destruction can occur due to immune causes (HIV infection, medications, diseases connective tissue, lymphoproliferative diseases, blood transfusions) or as a result of non-immune causes (Gram-negative sepsis, acute respiratory distress syndrome). Clinical and laboratory features are similar to those found in idiopathic thrombocytopenic purpura. Only a study of the medical history can confirm the diagnosis. Treatment is associated with correction of the underlying disease.

Acute respiratory distress syndrome

Patients with acute respiratory distress syndrome may develop nonimmune thrombocytopenia, possibly due to platelet deposition in the capillary beds of the lungs.

Blood transfusions

Post-transfusion purpura is caused by immune destruction similar to ITP, except for the presence of a history of blood transfusion within 3 to 10 days. Patients are predominantly women and lack platelet antigen (PLA-1), which is present in most people. Transfusions of PLA-1-positive platelets stimulate the production of PLA-1 antibodies, which (mechanism unknown) may react with the patient's PLA-1-negative platelets. The result is severe thrombocytopenia, which resolves within 2-6 weeks.

Connective tissue and lymphoproliferative diseases

Connective tissue (eg, SLE) and lymphoproliferative diseases can cause immune thrombocytopenia. Glucocorticoids and splenectomy are often effective.

Drug-induced immune destruction

Quinidine, quinine, sulfonamides, carbamazepine, methyldopa, aspirin, oral antidiabetic drugs, gold salts, and rifampin can cause thrombocytopenia, usually due to an immune reaction in which the drug binds to the platelet to form a new “foreign” antigen. This condition is indistinguishable from ITP except for the history of drug use. When you stop taking the medication, your platelet count increases within 7 days. Gold-induced thrombocytopenia is an exception, since gold salts can remain in the body for many weeks.

Thrombocytopenia develops in 5% of patients receiving unfractionated heparin, which can occur even when very low doses of heparin are given (for example, during arterial or venous catheter). The mechanism is usually immune. Bleeding may occur, but more often platelets form aggregates that cause vascular occlusion with the development of paradoxical arterial and venous thrombosis, sometimes life-threatening (for example, thrombotic occlusion of arterial vessels, stroke, acute heart attack myocardium). Heparin should be discontinued in all patients who develop thrombocytopenia or a decrease in platelet count by more than 50%. Since 5 days of heparin is sufficient to treat venous thrombosis, and most patients begin taking oral anticoagulants at the same time as taking heparin, heparin withdrawal is usually safe. Low molecular weight heparin(LMWH) is less immunogenic than unfractionated heparin. However, LMWH is not used for heparin-induced thrombocytopenia, since most antibodies have cross interaction with LMWH.

Gram-negative sepsis

Gram-negative sepsis often causes nonimmune thrombocytopenia, which corresponds to the severity of the infection. Thrombocytopenia can be caused by many factors: disseminated intravascular coagulation, the formation of immune complexes that can interact with platelets, complement activation, and platelet deposition on damaged endothelial surfaces.

HIV infection

Patients infected with HIV may develop immune thrombocytopenia, similar to ITP, except in association with HIV. The platelet count can be raised by administering glucocorticoids, which are often withheld until the platelet count drops below 1/µL, as these drugs can further reduce immunity. The platelet count also usually increases after the use of antiviral drugs.

Pathogenesis of thrombocytopenia

The pathogenesis of thrombocytopenia lies either in the pathology of the hematopoietic system and a decrease in platelet production by myeloid cells of the bone marrow (megakaryocytes), or in impaired hemodieresis and increased destruction of platelets (phagocytosis), or in sequestration pathologies and platelet retention in the spleen.

IN bone marrow healthy people An average of platelets are produced daily, but not all of them circulate in the systemic circulation: reserve platelets are stored in the spleen and released when needed.

When the examination of the patient does not reveal diseases that caused a decrease in platelet levels, a diagnosis of thrombocytopenia is made unknown origin or idiopathic thrombocytopenia. But this does not mean that the pathology arose “just like that.”

Thrombocytopenia, associated with a decrease in platelet production, develops with a lack of vitamins B12 and B9 (folic acid) in the body and aplastic anemia.

Leukopenia and thrombocytopenia are combined with impaired bone marrow function associated with acute leukemia, lymphosarcoma, and cancer metastases from other organs. Suppression of platelet production may be due to changes in the structure of hematopoietic stem cells in the bone marrow (the so-called myelodysplastic syndrome), congenital hypoplasia of hematopoiesis (Fanconi syndrome), megakaryocytosis or myelofibrosis of the bone marrow.

Symptoms of thrombocytopenia

Platelet disorders lead to a typical bleeding pattern of multiple petechiae on the skin, usually in to a greater extent on foot; scattered small ecchymoses in places of minor injuries; bleeding of mucous membranes (nosebleeds, bleeding in the gastrointestinal tract and genitourinary tract; vaginal bleeding), severe bleeding after surgical interventions. Severe bleeding in the gastrointestinal tract and central nervous system can be life-threatening. However, manifestations of significant tissue bleeding (eg, deep visceral hematoma or hemarthrosis) are atypical for platelet pathology and suggest the presence of disorders of secondary hemostasis (eg, hemophilia).

Autoimmune thrombocytopenia

The pathogenesis of increased platelet destruction is divided into immune and non-immune. And the most common is autoimmune thrombocytopenia. The list of immune pathologies in which it manifests itself includes: idiopathic thrombocytopenia (immune thrombocytopenic purpura or Werlhof's disease), systemic lupus erythematosus, Sharpe's or Sjögren's syndromes, antiphospholipid syndrome, etc. All these conditions are united by the fact that the body produces antibodies that attack its own healthy cells, including platelets.

It should be borne in mind that when antibodies from a pregnant woman with immune thrombocytopenic purpura enter the bloodstream of the fetus, transient thrombocytopenia is detected in the child during the neonatal period.

According to some reports, antibodies against platelets (their membrane glycoproteins) can be detected in almost 60% of cases. The antibodies have immunoglobulin G (IgG), and as a consequence, platelets become more vulnerable to increased phagocytosis by splenic macrophages.

Congenital thrombocytopenia

Many deviations from the norm and their result - chronic thrombocytopenia - have a genetic pathogenesis. The protein thrombopoietin, synthesized in the liver, encoded on chromosome 3p27, stimulates megakaryocytes, and is responsible for the effect of thrombopoietin on a specific receptor protein encoded by the C-MPL gene.

It is assumed that congenital thrombocytopenia (in particular, amegakaryocytic thrombocytopenia), as well as hereditary thrombocytopenia (with familial aplastic anemia, Wiskott-Aldrich syndrome, May-Hegglin syndrome, etc.) is associated with a mutation of one of these genes. For example, an inherited mutant gene produces persistently activated thrombopoietin receptors, which causes overproduction of abnormal megakaryocytes that are unable to produce sufficient platelets.

The average lifespan of circulating platelets is 7-10 days; cell cycle is regulated by the antiapoptotic membrane protein BCL-XL, which is encoded by the BCL2L1 gene. In principle, the function of BCL-XL is to protect cells from damage and induced apoptosis (death), but it turns out that when the gene is mutated, it acts as an activator of apoptotic processes. Therefore, platelet destruction may occur faster than platelet formation.

But hereditary disaggregation thrombocytopenia, characteristic of hemorrhagic diathesis(Glanzmann thrombasthenia) and Bernard-Soulier syndrome, has a slightly different pathogenesis. Due to a gene defect, thrombocytopenia is observed in children early age, associated with a violation of the structure of platelets, which deprives them of the ability to “stick together” to form a blood clot, necessary to stop bleeding. In addition, such defective platelets are rapidly utilized in the spleen.

Secondary thrombocytopenia

By the way, about the spleen. Splenomegaly - an increase in the size of the spleen - develops for various reasons (due to liver pathologies, infections, hemolytic anemia, obstruction of the hepatic vein, infiltration of tumor cells in leukemia and lymphomas, etc.), and this leads to the fact that it can retain up to a third of the total platelet mass. As a result, it happens chronic disorder blood system, which is diagnosed as symptomatic or secondary thrombocytopenia. When this organ is enlarged, in many cases splenectomy is indicated for thrombocytopenia or, simply put, removal of the spleen for thrombocytopenia.

Chronic thrombocytopenia can also develop due to hypersplenic syndrome, which means hyperfunction of the spleen, as well as premature and too rapid destruction of blood cells by its phagocytes. Hypersplenism is secondary in nature and most often occurs due to malaria, tuberculosis, rheumatoid arthritis or tumor. So, in fact, secondary thrombocytopenia becomes a complication of these diseases.

Secondary thrombocytopenia is associated with bacterial or systemic viral infection: Epstein-Barr virus, HIV, cytomegavirus, parvovirus, hepatitis, varicella-zoster virus (the causative agent of chickenpox), or rubivirus (which causes rubella measles).

When affecting the body (directly on the bone marrow and its myeloid cells) ionizing radiation and use large quantity alcohol, secondary acute thrombocytopenia may develop.

Thrombocytopenia in children

According to studies, in the second trimester of pregnancy the level of platelets in the fetus exceeds 150 thousand/μl. Thrombocytopenia in newborns is present after 1-5% of births, and severe thrombocytopenia (when platelets are less than 50 thousand / μl) occurs in 0.1-0.5% of cases. At the same time, a significant proportion of infants with this pathology are born prematurely or have had placental insufficiency or fetal hypoxia. In 15-20% of newborns, thrombocytopenia is alloimmune - as a result of receiving antibodies to platelets from the mother.

Neonatologists consider other causes of thrombocytopenia to be genetic defects of bone marrow megakaryocytes, congenital autoimmune pathologies, the presence of infections, as well as DIC syndrome(disseminated intravascular coagulation).

Most cases of thrombocytopenia in older children are symptomatic, and possible pathogens include fungi, bacteria, and viruses, such as cytomegalovirus, toxoplasma, rubella, or measles. Acute thrombocytopenia occurs especially often with a fungal or gram-negative bacterial infection.

Vaccinations for thrombocytopenia in children are given with caution, and in severe forms of the pathology, preventive vaccination by injection and cutaneous applications (with skin scarification) may be contraindicated.

Thrombocytopenia during pregnancy

Thrombocytopenia during pregnancy can have many causes. However, it must be taken into account that the average platelet count during pregnancy decreases (up to 215 thousand / μl), and this is normal.

Firstly, in pregnant women, a change in the number of platelets is associated with hypervolemia - a physiological increase in blood volume (on average by 45%). Secondly, platelet consumption during this period is increased, and bone marrow megakaryocytes produce not only platelets, but also significantly more thromboxane A2, which is necessary for platelet aggregation during blood coagulation (clotting).

In addition, in the α-granules of pregnant platelets, the dimeric glycoprotene PDGF, a platelet-derived growth factor, is intensively synthesized, which regulates cell growth, division and differentiation, and also plays a critical role in the formation blood vessels(including the fetus).

As obstetricians note, asymptomatic thrombocytopenia is observed in approximately 5% of pregnant women during normal gestation; in 65-70% of cases, thrombocytopenia of unknown origin occurs. 7.6% of pregnant women experience a moderate degree of thrombocytopenia, and 15-21% of women with preeclampsia and gestosis develop severe thrombocytopenia during pregnancy.

Purpura and other hemorrhagic conditions (ICD code D69)

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 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

D69.4 Other primary thrombocytopenias

Excluded: thrombocytopenia with absence 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

Thrombocytopenia: symptoms and treatment

Thrombocytopenia - main symptoms:

• Red spots on the skin
• Enlarged lymph nodes
• Fever
• Enlarged lymph nodes in the neck
• Minor hemorrhages on the skin and mucous membranes
• Blue spots on the skin

A disease that causes a decrease in the number of platelets in the blood is called thrombocytopenia. This is exactly what the article will talk about. Platelets are small blood cells that have no color and are significant components involved in blood clotting. The disease is quite serious, since the disease can lead to hemorrhage in the internal organs(especially in the brain), and this is a fatal ending.

Classification

Like most medical diseases, thrombocytopenia has its own classification, which is formed on the basis of pathogenetic factors, causes, symptoms and various manifestations.

According to the criterion of etiology, two types of disease are distinguished:

They are characterized by the fact that the primary type manifests itself as an independent illness, and the secondary type is provoked by a number of other diseases or pathological abnormalities.

According to the duration of the disease in the human body, there are two types of malaise: acute and chronic. Acute - characterized by a short duration of impact on the body (up to six months), but manifested by immediate symptoms. The chronic form is characterized by a prolonged decrease in platelets in the blood (over six months). Exactly chronic form is more dangerous as treatment takes up to two years.

According to the criteria for the severity of the disease, characterized by the quantitative composition of platelets in the blood, three degrees are distinguished:

• I - composition is 150–50x10 9 /l - the severity criterion is satisfactory;
• II - 50–20x10 9 /l - reduced composition, which manifests itself with minor damage to the skin;
• III - 20x10 9 /l - characterized by the appearance of internal bleeding in the body.

The norm of blood cells in the body is equal to 0.00/µl. But precisely in female body these indicators are constantly changing. The changes are influenced by the following factors:

Platelets appear in the body from the bone marrow, which synthesizes blood cells by stimulating megakaryocytes. The synthesized blood plates circulate through the blood for seven days, after which the process of their stimulation is repeated.

According to the International Classification of Diseases of the Tenth Convocation (ICD-10), this disease has its own codes:

• D50-D89 - diseases circulatory system and other types of deficiency.
• D65-D69 - blood clotting disorders.

Causes

Often the cause of the disease is allergic reaction body to various medical supplies As a result, drug-induced thrombocytopenia is observed. With such ailment, the body produces antibodies directed against the drug. Medicines that affect the occurrence of blood cell insufficiency include sedatives, alkaloids and antibacterial agents.

The causes of deficiency may also be problems with the immune system caused by the consequences of blood transfusions.

The disease manifests itself especially often when blood groups do not match. Autoimmune thrombocytopenia is most often observed in the human body. In this case, the immune system is unable to recognize its platelets and rejects them from the body. As a result of rejection, antibodies are produced to remove foreign cells. The causes of such thrombocytopenia are:

1. Pathological kidney failure and chronic hepatitis.
2. Lupus, dermatomyositis and scleroderma.
3. Leukemic diseases.

If the disease has a pronounced form of an isolated disease, then it is called idiopathic thrombocytopenia or Werlhof’s disease (ICD-10 code: D69.3). The etiology of idiopathic thrombocytopenic purpura (ICD-10:D63.6) remains unclear, but medical scientists are inclined to believe that the cause is a hereditary predisposition.

The manifestation of the disease is also typical in the presence of congenital immunodeficiency. Such people are most susceptible to the factors causing the disease, and the reasons for this are:

• damage to the red bone marrow from exposure to drugs;
• immunodeficiency leads to damage to megakaryocytes.

There is a productive nature of the disease, which is caused by insufficient production of platelets by the bone marrow. In this case, their insufficiency occurs, which ultimately develops into malaise. The causes are considered to be myelosclerosis, metastases, anemia, etc.

A lack of platelets in the body is observed in people with a reduced composition of vitamin B12 and folic acid. Excessive radioactive or radiation exposure to cause blood cell deficiency cannot be ruled out.

Thus, two types of causes influencing the occurrence of thrombocytopenia can be distinguished:

1. Leading to the destruction of blood cells: idiopathic thrombocytopenic purpura, autoimmune disorders, surgical interventions on the heart, clinical circulatory disorders in pregnant women and side effects of medications.
2. Contributing to a decrease in the production of antibodies by the bone marrow: viral influences, metastatic manifestations, chemotherapy and radiation, as well as excessive alcohol consumption.

Symptoms

Symptoms of thrombocytopenia disease include: different kinds manifestations. It depends:

• firstly, from the cause of occurrence;
• secondly, on the nature of the disease (chronic or acute).

The main signs of damage to the body are manifestations on the skin in the form of hemorrhages and bleeding. Hemorrhages are most often observed on the limbs and torso. Damage to a person’s face and lips is possible. To illustrate the manifestation of hemorrhages on the human body, the photo below is presented.

Thrombocytopenia is characterized by symptoms of prolonged hemorrhages after tooth extraction. Moreover, the duration of hemorrhage can be either one-day or accompanied for several days. It depends on the extent of the disease.

With symptoms, there is no increase in liver size, but very often doctors observe enlargement lymph nodes cervical region. This phenomenon is often accompanied by an increase in body temperature to subfebrile levels (from 37.1 to 38 degrees). An increase in the rate of red blood cell accumulation in the body is evidence of the presence of a disease called lupus erythematosus.

Symptoms of platelet deficiency are quite easily observed after taking blood for analysis. The quantitative composition will differ significantly from the maximum standards. When the number of platelets in the blood decreases, their size increases. This is reflected on the skin as the appearance of red and bluish spots, which indicates the transformation of blood cells. There is also destruction of red blood cells, which leads to a decrease in the quantitative composition, but at the same time the number of reticulocytes increases. There is a displacement phenomenon leukocyte formula to the left.

The human body with a reduced composition of blood cells is characterized by an increase in the composition of megakaryocytes, which is caused by frequent and extensive bleeding. The duration of blood clotting is noticeably increased, and the reduction in clotting of blood released from the wound is reduced.

According to the symptoms of the disease, three degrees of complications are distinguished: mild, moderate and severe.

Mild degrees are typical causes of the disease in women with prolonged and heavy menstruation, as well as with intradermal bleeding and nasal hemorrhages. But at the stage mild degree diagnosing the disease is extremely difficult, so the presence of the disease can only be confirmed after a detailed medical examination.

The average degree is characterized by the appearance of a hemorrhagic rash throughout the body, which consists of numerous pinpoint hemorrhages under the skin and on the mucous membrane.

Severe disorders are typical gastrointestinal tract caused by hemorrhages. The platelet count in the blood is up to 25x10 9 /l.

Symptoms of secondary thrombocytopenia have similar features.

Pregnancy and illness: symptoms

Thrombocytopenia in pregnant women is characterized by significant changes in the quantitative composition of cells in the blood of women. If there is no diagnosis of the disease in pregnant women, but the platelet composition indicator decreases slightly, this indicates that their vital activity is decreasing and their participation in the periphery of the blood circulation is increasing.

If there is a reduced composition of platelets in the blood of a pregnant woman, then these are direct prerequisites for the development of the disease. The reasons for the reduced number of platelets are the high rates of death of these bodies and low rates of formation of new ones. Clinical signs are characterized by subcutaneous hemorrhages. The causes of insufficiency of colorless cells are incorrect composition and nutritional standards or a small amount of food consumption, as well as damage to the immune system and various blood losses. Through this process, the corpuscles are produced by the bone marrow in small quantities or have an irregular shape.

Thrombocytopenia during pregnancy is very dangerous, so the issue of diagnosis, and especially treatment, is given maximum attention. The danger is that a lack of platelets in the mother’s blood during pregnancy contributes to hemorrhage in the child. The most dangerous hemorrhage in the womb is cerebral, the result of which is characterized by fatal consequences for the fetus. At the first sign of such a factor, the doctor makes a decision about premature birth in order to eliminate the consequences.

Childhood thrombocytopenia: symptoms

Thrombocytopenia in children is quite rare. The risk group includes school-age children, whose incidence is more common in winter and spring.

Thrombocytopenia and its symptoms in children are practically no different from adults, but it is important for parents to early stages development of the disease, diagnose it based on the first signs. Children's symptoms include frequent bleeding from the nasal cavity and the occurrence of small rash on the body. The rash initially appears on lower limbs body, and then they can be observed on the hands. With minor bruises, swelling and hematomas occur. Such signs most often do not cause concern to parents, due to the absence pain symptoms. This is an important mistake, because any disease in its advanced form is dangerous.

Bleeding gums indicate a lack of platelets in the blood in both children and adults. In this case, feces in a sick person, and more often in children, are excreted together with blood clots. Hemorrhage due to urination cannot be ruled out.

Depending on the degree of impact of the disease on the immune system, a distinction is made between immune and non-immune platelet deficiency. Immune thrombocytopenia caused by massive death of blood cells under the influence of antibodies. In such a situation there is no difference immune system own blood cells and are rejected from the body. Non-immune disease manifests itself through physical impact on blood platelets.

Diagnostics

A person should be diagnosed at the first signs and symptoms of the disease. The main method of diagnosis is a clinical blood test, the results of which show a picture of the quantitative composition of platelets.

If a deviation in the number of blood cells in the body is detected, an indication is given for a bone marrow examination. Thus, the presence of megakaryocytes is determined. If they are absent, then thrombus formation is impaired, and their presence indicates the destruction of platelets or their deposition in the spleen.

The causes of deficiency are diagnosed using:

• genetic tests;
• electrocardiograms;
• tests for the presence of antibodies;
• ultrasound examinations;
• X-ray and endoscopy.

Thrombocytopenia during pregnancy is diagnosed using a coagulogram, or in simple words speaking, a blood clotting test. This analysis allows you to accurately determine the composition of platelets in the blood. The course of the birth process depends on the number of platelets.

Treatment

Treatment of thrombocytopenia begins with therapy, in which a drug called Prednisolone is prescribed in the hospital.

Important! Treatment methods are prescribed strictly by the attending physician only after undergoing an appropriate examination and diagnosing the disease.

The dosage of the medication is indicated in the instructions, according to which 1 ml of the drug is taken per 1 kg of body weight. As the disease progresses, the dose increases by 1.5–2 times. In the initial stages, the ailment is characterized by a quick and effective recovery, so after taking the drug, you can notice an improvement in health within a few days. The drug continues until the person is completely cured, which must be confirmed by the attending physician.

The effect of glucocorticosteroids has a positive effect on the fight against malaise, but in most cases only the symptoms disappear, and the disease remains. Used to treat deficiency in children and adolescents.

Treatment of idiopathic chronic thrombocytopenia is carried out by removing the spleen. This procedure in medicine is called splenectomy and is characterized by its positive effects. In advance of surgery, the dosage of Prednisolone is increased threefold. Moreover, it is injected not into a muscle, but directly into a human vein. After splenectomy, administration of the drug in the same doses continues for up to two years. Only after the specified period has passed is an examination and certification of the success of the splenectomy performed.

If the removal operation is unsuccessful, the patient is prescribed immunosuppressive chemotherapy with cytostatics. These drugs include: Azathioprine and Vincristine.

When an acquired deficiency of a non-immune nature is diagnosed, thrombocytopenia is treated symptomatically by taking estrogens, progestins and androxons.

More severe forms idiopathic thrombocytopenia is caused by excessive hemorrhages. A transfusion is performed to restore blood. Treatment of severe cases requires discontinuation of medications that may negatively affect the ability of platelets to form clots.

After diagnosing the disease, the patient is registered and an examination procedure takes place not only of the patient, but also of his relatives to collect a hereditary history.

In children, the malaise can be treated well and without complications, but in some cases the possibility of symptomatic therapy cannot be ruled out.

Treatment of thrombocytopenia with traditional medicine also has its considerable achievements. First of all, to get rid of the problem of platelet deficiency in the blood, you should include honey and walnuts in your diet. Decoctions of nettle and rosehip leaves also help well. For preventive measures Birch, raspberry or beet juice is used.

If you think that you have Thrombocytopenia and the symptoms characteristic of this disease, then a hematologist can help you.

We also suggest using our online disease diagnostic service, which selects probable diseases based on the entered symptoms.

IDIOPATHIC THROMBOCYTOPENIC PURPURA ICD-10 CODE;

DIAMOND-BLACKFAN ANEMIA ICD-10 CODE

D61. Other aplastic anemias. Types of AA:

Congenital [Fanconi anemia (FA), Diamond-Blackfan anemia (DBA), dyskeratosis congenita, Shwachman-Diamond-Oski anemia, amegakaryocyte thrombocytopenia];

Acquired (idiopathic, caused by viruses, drugs or chemicals).

AA occurs with a frequency of 1-2 cases per 1,000,000 population per year and is considered a rare blood disease. Acquired AA develops with a frequency of 0.2-0.6 cases per year. The average annual incidence rate of AA in children in the period from 1979 to 1992 in the Republic of Belarus was 0.43±0.04 children. There were no differences in the incidence of AA in children before and after the Chernobyl disaster.

DBA is described under many names; partial red cell aplasia, congenital hypoplastic anemia, true erythrocyte anemia, primary red cell disease, erythrogenesis imperfecta. The disease is rare, L.K. Diamond et al. in the 60s XX century described only 30 cases of this disease; to date, more than 400 cases have been described.

For a long time, it was believed that the incidence of DBA was 1 case per living newborn. In 1992, L. Wranne reported a higher incidence of 10 cases in newborns. The incidence rate of DBA according to the French and English registries is 5-7 cases per living newborn. The gender ratio is almost the same. More than 75% of DBA cases are sporadic; 25% are familial in nature, and in some families several patients are registered. The registry of patients with DBA in the USA and Canada includes 264 patients aged from 10 months to 44 years.

D61.0. Constitutional aplastic anemia.

FA is a rare autosomal recessive disorder characterized by multiple congenital physical anomalies, progressive bone marrow failure, and a predisposition to the development of malignancies. The incidence of AF is 1 case per 000 000 population. The disease is common among all nationalities and ethnic groups. Minimum age of manifestation clinical signs- neonatal period™, maximum - 48 years. The register of patients with AF of the Research Institute of Pediatric Hematology of the Ministry of Health of the Russian Federation recorded the data of 69 patients. The average age of manifestation of the disease is 7 years (2.5-12.5 years). 5 familial cases were identified.

HEMORRHAGIC DISEASES Purpura and other hemorrhagic conditions

D69.3. Idiopathic thrombocytopenic purpura.

Idiopathic thrombocytopenic purpura (ITP), according to many hematologists, is a common hemorrhagic disease. However, the only study in our country shows that the incidence rate of ITP in the Chelyabinsk region is 3.82 ± 1.38 cases per year and does not have an increasing trend.

Thrombocytopenia

Thrombocytopenia: Brief description

Thrombocytopenia is a low platelet count in the peripheral blood, most common reason bleeding. When the platelet count decreases to less than 100´ 109/l, the bleeding time lengthens. In most cases, petechiae or purpura appear when the platelet count drops to 20–50´ 109/l. Serious spontaneous bleeding (eg, gastrointestinal) or hemorrhagic stroke occurs with thrombocytopenia less than 10´ 109/L.

Thrombocytopenia: Causes

Etiology and pathogenesis

Thrombocytopenia can occur as a manifestation of drug allergies (allergic thrombocytopenia), caused by the production of antiplatelet antibodies (autoimmune thrombocytopenia), caused by infections, intoxications, thyrotoxicosis (symptomatic).

In newborns, thrombocytopenia can be caused by the penetration of autoantibodies of a sick mother through the placenta (transimmune thrombocytopenia).

Pathology of thrombocytopoiesis Maturation of megakaryocytes is selectively suppressed by thiazide diuretics and other drugs, especially those used in chemotherapy, ethanol Special reason thrombocytopenia - ineffective thrombopoiesis associated with the megaloblastic type of hematopoiesis (occurs with a deficiency of vitamin B12 and folic acid, as well as with myelodysplastic and preleukemic syndromes). Morphologically and functionally abnormal (megaloblastic or dysplastic) megakaryocytes are identified in the bone marrow, giving rise to a pool of defective platelets that are destroyed in the bone marrow. Amegakaryocyte thrombocytopenia is a rare cause of thrombocytopenia caused by a congenital deficiency of megakaryocyte colony-forming units.

Anomalies in the formation of the platelet pool occur when platelets are eliminated from the bloodstream; the most common cause is deposition in the spleen. Under normal conditions, the spleen contains a third of the platelet pool. The development of splenomegaly is accompanied by the deposition of a larger number of cells with their exclusion from the hemostasis system. With a very large size of the spleen, it is possible to deposit 90% of the total platelet pool. The remaining 10% in the peripheral bloodstream has a normal circulation duration.

Increased destruction of platelets in the periphery is the most common form of thrombocytopenia; Such conditions are characterized by a shortened platelet lifespan and an increased number of bone marrow megakaryocytes. These disorders are referred to as immune or non-immune thrombocytopenic purpura Immune thrombocytopenic purpura Idiopathic thrombocytopenic purpura (ITP) - the prototype of thrombocytopenia due to immune mechanisms (no obvious external reasons destruction of platelets). See Idiopathic thrombocytopenic purpura Other autoimmune thrombocytopenias caused by the synthesis of antiplatelet antibodies: post-transfusion thrombocytopenia (associated with exposure to isoantibodies), drug-induced thrombocytopenia (for example, caused by quinidine), thrombocytopenia caused by sepsis (the incidence can reach 70%), thrombocytopenia in combination with SLE and other autoimmune diseases. Treatment is aimed at correcting the underlying pathology. It is necessary to stop taking all potentially dangerous drugs. GK therapy is not always effective. Transfused platelets undergo the same accelerated destruction Non-immune thrombocytopenic purpura Infections (eg, viral or malaria) Massive transfusion of preserved blood with low platelet content DIC Prosthetic heart valves Thrombotic thrombocytopenic purpura.

Genetic aspects

Thrombocytopenia (*188000, Â). Clinical manifestations: macrothrombocytopenia, hemorrhagic syndrome, rib aplasia, hydronephrosis, recurrent hematuria. Laboratory research: autoantibodies to platelets, shortened platelet life, increased clotting time, normal tourniquet test, defects in the plasma component of hemostasis.

May–Hegglin anomaly (Hegglin syndrome, B). Macrothrombocytopenia, basophilic inclusions in neutrophils and eosinophils (Döhle bodies).

Epstein syndrome (153650, Â). Macrothrombocytopenia in combination with Allport syndrome.

Fechtner family syndrome (153640, Â). Macrothrombocytopenia, inclusions in leukocytes, nephritis, deafness.

Congenital thrombocytopenia (600588, deletion 11q23. 3-qter, Â). Clinical manifestations: congenital dysmegakaryocyte thrombocytopenia, mild hemorrhagic syndrome. Laboratory studies: 11q23 deletion. 3– qter, increased number of megakaryocytes, giant granules in peripheral blood platelets.

Cyclic thrombocytopenia (188020, Â). Hemorrhagic syndrome, cyclic neutropenia.

Thrombocytopenia Paris–Trousseau (188025, deletion 11q23, defect of the TCPT gene, Â). Clinical manifestations: hemorrhagic syndrome, thrombocytopenia, hypertelorism, ear abnormalities, mental retardation, coarctation of the aorta, developmental delay in the embryonic period, hepatomegaly, syndactyly. Laboratory studies: giant granules in platelets, megakaryocytosis, micromegakaryocytes.

TAR syndrome (from: thrombocytopenia–absentradius - thrombocytopenia and absence of the radius, *270400, r). Congenital absence of the radius in combination with thrombocytopenia (pronounced in children, later smoothed out); thrombocytopenic purpura; in the red bone marrow there are defective megakaryocytes; Anomalies of kidney development and congenital heart disease are sometimes noted.

Thrombocytopenia: Signs, Symptoms

Clinical picture

Thrombocytopenia: Diagnosis

Diagnostics

Thrombocytopenia: Treatment Methods

Treatment

Pathology of thrombocytopoiesis. Treatment is based on eliminating the offending agent, if possible, or treating the underlying disease; The half-life of platelets is usually normal, allowing platelet transfusions in the presence of thrombocytopenia and signs of bleeding. Thrombocytopenia caused by deficiency of vitamin B12 or folic acid disappears when their normal levels are restored.

Amegakaryocytic thrombocytopenia responds well to treatment; antithymocyte immunoglobulin and cyclosporine are usually prescribed.

Anomalies in the formation of the platelet pool. There is usually no treatment, although splenectomy may resolve the problem. During transfusions, some platelets are deposited, making transfusions less effective than in states of reduced bone marrow activity.

Treatment of idiopathic thrombocytopenic purpura - see Idiopathic thrombocytopenic purpura.

Complications and associated conditions Decreased platelet production is combined with aplastic anemia, myelophthisis (replacement of bone marrow with tumor cells or fibrous tissue) and some rare congenital syndromes: Evans syndrome (Fisher–Evans syndrome) - a combination of autoimmune hemolytic anemia and autoimmune thrombocytopenia.

ICD-10 D69 Purpura and other hemorrhagic conditions

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A disease that causes a decrease in the number of platelets in the blood is called thrombocytopenia. This is exactly what the article will talk about. Platelets are small blood cells that have no color and are significant components involved in blood clotting. The disease is quite serious, since the disease can lead to hemorrhage in the internal organs (especially in the brain), and this is fatal.

Classification

Like most medical diseases, thrombocytopenia has its own classification, which is formed on the basis of pathogenetic factors, causes, symptoms and various manifestations.

According to the criterion of etiology, two types of disease are distinguished:

• primary;
• secondary.

They are characterized by the fact that the primary type manifests itself as an independent illness, and the secondary type is provoked by a number of other diseases or pathological abnormalities.

According to the duration of the disease in the human body, there are two types of malaise: acute and chronic. Acute - characterized by a short duration of impact on the body (up to six months), but manifested by immediate symptoms. The chronic form is characterized by a prolonged decrease in platelets in the blood (over six months). It is the chronic type that is more dangerous, since treatment takes up to two years.

According to the criteria for the severity of the disease, characterized by the quantitative composition of platelets in the blood, three degrees are distinguished:

• I - composition is 150–50x10 9 /l - the severity criterion is satisfactory;
• II - 50–20x10 9 /l - reduced composition, which manifests itself with minor damage to the skin;
• III - 20x10 9 /l - characterized by the appearance of internal bleeding in the body.

The norm of blood cells in the body is from 140,000 to 440,000/μl. But it is in the female body that these indicators are constantly changing. The changes are influenced by the following factors:

• menstruation;
• pregnancy;
• complications after pregnancy.

Platelets appear in the body from the bone marrow, which synthesizes blood cells by stimulating megakaryocytes. The synthesized blood plates circulate through the blood for seven days, after which the process of their stimulation is repeated.

According to International Classification of Diseases tenth convocation (ICD-10), this disease has its own codes:

• D50-D89 - diseases of the circulatory system and other types of insufficiency.
• D65-D69 - blood clotting disorders.

Causes

Often the cause of the disease is an allergic reaction of the body to various medications, resulting in drug-induced thrombocytopenia. With such ailment, the body produces antibodies directed against the drug. Medicines that affect the occurrence of blood cell insufficiency include sedatives, alkaloids and antibacterial agents.

The causes of deficiency may also be problems with the immune system caused by the consequences of blood transfusions.

The disease manifests itself especially often when blood groups do not match. Autoimmune thrombocytopenia is most often observed in the human body. In this case, the immune system is unable to recognize its platelets and rejects them from the body. As a result of rejection, antibodies are produced to remove foreign cells. The causes of such thrombocytopenia are:

1. Pathological kidney failure and chronic hepatitis.
2. Lupus, dermatomyositis and scleroderma.
3. Leukemic diseases.

If the disease has a pronounced form of an isolated disease, then it is called idiopathic thrombocytopenia or Werlhof’s disease (ICD-10 code: D69.3). The etiology of idiopathic thrombocytopenic purpura (ICD-10:D63.6) remains unclear, but medical scientists are inclined to believe that the cause is a hereditary predisposition.

The manifestation of the disease is also typical in the presence of congenital immunodeficiency. Such people are most susceptible to the factors causing the disease, and the reasons for this are:

• damage to the red bone marrow from exposure to drugs;
• immunodeficiency leads to damage to megakaryocytes.

There is a productive nature of the disease, which is caused by insufficient production of platelets by the bone marrow. In this case, their insufficiency occurs, which ultimately develops into malaise. The causes are considered to be myelosclerosis, metastases, anemia, etc.

A lack of platelets in the body is observed in people with a reduced composition of vitamin B12 and folic acid. Excessive radioactive or radiation exposure to cause blood cell deficiency cannot be ruled out.

Thus, two types of causes influencing the occurrence of thrombocytopenia can be distinguished:

1. Leading to the destruction of blood cells: idiopathic thrombocytopenic purpura, autoimmune disorders, cardiac surgery, clinical circulatory disorders in pregnant women and side effects of drugs.
2. Contributing to a decrease in the production of antibodies by the bone marrow: viral influences, metastatic manifestations, chemotherapy and radiation, as well as excessive alcohol consumption.

Symptoms

Symptoms of thrombocytopenia disease have different types of manifestations. It depends:

• firstly, from the cause of occurrence;
• secondly, on the nature of the disease (chronic or acute).

The main signs of damage to the body are manifestations on the skin in the form of hemorrhages and bleeding. Hemorrhages are most often observed on the limbs and torso. Damage to a person’s face and lips is possible. To illustrate the manifestation of hemorrhages on the human body, the photo below is presented.

Thrombocytopenia is characterized by symptoms of prolonged hemorrhages after tooth extraction. Moreover, the duration of hemorrhage can be either one-day or accompanied for several days. It depends on the extent of the disease.

With symptoms, there is no increase in the size of the liver, but very often doctors observe an enlargement of the lymph nodes of the cervical region. This phenomenon is often accompanied by an increase in body temperature to subfebrile levels (from 37.1 to 38 degrees). An increase in the rate of red blood cell accumulation in the body is evidence of the presence of a disease called lupus erythematosus.

Symptoms of platelet deficiency are quite easily observed after taking blood for analysis. The quantitative composition will differ significantly from the maximum standards. When the number of platelets in the blood decreases, their size increases. This is reflected on the skin as the appearance of red and bluish spots, which indicates the transformation of blood cells. There is also destruction of red blood cells, which leads to a decrease in the quantitative composition, but at the same time the number of reticulocytes increases. There is a phenomenon of a shift in the leukocyte formula to the left.

The human body with a reduced composition of blood cells is characterized by an increase in the composition of megakaryocytes, which is caused by frequent and extensive bleeding. The duration of blood clotting is noticeably increased, and the reduction in clotting of blood released from the wound is reduced.

According to the symptoms of the disease, three degrees of complications are distinguished: mild, moderate and severe.

Mild degrees are typical causes of the disease in women with prolonged and heavy menstruation, as well as with intradermal bleeding and nasal hemorrhages. But at the mild stage, diagnosing the disease is extremely difficult, so the presence of the disease can be confirmed only after a detailed medical examination.

The average degree is characterized by the appearance of a hemorrhagic rash throughout the body, which consists of numerous pinpoint hemorrhages under the skin and on the mucous membrane.

Severe grades are characterized by gastrointestinal disorders caused by hemorrhages. The platelet count in the blood is up to 25x10 9 /l.

Symptoms of secondary thrombocytopenia have similar features.

Pregnancy and illness: symptoms

Thrombocytopenia in pregnant women is characterized by significant changes in the quantitative composition of cells in the blood of women. If there is no diagnosis of the disease in pregnant women, but the platelet composition indicator decreases slightly, this indicates that their vital activity is decreasing and their participation in the periphery of the blood circulation is increasing.

If there is a reduced composition of platelets in the blood of a pregnant woman, then these are direct prerequisites for the development of the disease. The reasons for the reduced number of platelets are the high rates of death of these bodies and low rates of formation of new ones. Clinical signs are characterized by subcutaneous hemorrhages. The causes of insufficiency of colorless cells are incorrect composition and nutritional standards or a small amount of food consumption, as well as damage to the immune system and various blood losses. Through this process, the corpuscles are produced by the bone marrow in small quantities or have an irregular shape.

Thrombocytopenia during pregnancy is very dangerous, so the issue of diagnosis, and especially treatment, is given maximum attention. The danger is that a lack of platelets in the mother’s blood during pregnancy contributes to hemorrhage in the child. The most dangerous hemorrhage in the womb is cerebral, the result of which is characterized by fatal consequences for the fetus. At the first sign of such a factor, the doctor makes a decision about premature birth in order to eliminate the consequences.

Childhood thrombocytopenia: symptoms

Thrombocytopenia in children is quite rare. The risk group includes school-age children, whose incidence is more common in winter and spring.

Thrombocytopenia and its symptoms in children are practically no different from adults, but it is important for parents to diagnose it based on the first signs in the early stages of development of the disease. Children's symptoms include frequent bleeding from the nasal cavity and the appearance of small rashes on the body. Initially, the rash appears on the lower extremities of the body, and then they can be observed on the arms. With minor bruises, swelling and hematomas occur. Such signs most often do not cause concern to parents, due to the absence of pain symptoms. This is an important mistake, because any disease in its advanced form is dangerous.

Bleeding gums indicate a lack of platelets in the blood in both children and adults. In this case, feces in a sick person, and more often in children, are excreted together with blood clots. Hemorrhage due to urination cannot be ruled out.

Depending on the degree of impact of the disease on the immune system, a distinction is made between immune and non-immune platelet deficiency. Immune thrombocytopenia is caused by massive death of blood cells under the influence of antibodies. In such a situation, the immune system’s own blood cells are not recognized and are rejected from the body. Non-immune disease manifests itself through physical impact on blood platelets.

Diagnostics

A person should be diagnosed at the first signs and symptoms of the disease. The main method of diagnosis is a clinical blood test, the results of which show a picture of the quantitative composition of platelets.

If a deviation in the number of blood cells in the body is detected, an indication is given for a bone marrow examination. Thus, the presence of megakaryocytes is determined. If they are absent, then thrombus formation is impaired, and their presence indicates the destruction of platelets or their deposition in the spleen.

The causes of deficiency are diagnosed using:

• genetic tests;
• electrocardiograms;
• tests for the presence of antibodies;
• ultrasound examinations;
• X-ray and endoscopy.

Thrombocytopenia during pregnancy is diagnosed using a coagulogram, or, in simple terms, a blood clotting test. This analysis allows you to accurately determine the composition of platelets in the blood. The course of the birth process depends on the number of platelets.

Treatment

Treatment of thrombocytopenia begins with therapy, in which a drug called Prednisolone is prescribed in the hospital.

Important! Treatment methods are prescribed strictly by the attending physician only after undergoing an appropriate examination and diagnosing the disease.

The dosage of the medication is indicated in the instructions, according to which 1 ml of the drug is taken per 1 kg of body weight. As the disease progresses, the dose increases by 1.5–2 times. In the initial stages, the ailment is characterized by a quick and effective recovery, so after taking the drug, you can notice an improvement in health within a few days. The drug continues until the person is completely cured, which must be confirmed by the attending physician.

The effect of glucocorticosteroids has a positive effect on the fight against malaise, but in most cases only the symptoms disappear, and the disease remains. Used to treat deficiency in children and adolescents.

Treatment of idiopathic chronic thrombocytopenia is carried out by removing the spleen. This procedure in medicine is called splenectomy and is characterized by its positive effects. In advance of surgery, the dosage of Prednisolone is increased threefold. Moreover, it is injected not into a muscle, but directly into a human vein. After splenectomy, administration of the drug in the same doses continues for up to two years. Only after the specified period has passed is an examination and certification of the success of the splenectomy performed.

If the removal operation is unsuccessful, the patient is prescribed immunosuppressive chemotherapy with cytostatics. These drugs include: Azathioprine and Vincristine.

When an acquired deficiency of a non-immune nature is diagnosed, thrombocytopenia is treated symptomatically by taking estrogens, progestins and androxons.

More severe forms of idiopathic thrombocytopenia are caused by excessive hemorrhages. A transfusion is performed to restore blood. Treatment of severe cases requires discontinuation of medications that may negatively affect the ability of platelets to form clots.

After diagnosing the disease, the patient is registered and an examination procedure takes place not only of the patient, but also of his relatives to collect a hereditary history.

Thrombocytopenia is a term that refers to all conditions in which the number of platelets in the blood is reduced. Pathology occurs more often in women than in men. The detection rate in children is 1 case in 20 thousand.

Properties of platelets

Causes of primary thrombocytopenia

The causes of insufficient platelet levels in the blood are divided into 3 groups.

Factors causing increased cell destruction when:

• various autoimmune processes (rheumatoid polyarthritis, systemic lupus);
• blood diseases (thrombocytopenic purpura);
• taking medications (sulfonamides, heparin, antiepileptic drugs, some medications for the treatment of cardiovascular and gastrointestinal diseases);
• during preeclampsia in pregnant women;
• after heart bypass surgery.

Factors that interfere with platelet reproduction when:

• radiation therapy;
• blood cancer ();
• infectious diseases (AIDS, hepatitis C, chicken pox, mononucleosis, rubella);
• tumor chemotherapy;
• long-term use of alcohol;
• deficiency of vitamin B 12 and folic acid in food.

Other reasons:

• pregnancy();
• large volume of blood transfusion;
• enlarged spleen (splenomegaly) due to various diseases liver, infections, has the ability to capture and destroy platelets;
• thrombocytopenia in a newborn child is rare and is explained by a delay in the development of hematopoiesis due to the mother’s history of infectious diseases;
• hereditary causes are observed when thrombocytopenia is combined with bleached areas of hair, impaired pigmentation of the skin, retina, eczema, and a tendency to infections.

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A set of diagnostic and therapeutic measures for D69.3 Idiopathic thrombocytopenic purpura

Medical studies intended to monitor the effectiveness of treatment

Medicines prescribed

• tab. 250 mg, 100 pcs;

• solution for intravenous and intramuscular injection. 4 mg/1 ml: amp. 1 PC.

• tab. 20 mg, 10 pcs per pack

• tab. 50 mg, 10 pcs per pack

• tab. 500 mcg: 50 pcs.;

• solution for injection 4 mg/ml: amp. 25 pcs.;

• eye and ear drops 0.1%: drop bottle 10 ml

• lyophilisate for preparation. solution for intravenous and intramuscular injection. 500 mg, 1000 mg: vial. 1 PC. included with r-ritel

• lyophilisate for preparation. solution for intravenous and intramuscular injection. 125 mg: fl. included with r-ritel;

• tab. 4 mg, 16 mg, 32 mg: 10, 30 or 100 pcs.

• tab. 4 mg: 50 pcs.

solution for intravenous and intramuscular injection. 30 mg/1 ml: amp. 3 or 5 pcs.

Coding of thrombocytopenia according to ICD 10

Platelets play a vital role in the human body and are a group of blood cells.

• 0 – purpura caused by an allergic reaction;
• 1 – defects in the structure of platelets with a normal number;
• 2 – purpura of another, non-thrombocytopenic origin (in case of poisoning);
• 3 – idiopathic thrombocytopenic purpura;
• 4 – other primary platelet deficiencies;
• 5 – secondary lesions;
• 6 – unspecified variants of pathologies;
• 7 – other types of hemorrhages (pseudogemophilia, increased fragility of blood vessels, and so on);
• 8 – unspecified hemorrhagic conditions.

This group of diseases is located under the heading of pathologies of the blood, hematopoietic organs and immune disorders of cellular origin.

Danger of thrombocytopenia

Due to the severity of clinical manifestations, thrombocytopenia in the international classification of diseases contains emergency care protocols for severe hemorrhagic syndromes.

A danger to life with a strong decrease in the number of platelets appears even when scratches appear, since the wound is not healed by primary blood clots and continues to bleed.

People with a lack of white blood cells can die from spontaneous internal hemorrhages, so the disease requires timely diagnosis and adequate treatment.

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IDIOPATHIC THROMBOCYTOPENIC PURPURA

Idiopathic thrombocytopenic purpura (ITP) is an autoimmune disease with bleeding caused by a decrease in the content of platelets in the peripheral blood due to their destruction by macrophages with the participation of antiplatelet autoantibodies.

Symptomatic thrombocytopenic purpura or Werlhoff syndrome is a clinically similar situation when, in some autoimmune diseases(SKV, rheumatoid arthritis etc.) antiplatelet autoantibodies also arise, which leads to thrombocytopenia with clinical manifestations in the form of thrombocytopenic purpura.

ICD10:D69.3 – Idiopathic thrombocytopenic purpura.

The etiology of the disease is unknown. Not excluded viral infection as etiological factor AND SO ON.

Under the influence of an etiological factor, a breakdown of immune tolerance to the antigens of one’s own platelets occurs in the patient’s body. As a result, the maturation of plasma cells capable of synthesizing antiplatelet autoantibodies is activated. These are immunoglobulins IgG and IgA and, in small quantities, IgM. Antiplatelet autoantibodies bind to antigenic determinants on the platelet membrane. Platelets “labeled” in this way interact with fixed macrophages of the spleen and liver and are destroyed by them. The lifespan of platelets is reduced to several hours and even minutes instead of the normal 7-10 days.

Fixation of autoantibodies on the membrane negatively affects the functional properties of platelets. Therefore, not only thrombocytopenia, but also thrombasthenia of undestroyed platelets plays a role in the pathogenesis of bleeding.

The number of megakaryocytes in the bone marrow is usually normal or even slightly increased.

As a result of the weakening of the platelet link in the blood coagulation system, patients have a tendency to bleed in the form of bruises on the skin and hemorrhages in the tissue of internal organs.

The level of platelets circulating in the blood, below which thrombocytopenic purpura begins, is 50x10 9 /l.

Blood loss can lead to a sideropenic state, hypochromic anemia.

The disease can occur in acute or chronic forms. Acute form occurs in people under 20 years of age, most often in children 2-6 years old, and lasts no more than 6 months. Duration chronic form ITP for more than 6 months. It develops in people aged 20 to 40 years, more often in women.

Patients periodically develop multiple pinpoint hemorrhages and bruises for no apparent reason or with minor injuries. Most often they are localized in the skin or subcutaneous tissue, mainly on the limbs. But they can be on any part of the body. Bruises of varying sizes, usually large. They have different colors because they do not appear at the same time. The skin of patients becomes spotted, similar to the skin of a leopard.

The next most common are heavy menstruation and uterine bleeding. The disease can begin precisely with this clinical manifestation. And sometimes that’s all there is to it.

Recurrent nosebleeds often occur, less commonly - pulmonary, gastrointestinal, and renal bleeding. Hemorrhages in the brain and retina of the eyes are especially dangerous.

As a rule, there are no hemorrhages in the muscles and joints.

In approximately every third case of the disease, there is a moderate enlargement of the spleen.

During the period of exacerbation of the disease, the appearance of fresh hemorrhages may be accompanied by a moderate increase in body temperature.

Frequent and massive blood losses, or small ones, but lasting for a long time, can cause the formation of sideropenipic syndrome, hypochromic anemia. Anemia usually develops with frequent nosebleeds and prolonged uterine bleeding.

General blood test: hypochromic anemia, platelets less than 50x10 9 /l. If the platelet count is less than 10x10 9 /l, there is a risk of massive bleeding. Platelets have increased sizes, often an atypical shape, and poor specific granularity. Small fragments of platelets are found.

Urinalysis: hematuria.

Biochemical blood test: decreased serum iron content.

Immunological analysis: high titer of antiplatelet autoantibodies. Increased levels of immunoglobulins, usually IgG.

Sternal puncture: the number of megakaryocytes is increased, especially their young forms without signs of platelets being detached from them. The number of plasma cells may be increased.

Hemostasis study: absence or slowing of blood clot retraction. Blood clotting time was not changed. The duration of bleeding according to Duque is increased to minutes.

Ultrasound examination: moderate splenomegaly without disturbance of portal hemodynamics.

The diagnosis is established when a petechial-spotted type of bleeding is detected in combination with thrombocytopenia less than 50x10 9 / l in the absence of symptoms of another disease, part of the clinical manifestations of which is symptomatic thrombocytopenia.