What is Acquired Hemorrhagic Coagulopathy?
The most common acquired coagulopathies are secondary forms of coagulopathy, characterized by complex disorders in the blood coagulation system.
The mechanism of these forms of coagulopathy is more complex than that of hereditary hemorrhagic diathesis.
Deficiency of certain coagulation factors with acquired coagulopathies is quite rare.
Diagnosis of Acquired Hemorrhagic Coagulopathy
The diagnosis of acquired coagulopathies is facilitated by a detailed questioning of the patient, since the phenomenon of one or another deficiency of coagulation factors was preceded by some other disease that led to the observed hemostasis disorder in the patient.
Difficulties in the diagnosis of a particular type of pathology are encountered in the case of heterogeneous coagulopathic syndromes. These pathologies include hemostatic disorders in the postpartum period and in newborns, with leukemia, liver diseases, and immune pathology.
Symptoms of Acquired Hemorrhagic Coagulopathy
Classification of the main clinical situations in which most acquired coagulopathies are observed:
- in the neonatal period:
– deficiency of K-vitamin-dependent factors;
– immune thrombocytopenia;
– disseminated intravascular coagulation syndrome;
– hereditary disorders of hemostasis;
– penetration of maternal immune coagulation factor inhibitors into the fetal circulation; - infectious diseases (including viral) and all types of sepsis:
– disseminated intravascular coagulation syndrome (especially in severe forms with septic shock);
– purpura due to the development of specific infectious vasculitis (hemorrhagic fevers) or secondary immune disorders such as Shenlein-Genoch disease or erythema, less often secondary immune thrombocytopenia; - obstructive jaundice:
– before the development of severe damage to the liver parenchyma – deficiency of K-vitamin-dependent factors;
– with severe damage to the liver parenchyma – the development of a deficiency of other factors and the addition of disseminated intravascular coagulation; - severe enteropathies and medical intestinal dysbiosis caused by prolonged use of broad-spectrum antibiotics and other antibacterial drugs – a deficiency of K-vitamin-dependent factors or DIC;
- liver diseases – infectious, toxic, parasitic, autoimmune, cirrhosis and cancer of this organ:
– impaired synthesis in the liver of plasma coagulation factors – VII, X, IX, II (the defect intensifies with acholia), as well as factors V, XI and I and fibrinolysis inhibitors;
– disseminated intravascular coagulation syndrome;
– the appearance in the circulation of pathological proteins that violate the process of blood coagulation; - all types of shock, severe injuries, terminal conditions (including with heavy blood loss) – disseminated intravascular coagulation syndrome;
- acute renal failure, including hemolytic uremic syndrome and concomitant intravascular coagulation of blood;
- the bites of some venomous snakes – destruction of the walls of blood vessels in combination with disseminated intravascular coagulation syndrome;
- chemical burns of the esophagus and stomach – disseminated intravascular coagulation syndrome;
- acute intravascular hemolysis – disseminated intravascular coagulation syndrome;
- kidney disease:
– acute nephritis and exacerbation of chronic glomerulonephritis – disseminated intravascular coagulation syndrome;
– nephrotic syndrome – intravascular coagulation and (or) deficiency of factors X, VII or II, due to their large loss in the urine;
– uremia – thrombocytopathy, thrombocytopenia; - systemic amyloidosis – factor X deficiency;
- hemoblastosis:
– hyporegenerative (production) thrombocytopenia and thrombocytopathy;
– disseminated intravascular coagulation syndrome with thrombosis and the most severe forms of bleeding (especially often with acute promyelocytic leukemia); - myeloproliferative diseases and thrombocythemia:
– hyperaggregation of blood cells and blockade of microcirculation with a possible transformation into a protracted syndrome of disseminated intravascular coagulation;
– in the later stages – thrombocytopenia; - paraproteinemia (myeloma, Waldenstrom macroglobulinemia, “heavy chain” disease), dysglobulinemia, protein abnormalities in liver diseases and collagenoses:
– anticoagulant and antiplatelet effect of abnormal proteins;
– blockade of microcirculation due to high viscosity syndrome and precipitation of protein precipitates; - thrombotic thrombocytopenic purpura (Moshkovits disease) – platelet hyper-aggregation, complicated by disseminated intravascular coagulation syndrome;
- hemorrhagic vasculitis, immune capillaropathy with more or less pronounced syndrome of disseminated intravascular coagulation;
- rheumatoid arthritis, systemic lupus erythematosus and other immune and autoimmune diseases:
– disseminated intravascular coagulation syndrome;
– immune thrombocytopenia;
– the production of immune inhibitors of certain coagulation factors (most often factor VIII);
– paraproteinemia; - malignant neoplasms:
– disseminated intravascular coagulation syndrome;
– thrombocytopenia; - surgical interventions – disseminated intravascular coagulation syndrome;
- complications of pregnancy and childbirth:
– disseminated intravascular coagulation syndrome;
– immune thrombocytopenia;
– the appearance in the circulation of immune inhibitors of individual coagulation factors (often factor VIII); - complications of artificial termination of pregnancy – disseminated intravascular coagulation syndrome;
- drug non-immune effects:
– indirect anticoagulants – deficiency of K-vitamin-dependent factors VII, X, II and IX;
– direct-acting anticoagulants – blockage of the coagulation cascade at different levels;
– fibrinolysin and fibrinolysis activators – proteolysis of factors I, VIII, V, impaired transformation of fibrinogen into fibrin and hypofibrinogenemia, intensive consumption of plasminogen and antiplasmin;
– defibrinating drugs – artificial incomplete syndrome of disseminated intravascular coagulation with afibrinogenemia and secondary activation of fibrinolysis;
– overdose of protamine sulfate and other heparin antagonists – violation of the initial stages of the blood coagulation process;
– trasilol and other broad-spectrum antiproteases – inhibition of fibrinolysis, the initial stages of blood coagulation, kallikreinkininovoy system, increased platelet aggregation;
– preparations of disaggregated action; - immune drug effects:
– hemorrhagic vasculitis of drug origin with a more or less pronounced disseminated intravascular coagulation syndrome;
– immune drug thrombocytopenia;
– disseminated intravascular coagulation syndrome with drug disease;
– stimulation of the formation of immune inhibitors of certain blood coagulation factors; - massive transfusion syndrome.