Disseminated intravascular coagulation is a disorder of hemostasis associated with hyperstimulation and a shortage of reserves of the blood coagulation system, leading to the development of thrombotic, microcirculatory and hemorrhagic disorders. With disease, there is a petechial hematoma rash, increased bleeding, organ dysfunction, and in acute cases, the development of shock, hypotension, severe bleeding, ODN and OPN. The diagnosis is established by characteristic signs and laboratory tests of the hemostasis system. Treatment is aimed at correcting hemodynamics and disorders of the coagulation system (antiplatelet agents, anticoagulants, angioprotectors, blood transfusions, plasmapheresis, etc.).
Disseminated intravascular coagulation (DIC syndrome, thrombohemorrhagic syndrome) is a hemorrhagic diathesis characterized by excessive acceleration of intravascular coagulation, the formation of loose blood clots in the microcirculatory network with the development of hypoxic and dystrophic-necrotic measurements in organs. Pathology is a danger to the patient’s life due to the risk of extensive, poorly stopped bleeding and acute dysfunction of organs (mainly lungs, kidneys, adrenal glands, liver, spleen) with an extensive microcirculatory network.
Disseminated intravascular coagulation can be considered as an inadequate protective reaction aimed at eliminating bleeding when blood vessels are damaged and isolating the body from the affected tissues. The occurrence of DIC syndrome in various branches of practical medicine (hematology, intensive care, surgery, obstetrics and gynecology, traumatology, etc.) is quite high.
Disseminated intravascular coagulation develops against the background of diseases occurring with damage to tissues, vascular endothelium and blood cells, accompanied by microhemodynamic disorders and a shift in hemostasis towards hypercoagulation. The main cause is septic complications of bacterial and viral infections, shock of any nature. DIC syndrome often accompanies obstetric pathology – severe gestosis, presentation and premature placental abruption, intrauterine fetal death, amniotic fluid embolism, manual separation of the afterbirth, atonic uterine bleeding, as well as cesarean section.
The development of thrombohemorrhagic syndrome can be initiated by metastatic malignant tumors (lung cancer, stomach cancer), extensive injuries, burns, serious surgical interventions. Often, DIC-syndrome accompanies transfusion of blood and its components, transplantation of tissues and organs, prosthetics of blood vessels and heart valves, the use of artificial blood circulation.
Cardiovascular diseases that occur with hyperfibrinogenemia, an increase in viscosity and a decrease in blood flow, a mechanical obstacle to blood flow with an atherosclerotic plaque can contribute to the occurrence of DIC syndrome. Disease can be caused by taking medications (OK, ristomycin, diuretics), acute poisoning (for example, snake venom) and acute allergic reactions.
Failure of hemostasis in DIC syndrome occurs due to hyperstimulation of coagulation and rapid depletion of anticoagulant and fibrinolytic hemostasis systems.
The development of disseminated intravascular coagulation is caused by various factors that appear in the bloodstream and directly activate the clotting process, or carry it out through mediators acting on the endothelium. Toxins, bacterial enzymes, amniotic fluid, immune complexes, stress catecholamines, phospholipids, decreased cardiac output and blood flow, acidosis, hypovolemia, etc. can act as activators of DIC syndrome.
The development of disseminated intravascular coagulation occurs with a sequential change of 4 stages.
- I is the initial stage of hypercoagulation and intravascular aggregation of cells. It is caused by the release into the blood of tissue thromboplastin or substances that have a thromboplastin-like effect and trigger internal and external clotting pathways. It can last from several minutes and hours (in acute form) to several days and months (in chronic).
- II – stage of progressive consumption coagulopathy. It is characterized by a deficiency of fibrinogen, blood plates and plasma factors due to their excessive expenditure on thrombosis and insufficient compensation.
- III – critical stage of secondary fibrinolysis and severe hypocoagulation. There is an imbalance of the hemostatic process (afibrinogenemia, accumulation of pathological products, destruction of red blood cells) with a slowdown in blood clotting (up to complete inability to coagulate).
- IV – stage of recovery. There are either residual focal dystrophic and necrotic changes in the tissues of certain organs and recovery, or complications in the form of acute organ failure.
According to the severity and rate of development of DIC, the syndrome can be acute (including lightning-fast), subacute, chronic and recurrent. An acute form of thrombohemorrhagic syndrome occurs with a massive release of thromboplastin and similar factors into the blood (with obstetric pathology, extensive operations, injuries, burns, prolonged tissue compression syndrome). It is characterized by an accelerated change in the stages of DIC syndrome, the absence of a normal protective anticoagulation mechanism. Subacute and chronic forms of DIC syndrome are associated with extensive changes in the surface of the vascular endothelium (for example, due to atherosclerotic deposits), acting as an activating substance.
Disseminated intravascular coagulation can manifest locally (limited, in one organ) and generically (with damage to several organs or the entire body). According to the compensatory potential of the body, compensated, subcompensated and decompensated DIC syndrome can be distinguished. The compensated form is asymptomatic, micro-clots are lysed due to increased fibrinolysis, clotting factors are replenished from reserves and by biosynthesis. The subcompensated form manifests itself as a hemosyndrome of moderate severity; decompensated – characterized by cascade reactions of reactive fibrinolysis, failure of coagulation processes, non-coagulability of blood.
DIC syndrome can occur with the same activity of the procoagulant and vascular-platelet links of hemostasis (mixed pathogenesis) or with the predominance of the activity of one of them.
Clinical manifestations are determined by the rate of development and prevalence of the lesion, the stage of the process, the state of compensatory mechanisms, the layering of symptoms of the inducer disease. Disease is based on a complex of thrombohemorrhagic reactions and organ dysfunction.
In the acute manifest form, generalized DIC syndrome develops quickly (in a few hours), which is characterized by a state of shock with hypotension, loss of consciousness, signs of pulmonary edema and acute respiratory failure. Hemosyndrome is expressed by increasing bleeding, massive and profuse bleeding (pulmonary, uterine, nasal, gastrointestinal). The development of foci of ischemic myocardial dystrophy, pancreatic necrosis, erosive and ulcerative gastroenteritis is characteristic. The lightning-fast form of DIC syndrome is characteristic of amniotic fluid embolism, when coagulopathy rapidly (within a few minutes) passes into a critical stage, accompanied by cardiopulmonary and hemorrhagic shock. The mortality rate of mother and child in this form of DIC syndrome is approaching 80%.
The subacute form is local in nature with a more favorable course. Minor or moderate hemosyndrome is manifested by petechial or drain hemorrhagic rash, bruises and hematomas, increased bleeding from injection sites and wounds, bleeding from mucous membranes (sometimes – “bloody sweat”, “bloody tears”). The skin acquires a pale appearance, marbling, becomes cold to the touch. In the tissues of the kidneys, lungs, liver, adrenal glands, gastrointestinal tract, edema, sharp fullness, intravascular coagulation, a combination of foci of necrosis and multiple hemorrhages develop. The most common – the chronic form of DIC-syndrome often has an asymptomatic course. But as the background disease progresses, manifestations of hemorrhagic diathesis and organ dysfunction increase.
DIC syndrome is accompanied by asthenic syndrome, poor wound healing, the addition of purulent infection, the development of keloid scars. Complications include hemocoagulation shock, acute respiratory failure, acute respiratory failure, liver necrosis, gastric ulcer, intestinal infarction, pancreatic necrosis, ischemic stroke, acute posthemorrhagic anemia.
To establish DIC syndrome, a thorough collection of anamnesis with the search for an etiological factor, analysis of the clinical picture and laboratory data (general blood and urine analysis, blood smear, coagulogram, paracoagulation samples, ELISA) is necessary. It is important to assess the nature of bleeding, to clarify the stage of coagulopathy, reflecting the depth of violations.
DIC syndrome is characterized by petechial-hematomic bleeding, hemorrhages from several places at once. With a low-symptomatic course, hypercoagulation is detected only by laboratory methods. Mandatory screening tests include determining the number of platelets, fibrinogen, APTT, prothrombin and thrombin time, Lee-White clotting time. The study of intravascular coagulation markers – RFMC and PDF, D-dimer by ELISA and paracoagulation samples helps to confirm the DIC syndrome.
The criteria for disease are the presence of fragmented erythrocytes in a blood smear, platelet and fibrinogen deficiency, an increase in the concentration of PDF, a drop in the activity of antithrombin III in blood serum, lengthening of APTT and thrombin time, absence of formation or instability of a clot or in vitro. The functional state of the “shock organs” is evaluated: lungs, kidneys, liver, cardiovascular system, brain. DIC syndrome must be differentiated from primary fibrinolysis and other coagulopathic syndromes.
The success of the treatment of DIC syndrome is possible with its early diagnosis. Active therapeutic measures are required for severe symptoms in the form of bleeding and organ failure. Patients with DIC syndrome should be hospitalized in the ICU and, if necessary, ventilator, active antishock therapy. With a low-symptomatic DIC syndrome, the main treatment is the treatment of background pathology, correction of hemodynamic parameters and functional disorders of organs.
Acute DIC syndrome requires urgent elimination of its root cause, for example, emergency delivery, hysterectomy – with obstetric pathology or antibiotic therapy – with septic complications. To eliminate hypercoagulation, the administration of anticoagulants (heparin), disaggregants (dipyridamole, pentoxifylline), fibrinolytics is indicated. Patients should be under constant dynamic monitoring of hemostasis indicators.
As replacement therapy for DIC syndrome, transinfusions of freshly frozen plasma, platelet or erythrocyte mass (with a drop in platelet or Hb levels); cryoprecipitate (with heart failure), saline are used. In case of life-threatening bleeding, it is possible to prescribe antifibrinolytic agents (aminocaproic acid, protease inhibitors). For skin hemorrhages and wounds, bandages with ethamzylate and a hemostatic sponge are applied.
According to the indications, corticosteroids, oxygen therapy, plasmapheresis are used. To restore microcirculation and impaired organ functions, angioprotectors, nootropic drugs, and post-syndrome therapy are prescribed. In the case of acute renal failure, hemodialysis and hemodiafiltration are performed. In chronic DIC syndrome, it is advisable to use disaggregants, vasodilators, in the postoperative period – heparin therapy.
Prognosis and prevention
The prognosis of DIC syndrome is variable, it depends on the main etiologically significant disease, the severity of hemostasis disorders and the timeliness of treatment initiated. In acute DIC syndrome, a fatal outcome is not excluded as a result of uncoupled large blood loss, the development of shock, acute respiratory failure, acute respiratory failure, internal hemorrhages. Prevention of DIC syndrome consists in identifying patients at risk (especially among pregnant women and the elderly), and treating a background disease.