DIC-syndrome can be acute, exacerbating, prolonged and hidden. With all these options, especially in acute cases, repeated transitions from thrombotic to hemorrhagic complications are possible, and vice versa.
Classification
Stage I – hypercoagulation and platelet aggregation.
II stage – transitional. At this stage, increasing coagulopathy is observed with thrombocytopenia, multidirectional shifts in general coagulation tests.
Stage III – the stage of deep hypocoagulation. At this stage, the blood coagulation ability may be completely lost.
Stage IV – restorative. In the case of an unfavorable course of DIC, various complications form at this stage, leading in most cases to death.
It is almost more convenient to use the following key indicators:
- the state of the hemostatic system, which is determined by:
– according to general coagulation tests;
– by the content of soluble fibrin and plasma fibrinogen breakdown products;
– by the content of platelets and their aggregates in the blood with an approximate assessment of cell function;
– by the level of antithrombin III;
– by a reserve of plasminogen and its activators;
– to identify the inferiority of coagulation when recording thromboelastograms (anomalies in the structure, fixation and mechanical properties of the clot);
– by the ability of the patient’s plasma to accelerate or inhibit coagulation and clot formation in the thromboelastogram of normal blood or plasma; - the presence, severity and localization:
– thrombosis;
– bleeding; - the severity and duration of hemodynamic disturbances (decrease in arterial and central venous pressure, circulating blood volume, etc.), taking into account the leading mechanisms of their origin:
– the causative factor that caused the DIC syndrome (trauma, intoxication, anaphylaxis);
– blood coagulation;
– hemorrhagic; - the presence and severity of respiratory failure and hypoxia, indicating their form and stage;
- the presence and severity of damage to other target organs that are most affected by DIC:
– kidney (acute renal failure);
– liver
– brain
– heart
– adrenal gland and pituitary gland;
– stomach and intestines (acute ulcers, bleeding with increased permeability of the vascular wall); - severity of anemia;
- imbalance in blood electrolytes (sodium, potassium, chlorine, calcium) and acid-base balance.
The clinic of the DIC-syndrome consists of the symptoms of the underlying disease that caused it, signs of developed shock (in acute forms), deep disorders of all parts of the hemostatic system, thrombosis and bleeding, hypovolemia (decreased filling of the vascular bed) and anemia, dysfunction and dystrophic changes in organs, metabolic disorders.
The sharper the DIC syndrome, the more short-term the phase of hypercoagulation (increased blood coagulation) and the more severe the phase of severe hypocoagulation (reduced blood coagulation) and bleeding. Such acute forms are characteristic mainly for infectious-septic, obstetric, post-traumatic (crash syndrome, burns, bone fractures), surgical (for traumatic operations), toxic (snake bites) and all types of shock-induced (including cardiogenic shock) DIC. The severity of the DIC syndrome in such cases depends not only on the severity of the underlying pathology and the general initial state of the patient’s body, but also on the timeliness and adequacy of first aid, the completeness of pain relief and further anesthetic management, the timeliness and maximum atraumaticity of surgical interventions, monitoring of the hemostasis system and completeness prevention and elimination of its disorders, maintaining the rheological properties of blood, the fight against disorders of microcirculation and general hemodynamics.
The emergence and progression of DIC-syndrome is facilitated by the insufficiently quick and complete removal of the patient from shock and hypotension (decreased tone), increased trauma of surgical interventions (isolation of organs from adhesions by blunting with kneading and tearing, intensive massage of the uterus after childbirth), insufficient correction of hypovolemia and not shown transfusions of canned blood containing a huge number of microclots and exacerbating DIC, instead of plasma, albumin, reopoliglyukin and other solutions.
Acute DIC syndrome is also observed in destructive processes in organs, in lung destruction of staphylococcal and other origin, acute liver dystrophy of toxic or viral origin (hepatorenal syndrome), acute necrotic or hemorrhagic pancreatitis. These forms of pathology are very often combined with septicemia (the appearance of a pathological agent in the blood) and various forms of superinfection that are difficult to treat. With all these types of pathology, the wave-like course of the DIC is also possible – periods of severe hemostasis are temporarily replaced by a completely satisfactory condition of the patients, after which catastrophic deterioration occurs again.
In addition to the symptoms of the underlying disease, the clinical picture of the acute DIC syndrome consists of the following main components.
Hemocoagulation shock. It occurs as a result of a violation of blood circulation in microvessels of various organs, tissue hypoxia, with the formation of toxic products in the blood and from entering it from the outside, including those formed during blood coagulation (hemocoagulation) and fibrinolysis (melting of the formed blood clots). It is rather difficult to follow the transformation of the shock that caused the DIC syndrome into hemocoagulation, since they merge into a general acute breakdown of hemodynamics with a catastrophic drop in arterial and central venous pressure, impaired microcirculation in organs with the development of their acute functional failure. As a result, acute renal or hepatorenal (hepatic-renal) failure, shock lung, and other complications may develop. DIC-syndrome starting with shock always catastrophic than shock-free forms, and the harder and longer the shock, the worse the prognosis for the patient’s life.
If bleeding occurs, the hemocoagulation shock transforms into hemorrhagic immediately or after a temporary improvement.
Hemostasis disorders go through different phases – from hypercoagulation to more or less deep hypocoagulation up to a complete loss of blood clotting ability. The identification of hypercoagulation does not require much effort – it is already detected when blood is extracted from a vein: blood coagulates immediately in a needle or in a test tube. In such cases, the laboratory receives an answer that it is impossible to examine the blood coagulation system, since the blood sent has coagulated. If there was no technical error when taking blood, then this answer in itself has diagnostic value, indicating a pronounced hypercoagulation.
In the second phase, some coagulation tests reveal hypercoagulation, while others reveal hypocoagulation. The multidirectionality of these shifts, which confuses doctors when evaluating a coagulogram, is also a typical laboratory sign of DIC. There is moderate thrombocytopenia (decrease in platelet count), platelet aggregation function is significantly reduced.
In the hypocoagulation phase, the thrombin time is sharply increased, and other parameters of the coagulogram are violated to one degree or another — c-joints are small, loose, or not formed at all. The effect of “transfer” of the patient’s plasma is either accelerates the coagulation of normal plasma, or slows it down. In the third phase, thrombocytopenia deepens, platelet function is severely impaired. When coagulating with an efa, a large amount of blocked (soluble) fibrin is found. Part of soluble fibrin coagulates with strong thrombin (causing coagulation of normal plasma in 3-4 s).
True afibrinogenemia (the absence of fibrin in the blood plasma) with DIC is almost never, and there is more or less pronounced hypofibrinogenemia (a decrease in the amount of fibrin in the blood plasma) and the binding of a significant part of fibrinogen to soluble fibrin. A test with efa venom reveals both this blocked fibrinogen / fibrin and the ability of blood to coagulate on the background of heparin therapy (fibrin therapy). Only in the terminal phase of the DIC-syndrome does the coagulation sharply lengthen in the test with efa poison, which is a poor prognostic sign.
A decrease in plasma fibrinogen level compared to the initial one is always observed in acute DIC, and in cases of protracted and chronic forms it is rare. However, in acute forms that developed against the background of the initial hyperfibrinogenemia (increased amount of fibrin), this decrease only leads to the fact that the concentration of fibrinogen in the plasma reaches a normal level. Such forms are frequent, since hyperfibrinogenemia is observed in all septic and acute inflammatory diseases, myocardial infarction and other organs, pregnancy, especially with toxicosis, and immune diseases. Together, all these forms account for about 50% of cases of acute DIC.
Early and steadily in DIC, the level of antithrombin III in plasma, which is a physiological antiplatelet agent, decreases. It is used to inactivate all coagulation factors. Evaluation of this disorder is of great clinical significance, since antithrombin III depression of up to 75% and below reflects the severity of DIC.
Relatively early in plasma, the content of plasminogen and some of its activators decreases, which is detected by rapid tests. The level of endothelial activators of thrombus fusion is significantly increased in most cases. The content in the plasma of patients with von Willebrand factor is also naturally increasing, which indicates a deep damage to the inner lining of the blood vessels.
Hemorrhagic syndrome is a frequent and dangerous, but far from mandatory, manifestation of disseminated intravascular coagulation. In most cases, it occurs in acute DIC, often in the hypocoagulation phase, although often multiple and heavy bleeding is also recorded in the second phase against the background of a normal or slightly reduced plasma fibrinogen content. The most severe bleeding occurs, of course, with complete or almost complete blood coagulation. From a clinical point of view, it is important to clearly distinguish between local type bleeding associated with damage or destructive changes in organs, and the common hemorrhagic syndrome due to general changes in the hemostatic system.
Local type bleeding includes bleeding during injuries and surgical interventions, postpartum and post-abortion uterine bleeding, bleeding from acute ulcers of the stomach or duodenum, hematuria (the appearance of blood in the urine) due to kidney infarction. These bleeding are associated not only with general disorders of hemostasis, but also with local (organ) pathology, which should be detected in time, correctly evaluated by a doctor and taken into account when conducting complex therapy. So, for example, a frequent combination of DIC and uterine atony requires, in addition to hemostatic therapy, a complex of actions that restore the normal tone of this organ, with bleeding from acute stomach ulcers – local bleeding stop (through a fibrogastroscope) and a change in the general treatment tactics.
General bleeding is characterized by the appearance of bruises, bruises and hematomas in the skin, subcutaneous and retroperitoneal tissue, nasal, gastrointestinal, pulmonary and renal hemorrhages, hemorrhages in various organs (brain and its membranes, heart, adrenal glands, lungs, uterus), diffuse sweating of blood in the pleural and abdominal cavities, sometimes in the pericardial sac. Each patient is dominated by one or the other form of bleeding.
Bleeding leads to acute posthemorrhagic anemia, in severe cases – to hemorrhagic shock. A decrease in hematocrit below 15-17% and the inability to increase it by replacement therapy with an erythrocyte mass are prognostically unfavorable and speak of ongoing blood loss, although it is not always easily detected.
Disruption of microcirculation in organs with their dysfunction and dystrophy is another group of the most important disorders that determines the clinical picture, severity, outcome and complications of DIC. In different patients and with different pathogenetic forms of this syndrome, one or the other organs, designated in the literature as target organs, suffer.
Extremely often, such an organ is the lungs, into the vessels of which from the venous system a huge amount of microbunches of fibrin, blood cell aggregates, and proteolysis products are introduced. As a result, acute pulmonary circulatory failure develops – shortness of breath, cyanosis, decreased blood oxygen saturation, and then increased carbon dioxide in arterial blood; interstitial edema, pulmonary infarction, and other signs of a “shock lung” appear, often with the development of respiratory distress syndrome. Intensive transfusion therapy used for DIC syndrome often aggravates these disorders, increasing the accumulation of water, sodium, and albumin in lung tissue.
Patients often show a special sensitivity to intravenous fluid administration and massive blood transfusions, sometimes the extra 200,000 ml of fluid dramatically increase hypoxia and provoke pulmonary edema. In the pulmonary variant of the lesion, with particular care, one should compare the amount of injected fluid with diuresis and blood loss, add diuretics, lasix to the complex therapy in a timely manner. It is also necessary to timely transfer the patient to mechanical ventilation with the creation of positive pressure on the exhale.
Acute renal failure is the second most frequent organ lesion in DIC. It manifests itself in the form of a decrease in the amount of urine excreted up to complete anuria (lack of urination), excretion of protein and red blood cells in the urine. In this case, the water-electrolyte balance is disturbed, as well as the acid-base balance in the body, an increase in the level of creatinine, and subsequently, residual nitrogen and urea, is noted in the blood serum. In general, this syndrome does not differ from other types of acute renal failure.
The combined forms are more severe – “shock lung” with acute renal failure or hepatorenal syndrome (hepatic-renal failure). In these cases, metabolic disorders are more severe and diverse, which creates additional difficulties in the treatment of patients.
Gasser’s hemolitic-uremic syndrome, all types of acute intravascular hemolysis can be considered typical renal forms of DIC, but hemolysis is not uncommon in many other forms of DIC.
Less commonly, liver damage occurs with the development of parenchymal jaundice, and sometimes with acute pain in the right hypochondrium. The opposite phenomenon is more often observed – the development of DIC syndrome against the background of acute or severe chronic liver damage (acute toxic and viral hepatitis, terminal phase of liver cirrhosis).
Target organs include the stomach and intestines. These lesions are accompanied by deep focal dystrophy of the mucous membrane of the duodenum and stomach, the formation of microthrombi and stasis in their vessels, the appearance of multiple bleeding, which in severe cases turns into continuous hemorrhagic impregnation of organs, the formation of acute erosive and ulcerative defects, which are a source of repeated high bleeding, d . Large doses of glucocorticosteroids (in order to remove the patient from shock), drugs that cause erosion of the gastric mucosa (acetylsalicylic acid), as well as adrenostimulants (adrenaline, norepinephrine) increase and aggravate these formidable manifestations of DIC.
With DIC, the rest of the intestine is also seriously affected, which can become a source of not only heavy bleeding, but also additional intoxication due to paresis, villi rejection and massive autolysis.
Disorders of cerebral circulation, thrombosis and bleeding in this area give a wide variety of symptoms – from headache, dizziness, confusion and fainting to typical thrombotic or hemorrhagic strokes, meningism phenomena.
Lesions of the adrenal gland and pituitary gland, leading to a typical picture of acute adrenal insufficiency (prolonged collapse, diarrhea, electrolyte disturbances, dehydration) and diabetes insipidus, are observed mainly with DIC syndrome of septic and shockogenic origin. They are associated either with thrombosis of the vessels that feed these glands, or with hemorrhages in them.