DIC syndrome in newborns. DIC syndrome (consumptive coagulopathy): how it develops, course and clinical picture, diagnosis, treatment

Physiol. Features of the hemostasis system in children of the newborn period:

1. reduction of K-vitamin-dependent coagulation factors

2. smart. The values ​​of adhesive and aggregation. act-sti Tr

3. increased permeability, vessel fragility. Walls

4. hypercoagulation of whole blood in the first hours and days of life.

DVS-s-m-is a complex general pathologist. Non-specific. The process, having developed in many painful conditions, is accompanied by widespread blood clotting into the circulation. channel and development of blockade of microcirculation, tissue hypoxia, and organ function.

E:1. injuries Damage to tissues and blood vessels, fuss. At time Operations, etc. ----- massive. entry into the blood of tissue thromboplastin

2. infection processes and septic. condition. (nar-e microcirculation, change in blood rheology ----- blood clotting ----- hypoxia)

3. allergic conditions

4. lek. pr-you are influential. on the roll and p/rolled. system

F -ry, sleeping internal combustion engine in a newborn

1. underdevelopment of the distribution network

3. lack. capacity of compensatory synthesis by the liver of FSK

Development mechanisms:

activation of convolution Tissue thromboplastin systems.

activur. Air of bacteria, viruses

vascular deficiency

scattered intravascular coagulation, aggregation of Tr with an accumulation of microclottes and their blockade of the bloodstream in organs.

dystrophic people in the organs

compass nar-ya

coagulopathy endogenous intoxication with proteolysis products

Pathogenesis: stages that are maintained in DIC:

change in the structure of the endothelium;

forms Blood elements;

gain convolution blood sp-sti;

decrease in lumen potential

vasospasm and venous stagnation.

disturbance of blood flow speed

1. Stage of hypercoagulation - intensified. thrombin formation, increased Tr adhesiveness --- the beginning of the formation of a microcirculation block in organs.

2. Hypocogulation stage - depletion decomposition. FSK after their disposal in the process of thrombus formation (consumption coagulopathy) and fibrin-embolism in various organs. The clinic is hemorrhagic. cm.

3. Fibryolytic stage. Characterized by increased fibrinolysis and hypo-or afibrinogenemia.

With the flow:

Acute DIC (min, day)

Subacute ICE (1-3 weeks)

Chr. (more than 1 month)

K:1st - nar-e microcirculation, blood thrombosis in the needle

Hemorrhagic. syndrome and decrease in Tr (for stage 2), stasis, arterial-external. shunts, to AD, GUS, O. pech. N,ONE,O. Adrenal failure. Neurological symptoms

Causes of death:

blockage of great vessels

hemorrhagic Syndrome

Differential DS: hemorrhagic. Syndrome, blood diseases

Lab DS: blood coagulation test, coagulogram, DS for sepsis

1-etiotropic and pathogenetic treatment mainly. Diseases

2-anti-shock therapy and maintaining the required volume of blood volume

3-heparin therapy 5-10 units\kg\hour intravenously for 12-24 hours (antidote – protamine sulfate-1 mg\100 units of heparin - if administered in excess)

4-jet FFP infusions

5- according to indications - protease inhibitors (Gordox 5000 IU/kg), GCS (in phase 3)

6-previous use of drugs that improve microcirculation (trental)

7-replacement of Er loss, maintenance of Ht>22%

8-for hypocoagulations-Tr mass, contrical

9-plasmapheresis

10-carrying out local hemostasis

3. Obstructive pyelonephritis . Pyelonephritis is a non-specific infectious and inflammatory process in the kidney that occurs with primary damage to the interstitial tissue, CLS. For the development of PyeN it is necessary: ​​1.bacterial. infection, 2. obstruction to the outflow of urine (reflux, stone, urinary tract abnormalities) Class serous and purulent (apostematous nephritis, renal carbuncle, pyonephrosis). Apostematous nephritis - suppuration of the kidney parenchyma with the development of multiple foci in it, cat. m/t merges and forms an abscess, carbuncle. Clinic t=40-41, chills, showers. sweat, myalgia, arthralgia, apathy, lower back pain. Diagnostics - in urine L-uria, bacteriuria (or anuria); blood- leukocytosis, anemia, hypo- and dysproteinemia, azotoemia. Ro- the kidney is enlarged; excretory urography– kidney function is reduced, the level of obstruction Ultrasound: obstruction, angiography.Treatment– comprehensive 1.removal of obstruction to the outflow of urine by radical or palliative surgery (reconstructive plastic surgery for anatomy, obstructions in the pelvis or distal part of the ureter, bladder outlet obstruction, nefo- or cystostomy in case of severe condition -ii b-x and expression of decrease in kidney function). 2.adequate A/B therapy taking into account microflora. 3.immunomodulatory and membrane-stab therapy. 4.desensitization, vitamins. 5. correction of dysbacteriosis. Emergency conditions: Acute urinary retention This is a complete stop of urination in the presence of a painful urge to do so. Clinic- full bladder, sharp pain in the lower abdomen. delays may develop detrusor insufficiency + sphincter paresis Bladder and as a result, paradoxical ischuria (urinary retention + incontinence, urine is constantly released in drops. Diagnostics: Ultrasound of the MPO, excretory urography, cystoscopy, CT. Treatment: underlying disease + catheter into the bladder or epicystostomy. surge arrester - non-specialist syndrome is characterized by the inability of the kidney to regulate the homeostasis of the internal environment of the body (including with prolonged obstruction of the urinary tract). Clinic: 1. initial stage (symptoms of the main disease); 2. oligoanuric stage; (reduced D, severe pain in the waist, Pastern, apathy, depression. Adynamia, stupor, stupor, maybe clonic-tonic convulsions, increased blood pressure, rhythm disturbances, anorexia, nausea, vomiting, hyperhydration - pastiness, increased central venous pressure, hemorrhage syndrome, Lab-no: hypochromic anemia, increased urea, creatinine, urea nitrogen, residual nitrogen, hyperkalemia, hyperchloremia, metabic acidosis. 80% of deaths at this stage are from OSHF due to toxic myocarditis, cerebral edema, pulmonary edema, asphyxia during convulsions, hemorrhage in the brain, massive bleeding; 3. polyanuric stage; (stage restored diuresis, early polyuric, late polyuric), hypokalemia, dehydration, hypercoagulation; 4.restorative Intensive therapy: 1. Arrangement or prevention of overhydration; strict accounting of incoming and outgoing fluid – catheterization of the bladder, accounting for perspiration, secretions: prohibit drinking, limit enteral nutrition, infusion volume - 800 + diuresis. Stimulation of diuresis: furosemide 1-2 mg/kg/day aminophylline 5-10 ml 2.4% 4 times a day, stimulation of diarrhea - weakens; sweating stimulus. 2. Reducing the level of catabolism: infusion of 40% glucose + insulin. 3. Correction of microcirculatory disorders: - infusions of rheopolyglucin (up to 200 ml / day), novocaine solution, albumin, noshpa, heparin, aminophylline. 4. Treatment and correction of hyperkalemia (iv 40% glucose + insulin, 10% calcium chloride, stimulation of diuresis, gastric lavage, cleansing enemas, enterosorption, hemosorption, hemodialysis). 5. Reducing uremic intoxication (gastric lavage, cleansing enemas, enterosorption, hemodialysis). 6. Symptomatic therapy (anemia - Er overflow, hypoproteinemia - plasma infusion, ascorbic acid, heparin therapy, sodium bicarbonate)

4. MS is a viral infection - O. vir. obstruction with moderately severe symptoms of intoxication, predominant damage to the lower respiratory tract with frequent development of bronchiolitis and with a peculiar cytopathogenic effect of the virus - the formation of a syncytium from giant cells. Vobud-l- RNA virus fam. paramyxoviruses, poorly resistant in external environment. 2 serovars that have a common antigen. Epidemiology. East-k - b-oh or nos-l. Patients shed the virus until 10-14 days of illness. Fur-m – airborne, spring-winter seasonality. Children in the first months of life and newborns are most susceptible. 12-25% of all acute respiratory infections in young children. Highly contagious, outbreaks in closed groups. The immune system is strong and re-infection is possible. I/O chronic course of infection. Pathogenesis Vir. enters the body by airborne droplets, multiplies in the epithelium of the mucous membrane of the DP, causing their hyperplasia with the formation of symplasts, giant cells united in a single network (syncytium) and the phenomenon of hypersecretion. Classification 1. By severity (mild; moderate; severe;) With a mild form of body type N or subfeb-I, intoxication is not severe, according to the type of catarrh of the upper respiratory tract. With a moderate form of body temperature 38-38.5°C, severe intoxication, symptoms of bronchiolitis with DN I - II stage. In severe form: hyperthermia, convulsive syndrome (rarely), stage II-III DN. due to diffuse bronchiolitis. The course of the disease can be smooth, without complications, or complicated. Complications - when bacterial infections are attached. More often, otitis media, sinusitis, and pneumonia occur. Diagnostic criteria: I. Epidemiological2. Anamnestic incubation is 3-7 days, the onset of the disease is gradual; complaints of naked pain, weakness, slight chilling, and sometimes chest pain. The cough in older children is dry, persistent, prolonged, in children of the first year of life - from the first day the cough is dry, sneezing, then it becomes frequent and intrusive. 3. Clinical Intoxication is moderate and does not determine the severity of the disease. The temperature is not higher than 38°C, sometimes normal. The general condition suffers slightly. Catarrh - slight pastiness of the face, injection of a vessel into the sclera, scanty discharge from the nose. The mucus membrane of the pharynx is slightly hyperemic or unchanged. Bronchoobstruction sm – leading. In young children, damage to the NDP is manifested by the development of o. bronchitis, bronchiolitis, with significant symptoms of obstruction of the respiratory tract. 4. Lab. data: for express diagnostics of m-d fluorescein antibodies with detection of Ag in the cytoplasm of cells of the nasal mucosa; virologist MD: isolation of virus from nasopharyngeal swabs on tissue culture; serological MD: increase in AT titer. Diff.Ds with other acute respiratory viral infections (influenza, papainfluenza) Treatment etiotr Ribavirin (aerosol) for 12-18 hours daily for up to 7 days. Int-n leukocyte. RNAase. Oxolinic ointment. Posyndromic therapyRespiratory syndrome Nasal drops Antitussives (prescribed for dry, obsessive cough; contraindicated for wet cough with copious sputum): codeine, codipront, glaucine hydrochloride, tusuprex, sedotussin, fervex for dry cough, libexin, levopront, falimint, tussin, stoptussin. Expectorants: thermopsis, marshmallow root, mucaltin, licorice root, pertussin, leaves of coltsfoot, plantain, potassium iodide, Doctor Mom, breast elixir, etc. Mucolytics: bromhexine, acetylcysteine, carbocysteine, ambroxol, fluifort. Inhaled bronchodilators: salbutamol, terbutaline, fenoterol, berodual, alupent. Distractions: mustard plasters, foot baths or ozokerite “boots”; Gargling with a decoction of chamomile, sage, tincture of eucalyptus, calendula Alkaline inhalations 5-6 times a day

DIC syndrome, or disseminated intravascular coagulation syndrome, is a complex multicomponent pathological process in the hemostatic system, manifested increased thrombus formation in the vessels of the microvasculature.

This condition occurs quite often in the practice of doctors of any specialty; obstetricians-gynecologists, resuscitators, surgeons, and emergency doctors encounter it. It is also the most common form of blood clotting disorders (coagulopathies) in intensive care both in adults and children.

Coagulopathies are conditions accompanied by certain changes in the. The main types of coagulopathies are congenital (genetic) and acquired, one of the variants of which is DIC syndrome. In the literature you can find data on the so-called hypercoagulable coagulopathy, or hypercoagulation syndrome, which is characterized by laboratory signs of increased blood clotting, but thrombosis is most often absent.

DIC syndrome has complex development mechanisms, various clinical manifestations, and precise diagnostic criteria for it have not yet been identified, which causes significant difficulties in its recognition and treatment. This condition always complicates any other diseases, and therefore is not an independent disease.

Thrombosis: normal or pathological?

In order to understand what is the reason and what are the mechanisms of occurrence of such severe violation like DIC, you need to know the main stages of blood clotting.

A person is constantly faced with the risk of possible injury, from minor scratches or cuts to serious injuries, therefore nature provides special defense mechanism– thrombosis, that is, the formation of a blood clot at the site of vessel damage.

There are two oppositely directed systems in the body - coagulating And anticoagulant , the correct interaction of which promotes thrombus formation if necessary, as well as the liquid state of blood in the vessels in the absence of any damage. These hemostatic systems play a very important protective role.

In case of integrity violation vascular wall the coagulation system is activated, a whole cascade of reactions of which leads to the formation (of a clot in the lumen of a vessel or chamber of the heart). Plasma proteins, in particular, as well as platelets, coagulation factors produced in the liver, and various enzymes are directly involved in this. The result is the formation of a blood clot that closes the defect in the vascular wall and prevents further bleeding.

To maintain the fluid state of the blood and prevent the uncontrolled formation of blood clots, there are specific antithrombotic mechanisms, realized by the action of the so-called anticoagulants– substances that prevent the occurrence of massive thrombosis (plasma proteins, proteolytic enzymes, endogenous heparin). In addition, an obstacle to thrombosis is rapid blood flow and the so-called fibrinolysis, that is, the dissolution of the fibrin protein and its removal from vascular bed with the help of enzymes circulating in the blood plasma and secreted by leukocytes, platelets and other cells. The remains of fibrin after its destruction are absorbed by leukocytes and macrophages.

When the interaction of the components of the hemostatic system changes with various diseases and injuries, Discoordination occurs in the functioning of the coagulation and anticoagulation systems, which contributes to massive uncontrolled thrombus formation along with bleeding. These mechanisms form the basis of the pathogenesis of DIC syndrome, which is life-threatening complication.

Causes of DIC syndrome

Since DIC is not an independent disease, it does not occur without some effect that activates the coagulation system. Most common reasons its occurrence:

• Infections - septic shock, severe bacterial and viral lesions;
• Various types of shock (traumatic, infectious-toxic, hypovolemic, etc.), terminal conditions;
• Injuries, including traumatic surgical interventions(organ transplantation, heart valve replacement), use of artificial blood circulation and hemodialysis machines during surgical interventions;
• Oncological diseases, especially common forms of cancer;
• DIC syndrome in obstetrics - premature placental abruption;
• During pregnancy in case of occurrence (eclampsia, preeclampsia), ectopic pregnancy and etc.;
• Serious illnesses of cardio-vascular system, purulent-inflammatory processes internal organs.

Thus, DIC syndrome accompanies most severe diseases and terminal conditions (clinical death, subsequent resuscitation measures). At the stage of establishing their presence, hypercoagulation either already exists or will develop if appropriate preventive measures are not taken.

In newborns born healthy and at term, DIC syndrome is extremely rare. More often it occurs in severe birth injuries, amniotic fluid embolism (in this case, both the mother and the fetus will have symptoms), and respiratory disorders.

In children, hereditary coagulopathies are possible, in particular, and, accompanied by increased bleeding, while thrombohemorrhagic syndrome is relatively rare, and its causes can be severe infections and injuries.

Stages of development and forms of DIC syndrome

There are various approaches to the classification of thromboembolism hemorrhagic syndrome: according to etiology, features of pathogenesis and clinical manifestations.

Based on the mechanisms of occurrence, the following stages of DIC syndrome are distinguished:

1. – characterized by the entry of thromboplastin into the blood, which triggers the process of blood clotting and thrombus formation;
2. Consumptive coagulopathy – intensive consumption of coagulation factors, subsequent increase in fibrinolytic activity (as a protective mechanism against massive thrombosis);
3. Hypocoagulation stage - as a result of the consumption of components of the coagulation system, incoagulability and platelet deficiency occur ();
4. Recovery stage.

thrombodynamics of a fibrin clot during various states coagulation system

Thus, when exposed to a damaging factor, for example, injury or bleeding, a protective mechanism is triggered - but uncontrolled consumption of coagulation factors leads to their deficiency and inevitable hypocoagulation, which is expressed in severe bleeding. If the patient is lucky and receives all the necessary services in a timely manner qualified assistance, then a recovery phase will begin with residual thrombosis.

It is worth noting that the process of thrombosis occurs in the microvasculature and is generalized in nature, therefore all organs and tissues are involved in the pathological process, which creates severe disturbances in their work.

Clinical classification of DIC syndrome implies the identification of the following forms:

• Spicy;
• Subacute;
• Chronic;
• Recurrent;
• Latent.

There is a so-called fulminant DIC syndrome, which only takes a few minutes to occur. This option is especially common in obstetrics.

Acute DIC syndrome lasts from several hours to several days and accompanies injuries, sepsis, surgical operations, transfusions of large quantities of blood and its components.

Subacute course typical for chronic infectious processes, autoimmune diseases(for example,) and lasts several weeks.

Chronic ICE possible in case of severe diseases of the heart and blood vessels, lungs, kidneys, diabetes mellitus. This form can last for several years and is observed in therapeutic practice. As signs of thrombohemorrhagic syndrome increase, the disease that caused it progresses.

Clinical manifestations

In addition to these laboratory research methods, in the diagnosis of DIC syndrome important occupied by a clinic. In severe cases, when the lungs and kidneys are affected, characteristic skin changes and bleeding, the diagnosis is beyond doubt, however, in subacute and chronic forms During the course of the disease, diagnosis can be difficult and requires a careful assessment of clinical data.

Since the main pathogenetic link in the development of DIC syndrome is increased thrombus formation in the microcirculatory vessels, those organs in which the capillary network is well developed will suffer first of all: lungs, kidneys, skin, brain, liver. The severity of the course and prognosis depend on the degree of blockage of microcirculation by blood clots.

cutaneous manifestations of DIC syndrome are the most noticeable to a layman

The main clinical signs are quite typical and are caused by widespread thrombosis, bleeding and, as a consequence, failure of various organs.

• Leather, as a well-supplied organ, is always involved in the pathological process, a characteristic hemorrhagic rash appears in it due to minor hemorrhages, foci of necrosis (necrosis) on the face and limbs.
• Defeat lungs manifests itself as signs of acute respiratory failure, the symptoms of which will be severe shortness of breath up to respiratory arrest, pulmonary edema due to damage to small vessels and alveoli.
• With fibrin deposition in blood vessels kidney acute renal failure, manifested by impaired urine formation up to anuria, as well as serious electrolyte changes.
• Defeat brain is expressed in, leading to neurological disorders.

In addition to organ changes, there will be a tendency to external and internal bleeding: uterine, gastrointestinal, etc., as well as the formation of hematomas in internal organs and soft tissues.

In general, the clinical picture of DIC syndrome consists of symptoms of multiple organ failure and thrombohemorrhagic phenomena.

Diagnosis of DIC syndrome

To establish a diagnosis of thrombohemorrhagic syndrome, in addition to the characteristic clinical manifestations, great importance have laboratory tests . Using tests, you can determine not only the presence of hemostasis disorders, but also the stage and form of DIC, and also monitor how effective the treatment is.

Laboratory diagnostics includes the so-called orientation tests accessible to everyone medical institutions(coagulogram), and more complex and accurate confirming(determination of platelet aggregation properties, blood plasma tolerance to heparin, etc.).

In the first stage, a decrease in the number of platelets, increased coagulation and an increase in the amount of fibrinogen can be observed, while during the period of severe coagulopathy of consumption there will be a significant decrease in fibrinogen, severe thrombocytopenia, a decrease in the content of coagulation factors and, accordingly, an increase in blood clotting time.

Post-mortem diagnosis of DIC syndrome through histological examination of tissues makes it possible to detect characteristic microscopic signs: accumulation shaped elements in the lumens of small vessels, thrombosis, multiple hemorrhages and necrosis in the internal organs.

Since in the first hours of the development of the disease laboratory parameters may remain within normal limits, then it is important to ensure constant monitoring and monitoring of changes in hemostasis parameters, especially in patients who have high risk development of DIC syndrome. It is also necessary to monitor changes in the electrolyte composition of the blood, levels (indicators of kidney function), acid-base status, and diuresis.

Treatment

Due to the multifactorial origin of consumption coagulopathy, complicating the most various diseases And pathological conditions,There is currently no uniform treatment strategy for DIC syndrome.. However, taking into account the characteristic stages and features of the course, the main approaches to the prevention and treatment of such a dangerous complication have been identified.

It is important to eliminate the causative factor that caused the development of thrombohemorrhagic syndrome as early as possible, this will etiotropic direction of treatment:

1. Adequate antibiotic therapy for purulent-septic complications;
2. Timely replenishment of circulating blood volume during blood loss;
3. Maintaining cardiovascular function and blood pressure at various types shock;
4. Prevention of complications and timely surgical care in obstetric practice;
5. Adequate pain relief in case of various injuries and traumatic shock, etc.

Main directions pathogenetic And symptomatic treatment:

• The use of fibrinolytics and antifibrinolytic drugs depending on the phase of the disease;
• Replacement infusion therapy;
• Improving the rheological properties of blood, using drugs to normalize microcirculation;
• Extracorporeal detoxification.

An important principle in the treatment of DIC syndrome is the use of anticoagulant therapy. Heparin is most often used for these purposes, which restores normal blood clotting, prevents the formation of blood clots and helps remove existing ones, thereby improving the function of affected tissues and organs.

To eliminate the deficiency of blood coagulation factors, replacement infusion therapy is performed. The optimal drug for these purposes is fresh frozen plasma. Along with it, heparin and protease inhibitors can also be administered (they reduce enzyme activity and prevent the development of hypocoagulation, prevent the development of shock - contrical, gordox).

To improve microcirculation in tissues, aspirin, trental, chimes, etc. are used, as well as the introduction of rheological solutions (reopolyglucin, voluven).

Very important in complex therapy DIC syndrome methods of extracorporeal detoxification - plasmapheresis, cytapheresis, hemodialysis.

In general, the treatment of DIC syndrome is a very difficult task., and sometimes the decision on the regimen of drugs and their dosages must be made in a matter of minutes.

It is necessary to treat DIC syndrome in stages, since the prescription of a particular drug entirely depends on the patient’s state of hemostasis at a particular point in time. In addition, constant laboratory monitoring of blood coagulation, acid-base balance, and electrolyte balance should be carried out.

Urgent Care consists of cupping pain syndrome, combating shock, establishing infusion therapy, administration of heparin in the first phase of DIC syndrome.

Patients who have been diagnosed with thrombohemorrhagic syndrome or are at high risk of developing it should be immediately hospitalized and placed in the intensive care unit.

Mortality in thrombohemorrhagic syndrome, according to various sources, reaches 70% with Stage III, at chronic course – 100%.

Prevention This dangerous complication consists, first of all, in the earliest possible treatment of the diseases that led to its occurrence, as well as in restoring blood circulation and microcirculation in organs and tissues. Only early initiation of therapy and correct tactics contribute to the normalization of hemostasis and further recovery.

Video: lecture by A.I. Vorobyova about DIC syndrome

DIC syndrome is also called disseminated intravascular coagulation syndrome. It is not a separate pathology or nosological entity. It is a complex process consisting of several stages, during which increased thrombus formation is observed in the lumen of blood vessels. This is a fairly common situation. Most often, surgical doctors and pediatricians encounter it. Treatment of DIC syndrome is extremely complex, requiring early diagnosis of the process.

The causes of DIC syndrome are determined by the diseases that provoked it. The most common triggers are.

1. Severe infectious pathologies - sepsis, accompanied by a state of shock, viral processes.
2. Other types of shock, which is inherently the main cause of DIC. These include traumatic, hypovolemic, infectious-toxic and even painful.
3. Any terminal condition can provoke disseminated intravascular coagulation.
4. Surgical operations, especially massive ones, in which artificial blood circulation machines are used.
5. Cancer diseases.
6. Hemodialysis.
7. Excessive blood loss.
8. Against the background of massive blood transfusion, this pathology also occurs.
9. In obstetric practice, DIC syndrome occurs with placental abruption, a complication labor activity amniotic fluid embolism, toxicosis, Rh conflict.
10. Pathologies of the cardiovascular system.

Based on the foregoing, we can conclude that disseminated intravascular coagulation is caused by severe pathological processes or terminal conditions. At the same time, pathology practically does not occur in healthy newborn babies. Here it is important to correctly differentiate it from other coagulopathies, such as hemophilia or von Willebrand disease.

Stages of development and forms of DIC syndrome

Doctors classify this condition in different ways. All these divisions are based on etiological, pathogenetic features, as well as variants clinical course. Taking into account the mechanisms of pathology triggering, the following stages of DIC syndrome are distinguished.

1. First, hypercoagulation occurs.
2. It gives way to the so-called consumption coagulopathy, which gradually gives way to the third stage.
3. Hypocoagulation is the terminal stage of shock; if the patient is not helped at this stage, the mortality rate will be very high.
4. Restorative, includes the process of restoring the body after correction of the shock state.

Pathogenesis

The pathogenesis of DIC syndrome is based on mechanisms that occur during all its stages. The failure of the body's hemostatic system is due to increased stimulation of blood coagulation, as well as depletion of anticoagulant and fibrinolytic mechanisms.

The pathophysiology of DIC depends on many factors that serve as activators of the coagulation process. They act independently or act as mediators of effects on the endothelium of the vascular wall. Activators of all stages of DIC include toxins, bacterial waste products, immune complexes, decreased circulating blood volume, and many others. It is they who determine the flow options of the internal combustion engine.

The pathological component is based on the stages of the process.

1. The first phase of DIC is hypercoagulation, during which cells inside the vessels begin to stick together. It is triggered by thromboplastin entering the bloodstream. Its duration is several minutes.
2. The pathophysiology of DIC syndrome includes consumption coagulopathy, in which there is a pronounced deficiency of fibrinogen and other coagulation factors due to rapid consumption, and the body does not have time to replace them.
3. Secondary fibrinolysis is accompanied by hypocoagulation, the blood clots very slowly or does not clot at all.
4. Recovery is characterized residual effects or complications.

Clinical manifestations

The symptoms of DIC syndrome are not questioned when skin manifestations occur (they may be called hemorrhagic manifestations), decreased diuresis, or lung damage. These are the main signs of pathology.

The symptoms are due to the main link in the pathogenesis, this is increased blood clotting. Parenchymal organs and skin are the first to suffer. The severity of the condition depends on the severity of thrombus formation.

1. When the skin is involved, a hemorrhagic rash is observed, it resembles minor hemorrhages and areas of tissue necrosis.
2. The lungs react by developing acute respiratory failure. Shortness of breath occurs, severe cases are accompanied by pulmonary edema or respiratory arrest.
3. When there is an excess of fibrin in the blood plasma, kidney problems– renal failure, end stage will manifest as anuria and electrolyte imbalance.
4. Brain damage is determined by the presence of neurological symptoms.

In addition to the changes described above, the patient may develop massive external or internal hemorrhages and hematomas.

Diagnosis of DIC syndrome

To determine the presence of disseminated intravascular coagulation in a patient, it is necessary to carefully collect anamnestic data and establish a diagnosis that provoked this condition. DIC syndrome requires laboratory diagnostics, which includes a coagulogram, general analysis blood, study of blood clotting factors. Very important point is to determine the severity of the patient in order to prescribe adequate correction.

It is necessary to take into account that the patient may bleed from several places at once. Moreover, if a chronic process has developed or it is not very aggressive, then hypercoagulation can only be detected through laboratory diagnostics.

The doctor must prescribe:

• blood test to determine platelets;
• coagulogram, which will display the amount of fibrinogen, blood clotting time, thrombin level, prothrombin level, APTT.

There are specific tests - RFMC, D-dimer. They are performed using enzyme immunoassay.

Doctors consider the main criteria for DIC syndrome to be the identification of fragmented red blood cells, an insufficient number of platelets, and a decrease in fibrinogen concentration. Low activity of antithrombin-III, increased duration of aPTT and thrombin time are also noted. Weak clot formation or instability indirectly indicate a violation of hemostasis.

The doctor is obliged to check the functional performance of the organs that are first exposed to shock - the kidneys, liver, lungs.

Chronic DIC syndrome

The main characteristics of chronic DIC are:

1. Constantly increased entry into the systemic bloodstream of substances that act as activators of the hemostasis system.
2. Increased rate of fibrin formation inside blood vessels.
3. Decreased platelet consumption.
4. There is no secondary activation of fibrinolysis, as well as generalized intravascular fibrinolysis.
5. Fibrin blocks the microcirculation of parenchymal organs, causing their severe dysfunction.

The acute process is activated by thromboplastin, which enters the blood from tissues that have undergone decay due to various triggering factors. It could be injuries, burns, surgical procedures on target organs, destructive processes, obstetric diseases. Much less often, phospholipids of the endothelium of the vascular wall or blood cells become triggers of DIC syndrome. This mechanism is more typical for bacterial processes and shock conditions. Chronic disseminated intravascular coagulation is caused by less aggression of the above activation factors, which contributes to its slow onset and a better prognosis for the patient’s life.

Treatment

Successful treatment of DIC syndrome is only possible if the condition is diagnosed in the early stages of its development. Active actions medical personnel necessary for severe manifestations - bleeding, development of multiple organ failure. Emergency care for DIC is provided in an intensive care unit. The chronic process requires correction of hemodynamics, electrolyte disturbances, and symptomatic therapy.

At acute course It is necessary to quickly determine the cause and then eliminate it. This could be an emergency delivery, the appointment of powerful antibacterial drugs. Hypercoagulation is corrected with fibrinolytics, anticoagulants, and antiplatelet agents. Patients with such pathologies are under constant supervision of medical workers; their hemostasis system is monitored every 15-30 minutes.

Replacement therapy involves blood transfusions and antifibrolytic agents. Sometimes there is a need to use hormonal drugs, plasmapheresis, oxygen therapy. In order to restore microcirculation, functional state vascular and metabolic therapy is prescribed for internal organs. The chronic process requires the administration of vasodilators, antiplatelet agents, and heparins. It is important to understand that treatment of the condition is complex, requiring certain knowledge and skills on the part of the doctor. The patient’s life depends on his skill.

DIC syndrome is a severe pathological blood disease. The mechanisms of disease development are as follows:

• stimulation of platelet function;
• stimulation of coagulative properties

As a result of this process, the following changes occur:

• increased thrombin synthesis;
• blood clot synthesis

Small clots form and interfere with blood circulation. Thrombocytopenia is a pathology that occurs due to a decrease in coagulation factors.

In addition to thrombocytopenia, the following symptoms occur:

• the phenomenon of fibrinolysis;
• severe hemorrhagic syndrome

A pathological severe condition that requires emergency intervention - DIC - syndrome. Mortality rate is up to sixty-five percent.

Etiology of DIC syndrome

This pathology is a consequence of other diseases. The etiology of the disease is as follows:

• infections;
• purulent diseases;
• artificial termination of pregnancy;
• catheterization process;
• injuries to the walls of blood vessels;
• mechanical damage to organs;
• consequence of surgery;
• phenomenon of vascular prosthetics

Additional causes of the disease:

• state of shock;
• gynecological diseases;
• pathology of pregnancy;
• tumor;
• malignant neoplasms;
• the phenomenon of hemolysis;
• acute course of hemolysis;
• autoimmune pathologies;
• medicines;
• drugs;
• toxic pathologies

Shock conditions include:

• anaphylactic shock;
• septic shock;
• cardiogenic shock;
• traumatic shock;
• hemorrhagic shock

Gynecological diseases include:

• amniotic fluid embolism;
• process of separation of the placenta;
• placenta previa;
• placental abruption;
• operative delivery

Malignant neoplasms of the following types:

• pulmonary system;
• prostate pathology

Immune pathologies of the following nature:

• hemorrhagic vasculitis;
• glomerulonephritis;
• systemic lupus

Common reason of this disease– generalized septicemia.

DIC - syndrome - symptoms

The clinic indicator is the main cause of the disease. The main way the disease arises is through shock situations. Symptoms of the disease in the chronic stage are as follows:

• minor bleeding;
• hypovolemia;
• dystrophy;
• metabolic disorders

Symptoms of DIC - syndrome in acute stage the following:

• phenomenon of increased coagulation;
• decreased coagulation;
• bleeding is intense;
• cardiogenic shock

The provision of medical care influences the manifestation of this disease. Selected necessary treatment. This disease progresses in the following cases:

• injuries;
• lack of relief of hypovolemia;
• insufficient blood transfusion

DIC is a syndrome that can be variable in nature. In this case, this process is facilitated by:

• pancreas pathology;

Signs of hemocoagulative shock are as follows:

• impaired blood flow;
• oxygen starvation;
• kidney failure;
• liver failure

Death occurs in most percent of cases. The therapeutic effect is difficult to achieve. A severe condition occurs in patients in the following cases:

• diagnosis of the disease is untimely;
• untimely treatment with medications

Bleeding in this disease is profuse. The provocateur of hemorrhagic shock of a generalized type is a pathology of the hemostatic system. The intensity of bleeding varies; with gynecological diseases, uterine bleeding develops.

Treatment for the disease is as follows:

• hemostatic therapy;
• restoration of uterine tone;
• therapy for stomach ulcers

Signs of generalized hemorrhagic syndrome are:

• skin bruising;
• hemorrhages;
• cough;
• sputum;
• nosebleeds;
• sweating blood

Hemorrhages occur in the following areas:

• pulmonary system;
• brain;
• spinal cord;
• adrenal region;
• uterus

Sweating of blood affects the following system organs:

• pericardial system;
• abdomen;
• pleural cavity

Acute posthemorrhagic shock occurs with intense bleeding. In this case, emergency treatment is necessary. DIC, a chronic syndrome, is characterized as follows:

• presence of bleeding;
• permanent anemia;

For anemia, transfusion must be used. A mass transfusion of red blood cells is performed. As a result of disruption of the blood circulation process, organ function is affected. If the respiratory function of DIC is impaired, the syndrome is severe.

Signs of this condition are:

• breathing problems;
• sputum;
• acrocyanosis

Pulmonary edema is aggravated by transfusion of solutions. These solutions include:

• sodium;
• albumen

At in a state of shock pulmonary system requires the following therapy:

• mechanical ventilation event;
• diuretics

The kidney system is also affected in this disease. In this case, the following symptoms arise:

• accumulation of proteins in the urine;
• accumulation of red blood cells in the urine;
• impaired urination

With liver pathology, the following symptoms occur:

• kidney failure;
• liver failure;
• abdominal pain;
• icteric syndrome

When treated with hormones, the following symptoms occur:

• hemorrhages;
• bleeding;
• intoxication

Intoxication is a consequence functional disorders intestines. Signs of impaired blood circulation in the brain:

• headache;
• signs of meningitis;
• dizziness;
• impaired consciousness

Signs of septic lesions are as follows:

• platelet formation;
• electrolyte disturbances;
• dehydration process;
• adrenal insufficiency

DIC – syndrome – stages

There are signs for each stage. The initial stage is the hypercoagulative stage. Signs of the hypercoagulable stage:

• intravascular aggregation;
• various blood clots;
• fatal outcome

The second stage of DIC syndrome is a stage accompanied by a decrease in platelets. Their aggregation is increased. Signs of this stage:

• phagocytosis;
• microclot lysis process

The third stage of the disease is the fibrinolytic stage. Signs of the third stage of the disease:

• restoration of blood circulation;
• damage to clotting factors

The fourth stage of DIC syndrome is the recovery stage. The signs of this stage are as follows:

• necrosis;
• dystrophy;
• restoration of tissue function

Multiple organ failure is a consequence of the lack of proper treatment. The use of medications is the basis of treatment.

In pregnant women, DIC syndrome

The process of hemostasis disruption occurs during pregnancy. Gynecological pathologies are important. Causes of death as a result of this disease:

• bleeding is intense;
• development of blood clots

Periods of development of DIC syndrome:

• stage of pregnancy;
• period after childbirth;
• newborn period

Forms of development of this disease:

• lightning stage of damage;
• death;
• sluggish defeat;

Signs of chronic disease:

• pregnancy status;
• cardiac pathology;
• urinary system disorder

Acute blood loss is a provoking factor of DIC syndrome. The cause is intense uterine bleeding.

Possible etiological signs of the disease:

• infections;
• inflammatory phenomena;
• embolism;
• placental abruption;
• inflammation of the endometrium;
• purulent lesion

The duration of the hypercoagulable stage is up to three days. Signs of this stage:

• redness of the skin;
• cardiopalmus

Signs of the hypocoagulable stage of the disease:

• uterine bleeding;
• nose bleed;
• presence of hemorrhages;
• presence of rashes;

There are various sources of bleeding. Diagnosis of the disease in pregnant women:

• use of coagulogram;
• laboratory methods

Therapeutic therapy includes:

• drug treatment;
• non-pharmacological means

Hospitalization of a pregnant woman is necessary. A pregnant woman is hospitalized in a hospital.

The child has DIC syndrome

The risk group is children, especially the neonatal period. Children may have the following symptoms:

• infections inside the womb;
• viruses;
• low body temperature;
• oxygen starvation;
• signs of acidosis

The cause of the disease in children is cardiac shock. Processes influencing DIC syndrome:

• thrombin synthesis;
• vascular damage;
• increased coagulation;
• blood clot formation;
• oxygen starvation;
• reduction of coagulation factors;
• decrease in platelets;
• impaired hemostasis process

The clinic is a reflection of the stage of the disease. The underlying disease matters. Possible signs diseases:

• acrocyanosis;
• increased breathing;
• decreased blood pressure;
• urinary disturbance;
• liver enlargement;
• spleen enlargement

In the coagulopathic phase they turn blue skin. The development of hemorrhagic shock is possible. Bleeding in the brain is a dangerous consequence of this condition.

Mortality is increasing. With assistance, the outcome of the disease is favorable. The recovery phase occurs with proper treatment. The main focus of therapy in children is to exclude the underlying cause.

Blood transfusions are used. To do this, use the following means:

• plasma solution;
• pentoxifylline solution;
• drug dopamine

Treatment of the coagulopathy phase in a child:

• replacement transfusion;
• platelet transfusion;
• heparin

Heparin is administered under the control of a coagulogram. Treatment during the recovery period is symptomatic. Thrombolytic agents are used in in this case.

Diagnosis of DIC syndrome

Distinguish the following diseases with impaired hemostasis:

• sepsis;
• burn;
• bites

Diagnosis is complicated in the following pathologies:

• leukemia signs;
• lupus erythematosus;

Testing is used in this case. Methods for diagnosing this disease:

• lab tests;
• instrumental method;
• blood clot analysis;
• calculation of prothrombin time;
• paracoagulation tests

Used for rational treatment following methods diagnostics:

• antithrombin assay;
• plasma research;
• sensitivity determination

Basic diagnostics of the following type:

• determine hematocrit;
• level of hypoxemia;
• electrolyte level;
• biochemistry

Chronic DIC syndrome is diagnosed at the terminal stage. The signs of chronic DIC syndrome are as follows:

• oncological diseases;
• cardiac congestion;
• myeloproliferative diseases

Signs of myeloproliferative diseases:

• increased blood viscosity;
• increased hematocrit;
• infiltrative foci

A severe degree of DIC syndrome occurs during chronic hemodialysis.

Treatment of DIC syndrome

DIC is a syndrome treated by rheumatologists. The therapy room is intensive. The mortality rate is up to thirty percent. The basis of therapy for this disease is the exclusion of provoking factors.

Therapy for this disease is antibacterial, since purulent processes are possible. Sensitivity to drugs is determined. There are indications for the use of antibacterial agents:

• criminal abortions;
• discharge of amniotic fluid;
• intoxication

Intoxication symptoms are as follows:

• hectic fever;
• meningitis;
• lung damage

The following means are also used:

• intravenous infusions;
• antiprotease agents

The effect of these drugs is as follows:

• reduction of intoxication;
• reduction of the destructive process

Antishock therapy is required to reduce shock states. Drugs used to reduce shock conditions:

• drug reopolyglucin;
• glucocorticosteroids

Medicines to improve blood circulation:

• adrenoblockers;
• phentolamine;
• drug trental

Heparin is used only in the presence of laboratory control. A large dosage of heparin is used in combination with antiproteases. Heparin is not used for heavy bleeding.

Indications for discontinuation of heparin:

• collapse;
• decreased blood pressure;
• thrombocytopenic syndrome

The effect of using transfusions:

• stopping the destruction process;
• coagulation correction;
• increasing protective properties

Drugs used in the treatment of the hypercoagulable phase:

• saline solution;
• albumins

Transfusion is also performed. Indications for red blood cell transfusion:

• heavy bleeding

Plasmapheresis is used for chronic disease. Consequences of plasmapheresis:

• removal of proteins;
• clotting factor is activated

Effectively complex treatment the following drugs:

• dipyridamole;
• trental

Indication for surgical methods treatment - the presence of a source of bleeding. Methods of surgical treatment:

• gastrofibroscope method;
• hemostatic agents

The development of the syndrome in a newborn is possible due to factors in intrauterine development or pathologies after birth or during childbirth.

During puberty, the following factors contribute to the development of the disease:

• placenta previa,
• fetoplacental insufficiency,
• death of one child during multiple pregnancy,
• malignant neoplasms of the uterus with damage to its soft tissues,
• severe gestosis in late pregnancy,
• unreasonably prolonged stimulation of labor.

Reasons for the development of DIC syndrome in the perinatal and neonatal period:

• conflict Rh factor,
• oxygen starvation,
• premature birth,
• infection during childbirth,
• respiratory disorders,
• birth injuries resulting in disorders of the central nervous system.

Symptoms

If a pregnant woman has DIC syndrome, with a 90% probability we can say that her baby will also have this blood flow problem.

Immediately after birth, it is impossible to visually detect manifestations of the disease in a newborn. A prompt blood test is required, which will provide data on the composition of blood, plasma and the concentration of thromboplastin in it.

The newborn also goes through all stages of development of the syndrome.

• hypercoagulation - sticking together of blood cells,
• hypocoagulation - excessive blood thinning,
• fibrinolysis is the most critical stage with pronounced thrombocytopenia,
• recovery - normalization of platelet levels in the blood.

Diagnosis of DIC syndrome in a newborn

In a baby, these stages develop rapidly. With absence timely diagnosis the onset of the third stage becomes fatal for most infants, since the body itself cannot cope with the anomaly and multiple internal hemorrhages occur.

An immediate response from specialists to abnormalities in a newborn’s hemostasis can save a little person from serious complications and tragic consequences.

Complications

Intrauterine development DIC syndrome threatens pregnancy loss and premature birth.

If the disease is detected immediately after birth and treated immediately, the prognosis is quite favorable.

If the diagnosis is made late, then the probability of death of the baby is 30-50%.

Treatment

What can you do

A young mother needs to be extremely attentive, strictly follow all medical recommendations, agree with treatment tactics doctor and take necessary medications. Only in agreement with specialists can the baby’s blood clotting be restored as quickly as possible and without side effects.

Under no circumstances should you resort to traditional therapy. Her methods can only make the situation worse.

A young mother needs to remain calm to avoid difficulties with lactation. After all, breast milk is the best immunomodulator during infancy, as well as an excellent sedative, but only if the mother’s mental state is good.

What does a doctor do

A group of specialists is working on the treatment of DIC syndrome in a newborn. They draw up an individual treatment plan for each specific case. Therapeutic tactics depends on the stage of the disease, its causes and general condition newborn In any case, doctors adhere to the following principles.

• Immediate start of treatment after receiving the results of the blood test.
• Surgical removal of the causes of DIC syndrome. First of all, therapy is aimed at removing intoxication child's body and to get out of a state of shock.
• Calculation of possible risks, on the basis of which methods of treatment and elimination of symptoms are selected.

In any case, the treatment is complex. As a rule, therapy proceeds in several directions at once, which allow achieving a quick and good effect.

• anti-shock measures,
• maintaining the composition and volume of blood and plasma,
• treatment of the underlying disease,
• elimination of pathological abnormalities,
• heparin therapy,
• administration of medications,
• restorative therapy with medications, vitamins and physiotherapy.

Prevention

Syndromic disruption of homeostasis is easier to prevent than to treat. To avoid childhood pathology future mom must begin to take care of her child even before conception. Of course, care should continue after birth. To prevent DIC syndrome in a newborn, it is necessary:

• identify before pregnancy pathological abnormalities in your body and eliminate them,
• during pregnancy, visit a gynecologist, conduct healthy image life, eat right, protect yourself from negative influences. All this is done with the aim of normal pregnancy and fetal development.
• with the onset of labor, call an ambulance or get to the maternity hospital on your own, do not give birth at home,
• If necessary, after birth, immediately give consent to the treatment of the baby.