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Hemorrhagic diathesis appears due to changes in the links of hemostasis (such as damage to the vascular wall) and occurs in a state of increased bleeding in both an adult and a child’s body. Hemorrhagic disease is bleeding of the mucous membranes. It can be detected by passing a detailed blood test.

What are hemorrhages

In medicine, spontaneous bleeding from blood vessels in any part of the body is called hemorrhage. This pathological syndrome manifests itself in patients in response to external influences or in the presence of internal diseases. Hemorrhagic disease occurs due to damage to the integrity of the walls of blood vessels, a decrease in the number of platelets, and a violation of coagulation hemostasis. In this case, blood flows beyond the boundaries of the blood vessel through the damaged area. The types of abnormalities depend on which part of the body they appear in.

Hemorrhagic syndrome is typical for what diseases?

Among the forms of hemorrhagic diseases, hereditary and acquired disorders of hemostasis are distinguished. The latter are associated with multifactorial disorders of the blood coagulation system (for example, acute disseminated intravascular coagulation syndrome), damage to blood vessels of dysmetabolic, immune, toxic-infectious, immune complex origin, abnormalities of adhesive proteins in blood plasma, damage to platelets and megakaryocytes. Hereditary hemorrhagic diseases are caused by:

pathologies of plasma factors of the blood coagulation system;
hereditary disorder of hemostasis;
genetic structural changes in the vascular wall.

Hemorrhagic diathesis in children

Due to a lack of vitamin K, hemorrhagic syndrome of newborns can develop, among the signs of which are: hemorrhagic skin rashes, umbilical bleeding. Intestinal bleeding or intracerebral hemorrhage may occur. Doctors name the following reasons for the occurrence of hemorrhages in newborns: during pregnancy, the mother took phenobarbitals, salicylates or antibiotics. Hemorrhagic disease in children occurs when:

neoplastic lesions of connective tissue;
thrombocytopenia;
coagulopathies;
vasopathy;
hemophilia.

Pathogenesis of hemorrhagic syndrome

As a mechanism for the development of hemorrhagic syndrome and its manifestations, doctors describe the following picture of pathogenesis:

impaired coagulation (DIC) and platelet production;
changes in collagen structure, fibrinogen properties, vascular walls:
- for circulatory disorders;
- decreased neurotrophic function of the central nervous system;
- violation of the angiotrophic function of platelets.

Hemorrhagic diseases - classification

The following types of hemorrhagic syndromes have been described in medicine: hematoma, petechial-spotted, mixed bruise-hematoma, vasculitic-purpuric, angiomatous. The listed types differ in the nature of their manifestation and causes. In each individual case, it is necessary to follow the individual treatment tactics chosen by the attending physician. Description of hemorrhagic diathesis according to the type of disease:

The hematoma type is caused by chronic genetic bleeding. This serious disease due to decreased coagulability manifests itself in the patient in the form of painful sensations with hemorrhages in the joints (hemarthrosis), dysfunction of the musculoskeletal system. In case of injury, internal hematomas form extensive swelling in the soft tissues, which causes pain.
The petechial-spotted type is also called the bruise type due to external manifestations on the body in the form of bruises, as can be seen in the photo. Appears in cases of blood clotting disorders (lack of coagulation factors, hypo- and dysfibrinogenemia), thrombocytopathy and thrombocytopenia (thrombocytopenic purpura).
Microcirculatory-hematoma, or mixed bruise-hematoma bleeding develops in the presence of immune inhibitors of factors IX and VIII in the blood, an overdose of thrombolytics and anticoagulants, disseminated intravascular coagulation, von Willebrand's disease, severe deficiency of prothrombin complex factors and factor XIII. Externally, this type of disease manifests itself through petechial-spotted skin hemorrhages, large hematomas in the retroperitoneal region and intestinal wall, and petechial skin rash.
Symptoms of the vasculitic purpuric type are a red skin rash (erythema). With the disease, there is a tendency to bleeding in the intestines and inflammation of the kidneys (nephritis), immune and infectious vasculitis, and disseminated intravascular coagulation syndrome.
The angiomatous type develops in the area of arteriovenous shunts, angiomas, and telangiectasia. This type of disease is characterized by hemorrhages in the area of vascular anomalies and persistent bleeding of permanent localization.

Causes of hemorrhagic syndrome

Hemorrhagic symptoms may develop with vascular anomalies, disorders of coagulation hemostasis, enzyme activity, blood coagulation system, or when taking medications that interfere with platelet aggregation. Experts were able to identify a type of disease in which there is a high risk of hemorrhage:

hepatitis;
oncology;
severe viral infections;
cirrhosis of the liver;
lack of prothrombin in the blood;
hemophilia;
leukemia;
vasculitis.

The causes of hemorrhages depend on the primary or secondary form of the disease. The first is characterized by the presence of genetic determination: there is a defective gene in the body that can cause a hemorrhagic disease at any time. The secondary form occurs from damage to the walls of blood vessels (with an autoimmune process, mechanical damage, inflammation and chemical intoxication), with secondary thrombocytopenia, DIC syndrome, hemorrhagic vasculitis and deficiency of prothrombin complex factors.

Symptoms of hemorrhagic syndrome

There is a connection between the areas of localization of hemorrhagic diathesis and the clinical picture, intensity of manifestation, and specificity of symptoms of the disease. Signs of hemorrhage in the nasal cavity are manifested by recurrent bleeding from telangiectasia (dilation of small vessels). This manifestation of symptoms is also typical for hemorrhages in the lips, mouth, pharynx and stomach. At the age of up to 30 years and during puberty, the frequency of bleeding from telangiectasia increases. Other signs include:

dissecting hematomas;
skin manifestations;
delayed bleeding;
decreased platelet count;
superficial ecchymoses;
petechiae;
hemarthrosis.

Treatment of hemorrhagic syndrome

The treatment of hemorrhage depends on the symptoms and cause of the disease in patients. Complex therapy involves: immunoglobulin, plasmapheresis, glucocorticosteroids. For inflammation of blood vessels (vasculitis), non-hormonal immunosuppressants, non-steroidal anti-inflammatory drugs (NSAIDs) are taken, corticosteroid therapy (glucocorticoid) is used and attempts are made to reduce the symptoms of inflammation. For hemophilia A, the missing factor VIII is administered, and for hemophilia B, factor XI is administered. After a detailed blood test, the doctor helps the patient choose treatment tactics.

Among the fundamental principles of therapy are:

symptomatic treatment;
intravenous injection of a synthetic analogue of vitamin K - vikasol, calcium chloride and ascorbic acid;
if necessary, transfusions of blood, its components (platelet, erythrocyte mass) and plasma are carried out;
taking medications that help strengthen the walls of blood vessels (ethamzilate);
for local treatment of hemorrhages the following are indicated: dry thrombin, homeostatic sponge, aminocaproic acid.

Consequences of hemorrhagic disease

If hemorrhages are detected, you should not panic, but you should immediately consult a doctor. With a mild degree of the disease and timely treatment, the prognosis of the disease is favorable. However, there are cases when, with late detection of the disease, severe complications of hemorrhagic syndrome occur, which can lead to death.

Among these consequences are: massive internal bleeding, cerebral hemorrhages, cardiac dysfunction, adrenal insufficiency. The child may experience hypovolemic shock, which manifests itself through a decrease in blood pressure and body temperature, weakness, and pallor. To prevent the described consequences, it is necessary to immediately take the child for a consultation with a pediatrician as soon as symptoms are noticed.

Prevention of hemorrhagic syndrome

Compliance with simple preventive measures can protect against the development of pathologies. A blood test will help identify hemorrhagic bleeding, and you can reduce the risk of its occurrence if:

within half an hour after birth, attach the baby to the breast;
administer vitamin K by injection to children at risk;
administer vitamin K injections during parenteral (intravenous) nutrition;
administer intramuscular vitamin K during or before labor if the mother is taking anticonvulsants.

Video: Neonatal hemorrhagic syndrome

vitamin K deficiency in a newborn, hemorrhagic diathesis

One of the rather dangerous conditions in pediatrics is hemorrhagic disease of the newborn, which is manifested by a decrease in blood clotting and the occurrence of bleeding of various locations. The reason for this is a decrease in the synthesis of some factors of the coagulation system, which is largely due to a lack of vitamin K in the child’s body. The danger of the disease lies in the high risk of complications, which can cause death. Modern methods of prevention in most cases make it possible to avoid this terrible condition and its consequences.

This pathology is relatively rare - it is diagnosed in only less than 1.5% of born babies. In Western European countries and the USA, hemorrhagic disease is even less common (less than 0.1%). This is due to the mandatory use of vitamin K for its prevention in all newborns in the first day after birth.

The role of vitamin K

The main cause of the pathological condition is insufficient intake or formation of vitamin K in the baby’s body. Therefore, in ICD-10 this disease also has the second name “vitamin K deficiency in a newborn.” In 1943, scientists who established the cause of hemorrhagic disease were awarded the Nobel Prize.

Vitamin K performs an important function in the human body. This substance is primarily responsible for the activation of certain components of the blood coagulation system.
Vitamin K plays a decisive role in the implementation of their blood coagulation properties; its deficiency significantly increases the risk of bleeding.

The immediate cause of increased bleeding is the lack of the following components of the coagulation system:

antihemophilic protein B;
prothrombin;
Stewart factor.

In addition, with hemorrhagic disease, the process of activation of other coagulation factors is disrupted. In this case, calcium ions are not included in the process of blood clot formation, which causes bleeding.

Causes of hemorrhagic disease in newborns

Unfortunately, vitamin K does not cross the placenta well during pregnancy. In addition, breast milk contains very little of it on the first day; the concentration of the vitamin gradually increases only in the next day. That is why small children in the first days after birth, especially those who are breastfed, are extremely sensitive to its deficiency.

Depending on the root cause, this pathology can be primary or secondary. The main primary causes of hemorrhagic disease of the newborn are as follows:

mother taking anticoagulant medications during pregnancy;
premature birth;
delivery by caesarean section;
taking antibiotics or anticonvulsants by a pregnant woman;
liver and intestinal diseases in women;
dysbiosis in the mother;
late toxicosis of pregnancy.

Secondary pathology is often associated with impaired liver function in the child. This can occur due to infection (hepatitis) or congenital pathologies. In this case, the factors necessary for complete blood clotting do not form sufficiently, which becomes the cause of bleeding.

How does the disease manifest itself?

Depending on the time of appearance of characteristic symptoms, hemorrhagic disease occurs:

early - hemorrhagic disease of newborns manifests itself in the first 24-48 hours after birth;
classic - symptoms appear on the third to fifth day;
late - bleeding occurs in the first weeks or months of the child’s life.

In the early or classic version of the course, the symptoms of hemorrhagic disease of newborns are as follows:

vomiting blood;
the presence of blood in the stool (melena);
subcutaneous hemorrhages of various sizes (hematomas, “bruises”);
hematomas in the head area;
increased bleeding in the area of the umbilical wound;
blood in the urine;
internal bleeding (pulmonary, intracranial).

Late hemorrhagic disease of newborns in most cases is caused by insufficient intake of vitamin K in breast milk, as well as a violation of its formation in the intestines. In this case, the reasons may be the use of antibacterial agents, dysbacteriosis, or congenital enzymopathies. It manifests itself during the first months of the child’s life with the same symptoms as the early form of the disease.

Intracerebral hematomas

Hemorrhagic disease of newborns is especially dangerous because intracerebral hemorrhage can occur against its background. In some cases, this condition causes severe neurological deficits and even death.

Most often, bleeding is localized under the membranes (subarachnoid hemorrhage) or in the substance of the brain. In this case, against the background of signs of blood coagulation disorders, other symptoms appear, indicating the involvement of intracranial structures:

impaired consciousness of varying degrees;
frequent regurgitation, vomiting;
constant, causeless crying of the child;
fontanelle tension;
divergence of the sutures of the skull;
convulsive syndrome.

If there are signs of intracranial hemorrhage, the child must be urgently hospitalized in the neurosurgical department and undergo specific therapy aimed at eliminating vitamin K deficiency. Late presentation significantly worsens the prognosis for the child in terms of neurological manifestations and life.

How is it diagnosed?

You can suspect the presence of a hemorrhagic disease in a child by the presence of characteristic external signs: the appearance of “bruises” on the skin even with slight pressure, a petechial rash on the palate, increased bleeding in the area of the umbilical wound or injection. Some children also develop yellowing of the skin, which is associated with bleeding in the digestive tract, breakdown of the blood and increased bilirubin levels.

For additional diagnostics, a number of laboratory tests are indicated:

general clinical blood test with platelet count;
coagulogram and determination of prothrombin index;
determination of bleeding time;
APTT (activated partial prothrombin time).

Hemorrhagic disease of newborns is characterized by normal bleeding time and platelet count. However, clotting time and APTT are prolonged. With prolonged bleeding, a decrease in hemoglobin and the number of red blood cells may be detected.

The presence of an intracranial hematoma is determined using neurosonography. If intra-abdominal bleeding is suspected, endoscopic examination and ultrasound scanning of the abdominal organs are indicated.

Therapy

According to modern clinical recommendations, the main method of treating hemorrhagic disease of newborns is injections of vitamin K3 (Vikasol). The medicine is administered intramuscularly, the dosage is calculated by the neonatologist individually based on the child’s weight, the maximum daily dose is no more than 4 mg. The medicine is prescribed once a day, the duration of treatment usually does not exceed three to four days.

Additionally, if necessary, the following medications and blood products are used:

fresh frozen plasma;
red blood cell mass;
plasma substitutes;
prothrombin complex (“UMAN-complex D.I.”);
drugs to maintain cardiovascular activity.

In severe cases of the disease and the presence of complications, treatment of hemorrhagic disease of the newborn is carried out in the intensive care unit. The presence of intracranial hemorrhage with symptoms of dislocation of the midline structures of the brain requires urgent surgical intervention and removal of the hematoma.

Forecast

If the disease is detected in the early stages and specific therapy is carried out, the prognosis is favorable. As a rule, relapses of hemorrhagic disease do not occur in the future.

Late stages of hemorrhagic disease of the newborn can cause complications in some children in the form of damage to the central nervous system. Less commonly, the disease ends in death.

Prevention

Preventive measures are indicated primarily for children at risk:

having varying degrees of prematurity;
receiving antibiotic therapy;
with birth injuries;
born asphyxia or as a result of caesarean section;
if the mother’s pregnancy proceeded with complications;
whose mothers suffered from liver diseases, dysbacteriosis, and took anticoagulants or antibacterial drugs.

In addition, prevention is also indicated for children who are bottle-fed. Although breast milk contains small amounts of vitamin K, it contains high levels of factors necessary for blood clotting. Therefore, children who do not receive breast milk require additional administration of artificial vitamin K.

In some European countries and the United States, prevention of hemorrhagic disease is mandatory for all newborns. In this case, vitamin K is given orally in a dose significantly higher than its content in breast milk. This introduction is repeated three times:

in the first days after birth;
on the fourth to seventh day;
in the third to sixth week of life.

For newborns at risk, administration of vitamin K supplements is indicated even in the absence of obvious signs of hemorrhagic disease. "Vikasol" is administered intramuscularly for one to three days. The duration of treatment is determined individually based on laboratory data.

The consequences of hemorrhagic disease of the newborn can be quite serious and life-threatening for the child. In the absence of timely treatment, the disease can cause severe complications with subsequent disability or even death. That is why it is so important to identify the pathology in a timely manner and begin treatment measures as early as possible.

Fortunately, hemorrhagic disease of newborns is an infrequent phenomenon, occurring in only 2-5 children out of 1000, and doctors encounter its more dangerous late form even less often - 5-20 children per 100 thousand. “So this is definitely not about us,” you will think, and it’s good if you turn out to be right. Otherwise, only a lightning-fast reaction from parents to alarming symptoms will help save the baby... So, as they say: “forewarned is forearmed.”

Causes of hemorrhagic disease of newborns

The cause of hemorrhagic disease is vitamin K deficiency, which is necessary for normal blood clotting. Its lack leads to various bleedings that pose a danger to the child's life.

Factors contributing to the development of hemorrhagic disease include the mother taking a number of medications during pregnancy (indomethacin, phenytoin, acetylsalicylic acid, antibiotics), immaturity or prematurity of the newborn, perinatal hypoxia, asphyxia, untimely breastfeeding, as well as birth injuries.

Newborns who, according to doctors, are at risk are given a prophylactic dose of vitamin K immediately after birth ( Vikasol).

The causes of late hemorrhagic disease are somewhat different; we will dwell on them in more detail a little later.

Symptoms and treatment of hemorrhagic disease of newborns

Since classical hemorrhagic disease develops in 2-4 days after birth(rarely on the first day), that is, while the child is still in the maternity hospital, parents just need to trust the professionalism of the doctors and not interfere with the treatment of the baby.

The most common symptoms of classical hemorrhagic disease are nose and gastrointestinal bleeding, continuous bleeding from or after. Therefore, if the baby spits up with blood, his nose is bleeding, the injection site bleeds for a long time, the umbilical wound or there is blood on the diaper, do not wait for the next round, ask the neonatologist to examine the newborn unscheduled, because the sooner treatment begins, the greater the chances of success .

If a blood test confirms the diagnosis, the baby should be immediately they begin to treat. Treatment consists of intramuscular injection of vitamin K, plasma and blood transfusions (in especially severe cases). In addition, about 6 times a day the newborn is fed expressed breast milk, which helps stop bleeding due to the fact that it contains thrombokinase.

If the diagnosis is timely and the treatment of hemorrhagic disease is correct, newborns will quickly complete recovery occurs.

Late hemorrhagic disease of the newborn

Late hemorrhagic disease affects children aged 1 to 4 months, most often appearing at 2 months. However, exceptions are possible here too, that is, infants both older than the specified age and younger can get sick. The late form of the disease has a slightly different nature - it is caused by the fact that the intestinal flora is not able to synthesize vitamin K2 in sufficient quantity. This disease is more severe and much more dangerous than the classic version.

Who is at risk? As a rule, these are full-term children who did not receive a prophylactic dose of vitamin K in the maternity hospital and suffer from transient liver failure(an indirect sign of such a deficiency is jaundice that has not gone away by 1 month) and, oddly enough, located exclusively breastfed. What does breastfeeding have to do with it? It turns out that the intestines of children fed with mother's milk are populated by flora that does not cope well with the synthesis of vitamin K2, while with artificial feeding the situation is quite the opposite.

The danger of late hemorrhagic disease of newborns is that if treatment is not started as soon as possible, then large-scale intracranial hemorrhages can't be avoided. The high mortality rate from the late form of this disease is associated precisely with the difficulty of its recognition. Since this phenomenon is considered very rare, not every local pediatrician will be able to interpret the symptoms in a timely manner, and parents are often in no hurry to see a doctor, not realizing that in such a situation literally minutes count.

So, parents should be wary the appearance of bruises on the baby’s body- in any quantity and any size. There is no need to think about under what circumstances the baby could have received such an injury - rubbed with a button from a bodysuit, hit the crib, lay down on a rattle... Don’t look for excuses, but call an ambulance, as this is the first alarm bell!

If a baby's blood was taken for analysis, and my finger won't stop bleeding, then this is a sure sign of problems with blood clotting, which means a reason to urgently call doctors. Why such a rush? The fact is that the very first visible symptoms, such as bruises on the body, bleeding, etc., will develop into intracranial hemorrhage in just 1-2 days, so it’s better to “be on the safe side” in this matter.

And finally, I would like to wish your children good health. Let the knowledge gained from this article remain only theoretical, and you will never have the opportunity to put it into practice!

The occurrence of hemorrhagic syndrome in newborns should be considered in connection with the peculiarities of the formation and maturation of the coagulation and anticoagulation systems during the period of intrauterine and postnatal life. In newborns, the hemostatic system has a number of features. They are characterized by increased capillary permeability, decreased aggregation activity and platelet retraction ability, low procoagulant activity and, despite this, a tendency to hypercoagulation in the first days of life.

In the early neonatal period, there is a persistent decrease in the components of the prothrombin complex - true prothrombin, proconvertin (factor VII) and proaccelerin (factor V), low activity of factors IX and X due to functional immaturity of the liver. Despite the fact that in newborns the activity of the main blood coagulation factors is reduced and ranges from 30 to 60% of the adult norm, no bleeding phenomena are observed. It is believed that the rate of enzymatic reactions converting prothrombin into thrombin and fibrinogen into fibrin is much higher in them than in adults.

Premature children, unlike full-term ones, are characterized by a tendency to hypocoagulation due to lower levels of vitamin K-dependent blood coagulation factors, lower platelet aggregation activity, higher permeability of the vascular wall, more active fibrinolysis with low values of antiplasmins.

Of particular interest are data on the effect of hypoxia on the hemostatic system in the early neonatal period. In children who suffered asphyxia, a decrease in the concentration of fibrinogen and proconvertin, increased platelet aggregation and an increase in their functional activity were detected. A tendency to hypercoagulation in mild and hypocoagulation in severe asphyxia has been established. There is an increase in intravascular coagulation in acute hypoxia, a decrease in blood coagulation ability and an increase in fibrinolytic activity in chronic hypoxia.

Thus, increased bleeding in newborns can be caused by both isolated defects in the vascular-platelet and coagulation components of hemostasis, and their combined damage in various pathological conditions.

Hereditary coagulopathies in the neonatal period are detected extremely rarely. Manifestations of hemophilia in newborn boys can include prolonged bleeding from sites of injury to the skin and umbilical cord, umbilical bleeding, hematomas at the site of injury, cephalohematoma, and intracranial hemorrhage. Other hereditary hemostasis defects in the neonatal period may include afibrinasemia (absence of factor XIII) and afibrinogenemia.

Thrombocytopenic purpura. Thrombocytopenia of immune origin is more often observed in newborns. The most common are transimmune forms of thrombocytopenia, in which, due to maternal illness (idiopathic thrombocytopenic purpura, lupus erythematosus, etc.), transplacental transfer of antiplatelet antibodies to the fetus and platelet destruction occur, regardless of their antigenic structure.

Symptoms of bleeding in newborns appear in the first days of life in the form of petechiae and small ecchymoses on the skin and mucous membranes. Slight bleeding from the gastrointestinal tract, hematuria, and rarely nosebleeds may occur. The prognosis is usually favorable.

In the isoimmune form of thrombocytopenia, the mother is healthy, but is incompatible with the fetus for platelet antigens. The platelet factor PLA-1, inherited from the father, has pronounced antigenic activity. During pregnancy, fetal platelets enter the mother's bloodstream and stimulate the formation of antiplatelet antibodies. The transfer of these antibodies to the fetus causes platelet destruction and thrombocytopenia.

Clinically, in newborns with the isoimmune form of thrombocytopenic purpura, from the first hours of life, petechial and small-spotted hemorrhages are found mainly on the trunk. In severe cases, significant nasal, pulmonary and gastrointestinal bleeding, hemorrhages in the internal organs and brain are observed. The latter often lead to death.

With congenital thrombocytopathies caused by the mother taking various medications during pregnancy and before childbirth (acetylsalicylic acid, sulfa drugs, phenobarbital and some antibiotics), hemorrhagic manifestations in newborns are not pronounced.

Hemorrhagic syndrome, caused by the development of secondary thrombocytopenia, is most typical for intrauterine and postnatal infections. Children with large angiomas may develop thrombocytopenia due to the accumulation and death of platelets in the vascular tumor (Kasabach-Merritt syndrome).

Particular attention in recent years has been paid to DIC syndrome, which, according to general opinion, occurs more often in newborns than is diagnosed.

Disseminated intravascular coagulation syndrome is one of the most severe pathologies of hemostasis, characterized by widespread blood coagulation, deep microcirculation disorders, metabolic disorders, depletion of the coagulation, anticoagulation and fibrinolytic blood systems, which leads to profuse, sometimes catastrophic, bleeding.

Any serious illness in the neonatal period (asphyxia, intrauterine infections, sepsis caused by gram-negative flora, shock, SDD, etc.) can be complicated by DIC syndrome. The triggering mechanism of the cascade system of blood coagulation begins with a series of reactions leading ultimately to the formation of thrombin.

The reasons for the increase in blood coagulation potential in newborns are different. Tissue thromboplastin can enter the newborn’s bloodstream during premature placental abruption, from injured tissues, during resorption of large hematomas, administration of drugs with high thromboplastic activity (blood, plasma, red blood cells), and increased hemolysis of erythrocytes of various types.

The appearance of active thromboplastin in the bloodstream leads to an increase in the level of thrombin, under the influence of which serotonin is released from platelets, reflex excitation of the blood coagulation system occurs and adrenaline is released into the blood, activating factor XII. These reactions cause thrombinogenesis and, as a consequence, an increase in blood coagulation potential. Secondary hypocoagulation is a consequence of the protective reflex act of the anticoagulation system of the blood against thrombin formation.

Endogenous activation of contact factors (XII-XI) can occur in areas of damage to the vascular endothelium under the influence of bacterial, viral, allergic, immune and metabolic disorders. In many cases, the cause of the development of DIC syndrome is a violation of microcirculation. The activation of the blood coagulation system is especially pronounced during infectious-toxic (septic) shock caused by gram-negative bacteria.

DIC syndrome occurs in several stages. Stage I is characterized by increasing hypercoagulation, intravascular aggregation of blood cells, activation of the kallikrein-kinin system and complement. This phase lasts a short time, often has no clinical manifestations and is not diagnosed in a timely manner. Stage II is clinically manifested by hemorrhagic syndrome, a decrease in the number of platelets, a decrease in the level of fibrinogen, prothrombin, proaccelerin, antihemophilic globulin and fibrin-stabilizing factor are noted. In stage III, there is a catastrophic decrease in all blood coagulation factors. Hemorrhagic syndrome is pronounced: injection sites bleed, profuse bleeding from the lungs, intestines, nose, kidneys and other organs is possible. Fibrinogen, antithrombin III, platelets, prothrombin and other coagulation factors are critically reduced, and signs of pathologically activated fibrinolysis appear. Stage IV, if the patient does not die, is characterized by a return to physiological limits of the level and activity of all factors of the coagulation and anticoagulation systems of the blood.

Diagnosis of hemorrhagic syndromes in newborns presents certain difficulties due to the uniformity of clinical manifestations. Therefore, in differential diagnosis, anamnesis data play an important role in comparison with clinical and laboratory tests. Laboratory diagnostics are presented in table. 32.

Treatment. Therapeutic tactics depend on the cause, type and severity of hemorrhagic disorders. In cases where the causes of increased bleeding have not yet been precisely established, therapy is carried out through general and local influences. Preparations with a general hemostatic effect include vitamins K, C, rutin, and calcium salts. Preferably, intramuscular administration of vitamin K 1 (konakion) in a dose of 1-5 mg. In its absence, vitamin K 3 (vicasol) in the form of a 1% solution - 0.3-0.5 ml for full-term children and 0.2-0.3 ml for premature children. Local measures include the use of a variety of mechanical (tamponade, pressure bandages, suturing, cold, etc.) and hemostatic (thrombin solutions, hemostatic sponges, fibrin film and powder) agents.

In the uncomplicated course of hemorrhagic disease, in cases where hemorrhagic manifestations are moderate, vitamin K is indicated at the rate of 1 mg/kg body weight 2 times a day, for 3 days in full-term infants and 2 days in premature infants. For melena, a solution of thrombin and adroxon in e-aminocaproic acid is prescribed (an ampoule of dry thrombin is dissolved in 50 ml of a 5% solution of e-aminocaproic acid, 1 ml of a 0.025% solution of adroxon is added and a teaspoon is given 3-4 times a day). Children with melena are fed expressed breast milk, cooled to room temperature.

In case of massive gastrointestinal bleeding, warm heparinized blood or plasma is transfused for hemostatic purposes and to prevent shock at the rate of 10-15 ml/kg body weight. It is advisable to prescribe a prothrombin complex drug (PPSB) at a dose of 15-30 U/kg.

For hemophilia A, antihemophilic plasma (10-15 ml/kg) or cryoprecipitate (5-10 U/kg) is infused. For hemophilia B, plasma or PPSB is administered in the above doses.

For immunopathological thrombocytopenic purpuras, children are fed donor or pasteurized breast milk for 2-3 weeks. Then applied to the chest under the control of platelets in the peripheral blood. For mild manifestations of hemorrhagic syndrome, e-aminocaproic acid is prescribed orally (in a single dose of 0.05 g/kg 4 times a day), calcium pantothenate (0.005 g 3 times a day), rutin (0.005 g 3 times a day), dicinone (0.05 g 4 times a day), intramuscular adroxon (0.5 ml of 0.025% solution 1 time a day), 1% ATP solution (1 ml daily).

For profuse skin purpura, especially combined with bleeding of the mucous membranes, prednisolone is prescribed (1.5-2.0 mg/kg), 3 doses in the morning and 1 dose in the afternoon.

For isoimmune thrombocytopenia, an effective treatment measure is the transfusion of platelet mass devoid of PLA-1 antigens (maternal platelets or specially prepared platelet mass). The introduction of platelets from a random donor has no effect, since 97% of donors have the platelet antigen PLA -1.

In transimmune thrombocytopenic purpura, platelet transfusions are contraindicated. In case of life-threatening bleeding, a replacement blood transfusion is performed to remove antiplatelet antibodies and platelet breakdown products.

Issues of prevention and treatment of DIC syndrome in newborns have not been sufficiently developed. Due to the heterogeneity of clinical manifestations, a uniform approach to its treatment is impossible. Since in most cases DIC syndrome develops secondary to some disease, the main attention should be paid to its treatment and elimination of those factors that may contribute to its development.

In complex therapy of the underlying disease, a number of measures are carried out aimed at the early replenishment of blood volume, its rheological properties and microcirculation. For this purpose, it is better to use rheopolyglucin, crystalloid solutions, mild (pipolfen, diphenhydramine, novocaine) and more pronounced antiplatelet agents (chirantil, droperidol), vasodilators (aminophylline, nicotinic acid, complamin).

There is currently no consensus on the advisability of using low doses of heparin to prevent DIC syndrome. There are also indications of the ineffectiveness of heparin use in newborns in stages I and II of DIC syndrome.

At the same time, heparin therapy occupies a central place in all modern programs for the treatment of DIC syndrome.

In stage I, heparin is prescribed at a rate of 100-150 units/kg 4 times a day. The correctness of dose selection can be monitored by lengthening the blood clotting time according to Lee-White by 2-3 times compared to the initial one, but not more than 20 minutes. Studies are carried out every 6 hours. If the clotting time does not lengthen, then the dose of heparin is increased to 200 IU/kg. If the clotting time is prolonged by more than 20 minutes, the dose is reduced to 50-75 U/kg. After selecting an individual dose to maintain a constant concentration and avoid possible complications, it is better to administer heparin intravenously at a precisely specified rate during infusion therapy. A.V. Papayan and E.K. Tsybulkin recommend that to maintain a constant concentration of heparin, administer it by continuous infusion at a dose of 15 U/(kg-h). If the clotting time does not lengthen, then increase the dose of heparin to 30-40 IU/(kg-hour). If the clotting time extends beyond 20 minutes, then the dose of heparin is reduced to 5-10 units/(kg-hour).

In the treatment of stage III, heparin remains the main pathogenetic therapy. To correct the deficiency of plasma coagulation factors and antithrombin III, transfusions of fresh frozen or native plasma in a dose of 8-10 ml/kg, warm heparinized blood - 5-10 ml/kg are indicated.

In stage III of DIC syndrome, after correction of the level of antithrombin III by the introduction of the above drugs against the background of heparin therapy, it is permissible to prescribe proteolytic enzyme inhibitors - contrical, trasylol at a dose of 500 U/kg once, as well as glucocorticoids in normal doses. If blood transfusions are necessary (hemoglobin below 50-60 g/l), additional heparinization is indicated (500 units of heparin per 100 ml of blood).

In cases of favorable outcomes, in order to avoid the effect of hypercoagulation, heparin is discontinued gradually against the background of ongoing disaggregant, vasodilator and infusion therapy aimed at improving the rheological properties of blood and microcirculation.

There are indications in the literature of positive results in the treatment of DIC syndrome in newborns with exchange transfusions of fresh heparinized blood.