TASHKENT MEDICAL ACADEMY
DEPARTMENT OF OBSTETRICS AND GINECOLOGY
• Hemorrhagic shock
• Syndrome, disseminated intravascular
coagulation
Lector prof.,doctor of medicine Babadjanova G.S
TASHKENT-2013
Purpose:
To make out the questions of diagnostics and new methods of
treatment,profilactics.
Object:
To give the new classification
To say theories of etiology and patogenesis
Clinics of difference
Methods of treatment
Bases of prophylactic of hemorrhagic shock and of DIC syndrome
• Hemorrhagic shock
• Hemorrhagic shock is called the state associated with acute and
massive blood loss. To lead the development of shock blood loss
1000 ml or more, which means a loss of 20% of BCC.
•
• Etiology. Causes of hemorrhagic shock in obstetric practice are:
bleeding during pregnancy, childbirth, the third delivery and
postpartum periods. The most common cause of massive blood
loss are as follows: placenta previa, abruption normally located
placenta and stopped ectopic pregnancy, ruptured uterus or
birth canal, hypotonia of the uterus in early postpartum period.
Massive blood loss is often accompanied by clotting (or precedes
it, or is a consequence). Features of midwifery bleeding in the
fact that they are abundant, suddenly and are usually combined
with other hazardous pathology (gestosis, extragenital pathology,
family trauma, etc.).
• Classification:
• 1 - Stage - compensated shock.
• 2 - stage - reversible decompensated shock.
• 3 - stage – decompensated irreversible shock.
• The severity of blood loss
• 1 - blood loss up to 15% of blood volume is accompanied by tachycardia
• 2 - 20-25%, tachycardia, hypotension
• 3 - 30-35%, tachycardia, hypotension, oliguria
• 4 - more than 35-40%, tachycardia, severe hypotension, collapse, loss of
consciousness, life-threatening
• Pathogenesis
• -hemorrhage
• -peripheral vasoconstriction,
• -release of catecholamines,
• -centralization of circulation
• -autogemodilyutsiya, violation of Rheology, acidosis,
• -DIC, multiorgan failure
• Clinic of haemorrhagic shock
• Compensated shock (blood loss 800 - 1200 ml)
• decompensated:
•
- Reversible (1200 - 2000ml)
•
- Irreversible (more than 2000ml)
• Complications
• -microcirculation disturbance
• -metabolic disorder
• -acute renal failure
• -acute liver failure
• -acute respiratory failure
• -cerebrovascular accident
• -heart failure
• -"Shock" uterus
• The principles of treatment
• With continuous bleeding above all is the question of surgery (amputation,
hysterectomy, ligation a.iliaca interna c 2 sides)
• Transfusion of FFP - 1 liter, cryoprecipitate
• Preparations of starch - stabizol, Refortan
• Cryoprecipitate, packed red blood cells, albumin
• The ratio of transfused red blood cells and plasma should be 1:4
• Hepatoprotectors (Essentiale)
• Etamzilat, Dicynone
• Protease inhibitors (contrycal, gordox, trasilol)
• Dopmin, adrenaline
• ALV
• diuretics
• Transfusion only crystalloids is not sufficient
• Colloidal solutions increase the viscosity of the blood and thus, delay the
liquid in the vessel
• Adequate replenishment of blood loss and timely correction of
• coagulopatic disorders
• Restores BCC begins with the establishment of abnormal bleeding (0.7% or
more of body weight). This is based on a dynamic evaluation of the amount
of blood lost and losting of blood.
• Prophylaxis
• Identification of patients at risk of bleeding during childbirth, during the
pregnancy.
• The preventive treatment of EGD during the pregnancy
• The presence in the hospital a lot of fresh frozen plasma (FFP)
Syndrome, disseminated intravascular coagulation
• ETIOLOGY
• Severe forms of gestosis, premature detachment of the placenta,
hemorrhagic shock, amniotic fluid embolism, sepsis, diseases of the
cardiovascular system, kidneys, liver, Rhesus-conflict, transfusion of
incompatible blood, nondeveloping pregnancy, etc. The above mentioned
states lead to tissue hypoxia and metabolic acidosis, which in turn causes
the activation of blood and tissue thromboplastin.
• Mechanism of DIC
• I phase. The formation of active thromboplastin time - the longest phase of
hemostasis. It involved factors plasma. (XII, XI, IX, VIII, X, IV, V), and platelet
factors (3, 1).
• Phase II. The transition of prothrombin into thrombin. Occurs under the
action of the active participation of thromboplastin and calcium ions (factor
IV).
• Phase III. The formation of fibrin polymer. Thrombin (with the participation
of calcium ions (factor IV) and platelet factor (4) transforms fibrinogen into
fibrin monomer, which is under the influence of factor VIII plasma and
Change procoagulants in hemostasis, platelet activation leads to platelet
aggregation with the release of biologically active substances: kinins,
prostaglandins, catecholamines, etc. They affect the vascular system.
• platelet factor 2 is converted into insoluble threads of fibrin polymer.
• For slow flow of blood through the branching of small vessels is its
separation into plasma and red blood cells that fill different capillaries. Loss
of plasma, red blood cells lose their ability to accumulate in the movement
and the form of slowly circulating, and then noncirculation formations.
Stasis occurs, aggregation, and then lyse, releasing associated with ecoid
blood thromboplastin. Admission into the bloodstream thromboplastin
causes the process of intravascular coagulation.
• Dropping out that the threads of fibrin entangle lumps of red blood cells,
forming a "sludge" - lumps, settling in the capillaries and further violate the
homogeneity of the structure of blood. Important role in the development
of "sludge", the phenomenon is played by two interrelated phenomena reduced blood flow and increased blood viscosity (MA Repin, 1986). Is an
infringement of the blood supply of tissues and organs.
•
In response to the activation of the coagulation system includes safeguards
- fibrinolytic system and cells of the reticuloendothelial system.
• On the background of disseminated intravascular coagulation due to
increased consumption and increased fibrinolysis procoagulants develop
increased bleeding.
• Different authors proposed different classifications of stages during DIC,
although the clinical syndrome of DIC is not always manifested in a clear
manner.
• MS Machabeli selects 4 stages:
Stage I - hypercoagulable state associated with the emergence of a large
number of active thromboplastin.
• Stage II - consumption coagulopathy associated with a decrease
procoagulants because of their inclusion in microthrombi. Simultaneously
activated fibrinolysis.
• Stage III - a sharp decline in the blood of all procoagulants until
afibrinogenemia development against the background of pronounced
fibrinolysis. This stage is characterized by a particularly severe
hemorrhages. If the patient remains alive, thrombohemorrhagic syndrome
goes to the next stage.
• Stage IV - replacement. There is a gradual normalization of the blood
coagulation system. Often at this stage revealed complications endured DIC
- Acute liver failure, acute renal failure, acute respiratory failure,
cerebrovascular accident.
• Fedorova ZD et al (1979), Sergei BA (1981) suggest the
following classification of current ICE syndrome:
• Stage I - hypercoagulability. The duration of this phase is different. It was
observed to decrease clotting time, decreased fibrinolytic and
anticoagulant activity, shortening of the thrombin-test. Clinically, in this
stage, flushing of the skin, alternating with cyanosis, marbling, drawing
particularly on the upper and lower extremities, and sometimes chills,
anxiety, patient, tachycardia.
• Stage II - hypocoagulation. According to the coagulation observed
consumption of clotting factors, there are degradation products of
fibrinogen and fibrin (FDP), decreased platelet count, thrombin time
increases, decreases slightly during lysis of fibrin clots, reduces the activity
of antithrombin III. Clinically noted increased bleeding from the birth canal,
wound surfaces, there are hemorrhages in the skin, nasal bleeding,
petechial rashes on the sides of the chest, thighs, upper eyelid. Blood flows
from the uterus, has loose clusters, which are rapidly lysed.
• Stage III - hypocoagulation with a generalized activation of fibrinolysis.
Coagulation: a decrease in the number and the weakening of the functional
properties of platelets, decreased concentration and activity procoagulants,
the circulation of the blood of large amounts of degradation products of
fibrinogen and fibrin (FDP), a sharp increase in fibrinolytic activity
• further increases in the free heparin. Clinic - released fluid is not blood
clotting, are sometimes formed small isolated clusters, which are rapidly
lysed. There is a generalized bleeding the injection site, venesection,
surgical field, haematuria, there are hemorrhagic effusion in the chest and
abdominal cavities, the pericardium.
• Stage IV - full hypocoagualation of blood. Terminal stage. Hypocoagulation
extreme degree, combined with high fibrinolytic and anticoagulant activity.
The clinical picture is the same as in Stage III - generalized bleeding.
• I must say that in this classic pattern of development of syndrome of DIC
life is different and there is a set of clinical and laboratory options
syndrome flowing individually for each patient. During the syndrome
depends on the nature of obstetric pathology that caused the bleeding,
concomitant somatic diseases, especially during pregnancy, etc.
• The duration of clinical manifestations of DIC can reach 7-9 hours or more.
Changes in the system hemocoagulation determined using laboratory
techniques, remain longer than clinical. Therefore, laboratory diagnosis of
DIC is paramount: allows you to more accurately determine the level or
phase syndrome, and select the correct treatment.
• The diagnosis of chronic syndrome of DIC is put on the basis of laboratory
tests of hemostasis.
• In the pathogenesis of gestosis pregnancy plays a role chronic syndrome of
DIC. It is characterized by: generalized arteriolar spasm, prolonged
moderately hypercoagulability. In the microcirculation system formed
platelet mikrosvertki ("sludge"), which in severe gestosis results in necrosis
and hemorrhage in the parenchymatous organs, brain and placenta, which
leads to the formation of placental insufficiency. And with the development
of local acute DIC - a premature detachment of the placenta.
TREATMENT
• Treatment of DIC syndrome individual. It encompasses both conduct three
major activities:
• - Elimination of the main reasons that caused the engine.
• - Normalization of hemodynamics.
• - Normalization of blood clotting
• For the treatment of DIC syndrome in obstetric hemorrhage should be
considered a phase syndrome, in which treatment is started, the nature of
obstetric pathology. It is conducted under the supervision of laboratory
diagnostics. So in progressive chronic DIC syndrome in pregnant women
with gestosis, in the presence of a dead fetus in the uterus during
pregnancy nondeveloping appropriate early delivery vaginally.
• Pregnant women with chronic DIC in gestosis shown in the complex of
therapeutic measures used low-molecular blood substitutes
(reopoliglyukin, gemodez, polidez, zhelatinol) in combination with
antispasmodics, which improves blood rheology, prevent mikrotromboz
and help to improve tissue perfusion. Heparin, injected subcutaneously
with 5000-10000 IU every 12 hours normalizes platelet count and
fibrinogen. It is an anticoagulant of direct action, reduces platelet activity
has antitromboplastin and antithrombin activity, thereby normalizes blood
circulation in parenchymal organs and utero-placental complex.
• In acute forms of DIC, along with efforts to normalize the central and
peripheral hemodynamics, conduct restoration of blood coagulation
properties. You must stop the intravascular clotting, lower fibrinolytic
activity and to restore the ability of the blood coagulation. This is carried
out under the control of coagulation. Restoration of blood coagulation
properties reach replacement therapy - a transfusion of fresh frozen
plasma, red blood cells frozen, warm blood, blood svezhetsitratnoy,
antihemophilic plasma fibrinogen.
• Inhibition of fibrinolytic activity by introducing inhibitors of animal origin kontrikal, trasilol, Gordoks. A single dose of kontrikal - 2000 IU (daily - 6000
IU), trasilol - 2500 IU (daily - 10000 IU), gordoks - 100000 units (daily 500,000 units). Inhibitors of fibrinolysis are used strictly under the control
of coagulation.
• Intensive therapy and continued after the removal of DIC syndrome and
referred for treatment of renal and hepatic failure, pulmonary disease,
recovery of protein and electrolyte balance, prevention of infectious
complications.