You are on page 1of 11

Placenta circulation Divided to o o Uteroplacental circulation Feto-placental circulation

Uteroplacental circulation Known as the maternal circulation that flow through the intervillous space Has about 500ml of blood : 150ml in the intervillous space and 350ml in occupied vili system Spiral arteries that pierce basal plate randomly in numerous site and a secondary invasion of trophoblast between 12-16 week that extend up to radial arteries within myometrium Thus they are further converted to uteroplacental arteries

Fetoplacental circulation 2 umbilical arteries carry impure blood from fetus Present of membrane that separates the maternal and fetus blood Fetal blood flow through the placenta is 400ml per minute

The placenta main functions are: o Transfer of nutrient and waste products between the mother and fetus, takes part in respiratory, excretory, nutritive Barrier function block larger molecules of noxious agent from maternal blood to pass to fetal circulation Immunological function Produces or metabolise the hormones and enzymes necessary to maintain the pregnancy

o o

Fetoplacental insufficiency A syndrome caused by morphofunctional changes in the placenta and is the result of a complex reaction of fetus and placenta

Risk factors o Social and domestic factors : occupational hazard, smoking, alcohol, heavy work Physical history of chronic disease, extragenital disease Features of obstetric and gynecological history: menstrual disorders, infertility, gynecological disorders, surgery on the genital organs, miscarriages, stillbirths, low birth weight, endometriosis, fibroids, often recurrent genital infections Course of the pregnancy gestosis first half of pregnancy, the threat of miscarriage, late gestosis, anemia, multiple pregnancy, exacerbation of chronic and acute infectious diseases during pregnancy, perenashivanie pregnancy.

o o

Classification o Depending on in which the structural units of the pathological processes occur: Hemodynamic - a violation of uteroplacental vessels and fetoplacental circulation; Placental membrane - reduce ability of the placental membrane to transport metabolites; Parenchymal cell - disturbances of the trophoblast cell activity and the placenta.

On clinical and morphological features: Primary (early) failure - develops before 16 weeks of pregnancy. Occurs during implantation, the formation of the placenta during early embryogenesis under the influence of various factors (genetic, endocrine, infectious, etc.). Important in the development of the primary enzyme deficiency plays a FPN decidual tissue that occurs when hormonal ovarian function, anatomical irregularities of the structure, location and attachment of the placenta, vascular pathology and abuse of maturation chorion. It promotes the development of congenital malformations of the fetus, non-viable pregnancy. Clinically threatened abortion or miscarriage in the early stages. In some cases, the primary becomes the secondary FPN

Secondary - Late FPI - develops against the background of already-formed placenta after 16 weeks of pregnancy. The emergence of this form of FPN is influenced by factors such as infectious, extragenital diseases, the threat of termination of pregnancy, gestosis, anemia during pregnancy, environmental factors (chemical agents, radiation, stress, physical overload, etc.).

On the clinical course: Acute - there is an acute violation of the decidual and uterineplacental circulation (heart attacks caused by the placenta, premature detachment of normally situated placenta) Chronic fetoplacental insufficiency - takes place every third pregnant women at high risk. Develops from the second trimester of pregnancy and occurs in a long time. Its main role belongs to the origin of the violation of the compensatoryadaptive mechanisms in combination with circulatory disorders, degenerative changes involutive in the placenta, inflammation, and immune disorders.

During pregnancy and fetal disorders during long proceeding in the placenta are ambiguous and depend on many factors. In chronic placental insufficiency initially disrupted the trophic function of the placenta, and later joins a violation of gas exchange. Chronic FPN clinically delayed fetal development (in 5-17%), chronic intrauterine hypoxia (4-6%) or a combination there.

Fetal hypoxia (FH)

Occur when the fetus is deprived of an adequate supply of oxygen. FH may be due to a variety of reasons such as cord prolapse, cord occlusion, placental infarction and maternal smoking.

Intrauterine growth restriction (IUGR) may cause or be the result of hypoxia. Birth asphyxia may result due to prolonged labor, breech delivery in full-term infants; placental abruption, and maternal sedation in premature infants. Oxygen deprivation is the most common cause of perinatal brain injury Intrauterine hypoxia and birth asphyxia can cause hypoxic ischemic encephalopathy which is cellular damage that occurs within the central nervous system (the brain and spinal cord) from inadequate oxygen. This results in an increased mortality rate, including an increased risk of Sudden infant death syndrome (SIDS). Oxygen deprivation in the fetus and neonate have been implicated as either a primary or as a contributing risk factor in numerous neurological and neuropsychiatric disorders such as epilepsy, ADHD, eating disorders and cerebral palsy. Classification o By Pathogenesis: Hypoxic hypoxia - oxygen saturation of hemoglobin below normal levels. This form of fetal hypoxia develops pneumonia, asthma, anemia, increased pulmonary artery pressure during pregnancy; Circulatory hypoxia - oxygen is supplied to the tissues of the fetus in sufficient quantities, although it enough voltage in the arterial blood. Develops during the slowing down of blood flow in the vessels of the fetus at risk of miscarriage; Hemic (anemic) hypoxia - caused by a significant decrease in the number of red blood cells (eg, hemolytic disease of the fetus), or low hemoglobin in red blood cells, as well as reducing the ability of hemoglobin to bind oxygen; Tissue hypoxia - develops at the cellular level, the pathology that leads to a violation of the capacity of cells obtained ispolzvat oxygen

o Based on character :
1) acute - because of acute disorders of uteroplacental or fruitplacental circulation at birth (birth abnormalities of forces, or loss of clamping the umbilical cord, prolonged compression of the fetal head in the pelvic cavity, etc.) and more rarely - during pregnancy (at break cancer, premature detachment of the placenta); 2) subacute - usually develops 1-2 days before giving birth on the background and is characterized by the depletion of HFPN adaptive

capabilities of the fetus; 3) Chronic - develops against the background of pregnancy complications (such as gestosis, perenashivanie, immunologic incompatibility, infection of the fetus), extragenital diseases (diabetes, hypertension), adverse working and living conditions (toxic, profvrednosti) is associated with morphofunctional modifications in the placenta Clinical signs of fetal hypoxia are: 1) The complaint for pregnant women increased or decreased mobility of the fetus; 2) the changing nature of the fetal heart (according to auscultation and CTG); 3) The discharge of meconium (a pathognomonic sign of fetal hypoxia only in cephalic presentation) Intrauterine Growth Restriction ( IUGR ) Occurs in two forms: o Symmetric form (10-30% of cases) - is developing with early pregnancy and is characterized by a lag proportional to body weight and length of the fruit. The reasons for the symmetric form IUGR: intrauterine infection, chromosomal abnormalities, genetic syndromes, bad habits and poor maternal nutrition, maternal hypoxic disease (heart defects, asthma, exposure to high altitude) o The asymmetric shape (develops in 70-90% of cases) - is characterized by a lag in body weight of the fetus with a normal length (malnutrition), the delay in the development of individual organs (usually liver). Occurs mainly in the third trimester of pregnancy complications against the background (gestosis, multiple pregnancy, malformations of the placenta, bleeding in the third trimester) and extragenital diseases (often with abnormal blood vessels).

Severity IUGR: Grade I - the lag in development of the fetus up to 2 weeks; Grade II - the lag in development of the fetus within 2-4 weeks; Grade III - retardation of the fetus more than 4 weeks - permanent changes may be intrauterine fetal death.

IUGR clinical picture o The first signs may appear in 18-19 or 24-26 weeks. o By 28-29 weeks of pregnancy, fetal growth delay is usually symmetrical. o The emergence of IUGR at 32 weeks' gestation and is more typical for an asymmetric shape. Originally marked slowdown or lack of growth of the uterus (fetal gestational age discrepancy), and weight gain pregnant. o Then the symptoms of chronic fetal hypoxia. Often a delay of fetal development is accompanied by phenomena of threatened abortion.

Diagnosis of fetoplacetal insufficency

Anthropometry in the dynamics. Assesses the weight and a growth factor mothers to 12 weeks' gestation, and weight gain during pregnancy: 1) normosteniki (MRK 36 4%) - the best gain 16-17%; 2) giposteniki (MRK 28 3%) - 22-23% increase; 3) gipersteniki (MRK 45 4,5%) - increase of 12-13%. Dynamic performance evaluation of high standing uterus and abdominal circumference, taking into account the period of growth and pregnancy, fetal position, amount of amniotic fluid. Backlog of standing height of uterine fundus 2 cm or more compared with the normal growth or lack of it for 2 weeks show hypotrophy of the fetus o The height of uterine fundus above the vagina, depending on the gestational age when normally developing pregnancy. Ultrasonography with dynamic fetometry. The most informative indices are: the size of the fetal head biparietal (BDP), the average diameter of the chest - the DW (at the level of swing valves) and the abdomen J (at level of origin or location of the umbilical vein of fetal kidney). Indicators of malnutrition in the fetus are mismatch 2 weeks or more values of the fetal head BDP-gestational age, the disproportion

between the size of the head and abdomen (chest exposed underdevelopment, to a lesser extent than the head and abdomen). o At an early breach of growth restriction (IUGR twin shape), the main diagnostic sign on ultrasound is the proportional reduction in size as the head and abdomen of the fetus. Ratio of BDP / coolant in this case is not different from that in healthy fetuses of similar gestational age and less than 1. o Thus, the correct diagnosis of IUGR symmetrical form is only possible with dynamic ultrasound. In the late fetal malnutrition (asymmetric shape IUGR) is usually disrupted the growth of the stomach, but not the fetal head. Diagnosis of this type of IUGR is not difficult and is possible at the first ultrasound: correlation BDP / J with more than 1. Ultrasonography with dynamic placenta investigation. o Echographic maturity are 4 placenta, depending on the density of echogenic structures: 1) The placenta is a homogeneous structure with a flat plate, chorionic; 2) against the background of a homogeneous structure of the placenta there are small hyperechoic areas, chorionic plate is twisted; 3) hyperechoic areas in the placenta become more intense, chorionic plate gyrus penetrates the placenta, but do not reach the basal layer; 4) chorionic plate gyrus reach the basal layer, forming a circle, the placenta takes pronounced lobed structure. o The appearance of III degree of maturity of the placenta to 38-39 weeks of pregnancy, evidence of its premature aging and is a sign of placental insufficiency. In some cases, ultrasonography revealed cystic changes in the placenta. Cysts of the placenta it echo negative education in the placental tissue of different shape or size. Are due to hemorrhage, softening, heart disease and other degenerative changes. o More often detected in the fetus side of placenta. Valuable information is provided by ultrasonic sizing of the placenta (the thickness and area). After determining the insertion site of

placenta measured maximum density. At physiological pregnancy placental thickness increases continuously up to 3637 weeks of gestation. Then the growth stops and the placental thickness or it is somewhat reduced, or remains at that level, accounting for 3.5-3.6 cm thinning or thickening of the placenta at 0.5 cm and a point to dysfunction of the placenta, which requires the use of therapy and Ultrasound in the dynamics Auscultation of fetal heart rate, ECG, PCG, CTG fetus. o Auscultation of fetal heart rate can reveal only gross changes in heart rate (tachycardia, bradycardia, arrhythmia, marked) o ECG may be a straight line .On the PCG in fetal hypoxia detected changes in the amplitude, duration and increase the splitting tones of the heart. Disturbing noises, especially systolic, and chronic fetal hypoxia indicates severe his suffering. o The most accessible and informative method of assessing the fetal heart rate is CTG. In describing the condition of the fetus are evaluated the following parameters CTG: 1) The basal rhythm of heart rate - the average time between changes in the values of fetal heart rate that occur sporadically or periodically (in relation to contractions). Normocardiac are considered heart rate from 120 to 160 beats / min, moderate tachycardia - from 160 to 180 beats / min, severe tachycardia more than 180 beats / min, moderate bradycardia - from 120 to 100 beats / min, bradycardia - less than 100 beats / min ; 2) rate variability - frequency and amplitude of the instantaneous changes in fetal heart rate (instantaneous oscillation). Oscillation amplitude is determined by the magnitude of the deviation from the basal rate, the frequency the number of oscillations in 1 minute. In clinical practice, the following classification of types of variability of basal rhythm: a) (monotone) rhythm - is characterized by low amplitude - 0-5 beats / min; b) slightly undulate - 5.10 beats / min; c) undulating (wavy) - 10-25 beats / min;

g) saltatory (jumpy, pulsating) - 25-30 beats / min. o The most unfavorable is the silent rhythm of CTG, especially while reducing the amplitude (less than 3 beats / min) and the oscillation frequency (at least 6 of the oscillations in 1 minute). 3) Acceleration- periodic slow acceleration of the basal rate, reflecting the degree of compensatory possibilities of the cardiovascular system of the fetus. In the course of the physiological delivery acceleration observed almost continuously at a frequency of 4-5 and more than 30 minutes, the duration of their 20-60 s, amplitude - more than 15 beats / min. Periodic acceleration occur early in labor and are associated with uterine contractions or compression of the umbilical cord. Sporadic acceleration most commonly associated with motor activity of the fetus. Decreased acceleration or lack of them are poor prognostic signs; 4) Decelerations - slow-wave deceleration basal rate, indicating some abnormal fetoplacental system. Depending on the time of relatively isolated contractions are 4 types of decelerations: Allocate certain cardinal signs of intrauterine fetal hypoxia o Initial signs of intrauterine fetal hypoxia: Tachycardia (over 160 beats / min) or moderate bradycardia (from 120 to 100 beats / min); Increasing or decreasing rate variability (arrhythmia) Weakening of the reaction to the functional tests; The occurrence of late decelerations in response to uterine contractions (reflect the failure of uteroplacental blood flow). o Pronounced signs of intrauterine fetal hypoxia: A significant bradycardia (less than 100 beats / min); The monotony of rhythm (over 50% of records); The absence or paradoxical response to functional tests; Late decelerations in response to uterine contractions. o For antenatal fetal assessment uses a simplified point system assessment (on Saveleva) Table 5. Scoring system for assessing Saveleva

Score 8-10 points on the normal fetus, 5-7 points - at the initial signs of fetal heart rate, 4 points or less - for signs of change expressed by the fetus Diagnostic value of CTG is enhanced by a careful comparison of data from the CTG obstetric situation and other criteria for evaluating the condition of the fetus. The change in frequency, amplitude, rhythm, heart rate variability in fetal function tests: 1) nonstress test - when a perturbation in the fetal heart rate quickens 15-35 beats / min. Hypo-, hyper-, areactivity test show a decrease in adaptive abilities of the fetus; 2) Cold test - reduction of fetal heart rate by 10 beats / min. FPN at changes in the rhythm or no response is inadequate (perverse); 3) oxytocin test - normal subthreshold dose of oxytocin (0.05 IU in 5 ml of 5% glucose solution) does not alter the physiological fluctuations in heart rate of the fetus. FPN occur at increased frequency of heart rate over 160 beats / min or slowing of less than 120 beats / min, if you save the monotonous rhythm - an unfavorable prognosis; 4) breath holding test: breath-hold is slowing, and the delay in the exhalation - increased frequency of fetal heart rate to 7 beats / min. When a FPN is revealed paradoxical reaction, or no change in heart rate. 7. Assessment of uteroplacental blood flow through doplermetry. Decrease in the rate and magnitude of blood flow intervillous space, and change other parameters by 30% and more evidence of severe placental insufficiency.

Therapy for Fetoplacental insufficiency Treatment of pathological conditions that caused the development of FPN. Elimination and reduction of perfusion failure.

The elimination or reduction of diffusion impairment. Increase adaptive capacity in the "mother - placenta - fetus." A compulsory component of treatment is bed rest pregnant. This improves blood flow to the uterus. Vasodilators and resources, normalizing the microcirculation and blood rheology: o 2.4% aminophylline-ny 10 ml intravenous bolus or infusion solution of glucose for 10 days. To improve tissue respiration is shown at the same time maintaining cytochrome c, 5 mg in 20 ml of 40% glucose solution; o Magnesium sulfate; o Trental - intravenously for 7-14 days, or reopolyglukin; Heparin with symptoms of hypercoagulability, fibrinosis, chronic DIC controlled coagulation, reverse heparin for 2-3 days before the expected delivery and to gemostaziologichesky control; Of estradiol dipropionate and estradiol propionate in combination with ether (for faster absorption) - intramuscularly.