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National Pirogov Memorial Medical University, Vinnytsya

CHAIR OF OBSTETRICS and Gynecology №1


for practical lesson

« Diagnostic methods of well-being of fetus. Placental insufficiency. Newborn resuscitation. Abnormalities of the placenta, umbilical cord, and membranes»

MODULE 4: Obstetrics and gynecology

Topic 7

Aim: to know obstetrics terminology, the methods of external and internal examination of pregnant women. To be able to prescribe and assess of modern methods of diagnostics of fetal well-being in obstetrics for in-term revealing of pathological changes in pregnant woman's organism and fetal status; prescribe an adequate treatment to the pregnant women in the case of fetal hypoxia.

Professional motivation: learning the methods of obstetrics examination of pregnant women is necessary to diagnose and to estimate the given information. An appropriate interpretation of fetal well-being tests in light of the natural course of any antenatal problem provides a firm base on which decisions are made.

Basic level: Student must know:

1. Anatomic terminology in English and Latin

2. Methods of physical examination of patient.

3. The structure of fetal head (anatomy of the skull).

4. Conceptus, development.

5. Obstetric ultrasound examination and its assessment.

6. Fetal heart rate auscultation.

7. To prescribe an adequate therapy of fetal well-being impairment

Assessment of fetal well-being

Assessment of fetal well-being includes maternal perception of fetal activity and several tests using electronic fetal monitors and ultrasonography

Tests of fetal well-being have a wide range of uses, including the assessment f fetal status at a particular time and the prediction of fetal status for varying time intervals, depending on the test and the clinical situation.

An active fetus is generally a healthy fetus, so that quantification of fetal activity is a common test of fetal well-being. If, for example, the mother detects more than four fetal movements while lying comfortably and focusing on fetal activity for 1 hour, the fetus is considered to be healthy.

Techniques using electronic fetal monitoring and ultrasonography are most costly, but also provide more specific information. The most common tests used are the nonstress test, the contraction stress test (called the oxytocin challenge test if oxytocin is used), and the biophysical profile.

The nonstress test (NST) measures the response of the fetal heart rate to fetal movement. Interpretation of the nonstress test depends on whether the fetal heart rate accelerates in response to fetal movement. A normal, or reactive, NST occurs when the fetal heart rate increases by at least I5bpm over a period of 15 seconds following a fetal movement. Two such accelerations in a 20-minute span is considered reactive, or normal. The absence of these accelerations in response to fetal movement is a nonreactive NST. A reactive NST is generally reassuring in the absence of other indicators of fetal stress. Depending on the clinical situation , the test is repeated every 3 to 4 days or weekly. A nonreactive NST must be immediately followed with further assessment of fetal well-being.

Whereas the nonstress test evaluates the fetal heart rate response to fetal activity, the contraction stress test (CST) measures the response of the fetal heart rate to the stress of a uterine contraction. With uterine contraction, uteroplacental blood flow is temporary reduced. A healthy fetus is able to compensate for this intermittent decreased blood flow, whereas a fetus who is compromised is unable to do so, demonstrating abnormalities such as fetal heart rate decelerations. If contractions are occurring spontaneously, the test is known as a contraction stress test; if oxytocin infusion is required to elicit contractions,the test is called an oxytocin challenge test (OCT). The normal fetal heart rate response to contractions is for the baseline fetal heart rate to remain unchanged and for there to be no fetal heart rate decelerations.

The biophysical profile is a series of five assessments of fetal well-being, each of which is given a score of 0 or 2. The parameters include a reactive nonstress test, the presence of fetal movement of the body or limbs, the findings of fetal tone (flexed extremities as opposed to a flaccid posture). And an adequate amount of amniotic fluid volume. Perinatal outcome can be correlated with the score derived from these five parameters.

A score of 8 to 10 is considered normal, a score of 6 is equivocal requiring further evaluation, and a score of 4 or less is abnormal, usually requiring immediate intervention
Table 1. Biophysical profile

Biophysical Variable



Fetal breathing movements (FBM)

Norma 1 = 2

At least 1 FBM of at least 30 seconds duration in 30 minutes

Abnormal = 0

No FBM of at least 30-seconds duration in 30 minutes

Gross body movement

Normal = 2

At least 3 discrete body /limb movements in 1 30 minutes

Abnormal = 0

2 or less discrete body /limb movements in 30 minutes

Fetal tone

Of muscles

Normal = 2

At least 1 episode of active extension with return to flexion of fetal limbs/trunk or opening/closing of hand

Abnormal == 0

Either slow extension with return to partial flexion or movement of limb in full extension or no fetal movement

Reactive fetal heart rate

Normal = 2

Reactive NST

Abnormal = 0

Nonreactive NST

Qualitative amniotic fluid volume

Normal = 2

At least 1 pocket of amniotic fluid at least 1 cm in two perpendicular planes

Abnormal = 0

No amniotic fluid or no pockets of fluid greater 1 than 1 cm in two perpendicular planes


Placental insufficiency (PI) is a symptom complex conditioned by violations of transport, trophic, metabolic, and endocrine functions of the placenta due to structural it.

Reasons: gestoses, miscarriage threat, immunoincompatible pregnancy, intrauterine infection, mother's diseases (pyelonephritis, essential hypertension, diabetes niellitus, anemia), etc.


I. By the term of onset

  1. primary - develops in the terms of placenta formation (till the 16th week);

  1. secondary — usually develops after the processes of placenta formation have finished.

II. By the course: acute and chronic. Acute PI appears at. cute vio­lation of decidual perfusion, for instance, at abruption of placenta -sharp violation of blood supply leads to fetal hypoxia or death.

Chronic PI is characterised by gradual worsening of decidual per­fusion as a result of the reduction of compensatory-adaptive reactions of the placenta to the action of pathological conditions of the mater­nal organism, has a long-term course, is accompanied by disorders, chronic oxygen starvation of the fetus.

Chronic PI (depending on the condition, of compensatory-adap­tive reactions) includes:

1. Relative ~ compensatory-adaptive reactions are preserved in the placenta:

— compensated (the phase of persistent hyperfunctioning) devel­ops at a threat of miscarriage and not severe forms of gestoses in cases, when these complications are successfully medically corrected;

— subcompensated (the phase of exhaustion of compensatory mechanisms, which have begun) — is more often observed in the wo­men, in whom a complicated course of pregnancy is developing against the background of extragenital pathology.

2. Absolute (decompensated) — the severest form of PI charac­terised by derangement of compensatory-adaptive reactions and develops against the background of chorion ripening disorders at pla­centa damages of involutive-dystrophic, circulatory and inflamma­tory character.


  1. Regular clinical observation.

  2. Dynamic ultrasonography in the 1st, 2"d, and 3"1 trimesters.

  3. Dopplerometry.

  4. Investigation of the hemostasis system.

  5. Detecting the content of estradiol, progesterone, chorionic go­nadotropin, and a-fetoprotein in the blood serum.

  1. Investigation of estradiol secretion with urine.

  2. Detecting the content of oxytocinase, general and placental basic phosphatase in the blood serum.

  1. Colpocytologic investigation.

Detection of the height of uterine fundus standing (HUFS) is very important in PI diagnostics, the diagnostic value of this method a! the term of 32 weeks makes 76 %.

The main method of PI detection is ultrasonographic placento-nietry, which enables assessing placenta thickness, area, and struc-l uro. Placenta thickness from the 20th till the 36th week of pregnancy approximately equals the term of pregnancy in weeks: at 20 weeks — 20 mm, at 28 weeks — 28 mm, at 36 weeks — 36 mm, after this term the placenta does not thicken further. Placenta thinning (less than 20 nun) or thickening (more than 50 mm) testifies to PI, which ap­peared as a result of intrauterine infection, immunization, etc.

At placentography there is carried out the assessment of placenta maturity by structure density singling out 4 maturity degrees (0—3). The Is' degree is characteristic of the 28th-32nd week of pregnancy, the 2"'L 32nd - 37'1' week, the 3rd degree of placenta maturity is character­istic of the term of pregnancy of 38—39 weeks, if it is detected earlier, it testifies to premature placenta aging and fetoplacental insufficiency.

Ultrasonography also detects the biophysical fetal profile on the basis of its functional condition, qualitative and quantitative (in points) assessment of the indices of non-stress test, respiratory move­ments, motion activity, tone, amniotic fluid volume, placenta maturi­ty degree. Normal indices of biophysical profile make 9— 12 points.

Modern examination methods also include dopplerometric assess­ment of the blood flow. The essence of Doppler method consists in the feet that, depending on the speed of object moving relative to the source of wave radiation the length of the wave of reflected radiation changes. Such devices are used for the qualitative assessment, of blood flow in different vessels of the pelvic cavity of the pregnant woman: the uterine artery, carotid artery, umbilical artery, the descending part of the fetal aorta, medial cerebral artery. In case of necessity there are investigated the curves of speed performance of blood flow in the vessel under consideration.

Most often investigation is conducted in. the umbilical artery and medial cerebral artery. Blood flow in the umbilical artery is detected by the contractile function of the fetal heart and resistance of the ves­sels of the fetal part of placenta, whose vascular resistance plays the main role in fetoplacental hemodynamics. The condition of blood flow in this vessel is the most informative index of the vascular resistance of the placental bloodstream.

Diagnostic criteria:

Normal blood flow — a high diastolic component in the dopplero-gram relative to the isoline, the ratio of systole amplitude to diastole is not more than 3.

Pathological blood flow:

  1. decelerated blood flow — diastolic component reduction, the ratio of systole amplitude to diastole is more than 3;

  2. terminal blood flow testifies to a strong probability of antena­tal fetal death;

  3. zero blood flow stops in the diastole phase (there is no diastolic component in the dopplerogram);

4) negative blood flow acquires reverse direction in the diastole phase.

At PI blood supply to the medial cerebral artery increases. This brain-sparing phenomenon reflects the compensatory centralization of blood supply to the essential fetal organs.

Investigation of the content of placental hormones and fetopla­cental complex (estriol, placental lactogen, choriomammotropin, etc.) in biological fluids may diagnose violations of fetal condition at the presence of different pregnancy complications or extragenital patho­logy. The severity of fetal condition correlates with the amount of se­creted hormones.

Fetal development delay (FDD) or fetal hypotrophy is a patho­logical condition, at which the newborn's weight or biometric param­eters of the fetus are not up to gestational age.


  1. Symmetric - the weight and length of the fetus are propor­tionally reduced, all the organs are evenly reduced in size;

  2. Asymmetric — fetal weight reduction at normal indices of its length, unproportional dimensions of different fetal organs (Table 13).

Table 1. Differential FDD Diagnostics




2mi trimester

3"1 trimester


Delay of all dimensions increase

Delay of abdomen dimensions increase

Placental blood flow disorders

From the 24"1 25"' week

After 32 weeks

Amniotic fluid






At symmetric hypotrophy newborns have small body weight at birth, such a child cannot be differentiated from a premature new­born. The symmetric form is observed at severe disorders of intrauter­ine development beginning from the 2nd pregnancy trimester. At asym­metric FDD newborns have a considerable weight deficit at normal body length. This from is characteristic of the fetuses, in which unfa­vorable development conditions began in the 3rd pregnancy trimester.

3 degrees of FDD severity:

the 1st degree - delay by 2 weeks;

the 2nd degree — from 2 to 4 weeks;

the 3rd degree — more than 4 weeks.

FDD takes place due to the following reasons: chromosome anom­alies and hereditary metabolic disorders, congenital defects caused by other factors, prenatal viral infections, action of ionizing radiation and medicinal preparations, placenta pathologies, mother's diseases, intoxication, malnutrition.


If FDD is suspected, complex examination of the pregnant woman is conducted including:

  1. Detection of the HUFS and abdomen circumference in dy­namics (the weight of the woman should be taken into account). HUFS dimensions delay by 2 cm or the absence of any amount of growth during 2—3 weeks at dynamic observation allows suspecting FDD.

  2. Sonographic fetal biometry. To asses fetal biometry there are detected the biparietal diameter of the fetal head (BDFFI), diameter of the chest and abdomen, length of the fetal hip. Gestational age of the fetus is assessed by the complex of signs. If there is detected in­adequacy of one or a couple of basic fetometric indices to pregnancy term, extended fetometry is conducted, correlation of the frontooc-cipital and biparietal. dimensions, head and abdomen circumference, biparietal dimension and hip length, hip length and abdomen circum­ference is calculated.

  3. Assessment of the biophysical fetal profile.

  4. Detection of the level of hormones in the maternal organism and amniotic fluid.

  5. Dopplcrometry of the blood flow speed in the umbilical artery.


PI therapy should be begun with the treatment of the fundamen­tal illness and prevention of unfavorable factors influence. Medica-mental therapy consists in the administration of drugs, which im­prove the uteroplacental blood flow (sygethin), microcirculation in the placenta and rheological properties of blood (dipiridamol, aciove-gin, essentiale, chophytol), have antioxidant properties (tocopherol). The increase of the uteroplacental blood flow is also promoted by hy­perbaric oxygenation.


  1. Delivery through the natural passages is conducted under cardiomonitoring control of the fetal condition at normal or deceler­ated blood flow in the umbilical arteries, if there is no fetal distress (BFP assessment — 6 points and less).

  2. Indications to cesarean section:

  • critical changes of blood flow in the umbilical arteries (zero and reverse) — urgent preterm delivery is to be conducted irrespec­tive of the pregnancy term;

  • acute fetal distress (bradycardia < 100 bpm and pathological heart rate decelerations) irrespective of blood flow type (normal or decelerated) in the umbilical arteries during pregnancy;

  • pathological BFP (4 points and less) in the absence of biologi­cal maturity of the neck of uterus (after 30 weeks of pregnancy).

There is no efficient method of FDD treatment, therefore the key moment in managing such pregnant women is the clear assessment of fetal condition and timely delivery.


  1. Detecting of FDD risk factors and conducting dynamic con­trol over this group of pregnant women.

  2. The pregnant woman holding to the day regimen and rational nutrition.

  3. Giving up pernicious habits (tobacco smoking, alcohol con­sumption, etc.).



Presently all the violations of fetal functional condition are denoted by the term "fetal distress". It should be noted that with the help of modern noninvasive methods of investigation it is impossible to find the true reasons for fetal cardiac dysfunction. Therefore in clinical practice one should use the term "fetal distress" instead of "chronic fetal hypoxia" and "acute fetal, hypoxia", which are not clinical.

In its turn the term "fetal hypoxia" means the state conditioned by the reasons, which lead to acute or recurrent restriction of access of oxygen to the fetus or to the violation of fetal ability to use oxygen in cellular metabolism. The notions of "fetal hypoxia" and "postnatal asphyxia" must be clearly defined. It should be noted that the term "hypoxia" is to be used in relation to the intrauterine fetus, because, in spite of significant biochemical changes shown by blood analysis, hypocapnia and not hypercapnia declares itself. Concerning new­borns it is more correct to use the term "asphyxia", which means the violation of gas metabolism with the development of hypoxia, hyper­capnia, and acidosis.

Etiological factors of fetal hypoxia are divided into preplacental, placental and postplacental.


1. A group of pathological conditions leading to the violation of
oxygen transport to the uterus and placenta:

  • violation of maternal blood oxygenation (cardiovascular and pulmonary pathology of the mother);

  • hemic hypoxia of the mother — anemia of pregnancy at Hb < 100 g/L;

  • generalized circulatory injury (hypotension of pregnancy, es­sential hypertension, preeclampsia with predominant hypertensive syndrome).

2. Circulatory injury in the uterine vessels:

- pathological changes of the spiral arterioles in the area of the placental bed as a consequence of inflammatory diseases of the endo­metrium and abortions in the history;

- occlusive vascular violations of the spiral arterioles in the area of the placental bed, peripheral vasoconstriction (preeclampsia, over­
mature pregnancy, diabetic retinal angiopathy).

Placental proper.

- primary placental insufficiency caused by a disturbance of the development and maturation of the placenta (small placenta, placenta bipartite, angioma, etc.);

infectious-toxic injuries to the placenta in the late terms of pregnancy;

- detachment of placenta.

- flexure of the umbilical cord (prolapse, compression, winding,


- fetal malformations and pathologies.

By the rate of development there is differentiated acute and chronic hypoxia. The reasons for acute hypoxia:, placenta detachment, umbilical factors, inadequacy of the perfusion of the intervillous lacu­na of the maternal part of the placenta at acute maternal hypotension (anaphylactic shock, metrorrhexis).

All the other listed above factors lead to chronic fetal hypoxia.

The main clinical manifestations of fetal hypoxia are:

  1. the change of heartbeats character (heart rate, the change of heart sounds, arrhythmia);

  2. the change of fetal movements intensity;

  3. the appearance of meconium in the amniotic fluid (except for (he cases of pelvic presentation).

However, the diagnosis of fetal hypoxia only on the basis of these data not infrequently has erroneous results. In this connection to con­firm fetal hypoxia there are detected the indices of the acid-base balance in the blood taken from the skin of the fetal head. A characteristic sign of hypoxia is evident reduction of BE, pH of blood lower than 7.20.

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