MINISTRY OF PUBLIC HEALTH OF UKRAINENATIONAL PIROGOV MEMORIAL MEDICAL UNIVERSITY, VINNYTSYA

CHAIR OF OBSTETRICS AND GYNECOLOGY №1

METHODICAL INSTRUCTIONS

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

Score Explanation

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 Normal = 2 At least 1 episode of active extension with return to flexion of fetal

Of muscles 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 INSUFFIENCY

Placental insufficiency (PI) is a symptom complex conditioned by violations of transport, trophic,

metabolic, and endocrine functions of the placenta due to structural changes.in it.

Reasons: gestoses, miscarriage threat, immunoincompatible pregnancy, intrauterine infection,

mother's diseases (pyelonephritis, essential hypertension, diabetes niellitus, anemia), etc.

Classification

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.

Diagnostics

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.

6. 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 ap-

peared 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.

1.2. FETAL DEVELOPMENT DELAY

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.

Classification

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

Symmetric AsymmetricBeginning 2mi trimester 3"1 trimesterFetbmetty Delay of all dimensions increase Delay of abdomen dimensions increase

Placental

blood flow

From the 24"1 25"' week After 32 weeks

Amniotic Oligohydramnios NormMalformation Frequent Rare

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.

Diagnostics

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.

Treatment

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 hy-

perbaric oxygenation.

Delivery

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.

Prevention

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.).

2. FETAL DISTRESS. POSTNATAL ASPHYXIA

2.1. FETAL DISTRESS

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.

Preplacental:

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.

Postplacental:

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

knot);

- 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.

Fetal Distress in the Course of Pregnancy

For the diagnostics of fetal distress in the course of pregnancy the following methods are used:

1. Auscultation of heart. Junction (beginning from the 20th week of pregnancy) — heart rate bigger

than 170 bpm and less than 110 bpm testifies to fetal distress.

Auscultation of fetal heart function is carried out at each visil of an obstetrician-gynecologist or a

midwife.

2. BFP (from the 30th week of pregnancy) - the total of the

points for biophysical parameters is evaluated:

- 7-10 points - satisfactory fetal condition;

- 5-6 points - doubtful test, (to be repeated in 2-3 days); 4 points and less - pathological

evaluation of the BFP (the question of urgent delivery is to be decided).

3. Dopplerometnj of blood velocity in the umbilical artery (reflects the state of

microcirculation in the fetal part of the placenta, whose vascular resistance plays the basic role in

fetoplacental hemodynamics).

Diagnostic criteria:

1. Pathological blood flow:

- decelerated blood flow - reduced diastolic component; the ratio of systole to diastole makes

more than 3;

- terminal blood flow (testifies to a strong possibility of antenatal fetal death).

2. Zero — the blood flow in the diastole phase stops (no diastolic component in the

dopplerogram).

3. Negative (reverse) — the blood flow in the diastole phase acquires reverse direction (the

diastolic component below the isoline in the dopplerogram).

Management of pregnancy with fetal distress:

1. Treatment of concomitant diseases of the pregnant woman, which lead to fetal distress.

2. Staged case monitoring of the fetal condition.

3. Outpatient observation and prolongation of pregnancy is possible at normal indices of the

biophysical methods of fetal condition diagnostics.

4. At decelerated diastolic blood flow in the umbilical arteries BFP investigation should be

conducted:

— if there are no pathological BFP indices, repeated dopplero-metry is to be conducted with

an interval of S—7 days;

— if there are pathological BFP indices, dopplerometry is to be conducted at least once in

two days, the BFP — daily.

5. Detection of the deterioration of blood flow indices (onset of

constant zero or negative blood flow in the umbilical arteries) is an

indication to urgent delivery by means of cesarean section.

Treatment:

— Till 30 weeks of pregnancy the treatment of concomitant diseases which lead to fetal

distress

— After 30 weeks of pregnancy the most effective and justified method of fetal distress

treatment is timely operative delivery.

Delivery:

1. Is possible through the natural maternal passages (at cardiomonitor control over fetal

condition) at:

— normal or decelerated blood flow in the umbilical arteries, if there is no fetal distress (6

BFP points and less).

2. Indications to urgent delivery by means of cesarean section after 30 weeks of pregnancy

are:

— critical changes of blood flow in the umbilical arteries (zero and reverse);

— acute fetal distress (pathological bradycardia and heart rate deceleration) independent of

the blood flow type (normal or decelerated) in the umbilical arteries during pregnancy;

— pathological BFP (4 points and less) at the absence of biological maturity of the uterine

cervix.

Prevention:

1. Detection of the risk factors of arrested fetal development and conduction of case monitoring

of the patients of this group.

2. Adhering to the day regimen, rational nutrition.

3. Quitting bad habits (smoking, alcohol consumption, etc).

Fetal Distress in the Course of Delivery

To diagnose fetal distress in the course of delivery the following methods are used:

1. Auscultation of fetal heartbeats.

The technique of auscultation during delivery:

— calculation of cardiac beats is conducted for a full minute —

every 15 min during the active phase and every 5 rnin during the second stage of delivery;

— obligatory auscultation before and after a contraction or a labor pain;

— if there are any auscultative violations of fetal heartbeats a cardiographic investigation is

carried out.

2. Cardiotocography (CTG):

— at fetal distress in the course of delivery CTG usually shows one or a couple of

pathologic signs: tachycardia or bradycardia, per sistent rhythm monotony (recording width of 5

bpm and less), early, variable, and especially late decelerations with the amplitude bigger than 30

bpm.

Unfavorable prognosis is also testified to by:

— deceleration of fetal heart rate at the height of deceleration lower than 70 bpm irrespective of

the type and amplitude of deceleration relative to heart rate;

— transition of late or variable decelerations to persistent bradycardia.

3. Detection of meconium in the amniotic fluid at fetal sac rupture:

— the presence of meconium in. the amniotic fluid in combination

with pathological changes of fetal cardiac rate is an indication to urgent delivery at cranial

presentation.

Delivery management.

1. Avoid the dorsal position of the parturient woman.

2. Stop oxytocine introduction if it was administered earlier.

3. If the reason for pathological fetal cardiac rate is the mother's condition, appropriate treatment

is to be conducted.

4. If the mother's condition is not the reason for pathological fetal cardiac rate, and fetal heart

rate remains pathological during the last three contractions, one should carry out internal

obstetric examination to determine the obstetric situation and find out possible reasons for fetal

distress.

5. Fetal distress detection requires urgent delivery:

— at the first stage of delivery — cesarean section;

— at the second stage:

• at cranial presentation — vacuum extraction or obstetric forceps;

• at breech presentation — fetal extraction by the pelvic poll!.

2.2. POSTNATAL ASPHYXIA

Postnatal asphyxia is a syndrome accompanied by gas metabolism derangement with hypoxia,

hypercapnia, and acidosis.

The reasons for asphyxia may be classified in such a way: I. Central reasons, which are

accompanied by the primary inhibition of the respiratory centers as a result of:

a) fetal hypoxia;

b) immaturity of the fetal nervous system;

c) an injury of the fetal nervous system;

d) pharmacological depressions.

II. Peripheral reasons conditioned by the violation of oxygen supply to the fetal brain right after

birth:

a) airways obstruction resulting from the aspiration of the amniotic fluid, meconium, blood, fetal

coat fragments;

a) anatomical or functional immaturity of fetal lungs;

b) dysfunction of the fetal cardiovascular system (congenital heart disease, hypovolemia, shock,

delay of rearrangement of the fetal type of circulation into extrauterine);

b) severe fetal anemia;

c) congenital anomalies (choanal atresia, diaphragmatic hernia, etc.).

Irrespective of the reasons for fetal hypoxia, they result in the decrease of oxygen level in the

fetal blood, development of respiratory and metabolic acidosis, which increases the inhibition of

respiratory centres, is accompanied by further derangement of pulmonary ventilation,

augmenting of hemodynamic and metabolic disorders.

Postnatal asphyxia most often results from fetal hypoxia. Therefore till the moment of birth there

already exists overstrain or derangement of the adaptation mechanisms of the fetal organism in

response to intrauterine hypoxia.

The degree of asphyxia is evaluated by the Apgar score on the 1st and 5lh min after birth.

However, if on the 5th min of life the assessment does not exceed 7 points, additional evaluations

are to be conducted every 5 min. up to the 20th min of life (the final decision about the

inefficiency of resuscitation measures), or to double assessment of 8 and more points.

At the present stage the Apgar score is considered insufficiently informative in the prognosis of

asphyxia development. More exact information, is given, by finding the so-called multiple organ

insufficiency (MOI) caused by severe asphyxia at birth.

The main MOI criteria are: violations of the indices of the cardiovascular, respiratory, nervous,

homeostasis, urinary, and digestive systems, metabolic disorders (pHa 7.1 and less; BEa 15

micromole/L and less; the level of natrium in blood plasma < 130 micromole/L or > 150

micromole/L; the level of potassium in blood plasma < 3 micromole/L or >7 micromole/L; the

level of glucose in blood, under the condition of complete parenteral nutrition, < 3.5

micromole/L or > 12 micromole/L.

The newborns born, in asphyxia are treated in three stages:

—the 1st — resuscitation;

—the 2ni — intensive syndrome therapy;

—the 3rd — rehabilitation.

Preparation to neonatal resuscitation at a high degree of perinatal risk, and also at

complicated delivery before the child's birth: one is to prepare the place and means for

resuscitation, check the availability and perfect readiness of equipment and instruments, a set of

medicaments, beforehand turn on the heating system of the resuscitation table and conditioning

of the breathing gas. After evaluating the fetal condition the neonatal resuscitation department

should be signalled about the necessity of turning on the couveuse.

The problem of temperature rate requires special attention. The newborn supercools

easily in the process of resuscitation. This is promoted by the fact that the newborn is not even

wiped because of haste, and when the amniotic fluid evaporates, heat loss increases (about 540

calories are needed for the evaporation of 1 ml of water).

Intravenous introduction of solutions, whose temperature is not controlled, also promotes

the supercooling of the newborn. During artificial pulmonary ventilation (APV) there increases

the organism's loss of not only water, but also heat. Resuscitation and intensive therapy without

any special measures concerning the optimization of temperature rates is accompanied by the

increase of peripheric vessels spasm, which increases the acidosis degree.

At the present stage neonatal resuscitation is conducted by the ' neonatologist-resuscitator.

The basic components of the resuscitation help to the newborn are known as the "ABC-steps" of

resuscitation.

A. Airways patency recovery (A — airways).

B. Breathing stimulation or recovery (B — breathing).

C. Circulation support (C — circulation).

Resuscitation stages:

1. Provision of airways patency:

a) to evacuate the content of the oral cavity and pharynx from (he moment the fetal head is born,

not waiting for the shoulders birth;

b) to continue the suction in the "draining" position after the Ictus is born;

c) at massive aspiration the toilet is to be conducted using the guidance of a laryngoscope;

d) the toilet is to be finished with the suction of stomach content to prevent recurrent aspiration

after regurgitation or vomiting.

2. APV is conducted after the airways toilet if there is no indepen

dent breathing during 40-60 sec after birth. Respiratory systems of

different types are used for this. One is recommended to stick to the

following rules when conducting APV:

a) the newborn's head is given the position of flexion, for this it is the best to put the newborn on

a special table with a movable head support, or to put a roll of diapers under the head;

b) after APV beginning one is to conduct lungs auscultation and make sure of the full value of

the toilet and efficiency of ventilation, which allows timely change of the APV regimen in case

of need. In the newborns with pulmonary vessels hypoperfusion the APV in the regimen "active

inspiration — active respiration" (with negative pressure on expiration), at excessive blood

filling of the lungs and at continual atelectases the application of the APV with increased resis-

tance on expiration of 5—6 mm Hg is administered;

c) if masked APV is ineffective during 2—3 min, trachea intubation is performed under the

guidance of a laryngoscope (at a severe stage of asphyxia, massive aspiration, and even at the

presence of green amniotic fluid — right after birth), the correct position of the intratracheal tube

is controlled auscultativcly;

d) in case of need one carries out a repeated toilet of the airways and sanation of the

tracheobronchial tree through the intratracheal tube (the catheter diameter must make 2/3 of the

tube's diameter). If the aspirate is dense, isotonic natrium solution is previously introduced with a

sterile syringe into the intratracheal tube and then evacuated;

c) if APV through the intratracheal tube is ineffective, in immature newborns it is indicated to

use the helium-oxygen mixture containing 30 % oxygen, during 10—15 inspirations;

f) if the APV apparatus is absent or out of order, one must conduct iuou.th-to-mouth ventilation,

being especially careful when exhaling air into the intratracheal tube.

3. Cardiac resuscitation. In case of apparent death, single heartbeats or even at heart rate <

60 bpm one must conduct closed-chest cardiac massage simultaneously with APV. The chest is

pressed to the spine 2-3 times with the tips of two fingers in such a way that the recess

makes 1 cm. if cardiac function is not renewed, 0.2 ml of 0.1 % adrenaline hydrochloride

solution is stream introduced into the umbilical vein, 3-5 mg of 10 % glucose solution per kg of

body weight, 1 —2 ml of 10 % calcium gluconate solution, glucocorticoids (10 mg/kg of

body weight or hydrocortisone 4 mg/kg — prednisolone). If there is no effect, 0.2 ml of 0.1 %

adrenaline solution and 1— 2 ml of 4 % sodium bicarbonate solution are introduced into the car-

dial cavity, cardiac massage is continued. It is expedient to conduct APV with cardiac massage

during 10 min.

4. Correction of volemic and metabolic disorders.

Disorders in the newborn period

Preterm birth

Infants born significantly before term usually require neonatal care until around the

expected date of delivery. Following the introduction of surfactant coupled with the widespread

use of antenatal corticosteroids in the mid-90s mortality rates for these infants fell significantly

although in the smallest the risks of death remained high (Fig. 11.1). Rates in the twenty-first

century remain similar to those shown. Mortality in extremely preterm babies can be

significantly reduced if hypothermia is prevented at birth; this is only possible if the delivery

room is maintained at an appropriate temperature. Most survivors do not sufferlong-ter m

disability, but in infants of less than 28 weeks gestation some 20% suffer neurodevelopmental

impairment.

The stress on parents and family of having a baby who undergoes intensive care can be

immense. They have to suffer prolonged uncertainly about the infant’s survival as well as a loss

of control overtheirbaby’s and their own lives. Careful preparation of parents, with visits to the

intensive care unit and meetings with unit staff may help, but the difficulties forfamilies in this

situation should not be underestimated.

Respiratory disorders

Abnormal breathing is a common presentation of many illnesses in the newborn period.

Intermittent or periodic breathing is common and not usually significant. However, a respiratory

rate persistently above 60 breaths/min needs further investigation, as do periods of apnoea

lasting more than a few seconds, especially if associated with cyanosis and bradycardia.

Tachypnoea with recession and nasal flaring is frequently the presentation of respiratory or

cardiac disorders, while apnoea may be the presentation of a great many disorders such as

septicaemia, meningitis, gastrointestinal obstruction or heart disease.

SURFACTANT DEFICIENCY

The respiratory distress syndrome caused by inadequate surfactant production is mainly a

disease of the preterm infant. However, it can occur in term infants, particularly those of diabetic

mothers or after caesarean section without labour.

Affected infantsmayrequiremechanical ventilation and intensive care. The classical clinical

presentation is an infant with tachypnoea, subcostal and intercostal recession and nasal flaring

which becomes progressively worse over the first 60 h after birth, and a chest X-ray showing a

ground glass appearance with air bronchograms. It can be associated with pneumothorax,

bronchopulmonary dysplasia (BPD) and intracerebral haemorrhage although in more mature

infants it normally resolves without sequelae. The combined use of antenatal corticosteroids and

surfactant modify the illness, improving survival and reducing the rates of complication such as

pneumothorax and intracerebral haemorrhage but have little effect on reducing the incidence of

BPD.

CONGENITAL PNEUMONIA

Congenital pneumonia is a relatively common problem associated with a variety of

microorganisms. The infant presents with respiratory distress and a chest X-ray shows patchy

inconsistent shadowing. Treatment is with antibiotics and intensive care as required.

MECONIUM ASPIRATION

Inhalation of meconium before or during delivery can be an extremely severe problem if

pulmonary hypertension with reduced lung perfusion and severe hypoxaemia develop.

Meconium may block large and/or small airways and lead to a ventilatory deficit. Although

meconium aspiration may be apparent at birth, severe disease may present an hour or more

laterand it is important that babies suspected of having aspirated are carefully observed.

Treatment of meconium aspiration complicated pulmonary hypertension requires expert

intensive care. Early surfactant administration may be beneficial, high frequency oscillatory

ventilation and the administration of nitric oxide reduce mortality. When other measures fail

extracorporeal membrane oxygenation should be considered.

TRANSIENT TACHYPNOEA OF THE NEWBORN

Transient tachypnoea of the newborn is due to delayed reabsorption of lung liquid which

leads to a moderate degree of intracostal recession and tachypnoea. In the preterm infant this can

lead to marked respiratory distress, but in a term baby needing high inspired oxygen

concentrations other causes of respiratory distress should be excluded.

BRONCHOPULMONARY DYSPLASIA

This is a chronic condition affecting up to 50% of infants born at 26 weeks or less.

Prematuredelivery, pre-and postnatal inflammation and infection, ventilation, oxygen and poor

nutrition are among the many factors contributing to the development and persistence of BPD.

The underlying problem is an arrest in alveolar and peripheral vascular development. The

severity is variable ranging from the need forsupplementar y oxygen forsever al weeks to

prolonged respiratory support with a ventilator or continuous positive airways pressure and

death. A small proportion of babies are discharged home on supplementary oxygen; most

outgrow the need by 12 months of age. All babies born prematurely have an increased risk of

respiratory illness within the first few years of life. This is increased in the group with BPD and

respiratory problems may persist into adult life.

Cardiac disorders

Some form of congenital heart disease affects between 7 and 9 per1000 live births of

whom approximately one quarter will present in the newborn period. Fetal anomaly ultrasound

can detect many lesions; antenatally, however, some are more difficult to diagnose. Cardiac

disease in the newborn baby presents in five main ways:

CYANOSIS DUE TO REDUCED PULMONARY BLOOD FLOW

The commonest causes are transposition of the great arteries (TGA), right to left shunts

such as Tetralogy of Fallot and pulmonary or tricuspid atresia. Administration of 100% oxygen

fails to increase arterial saturation and a chest X-ray may show oligaemia. Tachypneoa may

occur; however, respiratory distress is often not a prominent feature of the presentation whereas

cyanosis may be profound. A measurement of blood gases is mandatory both to the diagnosis

and as a measure of the baby’s condition: metabolic acidosis is an ominous sign. Forthose

presenting in the neonatal period immediate treatment is required to prevent the ductus arterious

from closing with transfer to a specialist paediatric cardiac centre.

CARDIORESPIRATORY DISTRESS DUE TO INCREASED PULMONARY BLOOD

FLOW

Left to right shunting though septal defects with a consequent increase in pulmonary blood

flow decreases the compliance of the lung leading to chest recession and tachypnoea. The

homeostatic response to this shunt is fluid retention, leading to congestive cardiac failure with a

large liver and oedema. Infants with large left to right shunts are not particularly hypoxaemic

except when cardiac failure is severe. The commonest cause of large left to right shunts are large

ventricular septal defect, atrioventricular septal defects and patent ductus arterious.

CYANOSIS AND CARDIORESPIRATORY DISTRESS

Infants inwhommixing between systemic and pulmonary circulations is impaired can

present with breathlessness and cyanosis. Complex conditions such as transposition of the great

arteries may lead to this presentation.

SHOCK SYNDROME DUE TO LOW CARDIAC OUTPUT

The clinical picture of shock is a desperately ill infant with generalized pallor, cyanosis,

cool peripheries and weak or absent pulses. Breathing is laboured or gasping, and the infant is

hypotonic. Neonatal shock is usually due to major sepsis, significant blood loss ormajorinter

ruption to the circulation such as hypoplastic left heart syndrome, severe coarctation of the aorta

or complex cardiac defects. Shock can also be part of the later natural history of other cardiac

defects.

THE ASYMPTOMATIC MURMUR

Murmurs are common in newborn infants and are frequently innocent. A low-amplitude-

ejection systolic murmur is audible in some 60% of normal newborn infants. It is normally best

heard over the pulmonary area and may be due to a ductus arterious that has not fully closed or a

pulmonary artery branch flow murmur which disappears before 6 months of age. Innocent

murmurs are systolic, short, localized and may change. Infants may develop murmurs when

unwell, because of increased cardiac output or reopening of the ductus arterious. Other causes of

asymptomatic murmurs in the newborn period include septal defects, aortic or pulmonary

stenosis and Tetralogy of Fallot. A thorough search for other signs of cardiac disease should be

made and an expert opinion arranged where appropriate. It is important to remember that the

mention of a heart murmur can strike panic into even the calmest of parents and the situation

needs to be handled with great tact. Rapid definitive diagnosis by echocardiography is the

mainstay of successful management.

Neurological disorders

NEONATAL ENCEPHALOPATHY

Neonatal encephalopathy can be caused by hypoxia ischaemia due to birth asphyxia but

also by other conditions including metabolic disorders and infections. These conditions should

be excluded before a confident diagnosis of hypoxic ischaemic encephalopathy due to birth

asphyxia can be accepted.

Hypoxia-ischaemia followed by resuscitation may lead to apparent recovery followed by

inexorable deterioration beginning 6–8 h later and ending in severe cerebral injury.

Consequently, it is frequently difficult to determine the prognosis soon after birth on clinical

grounds alone. However, if asphyxia is severe or happened some time before delivery the infant

will not develop spontaneous breathing; therefore, if despite advance life support there is no sign

of spontaneous breathing 20 min after birth the outcome is extremely poor.

Hypoxic ischaemic encephalopathy is graded clinically using clinical signs. Infants with

grade 1 encephalopathy have a very good prognosis whereas infants with Grade 3 almost all die

or are severely impaired. About half the infants with Grade 2 have severe neurodevelopmental

impairment. Unfortunately a large number of infants at risk fall into Grade 2, limiting the utility

of the system.

If asphyxia is suspected, further investigation is required, preferably by paediatricians

specialized in neonatal neurology and with access to sophisticated equipment such as

electrophysiology, magnetic resonance imaging or magnetic resonance spectroscopy. Diagnosis

and an accurate guide to prognosis can then be obtained.

CEREBRAL PALSY

Cerebral palsy is a non-progressive brain syndrome which may not be apparent until after

the first year of life and which cannot be confidently diagnosed at birth. Population based studies

have shown that about 20% of all cases of cerebral palsy are due to birth asphyxia in the term

infant, approximately one third are associated with preterm birth, and the remainder have no

obvious fetal or perinatal antecedent.

CONVULSIONS

Convulsions occurring just after delivery in term infants may be due to hypoxic ischaemic

encephalopathy, metabolic disorders, infections, hypoglycaemia, hypocalcaemia,

hypomagnesaemia or pyr idoxine deficiency. Many otherwise idiopathic fits are caused by focal

cerebral infarction, which have a much better prognosis than generalized hypoxic ischaemic

injury but are difficult to diagnose without magnetic resonance imaging.

BRAIN INJURY IN PRETERM INFANTS

Preterm infants are at high risk of cerebral injury and approximately10%of infants born

pretermdevelop significant neurodevelopmental impairment and another 10% have minorneur

ological lesions: two classical lesions which occurin preterm infants. First, intracerebral

haemorrhagemayaffect only the germinal layers or ventricles in which case the prognosis is

good; however, haemorrhage into the brain parenchyma is caused by haemorrhagic infarction

and this is associated with neurodevelopmental impairment. Second, in periventricular

leucomalacia there is a general loss of white matter, sometimes with cavitation. Whereas

haemorrhagic parenchymal infarctions can be usually seen by cerebral ultrasonography,

periventricularleucomalacia is difficult to see and is probably under diagnosed. Both these

conditions seem to be becoming less common than a more subtle loss of cerebral matter; this

may present as dilated cerebral ventricles on cerebral ultrasonography but is often only apparent

with magnetic resonance imaging. The aetiology of this condition is poorly understood, the

extremely preterm infant seems to be most at risk. The usefulness of cerebral ultrasonography

alone to predict neurological prognosis in extremely preterm infants is therefore limited. The

more mature preterm infants with normal ultrasound scans at discharge from intensive care have

a very low risk of neurodevelopmental impairment whereas those with definable loss of brain

tissue from whatevercause have a greaterthan 50% chance of long-term impairment.

BRACHIAL PLEXUS INJURY

Brachial plexus injury occurs in 0.4–2.5 per 1000 live births. The commonest type, Erb’s

palsy, involves C5 and 6 nerve roots. The incidence has not declined over the past few decades;

however, the prognosis for recovery, has improved with full recovery expected in the majority of

babies with Erb’s palsy. Injury to the brachial plexus results in the characteristic waiters tip

position, a fracture to the clavical may also be present. Careful neurological examination is

needed to determine the level of the lesion as this affects the prognosis for recovery of function;

an associated Horner’s syndrome is a bad prognostic sign. Effects of maternal drug ingestion

Infants of motherswhotake drugs such as opiates, cocaine, amphetamines, barbiturates,

benzodiazepines and some othermedical drugs may develop a withdrawal syndrome with

irritability, poor feeding, apnoea and fits. The babies of mothers who have high alcohol or

nicotine intake may also exhibit withdrawal. Wherever possible the mother and baby should be

kept together; in many cases breastfeeding in not contraindicated. If a history of maternal drug

abuse was known antenatally a plan of management can be agreed before birth and a referral to

the social work team may be appropriate. Management of a baby at risk of drug withdrawal

involves careful observation and skilled nursing. If withdrawal is severe treatment with opiates

may be required. Naloxone should never be given to infants at risk of opiate withdrawal as it can

provoke convulsions. Many labourwar ds no longerstock naloxone forfearit will be given

inadvertently to an infant of a substance-abusing mother.

Jaundice

Jaundice beginning in the first 24 h after birth is pathological. It is usually unconjugated

and the commonest cause are haemolytic anaemia or infection. Jaundice beginning on days 2–5

is commonly physiological, but unconjugate hyperbilirubinaemia may have many causes

including haemolytic disease, ABO incompatability and G-6-P deficiency Guidelines forthe

management of neonatal jaundice are derived from the belief that bilirubin levels greate than 340

mmol/l in term infants can cause deafness an kernicterus. This is based on data established when

kernicteru due to severe rhesus disease was common bu it has not been demonstrated that 340

mmol/l is the critica level for nervous system injury in other conditions. It I generally believed

that in preterm infants critical levels ar lower than this, especially if the infants have intercurren

illness, while at term higher concentrations may be tolerate without neurological deficit provided

the infant does not have additional pathology such as infection oracidosis Many authorities now

advocate a more relaxed vie of neonatal jaundice in a well, term infant, but haemolyti jaundice

and jaundice in the sick or preterminfant should always be treated aggressively. Failure to

control bilirubin levels by phototherapy should lead to urgent exchange transfusion. Conjugated

hyperbilirubinaemia signifies liver disease and requires urgent specialist investigation. These

infants maybe at risk of complications such as significant bleeding and neurological damage.

Hypoglycaemia Blood glucose concentration is only one measure available of metabolic

fuel and in term infants who are able to produce and utilize ketones, it is not easy to define an

unequivocal level at which the baby is at risk of the neurological sequelae of hypoglycaemia.

Authorities differ, but a pragmatic solution is to consider term infants with two consecutive

blood glucose levels below 2 mmol/l ora single blood glucose level below 1 mmol/l in need of

intervention. The blood glucose must be measured using an accurate device as commercial test

strips are not adequate formaking the diagnosis of hypoglycaemia. Conditions commonly

associated with transient low blood glucose are hypothermia, infection, prematurity, intrauterine

growth retardation and maternal diabetes. Some infants develop transient hyperinsulinaemia,

particularly infants of diabetic mothers with poor antenatal control or those with severe rhesus

disease. Rare causes include the Beckwith-Wiedemann syndrome and metabolic defects such as

cortisol deficiency, galactosaemia and otherenzyme defects of glycogenolysis, gluconeogenesis

orfatty acid β oxidation. Preterminfants are much less able to mount a ketotic response and

hypoglycaemia should be treated promptly. Treatment is initially to give calories in the form of

milk oras intravenous glucose infusion. Rapid bolus injections of concentrated glucose solutions

(20–50%) are not recommended. If hypoglycaemia persists investigations, including insulin

measurements, are required.

Infections

Newborn infants are particularly prone to perinatal infection; risk factors include low-

birthweight infants, prolonged ruptured membranes, maternal fever or chorioamnionitis.

Iatrogenic infection is problematic for those undergoing intensive care; the presence of

indwelling cannulae, central venous lines and invasive mechanical ventilation increase the risk.

Organisms responsible for later neonatal infection frequently come from the skin or gut.

Breastfeeding helps promote normal gut flora and reduces the risk of acquired neonatal

infections. Adherence to good hand-washing practices by all staff, parents and visitors can

significantly reduce the risk of acquired infection.

SEPTICAEMIA

The signs of systemic sepsis are non-specific. Infants may present with apnoea,

bradycardia or cyanotic episodes; is a common association. They may be lethargic and hypotonic

and they are hyper or hypothermic. Sepsis frequently presents as a metabolic acidosis or shock

and occasionally causes petechial skin rash or severe jaundice. Organisms which commonly

cause infection in the newborn period are group B streptococci, and gram-negatives such as

Escherichia coli orKlebsiella. The prolonged user multiple changes of antibiotics in the antenatal

period may increase the risk of infection with resistant organisms. Rapid treatment with

antibiotics, immediate resuscitation and, frequently, mechanical ventilation is required.

Investigations include chest X-ray, blood cultures, urine culture, and examination and culture of

the placenta. A lumbar puncture is performed once the baby is stable and will tolerate the

procedure. The mortality of infants who develop septicaemia in the neonatal period is high with

a significant number of survivors developing subsequent impairment.

GROUP B STREPTOCOCCUS INFECTION

Mortality due to maternal colonization by Group B streptococcus (GBS) is reduced by

antibiotic therapy to the Mother during labour and early treatment of infants with evidence of

infection. About 2% of infants of colonized mothers develop infections, and 70% of these

manIFEST risk factors at birth such as preterm labour, prolonged rupture of the membranes or

meconium stained liquor. Urgent antibiotic therapy is indicated for these infants. Well infants

shown by surface cultures to be colonized, do not require treatment. Recurrent GBS infection

can occurbut more commonly GBS infection can occurlater in infancy when meningitis is the

presenting problem.

MENINGITIS

Signs of meningitis in newborn infants are non-specific with a bulging fontanelle;

opisthotonos and seizures occurlate in the disease. Meningitis usually presents as septicaemia

and can be complicated by cerebral oedema, cerebral infarction, brain abscess or deafness.

Common causal organisms are GBS and E. coli. Listeria monocytogenes is a rare cause of

perinatal infection in the United Kingdom.

URINARY TRACT INFECTION

Urinary tract infectionsmaypresent as jaundice, vomiting, poorfeeding orsepticaemia. The

main cause is believed to be spread of blood-borne organisms to the kidney during septicaemia.

Further investigation is essential as 35–50% are associated with urinary tract abnormalities such

as vesico-ureteric reflux or ureterocele. Breastfeeding offers a significant degree of protection.

EYE INFECTION

The majority of sticky eyes are not infected but are due to a blocked nasolacrimal duct. In

the absence of conjunctival redness orswelling investigation forinfection and treatment with

topical antibiotics is not required. Simple measures such as cleaning with boiled water and

lacrimal duct massage suffice with symptoms usually resolving in 3–6 months. Neonatal

conjunctivitis can be caused by such organisms as Staphylococcus aureus,Chlamydia

trachomatis, Haemophlus influenzae,Str eptococcus pneumoniae and Neisseria gonorrhoeae.

Gonococcal ophthalmia usually presents within 24 h of delivery with profuse purulent

conjunctival discharge and immediate diagnosis and treatment (systemic and topical) is required

to prevent damage to the cornea. Chlamydial ophthalmia which is now among the commonest

causes of neonatal conjunctivitis presents between 5 and 12 days postnatal age; some babies

infected as neonates will develop chlamydial pneumonia laterin infancy. Corneal scarring is rare;

14 days systemic and topical treatment is required. The identification of either N. gonorrhoeae or

chlamydia in the baby requires referral of motherand hersexual partnerforinvestigation and

treatment.

SKIN INFECTION

Simple hygienic methods such as bathing, hand washing and routine umbilical cord care

can prevent many skin infections. The infant’s skin is vulnerable to infection by Staphylococci,

which usually leads to small pustules or lesions but can also cause scalded skin syndrome with

severe exfoliation. Staphylococcal infections should therefore be treated with antibiotics after

appropriate cultures have been taken. Streptococci can also cause skin infection and both may

cause systemic illness. Infection of the umbilical cord is commonly limited to periumbilical

redness with a small amount of discharge. The presence of oedema indicating cellulitis can

occasionally lead to complications such as spreading cellulites of the abdominal wall, fasciitis

and septicaemia and requires treatment with systemic antibiotics. Candidiasis usually presents

after the first week of life with napkin dermatitis with or without oral thrush. Topical and oral

treatment is required to prevent the candidiasis returning as the gut is colonized with candidia.

Maternal nipple candidial infection can occur in breastfeeding mothers.

TUBERCULOSIS

Tuberculosis is a re-emergent disease and many hospitals now offerBacille Calmette-

Guйrin (BCG) immunization to newborn infants. Infants born to mothers infected with active

tuberculosis should be vaccinated with isoniazidresistantBCGvaccine and kept with the mother

while both receive treatment with appropriate drugs. Breastfeeding should be encouraged. Expert

advice on drug therapy is advisable as patterns of antibiotic susceptibility change overtime.

TETANUS

Neonatal tetanus due to infection of the umbilical stump by Clostridium tetanii is the result

of poor hygiene and is a distressing and severe condition with extremely high mortality.

Opisthotonus and muscle spasms of the jaw and limbs are presenting features and can appear

very rapidly after birth. Prevention centres on maternal vaccination during pregnancy and

education to improve hygiene and change of local cultural practices.

Gastrointestinal disorders

OESOPHAGEAL ATRESIA OR TRACHEO-OESOPHAGEAL FISTULA

These conditions should be suspected when there is polyhydramnios or excessive mucous

from the mouth at birth. The baby may show rapid onset of respiratory stress and cyanosis

particularly after the first feed. X-ray confirms the diagnosis, the naso- oror ogastric tube does

not pass into the stomach. A large bore nasogastric tube should be placed in the oesophageal

pouch, constant suction and regular aspiration help prevent aspiration pneumonia. Associated

congenital anomalies occurin 50% or more of infants. Surgery involves division of the fistula

and oesophageal repair; if primary anastomosis is not possible lengthened procedures are

required before later oesophageal repair. Common long-term complications are gastro-

oesophageal reflux and anastomotic stricture formation both of which may require further

surgical treatment and long-term medication. Survival is usually determined by the severity of

associated congenital anomalies and not the defect itself.

DIAPHRAGMATIC HERNIA

Herniation of the abdominal contents into the hemithorax leads to severe respiratory

difficulties with persistent pulmonary hypertension. Most cases present with respiratory distress

and cyanosis at birth. Essential early management is the passage of a large bore nasogastric tube

into the stomach to prevent gaseous distension, ventilation and rapid transfer to intensive care.

All these infants require tertiary level intensive care, with access to sophisticated mechanical

ventilation and modern vasodilator therapy such as nitric oxide. Surgery is delayed until the

infant’s respiratory status has been stabilized. Survival depends on the degree of underlying

pulmonary hypoplasia and the presence of associated congenital anomalies such as cardiac

defects. Long-term complications include persistent gastro-oesophageal reflux and respiratory

problem; neurodevelopmental problems can develop if neonatal hypoxia was severe.

ABDOMINAL WALL DEFECTS

Exopmhalos, in which part or all of the intestine and abdominal organs are in a peritoneal

sack outside the abdomen, should be differentiated from gastroschisis where a congenital defect

of the abdominal wall allows herniation of the abdominal contents without a peritoneal sac. The

former is frequently associated with other congenital defects, while the latter is not. Urgent

surgery is required if the amniotic sac has broken and for gastroschisis; immediate management

is to wrap the abdominal contents in a plastic wrapper taking care not to twist the bowel and

disrupt its vascular supply. This should help prevent hypovalaemia due to fluid loss from the

exposed bowel. A large bore nasogastric tube is passed and the baby’s circulatory status

constantly assessed. Hypovalaemia orexcessive nasogastric output should be treated with 20

ml/kg 0.9% sodium chloride bolus intravenous infusions. The risk of hypothermia is high unless

good thermal management is present from birth. Primary repair is not always possible if the

abdominal cavity is not large enough to accommodate all the contents; a silo made of sterile

prosthetic material is attached to the abdominal wall and the contents gradually reduced over 7–

10 days. Outcomes are worse for those requiring silo treatment as infected complications are

high. The long-term outcome for most with exopmhalos is determined by the presence of

associated congenital anomalies. In gastroschisis 90%ormor e now survive. However,

theirpostnatal course is often protracted and parenteral nutrition may be required for several

weeks with its risks and complications. In addition bowel atresias and necrotizing enterocolitis

may develop.

INTESTINAL OBSTRUCTION

Highintestinal obstructions usually present with vomiting whichmaybe bile stained, and

this ominous signdemands urgent investigation. Plain X-ray film of the abdomen can confirm the

presence of obstruction by showing a lack of air in the lower gut or a sign such as the ‘double

bubble’ of duodenal atresia. Hypertropic pyloric stenosis does not usually present until 2–6

weeks of age. Lower intestinal obstruction usually presents as failure to pass meconium within

24 h followed by abdominal distension with orwithout vomiting. Causes include Hirshprung’s

disease, meconium ileus due to cystic fibrosis low bowel atresia or hypoplasia and imperforate

anus. Ameconium plug can sometimes mimic obstruction especially in preterm infants.

NEONATAL NECROTIZING ENTEROCOLITIS

This poorly understood inflammatory condition is primarily a condition of

preterminfantsandthose with congenital heart disease. It presents as an acute abdomen in the

days or weeks after birth and varies in severity from mild to fatal. Diagnosis is clinical, aided by

characteristic X-ray changes such as airin the bowel wall orbiliar y tree. Treatment is

conservative with cessation of enteral feeding and with antibiotics orsur gery.

Common queries from parents

Many minor alterations to physiology cause alarm to parents. Some common questions and

responses to them are outlined in Table 11.6 and in the absence of disease, reassurance is all that

is required. It is wise to read your unit’s breastfeeding policy so as not to contradict the advice

given by midwives and lactation consultants.

Advanced life support

If mask ventilation fails to produce an adequate heart rate check again forevidence of

upperair way obstruction and aspirate the nasal passages and nasopharynx. Meconium present in

the trachea should have been aspirated under direct vision using a laryngoscope before

ventilation, but this may need repeating. If clearing of the airway and reventilation fails to

produce a normal heart rate, endotracheal intubation is required. This technique is not difficult

but requires practice and carries a considerable danger in inexperienced hands: the endotracheal

tube will enter the oesophagus easily and significantly inhibi ventilation. If an infant does not

rapidly improve after attempted endotracheal intubation, there is presumptive evidence of the

tube being in the oesophagus. It should be removed and intubation repeated. If there is doubt it

may be safer to concentrate on bag and mask ventilation while awaiting skilled assistance. Once

the endotracheal tube is placed, auscultate the chest overboth lungs to ascertain that breath

sounds are equal. Inequality implies that the tube has been inserted too far and entered one lung,

but could also suggest majorpr oblems such as pneumothorax orcongenital diaphragmatic hernia.

Endotracheal intubation secures access for mechanical ventilation. Initial ventilation should

include an inspiratory time of approximately 1 s todistend collapsed alveoli, and peak pressures

sufficient to visibly move the chest. Once the alveoli are expanded less pressure is required. Thus

the first breaths may require peak pressures of 30 cm of waterormor e in term babies, whereas

afterthis it is usually possible to ventilate the lungs with pressures of approximately half this, and

a respiratory time of 0.5 s at a rate of 40 breaths/min. If there is evidence or presumption of

surfactant deficiency, exogenous surfactant shouldbe administered early. Effective ventilation is

enough to resuscitate most infants and only rarely is cardiac massage or the administration of

blood because of bleeding required. On very rare occasions, endotracheal adrenaline may need to

be administered for persistent bradycardia and if this fails intravenous adrenaline may be given.

It is no longer good practice to administer sodium bicarbonate intravenously to infants unless

blood gases are measured or circulatory failure is very prolonged. Most low-risk infants who

require resuscitation can be extubated within a few minutes and can usually be nursed by their

mothers as long as (1) there is no specific problem such as meconium aspiration, prematurity or a

history of infection and (2) adequate observation can be maintained. Infants who cannot be

extubated successfully in this time or who continue to have respiratory problems require

admission to a neonatal unit.

Tests and Assignments for Self — assessment.

Multiple Choice.

Choose the correct answer / statement:

1-1. Which of the following approximates the incidence of major structural or functional abnor-malities found in neonates?a. <1 %b. 2 to 3%c. 5 to 8%d. 10 to 12%

1-2. Which of the following is NOT currently used for fetal therapy?a. cordocentesisb. fetal tissue biopsyc. stem cell transplantationd. vesicoamnionic shunting

1-3. In women with no obstetrical or family history of aneuploidy, which of the following is the most powerful maternal predictor of aneuploidy?a. ageb. racec. parity

d. socioeconomic status

1-4. Approximately what percentage of all conceptuses are aneuploid?a. 5b. 10c. 25d. 50

1-5. What percentage of stillbirths and neonatal deaths are attributable to chromosomal abnor-malities?a. 1 to 3b. 5 to 7c. 10 to 12d. 15 to 20

1-6. Your patient has just spontaneously aborted a 7-week gestation. You counsel her that aneu-ploidy accounts for approximately what percentage of first-trimester abortion?a. 30b. 50c. 70d. 90

1-7. The fetal death rate following amniocentesis approximates which of the following?a. 1:100b. 1:200c. 1:400d. 1:500

1-8. Women with which of the following characteristics should be offered amniocentesis for fetal karyotyping?a. previous child was 4~.XYYb. twin gestation regardless of maternal agec. will be 35 years or older at time of deliveryd. prior history of 3 first-trimester spontaneous abortions

1-9. At term what is the risk of delivering an aneuploid fetus in a 35-year-old woman?a. 1:50b. 1:100c. 1:200d. 1:400

1-10. What is the recurrence risk of trisomy, either the same involved chromosome or different, in a young mother who had a previous pregnancy complicated by an autosomal trisomy?a. 1%b. 3%c. 5%d. 10%

1-11. What is the approximate recurrence risk of structural abnormalities that are multifactorial in etiology?a. 0.5%b. 1%

c. 2 to 3%d. 10 to 15%

1-12. Your 25-year-old newly pregnant patient informs you that her cousin was born with anencephaly, which has a multifactorial etiology. How do you counsel her regarding her fetus' risk for this abnormality?a. is greater than that of the general populationb. warrants pregnancy terminationc. warrants amniocentesis at 14 to 16 weeksd. warrants MSAFP level measurement at 16 weeks

1-1. Isolated fetal structural dejects are most commonly found in which of the following organs?a. liverb. heartc. bladderd. neural tube

1-14. Your patient's first child had an atrioventricular defect. You counsel her that the risk of recurrence of the same defect in future pregnancies is which of the following?a. 20%b. 40%c. 60%d. 80%

1-15. Additionally, you counsel the patient in Question 14 that fetal ultrasonography and echocardiography should be performed in future pregnancies at what gestational age?a. 6 to 8 weeksb. 10 to 12 weeksc. 20 to 22 weeksd. 26 to 28 weeks

1-16. Your newly pregnant patient informs you that her sister was born with spina bifida. You counsel her which of the following regarding her fetus risk for this abnormality?a. risk is 10 to 15%b. risk equals that of the general populationc. warrants maternal serum alpha-fetoprotein (MSAFP) level measurementd. warrants MSAFP level measurement plus fetal ultrasonographic examination

1-17. Which of the following has NOT been associated with an increased risk of fetal neural-tube defects?a. concurrent trisomy 1b. poorly controlled diabetesc. first-trimester acetaminophen used. high maternal fever early in gestation

1-18. Exposure to which of the following drugs is associated with an increased risk of fetal neural-tube defects?a. carbamazepineb. isotretinoinc. valproic acidd. all of the above

1-19. The most common hemoglobinopathy in the US. is found among persons belonging to which crhnic or geographic background?a. Mediterraneanb. Middle Easternc. Southeast Asiand. African American

1-20. Individuals of Jewish ancestry are at increased risk for which of the following diseases?a. Canavanb. Gaucherc. Tay-Sachsd. all of the above

1-21. Which of the following fetal structures is NOT involved in the synthesis of alpha-fetoprotein (AFP)?a. liverb. yolk sacc. bone marrowd. gastrointestinal tract

1-22. AFP can be found in which of the following body fluids?a. fetal urineb. fetal serumc. maternal serumd. all of the above

1-23. At which gestational age is the highest level of amnionic fluid AFP observed?a. 7 weeksb. 11 weeksc. 1 weeksd. 17 weeks

1-24. At which gestational age is the highest level of MSAFP observed?a. 10 weeksb. 14 weeksc. 18 weeksd. 22 weeks

1-25. Levels of MSAFP are influenced by which of the following maternal factors?a. raceb. diabetic statusc. maternal weightd. all of the above

1-26. In screening your patient's fetus for neural-tube defects at 16 weeks gestation, you obtain an MSAFP result which is 3.0 MoM.Your patient has no history indicating an increased risk for this defect. Which of the following is the next best step in her management?a. repeat MSAFP level measurementb. amniocentesis for fetal karyotypingc. amniocentesis for amnionic fluid AFP level measurementd. ultrasonography and amniocentesis for amnionic AFP level measurement

1-27. Which of the following accounts for the largest portion of elevated MSAFP levels in the absence of fetal anomaly?a. fetal deathb. maternal obesityc. multiple gestationd. incorrect gestational dating

1-28. Which ,of the following is NOT a condition associated with an elevated MSAFP level?a. omphalocoeleb. cloacal extrophyc. oligohydramniosd. complete molar pregnancy

1-29. In screening your patient's fetus for neural-tube defects at 16 weeks gestation, you obtain an MSAFP result that is 4.0 MoM.Your patient has no history indicating an increased risk for this defect. Which of the following is the next best step in her management?a. ultrasonographic examinationb. repeat MSAFP measurementc. amniocentesis for fetal karyotypingd. amniocentesis for amnionic fluid AFP level measurement

1-30. Which of the following fetal cranial ultrasonographic findings is NOT associated with neural-tube defects?a. lemon signb. banana signc. cabbage signd. ventriculomegaly

1-31. Open spine defects are associated with specific cranial lesions in what percentage of cases?a. 5b. 33c. 67d. 99

1-32. In screening your patient's fetus for neural-tube defects at 17 weeks gestation, you obtain an MSAFP result of 5.0 MoM. Your patient has no history that points to an increased risk for this defect. Ultrasonography reveals a viable singleton gestation with no structural anomalies, normal amnionic fluid index, and fetal measurements consistent with gestational age. Which of the following is the next best step in her management?a. reassuranceb. repeat MSAFP level measurementc. amniocentesis for fetal karyotypingd. amniocentesis for amnionic fluid AFP level measurement

1-33. In a woman with an elevated MSAFP level and elevated amnionic fluid AFP, what further testing should be performed on the amnionic fluid?a. Δ OD 450b. fetal fibronectin assayc. C-reactive protein assayd. acetylcholinesterase assay

1-34. Unexplained elevated abnormal AFP levels are associated with which of the following

complications?a. fetal deathb. low birthweightc. preterm rupture of membranesd. all of the above

1-35. Which of the following maternal serum analytes is NOT included in the "triple screen" for Down syndrome?a. AFPb. placental lactogenc. unconjugated estriold. chorionic gonadotropin

1-36. What percentage of fetuses with Down syndrome can be detected in women older than 35 years using the triple screen?a. 50 to 55b. 65 to 70c. 75 to 80d. 90 to 95

1-37. Which of the following is a maternal serum marker used in first-trimester Down syndrome screening?a. placental lactogenb. acetylcholinesterasec. pregnancy-associated plasma protein Ad. all of the above

1-38. Ultrasonographic measurement of which of the following is commonly used in first-trimester Down syndrome screening protocols?a. femur lengthb. intraorbital distancec. nuchal translucencyd. placental sonolucencies

1-39. Cystic fibrosis is inherited via which genetic transmission pattern?a. imprintingb. X-Iinkedc. autosomal recessived. autosomal dominant

1-40. Antenatal cystic fibrosis screening should be offered when both members of a couple are from which of the following ethnic groups?a. Southeast Asianb. Ashkenazi Jewishc. African Americand. Hispanic American

1-41. Which of the following is the most common cause of familial mental retardation?a. trisomy 1b. Down syndromec. 47.XXY genotyped. fragile X syndrome

1-42. Which of the following patients need NOT be offered screening for fragile X syndrome?a. males with unexplained mental retardationb. females with unexplained mental retardationc. first-degree relative of patients with known fragile X syndromed. first-degree relatives of patients with unexplained mental retardation

1-43. What is the most rational initial approach when a major fetal malformation is discovered using ultrasonography?a. MSAFP testingb. fetal karyotypingc. parental karyotypingd. serial ultrasonographic examinations

1-44. What is the most rational initial approach when two minor structural abnormalities are discovered using ultrasonography?a. MSAFP testingb. fetal karyotypingc. parental karyotypingd. serial ultrasonographic examinations

1-45. Which of the following changes in the fetal nasal bone have been used as a marker for Down syndrome?a. absenceb. increased sizec. decreased sized. increased opacification

1-46. Which of the following is a risk associated with second-trimester amniocentesis?a. chorioamnionitisb. amnionic fluid leakagec. fetal needle stick injuryd. all of the above

1-47. Higher rates of which of the following is a disadvantage of early amniocentesis compared with second-trimester amniocentesis?a. fetal deathb. foot deformitiesc. membrane ruptured. all of the above

1-48. Increased risk of which of the following is associated with chorionic villous sampling performed after 9 weeks gestation?a. fetal deathb. limb-reduction defectsc. oromandibular defectsd. cavernous hemangiomas

1-49. What is an advantage of transcervical chorionic villous sampling compared with second-trimester amniocentesis?a. lower fetal death rateb. test results received at an earlier gestational age

c. able to perform even if vaginal bleeding is presentd. able to perform on an extremely anteverted or retroverted uterus

1-50. Which of the following procedures has the highest fetal death rate?a. second-trimester amniocentesisb. transcervical chorionic villus samplingc. transabdominal chorionic villus samplingd. all have approximately equivalent rates

1-51. In which of the following situations would cordocentesis be appropriate?a. red cell alloimmunizationb. nonimmune fetal hydropsc. suspected primary fetal CMV infectiond. all of the above

1-52. Fetal tissue biopsy has been used for antenatal diagnosis of which of the following diseases?a. muscular dystrophyb. epidermolysis bullosac. mitochondrial myopathyd. all of the above

1-53. Preimplantation genetic analysis techniques can use genetic material from which of the following?a. blastocystb. first polar bodyc. second polar bodyd. all of the above

1-54. Which of the following has NOT been shown to be an effective method for administering medications for fetal medical therapy?a. injection into fetal buttockb. injection into amnionic fluidc. injection into the umbilical cordd. oral administration to the mother

1-55. Fetal medical therapy is LEAST likely to show beneficial effects in which of the following fetal conditions?a. cardiac arrhythmiasb. maternal-fetal infectionc. posterior urethral valvesd. congenital adrenal hyperplasia

15-56. In assessing the usefulness of fetal surgery to correct or ameliorate major malformations, which of the following should be considered?a. maternal risksb. natural history and prognosis of the malformationc. associated high incidence of genetic abnormalitiesd. all of the above

1-57. Of the following conditions, which cannot be ameliorated by antepartum vesicoamnionic shunting?

a. urethral atresiab. renal cystic dysplasiac. posterior urethral valvesd. ureteropelvic junction obstruction

1-58. Thoracoamnionic shunting is performed to prevent which of the following?a. pectus carinatumb. congenital scoliosisc. pulmonary hypoplasiad. left ventricular hypertrophy

1-59. Which of the following statements in advocacy of antenatal repair of congenital diaphragmatic hernia is true?a. Less than 30% of neonates survive postnatal hernia repair.b. Antenatal surgery is associated with only a 15% incidence of preterm birth.c. Several antenatal repair procedures are associated with improved neonatal survival.d. None of the above are true.

1-60. Pulmonary sequestration and congenital cystic adenomatoid does NOT result in which of the following?a. fetal hydropsb. pleural effusionc. oligohydramniosd. pulmonary hypoplasia

1-61. Antenatal repair of spina bifida has been shown to be associated with which of the following?a. minimal maternal morbidityb. improved lower extremity mobilityc. reduced need for ventriculoperitoneal shunt placementd. none of the above

2-1. What is the goal of antepartum fetal surveillance?a. prevent fetal deathsb. prevent early deliveriesc. increase fees for obstetriciansd. delay delivery until lung maturity achieved

2-2. What is the negative-predictive value of antenatal fetal testing?a. 10%b. 40%c. 70%d. ~100%

2-3. What is the positive-predictive value of antenatal fetal testing?a. <10%b. 10 to 40%c. 40 to 80%d. 80 to ~100%

2-4. At what gestational age does passive, unstimulated movement begin?a. 3 weeks

b. 7 weeksc. 11 weeksd. 2 weeks

2-5. At which gestational age do fetuses begin to exhibit rest-activity cycles?a. <1.0 weeksb. 10 to 20 weeksc. 20 to 30 weeksd. 30 to 40 weeks

2-6. All of the following have been used to describe fetal behavioral states EXCEPTa. breathingb. heart ratec. eye movementsd. body movements

2-7. Quiescent sleep is described by which of the following behavioral states?a. 1Fb. 2Fc. 3Fd. 4F

2-8. Fetuses spend most of their time in which of the two states?a. 1F and 2Fb. 1F and 4Fc. 2F and 3Fd. 3F and 4F

2-9. What is the mean length of the quiet or inactive state for term fetuses (i.e., "sleep cyclicity")?a. 11 minb. 23 minc. 75 mind. 105 min

2-10. What is the range of normal weekly counts of fetal movement?a. 20 to 600b. 50 to 950c. 100 to 1000d. 200 to 1200

2-11. Using maternal perception to quantify fetal movement, the threshold for fetal well-being at term is which of the following?a. 10 movements in 1 hourb. 30 movements in 2 hoursc. 100 movements in 1 dayd. none of the above

2-12. Which of the following statements regarding fetal movement is true?a. Its highest rates are at term.b. It is affected by amnionic fluid volume.c. Maternal perception of movement generally correlates poorly with instrumental measurement.

d. All of the above are true.

2-13. All of the following are descriptions of respiratory movements in the fetus EXCEPTa. gaspingb. paradoxical breathingc. glossopharyngeal breathingd. irregular bursts of breathing

2-14. In normal fetuses, what is the length of time that fetal breathing movements may be totally absent?a. 20 minb. 60 minc. 120 mind. 200 min

2-2. Which of the following may affect fetal breathing movement rates?a. laborb. fetal hypoxiac. cigarette smokingd. all of the above

2-3. True statements regarding fetal breathing include which of the following?a. They are affected by sound.b. They are unaffected by maternal eating.c. The highest respiratory rates are at term.d. They are used in the assessment of the four fetal behavioral states.

2-17. Which of the following fetal activities is monitored during a contraction stress test?a. breathingb. eye movementsc. heart rated. body movements

2-18. In a contraction stress test, all of the following may be a source of contractions EXCEPTa. oxytocinb. fundal massagec. nipple stimulationd. spontaneous onset

2-19. What controls fetal heart rate acceleration?a. autonomic function at brainstem levelb. aortic baroreceptor reflexesc. carotid baroreceptor reflexesd. humeral factors such as atrial natriuretion peptide

2-20. Fetal heart rate accelerations during the nonstress test are affected by which of the following?a. fetal lieb. fetal acidemiac. fetal sexd. all of the above

2-21. What is the American College of Obstetricians and Gynecologists' (ACOG) definition of a reactive nonstress test (NST)?a. 1 acceleration in 20 minb. 2 accelerations in 20 minc. 8 accelerations in 20 mind. 2 accelerations in 20 min

2-22. What is the associated risk of perinatal pathology for a fetus with a nonreactive nonstress test for 90 minutes?a. 10%b. 25%c. 50%d. 90%

2—23. Investigators advocate which nonstress testing schedule?a. dailyb. once weeklyc. twice weeklyd. all of the above

2-24. Fetal death within 7 days of a normal nonstress test occurs most commonly with which indication for testing?a. postterm pregnancyb. gestational diabetesc. gestational hypertensiond. fetal growth restriction

2-25. During acoustic stimulation testing, what fetal response is measured?a. breathingb. heart ratec. eye movementsd. body movements

2-26. Which of the following is NOT a fetal biophysical variable used in the biophysical profile?a. heart rateb. breathingc. eye movementd. body movement

2-27. Which of the following best describes a biophysical score of 6?a. normal scoreb. acidotic scorec. equivocal scored. abnormal score

2-28. The modified biophysical profile is described by which of the following?a. contraction stress test and Doppler umbilical artery velocimetryb. acoustic stimulation nonstress test and amnionic fluid index determinationc. acoustic stimulation nonstress test and Doppler umbilical artery velocimetryd. none of the above

2-29. Which of the following results describes abnormal umbilical artery velocimetry?

a. absent end-diastolic arterial flowb. reversed end-diastolic arterial flowc. systolic/diastolic ratio greater than the 95th percentile for gestational aged. all of the above

2-30. According to the ACOG, Doppler yelocimetry may be beneficial in which of the following clinical situations?a. gestational diabetesb. postterm gestationc. fetal growth restrictiond. antiphospholipid antibody syndrome

2-31. According to the ACOG, which of the following is considered the BEST test to evaluate fetal well-being?a. modified biophysical profileb. contraction stress testc. umbilical artery Doppler velocimetryd. none of the above

2-32. The most important consideration in deciding when to begin antepartum testing is which of the following?a. prognosis for neonatal survivalb. type of maternal diseasec. severity of maternal diseased. none of the above

Chapter 3. Ultrasonography and Doppler

3-1. Abdominal ultrasonography is most commonly performed using transducers that generate which range of sound frequency?a. 1 to 3 mHzb. 3 to 5 mHzc. 5 to 7 mHzd. 7 to 9 mHz

3-2. What is the major biological hazard from fetal ultrasonography?a. noneb. chromosomal breakagec. impaired neonatal hearingd. early spontaneous abortion

3-3. Several studies have shown the utility of fetal ultrasonography for which of the following?a. assist in aneuploidy detectionb. decrease postterm delivery induction ratec. determine gestational age more accurately than the last menstrual periodd. all of the above

3-4. According to the American Institute of Ultrasound in Medicine (AIUM), assessment of fetal anatomy is best performed no earlier than what gestational age?a. 14 weeksb. 18 weeksc. 22 weeks

d. 26 weeks

3-5. According to AIUM, which of the following should be evaluated during a first-trimester ultrasound?a. fetal weightb. fetal presentationc. placental locationd. maternal adnexal evaluation

3-6. With transabdominal ultrasonography, the gestational sac is reliably seen in the uterus by which gestational age?a. 4 weeksb. 5 weeksc. 6 weeksd. 7 weeks

3-7. With transvaginal ultrasonography, fetal cardiac motion is reliably seen by which gestational age?a. 4 weeksb. 5 weeksc. 6 weeksd. 7 weeks

3-8. A standard fetal ultrasonographic examination includes evaluation of which of the following?a. gallbladderb. large colonc. umbilical cord insertiond. hand and foot digit count

3-9. In determining gestational age between 14 and 26 weeks, which of the following is the most accurate parameter to measure?a. femur lengthb. biparietal diameterc. crown-rump lengthd. abdominal circumference

3-10. Which of the following ultrasonographic views is used to measure the biparietal diameter?a. trans thalamicb. transcerebellarc. transventriculard. transhemispheric

3-11. Which of the following fetal measurements shows the greatest variation?a. femur lengthb. biparietal diameterc. crown-rump lengthd. abdominal circumference

3-12. During standard ultrasonographic examination which of the following cranial structures is NOT routinely evaluated?a. cisterna magna

b. pituitary glandc. choroid plexusd. lateral ventricles

3-13. What is the incidence of neural-tube defects in the United States?a. 0.8 per 1000b. 1.6 per 1000c. 8 per 1000d. 3 per 1000

3-14. Encephalocele is usually associated with which of the following?a. hepatomegalyb. hydrocephalusc. normal intelligenced. all of the above

3-2. Ultrasonographic findings of spina bifida and the lemon sign are suggestive of which malformation?a. anencephalyb. Budd-Chiaric. Arnold-Chiari Id. Arnold-Chiari II

3-3. Which of the following is used to describe an elongation and downward displacement of the cerebellum?a. lemon signb. pickle signc. melon signd. banana sign

3-17. What is the average diameter in millimeters of the lateral ventricular atrium at 2 weeks' gestation and older?a. 2 to 4b. 6 to 8c. 10 to 12d. 14 to 3

3-18. A free-floating or dangling choroid plexus is suggestive of which of the following?a. hydrocephalusb. cerebral atrophyc. aqueductal stenosisd. choroid plexus cyst

3-19. Cystic hygroma is the result of which of the following?a. lymphatic obstructionb. meningeal herniationc. arterial aneurysm formationd. cystic degeneration of the sternocleidomastoid muscle

3-20. What percentage of cystic hygromas are associated with aneuploidy?a. 20 to 30b. 40 to 50

c. 60 to 70d. 80 to 90

3-21. What is the most common chromosomal anomaly associated with cystic hygroma in second- or third-trimester fetuses?a. triploidyb. trisomy 18c. trisomy 21d. monosomy X

3-22. The lungs are best visualized beginning at which gestational age?a. 3 to 20 weeksb. 20 to 25 weeksc. 25 to 28 weeksd. 28 to 32 weeks

3-23. In greater than 90% of cases, congenital diaphragmatic hernias are located in which of the thoracic quadrants?a. left anteriorb. left posteriorc. right anteriord. right posterior

3-24. Which of the following is a specific ultrasonographic finding in fetuses with diaphragmatic hernia?a. cardiac displacementb. small abdominal circumferencec. absence of intra-abdominal stomach bubbled. all of the above

3-25. What is the incidence of congenital cardiac malformation in newborns?a. 8 per 100b. 8 per 1000c. 8 per 10,000d. 8 per 100,000

3-26. What percentage of congenital heart defects are due to multifactorial or polygenic transmission?a. 10b. 33c. 67d. 90

3-27. Ultrasonographic examination identifies a hypoplastic left heart in your patient's fetus at 18 weeks' gestation. The next most appropriate management step includes which of the following?a. Doppler aortic arch velocimetryb. amniocentesis for fetal karyotypingc. cordocentesis to assess level of fetal anemia d. amniocentesis for acetylcholinesterase level measurement

3-28. The four-chamber view of the heart is seen transversely at which fetal body level?a. 4th rib

b. T-8 vertebrac.immediately above the diaphragmd. branching of the main stem bronchus

3-29. Which of the following typically should NOT prompt fetal echocardiography?a. fetal arrhythmiab. maternal diabetesc. first-degree relative with heart defectd. elevated maternal serum alpha-fetoprotein level

3-30. Which of the following ultrasonographic findings has been most frequently associated with fetal heart defects?a. oligohydramniosb. mediastinal shiftc. left-axis deviationd. raised left hemidiaphragm

3-31. The ultrasonographic detection rate of fetal heart defects in a low-risk population approximates which of the following?a. 2%b. 35%c. 65%d. 85%

3-32. Nonvisualization of the fetal stomach during an ultrasonographic examination is common in all of the following EXCEPTa. anencephalyb. esophageal atresiac. diaphragmatic herniad. tracheoesophageal fistula

3-33. Which of the following is NOT associated with echogenic bowel seen ultrasonographically?a. trisomy 21b. cystic fibrosisc. thick meconium-stained fluidd. swallowed intra-amnionic blood

3-34. Gastroschisis is associated with which of the following?a. aneuploidyb. other bowel abnormalitiesc. poor postnatal survivald. all of the above

3-35. Which of the following is more likely to be associated with aneuploidy?a. anal atresiab. gastroschisisc. omphalocoeled. esophageal atresia

3-36. The "double-bubble" sign is an ultrasonographic finding of which of the following anomalies?

a. cystic hygromab. duodenal atresiac. aqueductal stenosisd. two-vessel umbilical cord

3-37. What percentage of fetuses with the "double-bubble" sign will have trisomy 21?a. 5b. 2c. 30d. 50

3-38. With which of the following anomalies is hydramnios NOT a typical associated finding?a. anal atresiab. anencephalyc. gastroschisisd. esophageal atresia

3-39. The fetal kidneys can routinely be visualized by what gestational age (weeks)?a. 8b. 12c. 18d. 22

3-40. Which of the following is NOT characteristic of Potter syndrome?a. tight skinb. abnormal fadesc. limb deformitiesd. pulmonary hypoplasia

3-41. Which of the following can NOT be reliably diagnosed antenatally?a. renal agenesisb. obstructive pyelectasisc. multicystic dysplastic kidney diseased. autosomal dominant polycystic kidney disease

3-42. Which of the following is the most common cause of neonatal hydronephrosis?a. posterior urethral valvesb. multicystic dysplastic kidneyc. collecting system duplicationd. ureteropelvic junction obstruction

3-43. Umbilical artery Doppler velocimetry is recommended in the evaluation of which of the following fetal indications?a. macrosomiab. growth restrictionc. suspected cyanotic heart lesiond. suspected pulmonary hypoplasia

3-44. Doppler evaluation has been used to screen inductus arteriosus constriction after exposure which of the following?a. heparinb. valproic acid

c. indomethacind. inhalation anesthetics

3-45. Peak velocities of blood flow through the fet middle cerebral artery have been shown by Doppler velocimetry to be increased in which of the following fetal complications?a. anemiab. cerebral palsyc. fetal alcohol syndromed. congenital HIV infection

References:

1. Danforth's Obstetrics and gynaecology. - Seventh edition.- 1994. - P. 289-304.

2. Obstetrics and gynaecology. Williams & Wilkins Waverly Company. - Thirdl Edition.- 1998.

- P. 118-130.

3. Basic Gynecology and Obstetrics. - Norman F. Gant7 F. Gary Cunningham, -j 1993. - P. 328-

397.

4. Obstetrics and gynecology. - Pamela S.Miles, William F.Rayburn, J.Christopher. Carey. -

Springer-Verlag New York, 1994. - P, 30-34.