BUKOVINIAN STATE MEDICAL UNIVERSITY
“Approved”
on methodological meeting
of Department of Obstetrics and Gynecology
with course of Infant and Adolescent Gynecology
“___”______________________ 201_ year
protocol #
T.a. The Head of the department
Professor
________________ O. Andriyets
METHODOLOGICAL INSTRUCTION
for practical lesson
“Placental dysfunction. Fetal growth retardation. Pathology of neonatal period.”
MODULE 4: Obstetrics and gynecology
CONTEXT MODULE 9: Pathological flow of pregnancy, labor and puerperium
Subject: Obstetrics and Gynecology
6th year of studying
2nd medical faculty
Number of academic hours – 6
Methodological instruction developed by:
ass.prof. Andriy Berbets
Chernivtsi – 2010
Aim: to learn the causes, clinic, diagnostic, treatment and preventing measures of placental
dysfunction and neonatal pathology, including asphyxia of the newborn.
Basic level:
1. Physiology of placenta.
2. Condition of normal newborn.
STUDENTS' INDEPENDENT STUDY PROGRAM
I. Objectives for Students' Independent Studies
You should prepare for the practical class using the existing textbooks and lectures. Special
attention should be paid to the following:
1. Obstetrics terminology.
2. External and internal obstetric examination.
3. Ultrasound examination
4. Cardiotocography
5. Biophysical profile of fetus
6. Physiology of placenta.
7. Methods of examination of placenta.
8. Definition of primary and secondary placental insufficiency.
9. Diagnostics of neonatal asphyxia.
10. Methods of resuscitation of the newborn.
11. The most common neonatal diseases.
12. Medications for placental insufficiency treatment.
Key words and phrases: Placental dysfunction. Fetal growth retardation. Pathology of neonatal
period.
PLACENTAL INSUFFIENCY (dysfunction)
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);
2) 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.
6. Investigation of estradiol secretion with urine.
7. Detecting the content of oxytocinase, general and placental basic phosphatase in the blood
serum.
8. Colpocytologic investigation.
Detection of the height of uterine fundus standing (HUFS) is very important in PI diagnostics,
the diagnostic value of this method a! the term of 32 weeks makes 76 %.
The main method of PI detection is ultrasonographic placento-nietry, which enables assessing
placenta thickness, area, and struc-l uro. Placenta thickness from the 20th till the 36th week of
pregnancy approximately equals the term of pregnancy in weeks: at 20 weeks — 20 mm, at 28
weeks — 28 mm, at 36 weeks — 36 mm, after this term the placenta does not thicken further.
Placenta thinning (less than 20 nun) or thickening (more than 50 mm) testifies to PI, which appeared as a result of intrauterine infection, immunization, etc.
At placentography there is carried out the assessment of placenta maturity by structure density
singling out 4 maturity degrees (0—3). The Is' degree is characteristic of the 28th-32nd week of
pregnancy, the 2"'L 32nd - 37'1' week, the 3rd degree of placenta maturity is characteristic of the term
of pregnancy of 38—39 weeks, if it is detected earlier, it testifies to premature placenta aging and
fetoplacental insufficiency.
Ultrasonography also detects the biophysical fetal profile on the basis of its functional
condition, qualitative and quantitative (in points) assessment of the indices of non-stress test,
respiratory movements, motion activity, tone, amniotic fluid volume, placenta maturity degree.
Normal indices of biophysical profile make 9— 12 points.
Modern examination methods also include dopplerometric assessment of the blood flow. The
essence of Doppler method consists in the feet that, depending on the speed of object moving
relative to the source of wave radiation the length of the wave of reflected radiation changes.
Such devices are used for the qualitative assessment, of blood flow in different vessels of the
pelvic cavity of the pregnant woman: the uterine artery, carotid artery, umbilical artery, the
descending part of the fetal aorta, medial cerebral artery. In case of necessity there are
investigated the curves of speed performance of blood flow in the vessel under consideration.
Most often investigation is conducted in. the umbilical artery and medial cerebral artery.
Blood flow in the umbilical artery is detected by the contractile function of the fetal heart and
resistance of the vessels of the fetal part of placenta, whose vascular resistance plays the main
role in fetoplacental hemodynamics. The condition of blood flow in this vessel is the most
informative index of the vascular resistance of the placental bloodstream.
Diagnostic criteria:
Normal blood flow — a high diastolic component in the dopplero-gram relative to the isoline,
the ratio of systole amplitude to diastole is not more than 3.
Pathological blood flow:
1) decelerated blood flow — diastolic component reduction, the ratio of systole amplitude to
diastole is more than 3;
2) terminal blood flow testifies to a strong probability of antenatal fetal death;
3) zero blood flow stops in the diastole phase (there is no diastolic component in the
dopplerogram);
4)
negative blood flow acquires reverse direction in the diastole phase.
At PI blood supply to the medial cerebral artery increases. This brain-sparing phenomenon
reflects the compensatory centralization of blood supply to the essential fetal organs.
Investigation of the content of placental hormones and fetoplacental complex (estriol,
placental lactogen, choriomammotropin, etc.) in biological fluids may diagnose violations of
fetal condition at the presence of different pregnancy complications or extragenital pathology.
The severity of fetal condition correlates with the amount of secreted hormones.
FETAL DEVELOPMENT DELAY
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 1).
Table 1. Differential FDD Diagnostics
Symmetric
Asymmetric
mi
Beginning
2 trimester
3"1 trimester
Fetbmetty
Delay of all dimensions increase
Delay of abdomen dimensions increase
Placental
From the 24"1
25"' week
After 32 weeks
blood
flow
Amniotic
Oligohydramnios
Norm
disorders
Malformation
Frequent
Rare
fluid
s
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 hyperbaric 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.).
FETAL DISTRESS. POSTNATAL ASPHYXIA
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 obstetriciangynecologist 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!.
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;
b) anatomical or functional immaturity of fetal lungs;
c) dysfunction of the fetal cardiovascular system (congenital heart disease, hypovolemia,
shock, delay of rearrangement of the fetal type of circulation into extrauterine);
d) severe fetal anemia;
e) 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 resistance 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 cardial 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
haemorrhage may affect 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 lowbirthweight 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.
Students must know:
1. Etyology and pathogenesis of placental disorders
2. Principles of diagnostics, treatment and management of women with placental disorders.
3.
Clinical picture, diagnosis and therapy of asphyxia of newborn, the most common
neonatal diseases.
Students should be able:
1. To evaluate the state of the fetus by the ultrasound examination an cardiotocography.
2. Principles of organization of the fetal department in the case fetal pathology.
3. Laboratory establishment of the diagnosis of placental insufficiency.
4. To prescribe the laboratory methods of examination.
5. To determine previous diagnosis of the disease of the newborn.
6. To perform emergency procedures of neonatal resuscitation.
References:
1. Danforth's Obstetrics and gynaecology. - Seventh edition.- 1994. - P. 560- 590|
2. Obstetrics and gynaecology. Williams & Wilkins Waverly Company. - Thin Edition.1998. -P. 157-179.
3. Basic Gynecoiogy and Obstetrics. - Norman F. Gant, F. Gary Cunningham. 1993. - P.
362-371.
4. Obstetrics.Edited by Prof. I. Ventskivska. – Kyiv. – 2008.