Asphyxia

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STATE ESTABLISHMENT «DNEPROPETROVSK MEDICAL
ACADEMY OF MINISTRY OF HEALTH UKRAINE »
“Сonfirmed;”
at methodical meeting
of hospital pediatrics №1 department
Сhief of department
professor _____________V. A. Kondratyev
“______” _________________ 2013 y.
METHODICAL INSTRUCTIONS
FOR STUDENTS` SELF-WORK
WHILE PREPARING FOR PRACTICAL LESSONS
Educational discipline
module №
Substantial module №
Theme of the lesson
Course
Faculty
pediatrics
2
8
Asphyxia of the newborn
5
medical
Dnepropetrovsk, 2013.
Asphyxia of the newborn
1. Actuality of the topic: Intrahospital hypoxia – polyetiologic phenomenon which occurs
quite often nowadays. It is hard to find a pregnancy which would pass without any
complications (mother’s illness, toxicosis, external influence on fetus and so on). Most often
chronic hypoxia is the affection factor of internal organs and systems, first of all – nervous
system, therefore the knowledge of asphyxia causes, ability to render urgent medical help to
a new-born baby, ability to diagnose abnormality in child’s health and carry our correcting
procedures are necessary skills for each doctor.
2. Certain purposes:
А. A student should know:
1. Basic causes which lead to oxygen hunger in intranatal period
2. Definition of term “asphyxia of a new-born baby”
3. Methodology of estimation of new born baby’s condition according to Apgar
4. Algorithm of rendering urgent help to a child born in asphyxia
5. Principles of intensive therapy and observation at early post-asphyxia period.
6. Consequences of new born baby’s asphyxia
- in nervous system
- in cardio-vascular system
- in respiratory system
- in kidneys
- in adrenal glands
- in gut
- in immune system
- in metabolism
7. Notion of hypoxic-ischemic encephalopathy
8. Mechanical formations of HIE
9. Clinical manifestations of HIE
10. Principles of treatment and rehabilitation of children with HIE
11. HIE outcomes
B. A student should be able:
1. To determine signs of asphyxia in new-born babies
2. To estimate condition of a new-born baby according to Apgar scale
3. To determine the degree of AN
4. To draw up a plan of rendering urgent aid to a certain child
5. To draw up a plan of further child’s treatment with AN
6. To reveal signs of HIE in a new-born baby
7. To reveal signs of post-hypoxic abnormalities in other systems and organs
8. To draw up a plan of in-patient observation over children who suffered new-born
asphyxia (AN)
3. Tasks for self-study work whilke preparing for the lesson
3.1. A list of basic terms, parameters, characteristics a student should master
while preparing for the lesson:
Term
1. Asphyxia of a new-born
Definition
Pathological condition caused by gas disorders in the need of 02
2
baby
2. Hipoxic-ischemic
encephalopathy
3. Antenatal hypoxia
4. Intranatal hypoxia
5. Cardiac-respiratory
syndrome
6. Syndrome of increased
nervous anxiety
7. Syndrome of general
depression
8. Hypertension syndrome
9. Hydrocephalic
syndrome
10. Cramp syndrome
11. Comatose condition
12. Neurosonography
necessity, superficiality of С02 which takes place along with metabolic
acidosis
Brain damage caused by perinatal hypoxia which is manifested by
morphological-functional disorders and signs of cerebral insufficiency
First revealed before birth
First revealed during the delivery
Mild asphyxia which develops due to depression of respiratory center
which most often occurs while using sedative, pain-killers, in narcosis
without acidosis development
It is manifested by worry, sleep disorders, regurgitation, painful cry,
increase of muscular tone, tremor of extremities and chin,
hyperreflexia
Most often it occurs in pre-term babies due to immaturity of CNS,
which is a generalized slow-down, languor, adynamy, hyporeflexia,
muscular hypotonia
It is manifested by the presence of a necessary condition – head is
thrown back, extremities are bent, fists are squeezed (a “boxer” pose),
presence of “cerebral” cry, regurgitation and vomiting, hyper and
tremor of extremities, vertical and rotator nystagmus, Grefe symptom
It develops closer to the end of acute period and it is manifested by
increase of head in volume, domination of cerebral cranium over
facial, bridge changes with hanging of forehead part, increase of
venous picture on the head, widening of liquor system and increase of
ventricular index according to data of brain ultrasound
It is most often manifested by generalized clonic-tonic cramps. More
seldom focal and multifocal, mioclonic cramps take place.
It develops in case of brain edema and it is characterized by
unconsciousness, absence of motor activity, cry, emotions and reaction
to pain
Ultrasound of brain structures with sensor in big fontanel
3.2. Theoretical questions to the lesson:
Definition of term “asphyxia of a new-born baby”
Reasons of new-born asphyxia
Reasons of chronic and acute intranatal fetus hypoxia
Pathogenesis of changes in case of fetus hypoxia
Use of contemporary diagnosing methods for fetus estimation (CT, ECG, US and so
on)
6. Clinical signs of asphyxia in new-born babies
7. Methodology of estimation of new born baby’s condition according to Apgar
8. Determination of asphyxia degree
9. Urgent help to a new-born child in asphyxia
10. Contemporary equipment used for reanimation and intensive care. Methods of ALV
11. Correction of metabolism disorders
12. Complications of asphyxia in new born children
- in nervous system
- in cardio-vascular system
- in respiratory system
- in kidneys
- in adrenal glands
1.
2.
3.
4.
5.
3
- in gut
- in immune system
- in metabolism
13. Complications of reanimation and intensive care
14. Notion of hypoxic-ischemic encephalopathy
15. Pathogenesis in development of hypoxic-ischemic encephalopathy
16. Clinical signs of hypoxic-ischemic encephalopathy. Neurological, somatic and
metabolism disorders
17. Contemporary methods of diagnosing CNS disorders (neurosonography, CT, NMR,
etc.)
18. Classification of hypoxic-ischemic encephalopathy
19. Treatment and rehabilitation of children with hypoxic-ischemic encephalopathy
20. Principles of treatment and control on pediatrics regions and its effectiveness
21. Outcomes of hypoxic-ischemic encephalopathy
4.3 . Practical works (tasks) which are performed on occupation:
1 To collect complaints, case history and personal (life) history
2. To inspect the child
3. To reveal early symptoms of asphyxia
4. To reveal the signs of the complications of asphyxia
5. To evaluate the condition of the child and available clinical symptoms.
6. To evaluate the results of the additional methods of investigation
7. To make the clinical diagnosis according to classification.
8. To make the plan of urgent therapeutic measures.
9. To make recommendations of dispensary supervision.
.
3. Maintenance of the subject:
Asphyxia of the newborn ICD-X Code: P21
Pathological life threatening condition caused by disorders of gas exchange in the form of
increased requirements in 02 and excess of C02 that is accompanied by metabolic acidosis.
The word "asphyxia" is translated as "without pulse", but this concept is traditionally means
"dyspnea".
Asphyxia in 80% of cases is the lasting fetal hypoxia, therefore it’s characterized by common
etiologic and pathogenetic factors.
1. The causes which lead to acute asphyxia of the newborns:
— blood supply interruption through an umbilical cord (the real knots of an umbilical cord,
its compression, tense cord encirclement round a neck or other parts of the infant);
- disorders of gas exchange through the placenta (premature complete or incomplete
placental separation, presentation, etc.);
- inadequate haemoperfusion of the maternal part of the placenta (excessively active labour,
hypotension or hypertension at mother of any etiology);
- deterioration of mother’s blood oxygenation (anemia, cardiovascular diseases, respiratory
failure);
- insufficiency of respiratory efforts of the newborn (iatrogenic - influence of drugs
administered to mother, antenatal brain disorder of the fetus, congenital defects of the
development of fetal lungs, etc.).
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Intranatal hypoxia. ICD-X code: P20
Causes of antenatal fetal hypoxia:
- overterm pregnancy;
- long-standing (more than 4 weeks) gestoses;
- multiple pregnancy;
- threat of interruption of pregnancy;
- diabetes in the pregnant women;
- bleedings and infectious diseases in the II—III trimesters of pregnancy;
- serious somatic disorders of the pregnant woman;
- smoking or other types of drug addiction of the pregnant woman;
- delay of intrauterine fetal development or other diseases revealed by ultrasonic or other
fetal investigations.
Causes of intranatal fetal hypoxia:
- Cesarean section (planned or urgent);
- pelvic, gluteal or others abnormal fetal position;
- premature or late birth;
- waterless interval more than 24 or less than 6 hours;
- first labor – if it is less than 4 hours at the woman who delivers for the first time and 2 hours
at repeated childbirth;
- presentation or premature detachment of the placenta, rupture of the uterus;
- usage of obstetric forceps, vacuum extractor and other obstetric interventions in labor;
- discrepancy of the sizes of the fetal head and sizes of pelvis of mother;
- acute hypoxia in childbirth at mother (shock, decompensation of somatic diseases,
poisoning, etc.)
- disorders of placental fetal (umbilical) blood circulation at tense cord encirclement, real
knots, a tension of a small umbilical cord on length, loss of its loops, pressing loops of
umbilical cord by fetal head to the walls of the birth canal
- fetal cardiovascular, respiratory diseases, diagnosed by ultrasonic investigation
- abnormal fetal heart rate;
- mekonium in waters, increased or decreased amount of waters;
- the narcotic and other analgetics, administered to the mother in 4 hours and less prior to the
delivery, the general anesthesia at mother.
2. Pathogenesis of fetal disorders at hypoxia:
At exposures of the specified mechanisms gas exchange is disordered and oxygen starvation
of tissues develops. At the hypoxia more differentiated and young tissues, namely a brain,
most often suffer. At the short-term hypoxia disorders of nervous system are reversible and
are manifested by disorders of blood circulation and liquor circulation (expansion and
overflow of vessels by blood, increase of permeability of the vascular wall, etc.). At longstanding oxygen deficiency there are irreversible changes of the brain and other fetal organs
(lungs, heart, kidneys, adrenal glands, liver) owing to hemorrhages, ischemia, edema,
dystrophy, necroses.
In the pathogenesis of hypoxia there is a short circuit of many "vicious circles" - disorders of
oxygenation leads to haemodynamical changes which, in turn, strengthen tissue acidosis.
Severe asphyxia breaks compensatory mechanisms, pathological acidosis, arterial
hypotension, disorders of permeability of cellular membranes, a hypovolemia, electrolytic
disorders occur. The most threatening complication is the brain ischemia resulting in
degenerative changes.
3. Main clinical manifestations of the fetal hypoxia:
Heart rate disturbances (at first tachycardia, then bradycardia), deterioration of sonority
of heart tones (at the beginning small strengthening, then - dullness of tones); occurance
of arrhythmia, mekonium in waters, change of parameters of acid-base balance of waters
and fetal blood.
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Aschyxia of the newborn is clinically manifested by the presence of signs of disorders of
vital systems: respiratory, cardiovascular, urinary, digestive, etc. for the first 3 days of
life; existence of clinical signs CNS disorders, and also presence of metabolic acidosis.
4 . Technique of an assessment of the newborn by Apgar scale. Definition of the degree
of asphyxia.
For the assessment of severity of asphyxia the Apgar scale is used which includes main
indicators of activity of the newborn: heart rate, breathing, muscular tone, reflexes, skin
color. Each of the above listed criteria is estimated by two-point system (0, 1, 2). Final
conclusion about the condition of the child is done on the basis of the score behind all 5
counted criteria. Assessment of the condition of the child should be carried out on the 1st
minute and in 5 minutes after the birth. Light asphyxia corresponds to the 6-7 points,
moderate - 4-5 points and severe - 1-3 points. Light asphyxia is regarded as the
cardiorespiratory syndrome owing to thedepression of the respiratory center which is mostly
seen at administration of sedative, anesthetizing preparations, an anesthesia. Unlike asphyxia,
acidosis isn't characteristic for this syndrome.
Clinical sign
Heart rate
Breathing
Muscular tone
The reflex
excitability
(reaction to the catheter)
Skin color
Table 1. V. Apgar scale (1953)
Assessment in points
0
1
2
Absent
Less than 100 in 1 More than 100 in 1 min
min
Absent
Bradipnoe,
Normal, loud cry
irregular
Absent
Easy flexing of
Active movements
extremities
Absent
Grimace
Sneezing, cough
Skin color of
Pink
Generalised pallor or color of the body,
Pink
cyanosis
cyanosis of
color of the body
extremities..
5. The urgent help at asphyxia of the newborn
The protocol of resuscitation actions at asphyxia of the newborn
At pure waters
At intensive meconial contamination of waters
1. To put the newborn under a source of radial 1. To suck contents of an oral cavity, a throat and a
heat on the horizontal dense surface.
nose cavity by the catheter after the birth of the head
2. To dry skin quickly by the warm diaper.
2. As soon as newborn it is located under the radial
3. To take away a wet diaper.
heater, immediately to provide its correct situation.
4. To provide the correct provision of the head 3. Under control of the direct laringoscopia
(as a rule, under shoulders enclose the roller).
to suck residual meconium from the throat, then to
5. To suck at first oral cavity contents, and then intubate trachea and respiratory airways directly
— nasal part of the throat (it isn't recommended through an endotracheal tube, then by special
deep and intensive suctions by a probe; negative aspirator to suck away residual meconium
pressure: at suction shouldn't exceed 100 mm
4. Quickly to dry up skin of the newborn by the
hg).
warm diaper.
5. To take away a wet diaper.
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6. To carry out short (no more than 2 times) tactile stimulation of the newborn (a percussion on a sole).
7. To estimate existence and character of independent breathing. In the absence of independent breath
or gasping breathing:
immediately to begin mechanical ventilation by the bag and the mask with the use of 90 — 100% of
oxygen (frequency 40-60 in 1 min.);
initial pressure of ventilation usually is 30-40 cm of water column, at children with the immature and
affected lungs and after the several first breaths inspiratory pressure has to be 20-40 cm of water
column.
If after mask putting on a child's face and carrying out several ventilations by the bag the thorax
doesn't move, such actions are recommended:
a) again to put a mask, providing its tight fitting to the person, and again to carry out ventilation; in the
absence of effect consistently to perform the actions provided below, each time checking efficiency of
ventilation;
b) to check the position of the head;
c) to check the presence of the secret in the oral cavity and if indicated to suck it;
d) to try to carry out ventilation with a half-open mouth with air duct use;
e) to increase inspiratory pressure.
In the absence of effect it is necessary to carry out an intubation of the trachea and to exclude existence
at the child of congenital anomalies. In 2 min. after initiating of mechanical ventilation by the bag and
the mask it is necessary to enter a probe into the stomach to prevent aspiration and stomach dilatation.
In the presence of adequate independent breath it is necessary to pass to item 9 at once.
8. To ventilate 15-30 times with 100% oxygen with the frequency of 40-60 in 1 min.
9 . To determine heart rate.
If heart rate is more than 100 in 1
min.
To evaluate skin color
Pink or local cyanosis
Central cyanosis
To observe for the presence of independent
breath, repeatedly to define heart rate, skin
color. To stop mechanical ventilation in the
presence of independent breath, to carry out
short tactile stimulation and to appoint a free
stream of oxygen
To appoint a free stream of oxygen (at least 80
%) with a speed of 5 l/min and to evaluate the
color of skin and mucous membranes. At
cyanosis reduction gradually to reduce the
concentration of oxygen, distancing an oxygen
tube from the face of the infant.
If heart rate is less than 100 in 1 min
Less than 60 in 1 min.
To begin (if independent breath is
adequate and mechanical ventilation
has not been carried out) or to continue
mechanical ventilation of 100%
From 60 to 100 in 1 min
Doesn't
increase
Increa
ses
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oxygen
To begin indirect heart massage of
with a frequency of 90 in 1 min if
mechanical ventilation has been
already carried out by 100% oxygen
within 15-30 s.
To continue
mechanical
ventilation by100%
oxygen with a
frequency 30 per 1
min.
To continue
mechanical
ventilation
by 100%
oxygen with
a frequency
of 40-60 per
1 min.
To begin indirect massage of the heart
with a frequency of 90 in 1 min, if
mechanical ventilation has been already
carried out, and heart rate is less than 80
in 1 min.
To begin administration of drugs if the heart rate is less than 80 per minute 30 seconds after the
initiating of mechanical ventilation by 100% oxygen and indirect massage of the heart
Equipment which is used for the resuscitation and intensive care
Resuscitation bags - standard and recommended equipment for mechanical ventilation of the
newborn (MV) during reanimation:
• can be filled with a stream or independenlyt;
• volume shouldn't exceed 750 ml;
• speed of the stream of oxygen in a bag has to be not less, than 5 l/minute;
• to provide lung ventilation by 90-100% oxygen, to athe bag which is filled independently,
attach the oxygen reservoir;
• resuscitation bags have to be equipped with at least one of the following mechanisms of
safety of lung ventilation of the newborn:
- the valve of restriction of pressure (in resuscitation bags of both types);
- the manometer (in resuscitation bags of both types);
- the control valve over the stream (in a resuscitation bag which is filled with a stream);
For carrying out MV of extremely preterms it is desirable to use the equipment with the valve
which creates positive pressure at the end of an exhalation. MV of the newborns through the
T-shaped adapter and the resuscitation mask, can regulate a stream of gas and limit
ventilation pressure.
• Use of devices of this kind provides effective and safe lung ventilation of the newborns,
especially, preterms (better controls parameters of ventilation and gives opportunity to use
positive pressure at the end of an exhalation).
• It is possible to use NEOPUFF devices or the similar standard equipment.
• The usage of such systems during resuscitation of the newborns should be preformed by the
trained personnel.
Resuscitation masks:
• sizes of masks: "1" - for the child with the weight >2500,0 g, "0" - for the child with the
weight <2500,0 g;
• preferable to use masks with soft edges;
• the round mask adjoins to the face of extremely preterms more hermetically, and for the
larger newborns the mask of the anatomic form should be used.
Equipment for the trachea intubation:
• for the tracheal intubation of the newborns direct blades of the laryngoscope are used: size
№0 for prematurely born and №1 for full-term newborns;
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• it is necessary to install the laryngoscope and to check lighting system;
• endotraсheal tubes without narrowing of four sizes
• in case of introduction in the conductor tube, it should be fixed reliably that the end didn't
get to the trachea during an intubation.
Correction of metabolic disorders.
1. Measures which normalize the vascular volume of blood
1.1. The indication to the usage.
• Hypovolemia:
- possibility of the development of this condition should be provided for all children, a
condition which doesn't improve after carried-out MV and indirect heart massage, especially,
if blood loss is possible;
- other symptoms of a hypovolemia - pallor, weak pulse filling and lack of signs of
improvement of peripheral blood circulation, despite all resuscitation measures
1.2 Drug therapy:
• 0,9% solution of sodium chloride (physiological solution);
• for the correction of considerable blood loss (available clinical signs of hemorrhagic shock)
there can be necessary an urgent transfusion 0 (І) II (-) erythrocytes;
• solutions which contain albumin, shouldn't be used during primary resuscitation as its
application is connected with the high risk of infectious neonatal mortality and morbidity.
1.3. Dosing and administration
• To prepare 40 ml of 0,9% of solution of sodium chloride in syringes or the system.
• Dose - 10 ml/kg.
• Introduction way - intravenous slowly, for 5-10 minutes.
2. Sodium hydrocarbonate
There are no sufficient scientific bases to recommend routine application of solution of
sodium hydrocarbonatis for primary resuscitation of the newborns.
2.1 The indications to the administration.
The probable or proved severe metabolic acidosis, during long-standing inefficient
resuscitation against adequate MV.
2.2 Dosing and administration.
Concentration of solution - 4,2% or 0,5 ml.
To prepare 20 ml in a syringe.
Dose - 4 ml/kg or 2 ml/kg.
Way of introduction - in the umbilical cord vein in the presence of the return blood flow.
Introduction rate slow, not quicker, than 2 ml/kg/minute.
3. Naloxone hydrochloride
3.1. The indications to the administration.
• Considerable depression of breathing at the newborn after restoration of normal heart rate
and skin color during MV if narcotic analgetics (opioids) were administered to the mother
for the purpose of labor pain relief for the last 4 hours prior to the birth of the child.
3.2. Dosing and administration.
• The recommended concentration of solution - 1,0 mg/ml.
• Dose - 0,1 mg/kg.
• Ways of administration:
- preferably intravenous;
- intramuscular - possible, but effect of the drug action will be slow;
- endotracheal adminstration of naloxon is inefficient.
3.3. It is impossible to appoint naloxon to the child from mother with suspicion to drug
addiction or from mother who gets long-standing supporting therapy by narcotic
preparations. It can cause seizures in the newborn.
6. Clinical consequences of perinatal asphyxia:
9
- CNS:
hypoxic-ischemic encephalopathy, brain edema, seizures, a syndrome of inappropriate
secretion of antidiuretic hormone, cerebral spastic infantile paralysis.
- Respiratory system:
pulmonary hypertension, surfactant system disturbances, mekonium aspiration, pulmonary
hemorrhage.
- Urinary system:
proteinuria, gematuria, oliguria, acute renal failure.
- Cardiovascular system:
insufficiency of the tricuspid valve, myocardium necrosis, arterial hypotension, left
ventricular dysfunction, sinuse bradycardia, rigid heart rhythm, shock.
- Digestive system:
necrotic enterocolitis, hepatic dysfunction, gastric or intestinal bleeding, reduced tolerance to
an enteral nutrition.
- Blood system:
thrombocytopenia, DIC-syndrome, polycytemia.
- Metabolic disorders:
Metabolic acidosis, hypoglycemia, hypocacemia, hyponatremia; increased potassium.
7. Concept about a hypoxic-ischemic encephalopathy
Hypoxic-ischemic encephalopathy (GIE) - the brain disorder caused by perinatal hypoxia
which is manifested by morphological functional disorders and signs of cerebral failure.
Pathogenesis of HIE:
- to decrease in the cerebral brain flow caused by the loss of ability to its autoregulation,
arterial systemic hypotonia, reduced ejection fraction through owing to the hypoxemic injury
of the myocardium, disorders of the venous outflow from the brain and increase of cerebral
vascular resistance;
- influence of prostaglandins, excessive synthesis of leucotriens by vessels, and also the role
of the antidiuretic hormone (ADG)
- localization of the affection at the brain – frontal and parietal regions the brain are mainly
damaged as the result of the the thinnest arterioles less developed net of capillaries. At the
chronic intranatal hypoxia typical changes in basal ganglia, thalamus occur which causes
increase of adaptational possibilities of haemodynamics. Ischemia occurs as the result of the
thromboses, hemorrhagic disorders, hematoencephalic barrier is damaged. These disorders
lead to edema, dystrophy and focal necroses of neurons of cerebral cortex, hypocampus, and
at preterms - periventricul regions;
- cytotoxic edema of the brain which can be caused by the cascade emission of aminoacids first of all, a glutamate combined with metabolic acidosis (PH less than 7,0);
- hemostatic disorders - low level of vitamins of K-dependent clotting factors and
trombocytic dysfunction, development of the DIC-syndrome can predispose to intracranial
hemorrhages.
Clinical signs of HIE. Neurologic, somatic and exchange disorders:
Clinical syndromes of the acute period of HIE:
1. Syndrome of increased neuroreflectory excitability is manifested by concern, disordered
sleep, eruction, constant cry, increase of the muscular tone, tremor of the extremities and the
chin, increased reflexes. These symptoms resolves within 5 days and corresponds to the light
form of HIE.
2. Syndrome of the general depression is observed at prematurely born children owing to
immaturity of CNS that is manifested by generalized depression. Characteristic signs are
weakness , adinamia, decreases reflexes, muscular hypotonia.
3. Hypertension syndrome. It is observed at almost 100% cases of HIE It is manifested by the
specific position of the child - the head is thrown back, extremities are flexed, the squeezed
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cams, "brain" cry, eruction and vomiting, increased tone and a tremor of extremities, vertical
and rotator nistagmus, Grefe symptom – the lag of an upper eyelid at eyeball movements
with the emergence of the scleral strip which is defined in rest, a symptom of "the sun which
sets" - the same, but at changed position of the body. At extreme degree of hypertension
generalized clonic seizures occur.
4. The hydrocephalic syndrome occurs at the end of the acute period and is manifested by the
increase in the size of the head, prevalence of the brain skull over facial part, sunken nasal
bridge with an overhang of the frontal site, dilatation of subcutaneous veins over the head,
and also dilatation ventricles index according to ultrasonic investigation of the brain.
5. The seizure syndrome at HIE is the most often manifested by generalized clonical-tonic
seizures. Focal, multifocal and myoclonic seizures occur less frequently.
6. The comatous condition develops at brain edema and is characterized by unconsciousness,
absence of physical activity, cry, emotions and reaction to the pain. Degree of severity of the
coma is defined by the level of the brain affection.
HIE classification:
There are three GIE clinical forms of HIE:
At light HIE signs of HIE are observed no more than 2-5 days. Hyperexcitability symptoms
prevail.
At moderate HIE disorders of the breathing rhythm, attacks of bradipnoe or bradycardia,
decreased physical activity can be observed during the first hours of life. Seizures, high-pitch
cry, eruction, tremor, chaotic movements appear later. Apnea attacks, symptoms of
intracranial hypertension or brain edema can occur until the end of the second - the beginning
of the third week of life.
Severe HIE is characterized by the absence of consciousness during the first 12 hours of life,
further some improvement of the condition of the child can be noted, but then, on 2 - the 3rd
week, the coma and seizures occur again. Especially unfavorable sign is the development of
generalized tonic seizures which are accompanied by the attacks of the secondary asphyxia
(breathing and heart arrest) - these symptoms testify to the presence of intracellular brain
edema with the involvement of brain stem structures. Symptoms of "weakness of shoulders",
"a short neck", "a hanging-down hand", "a sharp-clawed paw", hypotonia, paralysis of the
upper extremities can be evident at accompanying hypoxic-ischemic disorder of the cervical
part of the spinal cord.
Course of the disease and prognosis
The most unfavorable symptoms are the preservation of the 3 points or lower by Apgar scale
at 5 minute for the first 8 hours of the life, persistent muscular hypotonia. Later the child can
suffer from cerebral paralysis, a delay of psychomotor and intellectual development, epilepsy
HIE diagnostics.
The diagnosis can be established by the complex of anamnestic data (the course of pregnancy
and delivery, interventions in labor, drug therapy of mother during pregnancy and in labor,
etc.), the analysis of dynamics of the clinical picture at the child and the assessment of results
of such methods of diagnostics:
- cranial ultrasonography - ultrasonic scanning of the brain through the big fontanel. This
method is highly informative, noninvasive; without radial damage and gives the image of
various structures of the brain in sagital and in frontal position;
- computer tomography of the brain which allows to analyze a condition of the cranial bones,
and brain parenchyma;
- nuclear magnetic resonance and emission tomography - very exact research method,
allowing to reveal pathological changes in the brain, to define differences between white and
gray substance of the brain and to specify degree of a miyelinization (maturity) of various
sites of the brain;
- Electroencefalograpy (EEG).
8. HIE treatment
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1. Organization of the regimen: decrease in intensity of sound and light irritants; careful
inspection, swaddling and performance of procedures; minimizing of painful manipulations;
"temperature protection" that prevents cooling and overheating, participation of mother in
care of the child.
2. Nutrition depending upon the condition: parenteral; through the constant or disposable
probe; from the small bottle. The child shouldn't starve. At parenteral administration of
nutrition it is important to adhere to the regimen, not to overload with volume, to prevent
hypovolemia, hypotension, dehydration, hyperviscosity; not to administer heparin as even its
small doses (1-2 U/kg) increase risk of intracranial hemorrhages.
3. Monitoring supervision over the main physiological parameters: heart rate, blood pressure,
rate of breathing, temperature, etc.
4. Restoration of potency of respiratory airways and adequate ventilation of lungs.
5. At HE - support of adequate cerebral perfusion, correction of pathological acidosis and
other biochemical parameters (hypoglycemia, hypocalcemia, etc.); intravenous
administration of 10% glucose solution (for the first days of life up to 50 ml/kg)
6. In case of comatous condition and at brain edema mechanical ventilation is indicated in the
regimen of hyperventilation; barbiturates (phenobarbital 3-5 mg/kg each 6-8 hours) or
sibazone 0,5 mg/kg each 8-12 hours are also administered. Barbiturates reduce increased
intracranial pressure at brain edema. Intravenous dehydration with plasma, 10% albumin
solution, mannitol or furosemid (at normal peripheral blood pressure) is carry out. These
should not be administered if the cranial hemorrhage is present. When the symptoms of brain
edema are progressing osmotic diuretics in connection with corticosteroids (dexamethasone
in an initial dose of 0,2 mg/kg, then - 0,1 mg/kg with an interval of 6 hours) should be used.
8. Preparations which improve microcirculation: curantil (dipiridamol), trental, cavinton,
xantinoli nicotinatis, instenon.
9. Antihypoxants: sodium oxybutiratis, piracetam, cocarboxylase, ascorbic acid, actovegin.
10. Antioxidants, stabilizers of cellular membranes: tocopherol, tocopherol acetate, selenium,
unithiol.
11. Nootropic preparations (pantogam, piracetam) for the purpose of improvement of trophic
processes in the brain. Drugs which improve trophic processes and miyelinization of nervous
cells (cerebrolisin, encephabol, solcoseril) are administered after stabilization of the
condition of the child, not earlier than after the 14th- the 20th day of life.
Treatment of seizures:
1. Standard therapy for urgent stopping the esizures: 100-150 mg/kg of 20% of solution of
sodium oxibutiratis intravenously slowly with 5% glucose solution, in the absence of the
effect - 0,5 mg/kg of 0,5% of sibasone solution intravenously; then 15-20 mg/kg of oral
phenobarbital; if the standard therapy isinefficient - barbiturates (thiopental sodium - 15
mg/kg/day intravenously slowly) under control of blood pressure and heart rate.
2. At hypoglycemic seizures - 10-20 ml/kg of 10-20% glucose solution intravenously,
maintenance dose - 3-5 ml of 10% solution/kg/1 hour intravenously before level of glycemia
normalizes.
3. At hypocalcemic seizures - 1 ml/kg of 10% of solution of calcium gluconate intravenously
slowly.
4. At hypomagnemic seizures - 0,2 ml/kg of 25% of solution of magnesium sulfate
intramuscular or intravenous administration simultaneously.
5. At the pyridoxine dependent seizures - 2 ml of 5% of piridoxin solution intravenously or
intramuscularly; maintenance dose of the pyridoxine - 25 mg/kg.
Haemostatic therapy:
1. Fresh frozen plasma 10-15 ml/kg intravenously 1 time per day.
2. Vikasolum 0,2-0,5 ml (2-5 mg) of 1% solution intravenously or intramuscularly.
3. Etamsylate-sodium (dicinon) - 1 ml of 12,5% solution intravenously for receiving fast
effect. To enter 0,3-0,5 ml for the 3-5 days further.
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At intracranial hemorrhage, additional measures:
- subdural puncture;
- neurosurgical intervention for the purpose of blood evacuation;
- lumbar puncture for blood drainage from subarachnoid space for the purpose of the
prevention of adhesion and secondary hydrocephaly.
Complications of rescucitation
Long-standing mechanical ventilation in the rigid mode causes the development of
bronchopulmonary dysplasia.
The most common distant consequence of MV is the retinopathy.
When carrying out resuscitation actions different variants of traumatic complications are
possible.
Additional materials for the self-control
А. Clinical cases
Case 1
Infant I. was admitted in the department of pathology of newborns. From the
anamnesis it is known that the child was born from the 25 year old woman, from the first
pregnancy with toxicosis in 1st trimester, anemia (Hb - 98 g/l) in the second trimester, iron
preparations were administered during pregnancy. In 28 weeks there was an interruption
threat, was treated in the hospital. Timely delivery. Weakness of the birth activity. The fetal
hypoxia occurred, stimulation by oxytocin. The first period of labor - 8 hours, the second - 25
minutes, a waterless period - 10 h. 20 min., mekonium in waters. Birth weight – 3300 g,
length - 51 cm. Assessment by the Apgar scale - 6-8 points. The infant cried after suction of
mucus. After the birth the condition of the infant is moderate caused by neurologic
symptoms: tremor of hands, chin. Other physical investigation is unremarkable. At the 4-th
day the condition of the child deteriorated by the neurologic symptoms, and the child was
transferred to the hospital.
At admitting to the hospital the condition of the child is severe. Skin is with a grayish
colour, acrocyanosis, marble shade. Umbilical wound is dry. Hyperestezia. Pharynx is pale.
Breathing is puerile. Tones of heart are rhythmical, heart rate 152/min. The abdomen is soft,
the liver is 3 cm below the right costal arch, and the spleen isn't palpated. Stool is yellowish
with undigested lumps of food. In the neurologic status - crying monotonous, big fontanel is
2,0*2,0 cm, pulse, sagital fissure is opened. Grefe symptom is positive, transient strabismus.
Reflexes of the newborn are decreased, a muscular tone with a tendency to hypotonia, tendon
reflexes are S=D, moderate activity. Tremor of hands is noted at the tension. Seizures
weren't evident at inspection.
Complete blood count: Hb – 192 g/l, erythrocytes – 5,8*1012/l, colour index – 0,98,
leukocytes – 12,5*109/l, bands – 10%, segments – 56%, еosinophils – 1%, basophils – 1%,
lymphocytes– 29%, ESR – 6 mm/h.
Biochemical analysis of blood: the general protein – 62 g/l, bilirubin: the indirect – 51
mcmol/l, direst – absent, urea - 3,3 mmol/l, potassium - 6 mmol/l, sodium 136 mmol/l,
calcium - 1,1 mmol/l, phosphorus - 2,32 mmol/l.
Ultrasonic investigation of the brain at the age of 8 days: smoothed drawing of sulci and gyri.
Frontal horns are expanded to 6 mm. Depth of lateral ventricles at the level of bodies (S=D)
is 7 mm (normal - up to 5 mm). Local echogenous inclusions in the subcortical ganglia. Cyst
of the vascular plexus about 3 mm is noted. The echogenity of the periventricular sites is
moderately encreased.
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Questions:
1. What is your preliminary diagnosis?
2. What additional investigations need to be carried out for the confirmation of the
diagnosis? What are the possible results?
3. What factors indicated the development of this pathology in the newborn?
4. What features of the hematoencephalic barrier at the newborns?
5. What compensatory mechanisms are developing at acute hypoxia of the newborn?
6. Name the cellular composition of the spinal liquid of the newborn.
7. Should this patient have consultation of the ophthalmologist? If so, what changes are
possible?
8. Administer treatment.
9. What drugs are used for the dehydration at treatment of brain edema?
10. What is prognosis for this child?
B. Tests
Question 1. In the child who has suffered a severe hypoxic ischemic injury, which of the
following is true?
A. Liver and kidney damage are irreversible
B. Isolated brainstem function might be preserved
C. CT scans do not reveal abnormalities until after 1 mo following Injury
D Intracranial pressure monitoring improves outcome
Answer B. Explanation: The brainstem may be preserved in the presence of cortical cell
death. This is a controversial point in the discussion of brain death. Today we agree on the
legal definition of whole brain death, which includes the brainstem and obviously precludes
effective spontaneous ventilation.
Cortical brain death proponents want to recognize cortical death alone as the criterion for
legal death. The controversy has not been resolved.
Question 2. The best description of the Apgar score is that it:
A. Accurately predicts who will develop cerebral palsy
B. Assesses neonates in need of resuscitation
C. Accurately predicts a low umbilical cord pH
D. Is unaffected by maternal opiate pain relief
E. Accurately predicts neonates who will die in the neonatal period
Answer B. Explanation: The Apgar score helps to rapidly assess the need to resuscitate
neonates after birth. Although it has some value in predicting neonatal mortality and cerebral
palsy, it has a poor positive predictive value. Most children with cerebral palsy have had
normal Apgar scores, while neonates with low Apgar scores do not universally get cerebral
palsy.
Question 3. A term female is born by spontaneous vaginal delivery to a primiparous woman
who received two doses of meperidine 30 min and 2 hr prior to an abrupt delivery. The baby
is apneic and limp. The most important, immediate management is to:
A. Administer naloxone in the umbilical vein
B. Perform bag-mask ventilation
C. Administer naloxone in the endotracheal tube
D. Begin chest compressions
E. Obtain a cord pH
14
Answer B. Explanation: Apnea from any cause is treated with securing apatent airway and
instituting ventilation. If bag mask ventilation is ineffective, endotracheal intubation should
be performed. Naloxone (Narcan) can be given only after the baby is ventilated.
Question 4. Successful ventilation is determined by all of the following except:
A. Zero reading of end-tidal CO2 measurement
B. Pink color
C. Rising heart rate
D. Symmetric breath sounds
E. Good chest rise
Explanation: Indeed, one expects that with a successful intubation and ventilation, the endtidal (exhaled) CO2 will rise dramatically. This is now used in many neonatal resuscitations.
Complete cardiac onset with poor perfusion may also cause a low end-tidal CO2.
Question 5. An infant has the following findings at 5 min of life: pulse, 130/min; cyanotic
hands and feet; good muscle tone; and a strong cry and grimace. This infant's Apgar score is:
A. 7
B. 8
C. 9
D. 10
Answer C. Explanation: One point in the Apgar score is taken off for color.
Question 6. A girl is born via stat cesarean section to a 34-year-old mother whose pregnancy
was complicated by hypertension and abnormal fetal heart monitoring. At delivery she is
covered in thick, green meconium and is limp, apneic, and bradycardic. Which of the
following is the best
first step in her resuscitation?
A. Administer IV bicarbonate.
B. Administer IV naloxone.
C. Initiate bag-and-mask ventilation.
D. Initiate chest compressions immediately.
E. Intubate with an endotracheal tube and suction meconium from
the trachea.
Answer E. An attempt is made to remove the meconium from the oropharynx and the airway
prior to initiation of respirations. Ideally, the obstetrician will begin suctioning the meconium
upon delivery of the head, and the pediatrician will further remove meconium with an
aspirator or through endotracheal intubation with suction. Ventilation is initiated after
meconium is removed. The goal is to remove airway meconium and to prevent its aspiration
into the small airways where ventilation-perfusion mismatch may occur with deleterious
effects.
Question 7. A term male is delivered vaginally to a 22-year-old mother. Immediately after
birth he is noted to have a scaphoid abdomen, cyanosis, and respiratory distress. Heart
sounds are heard on the right side of the chest, and the breath sounds seem to be diminished
on the left side. Which of the
following is the most appropriate next step in his resuscitation?
A. Administer IV bicarbonate.
B. Administer IV naloxone.
C. Initiate bag-and-mask intubation.
15
D. Initiate chest compressions immediately.
E. Intubate with an endotracheal tube.
Answer E. The case describes diaphragmatic hernia. As a result of herniated bowel contents
into the chest, these children often have pulmonary hypoplasia. Bag-and-mask ventilation
will cause accumulation of bowel gas (which is located in the chest) and further respiratory
compromise. Therefore, endotracheal intubation is the best course of action.
Question 8. A 37-week-gestation boy is born after an uncomplicated pregnancy to a 33-yearold mother. At birth he was lethargic and had a slow HR. Oxygen was administered via bag
and mask, and he was intubated; his HR remained at 40 bpm. Which of the following is the
most appropriate
next step?
A. Administer IV bicarbonate.
B. Administer IV atropine.
C. Administer IV epinephrine.
D. Administer IV calcium chloride.
E. Begin chest compressions.
Answer E. If the HR is still less than 60 bpm despite PPV with 100% oxygen, then chest
compressions are given for 30 seconds. If the HR is still less than 60 bpm, then drug therapy
(usually epinephrine) is indicated.
Question 9. At 43 weeks’ gestation, a long, thin infant is delivered. The infant is apneic,
limp, pale, and covered with “pea soup” amniotic fluid. The first step in the resuscitation of
this infant at delivery should be
A. Suction of the trachea under direct vision
B. Artificial ventilation with bag and mask
C. Artificial ventilation with endotracheal tube
D. Administration of 100% oxygen by mask
E. Catheterization of the umbilical vein
The answer is A. Infants who are postmature (more than 42 weeks’ gestation) and show
evidence of chronic placental insufficiency (low birth weight for gestational age and wasted
appearance) have a higher-than-average chance of being asphyxiated, and passage of
meconium into the amniotic fluid thus places these infants at risk for meconium aspiration.
To prevent or minimize this risk, these infants should have immediate nasopharyngeal
suction as their heads are delivered. Immediately after delivery and before initiation of
respiration, their tracheas should be carefully and thoroughly suctioned through an
endotracheal tube under direct vision with a laryngoscope. Afterward, appropriate
resuscitative measures should be undertaken to establish adequate ventilation and circulation.
Artificial ventilation performed before tracheal suction could force meconium into smaller
airways.
Question 10. A 42-week gestation neonate is born by cesarean delivery following repeated
fetal heart rate decelerations. At rupture of membranes, thick meconium was noted. The
infant has no respiratory effort but slight movement and a heart rate of 90 beats per minute.
Of the following,which is the first intervention?
A pass an umbilical artery catheter to measure pH and Po2
B start bag-and-mask ventilation with 100% oxygen
C suction the mouth and trachea to remove the meconium
D intubate the trachea and begin ventilation with 100% oxygen
16
E establish monitoring with ECG and pulse oximeter
Answer C. After birth, intubation and tracheal suction decrease the risk of developing
meconium aspiration syndrome in infants who are not vigorous at birth. The infant described
in this case is
not vigorous (depressed respirations, depressed muscle tone, and/or a heart rate < 100 beats
per
minute), thus endotracheal intubation with suctioning to remove the meconium is indicated
after the infant is delivered.
Question 11. A 2,9-kg term male infant is born to a mother who developed polyhydramnios at 34
weeks' gestation. At birth, the Apgar scores were 9 and 9. The infant develops choking and cyanosis
with the first feed. In addition, is unable to place a nasogastric tube. What is the most likely
diagnosis?
A.Choanal atresia
B.Laryngomalacia
C.Esophageal atresia
D. Tracheal atresia
E. Respiratory distress syndrome
Question 12. In the 43rd week of gestation a long, thin infant was delivered. He is apneic, limp,
pale, and covered with "pea soup" amniotic fluid. The first step in the resuscitation of this infant at
delivery should be:
A.Suction of the trachea under direct vision
B.Artificial ventilation with bag and mask
C.Artificial ventilation with endotracheal tube
D.Administration of 100\% oxygen by mask
E.Catheterization of the umbilical vein
Question 13. A full-term baby was born with body weight of 3200 g, body length of 50 cm, Apgar
score - 8-10 points. What is the optimum time for the first breast-feeding?
A.First 6 hours
B.First 24 hours
C.First 30 minutes
D.First 48 hours
E.After 48 hours
Question 14. The child had Apgar scale of 8-9 points at time of birth. When should he be
breastfed?
A. Right after birth
B.After processing of the umbilical cord and performing profilaxis of gonoblennorea
C.After umbilical cord processing
D.30 minutes after birth
E. 2 hours after birth
Question 15. What medication should be administered to the baby, born by Caesarean section, if
he is at asphyxia and independent breathing is absent on the first minute of life?
A.Etimizole
B.Caffeine sodium benzoate
C.Cordiamin
D.Sodium bicarbonate
E.Naloxone a hydrochloride
Question 16. Newborn child experienced intranatal asphyxia. While suctioning the mucus from
the upper respiratory tract miconium is reveaked. Independent breath is absent. The further actions of
17
neonatologist provide:
A.External heart massage
B.Tracheal intubation, sanation of respiratory tract
C.Application of 100 %oxygen.
D.Adrenaline introduction.
E.Tactile stimulation of breathing.
Question 17. After birth the child is pale, has arrhythmic breathing which doesn't improve against
oxygenotherapy. Pulse is weak, tachycardia is observed, arterial pressure it barely measured. Edema
is absent. What is the most likely cause of these symptoms?
A.Congestive heart failure
B.Intracranial hemorrhage
C.Intrauterine sepsis
D.Asphyxia
E.Intrauterine pneumonia
Question 18 . Overterm infant, which was born at 43 weeks` gestation, has apnoe, pallor, the child
is covered by greenish amniotic fluid. The first steps in the newborn resuscitations include:
A.Mechanical ventilation using the mask and a bag
B.Mechanical ventilation using the endotracheal tube
C.Application of 100 % of oxygen
D.Umbilical vein cateterisation
E.Aspiration of tracheal contents
Question 19. The newborn which had asphyxia at the birth had apnea and the bradycardia (heart rate
70 per minute). Mechanical ventilation using 100 % oxygen with application of a mask and a bag of
Ambu was applied urgently. In 30 seconds the heart rate without improvement. What should be the
next step of resuscitatory measures?
A.Undirect heart massage
B.Tactile stimulation
C.Continue ventilation
D.Sodium hydrocarbonate intravenously
E.Epinefrin intravenously
Question 20. The term infant with cord encirclement round the neck since 1 minute of life has total
cyanosis, apnea, heart rate - 80 in minute, muscular hypotonia and absent reflexes. Signs of
meconium aspiration are absent. After sanation of respiratory tract breathing hasn’t restored. Your
following action?
A.Adrenaline introduction
B.Etamzilat introduction
C.Mechanical ventilation using the mask of 100 % О2
D. Intubation of trachea and mechanical ventilation
E.Irritation of the skin along the spinal cord
4. LITERATURE FOR STUDENTS
1. Nelson Textbook of Pediatrics. - 18th ed. / Ed. by R. Kliegman et al.-Philadelphia:
Saunders Co, 2007.- 3146 p.
2. Pediatry. Guidance Aid / За ред. О.В. Тяжка; О.П. Вінницька, Т.І. Лутай – К. : Медицина, 2007 . –
158 с.
3. Current Pediatric Diagnosis & Treatment (CPDT). - 18th ed./ Ed. By W.W.Hay et al. - The
McGraw-Hill Companies. – 2006.
4. Current pediatric therapy -18th ed. / Ed. by F.D.Burg et al. - Elsevier Inc. – 2007.
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5. Nelson Essentials of Pediatrics -5th ed. / Ed. by B.S.Siegel, J.J.Siegel. - Elsevier Inc. –
2007.
6. Examination of the Newborn. A Practical Guide / Ed. by Helen Baston and Heather
Durward. - the Taylor & Francis e-Library. - 2005.
7. Fetal and neonatal secrets. - second edition . / Ed. by R.A.Polin, A.R.Spitzer. - Elsevier.2006.
8. Key Topics in Neonatology / Ed. by R.H. Mupanemunda, M. Watkinson. - Oxford
Washington DC. -1999.
Performed by ass. Vaculenko L.I., ass. Tkachenko N.P.
Approved “_____”____________20____y.
Сhief of the department, professor
Protocol №_____
V. A. Kondratyev
Reconsidered
Approved “_____”____________20____р.
Сhief of the department, professor
Protocol №_____
V. A. Kondratyev
Reconsidered
Approved ““_____”____________20____р.
Сhief of the department, professor
Protocol №_____
V. A. Kondratyev
Reconsidered
Approved “_____”____________20____р.
Сhief of the department, professor
Protocol №_____
V. A. Kondratyev
Reconsidered
Approved ““_____”____________20____р.
Сhief of the department, professor
Protocol №_____
V. A. Kondratyev
Reconsidered
Approved “_____”____________20____р.
Сhief of the department, professor
Protocol №_____
V. A. Kondratyev
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