ASPHYXIA

 Asphyxia is characterized by progressive

hypoxia, hypercapnia, hypoperfusion and
acidosis.
 Conditions with anticipated high-risk birth
Antepartum factors:
 Maternal diabetes

 Maternal infections
 Pregnancy-induced hypertension
 Polyhydramnions
 Premature rupture of membranes
 Chronic hypertension
 Anemia or immunization
 Previous fetal or neonatal death
 Bleeding in second or third trimester
 Maternal cardiac, pulmonary, renal, thyroid or
neurological disease
 Post-term gestation
 Multiply gestation
 Size-dates discrepancy
 Drug therapy, s.as lithium carbonate,
magnesium, adrenergic-blocking drugs
 Fetal malformation
 No prenatal care
 Age <16 or >35
Intrapartum factors
 Emergency Caesarean section
 Forceps or vacuum-assisted delivery
 Breech or other abnormal presentation
 Premature labor
 Precipitous labor
 Chorioamnionitis
 Prolonged rupture of membrane (>18 hours
before delivery)
 Prolonged labor (>24 hours)
 Stressed mature
 As a result of some drugs, such as pain-killer,
anesthesia, anesthethics, antidepressant, magnesium
 As a result of mazolysis
 As a result of haemorrhagic shock
 Trauma – cerebral haemorrhage
 As a result of some fetus disease, such as congenital
abnormalities, trauma, infectious disease
 As a result of cardiorespiratory depression
 Unknown reasons
PATHOPHYSIOLOGY
 The ability of the fetus or infant to survive episodes
of asphyxia is related to the mechanism that regulates
blood flow to the organs of the body. These
mechanisms are designed to maintain oxygen
delivery to the vital organs (i.e. – the brain, heart,
adrenal glands) during periods of hypoxia.
 PATHOPHYSIOLOGY
 During periods of hypoxia or hypercapnia, blood flow to the
brain is increased. The result is a stable delivery of oxygen to the
brain to meet metabolic demands and maintenance of a normal
intracellular pH.
 Mild asphyxia. Adaptive changes in blood flow allow adequate
oxygen delivery to the brain, heart, adrenal gland. This is
accomplished through an increase in and a redistribution of the
cardiac output. Blood flow to the skin, muscles, kidney, and
gastrointestinal tract is sacrificed to maintain perfusion of the
vital organs. The development hypoxia in fetus leads to period of
rapid respiration. If hypoxia continuities, the respiratory
movements stop, heart beats decrease and fetus entrance to
period of primary apnea. If a child is born that the giving of
oxygen and tactile stimulation recover the spontaneous breathing.
PATHOPHYSIOLOGY
 During periods of severe or prolonged asphyxia, the under
perfuse (sacrificed) tissues and organs gradually become
acidosis because of anaerobic metabolism and lactic acid
production. This leads to myocardial depression and a gradual
decrease in blood pressure so that blood fails to perfuse the vital
organs, with resultant permanent tissue damage in such organs,
the deep rapid respiration-gasping occurs. The heart beats and
AP are decreasing. Then the breathing stops. During this
moment the infant doesn’t respond to tactile stimulation and
ABC-reanimation is necessary.
 Apgar score
Score 0 1 2

Respiratory effort none Slow, irregular Good, crying

Heart rate per absent <100 >100

minute

Color of the body Blue or pale Body pink, Pink

extermities blue
Muscle tone flaccid Some flexion Activity moving
the extermities
Reflex grimace Cries, coughs,
stimulation sneers
 Thescore must be carry out at 1st and 5th
minutes after birth. Normal babies have
an Apgar score of more than 8 at one and
5th minutes.
Degrees of asphyxia:

7-8 balls – disorder of adaptation

6-4 balls – asphyxia of middle degree
0-3 balls – sever asphyxia
International characteristic of asphyxia are:

1. Deep methabolic or mixed acidosis (pH 

7,0) in cord blood.
2. Persistence of Apgar score 0-3 balls during 5
minutes
3. multiply (numerous) disorders
cardiovascular system, lungs (respiratory
system), renal, gastro-intestinal tract, blood.
 CLINICAL SYNDROMS OF ASPHYXIA
Central nervous system Hipoxic-ischemic encephalopathy, the wet
brain, intracerebral heamorrhage,
periventricular leucomalation
Respiratory system Syndrom of lungs shunting, disorders of
surfactant, posthypoxic pneumopathya,
lungs hypertension
Cardiac system Lungs hypertension, heamathogenic shock,
policytemia, ischemic necrosis of
endocardium, disorders of cardiac rhythm.
Renal Oliguria, acute renal failure insufficiency

Gastro-intestinal system Vomiting, necrotizing enterocolitis,

disfunction of liver
Methabolism Pathological acidosis, high activity of lipid
peroxidation, hypoglycemia, hyponatriemia
 Salient Features of Sarnat Stages of Post-hypoxic Encephalopathy

Stage I Stage II Stage III

 
Level of hyperalert lethargic or obtunded stuporous
consciousness
Neuromuscular normal mild hypotonia flaccid
control mild distal strong distal intermittent
Muscle Tone flexion flexion decerebration
Posture
Stretch reflexes overactive overactive decrease or absent

Complex Reflexes
Suck weak weak or absent absent
Moro strong; low weak:incomplete high absent
threshold threshold
Autonomic generalized generalized both system
Function sympathetic parasympathetic depressed
Seizures none common; focal or uncommon
multifocal
 Hypoxic- ischemic encephalopathy
Mild HIE
 Muscle tone may be increased slightly and deep tendon
reflexes may be brisk during the first few days.
 Transient behavioral abnormalities, such as poor
feeding, irritability, or excessive crying or sleepiness,
may be observed.
 By 3-4 days of life, the CNS examination findings
become normal.
Moderately severe HIE
 The infant is lethargic, with significant hypotonia and
diminished reflexes
 The grasping, Moro, and sucking reflexes may be
sluggish or absent
 HIE
 The infant may experience occasional periods of apnea
 Seizures may occur within the first 24 hours of life.
 Full recovery within 1-2 weeks is possible and is associated with
a better long-term outcome.
 An initial period of well-being or mild period HIE may be
followed by sudden deterioration, suggesting ongoing brain cell
dysfunction, injury, and death; during this period, seizure
intensity may increase.
Severe HIE
 Stupor or coma is typical. The infant may not respond to any
physical stimulus.
 Breathing may be irregular, and the infant often requires
ventilatory support.
 Generalized hypotonia and depressed deep tendon reflexes are
common.
 HIE
 Neonatal reflexes (sucking, swallowing, grasping, Moro) are
absent.
 Disturbances of ocular motion, such as a skewed deviation of eyes,
nystagmus, bobbing, and loss “doll’s eye” movements may be
related by cranial nerve examination.
 Pupils may be dilated, fixed, or poorly reactive to light.
 Seizures occur early and often and may be initially resistant to
conventional therapy. The seizures are usually generalized, and
their frequency may increase during 24-48 hours of life after onset,
correlating with the phase of reperfusion injury.
 Involvement of multiple organs besides the brain is a hallmark of
HIE: severely depressed respiratory and cardiac function and signs
of brainstem compression suggest a life-threatening rupture of the
vien Galen with a hematoma in the posterior cranial fossa.
HIE

 Reduced myocardial contractility, severe hypotension, passive

cardiac dilatation, and tricuspid regurgitation are noted
frequently in severe HIE.
 Patients may have severe pulmonary hypertension requiring
assisted ventilation.
 Renal failure presents as oliguria and, during recovery, as
high- output tubular failure, leading to significant water and
electrolyte imbalances.
ABC’s of Resuscitation
A B C (A: Airway, B: Breathing, C: Circulation)
A - establish open airway
Position, suction
B - initiate breathing
Tactile stimulation
Oxygen
C - maintain circulation
Chest compressions
Medications
 Resuscitation at the delivery room
Suction equipment  Scissors
 Mechanical suction and tubing  Tape or securing device for
 Suction catheters, 5F or 6F, 8F,10F or 12F endotracheal tube
 8F feeding tube and 20 ml syringe
 Alcochol sponges
Medications
 Meconium aspirator  Epinephrine 1: 10 000 (0,1 mg/ml) 2
Bag and mask equipment ml or 10 ml
 Neonatal resuscitation bag with a  Naloxone hydrochloride
pressure-release valve or pressure  Dextrose 10%
manometer (the bag must be capable of  Feeding tube 5F
delivering 90 or 100% per cent oxygen) Umbilical vessels catheterization
 Face masks, term newborn and preterm supplies:
sizes  Sterile gloves
 Oxygen source with flowmeter and tubing  Scalpel or scisors
 Povidon-iodine solutions
Intubation equipment
 Umbilical tape
 Laryngoscope with straight blades №0  Umbilical catheters 3,5F, 5F
(for preterm) and №1 (for term)
 Three-way stopcock
 Extra bulbs and batteries for laryngoscope  Syringes 1, 3, 5, 10, 20, 50ml
 Endotracheal tube: 2.5, 3.0, 4.0 mm  Needles 25, 21, 18 gauge
internal diameter
 Algorythm

1. Provide warmth by:

 Placing the baby under pre-warmed radiant warmer
 Drying with a pre-warmed linen and recovering the wet
linen
2. Clear airway by:
 Suction of mouth, oropharynx and nose (mouth before
nose). Be gentle.
 Position the baby with head held in midline and
semiextended
3. If necessary (breath, shouting, crying are absent):
 Put a shoulder roll (1/2 or ¾ of inch) beneath the
scapula, so as to open airways
 Stimulate by flicking the toes, slapping on soles,
rubbing the trunk or tights gently (avoid continue
use of tactile stimulation in an apneic baby, as
this will waste valuble time)
 If central cyanosis is present give free flow of
oxygen at 5 L/min. This can be provided by
oxygen mask held firmly over the baby’s face or
oxygen tubing cupped closely over the baby’s
mouth and nose.
Posture
4. Ensure a good seal, and compress the bag
enough to cause a visible chest expansion at
the rate of about 40 breath per minute
5. Check list in case of non-expansion of chest
a) Airway blocked - YES -
oropharyngeal suction, check neck position
b) Leak in mouth seal - YES - reapply
face mask with proper seal
c) Insufficient inflation - YES - check
leak in bag, increase pressure applied
PPV
6. Indication to intubate baby at include;
a) Meconium stained baby who is not vigorous
b) Non-response to bag and mask ventilation
after 30 seconds of AVL
c) Congenital diaphragmatic hernia
7. Response to assisted ventilation is assessed
30 seconds initiating ventilation. Good
response to assisted ventilation (it is also an
indication to discontinue assisted ventilation)
in indicated by:
a) Appearance of spontaneous respiratory effort
b) Heart rate > 100 beats/min
c) Pink color
After 30 seconds of bag and mask
ventilation, evaluate heart rate:
1. If HR > 100 b/min, assess respiration and if it is
adequate – gradually wean of PPV by decreasing
the rate and pressure of PPV. If baby has
apnea/gasping – continue PPV.
2. If heart rate is between 60 to 100 b/min continue
PPV and re-evaluate after 30 seconds.
3. If heart rate is less then 60 per minute, begin chest
compression, at rate of 90 b/min in ratio of 3:1 with
PPV.
4. If HR after chest compression 60b/min – use
medication
MEDICATIONS

 Medications used in resuscitation are

epinephrine, volume expanders,
sodium bicarbonate, naloxone. There is
no role of atropine, dexamethasone, calcium,
mannitol, dextrose for resuscitation in the
delivery room.
Medication Indication Concentration Dose
Epinephrine HR below 60/min after 30 1:10000(i.e., 0.1 mL/kg to
(1:1000), IV or sees of ventilation and chest diluted x 10) 0.3mL/kg
IT compression 0.5 mEq per mL

Volume Evidence of acute bleeding 10 mL/kg

expanders with signs of hypovolemia
(Normal saline),
IV
Naloxone Respiratory depression with 0.25 mL/kg
(0.4mg/mL), IV, history of narcotic (i.e.,O.1mg/k
IT or IM administratior 4 hrs before g
delivery. Administer only
after positive pressure
ventilation has restored
oxygenation.
Sodium Documented metabolic 0.4 mg/ mL 4 mL/kg (i.e.,
bicarbonate (0.9 acidosis, Apgar 3 or less at 5 2 mEq per kg)
mEq per mL), IV min
Brain death

 Coma manifested by lack of response to pain, light or audio

stimulation
 Apnea confirmed by documentation of failure to breath when
pCO2 is more than 60 mm Hg tested for 3 minutes
 Bulbar movements and brainstem reflexes are absent
(including midposition or fully dilated pupils, no response to
light or pain, oculocephalic, caloric, corneal, gag, cough,
rooting, sucking reflexes are absent, baby hasn’t spontaneous
or induced movements)
Prognosis

 Depends on severety and term of hypoxia

Birth Trauma
Factors predisposing to injury include the following:
 Prima gravida
 Cephalopelvic disproportion, small maternal stature, maternal
pelvic anomalies
 Prolonged or rapid labor
 Deep transverse arrest of descent of presenting part of the
fetus
 Oligohydramnios
 Abnormal presentation (breech)
 Use of midcavity forceps or vacuum extraction
 Versions and extractions
 Very low birth weight infant or extreme prematurity
 Fetal macrosomia
 Large fetal head
 Fetal anomalies
Injuries with favorable long-term prognosis
 Soft tissue
 Abrasions
 Erythema petechia
 Ecchymosis
 Lacerations
 Subcutaneous fat necrosis
 Skull
 Caput succedaneum
 Cephalhematoma
 Linear fractures
 Face
 Subconjunctival
hemorrhage
 Retinal hemorrhage
 Musculoskeletal injuries
 Clavicular fractures
 Fractures of long bones
 Sternocleidomastoid injury
 Intra-abdominal injuries
 Liver hematoma
 Splenic hematoma
 Adrenal hemorrhage
 Renal hemorrhage
 Peripheral nerve
 Facial palsy
 Unilateral vocal cord
paralysis
 Radial nerve palsy
 Lumbosacral plexus injury
 Cephalhematoma

 Cephalhematoma does not cross suture

lines
 Well-demarcated, fluctuant swelling
 Most commonly occurs over parietal
bone
 No overlying skin discoloration
 Appears by day 2-3 of life
 No laboratory studies are usually necessary.
 Skull radiography or CT scanning is used if neurologic
symptoms are present.
 Usually, management solely consists of observation.
 Transfusion for anemia, hypovolemia, or both is necessary if
blood accumulation is significant.
 Aspiration is not required for resolution and is likely to increase
the risk of infection.
 Hyperbilirubinemia occurs following the breakdown of the RBCs
within the hematoma. This type of hyperbilirubinemia occurs
later than classic physiologic hyperbilirubinemia.
 The presence of a bleeding disorder should be considered.
Skull radiography or CT scanning is also used if concomitant
depressed skull fracture is a possibility.
 Brachial plexus injuries are most often classified according to spinal
nerve root involvement and into 3 main nerve groups:45
 Upper root injuries

 Erb's palsy or Erb-Duchenne palsy;

 Injury to C5 to C6 with shoulder and biceps weakness or
paralysis;
 Can involve C7 with forearm paralysis.
 Lower root injuries

 Klumpke's palsy;
 Paralysis of C8 to T1 (sometimes C7 also involved);
 Weakness of distal upper extremity only.
 Complete or total nerve injury (second most common)

 Erb-Klumpke's or total paralysis;

 Involves the complete plexus (C5 to T1);
 Associated with Horner's syndrome in one third of those severely
affected.
 Erb palsy (C5-C6)
 Erb palsy (C5-C6) is most common and is
associated with lack of shoulder motion.
 The involved extremity lies adducted, prone, and
internally rotated.
 Moro, biceps, and radial reflexes are absent on
the affected side.
 Grasp reflex is usually present.
 Five percent of patients have an accompanying
(ipsilateral) phrenic nerve paresis
 Klumpke paralysis (C7-8, T1)
 Klumpke paralysis (C7-8, T1) is rare and
results in weakness of the intrinsic
muscles of the hand;
 grasp reflex is absent.
 If cervical sympathetic fibers of the first
thoracic spinal nerve are involved, Horner
syndrome is present.
 Management
 Management consists of prevention of
contractures.
 Immobilize the limb gently across the
abdomen for the first week and then start
passive range of motion exercises at all
joints of the limb. Use supportive wrist
splints.
 Best results for surgical repair appear to
be obtained in the first year of life.
 Subdural haemorrhage
 Subdural haemorrhage occurs mainly in full-term infants and is most
frequently caused by a rupture of veins at their confluence into the
longitudinal cerebral sinus.
 Injury may occur to the internal cerebral veins, v. of Galen cerebral
tentorium or falx, sagittal sinus and/or laternal sinuses.
 Clinical manifestations accompanying the subdural haematoma
depend on the severity of haemorrhage and also on the onset of the
condition: acute, subacute or chronic.
 An acute development of haematoma occurs after 5 days from injury.
The newborn has impaired consciousness, seizures, dyspnoea,
opisthotonus, pinpoint pupils, movement of the eyeballs `towards the
haemorrhage site', and papilloedema at the fundi. Frequently,
haematoma may lead to coma.
 The newborn who survives the acute phase of the condition, may, in
infancy, develop hydracephalus secondary to a disturbed cerebral
flow or absorption of the cerebrospinal fluid.
 In subacute condition various nonspecific symptoms and
signs appear within 6 weeks from the injury, i.e.
vomiting, strabismus, a „setting sun sign ”.
 Later, a chronic haematoma is recognised. It is then very
difficult to diagnose considering even a 6-month period
from delivery, variability and nonspecificity of clinical
manifestations as well as difficulty in its visualisation on
the USG examination,
 When the location is very close to the cerebral surface,
computer tomography (CT) is the investigation of choice.
In such cases translumination with a diaphanoscope may
be used as an exploratory examination.
 Subarachnoid haemorrhage
 subarachnoid haemorrhage, or bleeding into the space filled with cerebro-
spinal fluid, on the cerebral surface and the spinal cord, usually originates
from veins or an arteriovenous involutional anastomosis.
 The primary subarachnoid haemorrhage occurs mainly in full-term infants
and is usually localised in the temporal and occipitaparietal regions, and
over the cerebellum.
 A small, but larger, gradually increasing subarachnoid haemorrhage does
not produce any clinical manifestations in the newborn. A larger, or
extensively progressing haemorrhage may (usually at two days of age)
result in convulsions. In that case the newborn's condition is usually
diagnosed as `good with convulsions'.
 In massive and rapidly increasing subarachnoid haemorrhage the course
of the condition may be severe and the outcome may be fatal. In the most
severe cases it is recommended to consider cerebral vascular defects,
including congenital haematoma.
 Secondary subarachnoid haemorrhage usually accompanies subtentorial
bleeding, develops simultaneously, and is associated with perinatal cranial
fracture. A USG examination in the diagnosis of subarachnoid
haemorrhage is useless.
Grade Hemorrhage Location

I Subependymal hemorrhage

II IVH without ventriculomegaly

III IVH with ventriculomegaly

IV IVH with parenchymal hemorrhage

 MOST COMMON TIME OF ONSET

ETIOLOGY DAYS 3 TO 7 DAYS 7 TO 10

Intracranial
hemorrhage X X
Hypoxic-ischemic
encephalopathy X
Hypoglycemia X (early) X (late)
Inborn errors of
metabolism X
Intracranial
infection X
Cerebral dysgenesis X X X
Anesthetic injection X
Drug withdrawal X
Neonatal epilepsy
syndromes X X
 Causes of Neonatal Seizures
PRETERM
ETIOLOGY TERM INFANTS OUTCOME
INFANTS
Hypoxic-ischemic
encephalopathy Most common Common Variable
Intraventricular
hemorrhage
(severe) Uncommon Common Poor
Subarachnoid
hemorrhage
(severe) Common Uncommon Good
Hypoglycemia Common Common Variable
Hypocalcemia Uncommon Uncommon Good
Intracranial
infection Common Common Variable
Cerebral
dysgenesis Common Common Poor
Drug withdrawal Uncommon Uncommon Variable