Asphyxia of the newborn

Hellou !
Definition

WHO: Asphyxia is incapacity of newborn

to begin or to support of spontaneous
respiration after delivery due to breaching
of oxygenation during labor and delivery
India: Asphyxia is absent or ineffective
respiration of newborn of 1 minute old with
Apgar score less than 4
Definition

Great Britain: Asphyxia is critical

insufficiency of oxygen in fetus during
delivery so severe that leads to
development of metabolic acidosis and
depression of spontaneous respiration
Definition

Canada: Asphyxia is breach of gas

exchange when hypoxia and hypercapnia,
and considerable metabolic acidosis occur
Definition

Australia: Asphyxia is a state with

mother has complications in perinatal
period that decrease provision with oxygen
and leads to acidosis
functional violation minimum 2 organs due
to acts of acute hypoxia
Definition

Ukraine: Asphyxia of newborn as a

nosological form is conditioned by causes
when fetus out and find (connect) with
severe maternal-placental and (or)
umbilical flow leads to increasing of
oxygen approach to fetus tissue and
hypoxia development
Definition
Asphyxia
 Asphyxia: means to be pulse less, but more
useful is a definition of impaired or interrupted
gas exchange.
 These situations can take place:
 a. Intrauterine: the gas exchange depends on
the function of placenta, and the blood-flow in
the umbilical vessels.
 b. Intrapartum
 c. Postnatal: after delivery the gas exchange
takes place in the pulmonary vesicles or alveoli
and depends on the function of the heart, lungs
and brain.
Causes of Asphyxia

 Fetal hypoxia:
 Mother: hypoventilation during anesthesia, cyanotic heart disease,
respiratory failure or carbon monoxide poisoning.
 Low maternal blood pressure as a result of the hypotension that may
compression of the vena cava & aorta by the gravid uterus
 Inadequate relaxation of the uterus to permit placental filling as a
result of uterine tetany caused by excessive administration of
oxytocin
 Premature separation of the placenta; placenta previa
 Impedance to the circulation of blood through the umbilical cord as a
result of compression or knotting of the cord
 Uterine vessel vasoconstriction by cocaine, smoking
 Placental insufficiency from numerous causes, including gestosis,
eclampcia, toxemia, postmaturity
 Extremes in maternal age (< 20 years or >35 years)
 Preterm or postterm gestation.
Causes of Asphyxia
 Intrapartus asphyxia:
 More frequently inadequate obstetric aid
 Using focerps, vacuum extraction, cresteller,
cesaring cection
 Trauma: narrow pelvis, presentation
 Extremely rapid or prolonged labor
 Multiple gestation
 Drags depression of CNS: anaesthesia, sedatics
& analgetics
 Meconium –stained amniotic fluid
Causes of Asphyxia
 Postnatal hypoxia:
 Anemia severe enough to lower the oxygen content of
the blood to a critical level due to severe hemorrhage or
hemolytic disease
 Shock severe enough to interfere with the transport of
oxygen to vital cells from adrenal hemorrhage,
intraventricular hemorrhage severe enough to age,
overwhelming infection or massive blood loss
 A deficit in arterial oxygen saturation resulting from
failure to breathe adequately postnatally due to a
cerebral defect, narcosis, or injury
 Failure of oxygenation of an adequate amount of blood
resulting from of cyanotic congenital heart disease of
deficient pulmonary function
Gas exchange.
Cell pathology
Cell pathology
Cell pathology
Cell pathology
Cell pathology
Cell pathology
Heart rate, breath movements and blood
pressure in fetus during primary and
secondary apnea
Virginia Apgar
Apgar Score of the Newborn

 SIGNSCORE 0 1 2
 Heart rate Absent <100 beats/min >100
Respiratory
 effort Absent Weak,irregular Strong cry
 Muscle tone Flaccid Some flexion Well
 Reflex irritability (response to catheter in nostril)
No Grimace Cough or sneeze
 Skin colour Blue, pale extremities blue pink
CRITERIAS OF SEVERE
ASPHYXIA:

 °Severe metabolic or mix acidosis pH ≤

7.00 in arterial blood of umbilical vessels
 °Assessment by Apgar is 0-3 during more
than 5 minutes
 ° Neurological symptoms such as general
hypotonic, lethargy, coma, seizures
 °Damage of vital organs (lungs, heart and
other) in fetus or newborn
Acute complications associated
with Asphyxia
 hypotension
 hypoxic encephalopathy
 seizures
 persistent pulmonary hypertension
 hypoxic cardiomyopathy
 ileum and necrotizing enterocolitis
 acute tubular necrosis
 adrenal hemorrhage and necrosis
 hypoglycemia
 polycytemia
 disseminated intravascular coagulation
Brain Edema
Periventricular leukomalacia
Morphologic substrate of Cerebral palsy
due to Asphyxia
DIAGNOSIS
 Clinical symptoms
 Metabolic derangement
 Renal and/or cardiac failure
 Assessment of the brain:
 a.. EEG EEG is useful particulary in the asphyxiated term
newborn.
Serial recordings are almost necessary.
 Low voltage. Burst-suppression patterns or electrical inactivity are
associated with bad prognosis.
 Rapid resolution of EEG abnormalities and/or normal interictal EEG
are associated with a good prognosis.
 b. Ultras onography: Ultrasound can be useful in premature
newboms
but is of more limited value in the term newborn.
 c. Computed tomography: CT is of major value both acutely
during the
neonatal period and later in childhood. The optimal timing of CT
scanning is
between 2 and 4 days.
DIAGNOSIS
 I. Intrauterine assessment
 A. Ultrasound and Doppler technique:
 Ultrasound: to measure the growth of the fetus. For this reason it is important have
a reliable gestational age. Early during pregnancy an ultrasound will be done to
date the fetus. This method safer than common clinical methods. The growth
retarded fetus is in a great risk of developing asphyxia.
 Doppler techniques: to measure the blood flow in the umbilical vessels or aorta. A
low flow or decreasing flow indicates a fetus in risk of asphyxia.
 B.Electrofysiological:
 Severe pathological fetus heart rate will lead to cessation of the delivery with
Caesarean section.
 Fetal heart rate: Episodes of bradycardia can be dangerous and lead to brain
damage. The problem is to do this type of measurement during long periods and on
every pregnant woman.
 II. Extrauterine assessment
 C. Biochemical
 - C blood sample drawn from the umbilical artery is an ideal way to evaluate
whether an intrapartum asphyxia exist or not. Low pH (< 7, 00) indicates the
intrapartum asphyxia.
 PC02 and P02 will also be deranged as you have a diminished gas exchange. The
low pH is the result of an increased level of H+ and lactate.
EEG
ABC resuscitation

A- Airways (maintenance of passable ness

of airway)
B- breathing (stimulation of breathing)
C- circulation (to support of circulation)
D-drug
ABC resuscitation

Step A- immediately after delivery the

infant’s head should be placed in a neutral
or slightly extended position
 Rolled towel under the shoulders
Step A- immediately after delivery the infant’s head
should be placed in a neutral or slightly extended
position
And airway established by clearing the mouth,

then the nose by rubber bag
If meconium is present in amniotic fluid, after sucking of
mouth and nose we must suck a pharynx by tube after
laryngoscopes
If it is inadequate we must use step B.
At first the tactile stimulation should be given to newborn, for
example-  gentle flicking of the feet or heel
ABC resuscitation

or rubbing of the back

If these measures are inadequate, mechanical ventilation
should be initiated, using mask and bag ventilation
If ventilation is adequate supplemental oxygen may be
given to improve heart rate or skin colour


If mechanical ventilation does not improve the respiration, heart
rate or colour skin, the following step is “C”-circulation. At first the
assessment of heart rate is necessary
If heart rate is less than 60 beats/minute, or between 60 and 80
beats and is not improving, cardiac compression is a lower on/third
of sternum

 Chest compressions with two fingers

ABC resuscitation

 Your big fingers must be lie on the sternum, other finder

should lie under the back of newborn
ABC resuscitation
 If heart rate is less then 80 beats per minute the cardiac
compression should be continued. If heart rate is 80 beats per
minute or more the cardiac compression should be stop .
Brain death
The clinical diagnosis of brain death is made on the basis
of
 - coma manifested by lack of response to pain, light, or
auditory stimulation;
 - apnea confirmed by documentation of failure to breathe
when pCO2 is greater then 60 mm Hg tested by 3
minutes;
 - absent bulbar movements and brainstem reflexes
(including midposition or fully dilated pupils with no
response to light or pain and with absent oculocephalic,
caloric, corneal, gag, cough, rooting and sucking
reflexes, flaccid tone and absence of spontaneous or
induced movements (excluding activity mediated at the
spinal cord level)
Different painless is possible
PROGNOSIS.
 Prognosis is difficult because of the inability to
establish the precise extent and duration of
cerebral insult and injury. At the time of delivery
low delayed Apgar scores between 0 and 3 at
10, 15 and 20 minutes' of age are associated
with significantly increased mortality and
morbidity, e.g. cerebral palsy. The single most
useful prognostic factor is the severity of the
neonatal neurological syndrome.
HI brain injure is the most impotent consequence of
perinatan Asphyxia

 Leads to increase lactate, fall in pH, ↓ATP, ↑

glucose utilization, loss of cerebrovascular
autoregulation
 Impairs ion pumps with accumulation Na,Cl,H2O,
Ca intracellularly
 ↑ amino acid neurotransmitters (glutamate,
aspartate)
 Generation of free radicals & leukotriens wich
they overwhelm endogeneous scavenger
mechanism
 Damage nucleic acids, lipids & proteins
HIE
Birth Trauma
Development of the CNS
Development of the CNS
Development of the CNS
Development of the CNS
Birth trauma

The term “Birth trauma” is used to denote

mechanical and anoxic trauma incurred by
the infant during labor and delivery.
Birth trauma

The incidence of B.T. has been estimated

at 2 – 7 per 1000 live births. Overall 5 - 8
per 100000 infants die of B.T. and 25 per
100000 die of anoxic injuries.
 Some injuries may be latent initially but
later result in severe illness or squealed
Birth trauma

The process of birth is blend of

compressions, contractions, and
tractions.
Birth trauma

 When fetal size, presentation, or

neurological immaturity complicate
this event, such intrapartum forces
may lead to tissue damage, edema,
hemorrhage or fracture in the
neonate.
Birth trauma

The use of obstetrical instruments may

further amplify the effect of such forces or
may induce injury by itself.
Although breech presentation carries
the greatest risk of injury, delivery by
cesarean section does not guaranteed an
injury – free infant.
The risk of birth injury

 Primiparity
 Small maternal stature
 Maternal pelvic anomalies
 Extremely rapid
 Prolonged labor
 Deep transverse arrest of descent of presenting
part of fetus
 Oligohydramnions
 Abnormal presentation (i.e. breech)
The risk of birth injury
Use of mid-forceps or vacuum extraction
Cesarean section
Versions and extraction
Very low birth weight infant or extreme
premature
Postmature infant (> 42 week of gestation)
Fetal macrosomia
Large fetal head
Fetal anomalies (see teratoma)
Teratoma
Classification of birth injuries

I. Soft-tissue injuries

- caput succedaneum
- subcutaneous and retinal hemorrhage,
petechia
- ecchymoses and subcutaneous fat
necrosis
Classification of birth injuries

II. Cranial injuries

cephalohematoma
fractures of the skull
Classification of birth injuries

III. Intracranial hemorrhage

subdural hemorrhage
subarachnoid hemorrhage
intra- and peryventricular
hemorrhage
parenchyma hemorrhage
Classification of birth injuries

 IV. Spine and spinal cord

fractures of vertebra
Erb-Duchenne paralysis
Klumpke paralyses
Phrenic nerve paralyses
 Facial nerves palsy
Classification of birth injuries

V. Peripheral nerve injuries

 VI. Viscera (rupture of liver, spleen
and adrenal hemorrhage)
 VII. Fractures of bones.
Birth trauma
Birth trauma
 Petechiae and ecchymosis are common
manifestation of birth trauma in the newborn. If
the etiology is uncertain, studies to rule out
coagulation disorders or infections etiology are
indicated. This lesions resolve spontaneously
within 1 week. Petechiae of the skin of the heard
and neck are common. All are probably
secondary to a sudden increase in intrathoracic
pressure during passage of the chest through
the birth canal. Parents should be assured that
they are temporary and result of normal hazards
of delivery.
Birth trauma

Subcutaneous fat necrosis. Although

not detectable et birth this irregularly
shaped, hard no pitting, subcutaneous
plagues with overlying dusky, red – purple
discoloration may by caused by pressure
during delivery. They appear during the
first 2 weeks of life usually in large babies
on the cheeks, arms, back, buttocks end
thinks.
Birth trauma

Caput succedaneum is a subcutaneous

extraperiosteal fluid collection with poorly
defined margins it may extend across the
midline over suture lines end is usually
associated with heat molding the soft
tissue edema will usually resolve over the
few days post partum.
Birth trauma
 Cephalohematoma is a subperiosteal collection of
blood secondary to rupture of the blood vessels between
the scull and pereostium, its extent will be delineated by
suture lines over days. The extent of hemorrhage may
be severe enough to present as anemia and hypotension
with secondary hyperbilirubinemia. It may be a focus of
infection leading to meningitis, particularly when there is
a concominant skull fracture. Skull X-rays should be
obtained if there are CNS symptoms, if the hematoma is
very large or if the delivery was very difficult. Resolution
occurs over 1 to 2 month, occasionally with residual
calcification as a thrombus.
Birth trauma
 INTRACRANIAL HEMORRHAGE occur in 20% to more
than 40% of infants with birth weight under 1500 gm but
is less common among more mature infants.
 Intracranial hemorrhage may occur in the subdural,
subarachnoid, intraventricular or intracerebral regions.
Subdural and subarachnoid hemorrhage follow head
trauma e.g., in breech, difficult and prolonged labor and
after forceps delivery. Other forms of intracranial
bleeding are associated with immaturity and hypoxia.
With better obstetric care intracranial bleeding has
become rare.
Predisposing factors of IVH

premature
respiratory distress syndrome
hypoxic ischemic or hypotensive injuries
reperfusion of damaged vessels
increased venous pressure
pneumothorax
hypervolemia, hypertensia
The etiologic factors with IVH in low-
birth-weight infants (Intravascular inflow
factors)
 impaired autoregulation
 seizers
 manipulation with infant
 infusion of hyperosmotic solutions
 rapid colloid infusion
 apnea
 presents of patent ductus arteriosus
 hypertension and use of ECMO
The etiologic factors with IVH in low-
birth-weight infants (Intravascular
outflow factors)
respiratory distress
pneumothorax
congestive heart failure
continuous positive airway pressure
labor/delivery
acute angle of the internal cerebral vein
The etiologic factors with IVH in low-birth-
weight infants (Vascular and extra vascular
structural factors)

 normal regression of germinal matrix

 relatively large blood flow to deep cerebral
structures
 hypoxic-ischemic injury to germinal matrix or its
vessels
 present of fibrinolitic enzymes
 poor structural support of germinal matrix
vessels
 abrupt termination of media in arteries proximal
to germinal matrix
Clinical manifestation IVH
Absent Moro reflex
Poor muscle tone
Lethargy
excessive somnolence
Pallor or cyanosis
Respiratory distress
DIC
Jaundice
Clinical manifestation IVH

Bulging anterior fontanel

Hypotonia
Weakness, seizures, muscular twitching
Temperature instability
Brain stem signs (apnea, lost extraocular
movements, facial weakness, abnormal
eye sing)
Laboratory correlates of blood loss

Metabolic acidosis
Low hematocrit
Hypoxemia, hypercarbia
Respiratory acidosis
Thrombocytopenia and prolongation of
protrombin time (PT) and partial
thromboplastin time (PTT)
Diagnosis IVH

History
Clinical manifestation
Transfontanel cranial ultrasonography
Computed tomography
Glucose level
Coagulogramma, hematocrit
Lumbal punction
Outcomes and prognosis

Patients with massive bleeding have a

poor prognosis. About 10-15% infants may
develop post hemorrhagic hydrocephalus
and chronic neurological pathology
Spinal cord
Strong traction exerted when the spine is
hyper extended or when the direction of
pull is lateral, or forceful longitudinal
traction on the trunk while the head is still
firmly, engaged in the pelvic, especially
when combined with flections and torsion
of vertical axis, may produce fracture and
separation of the vertebra. Tran section of
the cord may occurs with or without
vertebral fractures
Clinical data

Areflexia
Loss of sensation
Complete paralysis of voluntary motion
below the level of injury
Epidural hemorrhage
Apnea
Delivery room

If cord injury is suspected, effort in the

delivery room should immediately focus on
resuscitation and prevention of further
insult.
The head should be made immobile
relative to the spine and secured on a flat,
firm surface with padding of pressure
points.
Duchenne-Erb paralysis

Injury to the 5th and 6th cervical nerves

Affected arm is adducted, internally
rotated
Forearm is in pronation
Wrist is flexed
Arm falls limply to the side of the body
when passively adducted
Moro, biceps and radial reflexes absent
Cervix injury
Klumpke’s paralysis
 injury to the 7th and 8th cervical and 1st thoracic
spinal nerves
 Horner syndrom (ipsilateral ptosis and miosis) if
the thoraxic spinal nerve is involved

 Absent of movements of the wrist

Phrenic nerve palsy

Injury to the C3,C4 or C5

Brachial plexur injury
RDS
Paradox (upward) movement during
inspiration
Clavicular fracture

Most common
Crepitus, palpable bony irregularity
sternoclaidomastoid muscle spasm
Cry during movement of upper extremities
Long bone injures

Loss of spontaneous arm or leg movement

is usually the first sing of humeral or
femoral injury, following by swelling and
pain on passive motion
Intraabdominal injures – target organ

Liver
Spleen
Adrenal gland (breach presentation)
Intraabdominal injures

Sudden presentation
Shock
Abdominal distension
Bluish discoloration, jaundice, pallor
Poor feeding
Thachypnea, tachycardia
history: difficult delivery
HIE
Selective necrosis of the neurons of the
deeper cerebral cortical layers is the
hallmark of hypoxic injury to the perinatal
brain in full-term babies, parasagittal
cerebral injury occurs as a result of the
generalized reduction in the cerebral blood
flow. In preterm babies, the areas of
infarction involve the deeper
periventricular white matter. Neuronal
necrosis may also entail basal ganglia.
HIE

Some of the ischemic infants with

encephalopathy gradually improve while
others deteriorate. If not treated promptly,
20 to 30 percent of infants with severe
ischemia die.
HIE
HIE

HIE
HIE
HIE
HIE
 HYPOXIA-ISCHEMIA
 ANAEROBIC GLYCOLYSIS
 ATP

ADENOSINE ↑GLUTAMATE
 ↓↓
 HYPOXANTHINE NMDA
 ↓ RECEPTOR
 XANTHINE ↓
 Ca++
 LIPASES NITRIC OXIDE
 ↓ SYNTHASE
 ↑ARACHIDONIC INHIBITORS
 ACID
 ↓
 FREE RADICALS

Sarnat
 Level of consciousness
 Neuromuscular control
 Muscle tone
 Posture
 Stretch reflexes
 Segmental myoclonus
 Complex reflexes: Suck, Moro,
oculovestibular tonic neck
 Autonomic function
Sarnat
Pupils
Respirations
Heart rate
Bronchial & salivary secretions
Gastrointestinal motility
Seizures
EEG
Duration of symptoms
Sarnat

Outcome
Mild: About 100% normal
Moderate: 80% normal; abnormal if
symptoms more than 5 to 7 days
Severe: About 50% die; remainder with
severe sequel
Sarnat
Diagnosis.

 A thorough neurological examination

combined with a careful history is helpful
for the diagnosis. Ultrasound examination
of the brain, EEG, intracranial pressure
measurement and computed scanning arc
is valuable.
EEG
EEG
Treatment.
 Prevention of asphyxia remains the most important mode of
treatment. Careful monitoring of the fetus during labor and prompt
appropriate intervention at the earliest signs of fetal compromise is
important in preventing perinatal asphyxia.
 The rapid responders from anoxia need observation in the nursery
for only 12 to 24 hours. These babies become active, and start
accepting feeds within a few hours. The slow responders need more
aggressive management. Both: hypoxemia and hyperoxemia as well
as hypercapnia should be circumvented, since they affect cerebral
blood flow. These babies should be kept in ward, with a minimal
noise level or in the nursery. Intravenous fluids should be restricted
to two-third of the maintenance requirements and blood glucose
levels must be maintained at 75-100 mg/dL. Acidosis,
hypocalcaemia and hypoglycemia need correction. Seizures should
be controlled with phenobarbitone but not in preterm babies who are
severely disturbed and in those with decerebration.
Treatment
curative and protective regimen in newborn

 Children with severe A or BT should be undergo

strict regimen because the rest more frequently
associated with emergency position if baby
 The infant must lie on the hard surface with
fixated neck by collar
 The baby is observed in bed or incubator, is not
washed and sometimes is turned side to side.
The transport of this infant prohibitive.
 Oxygen (ingalation or mask or apparatus )
 Feeding throught catheter 40-50% daily calories
Treatment
curative and protective regimen in newborn

Baby with subcompensation of all function

must be undergo spareing regimen.
May be washed (in bad)
Feeding through catheter and spoon. If he
can suck he may be apply to mother brest
Common (general) regimen is
administrated for healthy child or
reconvalescents
Treatment
 Oxygenotherapy
 Hemostatics: 1% vit K 1mg/kg, dicinone 12.5
mg/kg
 Hypovolemia: 5% albumine, plasma, 5% glucose
– 1-10 ml/kg
 Protect of nerve cells and anticonvulsants: 20%
Natrium-oxybutirate 100 mg/kg, sibazone 0.3
ml/kg, Phenobarbital 20 mg/kg (5-10)
 25% Magnesia 0.2 ml/kg
Treatment (underlying problems
associated with BT)
Hypoglycemia – 5% glucose i/v 1-10 ml/kg
Hypocalciemia–10% Ca-gluconate 2 ml/kg
Acidosis- 4.2% Sodium bicarbonate
solution 2 meq/kg
Treatment (underlying problems
associated with BT)
RDS
Hypoxia
Hypothermia
Hypotension
Support cardiac output 0.5% dopamin 5
μg/kg/min & speed is 1 ml/hour
seizures
seizures
Treatment
I don’t want a trauma