Asphyxia of the newborn.
Birth trauma
Definition
 WHO: Asphyxia is incapacity of newborn
to begin or to support spontaneous
respiration after delivery due to
breaching of oxygenation during labor
and delivery
Asphyxia is absense or ineffective
respiration of newborn of 1 minute old
with Apgar score less than 4
Causes of Asphyxia
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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 cause compression of the vena cava & aorta by the
gravid uterus
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 forceps, vacuum extraction, cresteller,
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caesarean section (immediate)
Trauma: narrow pelvis, malpresentation
Extremely rapid or prolonged labor
Multiple gestation
Drugs depression of CNS: anesthesia, sedatives &
analgesics
Meconium-stained amniotic fluid
Causes of Asphyxia
Postnatal hypoxia:
 Anemia due to severe hemorrhage or hemolytic
disease
 Shock from adrenal hemorrhage, intraventricular
hemorrhage, overwhelming infection, massive blood
loss
 Failure to breathe due to a cerebral defect, narcosis or
injury
 Failure of oxygenation resulting from of cyanotic
congenital heart disease or deficient pulmonary
function
Predisposing risk
factors for asphyxia are:
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Multiple gestation;
Placental abruption;
Placenta previa;
Preeclampsia;
Meconium-stained amniotic fluid;
Fetal bradycardia;
Prolonged rupture of fetal membranes;
Extremes in maternal age (senior 35 y, junior 20 y);
 Maternal diabetes;
 Maternal use of illicit drugs;
Postnatal symptoms of ASPHYXIA
MILD ASPHYXIA
 ° The infant who experiences mild
asphyxia initially will be depressed.
This is followed by a period of
hyperalertness, which resolves within
1 or 2 days.
° Clinical symptoms:
 hyperalertness (jitteriness),
 increased irritability and tendon
reflexes,
 exaggerated Moro response;
 ° There are no local signs
 ° The prognosis is excellent for normal
(good) outcome.
CRITERIA OF MODERATE ASPHYXIA
° The infant who experiences moderate
asphyxia will be very depressed. This
is followed by a prolonged period of
hyperalertness and hyperreflexia.
° Clinical symptoms:
 lethargy, hypotonia ,Apgar is 4-7
 suppressed reflexes with or without
seizures
 Generalised seizures often occur 12 to
24 hours after episode of asphyxia,
but are controlled easily, resolving in
a few days regarding of therapy.
 ° The prognosis is variable (20-40%
with abnormal outcome).
CRITERIA 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 hypotonia, lethargy, coma,
seizures, brainstem, autonomous
dysfunction;
 ° Evidence of multiorgan system
dysfunction in the immediate
neonatal period - damage of vital
organs (lungs, heart and others) in fetus
or newbon;
CRITERIA OF SEVERE ASPHYXIA
 ° Severe
asphyxia is associated
with coma, intractable seizures
activity, cerebral oedema,
intracranial haemorrhage.
 ° The infant often became
progressively more depressed
over the first 1 to 3 days, as a
cerebral oedema develops, and
death may occur during this
period.
 Survival is usually associated
with poor long-term outcome
(100% with abnormal outcome);
Acute complications
associated with Asphyxia
 hypoxic-ischemic encephalopathy (HIE)
 hypotension
 seizures
 persistent pulmonary hypertension
 hypoxic cardiomyopathy
 necrotizing enterocolitis
 acute tubular necrosis
 adrenal hemorrhage and necrosis
 Hypoglycemia, polycytemia
 disseminated intravascular coagulation
Sarnat criteria
 Level of consciousness
 Neuromuscular control
 Muscle tone
 Posture
 Stretch reflexes
 Segmental myoclonus
 Complex reflexes: Suck, Moro, oculovestibular tonic
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neck
Autonomic function
Pupils
Respirations
Heart rate
Bronchial & salivary secretions
Gastrointestinal motility
Seizures
EEG
Duration of symptoms
DIAGNOSIS
 Clinical symptoms and metabolic derangement –
blood sample from the umbilical artery - low pH
(< 7, 00) - indicates the intrapartum asphyxia.
 Renal and/or cardiac failure
 Assessment of the brain: EEG
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.
Ultrasound and Doppler technique
 Ultrasound: to measure the growth of the fetus. The growth
retarded fetus is in a great risk of developing asphyxia.
Ultrasound can be useful in premature newborns.
 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.
 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.
perivascular edema
Dilated lateral ventricles
Classification of birth injuries
I. Soft-tissue injuries
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caput succedaneum
subcutaneous and retinal hemorrhage, petechia
ecchymoses and subcutaneous fat necrosis
II. Cranial injuries
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cephalohematoma
fractures of the skull
III. Intracranial hemorrhage
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subdural hemorrhage
subarachnoid hemorrhage
intra- and periventricular hemorrhage
parenchyma hemorrhage
Classification of birth injuries
 IV. Spine and spinal cord
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fractures of vertebra
Erb-Duchenne paralysis
Klumpke paralyses
Phrenic nerve paralyses
Facial nerves palsy
 V. Peripheral nerve injuries
 VI. Viscera (rupture of liver, spleen and adrenal
hemorrhage)
 VII. Fractures of bones.
Birth trauma
 Caput succedaneum is a subcutaneous extraperiosteal
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fluid collection in the presenting part of fetus
is caused by infiltration of subcutaneous soft tissue in the
presenting part resulting from pressure in birth canal
with poorly defined margins
it may extend across the midline over suture lines
This swelling is resolved rather quickly within several
days post partum.
Caput succedaneum
Cephalohematoma
 is a subperiosteal collection of blood
resulting from rupture of the blood
vessels between the skull and
pereostium
 its does not extend over suture lines
between adjacent bones.
 Its occurrence is commonly on one
side of the head
 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
concomitant 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
 Occurs in 20% to more than 40% of infants with birth weight
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under 1500 gm,
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.
Clinical manifestation of IVH
 Absent Moro reflex
 Weakness, seizures, muscular twitching
 Poor muscle tone
 Hypotonia
 Lethargy
 excessive somnolence
 Pallor or cyanosis
 Respiratory distress
 Jaundice
 Bulging anterior fontanel
 Temperature instability
 Hypotonia
 Brain stem signs (apnea, lost extraocular movements, facial
weakness, abnormal eye signs)
Diagnosis IVH
 History
 Clinical manifestation
 Transfontanel cranial ultrasonography
 Computed tomography
 Glucose level
 CBC - complete blood count
 Lumbar puncture
Spinal cord
Spinal cord injuries are commonly caused by strong traction when
 the spine is hyper extended
 forceful longitudinal traction on the trunk while the head is still
firmly engaged in the pelvic
 shoulder dystocia
Clinical data
 Reflex
 Loss of sensation
 Complete paralysis of voluntary motion below the level of injury
 Epidural hemorrhage
 Apnea
ANATOMY OF THE BRACHIAL PLEXUS
1
2
3
4
5
Roots
6
9
8
Trunks
7
Cords
Nerves
1
2
3
Upper
Middle
Lower
4
5
6
Lateral
Posterior
Medial
7
8
9
Ulnar
Median
Radial
Erb Palsy –
Upper trunk plexopathy
 Injury to the 5th and 6thcervical nerves (C5-C6 root
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avulsion)
Arm falls limply to the side of the body when
passively adducted
Affected arm adduction & internal rotation
Elbow extended & forearm pronated
Wrist is flexed
“Waiters tip” position
Moro, biceps and radial
reflexes absent
+/- Horner syndrome
Klumpke palsy
 Lower trunk (C8, T1) injury
Poor grasp, proximal function
preserved
 Absence of movements of the wrist
 Horner syndrome (ipsilateral ptosis
and miosis) if the thoracic spinal nerve
is involved
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Flail arm
• Injury to entire plexus