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INTRODUCTION BIRTH ASPHYXIA

The document presents a case of a 3-day-old neonate born at 43 weeks with a birth weight of 3.100 kg, who experienced a fit shortly after birth and had a history of not crying at birth. The infant was managed for potential birth asphyxia, with immediate and follow-up treatments outlined, including the use of dopamine and volume expanders. Additionally, the document discusses the pathophysiology and implications of hypoxic-ischemic encephalopathy (HIE) resulting from birth asphyxia.

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7 views8 pages

INTRODUCTION BIRTH ASPHYXIA

The document presents a case of a 3-day-old neonate born at 43 weeks with a birth weight of 3.100 kg, who experienced a fit shortly after birth and had a history of not crying at birth. The infant was managed for potential birth asphyxia, with immediate and follow-up treatments outlined, including the use of dopamine and volume expanders. Additionally, the document discusses the pathophysiology and implications of hypoxic-ischemic encephalopathy (HIE) resulting from birth asphyxia.

Uploaded by

cletusjoe968
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© © All Rights Reserved
We take content rights seriously. If you suspect this is your content, claim it here.
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PERSONAL DETAILS

Presenting the hx of 3 days old baby of


Matilda Simuliampondo
24 yr old primagravida
Resides in Woodlands
-SDA

Antenatal History

Booked at 6 months at Chilenge clinic


Attended total of 3 antenatal clinics
Pregnancy described as uneventful
No illness, fever, RVD & RPR both –ve
No hx of polydipsia, polyuria, polyphagia
Drug hx : Hematinics & Fansider

PMHx :No hx DM, Hyptn, TB, Asthma,


Heart disease
No hx of 3 rd trimester bleeding or bleeding
at any time during pregnancy.

INTRAPATUM HISTORY
Delivered post dates at 43 weeks
Hx of slow progressing labour lasting a total
of 19 hrs 50 mins
Entered labour at 10 20 hrs
AROM done at 13 00 hrs & augmented with
oxytocin
Clear liquor & not foul smelling
Delivered at 19 40 hrs

BIRTH HISTORY
Birth was SVD, cephalic presentation, episiotomy was indicated for
big baby
Birth wt :3.100 kg
Didn’t cry at birth
Apgar score at 1 min – 2/10 & at 5 min – 5/10
Experienced a fit 1 hr after birth characterised by fisting

Summary
Presented a 3 days old neonate born at 43
wks by SVD birth wt of 3.100 kg with a hx
of not crying at birth & a fit one hr after birth
characterised by fisting with a prolonged
labour & episiotomy for big baby. No hx of
maternal illness or DM.
Immediate Management
Place under a radiant heater to prevent
hypothemia
Dry the infant
Position head down & extended, clear the
air by suctioning & gentle tactile stimulation
eg. Rubbing the back
Assess & monitor infant colour, resp effort,
heart rate

Follow Up Management
Severe asphyxia may depress myocardial
function causing cardiogenic shock despite
recovery of heart & respiratory rate
Dopamine or Dobutamine administered as
continuous IV infusion (5 – 20
micrograms/kg/min) by umbilical cord
cannulation
Volume expanders (Normal saline, Ringers
lactate or whole blood) to improve cardiac
output in a poorly perfused infant
Restoration of oxygenation is the main
treatment for birth asphyxia associated
metabolic acidosis
Examination
Patient was in incubator so exam was by
inspection only
Flexed position looking pink & well perfused
No RD :no nasal flaring or subcostal
recession & no rash
No jaundice
Umbilical stump was dry
HC appeared correct for age, eyes open &
moving in response to sound
Patient had passed urine in first 24 hours

INTRODUCTION BIRTH ASPHYXIA

Birth asphyxia is a clinical syndrome resulting


from intrapartum oxygen deprivation i.e a
hypoxic – ischaemic insult producing lack of
perfusion to various
HIE is an acquired syndrome characterized by
clinical and laboratory evidence of acute brain
injury due to asphyxia (ie, hypoxia, acidosis).
Pathophysiology: Brain hypoxia and ischemia
from systemic hypoxemia and reduced cerebral
blood flow (CBF) are the primary triggering
events for HIE. In this regard, HIE is similar to
stroke syndromes in adults, except that in
neonates, the pathology is more generalized
and the causes are different. Initial
compensatory adjustments, which include
hypoxia (drop in partial pressure of oxygen
[PO2]) and hypercapnia (increased partial
pressure of carbon dioxide [PCO2]), are
important and powerful stimuli, increasing CBF
and thus oxygen delivery. During the early
phase of shock, the cardiac output is
redistributed and the systemic BP increases
(due to increased epinephrine release) to
maintain CBF.
Cerebral autoregulation of CBF maintains brain
perfusion (for awhile) in spite of an initial drop in
the mean BP. In experimental animals, CBF
autoregulation has been shown to be intact in
hypotension. However, the range of BP within
which CBF is maintained is unknown for human
infants. This range is likely to be narrower and
set at lower limits than the adult range (ie, 60-
100 mm Hg).
With prolonged asphyxia, the early
compensatory adjustments fail; CBF may
become "pressure-passive," at which time brain
perfusion is dependent on systemic BP. As BP
falls, CBF falls below critical levels and brain
hypoxia occurs. This results in intracellular
energy failure. During the early phases of brain
injury, brain temperature drops and local
release of the neurotransmitter GABA
increases; these changes reduce cerebral
oxygen demand, transiently minimizing the
impact of asphyxia.
At the cellular level, neuronal injury in HIE is an
evolving process. The magnitude of final
neuronal damage depends, first, on the extent
of the initial insult. The nature, severity, and
duration of the primary injury are extremely
critical in determining the extent of ultimate
residual damage. Following the initial phase of
energy failure from the asphyxial injury,
cerebral metabolism may recover, only to
deteriorate in the second phase.
Reperfusion injury is a second determinant of
the extent of brain damage. By 6-24 hours after
the initial injury, a new phase of neuronal
destruction sets in, characterized by apoptosis
(ie, programmed cell death). Also known as
"delayed injury," this phase may continue for
days to weeks. The severity of brain injury in
this phase correlates well with the severity of
long-term adverse neurodevelopmental
outcome in infants. Modern treatment
interventions are geared to reducing the
neuronal destruction that occurs during this
phase of HIE. Local and systemic factors such
as intrauterine growth retardation (IUGR),
preexisting brain pathology, or developmental
defects noted below (ie, low Apgar scores,
frank neurologic deficits) increase the
magnitude of neuronal damage.

A large cascade of biochemical events follow


HIE injury. Both hypoxia and ischemia increase
the release of excitatory amino acids (EAAs
[glutamate and aspartate]) in the cerebral
cortex and basal ganglia. EAAs begin causing
neuronal death immediately through the
activation of receptor subtypes such as kainate,
N-methyl-D-aspartate (NMDA), and amino-3-
hydroxy-5-methyl-4 isoxazole propionate
(AMPA). Activation of receptors with associated
ion channels (eg, NMDA) leads to cell death
due to increased intracellular concentration of
calcium. A second important mechanism for the
destruction of ion pumps is the lipid
peroxidation of cell membranes, in which
enzyme systems, such as the Na+/K+-ATPase,
reside. This leads to influx into the cell water,
cell swelling, and death. EAAs also increase
the local release of nitric oxide (NO), which may
exacerbate neuronal damage, although its
mechanisms are unclear.
It is quite possible that EAAs disrupt factors that
normally control apoptosis, increasing the pace
and extent of programmed cell death. The
regional differences in severity of injury may be
explained by the fact that EAAs particularly
affect the CA1 regions of the hippocampus, the
developing oligodendroglia, and the subplate
neurons along the borders of the periventricular
region in the developing brain. This may be the
basis for the disruption of long-term learning
and memory faculties in infants with HIE.

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