Download Post-Placental Hypoxia

INTRAUTERINE HYPOXIA
LABARAN KAMAL UMAR(MED)
10/05/2016
WHAT IS INTRAUTERINE HYPOXIA?
Intrauterine hypoxia occurs when the foetus is deprived of an
adequate supply of oxygen. It may be due to a variety of reasons
such as prolapse or occlusion of the umbilical cord, placental
infarction and maternal smoking. Intrauterine growth restriction
(IUGR) may cause or be the result of hypoxia. Intrauterine hypoxia
can cause cellular damage that occurs within the central nervous
system (the brain and spinal cord). This results in an increased
mortality rate, including an increased risk of sudden infant death
syndrome (SIDS). Oxygen deprivation in the foetus and neonate have
been implicated as either a primary or as a contributing risk factor in
numerous neurological and neuropsychiatric disorders such as
epilepsy, ADHD, eating disorders and cerebral palsy
CAUSES
Intrauterine hypoxia is associated with a variety of maternal,
placental, and foetal conditions which may manifest differently and
have different outcomes. Kingdom and Kaufmann [29] suggested to
classify hypoxic pregnancy conditions into 3 subtypes: (1)
preplacental hypoxia, where both the mother and her foetus will be
hypoxic (i.e., high-altitude, cyanotic maternal heart disease; etc.); (2)
uteroplacental hypoxia, where the maternal oxygenation is normal but
the utero-placental circulation is impaired (i.e., preeclampsia,
placental insufficiency, etc.); (3) post placental hypoxia, where only
the foetus is hypoxic. We will focus on the first 2 subtypes as the postplacental hypoxia is mainly related to foetal diseases rather than to
the direct impact of hypoxia onto the foetus.
Pre-Placental Hypoxia
Main causes of pre-placental hypoxia are a hypoxic environment
(high-altitude) and pre-existing maternal cardiovascular disease
such as cyanotic heart disease, heart failure, or pulmonary
hypertension. Maternal anaemia, infections, and chronic
inflammation may further limit the maternal oxygen uptake and
oxygen delivery to the foetus, thereby increasing the risk for
adverse pregnancy outcomes
Utero-Placental Hypoxia
Utero-placental hypoxia is related to abnormal placentation early in
gestation and to placental vascular disease later in pregnancy.
Abnormal placental implantation is a common finding in pregnancies
complicated by IUGR, by gestational hypertension, and by preeclampsia. There exists an increased risk for both the mother and the
foetus to develop cardiovascular disease later in life.
Post-Placental Hypoxia
In post-placental hypoxia, only the foetus becomes
hypoxic which is either related to diminished uterine
artery flow (i.e., mechanical compression, rupture, and
thrombotic occlusion), progressive foetal cardiac failure
(i.e., complete congenital heart block, complex
congenital heart malformations), or due to important
genetic anomalies. As mentioned earlier, we will not
further explore the post-placental hypoxia as it is
mainly related to foetal diseases rather than to the
impact of hypoxia onto the foetus
Effects of Hypoxia on the Foetus
A main consequence of chronic hypoxia is the failure of the foetus
to achieve its genetically determined growth potential. About 10%
of all babies grow poorly inutero and are born small for
gestational age. IUGR is associated with distress and asphyxia
and a 6- to 10-fold increased perinatal mortality . Frequent
hypoxia-mediated complications include meconium aspiration,
metabolic and hematologic disturbances, cognitive dysfunction,
and cerebral palsy. Acute and chronic hypoxia is also associated
with a variety of morphological and functional foetal cardiac
changes that aim either to compensate for the reduced
oxygenation of vital organs or are the result of hypoxia-mediated
foetal tissue damage
Fetal hypoxia is not a disease per se; it is a set of
pathological processes that take place within the
womb, causing the fetus to be seriously deprived of
oxygen for a period of time and causing resultant
damages and impairments. Organ activity and
metabolic processes become disordered and
congenital abnormalities may develop. Damages to
the central nervous system, including the brain and
breathing disorders are common, leading to
conditions such as hypoxic-ischemic encephalopathy,
cerebral palsy, ADHD, epilepsy, and numerous
neurological and neuropsychiatric conditions. The
mortality rate is high in many instances, and though
the child may survive birth, the risk for sudden infant
death syndrome (SIDS) is high.
CLINICAL FEATURES












poor muscle tone
Transient feeding
Crying and sleep abnormalities
Neurological findings only become close to normal after three to
four days after birth. Moderate levels of the disease produce a
lethargic infant, with nearly absent deep tendon reflexes
Sleep apnea and seizures occurring within 24 hours after birth.
Severe levels of this cellular, neurological disease are typically of
stupor or coma, no response to physical stimulus
Irregular breathing
Vision abnormalities
Seizures and no sucking ability.
The risks for severe forms are of irregular heartbeat,
blood pressure variability,
and cardiovascular failure.




TREATMENT
Initial treatments for foetal hypoxia infants are immediate
submersion of the birthed infant into hypothermic therapies to
increase the chances for survival.
Electrolytes are often severely low and require immediate
suffusions of sodium, potassium, and chloride as well as
treatments for severely reduced urinary output.
The infants usually need resuscitation and stabilization, careful
fluid management, supportive ventilation treatments, and
anticonvulsants for seizures.
Hypoglycaemia and hyperglycaemia are a risk and appropriate
treatments are usually begun immediately to get good nutrition to
the infant.