| Gorovitz & Borten, P.C. Attorneys at Law 400-1 Totten Pond Road Waltham, Massachusetts 02451 Tel: (781) 890-9095 |
| Fetal Asphyxia |
The placenta is the site of transfer of oxygen and carbon dioxide between the
mother and the fetus. The fetus depends on the adequacy of maternal
circulation for the delivery of oxygen and removal of carbon dioxide. Respiratory
changes during pregnancy facilitates the diffusion of oxygen from mother to
fetus and carbon dioxide from fetus to mother. Nonetheless, while a fetus has
adaptive mechanisms to grow in a low oxygen environment, a critical drop in
placental circulation critically reduces the availability of oxygen and produces an
accumulation of waste products, mainly carbon dioxide.
Under normal circumstances, fetal metabolism in an oxygen adequate
environment is called 'aerobic metabolism'. In the absence of adequate levels of
oxygen, the fetus continues to metabolize by a process called 'anaerobic
metabolism'. Anaerobic metabolism can be sustained only for a limited amount
of time. Accumulation of hydrogen causes a drop in pH to dangerous levels.
Normal pH levels in adults range from 7.35 to 7.45 and mean umbilical pH in
newborns ranges from 7.25 to 7.35.
Normally, uterine contractions produce a transient decrease in blood flow to the
placenta. Adequate relaxation of the uterus between uterine contractions
enables blood flow to recover with full fetal recovery from the temporary drop in
oxygen. A prolonged uterine contraction (tetanic contraction) or multiple uterine
contractions with insufficient uterine relaxation between them causes a
prolonged drop in oxygen (hypoxemia) and an increase in carbon dioxide
(hypercapnia) in the fetal blood.
Fetuses have adaptive mechanisms to deal with decreased levels of oxygen
(hypoxia). They include:
The effectiveness of these compensatory mechanisms depends on the duration,
frequency and intensity of the hypoxia and the health of the placental function.
A compromised placenta will not allow recovery compensation to take place
resulting in prolonged fetal hypoxia (asphyxia).
Intrapartum surveillance for fetal hypoxia include:
Asphyxia is the result of an impairment in the placental gas exchange that
produces significant changes in the fetal pH. Prolonged fetal asphyxia creates a
hostile environment to various vital organs. When the fetal heart is affected, a
decrease in cardiac output leads to fetal hypotension and further decrease in
fetal circulation and blood flow to the heart and the brain. Prolonged and/or
sustained hypoxemia results in decreased oxygen levels in the tissues (hypoxia)
that leads to fetal asphyxia.
Fetal asphyxia or intrauterine asphyxia is a common cause of long-term
neurologic dysfunction. Prolonged and uncorrected fetal asphyxia leads to
progressive cellular and tissue damage resulting in organ failure and ultimately
fetal death in-utero or severe disabilities if the fetus is born alive. Damage to the
fetal brain depends on the severity and duration of hypoxemia.
Severe degrees of fetal asphyxia resulting from decreased cerebral perfusion is
called 'Hypoxic-Ischemic Encephalopathy'. Uncorrected Hypoxic-Ischemic
Encephalopathy can cause 'Neonatal Encephalopathy' which is a syndrome
defined by disturbed neurologic function after birth. This syndrome includes:
Long term morbidity associated with Hypoxic-Ischemic Encephalopathy includes
permanent neurologic damage such as cerebral palsy. Cerebral palsy is the
abnormal control of movement and posture as a result of abnormal development
or damage to the area of the brain that controls movement and posture.
If the child's injury was the result of intrauterine fetal hypoxia (asphyxia), it was
diagnosable, avoidable, preventable and treatable. The injury may be the result
of a medical provider's mistake in handling an obstetrical condition. Your child
and you as parents of the child are entitled to receive compensation. If your
child's condition was the result of medical negligence, allow Dr. Borten and the
Boston area medical malpractice attorneys at Gorovitz & Borten help you assert
your rights and get the compensation you deserve.
mother and the fetus. The fetus depends on the adequacy of maternal
circulation for the delivery of oxygen and removal of carbon dioxide. Respiratory
changes during pregnancy facilitates the diffusion of oxygen from mother to
fetus and carbon dioxide from fetus to mother. Nonetheless, while a fetus has
adaptive mechanisms to grow in a low oxygen environment, a critical drop in
placental circulation critically reduces the availability of oxygen and produces an
accumulation of waste products, mainly carbon dioxide.
Under normal circumstances, fetal metabolism in an oxygen adequate
environment is called 'aerobic metabolism'. In the absence of adequate levels of
oxygen, the fetus continues to metabolize by a process called 'anaerobic
metabolism'. Anaerobic metabolism can be sustained only for a limited amount
of time. Accumulation of hydrogen causes a drop in pH to dangerous levels.
Normal pH levels in adults range from 7.35 to 7.45 and mean umbilical pH in
newborns ranges from 7.25 to 7.35.
Normally, uterine contractions produce a transient decrease in blood flow to the
placenta. Adequate relaxation of the uterus between uterine contractions
enables blood flow to recover with full fetal recovery from the temporary drop in
oxygen. A prolonged uterine contraction (tetanic contraction) or multiple uterine
contractions with insufficient uterine relaxation between them causes a
prolonged drop in oxygen (hypoxemia) and an increase in carbon dioxide
(hypercapnia) in the fetal blood.
Fetuses have adaptive mechanisms to deal with decreased levels of oxygen
(hypoxia). They include:
- Decrease in heart rate
- Reduction in oxygen consumption
- Redistribution of circulation to vital organs (heart, brain)
- Increased anaerobic metabolism
The effectiveness of these compensatory mechanisms depends on the duration,
frequency and intensity of the hypoxia and the health of the placental function.
A compromised placenta will not allow recovery compensation to take place
resulting in prolonged fetal hypoxia (asphyxia).
Intrapartum surveillance for fetal hypoxia include:
- Electronic fetal monitoring
- Fetal scalp blood sampling
- Fetal scalp stimulation
- Vibroacoustic stimulation
- Fetal pulse oxymetry
Asphyxia is the result of an impairment in the placental gas exchange that
produces significant changes in the fetal pH. Prolonged fetal asphyxia creates a
hostile environment to various vital organs. When the fetal heart is affected, a
decrease in cardiac output leads to fetal hypotension and further decrease in
fetal circulation and blood flow to the heart and the brain. Prolonged and/or
sustained hypoxemia results in decreased oxygen levels in the tissues (hypoxia)
that leads to fetal asphyxia.
Fetal asphyxia or intrauterine asphyxia is a common cause of long-term
neurologic dysfunction. Prolonged and uncorrected fetal asphyxia leads to
progressive cellular and tissue damage resulting in organ failure and ultimately
fetal death in-utero or severe disabilities if the fetus is born alive. Damage to the
fetal brain depends on the severity and duration of hypoxemia.
Severe degrees of fetal asphyxia resulting from decreased cerebral perfusion is
called 'Hypoxic-Ischemic Encephalopathy'. Uncorrected Hypoxic-Ischemic
Encephalopathy can cause 'Neonatal Encephalopathy' which is a syndrome
defined by disturbed neurologic function after birth. This syndrome includes:
- Difficulty in initiating respirations
- Difficulty in maintaining respirations
- Depression of muscle tone
- Depression of reflexes
- Poor or absent Moro's reflex
- Subnormal level of consciousness
- Abnormal cry and suck
- Stupor that develops within 72 hours after birth
- Seizures (quite often within the first days of life)
Long term morbidity associated with Hypoxic-Ischemic Encephalopathy includes
permanent neurologic damage such as cerebral palsy. Cerebral palsy is the
abnormal control of movement and posture as a result of abnormal development
or damage to the area of the brain that controls movement and posture.
If the child's injury was the result of intrauterine fetal hypoxia (asphyxia), it was
diagnosable, avoidable, preventable and treatable. The injury may be the result
of a medical provider's mistake in handling an obstetrical condition. Your child
and you as parents of the child are entitled to receive compensation. If your
child's condition was the result of medical negligence, allow Dr. Borten and the
Boston area medical malpractice attorneys at Gorovitz & Borten help you assert
your rights and get the compensation you deserve.
Contact Information
For a free confidential consultation and receive a response within 24 hours
(when possible), please contact us by phone, fax or e-mail with your question or
concern.
Telephone: 781-890-9095 - Fax: 781-890-9098
Directions
Electronic mail:
Questions or Inquiries to: inquiry@gbmedlaw.com
For a free confidential consultation and receive a response within 24 hours
(when possible), please contact us by phone, fax or e-mail with your question or
concern.
Telephone: 781-890-9095 - Fax: 781-890-9098
Directions
Electronic mail:
Questions or Inquiries to: inquiry@gbmedlaw.com
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Borten, P.C. for informational purposes only and are not intended, and should not be
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