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:
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
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.
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