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Timing Brain Damage (Continued from page 8)


labor and delivery period if tracings from the fetal heart monitor show there was a sudden deceleration of the heart rate to less than 110 beats per minute, a condi- tion called bradycardia.2 But even with partial prolonged as-


phyxia, you and your expert can look for telltale signs in the tracings that show injury was imminent—for example, when the tracing initially is reassuring and then becomes “non-reassuring” and gets progressively worse. In interpreting heart tracings, some


experts believe that decreased variability of the fetal heart rate is paramount, while others believe that decreased (or increased) baseline and an absence of normal accel- erations in the fetal heart rate following contractions are more important in deter- mining the condition of the fetus.3


The


key to timing injury based on fetal heart rate tracings is an understanding that a fetus has only a finite reserve—a limited time—to withstand a hypoxic condition.


2


F. Gary Cunningham Et Al., WILLIAMS OBSTETRICS 335 (21st ed. 2001).


The injury occurs some period of minutes (the length of which depends on the amount of the fetus’s reserves) after the fetal heart rate deteriorates from a good tracing to a bad one or from a bad tracing to a worse one. The question is how long the fetus can withstand a hypoxic insult before succumbing to brain damage. It makes sense that a fetus with a


perfectly normal (reassuring) heart rate tracing before a sudden deceleration or bradycardia begins will be able to hold up against a hypoxic insult longer than an infant who has a sudden deceleration after a period of non-reassuring tracings. One study concluded that an obstetrician has


3


See Jeffrey P. Phelan & Joo Oh Kim, Fetal Heart Rate Observations in the Brain-Dam- aged Infant, 24 SEMINARS IN PERINA- TOLOGY 221 (2000). Dr. Barry Schifrin, a popular defense expert, believes he can distinguish on a fetal heart rate tracing the difference between a hypoxemic but unin- jured fetus and an injured but nonhypoxic fetus. SeeBarry S. Schifrin, The CTG and the Timing and Mechanism of Fetal Neurological Injuries, 18 BEST PRACTICE & RES. CLINICAL OBSTETRICS & GYNECOL- OGY 437 (2004).


up to 18 minutes after an acute sudden insult to deliver a baby to prevent pos- sible brain damage.4


A more recent study,


however, found that a longer period of hypoxia may be required for brain damage to occur.5 Expect the defense to produce medical


witnesses who will say that use of fetal heart rate tracings has not led to a decrease in the rate of cerebral palsy; therefore, they are meaningless in determining when an infant suffered a brain-damaging injury. These witnesses ignore the fact that if one focuses on the incidence of cerebral palsy as a result of HIE, the rates of cerebral palsy have fallen with the use of fetal heart rate tracings.6


Blood acid levels Any lawyer who handles birth asphyxia


cases should be familiar with Neonatal En- cephalopathy and Cerebral Palsy (NEACP), a monograph published in 2003 by the American College of Obstetricians and Gynecologists (ACOG) in conjunction with the American Academy of Pediatrics (AAP). It will become the basis of your opponent’s causation defense and should be addressed from the outset of your case investigation.7 The NEACP asserts that four “essential”


criteria must be met before birth-related asphyxia can be identified as the cause of cerebral palsy:


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(Continued on page 12) 4


Anna S. Leung et al., Uterine Rupture After Previous Cesarean Delivery: Maternal and Fe- tal Consequences, 169 AM. J. OBSTETRICS & GYNECOLOGY 945 (1993).


5


That later study looked at 54,867 births be- tween 1990 and 1995. Among those births, there were 11 uterine ruptures. Five of those 11 births involved bradycardias lasting more than 18 minutes and up to 37 minutes. One child was lost to follow-up, but none of the others sustained permanent neurological damage. Cydney Afriat Menihan, Uterine Rupture in Women Attempting a Vaginal Birth Following Prior Cesarean Birth, 18 J. PERINATOLOGY 440, 441-42 (1998).


See Julie Smith et al., The Continuing Fall in Incidence of Hypoxic-Ischemic Encephalopathy in Term Infants, 107 BRIT. J. OBSTETRICS & GYNAECOLOGY 461 (2000).


7 Baltimore, MD 410-727-5735 www.etnet.com 10


Washington, D.C. 202-638-0902 Frederick, MD 301-696-1926 Belcamp, MD 410-272-1680


Trial Reporter


Other authors have discussed at length the shortcomings of the NEACP; therefore, this article confronts the NEACP only on the is- sue of umbilical cord blood gas. See generally Dov Apfel, Keep Junk Science Out of Cerebral Palsy Cases, TRIAL, May 2004, at 46.


Summer 2006


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