When the parents of a child diagnosed with brain damage in the first year of life come to your office for help, the first question is usually whether the damage could have been prevented. If it was caused by an injury during the perinatal period (around the time of birth) and could have been avoided with a timely delivery—for example, if the health care providers had reacted to worrisome fetal heart rate tracings—your prospective clients could have a viable medical negligence claim.

Birth-related brain damage can be caused by hypoxia and ischemia—decreased oxygen and blood flow to the infant’s brain. Defense experts often claim that this kind of brain damage—known as hypoxic ischemic encephalopathy (HIE)—is the result of unknown factors occurring during pregnancy. But the authors of a 2003 article published in the British medical journal The Lancet reported that “more than 90 percent of term infants with neonatal encephalopathy, seizures, or both, but without specific syndromes or major congenital defects, had evidence of perinatally acquired insults, and there was a very low rate of established brain injury acquired before birth.”1 In lay terms, this means that if a newborn suffers brain damage, it was probably caused by something that occurred near the time of birth.

• Fetal heart rate tracings
• Blood acid levels
• Radiological studies
• Nucleated red blood cells
• Seizures
• Meconium

• Frances Cowan et al., Origin and Timing of Brain Lesions in Term Infants with Neonatal Encephalopathy, 361 LANCET 736, 740 (2003).
• F. GARY CUNNINGHAM ET AL., WILLIAMS OBSTETRICS 335 (21st ed. 2001).
• See Jeffrey P. Phelan & Joo Oh Kim, Fetal Heart Rate Observations in the Brain-Damaged Infant, 24 SEMINARS IN PERINATOLOGY 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 uninjured fetus and an injured but nonhypoxic fetus. See Barry S. Schifrin, The CTG and the Timing and Mechanism of Fetal Neurological Injuries, 18 BEST PRACTICE & RES. CLINICAL OBSTETRICS & GYNECOLOGY 437 (2004).
• Anna S. Leung et al., Uterine Rupture After Previous Cesarean Delivery: Maternal and Fetal Consequences, 169 AM. J. OBSTETRICS & GYNECOLOGY 945 (1993).
• That later study looked at 54,867 births between 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).
• Other authors have discussed at length the shortcomings of the NEACP; therefore, this article confronts the NEACP only on the issue of umbilical cord blood gas. See generally Dov Apfel, Keep Junk Science Out of Cerebral Palsy Cases, TRIAL, May 2004, at 46.
• A “base deficit” occurs when bicarbonate (HCO3) concentration decreases to below normal. HCO3 levels decrease as the body uses bicarbonate to buffer organic acid in an attempt to maintain a normal pH level. CUNNINGHAM ET AL., supra note 2, at 390-91.
• See, e.g., Ronald E. Myers, Two Patterns of Perinatal Brain Damage and Their Conditions of Occurrence, 112 AM. J. OBSTETRICS & GYNECOLOGY 246 (1972).
• See, e.g., Robert C. Goodlin, Do Concepts of Causes and Prevention of Cerebral Palsy Require Revision?, 172 AM. J. OBSTETRICS & GYNECOLOGY 1830 (1995); T. Murphy Goodwin, Clinical Implications of Perinatal Depression, 26 OBSTETRICS & GYNECOLOGY CLINICS N. AM. 711 (1999).
• See Marcus C. Hermansen, The Acidosis Paradox: Asphyxial Brain Injury Without Coincident Acidemia, 45 DEVELOPMENTAL MED. & CHILD NEUROLOGY 353 (2003); Jeffrey P. Phelan et al., Birth Asphyxia & Cerebral Palsy, 32 CLINICS PERINATOLOGY 61, 64 (2005); Schifrin, supra note 3.
• Michael G. Ross & Rageev Gala, Use of Umbilical Artery Base Excess: Algorithm for the Timing of Hypoxic Injury, 187 AM. J. OBSTETRICS & GYNECOLOGY 1 (2002).
• Id. at 8.
• See PAUL GOVAERT & LINDA S. DE VRIES, AN ATLAS OF NEONATAL BRAIN SONOGRAPHY 241 (1997) (cerebral edema can occur “in the first hours of life”); PEDIATRIC NEURORADIOLOGY 251 (William S. Ball Jr. ed., 1997) (cerebral edema can occur “as early as the first day”); Alastair MacLennan, A Template for Defining a Causal Relation Between Acute Intrapartum Events and Cerebral Palsy: International Consensus Statement, 319 BRIT. MED. J. 1054, 1058 (1999) (cerebral edema can occur “within 6-12 hours”); N.K. Anand et al., Neurosonographic Abnormalities in Neonates with Hypoxic Ischemic Encephalopathy, 31 INDIAN PEDIATRICS 767, 769, 772 (1994) (cerebral edema can be found on “day one of life”); A. James Barkovich, MR and CT Evaluation of Profound Neonatal and Infantile Asphyxia, 13 AM. J. NEURORADIOLOGY 959 (1992) (cerebral edema can be found “less than 24 hours after injury”).
• Marilyn J. Siegel et al., Hypoxic-Ischemic Encephalopathy in Term Infants: Diagnosis and Prognosis Evaluated by Ultrasound, 152 RADIOLOGY 395 (1984).
• JOSEPH J. VOLPE, NEUROLOGY OF THE NEWBORN 349, 353 (4th ed. 2001). See also Goodlin, supra note 10, at 1836.
• AM. C. OBSTETRICIANS & GYNECOLOGISTS & AM. ACAD. PEDIATRICS, NEONATAL ENCEPHALOPATHY AND CEREBRAL PALSY: DEFINING THE PATHOGENESIS AND PATHOPHYSIOLOGY 59 (2003).
• See, e.g., Shannon E.G. Hamrick et al., Nucleated Red Blood Cell Counts: Not Associated with Brain Injury or Outcome, 29 PEDIATRIC NEUROLOGY 278 (2003).
• See, e.g., Kurt Benirschke, Placenta Pathology Questions to the Perinatologist, 14 J. PERINATOLOGY 371, 374 (1994).
• VOLPE, supra note 16, at 333-34.
• See, e.g., Myoung Ock Ahn et al., Does the Onset of Neonatal Seizures Correlate with the Timing of Fetal Neurological Injury?, 37 CLINICAL PEDIATRICS 673 (1998).
• DAVID K. STEVENSON & PHILIP SUNSHINE, FETAL AND NEONATAL BRAIN INJURY 181 (1989).
• See, e.g., Kazuyoshi Watanabe et al., Neonatal EEG: A Powerful Tool in the Assessment of Brain Damage in Preterm Infants, 21 BRAIN & DEVELOPMENT 361 (1999).
• KURT BENIRSCHKE & PHILIP KAUFMANN, PATHOLOGY OF THE HUMAN PLACENTA 295 (3d ed.1995).