Timing brain damage in birth injury cases

05-2006-29

By Zev Gershon and Wayne Willoughby

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 



Generally speaking, HIE cases fall into two categories: those involving near-total asphyxia and those involving partial prolonged asphyxia during labor and delivery. Near-total asphyxia occurs suddenly after events such as a cord prolapse, uterine rupture, or acute placental abruption. Partial prolonged asphyxia occurs over a period of time and can be due to such events as a partial umbilical cord occlusion. 

Blood gas test results and radiological films can help determine whether the injury occurred around the time of birth, but fetal heart tracings are the key to identifying more precisely when the injury occurred. Brain damage due to near-total asphyxia is relatively easy to time to the 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 condition called bradycardia.2 

But even with partial prolonged asphyxia, 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 “nonreassuring” 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 accelerations in the fetal heart rate following contractions are more important in determining 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. 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 nonreassuring tracings. One study concluded that an obstetrician has up to 18 minutes after an acute sudden insult to deliver a baby to prevent possible 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 withNeonatal Encephalopathy 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:

• 
  an umbilical cord arterial blood pH less than 7 with a “base deficit” greater than or equal to 12 mmol/L (millimoles/liter)8

• 
   


• 
  an early onset of encephalopathy


• 
  cerebral palsy of the spastic quadriplegic or dyskinetic type


• 
  exclusion of other etiologies

In the majority of HIE cases we have reviewed, the medical records reflect an early onset of encephalopathy, spastic quadriplegia, and the exclusion of other etiologies for the brain damage. As a result, our planned response to an anticipated NEACP defense usually centers on the umbilical cord blood gas analysis. 

When the laboratory report reflects that NEACP cord blood gas criteria are met, a health care provider will find it hard to defend the case on causation. If the laboratory results do not meet the criteria, the plaintiff must be prepared to explain why the jury should reject the laboratory report or reject the NEACP standard. 

Over the years, we have seen cases in which health care providers mishandled or mislabeled blood samples, resulting in unreliable blood cord gas results. In one case, the doctor drew blood from the placenta and improperly labeled it as umbilical cord blood. Direct evidence of such errors provides a ready explanation for why the NEACP criteria weren’t met. 

Even if there is no direct evidence of sampling error or lab error, there may be circumstantial evidence that the reported test results are unreliable and that an accurate reading of the cord blood gases would have met the NEACP criteria. 

For example, we have handled cases in which the fetus was in distress for a significant time before birth, but the umbilical cord blood pH at birth did not meet the NEACP criteria. Nevertheless, the initial arterial blood gases taken some period of time after birth were abnormally low even though the baby had undergone vigorous neonatal resuscitation and shown some improvement in his clinical condition. In other words, the blood gases taken 30 or 45 minutes after delivery were worse than those taken at birth—the opposite of the result one would expect when there was a significant period of distress before birth and proper resuscitation and clinical improvement after birth. 

Under these circumstances, neonatology experts opined that the reported umbilical cord blood gas results were probably wrong, and an accurate measurement would have met the NEACP criteria. These experts cite studies showing that arterial pH will fall about .04 units per minute in the presence of total asphyxia—in other words, it takes 10 minutes for a pH of 7.4 to fall to 7.9 

Even if an infant’s umbilical pH is 7 or above, he or she may still suffer HIE.10 Acidosis in the tissues due to lack of oxygen does not necessarily result in acidemia reflected by a low blood pH, especially when heart rate circulation is decreased.11 The decrease in heart rate circulation will be reflected in the fetal monitor strips. Therefore, even if the umbilical cord pH is 7 or above, if the fetal heart tracings reflect decreased heart rate circulation, you may still be able to time the injury to the labor and delivery period. 

If the umbilical cord blood pH is 7 or above but the base deficit meets the NEACP criterion—it is greater than or equal to 12 mmol/L—then a study by Michael Ross may be useful in proving causation. Ross concluded that “base excess values have a significantly greater usefulness than umbilical cord pH values” for timing HIE to labor and delivery.12 

Ross found that fetal stress (for example, repetitive, severe variable decelerations) may reduce the buffer base by about 1 mmol/L every 30 minutes; subacute fetal compromise may reduce the buffer base by 1 mmol/L every 6 to 15 minutes; and acute, severe compromise (for example, terminal bradycardia) may reduce the buffer base by as much as 1mmol/L every 2 to 3 minutes.13 

So even if the pH does not meet the NEACP criterion, a neonatologist or pediatric neurologist may be able to opine to reasonable medical certainty or probability when HIE began by applying the Ross algorithm to the reported base-deficit level and referring to an obstetrician’s opinion about the timing and nature of the fetus’s bradycardia. You can provide evidence of causation by showing that the injury is tagged to a point in time after which delivery should have occurred under the standard of care. 



Radiological studies 



Generally speaking, a child who has had a devastating hypoxic insult during labor and delivery initially will have a normal brain scan because the abnormality will not appear on the scan taken right after the injury. Also, the child will initially have a normal head circumference, but during the weeks and months following birth, the head fails to expand normally, and the child becomes microcephalic due to abnormal brain growth caused by the hypoxic insult. 

While no single brain scan can time injury to the exact minute or hour, a group of brain studies can be used to show whether the injury occurred before, during, or after birth. If the injury occurred before birth, one would expect to find advanced abnormalities on brain scans (and possibly an abnormally small head circumference at birth, depending on how long before delivery the injury occurred). Brain scans of babies who have suffered HIE near the time of birth usually reflect—at most—cerebral edema (brain swelling) to indicate an injury has occurred. 

Whether dealing with acute near-total or partial prolonged asphyxia, the defense will probably try to use an ultrasound, CT scan, or MRI of the brain taken during the child’s first day of life to undermine causation. Some defense-oriented medical witnesses rigidly claim that it takes at least 24 hours after an HIE event for any anomaly to appear on a brain study. They say that if a sonogram of the brain performed at 12 hours of life shows some brain swelling, then the brain injury must have occurred at least 24 hours before the study was taken (12 hours before birth). Such testimony can be a substantial hurdle to overcome. 

However, several studies have found that cerebral edema may appear within 24 hours after the injury occurred.14 Before using this literature, it is wise to have the defense medical witness clearly state—on the record—that cerebral edema will never show up on a brain scan within 24 hours of a birth-related brain injury. Otherwise, the defense witness will use the fallback position that that some edema may show up in less than 24 hours, just not the amount of edema shown on the brain scan in your case. 

Sometimes defense-oriented witnesses in the “no edema in 24 hours” camp will point to a “slit-like” appearance of the infant’s brain ventricles on the initial sonogram as evidence of edema (and thus an injury occurring 24 hours earlier). Although cerebral edema after an acute insult may compress the ventricles of a newborn’s brain and create the slit-like appearance, or even obliterate the ventricles altogether, one study reflects that slit-like ventricles occur in 62 percent of newborns with no cerebral edema.15 So if the only abnormal finding on the initial sonogram of the brain is slit-like ventricles, you can argue that the defense cannot use this finding to time the injury. 

The defense may also look to radiological studies for signs of periventricular leukomalacia (PVL), a condition marked by damage surrounding the brain ventricles, to support the assertion that the baby’s injuries are unrelated to HIE. PVL is usually described as an injury of prematurity, because many premature babies have the condition. Therefore, when a term baby has both HIE and PVL, defense witnesses will point to the PVL to claim that the injuries had to be unrelated to birth. 

Yet the renowned pediatric neurologist and author Joseph Volpe reports that PVL has been found in one-third to one-half of term infants who have suffered oxygen deprivation during labor and delivery.16 So the presence of PVL does not necessarily push the time of injury back from the perinatal period to the prenatal period. 



Nucleated red blood cells 



The issue of nucleated red blood cells (NRBCs) comes up in about half of the depositions we take. An NRBC is an immature red blood cell manufactured in the bone marrow. Some defense experts still try to time birth injuries based on the rise and fall of NRBCs, usually by claiming that insufficient time elapsed between labor and the newborn’s initial blood studies to account for the number of NRBCs found in the studies. Such experts can be confronted with the medical literature and even the NEACP. 

The NEACP reports that the data on the question of NRBCs is conflicting and that “The clinical utility of these measurements to determine the timing of neurologic injury should be considered investigational.”17 Other authors have written that NRBCs are unrelated to brain injury.18 Moreover, there is literature reporting quick rises in NRBC count shortly after an acute stress to the fetus—for example, in less than 1 1/2 hours after the insult.19 

Be careful, though, not to equate a rise in the NRBC count with the beginning of brain damage. While it is clear that asphyxia may cause elevated counts, it is also clear that not all asphyxia leads to brain injury. 



Seizures



In the past, defense medical witnesses often timed brain damage to the occurrence of the infant’s first seizure. This defense does not come up often now, but as with other fashion trends, it might resurface. 

Volpe reports that after an acute birth-related HIE event, seizures can be expected to occur by 6 to 12 hours after birth in 50 percent to 60 percent of the cases, and by 12 to 24 hours after birth in 15 percent to 20 percent of the cases.20 We emphasize the word “by” to stress the importance of reading the medical literature carefully. 

One well-credentialed defense pediatric neurologist we know has consistently testified that after an acute HIE event, it took 6 to 12 hours for seizures to occur, claiming Volpe as the basis for his opinion. So if a baby seized at two hours of age, this neurologist would testify that the injury must have occurred at least four hours before delivery. Not only did this expert misquote Volpe, he ignored literature that specifically says birth injury cannot be timed by reference to the onset of neonatal seizures.21 

Occasionally, a defense expert cites EEG tracings (showing what appears to be a more developed and chronic pattern of brain damage than an acute process) taken after birth to support an opinion that an injury occurred long before birth. Generally, it may be true that if a certain pattern persists, it may represent a chronic injury, whereas a worsening or improving pattern may represent a more acute phenomenon.22 Yet, the studies we are aware of attempt to time injuries by EEG tracings only in premature infants23; in the term baby, these studies are of questionable relevance. 



Meconium 



The defense may produce experts who will show that the baby or the placenta was stained with meconium, the infant’s first feces while still in the womb. Meconium in the amniotic fluid is a sign that the baby was under stress during labor and birth. 

Even if it can be shown that the meconium was produced many hours before birth, this does not necessarily rule out a birth-related brain injury. Fetal stress of a degree sufficient to produce meconium usually is not sufficient to produce brain damage. Nonetheless, if you have to fight the battle of timing by meconium staining, one reference is Benirschke’s placental pathology textbook that reports that staining of the outer amnion of the placenta can occur in an hour, the deeper chorion layer of the placenta within three hours, and the infant’s fingernails in four to six hours.24 Thus, the soft skin of a baby takes between one and four hours to stain. 

The attorney who investigates a claim on behalf of a child who suffered catastrophic injury at birth due to medical negligence faces many challenges. The battle will be fought on all fronts—standard of care, causation, injury, and damages—and at great expense. This is not a challenge that every attorney should take on, but for those willing and able to study the medical literature and give their client’s cause full effort, there is no greater satisfaction than pursuing justice for a child. 



Zev T. Gershon, a physician and lawyer, and Wayne M. Willoughby are partners in Gershon, Willoughby, Getz & Smith in Owings Mills, Maryland. © 2006, Zev T. Gershon and Wayne M. Willoughby.



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Notes

• 
  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).

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