Trial Magazine

Complexity, confusion, and ambiguity are the “three horsemen of defeat”—powerful weapons used by the defense to defeat plaintiffs’ claims.¹ These insidious enemies are inherent in birth injury cases, which are complex, confusing, and ambiguous by their very nature.

Proving that a medical provider’s negligence caused a newborn baby’s brain injury is always complicated. The defense often argues that events or conditions unrelated to the medical care caused the injury or that the injury occurred outside the time period when the medical providers should have intervened to protect the baby. Since establishing causation is the ultimate “end point” and usually the most complicated part of the case, begin with the end in mind: Determine the location, cause, mechanism, and timing of the injury.

A baby’s brain can be injured in various ways and due to various causes.² One common cause is hypoxic-ischemic injury or hypoxic-ischemic encephalopathy (HIE), which is a clinical diagnosis of damage to the baby’s brain (encephalopathy) due to insufficient oxygen in the blood reaching the baby (hypoxemia), insufficient blood flow reaching the baby (ischemia), or both.³ Asphyxia occurs when the lack of oxygen or blood flow causes significant metabolic acidosis, which then damages brain cells.⁴ Asphyxia can occur during the time period at or near birth and can often be prevented with proper medical care.⁵ It can result in HIE, cerebral palsy, and severe cognitive deficits.⁶

Location and Patterns of Injury

To support causation, it is critically important to identify the location and pattern of injury to the baby’s brain. Neuroimaging studies, such as head ultrasound and MRI, are used to identify the structures of the brain that are injured and the pattern of injury. Pediatric neuroradiologists, who have training and experience in reading neonatal radiology studies and assessing evolving patterns of injury associated with birth asphyxia and HIE, should review radiological studies of the baby’s brain.

The specific imaging studies performed on a baby with suspected hypoxic-ischemic brain injury may vary by patient or hospital institution, but often a head ultrasound is performed within several hours of birth followed by one or more MRI studies within the first few days or weeks after birth. The sequence and timing of the radiological studies can show the evolution of the injury pattern, which can approximate the timing of the injury.

In the neonatal intensive care unit, head ultrasound is often the first imaging study performed on a newborn with “neonatal encephalopathy,” a term for a syndrome of abnormal neurologic function consistent with a brain disorder.⁷ Head ultrasound is available at the bedside and allows for rapid evaluation, usually without sedating the baby. Head ultrasound can detect hemorrhage, brain malformations, and cystic changes in the brain tissue, as well as swelling or edema within 24 to 48 hours of the injury.⁸ It is useful as a screening evaluation for a baby with neonatal encephalopathy to rule out hemorrhage or malformation and to potentially identify edema (swelling) related to hypoxic-ischemic injury. However, it lacks sensitivity to define the full extent of the brain injury, particularly in the first 24 hours after the injury.⁹

MRI is a more accurate imaging modality and provides the best imaging resolution to identify hypoxic-ischemic injury in the newborn brain and other potential causes of neonatal brain injury.¹⁰ Various types of MRI studies are used, including conventional MRI (MR or magnetic resonance ¬parameters) and diffusion-weighted imaging (DWI). A conventional MRI shows edema and abnormalities from HIE within the first three to four days after injury but usually not on the first day after injury. However, DWI detects the movement of water molecules into and out of cellular spaces and can show abnormalities within the first 24 to 48 hours after injury, which helps identify the nature and extent of the injury early on.¹¹

Depending on the specific mechanism that causes HIE, the disruption of blood flow and oxygen can be rapid and severe or slow and progressive. Different mechanisms produce different injury patterns depending on the nature of the hypoxic-ischemic insult, the duration of the insult, and the gestational age of the baby.¹² There are three primary patterns of hypoxic-ischemic brain injury in ¬full-term babies.¹³

Pattern 1: ‘acute profound’ or ‘acute near-total asphyxia.’ Also referred to as the “deep gray matter” pattern, this pattern of injury results from a sudden and severe lack of oxygen that typically happens over approximately 10–25 minutes. Near-total asphyxia lasting more than 25 minutes is associated with significant injury or death.¹⁴ Acute profound asphyxia damages the central gray matter of the brain, including the basal ganglia, the thalami, and often the brain stem; however, there may be associated damage in the white matter.¹⁵

Pattern 2: ‘partial prolonged asphyxia’ or ‘watershed.’ A partial prolonged lack of oxygen is less acute and severe and occurs progressively over a longer time period. Injury from partial prolonged asphyxia can occur within 30 minutes to several hours after birth.¹⁶ Partial prolonged asphyxia causes damage to the white matter of the “watershed” zones around the anterior, middle, and posterior cerebral arteries.¹⁷ The damage may involve the cerebral cortex and the subclinical white matter.

Pattern 3: mixed. The mixed pattern involves a combination of the two patterns above. When there is overlap between the two, the baby may have features of both patterns of injury.

Timing of the Injury

Once you have identified the location, pattern, and evolution of the injury during the first days after birth, use this information to establish the timing of the injury. Acidosis produces cellular changes resulting in edema that generally appears within 24 to 48 hours after the injury, peaks between three to five days after injury, and resolves and normalizes by seven to eight days after injury.¹⁸ The neuroradiological picture of the injury changes over time, which is evidence of the cause and approximate timing of injury.¹⁹

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If an ultrasound performed within the first 24 hours of birth is normal, and a subsequent ultrasound or MRI shows abnormalities, that is radiologic evidence consistent with an injury happening at or near the time of delivery.

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Findings, or the absence of findings, on a head ultrasound can be evidence of the cause and the timing of injury. If an ultrasound performed within the first 24 hours of birth is normal, and a subsequent ultrasound or MRI shows abnormalities, that is radiologic evidence consistent with an injury happening at or near the time of delivery.

Serial or repeat MRI studies can be very helpful to pinpoint when the injury occurred. For example, if an initial MRI performed one or two days after the injury is normal, but a repeat MRI performed six to seven days after the injury shows evidence of edema or hypoxic-ischemic injury, that correlation is evidence that the injury likely occurred at or near the time of delivery because edema resulting from the injury evolves and normalizes over several days after the injury occurred.

Therapeutic hypothermia or “cooling” of the baby after injury is a neuroprotective therapy that has been shown to reduce the severity of HIE. Therapeutic hypothermia appears to decrease the incidence of gray and white matter abnormalities on MRI.²⁰ If the baby was cooled, consult with an experienced pediatric neuroradiologist to determine whether and how cooling may affect the neuroimaging evaluation of the injury.

Identify the Injury Mechanism

Once you have determined the injury pattern and the approximate timing, you must establish that a mechanism (event) that can cause that specific pattern of injury occurred and that the mechanism was preventable. Examine the mother’s and baby’s medical history and records to determine what events happened during the pregnancy, labor, and delivery that could cause the injury. The mechanism of the lack of oxygen must match the pattern of brain injury.

There are three key factors to look for in the medical records in considering the cause and the timing of the lack of oxygen as the cause of the brain injury:

• evidence of fetal distress or risk for lack of oxygen (for example: abnormal fetal heart rate patterns, sentinel events that are known to cause lack of blood flow and oxygen, and acidosis in the blood)
• the need for resuscitation after delivery, low Apgar scores, or both
• abnormal neurologic function in the first hours of life.²¹

The neurological syndrome after signs of asphyxia at or near birth is the single most useful indicator that a significant hypoxic-ischemic injury has occurred.²² This syndrome of abnormal neurologic function includes a depressed level of consciousness, which may range from stupor to coma and respiratory depression to respiratory failure and also result in abnormalities of muscle tone, feeding difficulties, and often seizures. Mechanisms capable of causing “acute profound asphyxia” and injury to the deep gray matter of the brain include conditions that can suddenly and severely disrupt the flow of blood and oxygen to the baby, such as uterine rupture, placental abruption, umbilical cord prolapse, and maternal cardiovascular collapse.²³ Babies who suffer acute profound asphyxia and have predominant deep gray matter injury generally have the worst cognitive and motor outcomes. Consistent with this finding, babies who have severe neonatal encephalopathy are more likely to have deep gray matter injury.²⁴

Mechanisms capable of causing “partial prolonged asphyxia” and injury to the watershed area of the brain include maternal high blood pressure or low blood pressure, preeclampsia, abnormal amniotic fluid levels, problems with placental function, umbilical cord compression, umbilical cord wrapped around the baby’s neck, strong and frequent contractions, and labor abnormalities. Babies who have predominant watershed white matter injury usually have more prominent cognitive deficits than motor deficits.²⁵

Attorneys handling birth injury cases also must be aware of and understand the application and implications of the American College of Obstetricians and Gynecologists’s (ACOG) and the American Academy of Pediatrics’s (AAP) 2014 publication, Neonatal Encephalopathy and Neurologic Outcome (NEANO).²⁶ The publication lists four criteria that are consistent with an acute lack of oxygen at or near delivery:

• an Apgar score of less than five at five minutes and at 10 minutes
• acidemia in the umbilical arterial blood
• neuroimaging evidence of acute brain injury consistent with HIE
• multisystem organ failure.²⁷

The NEANO publication also lists criteria that are indicative of the type and timing of contributing factors that are consistent with an acute lack of oxygen at or near delivery, including:

• a sentinel hypoxic-ischemic event immediately before or during labor and delivery
• fetal heart rate patterns consistent with an acute lack of oxygen
• imaging studies consistent with an acute event
• the lack of evidence of other contributing factors, such abnormal fetal growth, maternal infection¬, neonatal sepsis, chronic placental lesions, or feto-maternal hemorrhage
• spastic quadriplegia or dyskinetic cerebral palsy.²⁸

Many cases of hypoxic-ischemic injury occur at or near delivery when all of these “criteria” are not met, but a medical explanation often exists for why they are not met. Defense witnesses routinely claim that the NEANO criteria must be established to prove that events during labor and delivery caused HIE and resulting cerebral palsy. However, many medical experts and experienced birth injury attorneys disagree that the criteria are mandatory.²⁹

For example, in cases of severe, abrupt disruption of blood flow and oxygen to the baby such as uterine rupture, placental abruption, or umbilical cord prolapse, there may not be time for the baby’s neuroprotective “dive reflex” to shunt blood and oxygen away from nonvital organs to protect vital organs such as the brain and heart. As a result, there can be severe hypoxic-ischemic injury without multisystem organ failure, which NEANO lists as a criterion.³⁰ When screening and developing a case, determine the medical evidence that is needed to show what criteria were and were not met, and be prepared to address the relevancy and application of the criteria to your case.

Was the Injury Preventable?

Once you have identified the mechanism of the hypoxic-ischemic injury, determine whether the injury could have and should have been prevented with proper care. Research the standards of care applicable to doctors, nurses, and hospitals involved in the care and identify any violations. Sources for information about standards of care include publications of the American College of Obstetricians and Gynecologists; the Association of Women’s Health, Obstetric and Neonatal Nurses; the American Academy of Pediatrics; and ACOG and AAP Guidelines for Perinatal Care.³¹ Also look for obstetric and nursing textbooks, journal publications, and hospital policies. Several categories of standard of care violations unfortunately occur with predictable frequency in birth injury cases.

Failure to identify or plan for risk factors. A health care provider should have reviewed maternal history and paid careful attention during prenatal care to identify any risk factors. Risk factors are warning signs of foreseeable injury. The failure to identify these factors or to monitor for and act on signs and symptoms of potentially dangerous conditions related to risk factors is often a violation of the standard of care. For example, preeclampsia occurs when the mother develops hypertension and proteinuria or hypertension and end-organ dysfunction in the last half of pregnancy. The disorder is caused by placental and maternal vascular dysfunction. Preeclampsia increases the risk of fetal hypoxia and the risk of placental abruption. Medical providers should identify and treat the mother for preeclampsia and monitor the mother and the baby for signs of hypoxia or abruption. Failure to identify and plan for potentially adverse consequences of preeclampsia and to timely intervene to protect the mother and baby are violations of the standard of care.

Carefully review the prenatal and hospital records for evidence of risk factors including:

• prenatal risk factors
  • diabetes
  • hypertension
  • preeclampsia
  • small baby (intrauterine growth restriction)
  • large baby (macrosomia)
  • vaginal birth after cesarean section
  • premature rupture of membranes
  • preterm labor

• labor and delivery
  • use of medications to induce labor (Cytotec/Pitocin)
  • meconium (“baby poop” in the amniotic fluid)
  • abnormal fetal heart rate patterns on fetal heart monitoring strip
  • prolonged labor
  • use of vacuum extractor or forceps
  • shoulder dystocia
  • cesarean section (scheduled, urgent, emergent)

• family history
  • chromosomal or genetic abnormalities

• complications in past pregnancies
• maternal behaviors during pregnancy.

Risk factors also can foreshadow potential defense arguments. As previously mentioned, preeclampsia can cause hypoxia. The defense may argue that the baby’s hypoxic-ischemic injury occurred during pregnancy as a result of chronic, long-standing hypoxia due to preeclampsia before the mother was admitted to the hospital and under the care of the hospital’s medical professionals. In that scenario, analysis of the location, pattern, and timing of the injury is critical to determine whether the pattern is that of a partial prolonged hypoxia or an acute profound asphyxia and whether there is evidence that the injury occurred at or near delivery when timely intervention would have prevented the injury. In evaluating a potential case, determine whether risk factors played any role in causing the injury and analyze the potential defenses, including the evidence necessary to defeat each defense.

Failure to monitor. An unfortunately common violation of the standard of care is the failure of nursing staff to identify fetal heart rate patterns signaling that the baby is hypoxic and becoming acidotic. During labor and delivery, abnormal fetal heart rate patterns are warning signs that the baby may not be tolerating the intrauterine environment or labor and may not be getting enough oxygen. When medical providers do not identify or do not understand the abnormalities of the baby’s heart rate and fail to act in a timely manner, this can result in delays in intrauterine resuscitative measures (such as giving the mother oxygen or fluids, or maternal position changes), delay in delivery, or both, causing hypoxic-ischemic injury.

Failure to educate and train. Hospitals must provide nursing staff who are competent in monitoring and interpreting the baby’s heart rate. Nursing staff failures may be the result of an institutional failure to educate, train, and assess staff competency in fetal heart rate monitoring. This institutional failure is a violation of the standard of care.

Failure to communicate. Nurses and doctors share responsibility for monitoring the mother and the baby. Nurses are the “eyes and ears” of the doctors who aren’t always physically present in the labor and delivery department. Failure to accurately communicate information during labor and delivery is a common standard of care violation that results in delays in delivery and preventable injuries.

Birth injury cases are complicated and time-intensive for all parties. Screening cases thoroughly early on by examining the evidence regarding injury pattern, timing, and mechanism is essential.

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Laura Brown is a partner at Williams & Brown with offices in Houston and Waco, Texas. She can be reached at Brown@TrialFirm.com.

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Notes

1. Rick Friedman & Patrick Malone, Rules of the Road: A Plaintiff Lawyer’s Guide to Proving Liability 5 (2d ed. 2010).
2. Some other causes of injury to the brain at birth include trauma, hemorrhage, stroke, infection, prematurity, hyperbilirubinemia (kernicterus), hypoglycemia, metabolic disorders, and genetic abnormalities. See Joseph J. Volpe, Encephalopathy: An Inadequate Term for Hypoxic-Ischemic Encephalopathy, 72 Annals of Neurology 156, 157 (Aug. 2012).
3. See Terrie E. Inder & Joseph J. Volpe, Pathophysiology: General Principles, in Joseph J. Volpe et al., Volpe’s Neurology of the Newborn 325 (6th ed. 2018).
4. Id.
5. While there are many types of birth injuries, this article focuses on the evaluation of asphyxial injuries.
6. See Hannah C. Kinney & Joseph J. Volpe, Hypoxic-Ischemic Injury in the Term Infant: Neuropathology, in Volpe et al., supra note 3, at 484.
7. Volpe, supra note 2, at 156. 
8. Terrie E. Inder & Joseph J. Volpe, Hypoxic-Ischemic Injury in the Term Infant: Clinical-Neurological Features, Diagnosis, Imaging, Prognosis, Therapy, in Volpe et al., supra note 3, at 510, 520.
9. Id.
10. Id. at 524.
11. Id. at 528.
12. Id. at 510.
13. Linda S. de Vries & Floris Groenendaal, Patterns of Neonatal Hypoxic-Ischaemic Brain Injury, 52 Neuroradiology 555, 556–57 (June 2010).
14. Volpe, supra note 2, at 158.
15. Mary Rutherford et al., Magnetic Resonance Imaging in Perinatal Brain Injury: Clinical Presentations, Lesions and Outcome, 36 Pediatric Radiology 582 (July 2006).
16. Volpe, supra note 2, at 158.
17. Steven P. Miller et al., Patterns of Brain Injury in Term Neonatal Encephalopathy, 146 J. Pediatrics 453, 453 (Apr. 2005).
18. Volpe, supra note 2, at 159.
19. Id.
20. Mary Rutherford et al., Assessment of Brain Tissue Injury After Moderate Hypothermia in Neonates With Hypoxic-Ischaemic Encephalopathy, 9 Lancet Neurology 39 (2010).
21. Inder & Volpe, supra note 8, at 512.
22. Id. at 539.
23. Am. Coll. of Obstetricians & Gynecologists’ Task Force on Neonatal Encephalopathy, Neonatal Encephalopathy and Neurologic Outcome (NEANO) (2d ed. 2014) (These factors are listed as “sentinel events” in the NEANO publication) [hereinafter NEANO].
24. See Volpe, supra note 2, at 161.
25. Id.
26. NEANO, supra note 23.
27. Id. at 208.
28. Id. at 209.
29. See, e.g., Dov Apfel, Birth Injury Litigation Criteria Exposed, Trial 20 (May 2015).
30. See Volpe, supra note 2, at 161.  
31. Am. Acad. of Pediatrics & Am. Coll. of Obstetricians & Gynecologists, Guidelines for Perinatal Care (8th ed. 2017).