Obstetrical Malpractice

Obstetrical Malpractice

Nurse_with_babyObstetrical Malpractice

More often than not, having a baby is a time of great anticipation, high hopes, and joy for the parents and their families. It also represents a period during which many women, in the course of their prenatal care, experience their first long-term contact with a physician, midwife, or nurse practitioner. Because pregnancy is a normal physiological process, most women progress through their prenatal course with expectations that everything will be absolutely normal, and that the infant will be healthy. When these expectations are not met, and the baby or mother is injured, joy turns to despair and grief. Plaintiffs seek explanations of how, when and why it happened and who was responsible. If they cannot get reasonable answers from their healthcare providers, the plaintiffs may turn to the legal system for relief. The costs associated with caring for an injured infant or mother can be enormous. The death or persistent coma of a previously healthy woman can have a profound impact on the family. This factor alone can induce plaintiffs to consider legal action against the healthcare providers. There are many prenatal and perinatal factors that lead to cerebral palsy and other types of birth injuries. The obstetrical case must be carefully evaluated by both plaintiff and defense counsel.

There are many reasons for bad outcomes in obstetrics, not all of which are related to negligence by a health care provider. Plaintiff attorneys may be confronted with the sight of an obviously neurologically damaged infant brought into the attorney’s office by parents who are upset and interested in pursuing a lawsuit against the doctor, nurse, and/or hospital. The attorney should see the infant before filing suit to look for obvious genetic defects and to estimate the extent of damages. Family history is very important. The attorney should attempt to identify a pre-existing family disorder such as a history of genetic disorders or seizures determine if the infant was premature, and if so, how early the child was born. Prematurity is associated with substantial risk of injuries in direct correlation with the degree of prematurity. The earlier the delivery and the lower the birthweight, the greater the risk of intracranial hemorrhage, respiratory difficulties from immature lungs and other problems related solely to fetal age at the time of delivery (Peters, 1989).

Common defenses include attributing the child’s neurological deficits to genetic errors or in-tero exposure to environmental toxins such as alcohol, medications, recreational drugs, lawn sprays, household chemicals, pesticides, oral contraceptives, x-rays, or cigarettes. Viral infections can also cause fetal injuries. Falls blows to the abdomen or motor vehicle accidents may also have an impact on the developing fetus. The attorney’s legal nurse consultant should determine when these incidents occurred and their severity. Before proceeding with filing a case, plaintiff attorneys may have the parents and/or infant screened for possible genetic disorders or exposure to chemicals.

According to ACOG (American College of Obstetrics and Gynecology), obstetricians can expect an average of 2.53 medical malpractice lawsuits to be filed against them during their career. However, more than half of all claims (53.9%) were either dropped or settled without payment on behalf of the obstetrician. Obstetricians also won 65.5% of all claims resolved by arbitration, jury or court verdict (ACOG News Release, 2000). The expanded scope of nursing practice, in addition to the specialty technology involved, has also been associated with a greater degree of liability for professional practice. Perinatal nurses (those caring for women during the timeframe of labor and delivery) have historically experienced increased liability exposure and have some of the highest rates for nursing malpractice insurance premiums.

Brain Damage
When cases involving hypoxic brain damage first began to appear a number of years ago, insurance companies, physicians, and hospitals were reluctant to defend them. The thought of a severe brain damaged infant sitting in the courtroom was daunting. The insurance companies’ willingness to settle such cases provided positive reinforcement to plaintiff attorneys to file more cases. Successful defenses of these cases increased after the cost of not defending them became evident. The defense bar’s courage to begin fighting these claims and the defense successes that have occurred in the courtroom resulted in a decrease in the number of these lawsuits.

Plaintiffs usually contend that the cause of brain damage in the infant was perinatal trauma and/or hypoxia (reduced oxygen) that were in turn due to malpractice. The defense frequently argues that the act or omission did not occur and that the cause of brain damage was not of intrapartum (during labor and delivery) origin. Common causation defenses include:

  1. alleging that the infant was unavoidably premature, and damage was due to the fragility of the preterm infant’s neurological system
  2. the timing of the event, particularly in an intracranial hemorrhage, was prior to labor
  3. the fetus was growth retarded, particularly if there is evidence of prenatal infection
  4. the problem was caused by a prenatal incident or infection
  5. allegations that the mother used street drugs during pregnancy are often quite damaging to the plaintiff’s case
  6. the placental pathology report shows prenatal rather than a perinatal problem

The medical literature about placental pathology has provided a proximate cause argument that attributes some of the infant’s hypoxic damage to prenatal factors. For this reason, in anticipation of litigation, some obstetricians ask national experts to examine the placenta when a hypoxic infant is born (Fiesta, July 1995).

Besides the advances in placental pathology, there have also been other important research findings with defense implications. There is increasing evidence that in most cases the brain injury associated with cerebral palsy (CP) is not related to perinatal events (Perlman, 1997). CP has been defined as a non-progressive motor disorder of early onset that affects approximately 2 to 3 per 1000 school aged children. Brain injury resulting in CP may occur at any time during the pregnancy, labor or postnatal period. There is overwhelming evidence to suggest that in approximately 70 to 80% of CP cases, the origin has been attributed to the antepartum (prior to labor) period. This correlates to the proportion of CP being attributed to a perinatal event such as birth asphyxia as only estimated to be 20% (Perlman, 1997). The US Preventive Services Task Force (1996) reports that most cases of CP occur in persons without evidence of birth asphyxia or other intrapartum events.

Mental retardation is different from cerebral palsy. The etiology of severe mental retardation unaccompanied by CP is primarily genetic, viral, or developmental in origin and not related to perinatal events. Mild mental retardation also does not appear to be related to peripartum events, but rather to social and environmental conditions (Perlman, 1997).

Impaired cerebral blood flow is the principal mechanism attributed to intrapartum hypoxic ischemia (brain damage due to insufficient oxygen). This occurrence is most likely a consequence of interruption in placental blood flow and gas exchange, which is more commonly referred to as asphyxia. Most infants who have impaired cerebral blood flow will respond with adaptive systemic and cerebral circulatory responses to maintain cerebral perfusion. It has been seen that even when asphyxia is prolonged or severe, most newborn infants recover with minimal or no neurologic damage (Perlman, 1997). There are many factors that have been associated with these antenatal (before labor) hypoxic-ischemic cerebral injuries. These include maternal drug use (e.g. cocaine), multiple pregnancies and bleeding in the third trimester. However, in most cases, the cause is idiopathic (not known).

The incidence of hypoxic-ischemic cerebral injury in most cases of CP is before labor and delivery. Studies have shown that the timing of the antepartum insult is critical to the evolution of a specific lesion. In attempting to determine the issue of an intrapartum timing of asphyxia as a proximate cause of CP, there are a set of conditions that need to be met. These are:

  1. No clinical evidence for potential antenatal injury, i.e. microcephaly (small brain), multiple pregnancies, hypothyroidism, chromosomal disorders, etc.
  2. The absence of antenatal cerebral injury by neuroimaging.
  3. Evidence of severe perinatal asphyxia, i.e. umbilical cord arterial pH less than 7.00, depressed neonate requiring intensive resuscitation, a postnatal (after birth) syndrome of hypoxia-ischemic encephalopathy including seizures, and associated systemic abnormalities.
  4. Exclusion of other causes of neonatal encephalopathy.

Careful monitoring of patients in labor is performed to detect changes in the fetal heart rate pattern that might identify asphyxia in utero. The nurse has a great responsibility in the assessment, interventions, evaluation, and communication in a timely manner with the physician. Measures to identify infants at risk for asphyxia continue during the delivery process, and into the initial neonatal period.

Lymphocytes, normoblasts, and platelets
Some studies assist the defense when events during labor and delivery are being alleged as the cause of fetal injury. Dr. Richard Naeye, a renowned pathologist, has postulated that finding large numbers of lymphocytes and normoblasts in the blood of neonates should raise the possibility of severe hypoxemia within the 24 hours that preceded the finding. Dr. Naeye reports that the time of the hypoxemia (reduced blood oxygen) can be calculated by counting back 24 hours from the time blood lymphocyte counts rapidly decreased from high to normal or subnormal levels. Recent studies have shown that lymphocytes can apparently enter the blood in large numbers within 15 minutes and normoblasts within 30 minutes of the start of severe hypoxemia-ischemia. It was also identified that the interval between the start of severe hypoxia-ischemia and the first recognized neonatal seizure in most infants is between 20-30 hours (Naeye, 1997).

A study that appeared in a recent (2001) American Journal of Obstetrics and Gynecology issue presents Dr. Naeye’s current thinking on the determination of the timing of fetal brain damage from hypoxemia-ischemia. His study analyzed 55 children with cerebral palsy to evaluate methods for determination of the time before birth at which antenatal hypoxemia-ischemia damaged the brain. He found that basal ganglia lesions predominated when bradycardia (slow heart rate) lasted less than 30 minutes before birth. As the bradycardia duration lengthened, white matter and eventually watershed brain lesions predominated. Lymphocytosis appeared 25 minutes after the bradycardia began, and thrombocytopenia appeared at 20 to 28 hours. The lymphocytosis disappeared 14 to 18 hours after it first appeared. He concluded that counting back from the time that lymphocytosis ended and thrombocytopenia (reduced number of platelets) began can sometimes identify the time when hypoxemia-ischemia damaged the fetal brain. The defense can utilize this type of analysis to argue that a child’s hypoxic-ischemic brain damage took place before her mother entered a health care facility in labor.

There are several lines of evidence that suggest that medical malpractice during labor is rare. Even with the judicious monitoring of labor patients, there are sudden intrapartum fetal deaths. These are often associated with acute unpredictable obstetrical events that clearly do not represent negligence. Would a different management have altered the outcome in a positive manner, or was the outcome an unavoidable accident or an act of God? The fetus is a remarkable being, with many adaptive mechanisms to be able to maintain cerebral blood flow and metabolism. The fetus also has an inherent tolerance or resistance of the fetal brain to intrapartum asphyxia. Given these factors, it is difficult to render a medical legal opinion with any degree of certainty, as to whether an alternate medical strategy could have been altered, or whether the outcome was an unavoidable act (Perlman, 1997).

Recent research illustrates that perinatal hypoxic-ischemic cerebral injury that is secondary to intrapartum asphyxia that results in CP is a rare event in most delivery rooms and NICU’s (Perlman, 1997). However, when a plaintiff is successful, the award tends to be high, but not excessive given the serious nature of the injuries. Life care planners play a key role in calculating costs for maintaining a brain-damaged baby.

Current trends in obstetrical care (and health care in general) make some areas of practice vulnerable to mistakes and consequent litigation. The growth of managed healthcare and increased utilization of cost-containing short-stay programs have resulted in earlier hospital discharge for the postpartum mother and her newborn. It has become apparent that this is too little time for the careful evaluation and teaching of mother and baby that should take place. In response to this trend, some states, including New Jersey, have passed laws mandating a specific length of stay after a hospital delivery. Hospital downsizing and cost-cutting measures are a reality affecting nurse-patient ratios, staffing patterns, and numbers of experienced personnel available to work with patients.

Nurses are therefore charged with being advocates for both patients at a time when financial and other pressures will be high. Members of the nursing profession will do well to review, remember, and practice their profession based on both ethical and clinical care standards. Members of the legal profession will need to choose or defend their cases carefully, in light of the changes in both health care and nursing practice.

Modified from Obstetrical Nursing Malpractice Issues, in Nursing Malpractice, Fourth Edition, 2011, Lawyers and Judges Publishing Company, Tucson, AZ.

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ACOG news release (embargoed until January 31, 2000). ACOG’s latest professional liability survey reveals increase in liability claims. Washington, DC, The Author.

Fiesta, J. (1995, July). Obstetrical liability update-part I. Nursing Management, 26(7), 24.

Naeye, R. and Lin, H. (2001). Determination of the timing of fetal brain damage from hypoxeia-eschemia. American Journal of Obstetrics and Gynecology. Volume 184, 217-24.

Naeye, R. (1997). Hypoxic-ischemic antenatal brain injury: determining how and when it took place. American Association of Legal Nurse Consultants, Eighth National Educational Conference, Syllabus book.

Perlman, J. (1997). Intrapartum hypoxic-ischemic cerebral injury and subsequent cerebral palsy: medicolegal issues. Pediatrics, Volume 99, number 6.

Peters, J. (1989, May). Litigating the brain-damaged baby case. TRIAL, 32-40.

US Preventive Services Task Force (1996). Guidelines for intrapartum electronic fetal monitoring. Guide to Clinical Preventive Services. Second edition.

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