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What’s the VERDICT? Genetic testing and the future of cerebral palsy malpractice cases Would genetic testing have prevented this lawsuit? Joseph S. Sanfilippo, MD, MBA, and Steven R. Smith, MS, JD CASE Mixed CP diagnosed at age 6 months After learning that the statute of limitations was to run out in the near future, the parents of a 17-year-old with cerebral palsy (CP) initi- ated a lawsuit. At the time of her pregnancy, the mother (G2P2002) was age 39 and first sought prenatal care at 14 weeks. Her past medical history was largely non- contributory to her current pregnancy, except for that she had hypothyroidism that was being treated with levothyroxine. She also had a his- IN THIS tory of asthma, but had had no acute episodes ARTICLE for years. During the course of the pregnancy there was evidence of polyhydramnios; her initial Types of cerebral thyroid studies were abnormal (thyroid-stimulat- palsy ing hormone levels, 7.1 mIU/L), in part due to page 41 lack of adherence with prescribed medications. She was noted to have elevated blood pressure (BP) 150/100 mm Hg but no proteinuria, with BP Legal monitoring during her last trimester. considerations page 42 Dr. Sanfilippo is Professor, Department Avoiding of Obstetrics, Gynecology, and Reproductive Sciences, University of malpractice claims Pittsburgh, and Director, Reproductive page 46 Endocrinology and Infertility, at Magee-Womens Hospital, Pittsburgh, Pennsylvania. He also serves on the OBG MANAGEMENT Board of Editors. Mr. Smith is Professor Emeritus and Dean Emeritus at California Western School of Law, San Diego, California. The authors report no financial relationships relevant to this article. 10.12788/obgm.0091 CONTINUED ON PAGE 40 ILLUSTRATION: KIMBERLY MARTENS FOR OBG MANAGEMENT MARTENS KIMBERLY ILLUSTRATION: mdedge.com/obgyn Vol. 33 No. 5 | May 2021 | OBG Management 37 What’s the VERDICT? CONTINUED FROM PAGE 37 The patient went into labor at 40 3/7 weeks, that the obstetrician should have been informed after spontaneous rupture of membranes. In by the hospital staff during the course of labor, labor and delivery she was placed on a monitor, and the obstetrician should have been more and irregular contractions were noted. The initial proactive in monitoring the deteriorating circum- vaginal examination was noted as 1-cm cervi- stances. This included performing a CD based cal dilation, 90% effaced, and station zero. The on “the Category III fetal heart tracing.” obstetrician evaluated the patient and ordered At trial, the plaintiff expert argued that fail- Pitocin augmentation. The next vaginal exam ure of nursing staff to properly communicate several hours later noted 3-cm dilation and with the obstetrician led to mismanagement. 100% effacement. The Pitocin was continued. Furthermore, the obstetrician used poor judge- Several early decelerations, moderate variability, ment (ie, below the standard of care) in not per- and better contraction pattern was noted. Eight forming a CD. The defense expert argued that, hours into the Pitocin, there were repetitive late overall, the fetal heart tracing was Category decelerations; the obstetrician was not notified. II, and the events occurred in utero, in part The nursing staff proceeded with vaginal exami- reflected by the mother having polyhydramnios nation, and the patient was fully dilated at station and hypothyroidism that was not well controlled +1. Again, the doctor was not informed of the due to lack of adherence with prescribed medi- patient’s status. At 10 hours post-Pitocin initia- cations. The child in his wheelchair was brought tion, the patient felt the urge to push. The obste- into the courtroom. The trial went on for more trician was notified, and he promptly arrived to than 1 week, and the jury deliberated for several the unit and patient’s bedside. His decision was hours. (Note: This case is a composite of several to use forceps for the delivery, feeling this would different events and claims.) be the most expedient way to proceed, although FAST cesarean delivery (CD) was a definite consider- TRACK ation. Forceps were applied, and as the nurs- WHAT’S THE VERDICT? ing staff noted,” the doctor really had to pull to The jury returns a verdict for the defense. Hypoxic-ischemic deliver the head.” A male baby, 8 lb 8 oz, was Should anything have been done differ- encephalopathy delivered. A second-degree tear was noted and ently in this trial? accounts for less easily repaired following delivery of the placenta. than 10% of all Apgar scores were 5 and 7 at 1 and 5 minutes cases of cerebral after birth, respectively. Medical considerations palsy The patient’s postpartum course was Cerebral palsy is a neurodevelopmental dis- uneventful. The patient and baby were dis- order affecting 1 in 500 children.1 Other prev- charged on the third day postpartum. alence data (from a European study) indicate As the child was evaluated by the pedia- an incidence of 1.3–1.9 cases per 1,000 live- trician, the mother noted at 6 months that the births.1 The controversy continues with child’s head lagged behind when he was picked respect to the disorder’s etiology, especially up. He appeared stiff at times and floppy at when the infant’s magnetic resonance imag- other times according to the parents. As the ing (MRI) does not identify specific pathol- child progressed he had problems with hand-to- ogy. The finger is then pointed at HIE and mouth coordination, and when he would crawl thus the fault of the obstetrician and labor he seemed to “scoot his butt,” as they stated. and delivery staff. In reality, HIE accounts for The child was tested and a diagnosis of less than 10% of all cases of CP.2 Overall, CP mixed cerebral palsy was made, implying a is a condition focused on progressive motor combination of spastic CP and dyskinetic CP. impairments, many times associated with He is wheelchair bound. The parents filed a law- specific MRI findings.3 In addition, “MRI- suit against the obstetrician and the hospital, negative” CP is a more vague diagnosis as focused on hypoxic-ischemic encephalopathy discussed among neurologists. (HIE) due to labor and delivery management The International Consensus Definition being below the standard of care. They claimed of CP is “a group of permanent disorders of 40 OBG Management | May 2021 | Vol. 33 No. 5 mdedge.com/obgyn FIGURE 1 Types of cerebral palsy Type Description Damaged part of the brain Spastic Increased muscle tone; difficulty walking; may have hemiplegia/ Motor cortex hemiparesis or quadriplegia/quadriparesis Dyskinetic Problems controlling hands, arms, legs; athetoid, choreoathetoid, Ganglia and dystonic movements Ataxic Problems with balance and coordination Cerebellum Mixed Spastic and dyskinetic cerebral palsy Combination Spastic Dyskinetic Ataxic the development of movement and posture, remains unknown. Some affected children causing activity limitations, that are attrib- have intellectual disabilities, as well as visual, uted to nonprogressive disturbances that hearing, and/or speech impairment. occurred in the developing fetal or infant A number of risk factors have been brain.”4 The International Cerebral Palsy associated with CP (TABLE 1, page 42),3,6 Genomics Consortium have provided a con- which contribute to cell death in the brain sensus statement that defines CP based upon or altered maturation of neurons and glia, clinical type as opposed to etiology.5 Many resulting in abnormal white matter tracts times, however, ascribing an HIE cause to CP and smaller central nervous system (CNS) is “barking up the wrong tree,” in that we now volume or cerebellar hypoxia.6 One very know there are clear cut genetic causes of CP, important aspect of assessment for CP is spe- and etiology attributed to perinatal causes, cific gene mutations, which may vary in part in reality, are genetic in up to 80% of cases.3 dependent upon the presence or absence of Types of CP are addressed in FIGURE 1. environmental factors (insults).1 Mutations ILLUSTRATION: © SCIENCE SOURCE ILLUSTRATION: Overall, the pathophysiology of the disorder can lead to profound adverse effects with mdedge.com/obgyn Vol. 33 No. 5 | May 2021 | OBG Management 41 What’s the VERDICT? TABLE 1 Risk factors for cerebral palsy3,6 Risk factors Maternal Epilepsy, thyroid abnormalities, other medical diseases (diabetes) advanced maternal age, smoking, preterm delivery Prenatal Placental abnormalities, intra-uterine fetal growth problems, abnormal amniotic fluid levels, preeclampsia, TORCH infections, chorioamnionitis, multiple gestations Perinatal prolonged or traumatic delivery, breech, meconium, neonatal seizures, hypoglycemia Postnatal Stroke, head trauma, meningitis Paternal Advanced age resultant CNS ischemia and neuromotor dis- pathogenic variants in the sequencing.9 Thus, ability. In fact, genetics play a major role in we have a tool to identify underlying genetic determining the etiology of CP.1 Of interest, pathogenesis with CP. This theoretically can animal models who are subject to HIE induc- change the outcome of lawsuits initiated for tion have CNS effects resulting in permanent CP that ascribe an HIE etiology. Clinicians motor impairment.7 need to stay tuned as the genetic repertoire continues to unfold. DNA sequencing The DNA story continues to unfold with the concept that DNA variants alter suscepti- Legal considerations bility to environmental influences. These Although CP is not a common event, it has FAST insults are, for example, thrombosis or hem- been a major factor in the total malpractice TRACK orrhage, all of

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