A case hinges on the causes of a child's developmental delays.
Mr. Kaplan is a partner at Aaronson, Rappaport, Feinstein & Deutsch, LLP, specializing in medical malpractice defense and healthcare litigation. He welcomes feedback on this column via email to firstname.lastname@example.org.
From February 6, 2006 to July 5, 2006, a patient received prenatal care for a moderate-to-high-risk pregnancy (gravida 5 with 3 prior abortions and a normal spontaneous vaginal delivery [NSVD] in 1998). On May 2, 2006, at 22 weeks by last menstrual period and 19 weeks by ultrasound, the woman underwent a reproductive medicine consult, which noted the possibility of Down syndrome and/or neural tube defect. An amniocentesis performed 2 days later was negative.
At 6:55 am on July 6, 2006, at 28 1/2 weeks, the patient presented to the ob/gyn triage of the defendant hospital reporting that her membranes had ruptured at approximately 6:00 am, with clear fluid. Her blood pressure was normal but her pulse rate was 127. She reported mild abdominal cramping. After a soap suds enema, an examination (the last vaginal examination done until late in the course) revealed the patient to be 2- to 3-cm dilated, 75% effaced, with the infant at -1. The patient was admitted. A nonparty ob attending’s plan was for close monitoring and administration of dexamethasone, magnesium sulfate and penicillin G.
A perinatologist consulted on July 7th at 7:50 am reviewed the fetal heart rate (FHR) tracings, which were described as having occasional variable decelerations, with mild to moderate long-term variability, reducing at times. The perinatologist’s reading of the strip indicated intermittent, small (10 beats per minute) accelerations, as well as very infrequent contractions and intermittent and mild variable decelerations. The patient was seen by the perinatologist again at 9:55 am and continued to be followed, with the medication regimen as planned.
Pediatrics was then called and spoke to the patient concerning the risk of prematurity. The record indicates that she presented with an elevated white blood cell (WBC) count of 24.5 and includes a single indication of some tachycardia in the infant, at 11 pm July 8th. On July 9th at 9:40 am, a resident examined the patient and noted that she was 6- to 7-cm dilated and 100% effaced. An intrauterine pressure catheter was placed and Pitocin was started at 9:44 am. At 9:45 am, there was an indication of positive long-term variability with positive accelerations, probably because of stimulation of the infant by the mother’s now-active labor.
The codefendant ob took over care at that point and the plan was for amnioinfusion and Pitocin augmentation with anticipation of NSVD. The patient was placed on oxygen. Examination by a resident at 10:30 am revealed the patient to be 7 to 8 cm dilated and at 11 am, she was bearing down with contractions. The resident was called and delivered the infant at 11:03 am. The birth weight was 915 g (2.02 lb). The defendant ob testified that he was present for the delivery although he did not author a delivery note. The patient was discharged on July 11th without incident.
The infant was granted Apgars of 5 and 7. On initial examination, at 12 pm, she was active and on nasal continuous positive airway pressure CPAP. She remained on nasal CPAP, with various levels of positive endexpiratory pressure (PEEP), through August 18th, when she finally was weaned to room air.
Placental pathology revealed an immature placenta marked with acute chorioamnionitis, an infection in the placenta tissues, and amniotic fluid. The resident and defendant ob testified that there were no signs or symptoms of acute chorioamnionitis or signs of infection. The defendant ob also testified that the placenta was placed in an unrefrigerated box overnight until the pathology department opened the following morning.
The infant had a relatively benign course other than some incidence of abdominal distention, addressed with suppositories. The dexamethasone may have caused a unique elevation in the infant’s WBC count, leading the neonatologists to believe the infant might have sepsis, but she never ran significant fevers, and never became truly “septic.”
The first blood gas (55 minutes after delivery) indicated that the base excess was only -2.5, and the pH was 7.243. An August 8th head ultrasound revealed some prominence of the lateral ventricles, more so on the right side, with the choroid plexus bilaterally appearing to be slightly irregular. The indication was that the finding could be an artifact or related to a previous bleed. The prominence of the right-sided ventricles could be related to a leftsided weakness, although no comment was made concerning the presence of periventricular leukomalacia (PVL). The infant was discharged on September 11th.
Early intervention specialists evaluated the infant at 4 months and 26 days (an adjusted age of 1 month and 26 days). She had some delay in gross motor development (weakness in her neck muscles) and some clonus in her right ankle secondary to prematurity. She continued to receive physical, occupational, and speech therapy with early intervention specialists until the age of 3.
On October 23, 2009, magnetic resonance imaging showed a normal brain with gray-white matter differentiation and no evidence of gyral or sulcal effacement. There were no masses, mass effects, hemorrhages, or cortical infarcts.
The child continued to receive physical, occupational, and speech therapy in school. By November 2010, at age 4.9 years, she only had “mild to moderate receptive and expressive delays.” She was able to identify common objects and produce sentences of 4 to 5 words. She used her verbal skills spontaneously, and was able to talk about remote events.
The child’s memory was intact. She was able to use verbal skills functionally mostly in English, even though she came from a bilingual home. She understood spacial–object relationship and part/whole relationships. She had “decreased to normal muscle tone” and fair muscle strength throughout. She was able to catch and kick a ball, jump from a height, and climb stairs without rail support although she needed rail support to descend stairs.
The child progressed from being unable to do very much with writing utensils to being able to copy circles and squares, color within lines, connect dots, string beads, and cut on a line with 90% accuracy. She could cut the outlines of a circle and square precisely and accurately and was able to play with blocks appropriately. She was toilet trained and able to dress herself, albeit at times requiring assistance.
The plaintiff claimed the following permanent injuries: global developmental delays, brain damage, speech and language delays, need for special education and for physical/occupational/ speech therapy, diminished earning capacity, and loss of enjoyment of life. They alleged that the defendants failed to diagnose chorioamnionitis and should have either delivered this baby earlier by cesarean section or at the very least begun augmentation of a basically desultory labor earlier, which would then be claimed to be the cause of the infant plaintiff’s problems.
Our response to the placental analysis was that the delivery took place over the weekend, therefore, the results of the placental pathology report were connected to the unrefrigerated nature of the placenta and not to chorioamnionitis, which was not at all capable of being diagnosed based upon the signs and symptoms that the plaintiff was presenting with during her labor.
The plaintiff’s counsel spent a significant portion of the depositions of the ob resident and attending concentrating on chorioamnionitis. The ob attending testified that chorioamnionitis is an infection in the amniotic fluid. The signs and symptoms are a temperature greater than 104°F on 2 occasions, abdominal and back pain and foul- smelling amniotic fluid, none of which were present in this case. He stated that a contraindication for amnioinfusion was chorioamnionitis, but insisted that there were no signs of infection in the plaintiff. He also testified that it was not a contraindication to administer the amnioinfusion.
The surgical pathology department was not available on the weekends and that being the case, a placenta would typically sit in a box, unrefrigerated until Monday. (The infant in question was delivered on a Sunday). Both the resident and the attending testified that the FHR strips were benign and were reassuring for a status post-dexamethasone, magnesium sulfate 28-week-gestation fetus, and refuted the suggestion there were “saltatory” patterns on the strips.
The plaintiff’s pediatric neurology expert noted evidence of mild spastic diplegia most pronounced on the child’s right side related to PVL consistent with perinatal hypoxia/ischemia. The plaintiff’s neuropsychologist expert examined the child and concluded that her IQ was 91 (27th percentile). The plaintiff had the child examined by another psychologist, who found the child to have average intelligence, with average scores on some tests and below-average scores on others. Interestingly, although she was considered to have right hemiparesis, her ability to imitate hand positions was average on both sides.
Our pediatric neurologist examined the infant and described a completely nonfocal neurological examination, other than some diminished visual acuity for distance and a subtle hypertonicity of the right ankle with no significant functional limitation. Our neuropsychology expert examined the child and felt that the child’s IQ was 96 (39th percentile) and average. The child’s visual spatial orientation (as tested in multiple different ways) was intact, arguing against the possibility of cerebral palsy.
Our ob/gyn expert was able to defend the care and treatment rendered during the labor and delivery. In her opinion, the infant suffered from risks associated with a premature delivery (ie, developmental delays) and recovered very nicely. She commented that there was no evidence of hypoxia or fetal distress on the FHR monitoring strips. The medications administered and the dosages were all appropriate. There was no indication for a cesarean delivery. The amnioinfusion was also appropriately ordered. Our neonatology expert was also able to defend the care as the neonatal course was relatively benign and uncomplicated.
The blood gases were consistent with a labor and delivery and initial care of an infant delivered at 28 1/2 weeks. There was no evidence of metabolic acidosis or hypoxia. The pH of 7.243 was consistent with respiratory acidosis, which is secondary to fluid in the lungs from the transition from the womb to room air. The elevated WBC count was a result of the dexamethasone, which resolved by the time of discharge. Our pediatric neurology expert opined that chorioamnionitis did not have an effect on this patient because there was an absence of PVL on the head ultrasound in this premature infant.
The plaintiff’s demand for settlement was initially $6 million. That became increasingly more reasonable as the trial date approached, mostly because of the plaintiff team’s perception of the defensibility of their claims. The case ultimately settled as to the defendant hospital in the amount of $100,000. There has been no resolution as to the codefendant ob attending. As this issue went to press, the case was still pending.
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We felt that this was a case of damages looking for a theory of liability. We felt the theories revolving around fetal hypoxia and maternal infection could be successfully defended, particularly once our experts assured us that leaving the placenta unrefrigerated overnight could, in fact, result in the type of growth encountered (certainly a novel issue!). However, given the exposure in the case, the venue, and the concern (however moderate) that the codefendant ob might harbor criticism of the hospital and staff for “failing” to effectuate delivery prior to his arrival on July 9th, the decision was made to settle the claim reasonably for little more than litigation costs.