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A patient sues alleging that her child was in distress, became hypoxic and that a cesarean should have been performed much earlier.
The patient, age 43, presented to the emergency room at Defendant Hospital on 9/4/12 for confirmation of pregnancy diagnosed with an at-home test and for prenatal care. She already had 2 children1. Exam revealed a well-appearing, well-nourished female in no apparent distress with a closed os and no vaginal bleeding. A sonogram confirmed an intrauterine pregnancy, and lab work was positive for an early pregnancy and a urinary tract infection. The patient was discharged to home with antibiotics and Zantac (for acid reflux) and instructed to follow up in the high-risk clinic.
Screening by nursing staff on 9/5/12 documented the last menstrual period as 7/21/12 and an estimated date of confinement (EDC) of 4/27/13, with a current gestational age of 6w4d. Cervical length was normal. The patient’s pre-pregnancy weight was 142 lb. Urine HCG testing was positive and a maternal quad screen was positive for Down syndrome.2 The prenatal course was also noted to be significant for a low-lying placenta. The record stated that the patient wished to continue her pregnancy and declined amniocentesis.
On 9/24/12, the patient was 9w2d pregnant, weighed 141.5 lb and her blood pressure (BP) was 103/64. Exam revealed a fundal height of 9 cm. Fetal well-being was reassuring. The patient was reported to be at risk due to hypertension and cholestasis (believed to be from previous pregnancy). Because of her advanced maternal age, she was again referred to the high-risk clinic. She was started on ferrous sulfate, folic acid and prenatal vitamins. Prenatal testing appeared to be within normal limits.
On 10/2/12, the patient’s chest x-ray was negative for active tuberculosis. She was evaluated by genetics on 10/13/12 and the age-related risk for fetal aneuploidy was 1 in 30. The benefits/limitations of the maternal serum screen and fetal anatomy ultrasound were reviewed with her and she again declined amniocentesis.
The patient was evaluated in the high-risk clinic on 10/18/12 by Dr. A. At 14w1d both fetal activity and fetal heart beat were present. The patient was scheduled for a follow-up sonogram in 1 week and re-dated by sonogram to 12 weeks.
On 10/20/12, a maternal quad screen was positive for Down syndrome and negative for open neural tube defects. On her return to the genetics clinic on 11/7/12, the risk of Down syndrome was noted to be more than 1 in 10. Amniocentesis was again discussed and the woman declined.
At 18w1d, the patient was evaluated in the high-risk clinic by Dr. B. A fetal heartbeat and good movement were noted, and cervical length was normal at 4 cm. Pregnancy-induced hypertension labs and 24-hour urine were reported to be normal. Urine testing revealed trace protein. Vaginal progesterone was started due to the woman’s history of preterm birth.
On 11/29/12, 12/20/12 and 1/10/13, the patient was evaluated by MFM attending Dr. C in the high-risk clinic. On 11/29/12, her cervical length was reported as normal, with fetal and cardiac activity present and fundal height consistent with gestational age. On 1/10/13 Dr. C noted that the placenta was still low-lying and the patient was normotensive. Testing for syphilis was negative and a 1-hour glucose level was within normal limits. On 1/31/13, trace pedal edema and slightly decreased hemoglobin levels were noted by Dr. C and iron supplements were increased.
Dr. E evaluated the patient in the prenatal clinic on 2/14/13. At 31w1d, the fundal height was 30 cm and maternal BP was 108/61. The visit was normal and without issue.
On 2/25/13, the patient presented to labor and delivery triage at 11:40 AM with complaints of a cough and sore throat. Her BP was 109/67, heart rate was 101, and fetal activity was present. At 32w5d her total pregnancy weight gain was 18 lb. At 12:35 PM a nurse noted that the patient’s temperature was 100.3° and the fetal heart rate (FHR) was 182 beats per minute (bpm) with moderate variability. Tylenol was given, an intravenous (IV) was started and observation continued. Lab work revealed a white blood cell count of 19, a potassium level of 3.1 and total protein of 6.3. Chest x-ray revealed mild right lower lobe pneumonia. A sonogram done on admission indicated decreased fetal activity. Antibiotics and dexamethasone were administered. Electronic fetal monitoring (EFM) revealed initial persistent tachycardia and minimal variability throughout the night. The patient was placed on her left side and oxygen and IV fluid boluses were given. Staff monitoring was active and charted.
At 5:54 PM PGY 3 Dr. F reviewed prenatal labs and presenting symptoms and noted that the patient remained on vaginal progesterone. On exam, fetal tachycardia and a category II EFM tracing were noted. The patient continued to receive ceftriaxone and azithromycin for pneumonia. An 8 PM nursing note said that the chief resident was notified of the tracing, and IV fluids and monitoring were to continue.
Evaluation by attending Dr. G at 8:21 PM showed presence of fetal movement with persistent fetal tachycardia and no contractions, vaginal bleeding or loss of fluid. Report on a (presumed) sonogram revealed a vertex presentation, adequate amniotic fluid index and a posterior placenta. It was noted that the patient had a posterior complete placenta previa at 18 weeks, which resolved at 29 weeks. The plan was to admit to the MFM service, obtain a growth sonogram and continue antibiotics and monitoring.
A 2/26/13 nursing notes documented continued fetal tachycardia, 160-180s, with minimal to moderate variability. At 4 AM, the RN documented that Chief Resident was “notified the whole night about patient’s category II tracing of having minimal variability and very few accels <10. At 2:30 AM, by nurse’s note and on the EFM “Remarks,” Chief Resident came to the patient’s bedside and shook patient’s stomach and assessed patient. No orders were given, but to continue to monitor patient including Fetal Heart Monitoring. IVF was in progress at 125 cc/hr. Dr. G attending was notified as well.”
At 4:09 AM PGY1 documented the mother’s vital signs as BP 108/60, heart rate 82, respiratory rate 19 and temp 98.1. EFM indicated 150 bpm with minimal variability, no accelerations or decelerations. A BPP performed by PGY-1 was 8/8. The assessment was fetal well-being reassured in the setting of pneumonia. Nursing documented a category II tracing, and the patient remained on her left side with oxygen.
At 5 AM an RN documented a FHR of 153 with minimal variability and that the Chief Resident and Dr. G were aware of the tracing. A second dose of dexamethasone was given. At 6 AM an RN documented that Chief Resident was made aware that the patient was having variable decelerations at that time; the “MD” (unknown) evaluated the tracing and no action was needed. At 6:54 AM an RN noted that resident Dr. F, the covering MFM, was at the bedside and assessed the patient and tracing. As per Dr. F, the patient was to have a second official sonogram that morning.
The “official” BPP performed at 9 AM scored 4/8. MFM Dr. C was consulted and advised delivery. At 9:30 AM RN noted that Dr. S. (PGY3) was made aware and at 10 AM RN noted that Dr. I discussed the non-reassuring status with the patient, who gave consent for cesarean delivery. At 11:01 AM the patient had received two doses of dexamethasone; the FHR remained at 155 bpm with minimal variability, no accelerations and spontaneous variable decelerations. A low-lying placenta and estimated fetal weight of 1816 g were also noted.
At 11:48 AM on 2/26/13, at 32w6d, the patient underwent an emergency cesarean, performed by attending Dr. J and a resident, with spinal anesthesia. At 11:56 AM maternal placental cord pH was 7.37. The baby girl weighed 3.5 lb and had Apgars of 1, 2, 4, 4 and 4. Dr. J stated the baby was pink at delivery then decompensated. She was limp with very minimal respiratory effort, was resuscitated and then intubated and taken to the neonatal intensive care unit. Bilateral pneumothoraces were noted and a right chest tube was placed. The infant also had a seizure shortly after birth and was started on anti-seizure medications. She was treated for sepsis with antibiotics, although cultures were subsequently negative. She had no reflexes or spontaneous movements, fixed and dilated pupils, and occasional twitching. Diagnostic testing revealed severe hypoxic-ischemic encephalopathy2 and severe cerebral dysfunction. The infant had respiratory distress syndrome and was unable to tolerate weaning from the vent as she was unable to maintain her airway. She continued to have multiple episodes of bradycardia and desaturations and was diagnosed with aspiration pneumonia and feeding intolerance.
On 3/26/13 the infant was transferred from Defendant Hospital to Nonparty Hospital Center for possible lactobezoar. There, the medical staff had a conference with the family to discuss the infant’s neurological impairment and the proposed care plan. After a tracheostomy was performed and milk was found in it, a gastrostomy tube was placed. The infant remained at the Nonparty Hospital until May 25, 2013 but her neurological condition did not improve.
The child was then transferred to a Children’s Hospital for long-term care and constant stimulation, where she receives occupational, physical, massage, respiratory and musical therapy. The infant now weighs 28 lb. The mother and the staff discussed trying to wean the child off oxygen and getting her to move more, but to date, that has not been successful. The child continues to have multiple episodes of serious aspiration. Her prognosis for long-term survival is very poor.
The plaintiff alleged that the child was in distress, became hypoxic and that the cesarean should have been performed much earlier. They claimed that the first BPP should, at the least, have been reviewed by a more senior resident and/or attending. They also alleged an ongoing lack of significant variability in the FHR monitoring strips. The sole neonatal theory was that “brain cooling” or hypothermic therapy was indicated but not performed.
Our MFM felt that the ongoing pattern of moderate and overwhelmingly minimal variability was ominous the longer it persisted. Accepting the fact that this was a 32+ week gestation, he stated that the BPP of 8/8 called for greater observation, earlier use of the MFM and the difficult decision as to whether to deliver several hours earlier. He had no problem with the fact that PGY-1 performed the first BPP. He stated that, because the FHR strips lacked significant variability, the test should have been repeated then or within 1 to 2 hours. That being said, he felt that the fetus had a significant infection throughout the 2 days before birth and that it was the competent producing cause of the significant neurological presentation virtually immediately after birth. He stated that the child was not hypoxic at birth and an earlier delivery would have confronted the same issues.
Our neonatal infectious disease expert said that the mother’s pneumonia had nothing to do with the outcome. This baby was born limp and so hospital staff immediately assumed that there was sepsis and the infant was treated clinically and given antibiotics. The drugs were important because he said that they would also treat chorioamnionitis, which was never pathologically proven. He noted that after 10 days of antibiotics, the infant had negative cultures.
The expert did not believe the infant had cytomegalovirus or toxoplasmosis because of the sudden onset of fetal inactivity, meaning she was kicking and moving as the mother testified and then suddenly not moving. Those infections don’t usually present with a sudden onset. The infant had a 7.37 cord blood gas recorded approximately 8 minutes after birth, which is not indicative of hypoxia. By 12:12 PM, approximately 24 minutes later, the infant’s arterial blood gas was 7.05, which is hypoxic. Once damage is done to the brain, there is no chance of reversing it and in this case, the child was hypoxic within a short time of the cord being cut. By the time the arterial blood gas was taken 24 minutes later and registered at 7.05, she already had significant brain damage. However, he saw no signs of an infectious disease process causing neurologic injury.
Our neonatologist stated that, at delivery, the child was not hypoxic. The maternal cord gas was a normal 7.37 pH. Apparently, as soon as the cord was cut, the child decompensated. He believed that some unidentified condition in utero caused the severe manifestations – gasping, poor heart rate, inability to initially ventilate. He believed that it was this undiagnosed condition that led to the poor outcome with profound neurological impairment. While he was critical of some of the initial treatment of the child upon delivery for causing or exacerbating bilateral pneumothoraxes, he said that did not cause the child’s neurological impairment, as within a relatively short time, parameters such as color, heart rate and blood gas values, and the pneumothoraxes began to improve. He opined that the profound ongoing nature of the neurological impairment goes back to the child’s condition in utero. He stated that this was not a case where “brain cooling” should have been employed.
Plaintiff’s early demands were in the high 7- to low 8-figure range. After discovery and depositions, a series of mediations were held. Given the difficulties posed by the FHR strips, the lack of an alternative explanation for the child’s decompensation after birth beyond hypoxia and the significant exposure portended by a potential jury verdict, the matter was settled for $2.5 million.
1. 1992 twin, premature birth – Philippines – one child survived. 2009 birth; full term; preeclampsia; 7 lbs., 7 oz.; Apgars 9/9.
2. Again, it should be noted that the post-delivery cord PH was an appropriate 7.37.