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STATE OF MAINE
YORK, ss SUPERIOR COURT
DOCKET NO. CV-2015-114
CLAIRE HANSEN, Minor Child, et al :
YORK HOSPITAL, et al :
: PANEL BRIEF OF CLAIMANTS
This case comes before Panel as a result of a Notice of Claim filed under Maine's Health Security Act.
This case involves the labor of Tawni Hansen and delivery of Claire Hansen.
Tawni Hansen received prenatal care from Jennifer Eaton, DO at Coastal Obstetrics & Gynecology (hereinafter “Coastal”) beginning at approximately 7 weeks gestation in November, 2008. This was Mrs. Hansen's first pregnancy and her due date was determined to be July 7, 2009. Dr. Eaton was an obstetrician employed both by Coastal and York Hospital (Eaton deposition, 11:17-20)
Mrs. Hansen’s prenatal course was complicated by maternal phenylketonuria (PKU). Phenylketonuria is an autosomal recessive disorder of phenylalanine metabolism characterized by deficient activity of the hepatic enzyme, phenylalanine hydroxylase. The main treatment for maternal phenylketonuria is to restrict the consumption of phenylalanine which results in a decrease in serum phenylalanine levels. ACOG (American Congress of Obstetricians and Gynecologists) recommends that pregnant women with phenylketonuria be monitored in consultation with providers from experienced phenylketonuria centers.
Mrs. Hansen was co-managed at Maine Medical Center with maternal-fetal medicine specialists. Dr. Jennifer Eaton, the physician who provided prenatal care to Mrs. Hansen, testified in her deposition that York Hospital, where Mrs. Hansen delivered, was not an experienced phenylketonuria center. [27:2-3]
Dr. Eaton further testified in her deposition that Mrs. Hansen was the only patient she had ever delivered that had phenylketonuria. [27:8] By her own admission, Dr. Eaton states that phenylketonuria is considered a high risk condition [30:17]
Throughout her pregnancy, Mrs. Hansen complied with the physician instructions regarding her prenatal care and phenylketonuria. She was seen at Maine Medical Center by the maternal fetal medicine specialists in order to attain the highest level of patient safety for her and her unborn child.
On June 29, 2009, at approximately 38 5/7 weeks gestation, Mrs. Hansen presented to York Hospital for a non-stress test and biophysical profile to assess fetal status. All testing on this date of June 29, 2009 indicated fetal wellbeing. However, Mrs. Hansen's blood pressure was elevated to 148/100 indicating the possibility of preeclampsia.
Preeclampsia is a serious maternal condition that is characterized by an alteration in angiogenic factors which affects the placenta, kidneys, liver, blood and brain. The dysfunction of the maternal vascular endothelium with preeclampsia manifests as enhanced formation of factors such as endothelin, reactive oxygen species and augmented vascular sensitivity to angiotensin II. Maternal preeclampsia can have deleterious effects on the fetus as placental blood flow and thus, gas and nutrient exchange may be interrupted causing partial, and possibly prolonged inadequate oxygenation for the fetus.
With the addition of preeclampsia, Mrs. Hansen was now a high risk patient with two known high risk, complicating factors-- phenylketonuria and preeclampsia.
Due to Mrs. Hansen's preeclampsia, she was sent to York Hospital on June 30, 2009 for induction of labor. Mrs. Hansen was admitted at approximately 3:30 pm by Tawanna Gordon, MD. Mrs. Hansen's blood pressure was checked at the time of admission and was documented as 146/98 with a pulse of 96.
Dr. Gordon ordered Cervidil to be placed and used as the initial agent for Mrs. Hansen's induction of labor. Cervidil is a vaginal insert placed to start or continue the ripening of the cervix in pregnant women who are at or near the time of delivery and in whom there is a medical reason for inducing labor. The manufacturer’s information recommends lying down the first two hours after insertion to assure the insert remains in place. Cervidil can cause tachysystole and, in doing so, cause decreased oxygenation and cerebral perfusion to the fetus due to inadequate resting time between contractions to allow for adequate cerebral reperfusion and gas exchange.
The fetal status was checked on admission by placing an external electronic fetal monitor. Initially, the fetal heart rate baseline was determined to be 124 with average long term variability (6-25 beats per minute) and accelerations in the fetal heart rate with activity.
It is important to remember that the fetal brain modulates the fetal heart rate through an interplay of sympathetic and parasympathetic forces. Thus, fetal heart rate monitoring can be used to determine if a fetus is well oxygenated. In this case, the fetal monitor tracing at the time of admission revealed a well oxygenated fetus.
Fetal monitors use ultrasound Doppler when an external monitor is placed. Using the Doppler method, the transducer which is in transmittal mode emits sound waves into the body which are reflected by different tissues. The reflections known as Doppler echoes are picked up by the transducer. These echoes are then amplified and sent through a speaker to be heard. Synchronically, the echoes are processed by an autocorrelation algorithm in the computer within the fetal monitor to determine the fetal heart rate which is then displayed on the monitor and recorded on the fetal tracing. Nurses and healthcare providers assess the fetal wellbeing status by reading and interpreting the fetal tracing. The accuracy of the fetal tracing is therefore important to assure the accurate interpretation of the fetal status.
After maternal and fetal status were found to be reassuring, the Cervidil was placed as stated. Mrs. Hansen contracted during the night with a frequency noted to vary from 1-3 minutes to 5-6 minutes with a duration for the contractions noted to be from 40-120 seconds. Contraction frequency is measured from the beginning of one contraction to the beginning of the next contraction. For example, If a contraction begins at 1:00 pm and lasts 120 seconds it will end at 1:02 pm. Yet if the contractions are 1-3 minutes apart, the provider would note the contraction start at 1:00 pm and the next contraction (if 3 minutes apart) would start at 1:03 pm giving a minute of rest between contractions. During this resting time between contractions is when the brain reperfuses blood flow and gases are ultimately exchanged. When contractions are too frequent or too strong, the brain is not allowed enough time to reperfuse and damage occurs. Synchronically, the blood is not allowed enough time in the placenta to exchange oxygen and carbon dioxide leading to a low concentration of oxygen in the blood (hypoxemia) and a deficiency of oxygen reaching the tissues (hypoxia), again causing damage to the fetus.
Mrs. Hansen's water broke on July 1, 2009 at approximately 3:30 am and the fluid was noted to be clear. At 7:30am, Respondent Dr. Jennifer Eaton, assumed control of the care. CCM documented at 7:30 am that Mrs. Hansen was in active labor and that her cervix 3 cm dilated, 90% effaced with the baby’s head at 0 station. Her contractions are noted to be every 1-2 minutes.
At 9:00 am, the nurses documented that Mrs. Hansen continues to have an external fetal monitor in place showing a baseline fetal heart rate of 135 with average long term variability, accelerations and early decelerations.
Nurses and healthcare providers denote the presence of decelerations for the fact that medicine has shown that CO = SV X HR. (CO = cardiac output; SV = stroke volume; HR = heart rate). If the fetal heart rate decelerates, cardiac output decreases. Cerebral perfusion pressure (CPP) is the net pressure gradient that causes cerebral blood flow to the brain. If there is too little cerebral perfusion pressure the brain tissue can become ischemic; if there it too much cerebral perfusion pressure, the intracranial pressure rises. Therefore, CBF = CPP/CVR where CBF is cerebral blood flow and CVR is cerebrovascular resistance. CPP = MAP-ICP is also an important mechanism within the brain. MAP is mean arterial pressure and ICP is intracranial pressure. External pressure causes decreases blood flow through the vessels in the brain. Increased intracranial pressure causes decreased blood flow to the brain in the fetus by compressing the cerebral arteries which increases cerebrovascular resistance. Under normal conditions, autoregulation maintains sufficient blood flow and protects the brain from ischemia. During labor, the repeated compression of the fetal head during contractions must be released for enough time to allow complete reperfusion to occur (resting time between contractions).
At 9:30 am, CCM documented that Mrs. Hansen was 4-5 cm dilated, 100% effaced and 0 station. Contractions are documented to be every 1-2 minutes. Contractions continue to be every 1-2 minutes.
At 1:05 pm, nursing documentation revealed Mrs. Hansen's pulse was 130 and the fetal heart rate was identical at 130. Cross channel verification was not done at this time to identify if the fetal heart monitor was, in fact, monitoring the fetus or the mother. Fetal monitors can misidentify the maternal heart rate as a fetal heart rate when the maternal heart rate is within 15 beats of the fetal rate thereby causing misinterpretation of fetal status.
Fetal monitoring manufacturers’ state that the fetal monitor can, and does, pick up the maternal heart rate when an external transducer is placed on the maternal abdomen. The fetal monitors also have channels for maternal heart rate monitoring such as maternal ECG and pulse oximetry. Maternal verification of heart rate therefore needs to occur regularly to differentiate it from the fetal heart rate. Maternal verification can be achieved by using pulse oximetry on the mother to differentiate it from the fetus. It must be remembered, however, that if the maternal pulse is tachycardic, the fetal monitor may confuse the two. The pulse oximeter works by using light wave technology while the fetal transducer works be emitting sound waves. The technologies are different and can be imprecise which can lead to the readings from cross channel verification attempts being incorrect. In this instance, a maternal EKG or manual maternal heart rate to verify is the best course of action and considered to be the standard of care.
At 1:30 pm, Mrs. Hansen is again examined by CCM and found to be 7 cm dilated, 100% effaced, and at 0 station with every 1-2 minute contractions continued.
At 5:00 pm, CCM documented that Mrs. Hansen was very uncomfortable with contractions every 2-3 minutes and a cervical exam that revealed 7 cm dilation, 100% effacement and again, a 0 station. At this time "Arrest of dilation" is noted by Dr. Eaton and discussed with Mrs. Hansen. The details of this conversation are unclear other than a cesarean section was offered due to no cervical change in 3 hours. It was conceded by Dr. Eaton at deposition that there was actually no cervical change for 4 hours and 45 minutes (91:13-17). It was also clarified in deposition that while Dr. Eaton “offered” a cesarean section, Mrs. Hansen was told that the baby’s fetal heart rate tracing was healthy, and therefore she agreed to continue with the induction. At no time did Dr. Eaton insist on a cesarean section and at no time did Mrs. Hansen refuse to have a cesarean section (Eaton deposition, P. 93:24-P. 94:25).
Mrs. Hansen received an epidural at approximately 5:30 pm for pain management. This also lowered her blood pressure.
Magnesium sulfate drip was given for blood pressure management beginning at approximately 6:00 pm. Contractions were still strong and occurring every 3 to 4 minutes.
Even though Mrs. Hansen progressed from 7 centimeters at 5pm to 9 centimeters at 6pm and her contractions were strong, Dr. Eaton ordered Pitocin augmentation which was started at approximately 7:13 pm. Dr. Eaton conceded in her deposition that giving Pitocin can cause already strong contractions to be stronger (101:17-102:8), regardless whether she was prescribing it to increase frequency of contractions. As of 7pm, all evidence supports that the baby was neurologically intact. Pitocin was given at increasing dosages. The baby’s status began to deteriorate approximately an hour after Pitocin was introduced. There is minimal beat to beat variability (beginning at Tracing 248 around 8pm), there is evidence of uteroplacental insufficiency, there is evidence of tetanic contraction, contractions more frequent without rest in between, classic hypertonis, classic hyper uterine activity, evidence of hypoxia which continues without stopping the increasing doses of Pitocin or investigating evidence of maternal insertion into the fetal tracing (i.e. mistaking the mother’s tracing for that of the baby). Without investigating whether the tracings are mother rather than baby, the healthcare providers are blind as to the impact of the Pitocin they continue to layer on at increasing doses.
Limitations in the external fetal monitor include misrepresentation of the fetal heart rate pattern which can lead to a potential misinterpretation of the fetal condition. These limitations are due to the fact that the sound waves are reflected from any tissue moving towards or away from the transducer. This could be the heart valves of the fetus, blood coursing through the maternal abdominal aorta or even the maternal cardiac valves themselves. Because of this, the fetal tracing requires frequent, regular confirmation that the tracing is indeed that of the fetus. There are several ways to verify the source and accuracy of the fetal heart rate recording. The fetal heart rate can be verified using an obstetrical stethoscope, ultrasound imaging or a fetal scalp electrode.
Maternal insertion/misidentification of fetal heart rate can be rectified with the insertion of an internal fetal scalp electrode to verify the baby fetal heart tracings. There is strong evidence of maternal insertion and Dr. Eaton could not explain the appearance of accelerations at the peak of Mrs. Hansen’s contractions (Eaton deposition, 111-112). Fetal heart rates decelerate during contractions as the cord is compressed during the contraction. There is no physiological explanation for a fetal acceleration at the peak of a contraction and even if there were, it is too dangerous with Pitocin flowing at increasing doses not to verify the fetal heart rate tracings.
Ongoing evaluation of the fetal tracing is only useful to evaluate fetal wellbeing if the tracing is in fact recording the fetus. The following gives examples of when this is indeed questionable in this case.
Time Maternal Pulse Fetal Heart rate
1305 130 130
1400 121 140
1800 116 125
1825 119 125
1840 118 125
1930 112 120
1945 111 125
2000 115 120
2015 115 130
2030 114 125
2045 111 125
2100 117 125
2115 125 125
2130 123 125
2145 125 120
2200 131 140
2215 122 135
2230 162 130 Are these reversed--is mom or fetus 162?
2245 160 130
Mrs. Hansen starts pushing at 2245
It is important to remember that if the fetal heart moves out of the ultrasound beam, the autocorrelation algorithm may then pick up the maternal and record the maternal tracing as the fetal tracing. The maternal heart rate can imitate several conditions of the fetus and fetal tracing which can lead to an erroneous interpretation. Maternal heart rates can simulate a fetal heart rate deceleration. The maternal heart rate can also simulate a normal fetal heart rate pattern especially during the second stage of labor when the mother is pushing and her heart rate naturally increases to where it may equal or exceed the fetal rate. In this instance, the maternal tracing may show a normal tracing including accelerations while the fetus may actually be decelerating or even be dead.
By 10:30 pm, Mrs. Hansen's cervix was completely dilated. In this case, when Mrs. Hansen begins pushing at approximately 2245, this occurs--the heart rate of Mrs. Hansen is recorded and misidentified as that of the fetus. In this instance the use of cross channel verification to detect probably duplication in the tracing from both maternal and fetal heart rate should be employed in order to identify fetal status. Instead, the Pitocin continues at higher dose and the contractions increase to the point that there is no resting time in between for the baby to recover. There are periods of contractions with 5 or more in a 10 minute period. During this time the Pitocin continues to run at high doses and Mrs. Hansen is encouraged to push. The fetal monitor tracings are obviously maternal with accelerations at the peak of contractions.
The baby, Claire Hansen, is born not breathing, is resuscitated with first gasp not occurring for 30 minutes and sustained respiration not occurring until 34 minutes. Head cooling protocol for 72 hours is ordered. This is done because the pediatrician, Dr. Westinghouse believed the baby’s injury was an acute hypoxic ischemic encephalopathy (lack of oxygen and blood flow causing a brain injury during labor and delivery)
Placental pathology revealed meconium stained fetal surface with normal maternal surface; a 3 vessel umbilical cord with a velamentous insertion; focal mild acute chorioamnionitis and chorionic villi showing uneven accelerated maturation.
Respondent Dr. Eaton:
In November 2008, Jennifer Eaton, D.O. advised Claimant Hansen that she can deliver at York Hospital barring any other complications other than her PKU. When Claimant Hansen developed pre-eclampsia prior to delivery, Dr. Eaton did not transfer her care to a tertiary care hospital nor did she consult with a specialist regarding the pre-eclampsia. Pre-eclampsia, a complication of pregnancy, may deteriorate rapidly and need a specialist in an emergency when mother or baby may experience a seizure, stroke or other severe health risk for harm or death. Dr. Eaton deviated from the acceptable standard of medical care for her position of licensed doctor of osteopathy and these deviations were the direct and proximate cause of Claimant Hansen’s prolonged labor and the direct and proximate cause of all of baby Hansen’s injuries.
On or about July 1, 2009, Claimant Hansen’s labor begins to deteriorate with no progression of the baby in the birth canal; arrest in dilatation is apparent. Dr. Eaton determines that Pitocin, a stimulant to the uterus, which induces contractions, is the next choice of treatment versus a C-Section, which would have assured a healthy baby. Dr. Eaton deviated from the acceptable standard of medical care by not recognizing the need for a C-Section to assure a healthy baby. Her deviations of the standard of care for a licensed doctor of osteopathy were the direct and proximate cause of Claimant Hansen’s prolonged labor and the direct and proximate cause of all of baby Hansen’s injuries.
Respondent York Hospital:
Respondent York Hospital through its agents, servants and/or employees had a duty to provide protocols for the transfer of high-risk pregnant mothers such as Claimant Hansen. Protocols are necessary to assure mothers and babies are not subject to injury due to the lack of expertise, staff and/or equipment at the time of delivery and to assure the need for a C-Section is recognized early enough to prevent injury to the mother and baby.
Further, York Hospital through its agents, servants and/or employees were negligent in not providing a pediatrician at the time of baby Hansen’s birth, which resulted in additional oxygen deprivation. A pediatrician should have performed resuscitation and even intubation to assure oxygen was supplied to baby Hansen’s lungs and brain. While a pediatrician was finally provided by Respondent York Hospital 10 minutes after birth, the baby was still not breathing and its pediatrician did not intubate baby Hansen. This is supported by the actions of the Maine Medical Center staff who provided immediate treatments such as head cooling to baby Hansen.
THE LAW AND STANDARDS/BURDENS OF PROOF
The issues to be determined by the Panel are as follows:
Whether it is more likely than not that the acts or omissions of Respondents were negligent, i.e. more likely than not, a deviation from a course of conduct recognized as a standard of care; and
Whether it is more likely than not that the acts or omissions complained of proximately caused injury to Claire Hansen. 24 M.R.S. § 2855(1).
The Panel’s purpose is to operate as a screen, not a brick wall. To be entitled to a Panel Decree marked “Yes” on the Decree form, Claimant needs only to prove the course of treatment pursued by Respondents, or the judgment exercised by Respondents, more likely than not deviated from a course of conduct recognized as reasonable by ordinarily competent physicians performing under like conditions. (See, Medical Malpractice Instruction 7.75.)
The proof used by the Panel shall be the preponderance of the evidence – not clear and convincing proof, and not proof beyond a reasonable doubt. 24 M.R.S. § 2855(2). The Panelists must understand and honor the distinction in the low-level of evidence required to be entitled to a “Yes” on the Panel Decree, and apply it to the case at hand.
It would be entirely improper for a Panel Chair, to express or imply to a Medical Panelist untutored in the law that clear and convincing proof is required. It would be entirely improper for a Panel Chair to express or imply to a Medical Panelist untutored in the law that proof beyond a reasonable doubt is the requirement to impose on a Clamant. Indeed, it can be said without dispute that a Panel Chair has a duty and obligation to assure herself that the Medical Panelists understand fully and apply only the lowest burden of proof required, i.e. that a “Yes” checkmark on the decree is required if Claimant has shown simply that it is more likely than not that a departure from a standard occurred, and that is simply more likely than not that the departure caused some injury to the Claimant.
Particularly where Medical Panelists have not been trained in the law, it is important for Medical Panelists to know that, under Maine law, a negligent act of a physician will not be excused by the fact that a course of conduct is customary. See Woolley v. Henderson Woolley v. Henderson, 418 A.2d. 1123 (ME 1980) at 1130(n) 6. References to local standards in past Maine cases have long since been rejected. Rather, Medical panelists must be educated by Attorney members of the Panel that the standard of care applicable to a physician in a panel hearing is the standard of care of any ordinarily competent physician under like conditions. McLaughlin v. Sy, 589 A.2d 448-452 (ME. 1991).
Wide latitude must be afforded the parties by the panel in the conduct of the hearing. The Maine Rules of Evidence need not be strictly applied. Rather, evidence must be admitted if it is the kind of evidence upon which reasonable persons are accustomed to rely in the conduct of serious affairs. 24 M.R.S.A. §2854(1).
Michael H. Bereston, admitted Pro Hac Vice
Attorney for Plaintiff
Michael H. Bereston, Inc.
Annapolis, MD 21401
Christopher R. Largay, Bar No. 7348
Largay Law Offices, P.A.
Bangor, ME 04401
CERTIFICATE OF SERVICE
This is to certify that on _________ day of October, 2016 Claimants Panel Brief of Claimants was sent to:
Marilyn Ashcroft, Panel Chair
Second Panel Member
Third Panel Member
Karen Wolf, Esquire
One Portland Square
Portland, Maine 04112
Michael A. Pignatelli Rath Young and Pignatelli, PC 20 Trafalgar Square, Suite 307 Nashua, NH 03063
R. Peter Taylor, EsquireHoefle, Phoenix, Gormley & Roberts, P.A. 127 Parrott Avenue Portsmouth, NH 03802-4480
Michael H. Bereston dical Center staff who provided immediate treatments such as head cooling to baby Hansen.
Whether it is more likely than not that the acts or omissions of Respondents were ne