terms/definitions · 2018-04-03 · 9th annual aabc birth institute 10/1/2015 2 freeman’s 3rd ed...

9th Annual AABC Birth Institute 10/1/2015

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Julia K. McNelis, R.N., J.D. Kitch Drutchas Wagner Valitutti & Sherbrook

Mt. Clemens, Michigan

(Detroit, Marquette, Lansing, Chicago, Toledo)

HEAD COMPRESSION: PLAINTIFF’S NEW THEORY TO EXPLAIN CEREBRAL PALSY

9th ANNUAL AABC BIRTH INSTITUTEOCTOBER 1-4, 2015, SCOTTSDALE, AZ

OCTOBER 2, 2015

Terms/Definitions

• Freemans, 3rd Ed. 2003• NICHD 2008• ACOG 2009• Williams, 23nd Ed. 2010• Freeman’s, 4th Ed. 2012


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Freeman’s 3rd Ed (2003)• Primary function of ctx is expulsion of uterine

contents• Manual palpation has been traditional method of

monitoring ctx• During labor strength varies 30mm Hg average

early labor to 50 mm Hg later first stage• 50mm Hg to 80 mm Hg second stage• Once labor starts ctx become more frequent and

stronger

Freeman’s 3rd (2003) Fig 5.8


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NICHD (2008)

• Normal-5 or less ctx in 10 minutes, averaged over 30 minutes

• Tachysystole-> 5 ctx in 10 minutes, averaged over 30 minutes

• “Hyperstimulation” and “hypercontractility” are not defined and should be abandoned

ACOG # 107 (2009)

• Adopts NICHD definitions• Tachysystole should always be qualified

as to the presence or absence of associated FHR decelerations

• The term tachysystole applies to both spontaneous and stimulated labor


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Williams 23 Ed. 2010

• Ctx in normal labor-forces are greatest and last longest at the fundus and diminish towards the cervix

• The Montevideo group ascertained that the lowest limit of ctx pressure required to dilate the cervix is 15 mm Hg

Williams 23 Ed. 2010• Hypotonic uterine dysfunction: there is no

basal hypertonus and uterine ctx have a normal gradient pattern but pressure insufficient to dilate the cx (synchronous). (p 467)

• Hypertonic uterine dysfunction: either basal tone is elevated appreciably or pressure gradient is distorted. (p 467)

--Gradient distortion may result from contraction of the uterine midsegment with more force then the fundus.


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Freeman’s 4th Ed 2012

• At or near term baseline tone of uterus 8 to 12 mm Hg, with values is excess of 25 mm Hg defines as hypertonus.

• Palpation and patient sensation will be reliable with regard to frequency but will be less so for duration and intensity. (p 79)

Freeman’s 4th Ed 2012 Fig 5.6


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Jury awards $58 million to Norwalk couple in baby case, the largest verdict in state

history

$110 million verdict in Michigan Head Compression During Labor and

Delivery


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THE PLAINTIFF THEORY

Mechanical forces of labor cause fetal brain damage in spite of normal FHR monitoring, normal Apgar Scores, normal umbilical artery blood gas results, and a normal newborn course.

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• Baby bagged for 1 minute at birth• No additional oxygen needed• No acidosis:

– Venous cord gas pH 7.29– Bicarb 24

• No multiorgan involvement• Pitocin off at 3:30 p.m.• 5 min Apgar of 7• Genetic malformation of the posterior

fossa and cerebellar hypoplasia. (25% of brainstem missing.)

Schifrin-Glass Abstract


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FACTS

• 30 forensic cases. (SA p. 151 12/11)• Schifrin, Glass, Ater were experts.• Tried, settled, no cause.• NECP Criteria• Criteria for inclusion was pH >7.0 (SA p. 160

12/11)


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FACTS (Con’t)

• Descriptive Study” > Not controlled• All fetal heart rate patterns were interpreted by

Dr. Schifrin. (SA p. 160 12/11)• All cases had >4 hours of

hyperstimulation/tachysystole via Shifrin (irrespective of any fetal heart rate response). (SA p. 165 12/11)

• Hyperstimulation/tachysystole defined as either:– >6 ctx in 10 min or URT >25 mm by IUPC

FACTS (Con’t)

• All 30 pregnancies also had changes in fetal heart rate pattern with the hyperstimulation/tachysystole. (SA p. 168 12/11).– Not subtle. (p. 169)– Eventually clearly developed signs of decompensation on the

FHRM. (p. 169)• All 30 cases had protracted active phase of labor. (p.

171)• Six terminal bradycardias. (p. 180)• 86.7% of adverse outcomes were anticipated based on

FHR pattern alone. (p. 183)• Prolonged resuscitation and admission to the NICU

occurred in each case. (p. 185)


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Conclusion

The features of prolonged hyperstim, head trauma/compression, diverse

ischemic/hemorrhagic supratentorial lesions strongly suggest mechanical mechanisms of injury related to forces of the fetal head with

increased intracranial pressure and diminished perfusion.

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Conclusion (cont’d)

These data credibly suggest an intrapartum neurological injury may occur

without systemic hypoxia. Excessive uterine activity should be

scrupulously avoided irrespective of any FHR response.

(p. 190)


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Dr. Stephen Glass (6/28/2011)

It’s not peer reviewed. (p. 25)

It provides the “lowest level” of scientific evidence. (p. 26)

It is not something that would be offered or indicated as a high level of scientific rigor. (p. 26)

Q: In that regard, you would agree, then, Dr. Glass, that what is presented in your poster and abstract is not a scientific consensus of

opinion, correct?

A: No. Not intended as being that, nor do I believe that’s true. (p. 46).


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Deposition Testimony

Q: The hypertonus, in your opinion, did not result in a decrease in perfusion to the placenta, to the baby. It resulted in a cessation of perfusion to the placenta, to the baby at that time?

A: I believe because of – I don’t that that’s right, exactly what you said. I believe that – yeah, I believe that when the, around just before then, this baby never, his heart rate, his, his tone never got below 40 or so.

And during that period of time, with that high of tone, the baby was not getting ability to, because of the tone, the baby was not getting ability to, because of the tone, this flow through the placental bed by the maternal side was reduced, if no stopped completely, and essentially stopped ability for the baby to get oxygen as well as reduced CO2, which then caused the baby to become acidotic, and caused the heart to stop because of that.

The Foundation

• Volpe p. 178 (2008)– Intracranial pressures can lead to

deleterious consequences:1) Disturbances of CBF and2) Shifts of neural structures within the cranium. (Id. p. 175)


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Foundation (con’t)

– Disturbances of CBF• 1) Cerebral perfusion = mean arterial blood

pressure - the intracranial pressures.– ↑ICP ↓CPP– If ICP ↑markedly CPP ↓ below the lower

limit of autoregulation CBF becomes impaired


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Two Tachysystole Theories

1) ↓ resting period inability for placenta to refill

2) Contractions head compression

Tachysystole Theory No. 11) Tachysystole/Hypertonus

>5 CTX in 10 min. period ↓perfusion

• In utero placental insufficiency• Category 3 tracings• Recurrent variables/recurrent lates and absent

variability• Progressive hypoxia• Hypoxic Fetal Heart Rate Pattern!


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THE TWO OMINOUS PATTERNS

• Lates/No Variability - Freeman 3rd, p. 71

Variables/No Variability - Freeman 3rd, p. 76

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Tachysystole Theory No. 2

• Head Compression– The mechanism is not so much that the decelerations create

such a reduction in heart rate that you’re getting ischemia and systemic hypoxia or acidosis. The concern is that they’re more of a reaction to the increased intracranial pressure which is causing a reduction in blood flow inside the head. (SA p. 107 9/ 11)

• Engaged fetal head and contractions– Intracranial pressure = 2 to 4 times amniotic fluid pressure. (SA

p. 109 12/11)– Resting tone = 25 mm Hg → intracranial pressure = 100 mm Hg.– Pressure outside fetal head are up to 250 mm Hg. (SA p. 112

12/11)– “The baby’s head is in the vice grips of the maternal tissues and

maternal pelvis” (SA p. 110 12/11)

The “Support”• Kelly (1963)• Schwarz (1969)• Mann (1972)• Obrien (1984)• Carlan (1991)• Aldrich (1995)• Bakker (2007)• Simpson (2008), etc


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Kelly, Am J Ob Gyn 1963,85:867

The increased pressure is transmitted inside the calvarium where it may overcome the intravascular blood pressure resulting in arrest of the cerebral circulation.The ensuing development of anoxia and asphyxia may damage not only the brain cells, but also the blood vessel walls, making them liable to rupture when exposed to hypertension.

Kelly (1963)

• Discussion of forceps and head compression

• Concludes that compression of the fetal head during forceps causes rise in intracranial pressure, secondarily the systemic blood pressure….associated with a deceleration of the fetal heart rate.

• Unclear as to how much force is safe due to physiologic change of slowing heart rate to maintain normal perfusion.


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Schwarz (1969)

• Schwarcz, 1969, Uruguay• 18 full term vertex• 3 IUPCs between fetal head and membranes• Intra-amniotic pressure via catheter through

abdominal wall• FECG attached to buttock or head


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Schwarz (1969)• CTX ↑ pressure by cephalic receptor with ↑ in

amniotic pressure.• Closest receptor to equator of fetal head the

pressure was greater• Pressure at equator of fetal head > amniotic

pressure• FHR changes did not occur as long as pressure

received by fetal head < amniotic pressure• Pressure at fetal head > amniotic pressure

caused ↓ FHR• Pressure of 50 mm Hg = ↓ FHR

Schwarz (1969)-Conclusions

1) Transient falls in FHR are caused by strong compression exerted by the uterine contractions on the fetal head.

2) Cephalic compression > 40 mm Hg and higher than pressure rise in amniotic cavity causes ↓ FHR

3) Cephalic compression could cause ↑ intracranial pressure → ↓ cerebral blood flow → hypoxia and/or cerebral ischemia.


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Schwarz (1969) Issues

• Findings support ↑ CP early decelerations

• ↑ CP causes changes on FHR pattern• ↑ CP causes transient changes on FHR →

stimulating vagus center• No mention of outcomes• No evidence of ischemia or hypoxia in 18

neonates

Mann, OB/GYN, v. 39[5] (1972)

• 30 fetal sheep experiments• Force applied to fetal sheep via forceps• Intracranial pressure was recorded via needle into the brain• Found no changes in oxygen tension and pH in carotid artery• Heart rate decreased in 11 experiments increased in 12 and

remained unchanged in 7.• Blood flow decreased significantly due to increase in cerebral

vascular resistance.• Conclusions:

– External applied force causes marked reduction in cerebral blood flow– Following force, blood flow returned rapidly and brain was well

oxygenated.– EEG changes had appearance of slow waves with a decrease in

amplitude, diagnostic of fetal cerebral hypoxia.


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Obrien, AM J Perinatology, v. 1[3] (1984)

• 11 Lambs• Study effects of external cephalic compression• Uterus exposed through incision, exposing fetal head.• Inflatable cuff was applied to the parietal region of the skull and

incision was closed• Fetal heart rate, blood pressure, and pulse were recorded with

pressure transducers• Fetal arterial pH, PCO2, and PO2 were measured by a blood gas

analyzer• Cuff pressures of 200 mmHg, initial bradycardia, then sustained

tachycardia.• 95% decrease in blood flow to all cerebral tissues occurred during

bradycardia• All fetuses demonstrated normal blood gas values and normal heart

rates and blood pressures prior to and following cuff inflation• No change in cardiac blood flow.

Carlan, J Perinatology, 1991,11(2) p.105-11

• 29 yr old, G 5, para 0• At 29 weeks gestation US showed marked

fetal cranial elongation and normal appearing intracranial anatomy

• 31 week vaginal birth, Apgars 5 and 7• Conclusion…The preterm parietal bones

are capable of more deformation of presumably lower forces than at term via Braxton-Hicks ctx.

• At 6 months of life normal


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Aldrich, BJOG v. 12 pp.448-453 (1995)

• 10 term pregnancies• All ROM• 7 augmented• EFHM• Fetal optical probe → fully dilated cervix →

applied against fetal head during routine vaginal exam → two fiber optic bundles were mounted 3 to 5 cm apart.

• Data was compared from prior to push to during pushing efforts.

Aldrich (1995) Results

• Following pushing all 10 fetuses• Cerebral hmg ↑• Cerebral blood volume ↑• Cerebral O2 ↓• All infants Apgar’s > 7 and 9• pH mean was 7.27


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Aldrich (1995) Conclusions

• Pushing causes ↓ fetal cerebral oxygenation (↓ HMG, ↓ O2)

• Pushing → reduction in utero placental blood flow → ↓ rate of oxygen exchange

• However, since only 4/10 resulted in variable decelerations (cord compression)

• Explanations are:1) Cerebral blood volume increased due to: ↑

intrauterine pressure between thorax and head → ↓ cerebral venous drainage →↑ cerebral blood volume

2) Fetal Head compression against pelvic tissues → increased pressure →↑ cerebral blood volume

Freeman 3rd, p. 22 (2003)

• Although it has become a popular theory, there remains no scientific basis for the action that cerebral ischemia caused by the pressure of labor in the absence of fetal hypoxia is a cause of cerebral palsy.”


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Cumberbatch v. Blanchette825 NY S2d 744 (2006)

• Plaintiff appealed from an Order in Circuit Court granting Defendant’s Motion to Preclude Testimony of Dr. Shifrin alleging fetal distress resulting from head compression of an infant’s head due to labor contractions

Cumberbatch Cont’d• The Court of Appeals concluded:

– Plaintiff’s failed to meet their burden of proving that Dr. Shifrin’s theory of causation was generally accepted in the medical community

– Plaintiff’s expert could cite to no relevant scientific data that compression of the infant’s dead due to labor contractions, augmented by Pitocin, resulted in ischemia, which in turn, resulted in an infarction.


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Bakker 2007, AJOG, v. 196 p. 313

• IUP recordings of 1433 vaginal deliveries from 1993 to 2004 at University in Netherlands

• Objective to assess the role of uterine activity on fetal outcome

• Findings:– > uterine activity is associated with higher incidence of an

umbilical artery pH of 7.11 or less– pH of 7.11 = fetal acidosis– When contractions occur and they exceed 30 mm Hg, the

maternal spiral arteries are compressed and placental perfusion is strangulated

– Elevated UA during the first and second stage of labor increases the risk of adverse fetal outcome

Bakker (2007) Issues

• Arbitrary fetal acidosis pH set at 7.11?• Hypertonus may cause placental insufficiency. (Late

decels)• No mention of fetal outcome• Cites to Freeman 3rd Edition for proposition that when

CTX>36 mmHg, placenta perfusion is “strangulated.”– Excessive uterine activity may cause inadequate

placental perfusion giving rise to fetal hypoxia. (p. 59).– “The effects that these contraction patterns may have

on the fetus are most immediately reflected in heart rate….”


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K. Simpson, AJOG, [199:34] (2008)

• Retrospective study of 56 inductions• ISL/IUPC-FS02 sensor inserted• 2 Definitions of hyperstimulation/tachysystole

– >5<6 CTX in 10 minutes– >6 CTX in 10 minutes– Both >30 minutes

• 102 periods of 30 min. of group 1• 56 periods of 30 min. of group 2• After 30 minutes, pit d/c, O2, IV bolus, and/or lateral positioning• Results:

– More absent and minimal variability, fewer accelerations, and mote late and recurrent decelerations in both hyperstimulation groups

– Group 2 = < accelerations >recurrent decelerations– Fetal oxygen desaturation in both groups over time

Simpson (2008) Conclusion

• Hyperstimulation caused desaturation and negative effect on FHR patterns

• 30 minutes of hyperstimulation = 20 to 29% decrease in fetal oxygen saturation

• More intervention the better• 5 or more CTX in 10 minutes is best definition• Did not measure effects on fetus with > 30

minutes of hyperstim.


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ACOG 107 (2009)

– Tachysystole should always be qualified as to the presence or absence of associated FHR decelerations.

– If uterine tachysystole with Category III FHR tracings occur, prompt evaluation is required and intravenous infusion of Oxytocin should be decreased or discontinued to correct the pattern.

ACOG 116 (2010)

• In laboring women receiving oxytocin, management of tachysystole generally involves efforts to reduce uterine activity…

• If there is a Category II or III tracing, oxytocin should be reduced or stopped…

• If tachysystole induced FHR abnormalities do not resolve with these initial maneuvers, then tocolytic medications may be warranted.


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Stewart Gray Journal (2012)

• Robert Stewart. Parkland. Dallas• 584 women undergoing induction• First four hours of induction, looked at ctx

6 or more in ten minutes• Found more FHT decels• Found no association with adverse

outcomes.

David Miller, M.D. Contemporary OB/GYN (2012)

• The theoretical mechanism of injury directly contradicts the NECP task force and is inconsistent with existing scientific evidence and consensus in the literature.

• Complete lack of validity.• No study has demonstrated that ctx-related

pressure on the fetal head causes abnormal newborn brain function.


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Dr. Michael Ross

• Tachysystole should always be qualified as to the presence or absence of associated fetal heart rate deceleration. P. 232

• Increased uterine activity of any type DOES NOT infer fetal stress or distress. P. 233

• Increased uterine activity may be well tolerated by some fetuses, whereas other may demonstrate stress with uterine activity of a low intensity. P. 233

• When a reactive fetus does not respond to increased contraction frequency with a fetal heart rate change (i.e., tachysystole) the situation suggests that excellent compensatory mechanisms with hypoxia are operative. P. 237

Nelson NEJM September 2015

Continuous electronic fetal monitoring during labor was introduced to identify fetal asphyxia, with the expectation that timely Intervention would prevent CP. Unfortunately, that expectation has met with disappointment. Despite there being a marked increase in surgical deliveries, risks and costs, no decrease in numbers of live births with CP in last 3 decades.


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Figure 1, Elective and Emergency Cesarean Sections and Live Births with Cerebral Palsy in Western Australia, 1980-2009, Perinatal Factors in Singletons with Cerebral Palsy Born at or near Term, The

New England Journal of Medicine, Karin B. Nelson MD, et al., September 3, 2015

Tachysystole and/or HypertonusDefense Expert

• We see this all the time and it is very commonly seen and well tolerated by both the mother and the fetus.

• We know with certainty that acute changes in the acid-base status of the fetus and the oxygenation level of the fetus in a laboring woman are reflected directly in the fetal monitor tracing of the heart

• In the absence of those change, then one can conclude with confidence that the baby is neither hypoxic not acidotic despite what may be going on in the mother.

• The utero-placental unit is functioning well and it will be reflected in the heart rate.


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Risk Management Issues Going Forward

• Fetal Heart Rate Monitor v Auscultation• Tachysystole• Hypertonus• Induction/Augmentation• Internal Policies• Charting

• Tachysystole->5 contractions in 10 minutes averaged over 30 minutes


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• Hypertonus-? Definition

Oxytocin

• FDA High Alert drug• Oxytocin Package Insert• **Favorite Bad Guy in any case


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Oxytocin Package Insert

CONTRAINDICATIONS

Oxytocin is contraindicated in any of the following conditions:

• Significant cephalopelvic disproportion;

• Unfavorable fetal positions or presentations which are undeliverable without conversion prior to delivery, e.g. transverse lies;

• In obstetrical emergencies where the benefit-to-risk ratio for either the fetus or the mother favors surgical intervention;

• In cases of fetal distress where delivery is not imminent;

• Hypertonic uterine patterns;

• Hypersensitivity to the drug.

Internal Polices

• What does your birth center policy say regarding definitions

• What does the hospital policy say with regard to definitions? Induction of labor? Oxytocin?


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Charting

• Presence of Tachysystole• Fetal Heart Response• Management Plan• Reduction or Discontinuation of Pit• Use of Terbutaline• Notification of Attending

QUESTIONS?


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Julia K. McNelis, R.N., J.D. Kitch Drutchas Wagner Valitutti & Sherbrook

Mt. Clemens, Michigan

(Detroit, Marquette, Lansing, Chicago, Toledo)

Thank You!

terms/definitions · 2018-04-03 · 9th annual aabc birth institute 10/1/2015 2 freeman’s 3rd ed...

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