9th Annual AABC Birth Institute 10/1/2015 HEAD COMPRESSION: PLAINTIFF’S NEW THEORY TO EXPLAIN CEREBRAL PALSY 9th ANNUAL AABC BIRTH INSTITUTE OCTOBER 1-4, 2015, SCOTTSDALE, AZ OCTOBER 2, 2015 Julia K. McNelis, R.N., J.D. Kitch Drutchas Wagner Valitutti & Sherbrook Mt. Clemens, Michigan (Detroit, Marquette, Lansing, Chicago, Toledo) Terms/Definitions • Freemans, 3rd Ed. 2003 • NICHD 2008 • ACOG 2009 • Williams, 23nd Ed. 2010 • Freeman’s, 4th Ed. 2012 1 9th Annual AABC Birth Institute 10/1/2015 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 2 9th Annual AABC Birth Institute 10/1/2015 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 3 9th Annual AABC Birth Institute 10/1/2015 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. 4 9th Annual AABC Birth Institute 10/1/2015 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 5 9th Annual AABC Birth Institute 10/1/2015 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 6 9th Annual AABC Birth Institute 10/1/2015 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. 14 7 9th Annual AABC Birth Institute 10/1/2015 15 16 8 9th Annual AABC Birth Institute 10/1/2015 17 18 9 9th Annual AABC Birth Institute 10/1/2015 19 20 10 9th Annual AABC Birth Institute 10/1/2015 21 22 11 9th Annual AABC Birth Institute 10/1/2015 23 24 12 9th Annual AABC Birth Institute 10/1/2015 25 26 13 9th Annual AABC Birth Institute 10/1/2015 27 28 14 9th Annual AABC Birth Institute 10/1/2015 • 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 15 9th Annual AABC Birth Institute 10/1/2015 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) 16 9th Annual AABC Birth Institute 10/1/2015 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) 17 9th Annual AABC Birth Institute 10/1/2015 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. 35 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) 18 9th Annual AABC Birth Institute 10/1/2015 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). 19 9th Annual AABC Birth Institute 10/1/2015 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 and 2) Shifts of neural structures within the cranium. (Id. p. 175) 20 9th Annual AABC Birth Institute 10/1/2015 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 21 9th Annual AABC Birth Institute 10/1/2015 22 9th Annual AABC Birth Institute 10/1/2015 Two Tachysystole Theories 1) ↓ resting period inability for placenta to refill 2) Contractions head compression Tachysystole Theory No. 1 1) 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! 23 9th Annual AABC Birth Institute 10/1/2015 THE TWO OMINOUS PATTERNS • Lates/No Variability - Freeman 3rd, p. 71 Variables/No Variability - Freeman 3rd, p. 76 • 24 9th Annual AABC Birth Institute 10/1/2015 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 25 9th Annual AABC Birth Institute 10/1/2015 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. 26 9th Annual AABC Birth Institute 10/1/2015 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 27 9th Annual AABC Birth Institute 10/1/2015 Schwarz (1969) • CTX ↑ pressure by cephalic receptor with ↑ in amniotic pressure.