Medical malpractice: Preparation and trial of birth injury ... · partum hypoxic events and cerebral palsy. Ostensibly this was designed to provide the practitioner with definitions

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NOVEMBER 2014

BY JAMES BOSTWICK

Over the past three decades the de-velopment and trial of birth injury casesdue to intra-partum hypoxic ischemic en-cephalopathy has evolved dramatically.During the 1960s and early 1970s, theonly method of monitoring a fetus duringlabor was by auditory auscultation (listen-ing for changes in fetal heart rate duringthe contractions). In the late 1970s andearly 1980s, electronic fetal monitoringwas developed and it soon became a stan-dard method for monitoring fetal well-being during labor (recordation of thefetal heart rate and the uterine contrac-tion by either internal or external meanson a continuous paper strip). It becamewidely used because it provided the onlyavailable window as to the well-being ofthe fetus. Over time, certain abnormali-ties suggesting “fetal distress” becamerecognized and it was recommended thatintervention occur to prevent asphyxialinjury to the fetus.

During the 1990s, the American College of Obstetrics and Gynecology(ACOG) began to realize that this essen-tial monitoring tool was also providingrecorded evidence concerning the fetus’scondition for birth injury litigation. Con-siderable attention was devoted to devel-oping strategies which expert witnessesand defense lawyers could use to nullifyor lessen the impact of abnormal fetalheart tracings of children that laterproved to have cerebral palsy. Major ret-rospective studies were undertaken which

ostensibly provided evidence that overtime the use of fetal monitoring made little or no difference in the percentage ofchildren born with cerebral palsy. Exten-sive effort also went into the analysis ofthe pathology of the placenta, neonatalpresentation and neuro-imaging findings;these were studied extensively looking foralternative explanations or potentialmarkers which could suggest a given pa-tient had not suffered an intra-partum in-sult. Attorneys specializing in this areaover the decades have seen a variety ofinventive hypotheses put forth as the cau-sation defense du jour, including fetal nu-cleated red blood cells, infection,mediated cytokine cascade causing sys-temic inflammatory response (SIRS), aswell as claimed placental abnormalitiessuch as villitis, intravillus thrombi, lowplacental weight, umbilical cord abnor-malities, eccentric cord insertions, nuchalcord, cord knots, etc.

By the early turn of the 21st century,this collaborative effort to create a sys-tematic defense modality to counter successes in birth injury litigation culmi-nated in the 2003 ACOG Task Force publication: Neonatal Encephalopathyand Cerebral Palsy: Defining the Patho-genesis and Pathophysiology. This “whitepaper” purported to outline criteria thatwere deemed essential in order to estab-lish a causal link between claimed intra-partum hypoxic events and cerebralpalsy. Ostensibly this was designed toprovide the practitioner with definitionsof intra-partum asphyxia and cerebral

palsy. In reality it appeared to manyknowledgeable observers the goal was tocreate exclusive criteria which experts tes-tifying in birth injury cases would have touse to establish causation.

The publication listed certain “essen-tial criterion” that had to be met beforecerebral palsy could be attributed to anintra-partum event. They were as follows:1. Evidence of an umbilical cord pH ofless than 7 and a base excess (a compo-nent of the blood gas analysis intended to show the accumulation of lactic acidsufficient to cause brain damage) of 12 or greater.2. Early onset of severe or moderateneonatal encephalopathy in infants at 34 or greater weeks in gestation. 3. Spastic or dyskinetic cerebral palsy.4. Exclusion of other possible causes, suchas infection, metabolic coagulation andgenetic disorders. [The battles here werefought primarily concerning numbers 1and 4.]

According to this study, there werealso several “non-essential criteria”which, while not specific for an asphyxialinjury, collectively would suggest that aninjury had occurred during labor and de-livery:1. A sentinel hypoxic event occurring im-mediately before or during labor (such asa prolapsed cord, placental eruption or amaternal and/or fetal hemorrhage). 2. A sudden and sustained fetal bradycardia(reduced heart rate) or the absence of nor-mal variability in the fetal heart rate withpersistent, late or variable decelerations.

Medical malpractice:Preparation and trialof birth injury casesA look at continuing developments in the field, includinghistory of fetal monitoring and causation issues

3. Apgar Scores (the assessment of a newborn’s status on a scale of 0 to 10) of 0 to 3 when a baby is five minutes oldor older.4. Onset of multi-system organ damagewithin 72 hours of birth. 5. Early imaging studies showing anacute, non-focal cerebral injury. [The battles here were fought primarily onnumbers 2, 3, 4 and 5.]

These essential criteria had been de-veloped in earlier ACOG bulletins andother medical journal articles in order tobolster defense positions in birth traumalitigation. Both prior to the ACOG publications in January of 2003 and sub-sequent thereto, there were a multitude ofcriticisms concerning the various criteria. Many authors suggested that acord blood pH cut-off of less than 7 wasartificially low and failed to include manybabies who clearly had suffered intra-partum asphyxia. Apgar scores are noto-riously subjective and many children suffering clear intra-partum events andother signs of intra-partum hypoxic is-chemic encephalopathy are oftenawarded Apgars higher than 3 at fiveminutes.

Seizures are a common sign of intra-partum asphyxial injury and were noteven mentioned as one of the criteria.

Experienced observers noted that in clear cases of intra-partum asphyxiathere often was not a sudden and sus-tained fetal bradycardia; further, that thecomplete absence of variability in thefetal heart rate, when there are persistentlate or variable decelerations is rarelyseen in clearly asphyxiated children. In-vestigators have frequently argued that abase excess greater than 12 is highly sug-gestive of ongoing intra-uterine asphyxia,whether or not the blood pH was lessthan 7. (There are a variety of circum-stances that can artificially elevate the ar-terial cord gas pH in an asphyxial eventincluding variations in maternal bloodpressure and an occult or a frank cordprolapse.) There also was huge contro-versy about the significance of early imag-ing findings.

National Fetal MonitoringStandards

All but one of the criteria describedabove deal with the retrospective analysisof causation after the occurrence of a po-tential intra-partum event. Only one ofthe criteria, that which relates to fetalmonitoring, provides a prospective aswell as a retrospective tool for the analysisof fetal well-being. Only fetal monitoringcan potentially determine on a real timebasis whether a fetus may be sufferingintra-partum asphyxia and thereforeneeds immediate conservative and/oremergent intervention. In the litigationcontext, defense experts continued to citethe old studies, claiming there is no de-crease in the number of cerebral palsychildren since the advent of the use offetal monitoring. On the other hand,monitoring is widely used by all practi-tioners; indeed, not even the staunchestdefense experts are willing to forego fetal monitoring in the care of their own patients. Why? It is clearly the onlyhelpful tool that exists to provide evi-dence concerning fetal status. Studiesmake it clear that suboptimal EFM prac-tices contribute to the occurrence of fetalasphyxia and consequent birth injuries.

In Sweden, there was a study of 177children with severe labor-related as-phyxia; they found that approximately 50percent of the cases were related to physi-cian and nursing malpractice. It was theconclusion of the authors that the failureto identify ominous fetal heart rate pat-terns associated with fetal hypoxia andacidosis and to initiate appropriate inter-ventions had the clear potential to lead tosevere asphyxia, death and/or cerebralpalsy.1 Another Swedish study concludedthat intra-partum events are very impor-tant potential causes of post-natal neuro-logic symptoms because they arepreventable; they note that misinterpreta-tion of electronic fetal monitoring pat-terns is often a contributing factor incases of asphyxia.2

As far back as 1997, a Taskforce metand started the process of developing

standardized definitions for interpreta-tions of fetal heart rate tracings and fordefining the presence of abnormal elec-tronic fetal monitoring patterns as it re-lated to the prediction of the potential forfetal compromise. These very basic defi-nitions establishing a normal baseline(110-160 beats per minute), the (reassur-ing) importance of accelerations of morethan 15 beats per minute for at least 15seconds and the absence of prolongedvariable or late decelerations (non-reassuring), and of course, the impor-tance of normal fetal heart rate variability(short and long term variations of heartrate). They stated that guidelines neededto be developed for clinical managementof fetuses with tracings between the ex-treme of normal and the obvious omi-nous pattern, so that clinicians could bealerted to the development of intra-par-tum asphyxia and recognize it earlyenough to prevent injury or death.

In 2005, despite the fact that fetalmonitoring is utilized in about 85 percentof live births in the United States, ACOGpublished a New Practice Bulletin whichessentially stated that it was unrealistic toexpect that a non-reassuring fetal heartrate tracing could predict cerebral palsy.The practice bulletin went on to assertthat there was a wide variation in the wayobstetricians interpret and respond tofetal monitoring tracings. If true, this cer-tainly would seem to cry out for more de-finitive standards to prospectively helpthe practitioner deal with potentially con-cerning fetal heart rate patterns.

Finally, in 2008, ACOG updated thedefinitions for fetal monitoring from the1997 guidelines and proposed that clini-cians adopt a new three-tiered system forcategorizing fetal heart rate patterns.Those categories are:Category 1 is essentially normal fetalheart tones with a normal baseline rateand moderate fetal heart rate variability.There may be decelerations and eitherpresent or absent accelerations. Category 2 is (the large, gray area) de-fined as all patterns not classified as Cate-gory 1 or Category 3. These patterns are



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described as “indeterminate and don’tpredict abnormal fetal acid-base statusand require ‘evaluation and continuedsurveillance.’” These situations would in-clude bradycardia, provided that there’snot totally absent variability, tachycardia,decreased or minimal variability, absentvariability with no current decelerations,marked variability, absence of accelera-tions after scalp or other stimulation, re-current variable decelerations withdecreasing or minimal variability, pro-longed decelerations (less than 10 min-utes), recurrent late decelerations withdecreasing or minimal variability, andvariable decelerations with a slow returnto baseline. Category 3 tracings are considered to beabnormal and “may” predict abnormalfetal acid-base status at the time of obser-vation. These include sinusoidal patternsor absent variability with recurrent late de-celerations, recurrent variable decelera-tions or bradycardia. (Note here thatthey have tightened the definition ofbradycardia indicating abnormal statusonly includes low heart rates with absentvariability.)

For quality clinical care, it wouldhave been best to provide clear and com-prehensive guidelines especially in thegray areas of Category 2. The Category 3situations are already potential disasters.Many of the scenarios in Category 2 maybe developing situations that need inter-vention before it is too late to alter theoutcome. In addition, even though thebulletin clearly established that Category3 patients are abnormal and that they maypredict abnormal fetal basis acidosis status,all they required the clinicians to do is tomake an “effort to expeditiously resolvethe abnormal pattern.” In describing theappropriate interventions, they mentionall of the standard, conservative attemptsto change fetal status, such as administer-ing oxygen, change in position, discon-tinuing stimulation and treating maternalhypotension, but stunningly, they neverbothered to mention surgical interventionor other expedited delivery. It was evidentthat these “guidelines” were purposely

worded in a vague and ambiguous fash-ion, with little concern for the clinician ortheir patient and an overriding goal ofproviding no definitive statements thatmight be utilized in birth injury litiga-tion.

In the years after the 2008 Taskforcepaper was published, ACOG continued toemphasize the limitations of electronicfetal monitoring, its uncertain efficacy andits high false-positive statistics in their an-nual practice bulletins. Yet, in practice,most of the live births in America contin-ued to be assessed with electronic fetalmonitoring because clinicians were awarethis remained the only method to deter-mine the well-being of the fetus. Thepracticing obstetricians intuitively recog-nized the obvious explanation for thesemisleading statistics. The overall preva-lence of cerebral palsy failed to diminishwith the use of fetal monitoring simplybecause the greatest percentage of cere-bral palsy cases are caused by events be-fore the onset of labor, only a relativelymodest number can be in whole or inpart attributed to intra-partum events.The other obvious reason the incidenceof cerebral palsy has not decreased is theremarkable advances made in the neona-tal care of the premature infant. Manypremature children that would have diedin the past now survive; unfortunately,they often have the complications com-mon to survivors of early gestation, such ascerebral palsy. So, while fetal monitoringmay have improved the chances the terminfant that gets into difficulty during laborwill avoid cerebral palsy, the increasingnumber of premature children with cere-bral palsy has kept the overall statisticsfrom showing an improvement. In theyears after 2008 it continued to be clearthat clinicians needed more definitiveguidelines to help them make interventiondecisions, but ACOG continued to rely onits vague litigation-oriented definitions.

2014, a breath of fresh air

In March of 2014, the AmericanAcademy of Obstetrics and Gynecologyand the American Academy of Pediatrics

published a Second Edition entitledNeonatal Encephalopathy and NeurologicOutcome. In this document, there are fi-nally some major changes in the evalua-tion of neonatal encephalopathycausation and the eventual neurologicoutcome, particularly as it relates to the role of asphyxia occurring during intra-partum events.

In the First Edition, as discussedabove, the Taskforce outlined essentialcriteria necessary to establish a causal linkbetween intra-partum hypoxic events andthe subsequent development of cerebralpalsy. This Second Edition clearly reflectsa broader perspective put forth by thecurrent Taskforce. It proposes that thisprocess should involve a comprehensivemulti-dimensional assessment of neonatalstatus to determine the likelihood that anacute hypoxic event occurred in andaround the labor and delivery timeframeand contributed to a neonatal en-cephalopathy resulting in a long-termneurologic injury. They have redefinedportions of the essential and non-essen-tial criteria in some very specific waysthat are more inclusive and more reflec-tive of the scientific evidence that hasbeen available for the last two decades.They admit they do not have a definitive test or set of markers that reliably establish that neonatal en-cephalopathy is or is not attributable toan acute intra-partum event. They rec-ognize the importance of being able toassess that issue as a matter of probabilityand, in this publication, provide signifi-cantly more definitive and more inclusivetools to aid in making that determina-tion.

Case definitions

They now define neonatal en-cephalopathy as a syndrome of disturbedneurologic function in the earliest days oflife in an infant born at or beyond 35weeks of gestation, now manifested by asub-normal level of consciousness orseizures and often accompanied by diffi-culty with initiating and maintaining respiration and depression of tone and



NOVEMBER 2014

reflexes. This is the first time that theyhave presented seizures as an alternativepresentation of neonatal encephalopathyas opposed to just an altered level of con-sciousness. It is also the first time thatthey have used the word ‘often’ ratherthan demanding there be ‘difficulty ininitiating and maintaining respirationand depression of tone and reflexes.’They go on to note that the neonatal en-cephalopathy due to acute hypoxic is-chemia (related to intra-partum events)will be accompanied by abnormal neona-tal signs and be associated with contribut-ing events that were and are in closeproximity to labor and delivery. They areproposing that determining causationshould be a process of compiling a con-stellation of potential markers and con-tributing events combined with thedevelopmental outcome to see if the con-stellation is consistent with an acute hy-poxic ischemic event and is not explainedby other etiologies. The approach pro-vides that the more the various elementsfrom the pertinent categories are consis-tent, the more likely it becomes that anintra-partum event has played a role inthe development of the neonatal en-cephalopathy and ensuing injury.

Neonatal signs considered tobe ‘consistent with’ an acuteintra-partum event

They now define as ‘consistent’ with anacute intra-partum event an Apgar Scoreof less than 5 at five minutes and at tenminutes. They go on to say that if theApgar Score at five minutes is greater thanor equal to 7, it is ‘unlikely’ that an intra-partum hypoxic ischemic event played amajor role. There are several majorchanges evident here when comparedwith the 2003 criteria, which requiredApgar Scores of 0 to 3 at five minutes.Here, they have not only increased theApgar Score from 3 to less than 5, butsuggest a score of 5 or 6 may also be ‘con-sistent’ because they indicate a score of 7 is necessary to fall in the category of‘unlikely’ to be related to an intra-partum

hypoxic ischemic event playing a role incausing neonatal encephalopathy. Thisessentially has changed the Apgar Scorelimit from 3 to 6. Furthermore, appar-ently in recognition of the subjective na-ture of Apgar Scores in general, they havenot even eliminated Apgar Scores of 7 orgreater; rather, they have simply placedthem in the category of being ‘unlikely.’

There have been major changes inthe analysis of fetal umbilical arteryacidemia, as it related to intra-partum asphyxia. The 2014 Second Editionstates that “a fetal umbilical artery pH of less than 7.0 or a base deficit greaterthan or equal to 12 mmol/L, or both, in-creases the probability that neonatal en-cephalopathy has an intra-partumhypoxic component.” They go on tostate that lesser degrees of acidemia [only] de-crease that likelihood. Finally, they state that“if the cord arterial gas pH levels are above7.20, it is unlikely that intra-partum hy-poxia played a role in causing neonatalencephalopathy.” This is a sea change inthe analysis of the acid-base status of thefetus, as it relates to intra-partum HIE.The previous essential criteria, which hadto be present, demanded a blood pH of less than 7.0 and a base excess of 12 orgreater. This huge 2014 change recog-nizes that base excess is the most impor-tant component of the asphyxial analysisbecause if it is 12 or greater, there is obvi-ous clear evidence of acute metabolic aci-dosis – whatever the pH may be. Thereare a variety of reasons why the pH mayor may not show a level consistent withthat degree of metabolic acidosis (for ex-ample, interference with perfusion fromcord prolapse or severe maternal hy-potension, etc.). The 2014 Edition alsotakes the pH level up to just under 7.2 bystating that arterial gas pH above 7.2 isonly ‘unlikely’ to be related to intra-partum hypoxia.

I suspect there have been hundredsof cases in the last decade tried to verdictwhere the acid base status of the fetus was the subject of dramatically conflictingexpert witness testimony. I suspect many

of those cases resulted in defense verdictsat least in part based on expert testimonythis new criterion demonstrates to havebeen inaccurate.

Another factor which is noted to bean important part of this global assess-ment is neural imaging, evidence of acutebrain injury seen on MRI or MRS consis-tent with hypoxic ischemia. The new edi-tion states flatly that MRI is the bestdefinition of the nature and extent of cere-bral injury in neonatal encephalopathy.It states that cranial ultrasonography andCTs simply lack sensitivity for evaluation oftiming and the nature and extent of thebrain injury. It notes that there are dis-tinct patterns of neural imaging that aregenerally recognized in hypoxic ischemiccerebral injury (watershed type versusdeep gray matter). It points out that earlyMRIs obtained between 24 hours and 96hours of life may be more sensitive for thedelineation of the time of a peri-natalcerebral injury. It also clearly states thatthe ability to precisely time the occur-rence is really a matter of days rather thana matter of hours or minutes in a hypoxic is-chemic event. This recognizes the ad-vances that have been made in the use ofdiffusion imaging in MRI and clearly callsinto question the efforts of many defenseexperts to use CT or ultrasonography to tryand time a hypoxic ischemic event to indi-cate it could not have been related to anintra-partum occurrence. It is clear thesemodalities may still have some limited ap-plication in certain specified circumstances,but that a timely MRI will be the most help-ful in determining if there is any reason tosuspect that a given case of neonatal en-cephalopathy does or does not qualify as anintra-partum occurrence. This is a dra-matic change from the 2003 criterion,which made no distinction between the var-ious modalities of imaging available to theclinician.

Finally, they again point out that thepresence of multi-system organ failure isconsistent with hypoxic ischemic en-cephalopathy. This recognizes that afetus that has undergone a profound



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hypoxic ischemic event, sufficient tocause a brain injury, will also probablyhave had a ‘diving reflex’ response caus-ing a shunting of the blood to the brain.This tends to deprive other vital organs,such as the kidneys, liver, heart and thegut to be denied adequate perfusion andmay result in evidence of dysfunctionearly in the neonatal clinical presenta-tion. Importantly, the discussion in thisarea makes it clear that this is highly vari-able and often does not correlate with thedegree of injury to the brain. This, again,is a significant departure from the 2003criterion which simply stated that thereshould be an onset of multi-system organdamage within 72 hours of birth.

Type and timing of contributingfactors consistent with acuteintra-partum events

As before, one contributing factorthat is consistent with an acute intra-partum event is a sentinel hypoxic or is-chemic event, occurring just before orduring labor, such as a ruptured uterus,an abruption of the placenta, cord pro-lapse, or other well-known catastrophicevents.

The new edition contains dramaticchanges in the description of fetal heartrate monitor patterns which they deem tobe consistent with an acute intra-partumevent:

They state that Category 1 or Cate-gory 2 fetal heart rate tracings associatedwith Apgar Scores of 7 or higher at fiveminutes, or normal umbilical cord arterialblood gas measurements, is “not consis-tent” with an acute hypoxic ischemicevent. By inference, this leaves a numberof situations that would be ‘consistent’with acute hypoxia. This is a huge depar-ture from the 2003 requirements thatstated only a sudden and sustained fetalbradycardia or persistent late or variabledecelerations with absent variability quali-fied. The 2003 requirement was that youhad to have (what became in 2008) a“Category 3” presentation or this was notan intra-partum hypoxic ischemic event.

Indeed, the 2008 definition also requiredbradycardia to have absent variability.

Now they define Category 1 or Cate-gory 2 fetal heart rate tracing as “not con-sistent” with an acute hypoxic event only ifthere are good Apgars or normal umbilical cordarterial blood findings. This critical changemeans that the large grey area of Category2 patterns (which include patterns withminimal or decreased variability, tachycar-dia, bradycardia with decreased variability,marked variability, absence of accelerationafter stimulation, recurrent variable or latedecelerations with minimal or decreasedvariability, prolonged decelerations, decel-erations with slow return to baseline, etc.)all can be defined as consistent with anacute hypoxic ischemic event if the childshows evidence of depression at birth,namely Apgar Scores below 7 or abnormalumbilical cord arterial blood gases (as re-defined).

They point out that there are addi-tional fetal heart rate patterns that de-velop after an original Category 1presentation which may suggest intra-partum timing of a hypoxic ischemicevent. These include tachycardia with recurrent decelerations and persistentminimal variability with recurrent decel-erations. This again is a significantwidening of the inclusion criteria for fetalheart patterns suggesting intra-partumasphyxia.

While these definitions only relate tocausation, by inference this edition estab-lishes new categories of “non-reassuring”patterns that by definition can result in as-phyxial injury. Birth injury specialistsrepresenting brain injured children andtheir experts have been insisting for thelast decade that minimal or poor variabilitywith recurrent decelerations is an omi-nous pattern which should require aggres-sive intervention. Unfortunately, defensewitnesses relied on the 2003 and 2008definitions that variability had to be “ab-sent” and testified that therefore based onthese guidelines, standard of care did notrequire intervention. This resulted inmany defense verdicts which were based

on testimonial evidence that has now beenrevised to conform to reality.

Unfortunately, many practitionersout there in clinical situations alsoneeded to have guidance on how to dealwith the patient who presented with on-going persistent decelerations and de-creasing or minimal variability; many ofthem may have relied on the guidance ofACOG and chosen not to intervene be-cause the variability had not become “ab-sent.” Indeed, many of those childrenmight have avoided injury if ACOG hadprovided more definitive and inclusiveguidelines for the doctors and nurses inthe field.

The 2014 factors also include timingand type of brain injury patterns basedon imaging studies that are consistentwith the occurrence of an acute intra-partum event. They note that echogenic-ity can be found on ultrasonography ob-tained approximately 48 hours or longerafter an ischemic event. However, theyemphasize that ultrasound lacks sensitiv-ity for brain injury in the encephalo-pathic newborn. They also point out thatcomputerized tomography imaging lackssensitivity for brain injury in the newbornand is not helpful for timing because itwill often not reveal abnormalities in thefirst 24 to 48 hours after an injury.

Most importantly, they note that dif-fusion abnormalities on MRI are mostprominent between 24 hours and 96hours of life if the injury relates to anacute peri-partum or intra-partum event.However this can only provide evidenceas to a range of days from injury, nothours or minutes.

They also point out that there areseveral well-defined patterns that are rel-atively typical of hypoxic ischemic cere-bral injury. These include: deep graymatter injuries (which are often associ-ated with more acute or profound injuriesand usually present with relatively dra-matic motor compromise and oftenspared cognitive function); or watershedcortical injury (which is more typically as-sociated with partial prolonged asphyxial



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events and can produce global or moremodest encephalopathy often presentingwith both cognitive injuries and mild tosevere motor involvement). They alsonote that neuro-imaging cannot distin-guish the etiology of hypoxic ischemicevents, such as whether it was a placentalinsufficiency or an interruption of umbili-cal cord blood flow.

Next they again discuss the impor-tance of considering whether there areother potential causes of the neonatal en-cephalopathy. However, unlike the 2003“essential criterion” which required theexclusion of other possible causes, such asinfection, trauma, metabolic coagulation,and genetic disorders, the 2014 state-ment simply states that the coexistence ofother significant risk factors, such as ab-normal fetal growth, maternal infection,hemorrhage, sepsis, and/or chronic pla-cental lesions, simply lessen the likeli-hood that an acute intra-partum event isthe sole underlying pathogenesis of a neona-tal encephalopathy. In other words, thereis a clear recognition that two conditionsmay co-exist in a fetus. Indeed, abnormalfetal growth, maternal infection, chronicplacental lesions, etc., may in fact be theunderlying cause of intra-partum eventswhich culminate in neonatal asphyxia.The Second Edition acknowledges thatthis does not require an either/or analysis.

Finally, while in 2003 it was statedflatly that the neurologic presentationhad to be one of spastic or dyskineticcerebral palsy to qualify for intra-partumcausation, the 2014 Second Edition sim-ply states that “other subtypes of cerebralpalsy are less likely to be associated withacute intra-partum hypoxic ischemicevents.”

Summary

For attorneys who prepare and try intra-partum hypoxic ischemic en-cephalopathy cases, this 209-page tome isrequired reading. The Taskforce has fi-nally recognized that identification of thecerebral palsied child injured by an intra-partum event cannot be autocraticallylimited based on a narrowly defined setof markers perhaps inspired less by sci-ence than the perceived need to defendlawsuits. At long last, ACOG has chosento provide the clinician reasoned andthoughtful retrospective guidelinesgrounded on evidence-based medicine.This work makes it clear that neither sideof the legal process has all the answers.Sensibly, the authors have noted that amultitude of elements may, or perhapsmay not, combine to produce an intra-partum hypoxic ischemic event. The definition of causation in neonatal encephalopathy is clearly a work in

progress. This edition, however, hastaken a huge step forward in acknowledg-ing that fact as well as in recognizing thehuge variability of human response to as-phyxial insult. Most importantly, basedon these new definitions of the fetus atrisk, today perhaps the doctors andnurses out there in the field watching thatbaby’s heart rate during labor will havesubstantially more guidance in the deci-sion making process.

James Bostwick is a mem-ber of the Bar in Californiaand Hawaii and tries cases inmany different states. He is aFellow of The Inner Circle ofAdvocates, The InternationalAcademy of Trial Lawyers(President 2004), ABOTA, aFounding member of The

American Board of Professional Liability Attorneysand was Best Lawyers’s “Trial Lawyer of the Year” for 2012 and 2013. See profile in this issue.

Endnotes1 Sophie Berglund, et al., Severe Asphyxia due to Delivery Re-lated Malpractice in Sweden, 1990-2005, 115 Brit. J. Obstet-rics and Gynecology, 316 (2008).2 Hakan Noren, et al., Fetal Electrocardiography in Labor andNeonatal Outcomes: Data from the Swedish Randomized Con-trol File on Inter-Partum Fetal Monitoring. 188AM.J.Obstreticsand Gynecology. 183, 190 (2003).



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Medical malpractice: Preparation and trial of birth injury ... · partum hypoxic events and cerebral palsy. Ostensibly this was designed to provide the practitioner with definitions