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How to Handle Causation in Birth Asphyxia Cases

By Chemnick | Moen | Greenstreet

Published in Trial News, the monthlynewpaper of the Washington State TrialLawyers’ Association May, 2002

In evaluating possible birthasphyxia cases, one must notoverly focus on the eventsduring the perinatal period and assumethat if there was a delay in reasonablyresponding to signs of hypoxia and if thebaby was later found to have cerebralpalsy, then the two are likely related.

On the other hand, one should notdismiss a possible claim too readilyfor want of causation just because thenewborn’s clinical presentation doesnot mirror the published hallmarks ofhypoxic encephalopathy.

The purpose of this article is toexplore, in a general way, the basicquestions pertaining to causation inbirth asphyxia cases: (1) when didthe injury likely occur; and (2) if itoccurred at about the time of birth,was there a sufficient hypoxic eventduring labor and delivery to cause thatinjury? To address these questions,I will generally discuss the relationshipbetween birth asphyxia and cerebralpalsy, and the frequently cited criteriafor evaluating whether there wassufficient birth asphyxia to cause braininjury at birth.

Timing of Damage

It is estimated that the incidenceof cerebral palsy is somewhere between1 and 2 per 1000 live births(American College of Obstetricians and Gynecologists,1992). The damage may rangefrom slight to severe. Although intrapartumasphyxia is a significant causeof cerebral palsy, the vast majorityof infants with cerebral palsy have noevidence of intrapartum asphyxia, andmost infants who suffer intrapartumasphyxia develop no signs of permanentbrain damage. More common riskfactors are genetic abnormalities, congenitalmalformations,birth weight lessthan 2000 grams, gestational age lessthan 32 weeks, and infection.

It is estimated that somewherebetween 5 and 15% of cerebral palsyoccurs near the time of birth; however,a substantial portion of thesecases occur because of prematurity.In fact, largely because of the increasein survival of low-birthweight babies,the rate of cerebral palsy has notmaterially declined over the past 50years despite the advent of fetal heartmonitoring, the heightened concernover perinatal asphyxia, and the deliveryof approximately one out of four babiesby Cesarean section.

Different etiologies result in differingforms of cerebral palsy. In addition, thesame etiology at different gestationalperiods can result in differing formsof cerebral palsy because of changeswhich occur during the developmentof the fetal brain, and the relativesusceptibility of the different structuresto asphyxia. For example, asphyxiaduring the late second and early thirdtrimester may well result in injury tothe transitional germinal matrix whichlies along the lining of the cerebralventricles and is composed of primitivecells. These cells ultimately contributeto the formation of the basal gangliaand other neuronal structures ofthe brain. Depending upon thedevelopmental stage at the time of theprenatal asphyxial event, the fetus mayalso suffer direct injury to the basalganglia, and to the periventricularwhite matter. These structures areparticularly susceptible because of theirhigh metabolic demand for oxygen.

An asphyxial injury during thisstage of development may well resultin spastic diplegia. Children with thataffliction present with high tone in theirlower extremities, with or without othersignificant disabilities. Depending uponthe degree of hypoxia, the brain damagecan extend outward through thecerebrum to the cortex, and thereforemanifest itself as well in corticaldisabilities such as mental retardation,epilepsy and/or blindness.

Although children who have sufferedsevere hypoxia during the prenatalperiod may present with smaller thannormal heads at birth, that is not alwaysthe case. In fact, the child’s head can benormal size. An MRI, however, wouldlikely show increased ventricle sizeaccompanied by loss of periventricularwhite matter or areas of necrosis. Such child’s head size can be expected togrow at a slower than normal rate, andmay ultimately result in microcephaly.Indications that the fetus may havebeen subjected to prenatal asphyxiacan often be found through placentalpathology. The placenta should beevaluated for signs of degeneration,maternal infection, and inadequatefunctional capacity. Also of particularinterest is the location of cord insertion,number of vessels, and length of cord.

When the incident of severehypoxia does not occur until after 35weeks a different pattern of injury occursto the brain. This is because the germinalmatrix is no longer present, and thebasal ganglia and periventricular whitematter have become more resistentto hypoxic injury by that time.Consequently, severe hypoxia atterm is more likely to result in diffusecortical damage. Such asphyxia cancause disproportionate damage tothose areas of the cortex more remotefrom the main blood supply. This iscommonly referred to as a watersheddistribution and is analogized to theaffect of turning down the spigot onone’s sprinkling system. On the otherhand, a complete loss of blood supplyto the fetal brain at term, whetherfrom severe bradycardia or heart stoppage,can cause discrete injury to thedeep brain including the basal ganglia,thalami and putamen. Such injurycan result from as little as 10 minutesof anoxia such as might occur from acord prolapse or ruptured placenta.

An asphyxial injury at term maywell result in spastic quadriplegia,truncal hypotonia and athetosis.Generally, the more severe the asphyxialevent, the more serious the child’sphysical disabilities, and the more likelythe child is to have serious mentalretardation. There is some dispute,however, as to whether asphyxia cancause mental retardation or learningdisabilities in the absence of physicaldisability. Nevertheless, there is a widerange of outcomes from similar degreesof apparent asphyxia at birth, whichsuggests that certain children areconsiderably better able to withstandthe affects of asphyxia than are others.

How Serious Was the Birth Asphyxia? Why the Usual Criteria May Not Apply

Generally, the infant who sufferedacute brain injury at birth will be severelydepressed and difficult to resuscitatewhile those whose injuries are subacutetend to recover more quickly. Suchsevere depression will usually be instark contrast to a fetus which wasactive prior to birth by report of themother, and as evidenced by a normallytwisted cord. The difficulty comes whenone attempts to define objective criteriato judge whether or not the degreeof asphyxia at birth was sufficient tocause the child’s brain damage.

The most commonly used yardstickfor determining whether the extentof birth asphyxia was sufficient to causesignificant brain damage is that fromthe American College of Obstetricsand Gynecology (ACOG) TechnicalBulletin 163. That document states:

“In assessing a possible relationship between perinatal asphyxia and neurologic deficit in an individual patient, all of the following criteria must be present before a plausible link can be made:

  • profound umbilical artery metabolic or mixed acidemia (pH < 7.00). (Normal pH for a newborn is 7.25 to 7.35. Acidemia can be due to a buildup in the blood stream of carbonic acid formed by oxidative metabolism of carbon dioxide which is called respiratory acidemia, or by a build up organic acid from anaerobic metabolism which is called metabolic acidemia. Where both are present, it is called mixed respiratory-metabolic acidemia.)

  • Persistence of an Apgar score of 0-3 for longer than 5 minutes. (The Apgar score is named after Dr. Virginia Apgar who developed the scoring system in 1952. There are five signs which are evaluated with either 0, 1, or 2 points assigned to each one depending upon the findings at certain intervals, commonly 1, 5 and 10 minutes after birth. The five signs are heart rate, respiratory effort, muscle tone, reflex irritability, and color. A perfect score would be 10, but that is rarely assigned.)

  • Neonatal neurologic sequelae, eg, seizures, coma, hypotonia * Multi-organ system dysfunction, eg. Cardiovascular, gastrointestinal, hematologic, pulmonary, or renal”

Since these guidelines were published,however, numerous studieshave found that asphyxial injury canoccur without the presence of all fourof these criteria. In one study reportedin 2 Prenatal Neonatal Medicine 286-93 (1997), the medical records of 16severely neurologically impaired terminfants were reviewed. All had sufferedacute intrapartum asphyxia from adocumented event such as a cordprolapse or uterine rupture, and noother explanation for their brain injuries. Only one met all four criteria,and only four met three of the criteria.The study also found that: five had apH <7.00; five had a 5-minute Apgarof 5 or less; 14 had seizures within thefirst 24 hours; and half had no multiorgandysfunction.

In a separate study, the same groupof investigators reported in 9 Journalof Maternal-Fetal Medicine 101-06(1999) that of 47 neonates with adocumented acute asphyxial injuryresulting in permanent brain injury, 10met all 4 criteria, 14 met 3, 14 met 2, 8met 1, and 1 met none of the criteria.

The same study also tended todispel one of the previously commonlyheld assumptions relating to the timingof seizures; namely that an early onsetof seizures after birth was an indicationof an earlier asphyxial event. Theassumption was that seizures frombirth asphyxia resulted from the buildup of brain edema, which generallytakes a minimum of 6 to 8 hours tofully develop. If that were always thecase, then seizure activity within acouple of hours of birth would indicatethat the prenatal asphyxial event musthave taken place hours before the onsetof the second stage of labor when mostcord accidents occur and when fetalheart rate tracings are more apt toshow signs of fetal hypoxia.

While it is true that the level ofedema necessary to effect seizureactivity, by itself, can take that long todevelop, the more recent view is thatthe most serious asphyxial injuriesresult in seizures within the firstcouple of hours. In such cases, itis thought that the hypoxic injury issufficient to directly cause disruption ofbrain function rather than just leadingto the build up of edema which in turn precipitates seizure activity. In fact, thestudy showed that the medium timefor seizures following documentablesevere asphyxial events was 3.5 hours.Some infants demonstrated seizureactivity within 2 hours of the onsetof the asphyxial event. This generalconclusion regarding the timing ofseizures was also reported in 37Clinical Pediatrics 673-76 (1998). Inthe study of 25 infants who sufferedseizures following acute asphyxia, themean time between the event and theonset of seizures was 3.1 hours, afterexcluding one infant that did not seizefor 90 hours.

In addition, these studies demonstratedthat many infants can developbrain injury from asphyxia withoutcoincident acidemia reflected in alow pH value. Such conclusion isalso supported by a study reportedin 93 British Journal of Obstetricsand Gynecology. It concluded that thehighest frequency of neurologicallydamaged infants was found in the groupwith low Apgar scores but with lessabnormal pH values. Similar conclusionswere reported in 161 American Journalof Obstetrics and Gynecology 213-20 (1989). In this study, infants withacidemia but with very low Apgarscores fared better than those with amore normal blood pH and very lowApgar scores. More normal pH underthose circumstances might indicatesome inability on the part of the fetusto continue to exchange gasses betweenthe blood and the cells of the body,including those of the brain. Thismay be indicative of a lack of effectivecirculation. In addition, it is postulatedthat the presence of acidosis witheffective circulation may increaserelative blood flow to the brain, anddecrease brain oxygen demands.

It is of course one thing to generallyunderstand the medicine relating tocausation and quite another matterto effectively present that evidence attrial. Not only is it important to findexperts who are well credentialed,but it is at least as important to findones who will also take the time tothoroughly prepare and assist you tocommunicate a consistent, simplerexplanation of the medicine to thejury. Such expert witnesses may wellinclude a neuro-radiologist, a placentalpathologist, a neonatologist, and apediatric neurologist. The more expertsone calls, the more chance there is forinconsistent testimony. To avoid or toat least minimize those pitfalls, it isnecessary for the attorney to firstunderstand the complex nature of themedicine and of the medical facts of thecase before preparing the expertwitnesses to present their testimonyin a manner which will be understoodby the jury.

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