Birth asphyxia

Donald MF Gibb NIL> MRCP FRCOG MEW1

spliyxia mcans literally ‘stoppage o f the pulse’ and is defined as ‘the condition of suspended aninia- A tion produced by a deficiency of oxygen in the

blood; suffocation’ (Oxford English Dictionap9. ‘Birth asphyxia‘ is an unsatisfactory term because it has come to mean poor condition of the baby at birth irrespective of cause; there are many causes of a txhy being in poor condition at tirth. In common use it has implied asphyxia caused by birth rather than asphyxia found at birth. This has very important medicolegal implications. A preferable concept is birth depression, depression at birth: which demands consideration of various causes before treatment can be logically and effectively undertaken. The term ‘flat baby’ should not be used: it has no scientific basis and is used insensitively in the presence of parents and family. A baby may be clepressed at hirth by causes as diverse as diaphragmatic hernia. infection, maternal anaesthesia, del- ivery problems as well as liypoxia and birth trauma.

Depressed babies have poor Apgar scores, but it should be remembered that the Apgar score was devised as an objective indicator of the condition of the neonate at hirth and not as a marker of asphyxia.’ The term ‘liypoxic ischaemic encephalopathy‘ should be avoided until specific evidence for its origins becomes available. Neonatal encephalopathy may not be asphyxia1 in origin.2 ‘This revien7 considers birth depression due to hypoxia: ‘true’ birth asphyxia. The term ‘brain damage‘ is not helpfiil in the neonatal period until the evolution of the process is clear. Cerebral palsy is a non-progressive disorder of movement o r posture not evident until months or years after birth. It is clear that cerebral palsy has multiple aetio1ogies.j There are fen: countries where there has been adequate follow-up of children relating their subsequent condition to birth events. It is probable

that only about 10Y0 of cases of cerebral palsy are related to peripartum e\ ents,’ Our attention must turn to their prevention, as n-omen are often in our care and under supervision at this time

THE PROCESS OF BIRTH DEPRESSION ASSOCIATED WITH HYPOXIA The condition of a baby at birth is dependent on many factors. To be healthy, the baby must be intact genetically and constitutionally. Intrinsic fetal defects are important contrihutors to l~haviour after birth and t o later cerebral palsy. The fetus must be provided with a supply of nutrients and oxygen from the mother. ‘Upstream’ deficiencies of niaternal respiratory or cardiac function compromise supply through the placental unit. It is uncommon for these to be acutely interrupted befure latmur and there is more likely to be a chronic interruption with chronic asphyxia Poor placental function of long standing results in intrauterine growth restriction and fetal compensation. In a different scenario babies become asphyxiated in a period of time that may be hours or days before birth. This is called ‘chronic partial asphyxia‘. The signs of this may be subtle, such as a change in fetal movement, or there may be no sign at all. Such babies are usually well grown. Other babies suffer severe acute compromise with conditions such as placental abruption, umbilical cord prolapse or uterine rupture. These babies behave in different way-s after birth. The mechanisms that may lead to critical cerebral damage are essentially hypoxaemia and ischaemia (poor perhsion), resulting in tissue hypoxia and damage.

INTRAU’TERINE GROWTH RESTRICTION A clironically- asphyxiated fetus suffering from placental dysfunction manifest as poor growth shows a reduction in body movements and txeathing movements reducing energy consumption and oxygen demand. There is a redistribution of blood supply seen on Doppler examin- ation. There is increased blood flow to the brain, myo- cardium and adrenals. with reduced flow- through the descending aorta to the viscera. Changes are integrated, but loss of end-diastolic flow in the descending aorta occurs in chronic hypoxia,’ and significant changes in middle cerebral artery blood flow suggest acidosis.” In time, head growth slows. There is increased extraction of o q g e n from the blood with hypercapnia, acidosis, hyperlacticaemia and erythroblastosis.’

These babies at birth may have superimposed acute asphyxia, particularly if they have item exposed to

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labour. The Apgar scores will depend on this but may be in the intermediate range. These babies in general do not suffer from convulsions. Typically, they have temperature regulation problems with hypotherrnia due to decreased fat insulation, decreased stores of bron~n fat and glycogen and poor lipid metabolism. They also have metabolic problems such as hypoglycaemia, hypocalcaemia as nwll as polycythaemia and hyperbilirubinaeinia. These babies, when premature, may show periventricular leucomalacia on brain imaging and? if they develop cerebral palsy, it is of the spastic type.

CHRONIC PARTIAL ASPHYXIA 'These babies arc usually near term and show no major signs of compromise until there is an abnormal cardio- tocogram (CTG). Included are fetuses identified as compromised in pregnancy based on an abnormal antenatal CTG. There rnay be subtle indicators, such as vaginal bleeding or reduced fetal movements, but not enough concern to justify obstetric intervention. There may IIC an unreactive C'lG with. poor baseline variability from tlie start of labour.s The CTG may be unusual in labour but not indicative o f progressive hypoxia. The Apgar scores are reasonal-ile and in the neonatal period convulsions occur late. These babies may have suffered neurological injury prior to the start of labour.

ACUTE ASPHYXIA An acutelp asphyxiated fetus tiehaves in a different way. In monkeys stucliecl by Myers9 using total umbilical cord occlusion, t h e fetal heart rate fell almost immediately at the time of tlie asphyxia1 event; this was followed by a transient rise in blood pressure which was short-lived and the hlood pressure fell steadily from three minutes. The blood oxygen was largely depleted in the firs1 tliree minutes of total asphyxia. There was a rapid fall in pH but this was initially a respiratory acidosis. If relieved of' the insult at this point the animals sut-vived. The first evidence f o r damage to the brain following resuscitation and exterided survival in unanaesthetised term fetuses came after ten minutes of total asphyxia. Tlie cerebral injui-y appears to be clue to iscliaemia related to tlie period of hypotension. Those fetirscs asphyxiated for longer than 25 minutes die in thc early hours in the intensive care unit of progressive and intractable heart failure due to injury o f the myocardium. The nervous system damage produced by this asphyxia affects thaianiic, brainstem and spinal cord structures. The focus is on the tlialamic structures which are injured after 13 minutes of total asphyxia.

The liurnan fetus born after being exposed to acute severe asphyxia will have a low lieart rate and delnyed onset of respiration. The Apgar score at one minute will be depressed. Aggressive resuscitation and artificial vent- ilation are recluired. Umbilical artery 11load gas measure- ments are important. An acidosis (pH c7.10, base deficit >12 mmol/l) does not have a relationship with impaired

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neurodevelopmental outcome at 4% years of age."' However. there is evidence that a cluster of abnormal perinatal signs, including acidosis, has a poor prognosis.' These signs were umbilical arterial acidosis as defined above, low Apgar scores and neonatal encephalopathy. This suggests that the preceding events, severity and cause of the acidosis were as important as the presence of the acidosis itself. Neonatal enc:ephalopathy can he due to hypoxia-ischaemia, infections. drugs, central nenous system malformations, intracranial liaemorrhage and metabolic caciscs. A grading system has heen intrciduccd to describe the neurological abnot-tnality."

Hypoxic ischaemic encephalopathy

0 Grade I: Irritability, staring with mild hypotonia and

0 Grade 11: Lethargy, marked abnormalities o f tone, tube

0 Grade 111: Conia, severely hypotonic. requiring artificial

poor sucking; these liabies do not have seizures.

feeding and seizures.

ventilation and with prolonged seizures.

Grades TI and 111 hypmic ischaemic enceplialopathy confer an increased risk of death or serious handicap.13 Infants with a severe encephalopathy frequently have an adverse outcome. The blood flow to vital organs is preserved during acute asphyxia. Less vital organs arc deprived o f tilood flow. Multi-organ dysfunction becc )mes apparent, with renal failure, necrotising enterocolitis, persistent pulmonary hypertension, disseminated intravascular coagulation and various metabolic abnormalities. These abnormalities are markers of hypoxic ischaemia.

If such a child has the misfortune t o develop ceret~ril palsy then it will be of the spast.ic quadriplegia or a dyskinetic (athetoid) type.14 However, spastic quadri- plegia has other causes and only 24% of a series of cases of children with moderate or severe quadriplegia were considered to be related to intrapartuni events. li

BRAIN IMAGING Great advances have heen made in imaging techniques in recent years. Neonatal cranial ultrasound is now widely available. Cranial ultrasound may reveal abnormalities of txain structure or development that have been present frorn early pregnancy. Cerebral oedema that is :i conse- quence of asphyxia is recognised by an increase in echo- density, a loss o f anatomical landmarks. indistinct sulci

ion of the ventricles. Later ultrasound find- ings associated with a poor neurodevelopmental outcome include bilateral uniformly echogenic thalami represent- ing t>asaI ganglia hypoxic ischaernic injury.16

Magnctic resonance imaging (MKI) is making an important contriliution to understanding brain injuiy. In coiiiparison with ultrasound, early MRI WIS found to be superior at diagnosing cerebral arterial infarrts, cortical atrophy and basal ganglia lesions, altliough ultrasound proved more able

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to detect periventricular luemorrhage.'7 Partial hypoxic ischaemia acts on the heart, causing alteratiom in heart rate. Bradycardia in the fetus and newborn reduces cardiac output. Critical reduction of output lasting for more than one hour beyond the capacity for regulation of die cerebral blood flow in the term fetus (over 36 weeks of gestation) causes ischaernic damage in the border zones between the cortical distributions of the main cerebral arteries.

Profound hypoxic ischaemia as occurs with cardiac arrest or severe bradycardia causes global lack of cerebral circulation. This results in irreversible damage to cells as their metabolic reserve becomes insufficient to maintain cell wall function. Cell death occurs in proportion to the metabolic activity, which varies with the mahirity of the fetus. In die term fetus, active myelination is taking place in the basal ganglia, thalami and pie- and post-central white nutter in which damage commences after about ten minutes of profound asphyxia. Asphyxia lasting for longer than 25 minutes usually results in death or much more severe and diffuse brain damage.

Rctween about 26 and 34 weeks of gestation the o l i g - dendroglia in the cerebral white matter are particularly vulnerable to a variety of insults including hypoxic ischaeinia and infection, particularly chorio-amnionitis. l'his damage causes the typical clinical and imaging features o f periventricular leucomalacia. Leucomalacia is a much less coininon reaction in the more mature fetus so that when it is discovered in a baby who has been born near term it is considered to be indicative of an earlier insult unless there is oveim~helming clinical evidence to the contrary:.

These changes on MRI persist and can be seen much later in childhood and are considered in the rncdicolegal context.

Electroencephalograph), (EEG) may provide important prognostic information. Term babies suffering from asphyxia show reduced background activity, and the more discontinuous the background t h e poorer the associated outconie.lH

THE CONTINUUM OF HYPOXIA In a medicolegal context there should be appreciation of the continuing process of hypoxia. This has been recognised by the American College of Obstetricians and Gj7necologists. lo They have defined that a neonate who has had severe hypoxia proximate to delivery that is severe enough to cause severe hypoxic ischaernic encephalopathy will show other evidence of liypoxic damage, including all of the following:

Profound metabolic or mixed acidaernia (pH <7.00) on an umbilical arterial blood sample.

Persistent Apgar scores of 0-3 for five minutes or longer.

Evidence of neonatal neurological sequelae (e.g. seizures, coma, prolonged hypotonia and one or more of the following: cardiovascukai-. gasti-ointestinal, haemato- logical, pulmonary, or renal system dysfunction).

The Perinatal Society o f Australia and New Zealand, in collaboration with international experts, has published a document trying to define the relationship between acute intrapartum events and cerebral palsy.20 They suggest essential criteria and additional criteria.

Essential criteria:

of a metabolic acidosis in intrapartum fetal, arterial or very early neonatal cord samples

(pH <7.00, base deficit >12 mmol/l).

Early onset of severe or moderate encephalopathy in infants >34 weeks of gestation.

Cerebral palsy of the spastic quadriplegic or dystonic type.

Additional criteria:

A sentinel (signal) hypoxic event occurring immediately before or during labour.

A sudden, rapid and sustained deterioration of the fetal heart rate pattern usually following the hypoxic sentinel event where the pattern was previously normal.

Apgar scores of 0-6 for longer than five minutes

Early evidence o f multi-system involvement.

Early imaging evidence of acute cerebral abnormality.

One problem with this document is the concept of a sentinel event. There are events such as ruptured uterus, abruption and cord prolapse that are fairly discrete. But it also has to be recognised that there is a continuation of the labour process which is a cumulative challenge, especially when aided by oxytocin. Deterioration of the fetal ticart rate pattern need not be sudden, rapid and sustained to be seriously threatening to the fetus. Indeed, some of the worst outcomes are seen when there is a final deterioration to a bradycardia after some time of an abnormal Irace. There appears to he a continuum from stress with compensation to distress with time. This document is to he reviewed as more information becomes available and will need to address the important data becoming available from imaging studies of the subjects' brains.

After reviewing the records of 210 singleton children who had a diagnosis of cerebral palsy at five years of age, 35 (16.6%) were identified as those most likely to have cerebral palsy of intrapartum origin. In 26 of these there was evidence of suboptimal care in labour." A model was constructed to identify potentially preventable causes of intrapartum origin.

RISK MANAGEMENT ISSUES While birth depression and later cerebral palsy may be associated with poor care in labour, medical negligence can only be proved when there is causation as well as liability for the poor care. The jigsaw of hypoxia has to be studied carefully. The umbilical arteq7 blood gases are the best key we have. It cannot simply he a stand-alone pH

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value because acidosis is common and relatively innocuous. Respiratoi-y acidosis is particularly common and benign. Tlie hlood gases tilust include a base deficit. i t may not be cost-effective to perform umbilical artery hlood gas estimation on all cases but tho American College has proposed the following approach. which has iiiuch to comiuend ir."

' Techfziyrie: Irninediatcly after de1ivery o f the neon;lte, a segment of the umtiilical coi-ci should be doublj- claiiiped. divided, and placed on the de1ivei-y table pending

assignrrient of the five-minute @gar score. Values froin the uiiil)ilic;iI ~rtei-y provide the most

rrgtlrtling fetal and nemhorn acici-base status. A claiuped segment o f cord is stalile fur pII and Idood gas assessment

for at least 00 minutes. and a cord hlood sample in a syringe

flushed with heparin is stahle for LIP to hU minutes. IT the five-minute Apgar bcore is satisfxtory and the infrint

appears stable and vigorous, the segment of umbilical cord can lie discarded. If a serious abnorniality that arose in the tielivery process. or a problem with the neonate's condition,

or Imth: persist a t o r lw).ond five minutes. blood can lw wi thdrmn from the cord ,segment and analysed for 131 I and gases. Soine txsic training will be required in .\rcuring an arterial sample as it can sometimes be clifficult.'

Ideally, a sample should I x taken in all cases from both artcry and vein to vedy by their discordancy that one is arterial.23 This may not be possihle in many hospitals. In the important situation o f the delivery of' a gron-th-1-estrictecl baby: with small cord vessels, it is iisefiil to take the arterial s;iniple while the cord is still att:ichcd to the placenta even before the placenta is delivcrcd. Tlie sample may he obtained froin the vesscls on the chorionic surf;ice o f ~ h c placenta.

'l'he h p g a r scores, particularly at and after five minutes, although crude, do provide a guide to the sevcrity of the condition. The nced for transfer and treatrnenc of hypoxic ischaeniic encephalopathy in the neonatal intensive unit is also a marker of possible later prohlems. Early cranial ultrasouIid and EEG are feasible in many units. MRT will assume gre:it importancc in time and will become routine.

In o ~ r day-today practice, obstetricians, iiiidwives and paediatricians must not use the ternis fetd distress, birth

, flat loahy and brain damage. These terms have led t o serious misiimlerstandings with families and lawyers. We must strive t o prevent the portion of birth asp1iyxi:i md subsequcnt brain injury due t o events in labour ovcr which we may have some control.

Acknowledgements 'The author would like to acknowledge the advice received froin Dr Janet Rennie, Consultant Yeonxal Paecliatvichn at King's College Eiospitd, London, and nr Brian iiendall, Consultant Radiologist a t the Royal Free Hospital, London, in the preparation of this paper.

AUTHOR DETAILS Donald MF Gibb h i n MRCP FRCOG hik .a~ , I m k p e m h t C'o? zsu Itn t z t Obstetn L za I I Suite 207, Pa rliw ay Hou se , Sheen Lane, London SW14 8LS, LK

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Blair E, Stanley FJ. Inwaparmin asphyxia: a n r e cause of cerehrtd palsy. J Pediafr 1988;112:5lj-9 Jouppila P, Kirkincn P. Increased intravaxddr resistance in die descending aork o f the hunun fetus in hypoxia. U r J Ohski Gjnaecol1984;91:85M Fdvre R, Sclionenbeqer R, Siswantl 1, Lorenz U. Standard curves of cerebral Dopplcr flow velcxity waveforms and predictivc values for intrauterine gowth retardation and fetal acidosis. Fetal Diagn ?her 1'991;6:113-9 Sootliill PW, Nicolaidcs KH, Camplxll S. Prenatrtl asphyxia, hyperlacticaeniia, hypofilycdemia, and erythrobhstosis in growth retarded fetuses. BMJ 1987296: 1051-3 Bhekdn JIJ, A h MO. Peiinatd ot%icrvations in forty-eight neurok)gicdly impaired term infants. Am J Oh&l C~~ecol1994;171424-31 Myers RE. Two ptterns of perinaral brain damage and their conditions of occurrence. AmJ Obstef Gyiecol 1972;112:246-76 Dennis J, Johnson A, Mutch L, Yudkin P, Johnson J? Acid-tme status at birth and neurodwelopmental outcome at four and one-half YCdfS. Am J ObsteF c;4'tlc?co~ 198%161:213-20 Yudkin PL, Johnson A, Clover LM, Murphy KW. Clustcring of pcrinltal markers of birth asphyxia and outcome at age five years. UrJ Obs&t Gynacco11~,101:77&31 Levene MI, Kornberg J, Williams THC. 'Ilie incidence and severity of pst-asphyxia1 encephalopdthy in full-term infants. Rady Hum ULJU

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Evans DJ, Levene MI. Hypoxic ischemic injury. I n Rennie JM, Roberton ARC (Eds) Textbook of.Veonuro1ogyv, 3rd ed. Edinburgh: Churchill Livingstone; 1399. p. 1231-51 Kutlicrford MA, Pennock JM, Dub0)witz LMS. Crdnial ultrasound and nmgnetic resonance imaging in 1iypo)xic-ischaenlic encephlopathy: a comparison with outcome. Dev Med Child hreuro110')4;36:813-2S Wertheim D, M e ~ u r i E, Paundez JC, Rurhcrford M, Acolet I), Dubowits! I.. Prqpxstic values of continuous elecmxncephalo- gmpllic recordings in full term infianb with hypoxic ischacinic encephaloparhy. Arch Lhi Child 1334;71:F97-F102 American College o f Obstetricians and Gynecologists. Commiffee Opfnion 7.38. Washington, DC; 1991 MdcLemn A. A teinpbate for dcfining causal rebationship Iwtween acute intraparturn evcnls and cerebral palsy: international consensus statement. UMJ 1993;319:1054-9 Criffney G, MaveU V, Johnson A, Squier W, Sekrs S. Model to identify potentially preventable cerebral palsy of intr;lpamim origin. A n b D b Child 1935;73:F106-8 American College of Obstetricians and Gynecologists. Umbicd artery blood acid-base analysis. IWJ Cyzecol Obstet 1!996;52305-10 Westgate J, Garibildi JM, G m n e KR. Umbilical cord Id(xK1 gas analysis at delivery: a time for quality data. Br J Obsfef ~ ~ z a e c o l 1!M:101: 105443

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