Indian J Pediatr 1991; 58 : 51-62

Monitoring of Perinatal Asphyxia in the Hospital Meharban Singh

Department of Pediatrics and Neonatal Division, All India Institute of Medical Sciences, New Delhi

Birth asphyxia is the major cause of perinatal morbidity and mortality in India. The perinatal survival can be improved by reducing the incidence, early identification and effective management of birth asphyxia. This can be achieved by monitoring the fetus not only during labor (intrapartum) but also by assessing his well being during intrauterine (antepartum) period, t

12 hours recording is 86, 132 and 107 at 24, 32 and 40 weeks of gestation respectively.2 Three one hour periods of counting i.e., morning, noon and evening are recommended during third trimester of pregnancy. The total thus recorded is multiplied by 4 to give a daily fetal movement rate (DFMR). The DFMR of less than 10 (durhag 12 hours observation period) indicates fetal hypoxia and imminent risk to the fetus. Alternatively mother can be advised to count the fetal movements every day starting at 9 am in the morning until the total movements equal ten. If mother perceives less than 10 movements per day for two consecutive days, she is advised to report to the doctor. In case she does not appreciate any fetal movements in a day, she must contact her obstetrician immediately.3 In response to chronic asphyxia there is a decrease in fetal activity which tries to conserve oxygen consumption. The most common denominator of fetal inactivity is chronic uteroplacental insufficiency.

ANTENATAL MONITORING OF FETAL HYPOXIA Fetal Movement Count

Systematic recording of perceived fetal activity by the mother .is the most reliable and convenient method and must be widely popularised in our country in view of its feasibility. It promotes maternal bonding to her baby and gives a sense of responsibility and concern to her to look after her unborn baby. The main limitations are lack of experience of a primigravida mother and risk of anxiety in some over sensitive mothers. The median fetal movement count per

Real Time Ultrasonography

The utilization of fetal movements as a part of biophysical detailed analysis of fetal behaviour is a reliable parameter of fetal well being. Four specific body movements

Reprint requests : Dr. Meharban Singh, Professor and Head, Department of Pediatrics and Neonatal Division, All India Institute of Medical Sciences,New Delhi-ll0 029. 51

52

THE INDIAN JOURNAL OF PEDIATRICS

can be dei'med at 38 weeks of gestation : Yawning, stretching, startle, and fetal eye movements. 4 Fetal Heart Rate Non Stress test (NST). Demomtration of acceleration by 15 beats/min of fetal heart rate in association with fetal movements or spontaneous uterine contractions during a 20 minute period of observation is called a 'reactive' non-stress test. In case there are no movements or cardiac acceleration, fetus should be stimulated and watched for another 20 minute spell. If fetus remains 'non-reactive' even after stimulation, he should be subject to oxytocin challenge test.5,6 The uterine contractions can be induced by nipple stimulation. The recent demonstration of acceleration of fetal heart rate with acoustic stimulation and corelation of reactive acoustic stimulation test with conventional NST raise the possibility that acoustic technique may decrease the testing time and expense of this antepartum evaluation. In case of abnormal NST the test is repeated upto 120 minutes. If there is no fetal movement accompanying acceleration of fetal heart rate it is known as unsatisfactory of equivocal NST. 7 Stress Test. This test is now commonly used as a follow up evaluation when a fetus is docmnented to be non-reactive by NST. The uterine stimulation may be achieved by using 0xytoxin or nipple-stimulation. Maternal blood pressure is recorded at the start and at least every 10 minutes during the test. Base-line t~terine activity and FHR are recorded for 15-30 minutes on a cardiotocometer. Oxytocin is administered at an initial rate of 0.5 mu/min and doubled after every 15-20 minutes until uterine contractions last for at least 40-60 seconds and occur at a frequency of three

Voi. 58, No. 1

contractions every 10 minutes. 8 Interpretations. Drop in fetal heart rate corresponding to the peak of uterine contraction and complete recovery by the end of the contraction is known as negative stress test (early deceleration) and occurs due to compression of fetal head. In late deceleration the drop in fetal heart rate develops sometimes after the peak of uterine contractions with recovery occurring much after the contraction is completed. A persistent late dederation is considered as a positive OCT and is indicative of serious fetal distress. Variable fetal heart deceleration is indicative of cord compression and carries variable prognosis? A definitely negative OCT is a reliable indicator of fetal well-being. A positive OCT is suggestive of decreased uteroplacental reserve. When interpreted in conjunction with NST its sensitivity and specificity and is enhanced is likely to withstand labor and vaginal delivery better as compared to the fetus who has both a non-reactive NST with positive OCT. The OCT should be repeated at weekly intervals in high-risk patients. It is contraindicated in patients with placenta previa and in situations associated with high risk of premature labor e.g. twins, ruptured membranes, incompetent cervical os. Fetal Biophysical Profile A combination of ultrasonically monitored fetal biophysical variables i.e. fetal posture, breathing movements, gross body movements, heart rate reactivity and semiquantitative amniotic fluid volume are used to assess fetal risk. Each variable is coded normal and abnormal (Table 1). and awarded a score of 2 and zero respectively. The observation for each variable is made

SINGH : MONITORINGOF PERINATALASPHYXIA IN THE HOSPITAL T~.

53

1. Fetal Biophysical Profde Score (Manning score12or planning score)

Biophysical Variable

Normal

Abnormal

Posture

Flexed

Extended

FBM*

At least one episode of FBM of at least 30 sec duration in 30 rain.

Absent FBM or no episode of > 30 sec in 30 min.

Gross body movements

At least 3 discrete body/limb movements in 30 rain.

2 or fewer body movements or limb movements in 30 min.

Reactive FHR

At least 2 episodes of FHR acceleration of 15 bpm of at least 15 see duration associated with fetal body movements in 30 min.

Less than 2 episodes of acceleration of FHR or acceleration of < 15 bpm in30 rain.

Quantitative AFV**

At least one pocket of AF measuring No AF pocket or pocket < 1 cm in 1 cm in 2 perpendicular directions 2 perpendicular directions.

* FBM-Fetal Breathing Movements, ** AFV-Amniotic Fluid Volume for at least 30 minutes or till normal criteria is met? ~

Management Protocol Score 10 Normal fetus but test should be repeated at weekly intervals. Do the test twice weekly in case of diabetic and post-term pregnancy. Score 8 Normal fetus with low risk of chronic asphyxia. Repeat weekly or twice weekly in diabetic and post-dated, if oligohydramnios is present it is an indication for delivery if baby is mature. Score 6 It is indicative of chronic asphyxia. Repeat the score after 46 hour. If oligohydramnios is present immediate delivery should be done. Score 4 Compromised fetus. If > 36 weeks and L/S ratio is > 2 repeat within 2-4 hour. If the repeat score is also 4, delivery is mandatory.

Score 0-2 It is suggestive of severe degree of chronic asphyxia and testing time should be extended to 120 min : if score < 4 deliver the baby irrespective of gestational age. Biophysical Profde Score (BPS) is the most accurate guide for detecting a compromised fetus but requires the availability of a real time ultrasound which is not feasible in many centers in India. It is manda-

tory that all obste~cal units must acquire cardiotocometers for monitoring ~rST and OCT and should popularize and'promote fetal activity count by the mothers. Fetal Growth Detection of I U G R is of primary importance because infants are at grave risk to suffer from intrapartum asphyxia. They tolerate labor poorly as compared to normally grown infants. Clinical Evaluation. Monitoring of maternal weight gain during pregnancy,

54

THE INDIANJOURNALOF PEDIATRICS

uterine size (fundal height) and increase in abdominal girth are reliable clinical parameters to assess fetal growth. There is an urgent need to construct community based uterine growth charts among healthy pregnant women. Ultrasound Methods. (a) Slow rate of head growth (BPD) may be associated with IUGR but is not a sensitive index because brain growth is often spared in IUGR. t3 (b) GASA. Growth adjusted sonographic age is based on serial US observations and assures that fetal growth is maintained within a narrow percentile band, and deviation from this pattern is an early sign of IUGR. ~' (c) Amniotic fluid volume. Oligohydramnios is a clinical hall mark of prolonged or repetitive episodes of utero-placental insufficiency. It occurs due to diminished urine and pulmonary fluid production during episodes of fetal hypoxia (Table

2). Severe IUGR with definitive signs of fetal distress such as non reactive NST or positive OCT may necessitate delivery even T~

Vol. 58, No. 1

prior to 30 weeks. When IUGR is suspected, twice weekly antepartum heart rate monitoring and ultrasound observations are mandatory. (d) Elevated head-abdomen ratio. This occurs due to loss of liver mass with relatively normal head growth but lacks specificity to detect less severe growth. retardation. (e) Fetal ponderal index is being currently evaluated as a p~rameter to detect IUGR. It is a ratio of total length (reflected by femur length) and total mass or volume (head and abdomen)) 6 Fetal asphyxia due to dysfunction of fetoplacental unit is a major cause of morbidity and mortality. The hypoxic insults are likely to be episodic or intermittent with the intervening period in which the fetus is normoxic. The signs associated with hypoxia will, therefore, depend on the duration, severity and frequency of hypoxic episodes. These lead to cumulative effects of chronic hypoxia. Clinically utero-placental insufficiency is ill defined and believed to be secondary to maternal chronic vascu-

2. Types of IUGR Babies on Ultrasoundt5

Classification

US findings

Prognosis and Comments

Constitutional IUGR (normal small)

No maternal risk factors and no Constant BPD growth, low normal growth rate, normal AFV and normal special treatment is required. to grey zone total intrauterine volume.

Early insult IUGR

Low normal growth rate, grey zone abnormal total intrauterine volume but normal AFV.

Anomalies are common and prognosis is poor.

Dysmature IUGR

Initially normal BPD, increased H/A ratio and abnormal TIUV, and reduced AFV.

Occurs due to ulteroplacental insufficiency.Maternal risk factors are common. Extensive antenatal and intranatal monitoring is required.

H/A : Head to abdomen ratio, TIUV : Total intrauterine volume, AFV : Amniotic fluid volume.

SINGH : MONITORING OF PERINATAL ASPHYXIA IN T H E HOSPITAL

lar disease due to diabetes mellitus and hypertension. It should be suspected in toxemia, postdated pregnancy, diabetes mellitus, oligohydramnios, third trimester bleeding and history of previous still births. Acute fetal asphyxia is uncommon before labor except due to cord prolapse or abruptio placentae. Risk of cord prolapse may be identified prior to clinical occurrence by ultrasound. Detection of cord presentation forewarns against occurrence of cord prolapse. INTRAPARTUM MONITORING Fetal asphyxia during labor commonly occurs as a result of temporary reduction of passage of oxygenated maternal blood flow through umbilical vessels duc to cord compression. The risk of asphyxia increases during late phases of labor when frequency, strength and duration of uterine contractions increase the duration of hypoxia with reduced time available for recovery in between the contractions. Three cardinal clinical signs of fetal distress are : (a) Variations in fetal cardiac rhythm and rate : There is tachycardia, followed by slow and irregular heart, fixed heart rate and terminally cessation of heart beats. (b) Passage of meconium into amniotic fluid : Thick and long standing passage of mcconium is ominous. The yellow staining of umbilical cord and nails is associated with increased risk of birth asphyxia.17,Is Passage of meconium in breech delivery and occurrence of fetal diarrhea due to listeriosis are not indicative of fetal hypoxia. (c) Excessive or diminished fetal movements : It is mainly used during antenatal monitoring. Excessive movements are indicative of severe and acute anoxia e.g. in association with a major abruptio placentae. Exaggerated movements are followed

55

by slow and infrequent fetal movements which disappear terminally. Of these signs only fetal heart rate variability is truly objective and of real value. Fetal heart rate monitoring clinically and combined with tocography (measurement of frequency and strength of uterine contractions) is useful for identifying normally oxygenated or compromised fetus. Fetal heart rate can be monitored by auscnltatory and cardiotocographic methods.

Auscultatory Method The time honored intermittent auscultation with a fetoscope is often carried out rather infrequently and without diligence. The common practice of auscultating fetal heart rate for half to one min every 15 minutes is inadequate to detect fetal hypoxia. The more sensitive mode of auscultation is to count FHR over 15 sec period at 5 min intervals during and following uterine contractions, t9

Cardiotocographic Method Recordings are taken on an electronic machine on a graded graph paper, and fetal heart rate variability in relation to fetal movements and uterine contractions is recorded. Baseline variations. Normal fetal heart at term (120-160 beats/min) has a beat-tobeat variability of 8 beats per minute (normal range 5-12 beats/rain). Smoothing. The reduction in FHR variability to less than 5 beats/min is an early warning sign especially if associated with other high risk factors. It may be secondary to administration of analgesic/sedative drugs to mother (diazepam, pethidine). Long term variability. The number of oscillatory changes during a course of 1

56

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THE INDIAN JOURNAL OF PEDIATRICS

min are recorded. A regular undulating pattern with a frequency of 2-5 cycles per minute and amplitude exceeding 5 beats per minute is known as a sinusoidal pattern. Major sinusoidal pattern (greater than 25 beats/min) show a poor prognosis and severe fetal compromise.

prolonged and severe and are not influenced by alteration of maternal posture, they indicate fetal asphyxia. (c) Combined patterns : These account for 10% of fetal heart rate abnormalities when alterations cannot be classified satisfactorily.

Fetal heart rate. Tachyardia may be moderate (160-180 bpm) or severe ( > 180 bpm). Severe bradycardia ( < 100 bpm) is ominous and reliable hall mark of fetal distress and hypoxia.

Fetal Scalp Blood pH

Periodic variations. They include deviations of the fetal heart rate from the basefine during the uterine contractions,m

(a) Uniform patterns of deceleration (along with uterine contractions). (i) Early deceleration or type I early dips : The onset, nadir and recovery of FHR tracing to baseline corresponds to onset, peak and end of the uterine contractions. These are due to transient cord compression. Early deceleration is an indication for increased vigilance.

(ii) Late deceleration : The nadir in the fetal heart rate is reached well after the peak of uterine contraction and recovery to the base line is not achieved until after sometime of termination of uterine contractions. It suggests utero-placental insufficiency due to decreased villous blood flow and fetal asphyxia. If the fall in fetal heart rate commences 20 see or more after the onset of uterine contraction and there is base line tachycardia, it indicates severe intrauterine asphyxia and demands immediate action to save the fetus. (b) Non uniform pattern of deceleration : The deceleration is not related to uterine contractions. They are suggestive of cord compression. When the changes are

The normal fetal scalp blood pH during first stage of labor is 7.33 and may fall to 7.13 during second stage of labor. When there are cardiotocographic evidences of fetal distress, fetal blood sampling is indicated for determination of pH. 2mMaternal acidosis as a cause of fetal blood gas abnormalities must be ruled out. When there is a clear cut evidence of fetal distress like persistent occurrence of late deceleration, scalp pH may not be done as the fetus may be further jeopardised by unnecessary delay due to sampling. Estimation of scalp blood pH is mandatory when less ominous changes fike persistent tachycardia or bradycardia with type I dips or mixed pattern are present. The scalp pH of greater than 7.25 indicates that labor should be observed; pH between 7.20 to 7.25 is an indication for repeat sampling within 15 rain. If the scalp pH is less than 7.20 the baby should be immediately delivered either by forceps or cesarian section depending upon the stage of cervical dilatation. A non invasive continuous monitoring of scalp tissue oxygen and pH is feasible. The tissue pH tends to be lower than blood pH by 0.04 and when low it should always be cross checked by doing blood pH before taking a management decision. The measurement of lactic acid in scalp blood, fetal ECG and EEG are investigative tools with limited utility in clinical practice.

SINGIt : MONITORING OF PERINATALASPHYXIAIN 1"HEHOSPITAL MONITORING BABIES WITH BIRTH ASPHYXIA

Apgar Score It is the traditional and time honored system for evaluating the condition of the baby at birth. =~ Five clinical parameters comprising of respiratory rate, heart rate, muscle tone, response to stimulus and color are assessed at 1-minute and awarded a score of 0, 1, 2 (Table 3).

57

reflex stimulus are dependent upon gestational maturity of the baby. It gives identical s~ares to centrally blue and totally pale babies although latter are much more compromised due to combined cardio-respiratory failure. In view of inherent limitations of Apgar scoring system, it is suggested that an action-oriented assessment with major emphasis on breathing and heart rate as outlined in Table 4, should be used for evaluation of newborn babies at birth. 25

T~u~ 3. Apgar Scoring System T~t.~ 4. AIIMS Action-Oriented Assessment Score Item

0

1

2

Breathing

nil

slow, gasping, crying

Heart rate nil

< 100/rain

z00/min

Tone

flaccid

in between

flexed

Reflex response* Color

nil

grimace

cry

pale or blue

peripheral cyanosis

pink

* Response is best elicited by tapping the soles of feet. When 1 rain Apgar score is low, it should be reassessed after every 5 minutes till the score is more than 7. One-minute Apgar score of less than 3 indicates severe birth asphyxia. A low Apgar score at 15 to 20 rain may be associated with neuromotor developmental retardation. Apgar scoring system has several limitations.25 The respiratory efforts and cardiac status are most critical determinants of neonatal condition and muscle tone, response to stimulus and color are dependent upon cardio-respiratory status of the baby. It ignores the time of fn'st cry which is important to differentiate between primary and terminal apnea. Tone and response to

Fetal distress Yes/No Criteria Duration Pethidine/ Morphine

Yes/No Dose

Hours before birth

First cry

Min after birth

Respiratory effort

Absent/slow-gasping/

Heart rate

Nil/(100/) 100 per min

crying

On the basis of this assessment the babies at birth should be classified as followsfl Status of the baby

Respiratory effort

Heart beat

Normal

Crying

Normal

Moderate Slow gasping, (i) normal (> 100/ birth breathing rain) asphyxia (ii) slow ( < 100/ min) Severe birth No breathing (i) slow < 100/min asphyxia (ii) nil (fresh still birth)

Monitoring of early Neurological Behavior of Asphyxiated Newborn Babies Apart from monitoring of vital signs, the

58

THE INDIANJOURNALOF PEDIATRICS

neurological behavior should be closely monitored every day by Sarnat and Sarnat staging system (Table 5). The observations regarding automatic neonatal reflexes, sucking behavior, alertness and muscle tone should be recorded every day. The occurrence of seizures (majority have onset during first 24 hours of life) and persistence of abnormal neurological behaviour for more than one week is associated with increased risk of neuromotor retardation on follow up. The neurological behaviour during early neonatal period is the most reliable predictor of neurodevelopmental prognosis in babies with birth asphyxia, z7

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Monitoring of lntracranlal Pressure and Cerebral Perfusion There are no simple and reliable methods to monitor ICP and cerebral perfusion in babies with birth asphyxia. They are mostly investigative tools limited to some regional perinatal centers. Most deaths due to asphyxia occur during first 72 hours of life.

Ultrasound and CT Monitoring of Brain When facilities are available, an ultrasound examination of head is mandatory in all asphyxiated babies during 1-2 weeks of life. The examination is desirable whether the infant was symptomatic or asympto-

TABLE5. Sarnat and Sarnat Clinical Staging of Post Hypoxic-ischemic Encephalopathy 2~ Sign

State I

Stage II

Stage III

Level of consciousness

Alert

Lethargy

Coma

Muscle tone

Normal

Hypotonia

Flaccidity

Tendon reflexes

Increased

Increased

Depressed or absent

Myoclonus

Present

Present

Absent

Active Exaggerated Normal or exaggerated Normal

Weak Incomplete Incomplete Over reactive

Absent Absent Absent Reduced or absent

Pupils Respiration

Dilated Regular

Variable or fixed Jerky, apneic

Heart rate Seizures

Normal or tachycardia None

Constricted Variation in rate and depth, periodic Bradycardia Common Low voltage, Periodic and]or paroxysmal

Periodic or isoelectric

Automatic reflexes Sucking Moro's response Grasp Doll's eyes Autonomic function

EEG

Normal

Bradycardia Common

SINGH : MONITORINGOF PERINATALASPHYXIAIN THE HOSPITAL matic during neonatal period. The evidences for intracranial hemorrhage, infarction, periventricular leukomalacia and selective neuronal damage should be looked for. ~3~ The ultrasonic observations should be correlated with antenatal and intrapartum evidences of hypoxia, severity of birth asphyxia and features of neurological abnormalities during neonatal period and follow up.

Auditory and Visual Evoked Responses If facilities are available, the auditory and visual evoked responses should be evaluated during first week of life and on follow up. The latency between the stimulus and appearance of response, interwave latency and abnormalities in evoked responses should be correlated with clinical and ultrasonic/CT scan abnormalities. Early detection of abnormalities on auditory and visual evoked responses, can identify minimally damaged babies at an early age so that appropriate stimuli can be provided to them for their optimal rehabilitation.

EEG Changes The initial abnormalities on EEG in infants with hypoxic ischemic encephalopathy is voltage suppression and decrease in the frequency (slowing) of waves. After 24 hours or so, periodic pattern appears, characterised by periods of greater voltage suppression interspersed with synchronous bursts of sharp and slow waves. The periodic pattern becomes prominent with more severe voltage suppression and fewer bursts of spikes and slow waves. The 'burst suppression' pattern is omninous and may progress to isoclectric tracing with hopeless prognosis.32 Those infants in whom EEG revert to normal within one week have good neurological outcome.

59

NEURODEVELOPMENTAL ASSESSMENT It is essential that all neonatal units should establish appropriate facilities for assessment of neurodevelopment of all high risk infants.33 A detailed neurological assessment with special emphasis on evaluation of motor functions, special senses palsy (sight and hearing) and early markers of cerebral palsy should be identified?4 A psychologist experienced in the art of developmental assessment should evaluate all asphyxiated babies on a modified Bayley's infant scale and Gessel's developmental kit.35

Steps For Monitoring Asphyxia (A) 1.

of Perinatal

Intrauterine Monitoring

High risk factors Placental insufficiency (PIH, post maturity), APH, premature labor, malpresentation, cord prolapse, rhesus iso-immunization, twins, bad obstetrical history, instrumental or operative delivery, maternal analgesia and anesthesia etc. The mothers with increased risk of perinatal asphxia to the baby should be closely monitored during third trimester of pregnancy. 2. Fetal movement count Maternal perception and ultrasonography 3. Fetal heart rate (cardiotocometery) (i) Non stress test (ii) Oxytodn challenge (or nipple stimulation) test 4. Fetal biophysical profile (Manning or Planning score on ultrasound examination) Fetal posture, body movements,

60

breathing movements, FHR, amniotic fluid volume. Fetal IUGR Gravidograms, abdominal girth, maternal weight gain, ultrasound evaluation of BPD, femur length, head/ abdomen ratio, total intrauterine volume, amniotic fluid volume, fetal ponderal index.

5.

lntrapattum Monitoring

(B) 1.

Clinical signs of fetal distress Cardiac rate (tachycardia followed by bradycardia and fixed heart rate) and rhythm disturbances (ii) Passage of meconium in-utero (iii) Fetal movements (excessive quickening followed by reduced movements) 2. Cardiotocometery (i) FHR. Reduction in beat-to-beat variability, tachycardia, bradycardia, rhythm disturbances (ii) Variations in FHR during uterine contractions (spontaneous or induced) (a) Early deceleration. Compression of fetal head. (b) Late deceleration. Fetal hypoxia. (c) Variable or non uniform deceleration. Cord compression. 3. Fetal scalp blood pH Sampling through fetoscope or transcutaneous fetal scalp monitoring. 4. Fetal blood lactic acid, ECG, EEG are investigative techniques. (i)

(C) Monitoring at birth 1. 2. 3.

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THE INDIAN JOURNAL OF PEDIATRICS

Apgar scoring system. AIIMS action-oriented assessment. Classification of babies into moderate and severe birth asphyxia.

(D) Monitoring during neonatal period 1.

Monitoring for systemic consequences of birth asphyxia. Vital signs, cardiac disturbances including CHF, hematuria and ARF, aspiration and congenital pneumonia, NEC, SIADH, metabolic disturbances (monitor electrolytes, acid base parameters, glucose, calcium, lactate). Early neurological behaviour Sarnat and Sarnat scoring system Monitoring of ICP and cerebral blood flow is experimental Imaging of brain by ultrasound, CT Scan and radionuclide (technetium) scan depending upon available facilities. Auditory and visual evoked responses. E.E.G. changes

2. 3. 4.

5. 6.

(E) Neurodevelopmental assessment during

infancy and childlzood (i)

(//)

(iii) (iv)

Neurological assessment to identify early markers of cerebral palsy (persistent neck tonic posture, clenching of fists, persistence of neonatal automatic reflexes, alterations or asymmetry of muscle tone) and disturbances in spedal senses. Neurodevelopmental assessment with modified Bayley's infant scale and Gessel's scale Assessment of cognitive functions and evidences of minimal brain dysfunction School performance I~FgazNCES

i. Singh M. Hospital-based data on perinatal and neonatal mortality in India. Indian Pediatr 1986; 23 : 579-584.

SINGH : MONITORING OF PERINATAL ASPHYXIA IN THE HOSPITAL 2. Sadovsky E, Yaffe H, Polishuk WZ. Fetal movement monitoring in normal and pathological pregnancies. Int J Obstet Gynecol 1974; 12 : 75-81. 3. Singh M. Fetal monitoring. In : Singh M (ed.)Care of the Newborn. New Delhi : Sagar publications, 1985; pp 31-41. 4. Campbell S. The assessment of fetal development by diagnostic ultrasound. Clin Perinatal 1974; 1 : 507-516. 5. Lee CY, Diloreto PC, Logrand R. Fetal activity acceleration determination for evaluation of fetal reserve. Obstet Gynecol 1976; 48 : 19-26. 6. Pratt D, Dimond F, Yen H et al. Fetal stress and non stress tests : An analysis and comparison of their ability to identify fetal outcome. Obstet Gynecol 1979; 54 : 419-423. 7. Rochard F, Schifrin BS, Goupil F et al. Non stress fetal heart rate monitoring in antenatal period. Am J Obstet Gynecol 1976; 126 : 699-706. 8. Braly P, Freeman RK..Significance of fetal heart rate reactivity with a positive OCt. Obstet Gynecol 1977; 50 : 689-693. 9. Freeman RK, Gobelsman U, Nochimson D et al. An evaluation of significance of positive OCT. Obstet Gynecol 1976; 47 : 8-13. 10. Manning FA, Mossion I, Lange I, Hatman CR. Fetal biophysical profile mortality. Abstracted from : Proc Soc of Obstetricians and Gynecologists of Canada, Vancouver BC, June 1983. 11. Manning FA, Morrison I, Langer IR. Fetal biophysical profile score : a prospective study in 1184 high risk patients. Am l Obstet Gynecol 1981; 140 : 289-294. 12. Manning FA, Morrision I, Lange IR. Antepartum determination of fetal health : composite fetal biophysical profile score. Clin Perinatol 1982; 9 : 288-294. 13. James DB. Ultrasound fetal measurements and IUGR. In : Nabile F. Maillad (ed.) Clinics in Diagnostic Ultrasound 1986; 19 : 11. 14. Robilson HP, Flemming JEE. A critical

15.

16.

17. 18.

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27.

28.

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evaluation of sonor crown-rump length measurements. Br J Obstet Gynecol 1975; 82 : 702-710. Sabbagha RE. Intrauterine growth retardation : Antenatal diagnosis by ultrasound. Obstet Gynecol 1978; 52 : 252-256. Champbell S, Newman CB. Growth of fetal biparietal diameter during normal pregnancy. BrJ Obstet Gynecol 1971; 78 : 513-519. Fenton AN, Steer CM. Fetal distress. Am J Obstet Gynecol 1962; 83 : 354-362. Miller FC, Sacks DA, Yeh SY et al. Significance of meconium during labour. Am J Obstet Gynecol 1975; 122 : 573-580. Schifrin BS, Dame L. Fetal heart rate patterns : Predictions of Apgar Score. JAMA 1972; 219 : 1372-1379. Paul RH, Khazin SA, Yeh Set al. Clinical fetal monitoring : VII. The evaluation and significance of intrapartum baseline fetal heart rate variability. Ant J Obstet Gynecol 1975; 123 : 206-210. Bread RW, Morris ED, Clayton SG et al. Fetal capillary pH as an indicator of the condition of fetus. J Obstet Gynecol Br Common Wealth 1967; 74 : 812-817. Kubli FW, Hon EH, Khazin AF et al. Observations on heart rate and pH in human fetus during labour. Am J Obstet Gynecol 1969; 104 : 1190-1206. Apgar V, James IS. Further observations on newborn scoring system. Am J Dis Child 1962; 104 : 419-428. Nelson KB, EUenberg JH. Apgar scores as predictors of chronic neurological disability. Pediatrics 1981; 68 ."36-42. Singh M. Resucitation of an asphyxiated newborn. In :Singh M, (ed). Medical Emergencies in Children. New Delhi : Sagar Publications, 1988 : pp. 43-54. Sarnat HB, Sarnat MS. Neonatl encephalopathy following fetal distress. Arch Neurol 1975; 33 : 696-703. Volpe JJ. Perinatal hypoxic-ischemic brain injury. Pediatr Clin North Am 1976; 23 : 383-389. Bada HS, Hajjar W, Chua C et al. Non

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THE INDIANJOURNALOF PEDIATRICS invasive diagnosis of neonatal asphyxia and intraventrieular hemorrhage by Doppler ultrasound. J Pediatr I979; 95 : 775779. 29. Fitzhardinge PM, Flodmark O, Fitz CR et al. The prognostic value of computed tomography as an adjunct to assessment of the term infant with post asphyxial eneephalopathy.JPediatr 1981; 99 : 777. 30. Schrumpf JS, Schring S, Killpack Set al. Correlation of early neonatal outcome and CT findings in neonatal brain hypoxia and injury. J Comput Assist Tomogr 1980; 4:445. 31. Despland PA, Galambos R. The auditory brainstem response is a useful diagnostic tool in intensive care nursery. Pediatr Res 1980; 14 : 154-160.

32. Harbek A, Karlberg P, Kjellmer I e t al. Clinical application of evoked electroencephalographic responses in newborn infants with perinatal asphyxia. Dev Med Child Neutol 1977; 19 : 34-41. 33. Brazelton "lB. Neonatal behavioural assessment scale. In : Clinics in Developmental Medicine, Philadelphia : Spastics International Medical Publication, JB Lippinoctt, 1973 : 34. Desouza SW, McCartney E, Nulan M e t al. Hearing, speech and language in survivors of severe perinatal asphyxia. Arch Dis Child 1981; 56 : 245-252. 35. Thompson AJ, Searle M, Russell G. Quality of survival after severe birth asphyxia. Arch Dis Child 1977, 52 : 62.0-626.

IgG SUBCLASSDEFICIENCYIN ASTHMA Eighty-two asthmatic children (1.5 to 6.3 years of age) were studied. Asthma had to be serious enough to warrant maintenance of asthma medications. This was determined by children having at least one asthraa attack per month or nearly daily symptoms. Half the children had symptoms of rhinitis, and half the children had eczema or a history of eczema. Seventy-six healthy controls (1 to 6.8 years of age) were used. Concentration of IgG1, IgG2, IgG3, and total lgG were lower in asthmatic children and lgG2 was lower in asthmatic children aged 5 to 7 years. Twenty-eight asthmatic children had significant deficiency of total IgG or lgG subclass, with IgG2 deficiency being most commonly seen (n = 26). Five of the children with IgG2 defidency had IgA deficiency as well. Based on the results of this study, children aged 7 years or less with moderate asthma may well have a significant abnormality of the immune system. In this study the most common abnormality was a deficiency of lgG2. This study would have been more complete if the authors had evaluated patient responsiveness to protein and polyscaccharide vaccines. Moderately asthmatic children who are unable to make specific antibody and who do not respond to aggressive antiasthma therapy as well as prophylactic antibiotics would be candidates for intravenous ?-globuline. Abstracted from : Loftus BG et al. Arch Dis Child 1988; 63 : 1434-1437.