Odendaal, E S

Odendaal, H J

Steyn, D W

South African Medical Journal (SAMJ)

ORIGINAL ARTICLESPreterm delivery is the most important cause of perinatalmortality and morbidity in the developed world.1 Theprevalence of preterm delivery in First-World countries is 6 - 10%.2 In developed countries very-low-birth-weight (VLBW)babies account for only 1 - 2.5% of all births.3,4 However, morethan half of prematurity-related deaths, morbidity andeconomic costs are due to VLBW neonates.4The total perinatally related wastage at Tygerberg Hospital is31.5 per 1 000 deliveries. Sixty per cent of these deaths arebabies with a very low birth weight.5 The mortality rate forsevere respiratory distress syndrome is about 50%. Theprevalence of other complications are periventricularhaemorrhage (30%), patent ductus arteriosus (20%) andnecrotising enterocolitis (5 - 10%).3Although the mortality rate for VLBW babies has decreasedover the past decades, there is still a high proportion ofseverely handicapped infants.4 According to data from theNational Institute of Child Health and Human Development(NICHD) neonatal networks, 90% of babies with a birth weightbetween 1 000 g and 1 500 g survived and only 20% had majorhandicaps. The survival rate was 77% for babies weighing 731 - 1 000 g, and the morbidity rate 35%. In the 501 - 750 ggroup, 39% survived, but 53% had major morbidity.4VLBW babies are a group with heterogenic aetiologies andinclude neonates who are preterm, small for gestational age, orboth.3 Attempts to reduce the incidence of the delivery of verysmall babies can only succeed once the causes are identified.We conducted this study to determine the primary reasons forthe delivery of VLBW babies at Tygerberg Hospital.Patients and methodsA cross-sectional descriptive study was done at TygerbergHospital over a 6-month period. The decision that 6 monthswas sufficiently long was taken after reassessment of availabledepartmental data sets which showed no seasonal variation inthe occurrence of VLBW babies. Immediately after delivery,data were collected from files of mothers who delivered babiesweighing between 500 g and 1 499 g. Data were charted on adata sheet which was then used for analysis. All live-bornbabies were also followed up for the first 7 days of the neonatalperiod.The following primary causes were recorded and clearlydefined.1. Preterm labour — onset of labour before 37 completedweeks of gestation.2. Preterm prelabour rupture of membranes (PPROM) —rupture of membranes before 37 completed weeks of gestation61January 2003, Vol. 93, No. 1  SAMJObjective. To determine the primary reasons for the deliveryof very-low-birth-weight (VLBW) babies.Design. Cross-sectional descriptive study.  Study period. 1 March 1997 - 31 August 1997. Methods. Data were collected from all mothers who deliveredbabies weighing 500 - 1 499 g. The following primary causeswere selected and clearly defined: spontaneous pretermlabour, preterm prelabour rupture of membranes,hypertensive disease, antepartum haemorrhage, intrauterinedeath and congenital abnormalities. A total of 227 patientswere admitted to the study. One patient was excluded fromthe study as the data in her file were inadequate. Of theremaining 226 patients, 210 had singleton pregnancies and 16had twin pregnancies. In total 242 babies were delivered;however, 6 babies from the twin pregnancies were excludedfrom the analysis as they had a birth weight exceeding 1 499 g. Results. Primary causes of delivery were  hypertensive diseasein 101 patients (44.7%), spontaneous preterm labour 65(28.8%), preterm prelabour rupture of membranes 21 (9.3%),intrauterine death 17 (7.5%), antepartum haemorrhage 10(4.4%), congenital abnormalities 3 (1.3%), and other 9 (4%). Ofthe hypertensive cases, 43 were delivered for fetal distress, 16for fetal distress due to abruptio placentae, 20 for maternalreasons, 19 for intrauterine death and 3 for both fetal andmaternal reasons.Conclusion. Hypertension, preterm labour and prelabourrupture of membranes were the main causes of delivery ofVLBW babies. Further research should address methods toreduce the number of these deliveries.S Afr J Med 2003; 93: 61-64.Department of Obstetrics and Gynaecology, Tygerberg Hospital and University ofStellenbosch and Medical Research Council Unit for Perinatal Mortality,Tygerberg, W CapeE S Odendaal, MB ChB, MMed (O & G)D W Steyn, MB ChB, MMed (O & G), FCOG (SA), MDH J Odendaal, MB ChB, MMed (O & G), FCOG (SA), MD, FRCOGObstetric causes for delivery of very-low-birth-weight babies atTygerberg HospitalE S Odendaal, D W Steyn, H J Odendaal62January 2003, Vol. 93, No. 1  SAMJORIGINAL ARTICLESand at least 1 hour before the onset of contractions.3. Hypertensive diseases were considered as primary causewhen the delivery was attributed to the hypertensive conditionor to the complications of its management. Hypertension wasdefined as a diastolic pressure of 90 mmHg, taken on twooccasions at least 6 hours apart, or a single diastolic pressure of110 mmHg. Pre-eclampsia was defined as hypertension in thepresence of significant proteinuria, that is 2+ or more on urineDipstix or > 300 mg in a 24-hour urine sample. Whenconditions such as abruptio placentae, fetal distress orintrauterine death occurred in patients with underlyinghypertensive disease, the latter was considered to be the causeof delivery. The diagnosis of fetal distress, severe enough towarrant delivery, was made in the presence of fetal heart ratebaseline variability of less than 5 beats per minute  continuingfor at least 60 minutes, or repeated late decelerations.4. Antepartum haemorrhage included bleeding due toabruptio placentae, placenta praevia and antepartumhaemorrhage of unknown origin. Patients with an underlyinghypertensive condition were included in the hypertensiongroup and excluded from the antepartum haemorrhage group.5. Intrauterine deaths, stillbirths and late abortions ofnormally formed fetuses in whom the death was not due tohypertensive disease, antepartum haemorrhage, pretermlabour or PPROM.6. Congenital abnormalities.7. Other causes included maternal illness and intrauterinegrowth restriction unrelated to a hypertensive disease.In patients with preterm labour and PPROM an attempt wasmade to diagnose the causes or co-factors that could have ledto the onset of labour.ResultsFrom 1 March to 31 August 1997, 2 589 mothers deliveredbabies at Tygerberg Hospital. During this period, 227 mothers(8.8%) delivered VLBW babies. One patient was excluded fromthe study as the data in her file were inadequate. Of theremaining 226 patients, 210 had singleton pregnancies and 16had twin pregnancies. Six babies from the twin pregnancieswere excluded from the analysis as the birth weight exceeded 1 499 g (Fig. 1).Patient profileOne hundred and sixty patients (70.8%) were from the Capemetropolitan area, and 66 patients (29.2%) were referred fromoutside areas.The mean age of our patients was 26.5 ± 6.3 years (range 14 -42 years). The range of the gravidity was 1 - 8, and of the parity0 - 5, with a mean of 2.6 and 1.3 respectively. Sixty-five patients(28.7%) were primigravidas. One hundred and eighty-sixpatients (81.6%) attended antenatal clinics. The median numberof clinic visits was 4 (range 1 - 14). Twenty patients (8.8%) werediagnosed as having syphilis. In our study group 89 patients(39%) were married, 91 (40%) were smokers and 15 (7%)admitted that they abused alcohol during the pregnancy.Previous obstetric history of noteForty-nine patients had a total number of 68 miscarriages intheir previous pregnancies. In 42 patients, hypertensivediseases had complicated one or more of their previouspregnancies. Preterm labour or PPROM occurred in 10 patientsin their previous pregnancies.Antepartum courseEighteen patients had urinary tract infection. In 11 patients,Escherichia coli was cultured. Vaginitis occurred in 56 patients.In 31 patients, chronic hypertension or pregnancy-inducedhypertension was diagnosed and 22 patients subsequentlydeveloped superimposed pre-eclampsia. A total number of 103patients had pre-eclampsia.A Doppler resistance index of the umbilical artery wasperformed in 79 patients. Thirty patients had absent-enddiastolic flow velocity.Primary cause of delivery (Table I)Hypertensive diseases and complications of hypertension and227 MothersOne patient withincomplete information210 Singletonpregnancies10 VLBWbabies6 Babies> 1 499 g16 Twinpregnancies226 Mothers foranalysisFig. 1. Summary of the distribution of patients (VLBW = very lowbirth weight).Table I. Primary causes of delivery in 237 patientsPrimary cause No. of patients (%)Hypertensive disease 101 (44.7)Preterm labour 65 (28.8)Preterm prelabour rupture of membranes 21 (9.3)Intrauterine death 17 (7.5)Antepartum haemorrhage 10 (4.4)Congenital abnormalities 3 (1.3)Other 9 (4)ORIGINAL ARTICLESpre-eclampsia were the primary cause of delivery in 101patients (44.7%). Forty-six of these patients were referred fromoutside areas.Of the hypertensive cases, 43 were delivered for fetaldistress, 16 for fetal distress due to abruptio placentae, 20 formaternal reasons, 19 for intrauterine deaths and 3 for both fetaland maternal reasons. Maternal reasons included complicationssuch as the HELLP (haemolysis, elevated liver enzymes andlow platelet) syndrome, renal failure and pulmonary oedema.Intrauterine death complicated the pregnancy in 19 patients.Abruptio placentae caused 9 of the 19 intrauterine deaths.Eighty-one patients with hypertensive disease  were deliveredat 28 weeks’ gestation or later.Antepartum haemorrhage without underlying hypertensivedisease occurred in 10 patients (4.4%). Of these patients, 6 hadintrauterine deaths and 3 fetal distress due to abruptioplacentae. Placenta praevia was diagnosed in 1 patient.Intrauterine death, not related to any of the other primarycauses for delivery, occurred in 17 patients (7.5%).Congenital abnormalities were diagnosed in 3 patients(1.3%) (2 singleton and 1 twin pregnancy).Maternal and fetal complications unrelated to hypertensivedisease was the primary cause of delivery in 9 patients (4%).Preterm labour occurred in 65 patients (28.8%) and PPROMin 21 patients (9.3%). The median time from onset of symptomsto admission was 7 hours (range 0 - 336 hours). This delay wasmainly due to a lack of transport and long travelling distance.The mean cervical dilatation on admission was 5.7 ± 3 cm. In31 patients the cervical dilatation was more than 6 cm onadmission. In 37 patients (43%) infection was demonstrated atthe time of preterm labour or PPROM — this includedvaginitis (13), urinary tract infections (7), chorioamnionitis (8),pulmonary tuberculosis (2), congenital syphilis (6) and AIDS(1). In 12 patients an abruption was seen on the placenta atdelivery. Cervical incompetence was diagnosed in 9 patients,multiple pregnancies in 9 patients and 2 patients had aplacenta praevia.Mode of deliveryCaesarean section was the mode of delivery in 90 patients(39.6%). In 74 patients the indication for caesarean section wasfetal distress. One hundred and three patients (45.4%) hadnormal vertex deliveries and 33 (14.5%) breech deliveries.Neonatal outcomeThe mean gestational age at delivery was 23.44 ± 3.09 weeks(range 21 - 41 weeks). Of the 236 babies born, 189 (83.3%) wereat a gestational age of 25 - 32 weeks. Fifteen babies weredelivered after 32 weeks, 3 with congenital abnormalities. Fiveof these babies were born to mothers with severe hypertensivedisease; 2 of these babies had absent-end diastolic flow velocityon umbilical artery Doppler studies. Thirty-two babies wereborn before 25 weeks’ gestation.The perinatal outcome for all age groups was: intrauterinedeaths 89 (37.7%), early neonatal death 29 (12.3%) and alive onday seven 118 (50%). Morbidity or mortality was caused byrespiratory distress syndrome in 94 babies (63.9%).The most important causes of delivery before 28 weeks’gestation were preterm labour in 35 patients (47.9%) andhypertensive diseases in 20 patients (27.4%). After 28 weeks’gestation these percentages were reversed. Hypertensivediseases were the cause of delivery in 81 patients (52.9%) andpreterm labour in 30 patients (19.6%).DiscussionSixty per cent of perinatally related wastage at TygerbergHospital occurs in VLBW babies.5 It is clearly a clinical andresearch priority. However, there may be various underlyingcauses leading to the birth of VLBW babies. While the logicalapproach to preventing an unfavourable outcome in anycondition would be an attempt to prevent the disease, a greatdeal may also be achieved by approaching those complicationswhich contribute most significantly to the unfavourableoutcome which is to be prevented.Previous studies have emphasised the role of preterm labourand PPROM in the incidence of preterm or VLBW babies.6-8 Inthis study, complications of hypertensive disease mandateddelivery in 101 patients (44.7%). This figure may be falselyhigh, because there may have been patients, for example, withpreterm labour, PPROM and intrauterine deaths who deliveredbefore referral to Tygerberg Hospital. Even after consideringthis possibility, this study once again emphasises theimportance of hypertension and pre-eclampsia in ourpopulation.While there seems to be general agreement that low birthweight is associated with poorer outcome, there are a paucityof data regarding the underlying causes. In a study byDobbelaere et al.,6 the primary reasons for the delivery of 550low-birth-weight babies, also over a 6-month period, werespontaneous preterm labour (28%), hypertensive diseases(19%) and PPROM (18%). However, from their report it is clearthat the exact birth weight as well as the presence of multiplepregnancy influenced the ratio between spontaneous pretermlabour and hypertensive diseases. Among the 466 singletonpregnancies, 230 babies (49.4%) weighed less than 2 000 g. Theprimary obstetric cause of the delivery was preterm labour in57 (24.8%) and hypertensive disease in 55 (23.9%) of thesecases. In contrast, 72 (30.9%) of the 233 singletons weighingmore than 2 000 g were delivered due to spontaneous pretermlabour, while hypertension was the underlying cause in only 32cases (13.7%). Spontaneous preterm labour resulted in the birthof 19 of the 55 babies from twin pregnancies (34.5%) weighing63January 2003, Vol. 93, No. 1  SAMJ64January 2003, Vol. 93, No. 1  SAMJORIGINAL ARTICLESless than 2 000 g, in comparison with only 4 (7.3%) due tohypertension. The respective statistics for babies larger than 2 000 g were 45.7% and 13.3%. It seems from their data thatthere may be a trend towards a higher ratio of hypertensivedisease with decreasing birth weight.It is clear that our approach to the prevention of small-for-gestational-age babies will differ from units where theunderlying causes are different. Much work has been donetowards improving perinatal outcome in pregnanciescomplicated by maternal hypertension. We have shownrepeatedly that gestational age at birth is the most importantfactor  determining perinatal outcome.9,10 It is also well knownthat expectant management of carefully selected patients withearly onset pre-eclampsia results in a decline in the perinatalmortality rate.9 Meticulous control of maternal blood pressureand frequent monitoring of the fetal heart rate pattern withcardiotocography for early diagnosis of abruptio placentae areessential when adapting this approach. A Doppler resistanceindex of the umbilical artery can identify those babies withintrauterine growth restriction at risk of fetal distress andintrauterine death.11Studies of interventions to prevent the development of pre-eclampsia in patients considered to be at high risk havegenerally been disappointing. However, there have been somepromising messages as well. While the role of low-dose aspirinin preventing pre-eclampsia is clearly limited, it may be ofvalue in women at high risk of early onset pre-eclampsia.12Perhaps earlier and more aggressive treatment of early onsethypertension with or without proteinuria may reduce theincidence of complications. In our study, 22 patients developedsuperimposed pre-eclampsia after the initial diagnosis ofchronic hypertension or pregnancy-induced hypertension wasmade. In 14 mothers the babies had absent-end diastolic flowand were growth restricted.Preterm labour and PPROM complicated the pregnancies in28.8% and 9.3% of patients respectively in our study. Even ifthe labour was theoretically preventable, suppression of labourwas only attempted in 23 patients (37.4%) with preterm labouror PPROM. The main reasons for non-suppression of labourwere ruptured membranes with the risk of chorioamnionitisand cervical dilatation of more than 8 cm on admission.Infection was demonstrated in 43% of patients with pretermlabour or PPROM.Screening methods for the earlier detection of lower genitaland urinary tract infections must be implemented at antenatalclinics. Patients with a previous history of preterm labour orPPROM are especially at risk. Hulsey et al.13 reported thatpreterm labour recurred in 24.6% of patients with previouspreterm labour.Abruptio placentae was diagnosed in 46 patients (20.4%).Twenty-five patients had hypertension or pre-eclampsia. In 9patients the abruption was unrelated to an underlyinghypertensive disorder. Abruptio placentae was a causal orcofactor in 12 patients with preterm labour or PPROM. Thehigh incidence of abruptio placentae necessitates furtherresearch into the pathophysiology of this problem.VLBW babies are a group with heterogenic aetiologies, butwith one common parameter — increased mortality andmorbidity. Interventional strategies must be planned on thebasis of the primary obstetric reason for delivery, not only toincrease the survival, but also to decrease the morbidity due tohandicaps.Hypertension, preterm labour and preterm rupture ofmembranes were the primary causes for delivery of 82.8% ofVLBW babies. Research on how to reduce these factors isurgently needed.References1. Danielian PJ, Hall MH. The epidemiology of prematurity. Curr Obstet Gynecol 1996; 6: 133-136.2. Pitman MC, Steer PJ. Prematurity: Assessment of uterine activity. Curr Obstet Gynecol 1996; 6:137-142.3. Halliday HL. Management of the very low birthweight neonate. Curr Obstet Gynecol 1992; 2:207-211.4. Novy MJ, McGregor JA, Iams JD. New perspectives on the prevention of extremeprematurity. Clin Obstet Gynecol 1995; 38: 790-808.5. Prins CA, Theron GB, Steyn DW, Geerts LTGM, De Jong G. Total perinatally related wastageat Tygerberg Hospital — a comparison between 1986 and 1993. S Afr Med J 1997; 87: 808-814.6. Dobbelaere A, Pattinson RC, Makin JD, Quintelier J. The potential for preventing the deliveryand perinatal mortality of low-birth-weight babies in a black urban population. S Afr Med J 1996; 86: 536-539.7. Berkowitz GS, Lapinski RH. Relative and attributable risk estimates for preterm birth. PrenatNeonat Med 1998; 3: 53-55.8. Tucker JM, Goldenberg RL, Davis RO, Copper RL, Winkler CL, Hauth JC. Etiologies ofpreterm birth in an indigent population: Is prevention a logical expectant? Obstet Gynecol1991; 77: 343-347.9. Odendaal HJ, Steyn DW, Norman K, et al. Improved perinatal mortality rates in 1 001patients with severe pre-eclampsia. S Afr Med J 1995; 85: 1071-1076.10. Hall DR, Odendaal HJ, Kirsten GF, Smith J, Grove D. Expectant management of early onset,severe pre-eclampsia: Perinatal outcome. Br J Obstet Gynaecol 2000; 107: 1258-1264.11. Hay WW. Etiologies of preterm birth: Intra-uterine growth restriction. Prenat Neonat Med1998; 3: 121-124.12. Louden KA, Kilby MD. Low-dose aspirin: The rationale for preventing pre-eclampsia andintra-uterine growth retardation: A role after CLASP? In: Bonnar J, ed. Recent Advances inObstetrics and Gynaecology No 19. Edinburgh: Churchill Livingstone, 1995: 15-33.13. Hulsey TC, Alexander GR, Van Dorsten P. ‘Cause’ of preterm birth in first and seconddeliveries. Prenat Neonat Med 1998; 3: 134-137.Accepted 18 August 2002.

Obstetric causes for delivery of very-low-birth-weight babies at Tygerberg Hospital

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Obstetric causes for delivery of very-low-birth-weight babies at Tygerberg Hospital

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