Please cite as: Smith V, Devane D, Higgins S, Begley C Preterm birth: the
risk factors The Practising Midwife, 2005; 8 (9): 12 – 16 ________________________________________________________________
Risk factors for preterm birth
Valerie Smith RM, RGN, BNS, BSc(Hons).* Midwifery Research Student.
Declan Devane RM, RGN, RNT, DipHE, BSc(Hons), PgDip(Stats), MSc. Doctoral Student/Midwifery Research Assistant. Shane Higgins MB, BCh, BAO, MRCOG, FRANZCOG. Consultant Obstetrician/Clinical Director Department of Obstetrics, Our Lady of Lourdes Hospital, Drogheda, Co-Louth, Ireland. Cecily M. Begley RGN, RM, RNT, FFNRCSI, MA, MSc, PhD, FTCD. Professor of Nursing and Midwifery/Director School of Nursing and Midwifery, The University of Dublin Trinity College 24 D’Olier St. Dublin 2 Ireland. *off print requests to
[email protected]
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Introduction Preterm birth poses a major challenge for both health care providers and the health care service. It is a major cause of perinatal mortality and serious morbidity and is responsible for 75-90% of all neonatal deaths not attributable to congenital abnormalities. (Lindsey 2004). With advances in technology and neonatal intensive care the rate of preterm birth and in particular the number of very preterm babies born, who subsequently survive, has increased. This has resulted in growing pressure on resources in terms of psychological support for parents and financial pressure for both parents and the health care service. The World Health Organisation defines preterm birth as birth before 37 weeks gestation (World Health Organisation 2003). However, such a definition is problematic in that it does not differentiate between a spontaneous abortion and a birth, a transition which, in itself, varies between countries (Lumley 2003). Over the past 20-30 years the incidence of preterm birth in most developed countries has been approximately 5-7% of live births with the incidence in the United States slightly higher at 11-12% (Goldenberg 2002, Tucker & McGuire 2004). A number of risk factors have been associated with preterm labour and birth, and these may be related to maternal or fetal circumstances. Many of these factors are not necessarily modifiable causative factors, but rather indicators as to those women who may be at an increased risk of preterm birth. Furthermore preterm birth can be multifactorial and it is often difficult to disentangle the effects of one single risk factor for preterm birth from other factors. Approximately 40-50% of all preterm births result from spontaneous preterm labour with the remainder resulting from either preterm premature rupture of membranes (PPROM) (25-40%) or obstetrically indicated/iatrogenic reasons (20-25%) (Tucker et al 1991). Iatrogenic reasons for preterm delivery can occur when problems such as pre-eclampsia, or severe intrauterine growth restriction occur. In such circumstances the safety and well-being of the mother or baby may over-ride the need for the pregnancy to continue leading to an elective preterm birth, usually by caesarean section. Iatrogenic reasons may also occur due to pregnancy complications as in the case of placental abruption, or cord prolapse, where immediate delivery of the baby is necessitated.
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This paper will explore risk factors associated with spontaneous preterm labour and birth including infection, behavioural and socioeconomic factors, multiple gestation, past obstetric history, the presence of cervicovaginal fetal fibronectin and asymptomatic cervical shortening. Infection The association between preterm birth and infection is well documented throughout the literature (Kurki et al 1992, Sheehan & Lamont 1996, Gibbs & Eschenbach 1997). Infection may account for up to 50% of preterm births (Lockwood 2002) and is associated more with early preterm birth (before 32 weeks gestation) than with late preterm birth (after 32 weeks gestation) (Goldenberg et al 2000). The pathophysiology of infection leading to preterm birth, although largely unclear, centres on activation of the mother’s immune system. Bacteria present in the amniotic fluid, membranes or placenta are recognised by the body as foreign and, in response the immune system releases a number of inflammatory mediators. These include Interleukin-1, Tumour Necrosis Factor, Interleukin-6 and Platelet Activating Factor, all of which are thought to play a role in the initiation of labour at term (Carson 1997). Furthermore these inflammatory mediators have been shown to stimulate prostaglandin synthesis in the amnion, chorion, decidua and myometrium. Prostaglandins are known to cause myometrial contractions, which may lead to cervical dilatation and membrane exposure/rupture, resulting in greater entry of microbes into the uterine cavity, and ultimately premature labour and preterm birth (Carson 1997, Klein & Gibbs 2004). The main microorganisms associated with preterm birth include Ureaplasma urealyticum, Mycoplasma species, Chlamydia Trachomatis, Trichomonas, Escherichia Coli, Group B Streptococcus, and most notably anaerobes such as Fusobacterium, Bacteriodes, anaerobic Streptococci, and Mobiluncus (Iams 2002, Goldenberg et al 2000). The spread of bacteria and infection to the uterus may occur via a number of routes. There may be spread from an ascending lower genital tract infection to the upper genital tract and passage through the cervix. In addition, haematogenous spread through the placenta may occur. For example there is a growing body of evidence associating periodontal disease with preterm birth (Jeffcoat et al 2001, Boggess 2003) where infection from this distant site is blood-borne to the uterus via the placenta. There may be migration of bacteria from the abdominal cavity through the fallopian tubes and there can be inadvertent needle contamination at the time of amniocentesis or chrionic villus sampling (Goldenberg et al 2000). Goldenberg (2002) suggests that clinical chorioamnionitis complicates 1-5% of term pregnancies, but 25% of preterm births. This is supported by Guzick and Winn (1985) who, in a survey of 2,774 women, found that histological chorioamnionitis was more common in preterm deliveries than in term, the incidence being 32.8% compared to 10%. A study at a North London hospital, where all women were offered screening for bacterial vaginosis at
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booking, reported that 20% of the 800 women screened had abnormal genital tract colonisation on Gram stain (Sheehan & Lamont 1996). Of those, 16% subsequently experienced a miscarriage or an early preterm birth. Behavioural/Socioeconomic factors Smoking has been linked as a risk factor for preterm birth. Tobacco smoking in pregnancy induces fetal hypoxia by vasoconstriction due to the effect of nicotine on adrenergic neurones (Stables 1999). Vasoconstriction reduces placental blood flow leading to placental underperfusion. The prolonged effect of continuous smoking in pregnancy results in an increase in carboxyhaemoglobin causing a sustained reduction in the availability of oxygen to the fetus (Stables 1999) and ultimately a reduction in the length of pregnancy. In a retrospective analysis of 36,059 women, which sought to explore the contribution of maternal smoking to preterm birth amongst Aboriginals and non-Aboriginals in South Austraila, Chan et al (2001) found that Aboriginals had a much higher rate of smoking during pregnancy (57.8% v 24.0% at the first antenatal visit). The preterm birth rates were 20% in the Aboriginal women compared with 11% in the non-Aboriginal group. Kyrklund-Blomberg et al (2005) describe a dose dependant association between smoking and the risk of very preterm birth. Heavy smokers (>10 cigarettes/day) had a threefold increased risk compared to non-smokers. Their study further demonstrated that compared with non-smokers, heavy smokers faced an almost five-fold increase in risk of very early preterm (
