Despite improvements in services for people with diabetes and an increased focus on care of diabetes in pregnancy, there has been no significant reduction in neonatal complications after pregnancy complicated by maternal diabetes. Some complications are severe and life threatening or lead to long-term difficulties, whilst others are transient and are unlikely to lead to long-term harm, if managed according to standard guidelines. Most neonatal complications are, in theory, avoidable by optimal diabetes care, those that arise directly as a result of poor control of diabetes in pregnancy or as a result of obstetric interventions related to maternal diabetes control. Of greater concern are iatrogenic complications that arise from decisions which have no clear rationale (e.g., ‘routine’ admission of a baby to a neonatal unit). Planning for neonatal management must take into account known risks and the likelihood of occurrence, start in advance of delivery, involve all relevant groups of professionals and be centred on the needs of the mother and baby and not upon historical organisational policies.
There are risks to the fetus and neonate whether diabetes predates pregnancy or develops during pregnancy. As the population of women with type 2 diabetes becomes younger, particularly in some ethnic groups, type 2 diabetes now represents approximately one-third of pregnancies complicated by pre-existing diabetes. Perinatal mortality rates and rates of fetal macrosomia for these pregnancies are no different to those affected by type 1 diabetes. Equally, complications occur after gestational diabetes, if the gestational diabetes is not recognised and well managed.
Factors leading to risk for the fetus and the neonate fall into three groups – the directly harmful metabolic environment, the obstetric interventions required when maternal control of diabetes is poor or inappropriate ‘routine’ practices ( Table 1 ). Optimising diabetic control before and during pregnancy minimises risks to the mother and fetus, and reduces the risk of postnatal complications described below. In many cases, this is achieved and complications are avoided. However, it is important to be aware of the complications which can occur. Adequate antenatal screening and assessment should indicate the pregnancies at greatest risk so that an antenatal plan may be made and, at all places of birth, there should be staff trained and competent to recognise and stabilise babies with unexpected complications.
| Directly related to diabetes in pregnancy: | |
| Congenital anomalies | (short and long term) |
| Intrauterine growth restriction | (short and long term) |
| Intrapartum hypoxia-ischaemia | (short and long term) |
| Birth injury | (usually short term) |
| Polycythaemia/jaundice | (short term) |
| Hypoketonaemic hypoglycaemia | (usually short term) |
| Hypocalcaemia, hypomagnesaemia | (short term) |
| Hypertrophic cardiomyopathy | (short term) |
| Complications of obstetric interventions: | |
| Complications of preterm delivery | (short and long term) |
| Complications of caesarean section | (short term) |
| Iatrogenic: | |
| Complications of unnecessary obstetric interventions | |
| Inappropriate separation of mother and baby | |
| Inappropriate formula supplementation | |
| Reduced breast feeding | |
| Over-feeding | |
Almost all of the complications have implications for neonatal management. Whilst some complications continue to have lifelong implications, new risks emerging later in childhood or as an adult after a healthy newborn period are less common.
However, it must be stated that the majority of women with diabetes in pregnancy do not have babies who develop complications, especially when diabetes control before and during pregnancy is good. The challenge for these babies is to avoid iatrogenic harm.
Care of the healthy, low-risk baby
For many women, especially those who access prenatal counselling and enhanced diabetes care and then continue to have good control of diabetes during pregnancy, the fetus and neonate are at low risk of complications. It is important to recognise that these babies should be managed according to normal standards for the healthy newborn baby. There is no indication for routine attendance of paediatricians at the delivery or routine admission to a neonatal unit. It is important to avoid unnecessary separation of mother and baby, and also to facilitate successful breast feeding if this is the mother’s chosen method of feeding. The iatrogenic complications, which arise as a result of failure to follow these principles, are discussed below.
Short-term risks
Despite the aspiration that improved maternal diabetes care will minimise perinatal morbidity and mortality, recent data suggest that notwithstanding some improvements over time, insufficient progress has been made since the first cohort studies which highlighted the risks of diabetes in pregnancy ( Table 2 ). Some fetal and neonatal complications are the direct result of the abnormal metabolic environment that the fetus is exposed to, and these include congenital anomalies, macrosomia, the effects of intrauterine and intrapartum hypoxia–ischaemia and neonatal hypoglycaemia. Others arise from the effects of being born preterm or by caesarean section and are not specific to diabetes. Finally, some neonatal problems are iatrogenic.
| IDM | UK- average | Rate ratio | |
|---|---|---|---|
| Neonatal death | 9.3/1000 | 3.6/1000 | 2.6 |
| Preterm delivery | 37% | 7.3% | 5 |
| Congenital anomaly | 5.5% | 2.1% | 2.6 |
| Birthweight >90th %ile | 52% | 10% | 5.2 |
| Shoulder dystocia | 7.9% | 3% | 2.6 |
| Erbs palsy | 4.5/1000 | 0.42/1000 | 11 |
| Apgar <7 at 5 mins | 2.6% | 0.76% | 3.4 |
| Admission NNU | 56% | 10% | 5.6 |
| Term admission SC a | 33% | 10% | 3.3 |
a 67.1% of admissions of full term babies to special care were assessed as avoidable.
Perinatal mortality
The fertility and well-being of women with diabetes dramatically improved with the availability of insulin, but a high perinatal mortality rate of 20–25% persisted until the 1960s. Although perinatal mortality rates have fallen over more recent decades, these vary between countries and regions and progress has been disappointing .
Most recent UK Confidential Enquiry into Maternal and Child Health (CEMACH) data indicate that the overall UK perinatal mortality rate (stillbirths and first-week neonatal deaths) with diabetes in pregnancy was 31.8/1000 compared with a national rate of 8.5/1000 (rate ratio 3.8, confidence intervals 3.0–4.7). This was similar to the rates in cohort studies from the Netherlands, Scotland (1979–1995 and1998–199 cohorts), UK northern region (1994 and 1996–2004 cohorts) and Northwest England. For the group of babies from the CEMACH cohort undergoing a more detailed enquiry, the most common causes of death were related to congenital abnormality and intrapartum complications, and therefore could be assumed to be preventable with optimal care ( Table 3 ).
| Cause of death a | Number (%) in enquiry N = 98 | Number (%) in UK popn N = 5756 | p value for difference |
|---|---|---|---|
| Unexplained | 58 (59%) | 2516 (44%) | 0.002 |
| Congenital anomaly | 18 (18%) | 1087 (19%) | 0.68 |
| Intrapartum causes | 10 (10%) | 429 (8%) | 0.30 |
| Immaturity | 4 (4%) | 1027 (18%) | <0.001 |
| Infection | 1 (1%) | 252 (4%) | 0.10 |
The stillbirth rate for women with types 1 and 2 diabetes in the UK 2002–2003 cohort was 26.8/1000, compared with a national rate of 5.7/1000 (rate ratio 4.7, confidence intervals 3.7–6.0). Similar rates have been reported in other UK studies and in a European study.
In the UK 2002–2003 cohort, the neonatal death rate was 9.3/1000 for babies born to mothers with diabetes, compared with a national rate of 3.6/1000 (rate ratio 2.6, confidence intervals 1.7–3.9). Neonatal mortality rates were very similar to this in the Dutch and Scottish cohort studies.
Congenital anomalies
It has long been recognised that there is a higher incidence of congenital anomalies in pregnancies complicated by diabetes than in the general population. Despite more recent major improvements in the care of diabetes in pregnancy, there has been little overall change in the incidence of congenital anomalies. Congenital anomalies in the offspring of women with diabetes occur with a frequency up to 10 times that observed in the general population. Most recent UK data demonstrate that 4–6% of fetuses of diabetic mothers had one or more major congenital anomalies. The reported incidence was even higher in the Netherlands and in less recent UK cohort studies from the UK Northern region and Northwest England. This has become more relevant as the overall perinatal mortality has fallen and congenital anomalies (along with intrapartum causes) now account for a large proportion of perinatal losses and have replaced respiratory distress syndrome (RDS) as the leading cause of perinatal loss.
The cause of diabetic embryopathy is not fully understood. Genetic factors (diabetes-related genes) are unlikely to play a role, as the incidence of birth defects is not increased in babies of fathers with diabetes. It is likely that congenital anomalies are related to the diabetic intrauterine environment during the period of organogenesis, before the seventh week of gestation. Therefore, most occur before the pregnancy is recognised and intensified diabetes treatment is initiated. Some reports suggest that early first-trimester improvement in glycaemic control, combined with prenatal diagnosis of anomalies using serum α-fetoprotein determinations and ultrasound scanning, could reduce the impact of congenital anomalies.
The teratogenic effect of hyperglycaemia has been suggested by human studies, and has been confirmed in animal studies. However, animal studies have demonstrated additional factors such as hyperketonaemia, increased levels of somatomedin-inhibiting factors and decreased myoinositol concentration in the neuroectoderm.
Insulin cannot be teratogenic, because the human placenta is impermeable to insulin at early gestation and fetal pancreatic β cells are not present before the 10th week. However, disturbances in the secretion of relaxin, an insulin homologue, have been suggested to be teratogenic.
Finally, hypoglycaemia can also be embryotoxic in experimental animals but data from human studies are reassuring.
The most common anomalies are congenital heart disease with an incidence in CEMACH cohort of 1.7%, 3 times more common than in the general population, and anomalies of limb musculoskeletal system or connective tissue (incidence 0.7%). Neural tube defects, although numerically rare, are more common (by a factor of 3.4 in the UK cohort) than in the general population.
To minimise risk, it is clear that efforts to prevent birth defects should start before conception, with contraceptive advice offered so that every pregnancy can be planned in advance with optimum periconceptual metabolic control. In planning for postnatal care, it is important that the obstetrician and neonatologist ensure that there has been adequate counselling of parents, involving the specialist team who will care for the baby postnatally and ensure that delivery takes place at an appropriate centre (dependent on the nature of the anomaly) to enable early access to specialist care, including neonatal surgery, should it be required. Routine postnatal echocardiography to screen for congenital heart anomalies is not indicated, unless an abnormality has been suspected on antenatal scanning or the baby presents with clinical signs of congenital heart disease.
Effects of antenatal and intra-partum hypoxia-ischaemia
Hypoxia–ischaemia is the combined pathology of impaired oxygenation of the blood and reduced perfusion (secondary to the effect of hypoxia on cardiac function). This is potentially damaging to all organ systems, particularly the brain. Macrosomia and obstructed labour may further contribute to intrapartum hypoxia–ischaemia.
In the UK CEMACH enquiry, 10% of perinatal deaths were related to intrapartum causes. In addition, many babies affected by intrapartum hypoxia–ischaemia will be born alive but will require expert resuscitation. This is one of the reasons why delivery of babies of diabetic mothers must occur in units where advanced neonatal life support is available and, often, the baby will need ongoing intensive care. Total body cooling has become an established treatment for hypoxic–ischaemic encephalopathy, and commencement of this treatment at a specialist centre is time critical.
Relative cellular hypoxia, secondary to insulin-induced high glucose uptake and metabolic rate or a direct effect of insulin on erythroid progenitors, causes increased erythropoietin secretion and, in turn, increased fetal red cell production. The resulting neonatal polycythaemia may then cause excessive neonatal jaundice (as the red cell burden is lysed) and, occasionally, hyperviscosity syndrome. Renal vein thrombosis or thrombosis in other vessels is rare, but occurs more frequently in babies whose mothers have diabetes than in those of mothers who do not.
Clinicians caring for babies after diabetes in pregancy must be alert to the complications of polycythaemia and measure the haematocrit if there are abnormal clinical signs, such as irritability, lethargy and poor feeding. The effects of polycythaemia and hypoglycaemia may be additive in terms of reduction of glucose delivery to the brain. Polycythaemia associated with clinical signs, such as irritability or lethargy, must be treated with partial exchange transfusion, according to standard neonatal guidance.
Pre-term delivery
In the UK CEMACH cohort (2002–2003), the rate of pre-term delivery (<37 weeks gestation) for babies born to mothers with pregestational diabetes was 4.8 times greater than the rate in the general population (35.8% vs. 7.4%). The Netherlands cohort study has provided similar data.
As with other maternal conditions which affect pregnancy, there is always a balance between continuing a pregnancy until term and reducing the time that both fetus and mother are exposed to a harmful environment. If pre-term delivery is planned, this must be in a unit that can provide the appropriate level of specialist neonatal care, which may require transfer of the mother to another maternity unit, preferably within a perinatal network system as operates in the UK.
There have been concerns regarding potential worsening of maternal glycaemic control and resulting perinatal and maternal morbidity if steroid therapy is given to aid fetal lung maturity. In the UK cohort, for 5 of the 68 women where steroids were not given, the reason cited was “health professionals concerned about effect of steroids on maternal glycaemic control.” However, it is now accepted that maternal diabetes is not a contraindication to maternal steroid administration if pre-term delivery is anticipated. This has resulted in babies of diabetic mothers not experiencing significantly worse surfactant deficiency than other babies of equivalent gestation. In the UK cohort, 70% of women who delivered live babies between 24 and 34 weeks’ gestation received prophylactic antenatal steroids.
There is no evidence that the other complications of prematurity are more severe than for a baby born at a similar gestational age to a mother who does not have diabetes. Pre-term babies of diabetic mothers should be managed according to standard protocols; in particular, mothers should be encouraged to express and store breast milk. However, additional problems specific to the baby of a diabetic mother may be present and need appropriate management.
Effects of delivery by caesarean section
In the 2002–2003 UK cohort, the caesarean section rate for women who have diabetes was 42.7% and in the Netherlands study 44.3%, compared with the overall UK national rate of around 20%. Even in pregnancies complicated by gestational diabetes (rather than pre-existing diabetes), there is a significant excess in caesarean section rate.
Whilst the baby may be protected from hypoxic–ischaemic brain injury by avoiding labour and vaginal delivery, the potential adverse impacts on the baby of unnecessary caesarean section are twofold – delayed and disrupted breast feeding and respiratory morbidity (transient tachypnoea of the newborn or surfactant deficiency). Therefore, there must be careful consideration of the balance of benefit and risk to mother and baby when planning birth by caesarean section.
Macrosomia
Having macrosomia and being large for gestational age are not interchangeable terms. Macrosomia describes a baby who is heavier than its genetically determined birth weight, and has a clinical appearance of somatic growth (involving mainly fat and abdominal organs) in excess of head growth. It may be present in a baby of ‘normal’ birth weight. Macrosomia and organomegaly attributed to fetal hyperinsulinaemia are well-recognised characteristics of pregnancies complicated by diabetes.
Glucose crosses the placenta by facilitated diffusion; therefore, maternal hyperglycaemia imposes a carbohydrate surplus on the fetus. The fetus responds with increased secretion of insulin. Because insulin is an anabolic hormone, fetal hyperinsulinaemia stimulates protein, lipid and glycogen synthesis to cause macrosomia. Although this classic maternal hyperglycaemia–fetal hyperinsulinism theory of Pedersen is widely accepted, the metabolic and endocrine disturbances are much more complex. For example, free amino acids also have a stimulatory effect on the development of the β cell, and the anabolic actions of insulin. In utero at least, this could, in part, be mediated through the insulin-induced release of insulin-like growth factors. In addition, birth weight is positively correlated with maternal concentrations of triglycerides and free fatty acids.
Evidence is inconsistent regarding the potential contribution to these morbidities by diabetic control and duration of diabetes. The rate of macrosomia (defined as birth weight above 90th centile) was 52% in the most recent UK cohort.
Macrosomia increases the risk of complications during labour and delivery, such as shoulder dystocia, obstructed labour, perinatal hypoxia–ischaemia and birth injury (e.g., brachial plexus injury and fractured clavicle or humerus). Recent UK cohort data provide rates for some of these – shoulder dystocia 7.9% (over twice the rate in the general population), Erbs palsy 4.5/1000 births (10 times the rate in the general population) and fractures (usually of the clavicle and humerus) 7/1000 births.
Neonatal management of these complications is covered in standard neonatal texts, but long-term effects also must be considered (see below).
Hypertrophic cardiomyopathy
Hypertrophic cardiomyopathy, characterised by hypertrophied septal muscle, which obstructs the left-ventricular outflow tract, has been related to maternal diabetes control and to fetal and neonatal hyperinsulinaemia. It may be sufficiently severe to cause fetal or neonatal death. In less severe cases, the presentation is usually within the first weeks of postnatal life with cardiorespiratory distress and congestive heart failure. The majority of infants need supportive care only, as resolution of the signs can be expected in 2–4 weeks. The septal hypertrophy regresses within 2–12 months. Routine postnatal echocardiography is not required unless there are clinical signs.
Intrauterine growth restriction
Placental insufficiency may be a feature of pregnancy complicated by diabetes, resulting in a baby who is small for gestational age. This intrauterine growth restriction carries increased risks, especially if the baby is pre-term. The fetus is more vulnerable to hypoxia–ischaemia and, postnatally, is likely to have more severe and persistent hypoglycaemia (see below). Delivery must be planned at a unit that provides the appropriate level of specialist neonatal care.
Impaired postnatal metabolic adaptation
With the cessation of placental nutrition at birth, the healthy newborn baby undergoes metabolic adaptation to ensure energy provision to vital organs, and subsequently to sustain growth and further development. The key fuels are glucose and ketone bodies (the latter being the product of beta-oxidation of fatty acids). The infant of the diabetic mother is at risk of transient hyperinsulinism, which, in turn, causes a high rate of glucose uptake and conversion to fat, reduced hepatic glucose production and reduced lipolysis and, thus, reduced ketone-body production ( Table 4 ).
Hypoketonaemic hypoglycaemia, if it occurs, in turn results in reduced fuel availability for the brain and other vital organs. However, in practice today in the UK, very few babies develop clinically significant hypoglycaemia associated with clinical signs. Reasons for this are likely to include standards of maternal diabetic control during labour such that significant postnatal hyperinsulinism is avoided, the transient nature of hyperinsulinism, and early preventive management (as described below).
The ultimate concern is that of brain injury and long-term neurodevelopmental sequelae (see below). Whilst it is clear that untreated hypoglycaemia that is sufficiently severe and prolonged to cause clinical signs may cause brain injury, there is no evidence that brain injury occurs in the absence of clinical signs (‘asymptomatic hypoglycaemia’). The purpose of clinical monitoring (see below) is to detect hypoglycaemia at an early stage before it becomes clinically significant, and to institute appropriate management. Clinical signs suggestive of (but not specific to) hypoglycaemia are abnormal tone, abnormal level of consciousness, poor oral feeding and fits, which may be atypical, for example, presenting as apnoea.
There are no clinical studies of sufficient rigour to provide evidence for the circumstances in which neonatal hypoglycaemia may cause brain injury and, thus, it is not possible to provide evidence-based guidelines for the prevention and management of clinically significant neonatal hypoglycaemia following maternal diabetes. Therefore recommendations in this chapter, from referenced texts written by clinical experts and from the UK CEMACH survey and UK National Institute for Health and Clinical Excellence (NICE) guidelines, remain empirical, urging clinicians to individualise management for each baby, emphasising the importance of careful clinical evaluation.
Clinical monitoring
Unless the baby has clinical complications sufficiently severe to require admission to a neonatal unit, mother and baby should remain together. This may be on a postnatal ward, provided there is sufficient midwifery or nursing resource to allow regular clinical monitoring of mother and baby, as required. Some hospitals elect to look after these babies and mothers on transitional care units, where enhanced midwifery or nurse staffing is available.
Those caring for the baby must regularly monitor the baby for feeding behaviour and abnormal neurological signs, and must document their findings. Unless there are risk factors for other complications (e.g., infection) and as long as the baby appears well, it is not necessary to monitor vital signs (temperature, pulse and respiration rate) or to screen for other potential complications, for example, polycythaemia. If, at any stage, there are abnormal clinical signs, the blood glucose level must be measured and an urgent paediatric review arranged.
UK NICE guidance is that infants of diabetic mothers should have regular blood glucose monitoring ( Table 5 ).
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Blood glucose monitoring must be by an accurate, laboratory-based method. No near-patient testing device has been demonstrated to be sufficiently accurate to diagnose or exclude neonatal hypoglycaemia. Some neonatal units have an accurate and quality-assured analyser situated in the unit laboratory to allow rapid but accurate blood glucose monitoring. This is the recommended standard. However, recent data indicate that only approximately 25% babies have blood glucose monitoring using accurate methods.
Blood glucose monitoring should be commenced at around 3–4 h of age. To commence sooner than this is not informative as all babies experience a physiological transitional fall in blood glucose level in the first hours after birth, often to levels below 2 mmol/l. Therefore, in an otherwise healthy baby, a low blood glucose level in the first 3–4 h does not help to differentiate a baby who has significant hyperinsulinism from a baby who is not affected by hyperinsulinism.
Blood glucose monitoring should be pre-feed to detect a nadir in blood glucose level. In a baby with no clinical signs, a post-feed glucose level is not helpful and exposes the baby to excessive heel stabs.
If hyperinsulinism occurs, it will usually present in the first 1–2 days postnatally and will be transient, lasting a maximum of a few days. Therefore, if a baby is clinically stable and has shown no evidence of clinically significant hypoglycaemia, blood glucose monitoring may be discontinued when accurately measured blood glucose levels are persistently above 2.0 mmol/l, and, in these circumstances, discharge to community care from 24 h of age is appropriate, if all else is well.
Clearly, babies, who are pre-term or unwell and admitted to neonatal units, will undergo blood glucose monitoring as part of their clinical care.
Feeding
Breast feeding is the method of choice for all babies (barring rare exceptions such as maternal human immunodeficiency virus (HIV) infection). However, in the UK cohort, only 53% of mothers with diabetes intended to breast feed, and, at 28 days, only 27% of term babies were breast fed.
Mothers should be encouraged antenatally to consider breast feeding their baby and should receive sufficient information regarding the benefits to make their choice. Immediately after delivery, a healthy baby should be placed skin–skin with mother and an early breast feed offered, with assistance to ensure that the baby achieves an effective latch. Breast feeds should be offered every 3–4 h (or more frequently if the baby demands), again with support, if necessary.
Formula supplements to breast feeds are required only if there are clinical indications, including intervention for hypoglycaemia. Formula supplements often result in reduced frequency of and hunger for breast feeding, thus reducing breast milk supply and suppressing normal neonatal metabolic adaptation. Therefore, if formula supplementation is required, this must be of the volume required and no more. If a mother elects to formula feed, requirements are not usually in excess of 100 ml kg −1 day −1 , but volumes should be adjusted according to clinical monitoring.
If a mother and baby are separated, or if the baby requires formula supplements to breast feeding, the mother should be encouraged to express breast milk, which allows lactation to be sustained, and which provides breast milk which can be given to the baby.
Operational thresholds for management
There is no doubt that a low blood glucose level associated with clinical signs (listed above) must be treated. In the absence of abnormal clinical signs, recommendations for blood glucose thresholds at which to intervene must be pragmatic, and must balance the risks of developing clinically significant hypoglycaemia against the risks of disrupting breast feeding and separating mother and baby. Most recent UK guidance advises that, in the absence of clinical signs, two consecutive blood glucose levels below 2.0 mmol/l at least 3–4 h after delivery require intervention to aim to raise the blood glucose level.
Management of clinically significant hypoglycaemia
Management of a low blood glucose level associated with abnormal clinical signs (listed above) is a medical emergency necessitating full clinical evaluation and transfer to a neonatal unit for intravenous glucose. If the blood glucose level is low but there are no clinical signs, it is reasonable to assess the effect of increasing milk intake before proceeding, if necessary, to intravenous glucose. Intravenous glucose, if required, should be started at 5 mg kg −1 min −1 of glucose (equivalent to 3 ml kg –1 h −1 of 10% dextrose) but increased as indicated by frequent blood glucose monitoring. Intramuscular glucagon (200 mcg kg −1 ) is useful if there are clinical signs and a delay in achieving intravenous access, in that glycogen will be broken down to release glucose, but the effect will be transient lasting less than 1 h.
Hypocalcaemia and hypomagnesaemia
Transient neonatal hypocalcaemia has been reported as a finding following diabetes in pregnancy and both its incidence and severity appear to be related to the degree of maternal diabetes control. It is usually associated with hyperphosphataemia and occasionally with hypomagnesaemia. The aetiology is not entirely clear, but neonatal hypoparathyroidism has been demonstrated and may, in part, be secondary to maternal magnesium loss.
Published studies and clinical experience indicate that hypocalcaemia and hypomagnesaemia are rarely of clinical significance, unless the baby has other complications, e.g., perinatal hypoxia–ischaemia. Therefore, there is no indication to screen for them in the healthy baby. If associated with clinical signs, the deficits must be corrected, as recommended in standard neonatal textbooks.
Iatrogenic complications
It will be seen from the discussion above that the timing and method of delivery often impact upon neonatal morbidity. Occasionally, decisions are made on fetal grounds but more often are related to maternal complications. However, in a number of cases, there are no clear maternal or fetal reasons for pre-term delivery or delivery by caesarean section. Each places neonatal well-being at risk. In the UK study, 9% of caesarean sections were not explained by maternal or fetal compromise and 4% were “routine for diabetes” or “maternal request.” A number of these “routine” caesarean sections were at a pre-term gestation. In the same UK cohort, 19% of mothers had pre-term delivery that was not spontaneous or explained by maternal or fetal compromise, and thus could have been avoided. This would have prevented some 235 admissions to neonatal care over the study period.
Even if there are no significant maternal or fetal complications and the pregnancy goes to term or near-term, the evidence would suggest that the baby is still exposed to potential iatrogenic harm. The UK CEMACH enquiry demonstrated frequent failings in medical and midwifery care, which impacted upon the baby’s postnatal course and, in particular, establishment of feeding. These included:
- –
‘Routine’ admission of babies to neonatal units;
- –
‘Routine’ supplementation or replacement of breast feeds with formula;
- –
Delayed ‘skin to skin’ contact and first feed;
- –
Poor management of temperature control;
- –
And the testing of blood glucose with subsequent response to this too soon after delivery.
In addition to the harmful effects of these practices for mother and baby, they represent an avoidable use of neonatal unit resource ( Table 6 ).
