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Potential Fetal Complications

Fetal complications seem to be subtle or uncommon based on current research. They can result from hyperemesis gravidarum (HG) if the mother's symptoms are severe, inadequately treated, or there is a delay in medical interventions. Some problems may also be related to treatment (e.g. IV infection, medication-related defects), but seem to be more of the exception. Several sporadic complications or associated conditions have been identified in a few research studies, but these mostly focus on what is noted at birth. No long-term follow-up studies have been done to date on children born to hyperemetic women. Most complications seem to be related to the severity of maternal malnutrition, thus mothers who lose more than 10% of their body weight and fail to gain adequate weight before delivery, will have a greater risk of fetal complications. If women with HG are given early medical care sufficient to manage their symptoms and minimize nutritional deficiencies, both mother and child will likely be healthy now and in the future.

Fetal Programming

Research is now suggesting that prolonged stress, malnutrition and dehydration in the mother can potentially put an unborn child at risk for chronic disease (e.g. diabetes, heart disease) in later life. This has been termed "fetal programming" by researchers around the world, and is a relatively new field of study. Although research has not directly linked fetal programming to hyperemesis gravidarum, mothers with HG experience many of the conditions linked to these potential chronic health conditions and it is likely only a matter of time before a correlation is established.

Other Potential Fetal Complications:

Early delivery
Congenital heart disease
Integumentary (skin) abnormalities
Low birth weight
Shorter length
Undescended testicles
Hip dysplasia
Large for age infant
Neurodevelopmental sequelae
Neural tube defects
Central nervous system malformations
Skeletal malformations
Perinatal death
Testicular cancer
Behavioral/emotional problems

Offsite Research:

Prenatal maternal stress: effects on pregnancy and the (unborn) child.
Mulder EJ, Robles de Medina PG, Huizink AC, Van den Bergh BR, Buitelaar JK, Visser GH.
Department of Perinatology and Gynaecology, University Medical Centre, Utrecht, The Netherlands
Early Human Development 2002 Dec;70(1-2):3-14

Animal experiments have convincingly demonstrated that prenatal maternal stress affects pregnancy outcome and results in early programming of brain functions with permanent changes in neuroendocrine regulation and behaviour in offspring. Recent well-controlled human studies indicate that pregnant women with high stress and anxiety levels are at increased risk for spontaneous abortion and preterm labour and for having a malformed or growth-retarded baby (reduced head circumference in particular). Evidence of long-term functional disorders after prenatal exposure to stress is limited, but retrospective studies and two prospective studies support the possibility of such effects. A comprehensive model of putative interrelationships between maternal, placental, and fetal factors is presented. CONCLUSIONS: Apart from the well-known negative effects of biomedical risks, maternal psychological factors may significantly contribute to pregnancy complications and unfavourable development of the (unborn) child. These problems might be reduced by specific stress reduction in high anxious pregnant women, although much more research is needed.

Prenatal programming of postnatal endocrine responses by glucocorticoids.
Bertram CE, Hanson MA.
Centre for Fetal Origins of Adult Disease, Mailpoint 887, Princess Anne Hospital, Coxford Road, Southampton SO16 5YA, UK. (e-mail: c.bertram@soton.ac.uk)
Reproduction 2002 Oct;124(4):459-67

Epidemiological studies have led to the hypothesis that a major component of the risk of diseases such as hypertension, coronary heart disease and non-insulin-dependent diabetes (the 'metabolic syndrome') is established before birth. Although the underlying mechanisms of this 'programming' of disease have not yet been conclusively determined, a reduced fetal nutrient supply as a consequence of poor placental function or unbalanced maternal nutrition is strongly implicated. It has been proposed that one outcome of suboptimal nutrition is exposure of the fetus to excess glucocorticoids, which restrict fetal growth and programme permanent alterations in its cardiovascular, endocrine and metabolic systems. This review focuses on the effects of endogenous and exogenous glucocorticoid exposure in utero on postnatal hypothalamo-pituitary-adrenal (HPA) axis activity, both in humans and experimental animals. The physiological consequences and proposed underlying molecular and cellular mechanisms are discussed. Current data indicate that key targets for programming may include not only the HPA axis but also glucocorticoid receptor gene and 11beta-hydroxysteroid dehydrogenase type 2 (11betaHSD2) gene expression in a range of tissues.

Endocrine programming and fetal origins of adult disease.
David I.W. Phillips
Trends in Endocrinology and Metabolism 2002, 13:363

Nutrition in early life. How important is it?
Novak D.
Division of Pediatric Gastroenterology, Department of Pediatrics, Box 100296, University of Florida College of Medicine, Gainesville, FL 32610-0296, USA. (e-mail: novakda@peds.ufl.edu)
Clinics in Perinatology 2002 Jun;29(2):203-23

While few would argue the importance of nutrition during adult life, temporary excess or deficiency has typically been thought to be of little long-term consequence. Recent data, summarized above, suggests that this may not be the case during in utero life, when alterations in the quantity or quality of nutrients provided may have life-long consequences. Perhaps even more surprisingly, decisions made in the neonatal period, such as whether to breastfeed or bottle feed, may have impacts on later health that, while small individually, have huge public health implications.

Fetal nutrition and adult disease.
Godfrey KM, Barker DJ.
MRC Environmental Epidemiology Unit (University of Southampton), Southampton General Hospital, Southampton, United Kingdom. (e-mail: kmg@mrc.soton.ac.uk)
American Journal of Clinical Nutrition 2000 May;71(5 Suppl):1344S-52S

Impaired growth and development in utero seem to be widespread in the population, affecting many babies whose birth weights are within the normal range. Although the influences that impair fetal development and program adult cardiovascular disease remain to be defined, there are strong pointers to the importance of the fetal adaptations invoked when the maternoplacental nutrient supply fails to match the fetal nutrient demand.

In utero programming of chronic disease.
Barker DJ.
MRC Environmental Epidemiology Unit, University of Southampton, Southampton General Hospital, Southampton, SO16 6YD, U.K.
Clinical Science (Lond) 1998 Aug;95(2):115-28

1. Many human fetuses have to adapt to a limited supply of nutrients. In doing so they permanently change their structure and metabolism. 2. These 'programmed' changes may be the origins of a number of diseases in later life, including coronary heart disease and the related disorders stroke, diabetes and hypertension. 3. This review examines the evidence linking these diseases to fetal undernutrition and provides an overview of previous studies in this area.

Fetal undernutrition and disease in later life.
Barker DJ, Clark PM.
MRC Environmental Epidemiology Unit, University of Southampton, Southampton General Hospital, UK.
Reviews of Reproduction 1997 May;2(2):105-12

Recent findings suggest that coronary heart disease and stroke, and the associated conditions, hypertension and non-insulin dependent diabetes, originate through impaired growth and development during fetal life and infancy. These diseases may be consequences of 'programming', whereby a stimulus or insult at a critical, sensitive period of early life results in long-term changes in physiology or metabolism. Animal studies provide many examples of programming, which occurs because the systems and organs of the body mature during periods of rapid growth in fetal life and infancy. There are critical windows of time during which maturation must be achieved; and failure of maturation is largely irrecoverable.

Nutrition and the early origins of adult disease.
Newnham JP, Moss TJ, Nitsos I, Sloboda DM, Challis JR.
School of Women's and Infants' Health, University of Western Australia, King Edward Memorial Hospital for Women, Subiaco, Perth, Western Australia Institute of Human Development, Child and Youth Health, University of Toronto, Toronto, Ontario, Canada.
Asia Pacific Journal of Clinical Nutrition 2002 Dec;11 Suppl 3:S537-S542

There is now overwhelming evidence that much of our predisposition to adult illness is determined by the time of birth. These diseases appear to result from interactions between our genes, our intrauterine environment and our postnatal lifestyle. Those at greatest risk are individuals in communities making a rapid transition from lives of 'thrift' to a lives of 'plenty'. From a global perspective, such origins of diabetes, coronary heart disease and stroke, should render research in these fields as one of the highest priorities in human health care. Prevention will be enhanced by elucidation of the mechanisms by which the fetus is programmed by the mother for the life she expects it to live. At the present time, there is evidence that fetal nutrition and premature exposure to cortisol are effective intrauterine triggers, but a multitude of alternative pathways require investigation. It is also likely that programming extends across generations, and may involve the embryo and perhaps the oocyte. An oocyte that becomes an adult human develops in the uterus of its grandmother, so further research is required to describe the role of environments of grandmothers and mothers in predisposing offspring to health or illness in adult life.

Updated on: Sep. 15, 2022