Summary
Alcohol (ethanol) is a recreational substance and is also used for a range of industrial, scientific, and medical applications. Alcohol is an established human teratogen. Due to a lack of data to facilitate the definition of a ‘safe’ level of drinking, UK government guidelines recommend complete abstinence from alcohol consumption during pregnancy. Topical application of alcohol would not be expected to result in systemic absorption and is not known to cause adverse fetal effects.
Alcohol consumed by the mother at any point in pregnancy has the potential to reach the fetus. Up to around week ten of gestation the pregnancy is maintained by yolk-sac nutrition, where maternally-ingested substances reach the embryo via diffusion. From around week ten to twelve, the placenta is functional and actively transports ingested substances to the fetal blood supply. Alcohol levels in the fetal compartment can reach levels higher than in the maternal bloodstream due to reduced fetal enzymatic activity and a slower elimination rate. Fetal exposure is also compounded by swallowing of excreted xenobiotics in amniotic fluid.
Fetal Alcohol Spectrum Disorders (FASD) encompass a continuum of adverse physical and neurodevelopmental outcomes that have been observed following prenatal alcohol exposure. At the most severe end of the spectrum sits Fetal Alcohol Syndrome (FAS), most often associated with chronic high (>5 units/day) alcohol consumption during pregnancy. Affected individuals exhibit pre- and postnatal growth retardation, characteristic facial features, and central nervous system abnormalities which can manifest as a range of neurobehavioural problems. Other diagnoses on the FASD spectrum encompass subgroups of these features and include partial fetal alcohol syndrome (pFAS), alcohol-related neurodevelopmental disorder (ARND) (up to 90% of FASDs), and alcohol-related birth defects (ARBD). The currently available data are not detailed enough to support a robust analysis of whether the likelihood and/or severity of these FASDs is linked to a particular drinking pattern.
Other factors which may affect interpersonal variation in the risk and severity of FASD include the duration and stage of pregnancy at exposure, maternal health and nutritional status, maternal body weight and size, co-exposure to medications, and the genetically determined alcohol detoxification capacity of both mother and fetus.
In addition to the features of FASD, gestational exposure to alcohol has been associated with miscarriage, stillbirth, and preterm delivery.
Occasional binge drinking is often reported to have occurred prior to recognition of a pregnancy. The limited available data relating to early pregnancy exposure to occasional binge drinking are not, overall, suggestive of harm. While healthcare professionals can offer some reassurance that this type of exposure is common, and that the currently available data do not confirm adverse effects, the limitations of the data (including low number of pregnancies and limited outcomes studied, as well as possible insensitivity of current neurodevelopmental tests for the detection of subtle effects) should also be discussed.
Following confirmed alcohol exposure in pregnancy, the need for enhanced antenatal surveillance will be determined by a clinical assessment of the magnitude of risk to the fetus. Postnatally, there are no definitive diagnostic tests for FASD. Where FASD is a possible diagnosis, differential diagnoses (such as an underlying genetic disorder) should also be considered, especially in cases where prenatal alcohol exposure is unconfirmed. Referral to a paediatrician or clinical geneticist is recommended.
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