Explain the effects of smoking, alcohol, medications, and drugs of abuse on pregnancy; and advise on cessation

Clinical overview

Substance use is one of the most under-asked, under-documented and clinically consequential exposures in South African antenatal care. Tobacco, alcohol, prescribed and over-the-counter medication, and illicit drugs each alter the maternal-placental-fetal unit through distinct mechanisms, yet they cluster together — the woman who smokes is more likely to drink, the woman who uses methamphetamine ("tik") is more likely to use tobacco and cannabis — and they cluster with poverty, intimate-partner violence, untreated mental illness and HIV. South Africa carries one of the highest documented prevalences of fetal alcohol spectrum disorder (FASD) in the world, with community studies from the Western Cape winelands reporting rates an order of magnitude above global estimates. The Saving Mothers reports (NCCEMD) remind us that substance use rarely appears as a direct cause of maternal death but sits behind many — through late booking, non-attendance, trauma, and the medical complications it accelerates.

Your task as a registrar is not to moralise but to explain the effects accurately to the woman and the team, and to advise on cessation with the specific, evidence-based, non-judgemental approach that actually changes behaviour. Detection requires you to ask everyone, every booking, in a way that invites honesty. The single most powerful obstetric intervention here is helping a woman stop smoking; the single most preventable cause of lifelong neurodevelopmental disability is prenatal alcohol exposure. Both are missed when we do not ask. This chapter sits alongside antenatal-booking, high-risk-pregnancy-risks and gbv-mental-health-pregnancy.

Core knowledge

Tobacco / smoking

Cigarette smoke delivers nicotine (a potent vasoconstrictor and addictive stimulant) and carbon monoxide (which binds haemoglobin as carboxyhaemoglobin, shifting the oxygen dissociation curve left and reducing fetal oxygen delivery), among thousands of other toxins. The dominant obstetric mechanism is chronic uteroplacental hypoperfusion and relative fetal hypoxia, compounded by direct toxic effects on trophoblast invasion.

Consequences, dose-dependent across all of these (standard teaching, with effect sizes broadly consistent across NICE NG201 and SA guidance):

Fetal growth restriction and reduced birthweight — the most reproducible effect; see intrauterine-growth-restriction.
Preterm birth and preterm prelabour rupture of membranes (preterm-birth-and-pprom).
Placental abruption and placenta praevia — smoking is a classic modifiable risk factor for both (antepartum-haemorrhage).
Miscarriage, ectopic pregnancy (tubal ciliary toxicity) and stillbirth.
Sudden infant death syndrome (SIDS) postnatally, increased by both antenatal and environmental (passive) smoke.
A paradoxical, non-protective small reduction in pre-eclampsia incidence is described but must never be presented as a benefit — outcomes are uniformly worse.

Quitting at any gestation helps; quitting before or early in pregnancy largely normalises birthweight. The benefit is immediate and continuous, which is the message to give.

Alcohol

Ethanol and its metabolite acetaldehyde are direct teratogens and neurotoxins that cross the placenta freely, reaching fetal concentrations approximating maternal levels; the fetus clears them slowly. Alcohol disrupts neuronal proliferation and migration, causes oxidative stress and apoptosis in developing neural tissue, and interferes with cell adhesion — producing the midline craniofacial dysmorphology and diffuse central-nervous-system injury that define the spectrum.

Fetal alcohol spectrum disorder (FASD) is the umbrella term; fetal alcohol syndrome (FAS) is the most severe, classically defined by three features (standard diagnostic teaching): the characteristic facies (short palpebral fissures, smooth philtrum, thin vermilion upper lip), pre- and/or postnatal growth restriction, and CNS/neurodevelopmental abnormality, in the context of confirmed or probable prenatal alcohol exposure. The neurodevelopmental harm — intellectual disability, executive-function deficits, behavioural and attentional disorders — is the lifelong burden and is the most common preventable cause of intellectual disability.

Critically, no safe threshold and no safe trimester have been established. Binge drinking is especially harmful, but harm is documented at lower exposures and the first trimester (organogenesis and early brain development) is high-risk while the third trimester (rapid brain growth) is also vulnerable. The honest advice is therefore complete abstinence throughout pregnancy and when trying to conceive. South African prevalence makes this a national priority.

Medications

Prescribed and over-the-counter medicines must be judged on a benefit–risk balance, never reflexively stopped, because abrupt withdrawal of treatment for epilepsy, hypertension, psychiatric illness or thromboprophylaxis can be more dangerous than the drug. Teratogenic risk is highest during organogenesis (roughly the first trimester); later exposures cause growth, functional and neonatal-adaptation effects. Key worked examples (mechanisms are standard teaching; cite specific drug doses only from guidelines):

Sodium valproate — high neural-tube-defect and neurodevelopmental risk; avoid in women of childbearing potential where possible. Epilepsy management in pregnancy follows RCOG GTG 68; counselling, folate and specialist co-management are essential. See medical-complications-in-pregnancy.
ACE inhibitors / ARBs — fetopathy (renal dysgenesis, oligohydramnios, skull hypoplasia), especially second/third trimester; switch antihypertensives per hypertension-in-pregnancy (NICE NG133 favours labetalol, nifedipine, methyldopa).
Warfarin — embryopathy in the first trimester and fetal bleeding risk later; relevant to mechanical valves and VTE.
Retinoids (isotretinoin) — among the most potent human teratogens; strict pregnancy-prevention required.
NSAIDs — premature ductus arteriosus constriction and oligohydramnios when used in late pregnancy.
SSRIs — generally continued where indicated; small risks of neonatal adaptation syndrome and (debated) persistent pulmonary hypertension must be weighed against the substantial harm of untreated antenatal depression (gbv-mental-health-pregnancy).

The practical rule: check every drug against a reputable teratogen resource, optimise to the lowest effective dose of the safest agent, and never stop essential treatment without a plan. Beware traditional and complementary medicines, which are common in SA and include uterotonic herbal preparations (e.g. those historically associated with uterine hyperstimulation) that women may not volunteer as "medication."

Drugs of abuse

Cannabis (dagga) — the most commonly used illicit drug in SA pregnancy. Associated with low birthweight and possible neurodevelopmental effects; advise cessation, and note that it is frequently co-smoked with tobacco.
Methamphetamine ("tik") and cocaine — sympathomimetic vasoconstrictors causing placental abruption, growth restriction, preterm birth and stillbirth; cocaine is specifically associated with abruption and maternal hypertensive/cardiac events.
Opioids (heroin, codeine, tramadol, prescribed opioids) — fetal growth effects, and crucially neonatal abstinence syndrome (NAS) after delivery. Abrupt maternal opioid withdrawal can precipitate fetal distress and demise, so unsupervised "cold turkey" is discouraged in favour of stabilisation.
Benzodiazepines — sedation, floppy-infant syndrome and neonatal withdrawal.

Polydrug use is the norm rather than the exception, and injecting use raises HIV, hepatitis B/C and sepsis risk — integrate with hiv-in-pregnancy.

Figure I7.1 — Exposure map linking tobacco, alcohol, medicines and drugs of abuse to placental, fetal and neonatal harms.

Assessment

Ask everyone, well

Universal, routine enquiry at antenatal-booking and revisited each trimester is the standard — selective screening based on appearance misses most users and entrenches bias. Use a normalising, structured opening ("Many women use some tobacco, alcohol or other substances; it helps me look after you and the baby to know what you use") and quantify: type, amount, frequency, route, last use, and previous quit attempts.

Alcohol — a validated brief screen such as AUDIT-C (standard tool) quantifies risk; ask about binge episodes specifically and about use before pregnancy was recognised.
Smoking — record cigarettes/day and exposure to household smoke; where available, an exhaled carbon monoxide (CO) monitor objectively identifies smokers and passive exposure and is a motivational tool (recommended in NICE NG201).
Drugs — non-judgemental enquiry into illicit, prescribed and traditional medicines; document injecting use.

Examination and investigation

Track symphysis-fundal height and arrange serial growth ultrasound with umbilical artery Doppler where exposure suggests FGR (intrauterine-growth-restriction, gestational-age-assessment).
Examine for signs of intoxication, withdrawal, injection sites, and the stigmata of chronic alcohol use.
Offer and repeat HIV testing (TLD-based ART per SA guidelines) and screen for hepatitis B, syphilis and other STIs in injecting/high-risk women.
Screen for the near-universal co-travellers: depression, anxiety and intimate-partner violence (gbv-mental-health-pregnancy).
Urine toxicology may inform care but is not a substitute for honest history and must be done with consent and clear purpose, not as covert surveillance.

A multidisciplinary, continuity-of-care model — linking the antenatal clinic with social work, mental-health and addiction services — is what the evidence supports for the highest-risk women.

Figure I7.2 — Universal assessment workflow for asking, quantifying exposure, screening co-travellers and using toxicology ethically.

Management

The objective's verb is to advise on cessation, so management is overwhelmingly about counselling, behavioural support, and safe pharmacological help — delivered without judgement, because shame drives disengagement and late booking.

The cessation conversation (apply to every substance)

Use a brief-intervention structure such as the 5 A's (standard teaching): Ask (universal enquiry), Advise (clear, personalised, non-judgemental advice to stop), Assess readiness, Assist (set a plan, refer, prescribe where appropriate), and Arrange follow-up. Frame benefits positively and immediately ("stopping smoking today improves your baby's oxygen this week"), reinforce at every visit, and document. Motivational interviewing — exploring the woman's own reasons and ambivalence rather than lecturing — outperforms instruction.

Figure I7.3 — Cessation ladder showing brief intervention, safe referral and the key "never abruptly stop" pitfalls.