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Imagine meeting a pregnant woman on long-term lithium who has just found out she is expecting. Stopping the drug risks a relapse of severe mood illness; continuing it carries a small but specific risk to the developing baby. Neither option is risk-free, and the job of the clinician is to weigh both risks explicitly rather than defaulting to either extreme.

Lithium is a mood stabiliser used mainly for bipolar affective disorder, an illness of recurring mood episodes swinging between mania and depression. Teratogenicity (the capacity of a drug to cause birth defects) describes the specific fetal risk that has to be weighed against the very real risk of stopping a mood stabiliser suddenly in pregnancy.

The trap is treating this as "stop the drug because it is dangerous." It isn't. Because abrupt lithium discontinuation carries its own well-documented risk of rapid relapse, particularly manic relapse, guidance does not recommend stopping lithium reflexively on discovery of pregnancy. The management principle to hold onto is informed, monitored continuation for most women, with a specific, low-absolute-risk cardiac anomaly screened for by ultrasound imaging rather than assumed.

First-trimester lithium exposure, exposure during the first twelve weeks of pregnancy when the fetal heart is forming, is linked to Ebstein's anomaly, a rare congenital malformation of the tricuspid valve (the valve between the right atrium and right ventricle of the heart) in which the valve sits abnormally low and often leaks. While the RELATIVE risk of Ebstein's anomaly is raised compared with the general population, the ABSOLUTE risk remains low: current estimates put it at roughly 1 in 1000 to 2000 exposed pregnancies, considerably lower than earlier decades of psychiatric teaching assumed. A drug can meaningfully raise the relative risk of a rare event while the actual chance of that event happening to any one pregnancy stays small.

Imagine a woman established on lithium with a therapeutic serum level who becomes pregnant. Rather than stopping, her team arranges fetal echocardiography (an ultrasound scan of the fetal heart, looking specifically for Ebstein's anomaly and other structural cardiac defects) around 16 to 20 weeks, uses the lowest effective dose, and advises avoiding dehydration, which raises serum lithium concentration by reducing the volume it is dissolved in. Lithium levels naturally fall across pregnancy as blood volume expands, then rise sharply again around delivery as that extra fluid is lost, so monitoring plans anticipate this shift, with levels checked more often than in a non-pregnant patient and adjustments planned around labour. Postnatally, lithium passes into breast milk, and the infant's immature renal clearance means it can accumulate to a much greater degree than in an adult; this does not make breastfeeding automatically unsafe, but it requires a discussion between the mother and her clinical team, with monitoring of the infant for signs of toxicity such as poor feeding, lethargy, or tremor if breastfeeding continues.

Lithium's teratogenic profile looks different when set against the other major mood stabilisers used in bipolar disorder. Sodium valproate is the most strongly teratogenic of the group, associated with major congenital malformations and later neurodevelopmental problems in the child, and is now subject to strict prescribing restrictions in women of childbearing potential. Lamotrigine, by contrast, carries a comparatively lower teratogenic risk profile and is often preferred where a mood stabiliser is still needed in pregnancy. Imagine a clinician who, out of unexamined caution about lithium's reputation, switches a stable patient onto valproate instead; this would actually INCREASE, not reduce, the risk to the fetus, since valproate's teratogenicity is worse-established than lithium's. Recognising this ordering, lithium sitting in the middle rather than at either extreme, is one of the most heavily tested facts in perinatal psychiatry.

Diagnosis here is imaging-based, not clinical guesswork: fetal echocardiography is the specific investigation used to look for Ebstein's anomaly after first-trimester lithium exposure, typically performed around 16 to 20 weeks of pregnancy. Ongoing diagnostic monitoring also means more frequent serum lithium level checks than in a non-pregnant patient, tracking the physiological fall in levels across pregnancy and the rise around delivery, alongside routine renal function and thyroid function monitoring that accompanies long-term lithium use in general.

NICE CG192, the guideline on antenatal and postnatal mental health, sets out the framework for these decisions: explicit discussion of relapse risk against teratogenic risk, specialist psychiatric and obstetric input, fetal echocardiography where first-trimester exposure has occurred, and close monitoring of serum lithium levels through pregnancy and around delivery, alongside the BNF's prescribing cautions in pregnancy. Treatment decisions rest on individualised risk-benefit discussion rather than a fixed rule, weighing maternal mental state, illness severity, and the practicalities of monitoring both mother and baby.

The examiner's favourite trap is a candidate who "plays it safe" by switching lithium to valproate in pregnancy. That's backwards: valproate is the WORSE teratogen of the two. If a stem describes first-trimester exposure, jump straight to Ebstein's anomaly and fetal echocardiography, not automatic discontinuation.

Lithium in pregnancy is managed by informed, monitored continuation, not automatic stopping: the specific fetal risk is Ebstein's anomaly (absolute risk still low, roughly 1 in 1000-2000), screened for with fetal echocardiography, under NICE CG192.