Hormone-associated venous thromboembolism in women: an evidence-based review

Introduction

Venous thromboembolism in a young woman is, more often than not, a hormonal event. The combined oral contraceptive, pregnancy, the puerperium and, later in life, menopausal hormone therapy account for most first events in women who are otherwise well, and each is a choice or a state that can be anticipated. That gives clinicians two opportunities most thrombosis does not: to choose a lower-risk preparation before the event, and to use the hormonal context to judge how long to anticoagulate after it.

This review brings together the evidence on the size of the risk for each hormonal exposure, the interaction with thrombophilia and other risk factors, venous thromboembolism in pregnancy and after delivery, and the management questions that follow a hormone-associated event: duration of anticoagulation, contraception, hormone therapy and menstrual bleeding during treatment. The strength of evidence is stated with each claim. Most of the risk data are observational, and relative risks from case–control studies should be read alongside the absolute rates from cohorts.

The background risk

In the Olmsted County population, the age- and sex-adjusted incidence of venous thromboembolism was 117 per 100 000 per year, lower in women than men overall (110 vs 130).¹² About a quarter of community cases have no identified cause.¹³ In women of reproductive age the background rate is much lower. Danish national cohorts put it at 2·1–3·0 per 10 000 woman-years in women not using hormonal contraception,^1,4 and two cohorts in a network meta-analysis gave 1·9 and 3·7 per 10 000.³ This is the denominator that every relative risk below multiplies. A three-fold relative risk on a baseline of 3 per 10 000 is 6 extra events per 10 000 women a year.

Combined hormonal contraception

Overall risk and duration

In the Danish national cohort (10·4 million woman-years), current users of combined oral contraceptives had 6·29 events per 10 000 woman-years against 3·01 in non-users. The rate ratio fell with duration of use, from 4·17 (95% CI 3·73–4·66) in the first year to 2·76 (2·53–3·02) after 4 years.¹ Estimates of the overall relative risk vary with design: 5·0 (4·2–5·8) in the Dutch MEGA case–control study,¹⁴ 2·97 (2·78–3·17) in two UK nested case–control studies,² and 3·5 (2·9–4·3) in a network meta-analysis of 26 studies.^3,15

The progestogen

For the same oestrogen dose, risk depends on the progestogen (Table 1). Four independent sources agree on the order. Levonorgestrel, norethisterone and norgestimate carry the lowest risk; desogestrel, gestodene, drospirenone and cyproterone acetate carry 50–80% more.³ In absolute terms, the UK data give 6 extra cases per 10 000 women a year with levonorgestrel or norgestimate against 14 with desogestrel or cyproterone.² The Cochrane review drew the practical conclusion that a pill with 30 µg ethinylestradiol and levonorgestrel is the preferred combined pill.¹⁵ Risk also rises with ethinylestradiol dose.^3,14

Estradiol-based pills and non-oral routes

Pills containing estradiol rather than ethinylestradiol may carry less risk. In a pooled analysis of two post-authorisation cohorts, estradiol valerate with dienogest had a lower risk than ethinylestradiol with levonorgestrel (HR 0·46, 0·22–0·98).¹⁶ These were industry-sponsored observational studies, and the result needs replication. We found no published venous thromboembolism data for estetrol-containing pills.

Non-oral combined methods do not avoid the risk. In Danish registry data, the transdermal patch carried a rate ratio of 7·9 (3·5–17·7) and the vaginal ring 6·5 (4·7–8·9) against non-users, higher than a levonorgestrel pill (adjusted RR 2·3 and 1·9 respectively).⁴ The route that protects in menopause (see below) does not protect here, because these methods deliver ethinylestradiol.

Progestogen-only contraception

Progestogen-only methods, apart from injectables, do not measurably raise risk. A meta-analysis of eight observational studies found an overall relative risk of 1·03 (0·76–1·39) for progestogen-only contraception, 0·90 (0·57–1·45) for the pill and 0·61 (0·24–1·53) for the levonorgestrel intrauterine system, but 2·67 (1·29–5·53) for injectable progestogen.⁵ Danish data gave a rate ratio of 0·6 (0·4–0·8) for the levonorgestrel intrauterine system and 1·4 (0·6–3·4) for the subdermal implant,⁴ and MEGA found an odds ratio of 3·6 (1·8–7·1) for depot medroxyprogesterone acetate.¹⁷ A systematic review for the US Centers for Disease Control and Prevention reached the same conclusions, and noted that progestogens used at the higher doses given for gynaecological conditions, rather than for contraception, may raise risk.¹⁸

Thrombophilia and other modifiers

Inherited thrombophilia

In 1994, a Dutch case–control study showed that oral contraceptive use (RR 3·8) and factor V Leiden (RR 7·9) multiplied rather than added: carriers taking the pill had a relative risk of 34·7 (7·8–154).¹⁹ A 2016 meta-analysis found relative risks of 5·89 (4·21–8·23) for mild thrombophilia (heterozygous factor V Leiden or prothrombin G20210A) and 7·15 (2·93–17·45) for severe thrombophilia (antithrombin, protein C or protein S deficiency, or combined defects) in pill users, against non-thrombophilic non-users. In family cohorts, the absolute risk in pill users was 4·3–4·6 per 100 pill-years with severe thrombophilia and 0·49–2·0 with mild. The authors advised against combined pills in severe thrombophilia but not necessarily in mild thrombophilia when alternatives are poorly tolerated.²⁰ These absolute rates come from relatives of affected probands and will overestimate risk in women found to carry a variant by chance.

Screening every woman before prescribing is not justified. In the UK TREATS health technology assessment, universal thrombophilia screening before combined oral contraception was the least cost-effective of all the strategies modelled, at £202 402 per event prevented; screening restricted to women with a personal or family history was more cost-effective in every group.²¹ A careful family history is the practical screen.

Obesity and polycystic ovary syndrome

Obesity doubles the risk of venous thrombosis (RR 2·0, 1·5–3·4), and in women with a body-mass index over 25 kg/m² who take oral contraceptives the risk rose about ten-fold.²² Women with polycystic ovary syndrome had a higher risk than other users of combined pills (RR 2·14, 1·41–3·24; 23·7 vs 10·9 per 10 000 person-years) and a higher risk even without the pill (RR 1·55, 1·10–2·19).²³ This matters because the pills most often prescribed for the syndrome contain cyproterone acetate or drospirenone (Table 1). We found no verifiable quantitative estimate of the interaction between smoking and oral contraceptives for venous thrombosis, as distinct from arterial disease, and do not give one.

Menopausal hormone therapy

The randomised evidence

In the Women's Health Initiative, conjugated equine oestrogen with medroxyprogesterone acetate roughly doubled venous thromboembolism (HR 2·06, 1·57–2·70; 3·5 vs 1·7 per 1000 person-years).^24,25 Risk was greatest in older and heavier women: against placebo users aged 50–59 years, the hazard ratio was 7·46 in treated women aged 70–79 years, and 5·61 in obese treated women; factor V Leiden carriers on treatment had a hazard ratio of 6·69.²⁴ Oestrogen alone, in women without a uterus, gave a smaller increase (HR 1·32, 0·99–1·75), significantly less than oestrogen with progestogen.²⁶

Route, oestrogen and progestogen

Route of administration is the single most important choice (Table 2). In the French ESTHER case–control study, oral oestrogen gave an odds ratio of 4·2 (1·5–11·6) and transdermal oestrogen 0·9 (0·4–2·1).²⁷ A meta-analysis confirmed this: oral oestrogen 2·5 (1·9–3·4), highest in the first year of use (4·0), and transdermal 1·2 (0·9–1·7). Transdermal oestrogen did not seem to add risk even in women with thrombogenic mutations or obesity.²⁸ In the largest study, with 80 396 cases, oral therapy gave an odds ratio of 1·58 (1·52–1·64) and transdermal therapy 0·93 (0·87–1·01), consistent across regimens.⁶ The usual explanation is that oral oestrogen passes through the liver first and raises hepatic synthesis of coagulation proteins; this is a mechanistic account and has not been tested directly in these studies.

The type of oestrogen and progestogen also matters. Oral estradiol carried less risk than conjugated equine oestrogen,⁶ as did esterified oestrogens in an earlier US study,²⁹ and the combination of conjugated equine oestrogen with medroxyprogesterone acetate, the regimen tested in the Women's Health Initiative, had the highest risk of all (OR 2·10, 1·92–2·31); estradiol with dydrogesterone had the lowest among oral combinations (1·18, 0·98–1·42).⁶ Micronised progesterone did not raise risk in ESTHER, whereas norpregnane derivatives did (OR 3·9, 1·5–10·0).²⁷ Tibolone did not change venous thromboembolism in a randomised trial in older women, although it raised stroke.³⁰

Tamoxifen, raloxifene and aromatase inhibitors

Selective oestrogen-receptor modulators raise risk. In the tamoxifen prevention trial, pulmonary embolism and deep vein thrombosis were more frequent with tamoxifen, mainly in women aged 50 years or older.³¹ In the RUTH trial, raloxifene raised venous thromboembolism (HR 1·44, 1·06–1·95; 1·2 extra events per 1000 woman-years).³² In adjuvant breast cancer treatment, anastrozole caused significantly fewer venous thromboembolic events than tamoxifen.³³ For a woman who has had venous thromboembolism, an aromatase inhibitor is therefore the lower-risk endocrine option where the oncological indication allows.

Pregnancy and the postpartum period

Size and timing of the risk

Pregnancy raises risk about four- to five-fold overall, but the risk is concentrated after delivery (Table 3). In Olmsted County the standardised incidence ratio was 4·29 (3·49–5·22), and the annual incidence after delivery was five times that during pregnancy (511·2 vs 95·8 per 100 000).³⁴ In MEGA, risk was raised five-fold during pregnancy, highest in the third trimester (OR 8·8), and 84-fold in the first 6 weeks after delivery.⁷ UK primary-care data found little increase in the first two trimesters, a six-fold increase in the third, and a 22-fold increase in the first 6 weeks after delivery, peaking in the first 3 weeks.³⁵ The sharpest peak is around delivery itself: in Swedish national data, the relative risk of venous thrombosis from 2 days before to 1 day after delivery was 115.³⁶ Risk does not end at 6 weeks. In 1·7 million Californian deliveries, the odds of a thrombotic event were 10·8 in the first 6 weeks and 2·2 (1·5–3·1) from 7 to 12 weeks, with no increase after that; the outcome combined stroke, myocardial infarction and venous thromboembolism, of which venous events made up most.⁸

Thrombophilia amplifies pregnancy risk as it does the pill's: in MEGA, pregnant or postpartum carriers of factor V Leiden had a 52-fold and carriers of prothrombin G20210A a 31-fold increase.⁷ Among obstetric factors, stillbirth was the strongest postpartum risk factor in UK data (IRR 6·2), followed by medical comorbidity, obesity, obstetric haemorrhage, preterm delivery and caesarean section.³⁸ Danish national data added pre-eclampsia (IRR 5·0), multiple pregnancy, hyperemesis, hospital admission and infection.³⁹ A UK prediction model for postpartum risk performed about as well as the Royal College of Obstetricians and Gynaecologists algorithm, with modest discrimination (C-statistic 0·67).⁴⁰

Assisted reproduction raises risk mainly in the first trimester. After in vitro fertilisation, venous thromboembolism occurred in 4·2 per 1000 pregnancies against 2·5 per 1000 after natural conception, and first-trimester pulmonary embolism was seven times more frequent.³⁷ Ovarian hyperstimulation syndrome, which complicated 6–7% of successful cycles, carried a roughly 100-fold increase in first-trimester risk.⁴¹

Diagnosis in pregnancy

Two prospective management studies have validated strategies that let some pregnant women avoid CT pulmonary angiography. In the Artemis study (498 women), a pregnancy-adapted YEARS algorithm avoided CT in 39% of women, 65% of those presenting in the first trimester and 32% in the third, and only one of those left untreated developed venous thromboembolism at 3 months.⁴² In the CT-PE-Pregnancy study (395 women), a strategy of clinical probability, D-dimer, compression ultrasound and CT gave a 3-month event rate of 0·0% (0·0–1·0) among untreated women.⁴³ The pregnancy-adapted Geneva score derived from that cohort discriminated better than the original score (area under the curve 0·795 vs 0·684) but has not yet been prospectively validated.⁴⁴ For suspected deep vein thrombosis, the LEFt rule (left leg, calf circumference difference ≥2 cm, first trimester) identified a low-probability group but was a derivation study that its authors said needed validation.⁴⁵

Not everyone agrees. The UK DiPEP study concluded that clinical features, decision rules and biomarkers do not accurately or cost-effectively select pregnant or postpartum women for imaging, and found D-dimer to have a specificity of only 8·8% at the standard threshold.⁴⁶ The two positions differ partly because DiPEP was a case–control diagnostic-accuracy study, whereas Artemis and CT-PE-Pregnancy tested whole strategies prospectively against clinical outcomes. On fetal safety, no case of neonatal hypothyroidism occurred among 151 newborns exposed to CT pulmonary angiography in utero.⁴⁷

Treatment in pregnancy

The American Society of Hematology (ASH) 2018 guideline makes a strong recommendation for low-molecular-weight heparin over unfractionated heparin for acute venous thromboembolism in pregnancy. It makes conditional recommendations that either once-daily or twice-daily dosing is acceptable, that low-risk patients can start treatment as outpatients, and against routine anti-factor Xa monitoring to guide dosing.⁴⁸ The earlier American College of Chest Physicians guideline suggested continuing anticoagulation for at least 6 weeks after delivery and for a minimum of 3 months in total (grade 2C).⁴⁹ That convention remains standard. By convention, oral anticoagulants are not used during pregnancy, low-molecular-weight heparin and warfarin are the usual choices while breastfeeding, and we found no published human data on direct oral anticoagulants in breast milk.

Prophylaxis

The ASH guideline makes a strong recommendation, on low-certainty evidence, for antepartum prophylaxis in women with a previous unprovoked or hormone-associated venous thromboembolism, and a conditional recommendation against it when the previous event was provoked by a transient non-hormonal factor that has resolved.⁴⁸ The distinction matters for this review: a previous hormone-associated event counts as a reason for antepartum prophylaxis because pregnancy reproduces the hormonal trigger.

The dose was settled by the Highlow trial. In 1110 pregnant women with previous venous thromboembolism, weight-adjusted intermediate-dose low-molecular-weight heparin did not reduce recurrence compared with fixed low-dose prophylaxis (2% vs 3%; RR 0·69, 0·32–1·47), with similar major bleeding (4% in each group). The investigators concluded that low-dose prophylaxis is the appropriate dose.⁵⁰ For other indications the evidence is weak. A Cochrane review of 29 trials rated all evidence on prophylaxis in pregnancy and after delivery as very low certainty,⁵¹ and a UK value-of-information analysis found the largest uncertainty in high-risk antepartum women and obese postpartum women.⁵² A pilot trial of low-dose aspirin after delivery showed that a large trial is feasible; it was not designed to show efficacy.⁵³

After a hormone-associated event

Recurrence and duration of anticoagulation

Recurrence is lower after a hormone-associated event than after an unprovoked one. In an individual-patient meta-analysis of 2554 patients, women had lower recurrence than men (5·3% vs 9·5% at 1 year), and women whose event was associated with hormone use and no other risk factor had half the recurrence of women with an unprovoked event (HR 0·5, 0·3–0·8).⁵⁴ A meta-analysis of 14 studies of women whose event was associated with oestrogen-containing contraception gave a pooled recurrence of 1·57 per 100 patient-years after stopping anticoagulation (1·10–2·23), which the authors judged low enough to favour short-term treatment.⁵⁵ A smaller French cohort found no significant difference between women who had and had not been using the pill (17·9 vs 17·6 per 1000 per year),⁵⁶ so the reduction is not certain for every woman.

For women with an unprovoked event, recurrence rules help decide who can stop. In the REVERSE II management study, women with none or one HERDOO2 criterion (post-thrombotic signs, D-dimer ≥250 µg/L on anticoagulation, body-mass index ≥30 kg/m², age ≥65 years) who stopped treatment had a recurrence of 3·0% per patient-year (1·8–4·8).^57,58 The DASH score counts an event not associated with hormones as a risk factor for recurrence.⁵⁹ Taken together, 3 months of anticoagulation is reasonable for a first event clearly associated with hormonal therapy once the hormone has stopped. This is a judgement from observational data; no trial has randomised duration in this group.

Hormones while anticoagulated

Women need reliable contraception while taking anticoagulants, because vitamin K antagonists can harm the fetus.⁹ In 1888 women under 60 years treated in the EINSTEIN trials, recurrence was 3·7% per year on hormonal therapy and 4·7% off it (adjusted HR 0·56, 0·23–1·39), with no difference between oestrogen-containing and progestogen-only therapy. The authors noted that World Health Organization guidance classes oestrogen-containing contraception during established anticoagulation as an unacceptable risk, despite the absence of data at the time.⁹ The 2024 US Medical Eligibility Criteria revised their recommendations for women with deep vein thrombosis or pulmonary embolism with or without anticoagulant therapy;⁶⁰ we could not verify the category assigned to each method from the indexed record. Panel 1 sets out a practical approach.

Heavy menstrual bleeding on anticoagulants

Abnormal uterine bleeding is the commonest bleeding complication in anticoagulated women of reproductive age. In the EINSTEIN analysis it was more frequent with rivaroxaban than with enoxaparin and warfarin (HR 2·13, 1·57–2·89), and hormonal therapy did not change it (HR 1·02).⁹ In a Polish prospective cohort, 41% of women on rivaroxaban reported heavy menstrual bleeding against 18% on warfarin, more needed interventions, and heavy menstrual bleeding on rivaroxaban predisposed to recurrent venous thromboembolism (OR 5·3, 1·1–33·3), probably because women interrupted their anticoagulant for 2–3 days during menstruation.⁶¹ The MEDEA trial is testing a switch to dabigatran or the addition of tranexamic acid against no change in women with heavy menstrual bleeding on factor Xa inhibitors; we found no published results.⁶² Management options include tranexamic acid, a hormonal intrauterine system, hormonal suppression while anticoagulated, or a change of anticoagulant.⁶³ Women should be asked about menstrual bleeding and told not to stop their anticoagulant on their own during menstruation.

Hormone-associated cerebral venous thrombosis: management and long-term sequelae

Cerebral venous thrombosis is the form of hormone-associated thrombosis with the most lasting consequences, and it is covered in full in our separate review. This section deals with what is specific to women whose thrombosis followed hormonal exposure, and with what happens after the acute phase.

Oral contraceptives are the dominant risk factor in young women. Case–control studies give odds ratios of 13 (5–37)⁶⁴ and 22·1 (5·9–84·2),⁶⁵ and a meta-analysis a pooled 7·59 (3·82–15·09).⁶⁶ The risk multiplies with thrombophilia (odds ratio 149 with prothrombin G20210A)⁶⁵ and with obesity (adjusted odds ratio 29·3 in obese women taking the pill, with no association in non-users).⁶⁷ In the International Study on Cerebral Vein and Dural Sinus Thrombosis (ISCVT), 65% of women had a sex-specific risk factor (oral contraceptives, pregnancy, the puerperium or hormone replacement), and these women did better. Complete recovery was 81% in women against 71% in men, the difference was confined to women with a sex-specific factor, and the absence of such a factor predicted poor outcome (odds ratio 3·7, 1·9–7·4).⁶⁸ In a recent cohort of 1525 adults, the absence of a female-specific risk factor also predicted death after the acute phase.⁶⁹ A hormonal cause is therefore, on average, a favourable prognostic sign. It is not a reason to expect full recovery, as the sections below show.

Acute management

Acute treatment does not differ by cause. Parenteral anticoagulation, preferably low-molecular-weight heparin, is given even when there is haemorrhage from venous congestion; decompressive surgery is used for impending herniation; and corticosteroids are not given.^70,71 After the acute phase, dabigatran was as safe and effective as warfarin in a randomised trial,⁷² and direct oral anticoagulants were associated with less major bleeding in a large cohort.⁷³ Three points are specific to the hormonal setting. Oestrogen-containing contraception should be stopped at diagnosis, and the European Stroke Organisation (ESO) guideline suggests avoiding it afterwards.⁷⁰ Thrombocytopenia at presentation should prompt consideration of vaccine-induced or heparin-induced thrombocytopenia before heparin is given (see the separate review). And if pregnancy is possible, it should be excluded before an oral anticoagulant is started, because vitamin K antagonists can harm the fetus.⁹

Duration of anticoagulation and recurrence

No randomised trial has defined the duration of anticoagulation after cerebral venous thrombosis, and the ESO guideline made no recommendation.⁷⁰ The EXCOA-CVT trial, comparing 3–6 with 12 months, had not published results by September 2026.⁷⁴ Recurrence is uncommon. In ISCVT, recurrent cerebral venous thrombosis occurred in 2·2% and any venous thromboembolism in 5·8% over a median of 14 months, and male sex was a predictor of recurrence.⁷⁵ After anticoagulation was stopped, an Italian cohort found recurrent cerebral venous thrombosis at 0·53 per 100 person-years.⁷⁶ In children and young people with provoked sinovenous thrombosis, a subgroup of a randomised trial found no recurrence with either 6 weeks or 3 months or more of anticoagulation.⁷⁷ Those were patients under 21 years and the result should not be applied directly to adults. For a first cerebral venous thrombosis associated with hormonal contraception that has been stopped, 3–6 months of anticoagulation is a reasonable convention; the evidence is observational and the ESO guideline makes no recommendation on duration.

Long-term sequelae

The modified Rankin Scale understates what patients live with. In a Helsinki cohort, 84% had a score of 0–1 at a median of 39 months, but 42% reported residual symptoms and only 57% were employed.⁷⁸ Most patients with hormone-associated thrombosis are young women of working age, so these sequelae matter for most of their lives (Table 4).

Cognition, mood and fatigue. A 2025 meta-analysis of 12 studies (801 patients) found cognitive impairment in 19% in studies at low risk of bias and 29% overall, most often affecting memory and executive function. It was present in 29% of patients with a modified Rankin Scale score of 0.¹⁰ Among functionally independent patients followed for a median of 5 years, 75% reported problems with concentration, 30% depression and 30% fatigue, all more often than in matched controls.¹¹ In the long-term follow-up of the heparin trial, 35% had cognitive impairment and 40% could not resume their previous work.⁸² Smaller series confirm deficits of memory and executive function in patients with good functional recovery.⁸⁵ These problems are easily missed when follow-up is limited to the neurological examination.

Return to work. In a Swedish cohort, 71% returned to work, after a median of 7 months. Women were less likely to return (hazard ratio 0·50, 0·25–0·99), as were patients with a parenchymal lesion (0·45, 0·24–0·82), and those who returned reported better quality of life and less fatigue, depression and anxiety.⁸¹ A 2025 review summarised the literature as 20–40% of patients not resuming full-time work.⁸⁶

Headache. At 3 months, 46% of patients in a Portuguese cohort had headache. Most was a new headache of tension-type or migraine pattern, but 10% had a secondary cause: dural arteriovenous fistula, intracranial hypertension or recurrent thrombosis. Pre-existing depression raised the odds of persistent headache (odds ratio 7·9), and the degree of recanalisation did not predict it.⁷⁹ A new or changed headache after cerebral venous thrombosis should therefore be investigated before it is attributed to a primary headache disorder. We found no trial of headache treatment specific to this group; treatment follows the headache phenotype.

Seizures and epilepsy. Late seizures, occurring more than 7 days after diagnosis, affected 11% of 1127 patients in an international cohort, a median of 5 months after diagnosis. Acute status epilepticus (hazard ratio 7·0), decompressive surgery (4·2), acute seizures (4·1), subdural haematoma (2·3) and intracerebral haemorrhage (1·9) predicted them, and 70% of patients with a late seizure had a recurrence despite antiseizure medication.⁸⁰ The DIAS3 score, derived from 1128 patients and externally validated in two further cohorts, predicts post-thrombotic epilepsy from six acute-phase variables.⁸⁷ In one retrospective series, unprovoked late seizures were more frequent in women who had taken hormonal contraceptives (p=0·047); the association is weak and needs confirmation.⁸⁸ Enzyme-inducing antiseizure medicines reduce the effectiveness of hormonal contraception, so the choice of antiseizure medicine and of contraception should be made together. This is a known pharmacological interaction; we did not review it systematically here.

Vision and intracranial pressure. In ISCVT, persistent visual deficits were more frequent in patients diagnosed later,⁸⁹ which makes visual assessment part of both acute care and follow-up in patients who present with papilloedema. The ESO guideline suggests not using acetazolamide to reduce death or dependency;⁷⁰ its use for vision-threatening intracranial hypertension is a convention extrapolated from idiopathic intracranial hypertension.⁹⁰ For persistent intracranial hypertension with sinus stenosis after thrombosis, venous stenting improved headache in 78% and visual symptoms in 92% of 17 patients, but one patient died of cerebellar haemorrhage.⁹¹ It remains a procedure for selected patients at experienced centres.

Recanalisation and dural fistula. A meta-analysis of 19 cohorts found recanalisation in 85% (77% in higher-quality studies), and recanalisation was associated with a favourable outcome (odds ratio 3·3, 1·2–8·9). Data on whether incomplete recanalisation predicts recurrence were too scarce to analyse.⁸³ Dural arteriovenous fistula is a recognised late complication, but in the RE-SPECT CVT imaging substudy no new fistula was found in 112 patients at 6 months, and the investigators judged routine follow-up angiography to have a very low yield.⁸⁴ Follow-up imaging is therefore better directed at new symptoms (pulsatile tinnitus, a change in headache, new focal signs) than scheduled for screening.

Contraception, pregnancy and hormone therapy after cerebral venous thrombosis

The ESO guideline suggests avoiding oestrogen-containing contraception after cerebral venous thrombosis.⁷⁰ The alternatives discussed above (the levonorgestrel intrauterine system, the implant, the progestogen-only pill, or a copper device) apply equally here; depot medroxyprogesterone acetate is best avoided.^4,5 We found no study that compared continuing with stopping hormonal contraception after cerebral venous thrombosis, and no outcome data on menopausal hormone therapy after it. If hormone therapy is needed later in life, the transdermal route is the lower-risk choice by extrapolation from venous thromboembolism at other sites.^6,28

Pregnancy after cerebral venous thrombosis is possible and usually safe. In a systematic review of 13 studies, recurrent cerebral venous thrombosis occurred in 9 per 1000 subsequent pregnancies and other venous thromboembolism in 27 per 1000; the risk is low in absolute terms but well above background.⁹² The ESO guideline suggests that later pregnancies are safe and that prophylactic low-molecular-weight heparin be considered throughout pregnancy and the puerperium,⁷⁰ and the Highlow trial supports a fixed low dose in women with previous venous thromboembolism.⁵⁰ Because obesity multiplies the thrombotic effect of oral contraceptives,⁶⁷ weight is also worth addressing in women who will later need contraception.

Transgender women

Oestrogen therapy for gender affirmation carries a risk of venous thromboembolism, estimated in one review at 2·3 per 1000 person-years with wide uncertainty because the underlying studies differ.⁹³ By extrapolation from cisgender women, transdermal estradiol appears least thrombogenic and oral ethinylestradiol most, and progestogens add risk.⁹⁴ We could not verify the primary cohort studies for this review, and the evidence in this group remains weaker than for cisgender women.

Uncertainties and future research

• Estradiol-based and estetrol-based pills. Early data suggest lower risk than ethinylestradiol pills, but they come from sponsored observational studies.¹⁶ Independent comparative data are needed.
• Prophylaxis in pregnancy. Apart from the Highlow dose comparison, evidence on who benefits from antepartum or postpartum prophylaxis is of very low certainty.^51,52
• Diagnostic strategies. Prospective management studies and the UK diagnostic-accuracy study disagree on whether D-dimer and decision rules can safely reduce imaging in pregnancy.^42,43,46
• Cerebral venous thrombosis after hormones. No study has reported sequelae separately for hormone-associated disease or compared continuing with stopping hormonal contraception, and the duration trial (EXCOA-CVT) has not reported.⁷⁴
• Heavy menstrual bleeding. Which anticoagulant, and which adjunct, is best for women of reproductive age awaits trial results.⁶²
• Regional data. All the risk estimates here come from Europe and North America. We found no population data from the Arabian Peninsula on hormonal contraceptive use, pregnancy-associated venous thromboembolism or thrombophilia prevalence, and the absolute risks above may not transfer unchanged.

Conclusion

Hormone-associated venous thromboembolism is common, largely predictable and, for the most part, preventable by choosing the right preparation. The practical rules follow directly from the evidence: prefer levonorgestrel or norgestimate when a combined pill is wanted; use progestogen-only methods other than injectables, or a copper device, after a thrombosis; use transdermal rather than oral oestrogen in menopause; recognise the weeks after delivery as the time of highest risk; and use the hormonal context to shorten, not lengthen, anticoagulation after a first event. The questions that remain concern the newer estrogens, prophylaxis in pregnancy and menstrual bleeding during treatment, and each needs a trial.

References

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