Chronic venous insufficiency in pregnancy
Chronic venous insufficiency (CVI) is one of the consequences of pregnancy-related haemodynamic and physical changes, which can be treated in a safe and simple way by compression therapy. At the current global medical online hub (MOH) webinar “CVI, DVT and nausea in pregnancy: What to expect and how to deal with it?” on June 4, 2022, Prof Dr Caitlin W. Hicks, Associate Professor of surgery at The Johns Hopkins University School of Medicine in the US, provided detailed insights on the mechanisms leading to venous insufficiency and how compression therapy may help.
Up to 80% of pregnant women suffer from CVI. Mostly, symptoms of venous insufficiency affect the lower extremities with appearance of varicose veins, itchy skin, swelling, leg pain, or cramps. These symptoms appear from early pregnancy on and become worse with progressing pregnancy. The lower extremity vein system consists of superficial, deep and perforator veins. All of these contain valves, which ensure that the blood flows directly back to the heart. With repeated insults to the valves and veins and further pregnancies, the risk of developing CVI increases.
Superficial thrombophlebitis (or superficial venous thrombosis, SVT) is a serious consequence of CVI. Patients with SVT are at risk of developing deep vein thrombosis (DVT), which represents one type of venous thromboembolism (VTE). Thus, CVI is associated with a five-times higher risk of VTE development. VTE is responsible for 19.6% of pregnancy-related deaths and caused by a combination of stasis, hypercoagulability, and injuries in the endothelial wall, known as Virchow’s Triad. Dr Hicks explained that all three factors are present during pregnancy: The venous return is reduced due to increased venous volume and diameter in consequence of elevated oestrogen levels as well as reduced systemic vascular resistance. Additionally, the endothelial walls get injured as a result of increased blood plasma volume caused by the activation of the RAAS system due to elevated oestrogen. Hypercoagulability occurs due to significantly increased levels of pro- and anticoagulant as well as fibrinolytic factors and adhesive proteins, potentially to prevent extensive maternal bleeding during delivery.
Preventive and treatment options of CVI, SVT and VTE are limited in pregnancy. In particular, with regard to pharmacological options, the data is sparse. Furthermore, the effect on foetal growth promotion is questionable. Hence, pharmacological intervention in pregnant women is generally not recommended, except in case of advanced and severe disease.
Medications to treat SVT, which are safe during pregnancy include acetaminophen and naproxen (restricted to first and second trimester). Unfractionated heparin (UFH) and low molecular weight heparin (LMWH) are available to treat severe SVT and prevent and treat VTE, both of which are safe to use while breastfeeding.
Non-pharmacological measures to prevent VTE include staying active (swim, hike, walk) and elevating legs as often as possible. In addition, wearing compression stockings has a preventive effect and is even used to treat CVI, SVT, and VTE, alone or supportively.
Prof Hicks recommended starting compression therapy as early as possible and choosing a moderate compression grade (in USA 20-30 mmHG), while a low compression grade (15-20 mmHG) is less, but still effective. To prevent VTE in patients with prior unprovoked DVT, factor V Leiden, prothrombin gene mutation, or antiphospholipid syndrome, compression should be combined with anticoagulant therapy.
The presentation was followed by a lively discussion that showed consensus on the use of compression therapy to improve venous diseases during pregnancy and breastfeeding, during which the body also undergoes various physical changes. If you missed this interesting talk, you are welcome to watch it the full session.
Take Home Messages
- Up to 80% of pregnant women suffer from chronic venous insufficiency (CVI)
- CVI is associated with 5x higher risk for venous thromboembolism (VTE)
- VTE is responsible for 19.6% pregnancy-related deaths
- VTE is caused by Virchow’s Triad (stasis, hypercoagulability and endothelial wall injuries), which is present during pregnancy due to:
- Oestrogen-related increased venous volume and diameter as well as reduced systemic vascular resistance (up to 30%)
- Increased pro- and anticoagulant as well as fibrinolytic factors and adhesive proteins
- Increased blood plasma volume (cardiac output up to 31% increased) resulting from oestrogen-related activation of the RAAS system
- Preventive and treatment options of CVI and VTE are limited:
- Pharmacological intervention in general is not recommended in pregnant women, except in case of advanced disease
- Safe alternatives are acetaminophen, naproxen (restricted to first and second trimester), unfractioned heparin (UFH) and low molecular weight heparin (LMWH)
- Most effective non-pharmacological measures are staying active (swim, hike, walk) and compression therapy
- Dr Hicks recommended moderate compression (20-30 mmHG)
- Compression therapy should be started as early as possible