By Manu Aggarwal

There are a few things that make me take a longer pause in venous medicine. Of all venous disease complications, one of the top concerns is the pregnant patient. In the last year, I have seen a handful of pregnant patients with variable superficial venous thrombophlebitis (SVT) of truncal veins, varicose veins and labial veins. Early recognition and management are key in these patients.

A patient, about two weeks out from a vaginal delivery, presented with terribly tender labia that were very firm to palpation. She had difficulty sitting, sleeping and breastfeeding. Ultrasound of the deep system was normal without evidence of deep venous thrombosis. However, scanning her labia showed multiple non-compressible veins. Her review of systems was negative for chest pain, shortness of breath, abdominal pain or fevers and chills. She was examined by her obstetrician who sent her to our office for evaluation/treatment. This was the patient’s second pregnancy. She had labial varicose veins with her first pregnancy but did not have any of the concerns she presented to us with after this second pregnancy.

We ordered a CT Venogram to rule out any progression of the thrombus. We do not have abdominal venous ultrasound available to give us further information. The CTV report was completed the same day and was negative for any propagation.

The SVT was confined to varicose veins on the labia. The patient was instructed to use a heating pad to the area and use a tighter-fitting panties or leggings to provide compression. We discussed that creating compression on the labia will be difficult with the over the counter compressions and she may consider creating a v-shaped strap to provide compression. The patient presented within a few weeks later for follow-up and she was feeling much better. Upon initial presentation, we discussed with her obstetrician whether to anticoagulate this patient for the next six weeks (post-partum time). There were no guidelines that we could find, the SVT was limited to the varicose veins of the labia and the patient was already feeling slightly better between the appointment with her obstetrician and our office – so we opted not to treat the patient with anticoagulation.

Another patient presented to us as a referral from her obstetrician with a several month-long-history of venous eczema and firm, tender varicose veins. She was wearing compression stockings occasionally because the itching was so intense. She was using a steroid cream sparingly due to pregnancy per her obstetrician. She had significant great saphenous vein insufficiency that was not addressed prior to her pregnancy – and she had a similar presentation during her last pregnancy.

The patient was scheduled to deliver in the next two weeks after her presentation, thus it was opted to keep the patient on compression stockings and to use an over-the-counter hydrocortisone cream to help with the itching. She was also told to discuss her concerns with her obstetrician to assure that such potency of the hydrocortisone cream would not be a concern during pregnancy because there was a concern by her obstetrician.

The patient presented three months after delivering where an endovenous laser ablation was performed on the great saphenous vein and ambulatory phlebectomy was performed on the varicose veins. At her one-week and at three-month follow-up post procedure, she was much more comfortable, and her leg felt less heavy, swollen and had improved skin discoloration.

Superficial venous thrombophlebitis affects more than 125,000 people in the United States. The number is likely higher because it is highly unrecognized and undertreated – which can be scary – when we know the likelihood of SVT progressing into at DVT can be 6-40 percent of the time or symptomatic pulmonary emboli in 2-13 percent of patients.

In addition to pregnancy, hypercoagulable states are found in up to 35 percent of patients with SVT. The most commonly inherited forms of coagulopathy are Factor V and Prothrombin gene mutation. The most common acquired form of coagulopathy is antiphospholipid syndrome. Where pregnancy is a coagulopathy — alone or with a coagulopathy on top of it all – the condition predisposes patients to thromboses. Pregnancy itself increases the opportunity for a venous thromboembolism by four-to-five-fold. Add a coagulopathy to that and the increase in risk is cringe-worthy.

An interesting fact in my research is that most VTEs occur within the first trimester and early second, with the most likelihood between 11- and 15-week gestation. These findings, however, are not reliably consistent. The multifactorial nature of VTE doesn’t stop with pregnancy. Obesity, smoking and maternal cardiac disease, personal history of VTE and premature delivery increase the risk of VTE during pregnancy.

At first. I had some difficult finding any definitive guidelines. The United Kingdom Centre for Maternal and Child Inquiries 8^th Report on Confidential Inquiries into Maternal Deaths in the U.K., VTE was the leading cause of direct maternal death in the United Kingdom for all but the final of the two-year eras reported from 1985 to 2008. Maternal death from VTE was more common than death from sepsis, preeclampsia, amniotic fluid embolism or hemorrhage. There was also a significant decrease in maternal death due to VTE in 2006-2008 era after the first publication of the Royal College of Obstetricians and Gynecologist Green Top Guideline “Thromboprophylaxis during Pregnancy, Labour and after Vaginal Delivery” in 2004.

In the United States, ACOG and ACCP have guidelines for the prevention of thromboembolism that can help reduce the rates of VTE-related morbidity and mortality. The following recommendations are based on the “American College of Chest Physicians Evidence-Based Clinical Practice Guidelines” (9^th Ed) for venous thromboembolism, thrombophilia, antithrombotic therapy and pregnancy.

Going back to my first patient with the labial SVT, ordering a CTV was to rule out any pelvic VTE. In pregnancy – up to 12-18 percent of DVT are pelvic DVT. Fortunately, her testing was normal. A d-dimer was not ordered because I felt like it would be falsely elevated anyway, and it wouldn’t change my management (ordering a CTV).

If she would have presented with this during pregnancy, based on the guidelines, she could have been managed with conservative treatments (heat, compression) and followed closely. However, if she had a strong family history of VTE or a personal history or confirmed lab coagulopathy, she would have been placed on LMWH or UFH. If she was close to delivery, one may argue to use UFH due to proximity of delivery. Once placed on anticoagulation, it would have to be continued for at least six weeks post-partum time, for a total minimum duration of six months. If she would have had an antithrombin deficiency, she would have required antepartum and post-partum anticoagulation.

Patients with recurrent pregnancy loss (greater or equal to three miscarriages) and women with severe or recurrent preeclampsia, placental abruption or otherwise unexplained intrauterine growth retardation should be screened for thrombophilia and antiphospholipid antibodies. Women with antiphospholipid antibody syndrome and a history of multiple greater than or equal to two early-pregnancy losses, or greater than or equal to one late pregnancy loss, preeclampsia, intrauterine growth retardation (IUGR), or abruption, require antepartum aspirin plus prophylactic or intermediate-dose UFH or LMWH. Women with APLAs and a history of VTE who are usually receiving long-term oral anticoagulation therapy, should be treated with adjusted-dose LMWH or UFH therapy plus low-dose aspirin and resumption of long-term oral anticoagulation therapy postpartum.

Given the extent of this patient’s labial SVT and prolonged course of recovery (close to 3 months until resolution of firmness), her second time with labial varicose vein symptoms (with this time being much more symptomatic), her obstetrician and I decided for her be tested for thrombophilia prior to another pregnancy.

For my patient who presented with significant venous eczema and SVT of the varicose veins, we opted to watch her conservatively because she was within two weeks of delivery. If the great saphenous was involved (greater than 5cm) or within 3-5cm of the SFJ, she would have needed anticoagulation. Perhaps the best would have been UFH due to the shorter halflife than LMWH because she was so close to delivery.

VTE in pregnancy is a significant cause of mortality – if not the No.1 cause of maternal mortality based on some statistics. The early recognition and treatment is key in improving patient outcomes. I would encourage all of us to work with your local obstetricians and gynecologists to come up with a standard of care based on the current guidelines that can be agreed upon for community-wide care. VTN

Manu Aggarwal, MHSA, MD, is a board-certified family physician and ABVLM-certified physician at the Vein Care Center Laser Specialists. Since 2007, the VCC has been an IAC-accredited vascular laboratory. In 2015, the VCC was one of the first 50 practices in the country to also be Vein Center accredited. The VCC has been dedicated to venous disease and laser treatments since 2004, and is in Lima, Ohio, with a satellite office in Celina, Ohio. She may be contacted at yourveincarecenter.com .