During the next 2 days, the patient had a persistent low-grade fever and continued to report mild RLQ abdominal pain. On the 4th day after delivery, the patient's temperature rose to 38.9 °C, and laboratory evaluation showed a white blood cell (WBC) count of 11,600/L. Increased RLQ abdominal pain was noted upon physical examination, although peritoneal signs were absent. An ultrasonographic examination produced no diagnostic findings. The primary care team (Obstetrics and Gynecology) performed a laparoscopic examination to rule out tubo-ovarian abscess and appendicitis; the findings from that examination were also nondiagnostic.

On the 5th day after childbirth, the patient still had a low-grade fever and RLQ abdominal pain. A contrast-enhanced computed tomographic (CT) scan documented filling defects in an enlarged right ovarian vein and in the inferior vena cava (IVC) (Figs. 1 and 2). The patient was given intravenous heparin and was referred to the cardiovascular surgery clinical service for evaluation and treatment of ovarian vein and IVC thrombosis.

At that evaluation, the patient had a temperature of 38.4 °C and a heart rate of 100 beats/min. Her WBC count was 11,900/L, and physical examination revealed mild, diffuse tenderness of both lower abdominal quadrants and a patent right femoral vein. A venogram (Fig. 3) showed a filling defect, which suggested a clot in the right ovarian vein that extended into the IVC.

Comprehensive discussions with the patient, her family, and the primary care team led us to believe that the patient might be unable to comply with medical management and with laboratory monitoring of her anticoagulation after hospital discharge. The consensus among the clinicians was that surgery would provide the best opportunity to achieve a complication-free outcome.

In the operating room, a midline abdominal incision was made, the right white line of Toldt was divided, and a right-to-left medial-visceral rotation was performed to expose the right ovarian vein and IVC (Fig. 4). The ovarian vein was distended, with intraluminal contents that felt semi-formed and gelatinous to palpation (consistent with thrombus). The right ovarian vein was transected and ligated, a caval thrombectomy was performed, and an IVC filter was placed. Intraoperative venography and fluoroscopy provided guidance and verification of complete thrombectomy and optimal positioning of the IVC filter (Fig. 5).

In 1854, Virchow³ described the importance of blood flow stasis, intimal injury, and altered coagulation in the pathogenesis of thrombosis. Virchow's triad can effectively explain the occurrence of postpartum ovarian vein thrombosis.

The ovarian veins arise from venules draining the ovaries, the broad ligament, and the infundibulopelvic brim. The right ovarian vein usually enters the anterolateral IVC at the L2 level, and the left ovarian vein usually enters the left renal vein. Both vessels are long and unbranched, and have incompetent valves. During pregnancy, the ovarian vein diameters increase 3-fold, flow capacity becomes 60 times greater, and valvular incompetence is exacerbated. After childbirth, blood flow in the ovarian veins immediately decreases, leading to venous collapse and stasis (the 1st component of Virchow's triad). Altered coagulation (the 2nd component) is usual after pregnancy. Hypercoagulability is present for 6 weeks postpartum, caused by increased production of coagulation factors 1, 2, 7, 10, and 11 and an increase in platelet adhesiveness. These changes usually peak on the 4th postpartum day. The 3rd component of Virchow's triad, intimal injury, is often due to exogenous factors. For example, the most commonly identified predisposing factor for postpartum ovarian vein thrombosis is intrauterine bacterial infection. It is theorized that the infection may cause local sepsis, producing inflammation and leukocyte infiltration that result in venous intimal injury.⁴

The symptoms of ovarian vein thrombosis usually develop within 4 weeks of delivery, most frequently within the first 4 days. Symptoms typically have an abrupt onset and include chills, fever, and abdominal discomfort. Thrombosis has been most frequently identified in the right ovarian vein and is associated with RLQ pain. The right-sided prevalence is due to the physiologic dextrorotation of the uterus during pregnancy, which may compress the ovarian vein on that side, and also to the direction of postpartum blood flow, which is antegrade in the right ovarian vein and retrograde in the left ovarian vein. It is estimated that ovarian vein thrombosis occurs in 0.05% to 0.16% of all pregnancies that result in live births.^5,6

Ovarian vein thrombosis is often difficult to distinguish from endometritis, acute appendicitis, hydronephrosis, right-sided ureteral obstruction, or pyelonephritis. A high index of suspicion and the ability to rule out other processes that may produce similar symptoms is important, because untreated ovarian vein thrombosis can have catastrophic consequences. Miller and colleagues,⁷ upon reviewing the cases of 182 untreated patients, found that 95 (52%) died.

Before the introduction of antibiotics and anticoagulants, treatment of ovarian vein thrombosis included bed rest, surgical ligation of the ovarian vein, and IVC ligation. This treatment was frequently associated with such complications as postoperative edema, recurrent thrombophlebitis, leg ulcers, stasis dermatitis, venous claudication, and a late mortality rate of 15%.⁴ The use of IVC filters rather than IVC ligation greatly decreased the incidence of these problems.⁸ However, the introduction of antibiotics, heparin, and the extended use of oral anticoagulation therapy into the treatment regimen led to a dramatic shift from operative to pharmacologic management. This approach has produced post-treatment outcomes and long-term results equivalent to those of surgery.^1,4,9 The development, application, and proven efficacy of thrombolytic therapy for the treatment of IVC thrombosis caused by extension of thrombus from the ovarian vein has further contributed to the shift from a surgical to a pharmacologically based therapeutic regimen.^10,11 Surgical treatment for this condition is generally reserved for patients in whom anticoagulation is contraindicated, and for those who have recurrent pulmonary emboli despite medical management, complications related to medical management, a “free-floating” thrombus, or a low likelihood of postoperative compliance or follow-up, as in the patient in this report.

In an ideal situation, we would have continued low-level anticoagulation after surgery and hospitalization. A recent multicenter study, the Prevention of Recurrent Thromboembolism (PREVENT) trial, showed a 64% reduction of recurrent deep venous thrombosis or pulmonary embolus in patients who continued either low-dose warfarin or dalteparin, compared with those taking placebo.^12,13 For reasons discussed above, this regimen was not feasible in our patient.