A 31-year-old female presented four days after uncomplicated vaginal delivery complaining about postpartum lower abdominal pain at the right iliac fossa and flank region, irradiating to the suprapubic area. There was accompanying fever. Initial laboratory tests showed an elevated C-reactive protein (CRP) with mild leucocytosis.
Ultrasound (US) showed an enlarged noncompressible tubular structure with central hypoechoic thrombosis at the right ovarian vein, extending superiorly from the right adnexa and lateral to the inferior vena cava (IVC) without flow on Colour-Doppler (CDUS) (Figure 1A, 1B).
Subsequent contrast-enhanced computed tomography (CT) demonstrated an enlarged right ovarian vein with central hypodensity, in keeping with thrombosis, extending up to the inferior caval vein, with adjacent inflammatory changes in retroperitoneal fat surrounding the right ovarian vein. The IVC, the right renal vein, and the left ovarian vein were normal with no signs of thrombi. (Figures 2A, 2B, 2C).
Axial T2-weighted Magnetic Resonance Imaging (MRI) showed low signal intensity of the wall of the enlarged right ovarian vein with a central hyperintense focus (Figure 3A). Apparent diffusion coefficient (ADC) map showed central hypo-intensity within the right ovarian vein (Figures 3B).
Postpartum ovarian vein thrombosis (POVT) is a serious complication following delivery . Pathophysiology of POVT is attributed to hypercoagulability status. The main risk factors are hormonal changes accompanying pregnancy, ovarian vein stasis, and endothelial injury during delivery . Caesarean section also increases the risk of thrombosis .
Due to compression by the enlarged uterus, 80-90% of POVT occur in the right ovarian vein, 6% in the left ovarian vein, and approximately 14% are bilateral .
Clinical features of POVT are nonspecific and include lower quadrant and flank pain and tenderness, fever, nausea, and vomiting. Elevated CRP and leucocytosis are the main laboratory findings [2, 3, 4].
US Doppler shows an enlarged, noncompressible tubular structure extending superiorly from the adnexa, containing a hypoechoic thrombosis and no blood flow on Doppler [3, 4, 5].
Postpartum bowel distension and uterus enlargement may hamper visualization of ovarian veins and possible thrombi, necessitating the use of other imaging modalities such as contrast-enhanced CT [4, 5, 6].
An ovarian thrombosis appears on contrast-enhanced CT imaging as a central hypodense filling defect within an enlarged ovarian vein. Irregularity and significant enhancement of the venous wall are usually remarkable. Venous tortuosity, perivascular oedema, and inflammatory changes in retroperitoneal fat surrounding the ovarian vein can also be present [1, 2, 3, 4].
When administration of intravenous iodine contrast is contraindicated, MRI is a useful alternative method to confirm the diagnosis. The venous thrombus in an enlarged puerperal ovarian vein may manifest as an inverted target sign on T2-weighted images with central hyperintense focus and peripheral hypointense rim, attributed to the central accumulation of extracellular methaemoglobin and peripheral hemosiderin. On diffusion-weighted images (DWI), the thrombus may show diffusion restriction. On gadolinium contrast-enhanced T1-weighted images, the thrombus appears as a hypointense filling defect . The use of gadolinium contrast should be restricted to cases where the diagnosis is not clear on non-enhanced imaging. There is no evidence to discontinue breastfeeding for 24 hours .
POVT complications could be life-threatening, including hematosepsis and extension of the thrombus to the inferior vena cava and/or renal veins, potentially leading to pulmonary embolism [3, 5]. Therefore, early diagnosis of POVT is pivotal to allow appropriate therapy in a timely manner. The current treatment of choice is intravenous anticoagulation and antibiotics [1, 2, 4].
In conclusion, postpartum fever with abdominal pain should always alert the referring physician and the radiologist to potential POVT.
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