Septic pelvic thrombophlebitis

Septic pelvic thrombophlebitis (SPT) is an inflammatory process that, in conjunction with the physiological conditions of postpartum and proximity with potentially infected tissues (e.g. endometrium, chorion, amniotic fluid), leads to the formation of a clot blocking the ovarian vein. Injury of the ovarian vein endothelium during delivery or pelvic operations and bacterial invasion from nearby tissues triggers an inflammatory response within the vein wall. Bacteria, viruses and physical trauma can trigger prothrombic processes within the body through inflammation and tissue factor expression on endothelial cells and monocytes that activates the intrinsic coagulation pathway.[6]

In addition to the intravascular vessel wall damage, Virchow's triad of thrombogenesis is completed by the hypercoagulable state of pregnancy up to 6 weeks postpartum and blood stasis from both laying down in a hospital bed for an extended amount of time without walking and pregnancy-induced ovarian venous dilatation.[7] Deep vein thrombosis is generally a concern in operations involving the pelvis or lower extremities wherein during recovery, a person's ability to ambulate is limited after the operation. Blood stasis and thrombogenesis within the ovarian vein specifically is especially of concern after cesarean sections due to the combination of inevitable physical trauma to the intima of pelvic blood vessels, the three-fold increase in diameter if the ovarian veins, and that pooling of the blood in the pelvis as this is the lowest part of the person while laying in a hospital bed. Notably, most cases of SPT involve the right ovarian vein rather than the left ovarian vein due to its greater length, weaker valves, and left-to-right venous flow in the pelvic region while sitting in the upright position.[8]

Ovarian veins have close connections with the uterine and vaginal venous plexuses that are in proximity to tissues commonly host to pathogens, notably in cases of vaginosis or endometritis. Pathogens from these adjacent tissues infect the forming clot, and contributing to a positive feedback loop of inflammation. Bacterial organisms associated with SPT include anaerobic and aerobic streptococci, Proteus species, Bacteriodes species, staphylococci, E. coli, and Klebsiella.[9] Sepsis occurs after the pathogens infect and proliferate in the thrombus within the lumen, leading to persistent bacteremia.  Fatal complications include septic shock and septic pulmonary embolism, leading to acute respiratory distress syndrome.

Septic pelvic thrombophlebitis (SPT) is often difficult to diagnose due to the absence of physical signs and symptoms.[10] SPT initially and most commonly presents as a fever anywhere from 5 to 21 days after delivery.[11] Temperatures of fever have been reported to be within 103 °F to 104 °F.[12]

The symptoms of SPT are similar to those of endometritis. Clinical signs include:

• prolonged spiking fever
• pain on palpation of uterus
• midline lower abdominal pain
• malodorous lochia (vaginal discharge)
• tachycardia
• tender abdominal mass[10]
• shortness of breath[13]

In rare cases, more serious postpartum complications may occur as a result of SPT such as pulmonary embolism.[13]

Septic pelvic thrombophlembitis (SPT) occurs most often in bedridden patients after giving birth, or after having undergone a Caesarean section. The main risk factor of developing SPT is postpartum endometritis, which in turn is most commonly caused by a Caesarean section. The blood often pools in the pelvis as this is the lowest part of the patient while laying in a hospital bed. Other risk factors for developing endometritis, and subsequently SPT include:

• Bacterial vaginosis
• Chorioamnionitis[14]
• Large amount of meconium in amniotic fluid
• Manual removal of the placenta
• Prolonged labor
• Multiple cervical examinations
• Multiple gestations
• Pre-eclampsia[15]
• pelvic inflammatory disease[16]
• intrauterine device insertion[17]

Septic pelvic thrombophlebitis (SPT) is mostly suspected when a spiking fever is not resolved using a broad spectrum antibiotic therapy. People often experience flank or abdominal pain which is non-colic and constant. The pain can vary in intensity and location.[10] Most often, SPT is diagnosed by the presence of fever, leucocytosis or positive blood cultures despite treating them with the standard antibiotic therapy.[6] Due to the nature of SPT, such as rare incidence and lack of specific clinical signs and symptoms, it is often misdiagnosed.[13]

SPT is very complex and difficult to see through scans because sometimes small blood clots cannot be detected by these machines. Due to the difficulty in suspecting thrombi in the ovarian veins, sometimes a presumptive diagnosis can be made in persons, especially in postpartum women.[18] This is the reason even healthy postpartum women are considered for anticoagulation therapy without no visualization of a thrombus in their scans.[18]

Septic pelvic thrombophlebitis is a rare complication of pregnancy. A report states that a pregnant woman undergoing a cesarean section increases the risk of developing SPT . The incidence of SPT occurred in about 1 per 9000 vaginal deliveries and 1 per 800 cesarean sections.[24] The overall incidence of SPT was 1 per 3000 deliveries.

In a study that involved 44,922 deliveries, fifteen women were diagnosed with pelvic thrombophlebitis. However, no complications or deaths were reported.[10]

Septic pelvic thrombophlebitis was first described and diagnosed by von Recklinhausen at the end of the 19th century.[10] It was initially described as a pelvic infection where there was the presence of a thrombosis in one or both of the ovarian veins. This disease had a high incidence and mortality during this time period. Since this discovery occurred prior to the antibiotic era, von Recklinhausen proposed surgical excision as the preferred treatment. In 1951, Collins published and advocated the practice of ligature of the inferior vena and ovarian veins as the most effective treatment. It was reported that there was a 90 percent survival rate after the surgery. It was not until the late 1960s that combination antibiotic and heparin therapy became the preferred treatment plan for SPT. After pharmacological therapy became the preferred treatment for SPT, mortality rates drastically decreased. Furthermore, the advances in diagnostic tools (e.g. computed tomography and magnetic resonance imaging) and understanding of the disease contributed to improving treatment outcomes. Although the management of this disease has seen much improvement since its discovery at the end of the 19th century, there is still controversy in deciding what the most optimal treatment plan is. Antibiotic therapy is still the preferred treatment if SPT is expected, but adding on heparin is still up for debate because of conflicting evidence of whether or not it provides a therapeutic benefit.