Introduction As a single agent, fluorouracil has been documented to have a small but present chance of causing extravasation of the port when not properly administered. It has also been shown that cancer patients receiving chemotherapy are at increased risk of deep vein thrombosis, symptomatic or silent. Case report A 43-year-old male patient with stage III colon cancer receiving FOLFOX developed a saddle pulmonary embolism involving possible extravasation that was discovered following cycle 3 of chemotherapy. CT scan and lower extremity Doppler confirmed non-occlusive deep vein thrombosis along with saddle pulmonary embolism. Management and outcome: For acute management, patient underwent bilateral pulmonary artery thrombolysis. Following this, the patient was initiated on rivaroxaban indefinitely. The right subclavian port was removed, and a new port was placed in the left subclavian. Patient went on to receive three more cycles of chemotherapy. Discussion Fluorouracil, an inflammitant, has been shown to have damaging potential, especially in terms of the integrity of the endothelium. Over time, this can lead to serious complications such as cardiotoxicity, including deep vein thrombosis formation. Based on how and when the thrombi were discovered, it is not possible to deduce whether the port, the 5-FU, extravasation or other factors were the precipitators of the formation of the thrombi. The combination of chemotherapy treatment along with CVC placement appears to have an additive risk to the formation of a thrombus. Practitioners should take caution when evaluating for extravasation and CVC integrity and note other potential differentials for causes, including deep vein thrombosis/saddle pulmonary embolism formation.
Postmortem Demonstration of the Source of Pulmonary Thromboembolism: The Importance of the Autopsy
