A 21-year-old female college student presented to the emergency department (ED) with severe pain in her left hip, thigh, and calf. The pain started suddenly when she was playing basketball a few hours earlier. She twisted her torso to shoot the ball and heard a “pop” in her left hip with immediate onset of pain, and she subsequently fell to her knees. She was initially able to ambulate but had worsening pain and rapid progression of swelling and mottling in the left leg from her hip to her ankle. She denied any pain or swelling in that extremity prior to the injury during the basketball game. With the exception of oral contraceptive use, she had no significant medical or family history.\nOn examination her left extremity was mottled, dusky, and cool to the touch from the hip to the toes and she had decreased dorsalis pedis and posterior tibial pulses when compared with the right extremity. The leg was markedly tender to palpation and sensation to light touch was diminished. Passive range of motion of the hip, knee, and ankle elicited severe pain.\nPOCUS was performed at the bedside to evaluate for arterial blood flow and deep venous thrombosis. This demonstrated normal color flow in the femoral and popliteal arteries (), but echogenic material was noted within the left common femoral vein extending distally to the popliteal vein and the veins were non-compressible (). Vascular surgery was immediately consulted, and while awaiting their arrival to the ED the patient was sent for an emergent computed tomography (CT) angiogram, which confirmed arterial patency and extensive deep venous thrombosis in the left popliteal, femoral, and iliac veins (). A heparin bolus was given and the patient was then taken to interventional radiology where she underwent partial thrombectomy, catheter-directed tissue plasminogen activator (tPA) treatment, and placement of an inferior vena cava (IVC) filter. By the next morning her leg was noted to be well-perfused, non-tender, and without swelling, and her pain had resolved. A workup for hypercoagulable states revealed heterozygosity for the Factor V Leiden mutation. She was discharged one week later on warfarin after bridging from enoxaparin.
A 49-year-old woman presented with acute coronary syndrome for which she received aspirin, clopidogrel, atorvastatin, enoxaparin, and tenecteplase at another facility. She was then transferred to our institute for further management. She underwent coronary angiography which was suggestive of triple vessel disease. As the patient was in acute congestive heart failure (Killip IV) with pulmonary edema, she was intubated and mechanically ventilated. She underwent coronary artery bypass grafting surgery the following day where she received 20,000U of unfractionated heparin.\nOn postoperative day (POD) 6, the patient developed right pedal edema with cyanosis. Bilateral lower limbs Arterial Doppler was normal. Venous Doppler of the right lower limb was suggestive of thrombosis of the right Common Femoral, Superficial Femoral, Popliteal, and Great Saphenous Veins. She also had progressively worsening thrombocytopenia in which the platelet count dropped from 297 × 109/L on day 1 of postenoxaparin exposure to a nadir of 20 × 109/L on day 8. With a suspicion of HIT and thrombosis (HITT), enoxaparin was replaced with fondaparinux on POD 7. She tested positive for HIT type 2 antibodies on day 10. Her platelets started improving by POD 11 [].\nOn POD 13, two-dimensional echocardiography done was suggestive of a left ventricular thrombus (with an ejection fraction of 25%) which resolved completely by POD 44 with anticoagulation. Fondaparinux was bridged with oral Vitamin K Antagonist-Acenocoumarol for HITT and PCD. Once there was a line of demarcation for gangrene, she underwent a right forefoot amputation on POD 34.\nThe patient was discharged on POD 47 with medications for cardiac failure along with acenocoumarol.