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.
A 64-year-old man with a history of obesity (BMI 38 Kg/m^2), arterial hypertension, atrial fibrillation, type 2 diabetes, chronic kidney disease, obstructive sleep apnea, and chronic venous insufficiency presented to the Emergency Department complaining of dyspnea, fever, and chest pain which started 7 days before. The patient was hypoxemic in room air (SpO2 80% and PaO2 43 mmHg). Inferior limbs appeared normal. A molecular swab formalized diagnosis of SARS-CoV2-related pneumonia. Respiratory distress progressed despite non-invasive-ventilation and hemodynamic instability requiring vasoactive support ensued. The patient was intubated and transferred to the ICU. The patient received invasive protective ventilation and hemodynamic support with noradrenaline. Gas exchange progressively worsened to a PaO2/FiO2 ratio of 70 mmHg. He developed a shock, and his lower limbs started to appear mottled. Lung and cardiac ultrasound were compatible with severe interstitial pneumonia and with no signs of pressure overload of the right heart. His coagulation profile was highly altered, as both aPTT and INR were elevated (respectively 2.28 seconds and 6.42), platelets were 164,000/mm3, and D-dimer was 117,521 UI/ml. Coagulation parameters continually worsened (), and treatment with one unit of fresh frozen plasma and vitamin K was required. Inferior limbs’ color progressively worsened, becoming frankly cyanotic, while pulses were still normal. Doppler ultrasound showed bilateral thrombosis of tibial and small saphenous veins. A continuous infusion of iloprost was started, as PCD was suspected (). Continuous infusion of unfractionated heparin was instituted, at a dose of 500-1000 IU per hour, according to aPTT, as well as continuous veno-venous hemodiafiltration as the patient developed acute kidney injury. The patient’s general conditions worsened (), and despite maximal treatment, he passed away after eight days of ICU care.