A 65-year-old woman with a medical history significant for diabetes mellitus, hypertension, peripheral vascular disease, and stage IV chronic kidney disease was scheduled for urgent coronary artery bypass grafting surgery (CABG). She was found to have severe triple vessel coronary artery disease after she sustained a non-ST elevation myocardial infarction three days postoperatively from a left lower extremity revascularization procedure. She had had a prior revascularization procedure on the left lower extremity for which she was taking clopidogrel. The clopidogrel was stopped 5 days prior to her most recent revascularization procedure.
The postoperative myocardial infarction was initially managed medically and therapy included a heparin infusion. On day 3 of heparin therapy, her platelet count dropped greater than 50% from a baseline of 197,000/cmm reaching a nadir of 36,000/cmm on day 4 of therapy. At this point HIT was suspected and heparin therapy was discontinued. Argatroban was selected for continued anticoagulation therapy because the patient had significant renal disease. Argatroban infusion was started at 0.8 mcg/kg/min and kept between 0.8 and 1.5 mcg/kg/min to maintain a target aPTT of 48-78 s.
The patient was brought to the operating room where she underwent an uneventful induction of general endotracheal anesthesia. Her baseline lab work included the following: aPTT 42.1 s, PT 14.7 s, and INR 1.4. Her ACT measured using a Hepcon  HMS Plus System (Medtronic Inc., Minneapolis, MN) was 161 s. Aminocaproic acid (Amicar , American Reagent Inc., Shirley, NC) bolus of 5 mg was given on skin incision, followed by infusion of 1 gm per hour for the duration of the surgery. In preparation for CPB, an initial bolus of 6.5 mg argatroban (0.1 mg/kg) was administered, followed by the commencement of a 5 mcg/kg/min infusion with a goal ACT greater than 500 s. Thirty minutes after the initial bolus, the ACT was found to be 313 s, prompting an additional 3 mg argatroban bolus and an upward adjustment of the infusion to 7.5 mcg/kg/min. A sample drawn 20 min after the second bolus returned an ACT of 765. At this point, retrograde arterial and venous autologous priming of the CPB was done and CPB was started.
The CPB circuit consisted of a Sarns disposable centrifugal pump with Capiox  RX25RW hollow fiber oxygenator and hardshell venous reservoir, arterial filter, and tubing. All of these listed components were X-coatedTM from Terumo (Terumo Cardiovascular Systems, Ann Arbor, MI, USA). The circuit was primed with 1000cc of Normosol  -R (Hospira, Inc., Lake Forest, IL, USA), 12.5G/250cc albumin (Telecris Biotherapeutics, Inc., Research Triangle Park, NC, USA), and 50meq NaHCO3. Hypothermia was permitted to 32.5 C measured rectally. After about 15 min of CPB, a clot was noted to be forming on the mesh sock of the venous reservoir. At the same time, the ACT results on the blood that was drawn earlier came back at 409 s, which prompted administration of a 3 mg bolus of argatroban. About 12 min later, blood was redrawn to check the ACT and other labs. The hematocrit values had fallen to 20% from the initial bypass hematocrit of 24%; so, two units of packed red blood cells were added to the CPB circuit. The repeat ACT values after the 3 mg argatroban bolus had increased only marginally to 499 s; so, another bolus of 1.5 mg was given followed by an upward adjustment of the infusion to 10 mcg/kg/min. This increased the ACT to 605 when measured 20 min later.
As there was no further evidence of a compromised CPB circuit, and because of the risks of changing the CPB circuit including the need for circulatory arrest, a decision was made to continue with the present CPB circuit while carefully monitoring the clot in the reservoir and other CPB circuit parameters that would indicate further problems. After the clot discovery, another ACT machine was brought into the room, and the two machines were run in a staggered fashion to prevent the delay in obtaining results. Additionally, given that clot formed with an ACT between 409 and 499 s, the remainder of the bypass run was carried out with an ACT greater than 600 s with a peak of 775 s. Ultrafiltration was started midway through the case, followed by zero balance ultrafiltration with Hemoflow F50NR Fresenius Polysulfone  Capillary Dialyzer (Fresenius Medical Care, Inc, Waukegan, IL) and a total of about 1200 cc of ultrafiltrate was removed by the end of bypass. Anastomosis of the grafts proceeded uneventfully. In order to avoid prolonged coagulopathy in the postoperative period and because of ACTs consistently staying above 600 s, we decided not to continue the argatroban infusion until the termination of bypass. Thus, the argatroban infusion was stopped about 15 min after removal of aortic cross clamp and recovery of patient's native rhythm. CPB was continued for another 40 min after cessation of the argatroban infusion because of trouble in achieving hemostasis by the surgeon. The subsequent separation from CPB was successful on first attempt with a total bypass time of 150 min. BRAT 2  Autologous Transfusion System (Sorin Group USA, Inc., Arvada, CO) was employed during the case for recovery of shed blood, using acid citrate dextrose solution as anticoagulant instead of heparin, but a decision was made to not reinfuse the processed blood. During the latter half of the CPB, relatively lower hematocrit levels were deliberately tolerated in order to preserve packed cells for after bypass. The hematocrit at the time of CPB termination was 20%; so, two units of banked packed cells were transfused immediately thereafter by the anesthesiologist. In the postbypass period, there was considerable difficulty in achieving hemostasis, which required further transfusion of 6 units of fresh frozen plasma, 5 units of platelets, and 8 more units of packed red cells. The last ACT before leaving the OR was 447 s. Drainage of the bypass circuit revealed no visible clots in the circuit other than the original one in the hardshell venous reservoir which appeared attached to the mesh material [Figure 1].
The aPTT on arrival to the ICU was more than 200 s and the ACT done 2 h later was 227 s. The first 24 h of the ICU stay required transfusion of 9 units of packed red cells, 10 units of fresh frozen plasma, and 10 units of platelets in order to correct the coagulopathy. The coagulation parameters did stabilize by post-op day 1 and so did the bleeding. She was subsequently discharged home on post-op day 26 without any obvious neurological deficits. Her delayed hospital discharge was because other medical conditions unrelated to coagulopathy.