In December 2005, a 47-year-old woman (height, 160 cm; weight, 57 kg) was transported to our institution, 1 week after she had experienced an acute myocardial infarction and subsequent emergency 3-vessel CABG in her native country. After the CABG, cardiogenic shock ensued, and she was referred to us for further treatment and an evaluation for cardiac transplantation.
Her medical history included hypertension, 2 myocardial infarctions 6 years earlier, and percutaneous transluminal coronary angioplasty with the insertion of 3 stents. Her surgical history included the repair of a herniated L5-S1 disk 6 months before the current admission, a hysterectomy 6 years previously, and a tonsillectomy. Before her spinal surgery, she had been fairly active physically. Her use of tobacco (15 pack-years) ended 6 years before the current admission, and she still occasionally consumed alcohol.
Upon arrival at our hospital via helicopter, the patient was receiving IABP and intravenous inotropic support, and she was dependent upon mechanical ventilation. Echocardiography after her hospital admission showed severely depressed LV function and an estimated LV ejection fraction of less than 0.10. The LV was mildly to moderately enlarged. The right and left atria were normal in size, and there were no structural valve abnormalities. Cardiac output was 3.3 L/min, cardiac index was 2.1 L/(min·m2), pulmonary artery mean pressure was 18 mmHg, and systemic vascular resistance was 2,133 dyns × sec/cm5. She experienced an episode of atrial fibrillation that converted after the administration of amiodarone and digoxin. Because of her recent sternotomy and the concomitant insertion of multiple invasive lines, she was at high risk for infection. In accordance with our infectious-disease service's recommendations, the patient underwent panculture and was given intravenous antibiotics. To treat the heart failure, inotropic solutions, vasopressors, diuretics, and IABP support were continued. Nutrition was maintained via total parenteral nutrition and nasogastric tube feedings.
Despite maximal medical therapy, the patient's end-organ function continued to deteriorate. She became oliguric and required continuous venovenous hemodialysis. A tracheostomy was performed to enable long-term mechanical ventilatory support. Elevated liver enzyme levels indicated shock liver syndrome, and she also developed thrombocytopenia. Our hematology service concluded that the decreased platelet count (14,000 μL) was multifactorial and likely unrelated to heparin antibodies (antiplatelet factor 4, 0.529 optical density units). The thrombocytopenia was probably related to vancomycin therapy, the use of the IABP, and possible sepsis with disseminated intravascular coagulation (dimerized plasmin fragment D, >20.0 mg/L fibrinogen equivalent units). The increased prothrombin time (21.7 sec) and partial thromboplastin time (40.5 sec) were attributed to shock liver syndrome.
The patient's heparin was discontinued, and bivalirudin was started as anticoagulation therapy. She was weaned from the IABP and remained on inotropic support. Although her renal function improved, she underwent dialysis intermittently. She was lightly sedated and was arousable; although she had little ability to communicate, she followed oral commands. Her left foot became cyanotic, and no arterial pulses or Doppler signals were noted. She was taken to the operating room for left femoral embolectomy. Postoperatively, she had good femoral pulses but no posterior tibial pulses. The diagnoses of critical-illness neuropathy and bilateral lower-extremity ischemia with gangrene were made.
In addition to these complications, the patient experienced episodes of atrial fibrillation amenable to chemical cardioversion. Her condition remained critical but stable, with slow improvements until, 40 days after admission, she experienced a hypotensive episode, became acidotic, and went into cardiac shock. An IABP was reinserted, vasopressors were started for hemodynamic support, and inotropic support was increased. Despite these measures, her condition continued to deteriorate, and the medical and surgical teams agreed that a circulatory assist device was needed if she were to survive.
Due to her severely coagulopathic state, unstable hemodynamic condition, and multiorgan failure, an invasive LVAD implantation posed an extremely high surgical risk. To support her LV function, the decision was made to replace the IABP with a TandemHeart pVAD.
The procedure was performed in the operating room under fluoroscopic C-arm guidance, in accordance with the manufacturer's protocol.9 Percutaneous access was not attempted, due to the patient's lower-extremity ischemia and small vascular structures. Her left groin was incised, and the left femoral artery (LFA) and vein were surgically exposed. A 7F sheath was introduced into the left femoral vein, through which a long J wire was advanced into the right atrium under C-arm guidance. A transseptal puncture was performed, and the outflow TandemHeart catheter was advanced into the left atrium. The LFA was too small for safe insertion of the sheath for the inflow cannula. Instead, the femoral artery was clamped with a partial occlusion clamp, and an 8-mm, reinforced GORE-TEX graft was sewn to the LFA with a running 5–0 polypropylene suture in end-to-side fashion and was attached with a connector to the TandemHeart inflow cannula (Figs. 1 and 2). The patient was thrombocytopenic, and tests for heparin antibodies remained negative; nevertheless, in accordance with the recommendations of our hematology service, we administered bivalirudin intravenously as anticoagulation therapy.
| Fig. 2 Postoperative photograph of the groin-access graft shows the left inguinal region and left upper leg, with the incision below the inguinal ligament. The TandemHeart's outflow cannula is in the left femoral vein (LFV), and the inflow cannula is (more ...) |
The successfully implanted TandemHeart induced stable flows of 2.5 to 3.0 L/min. Due to the patient's coagulopathy and bleeding from the left groin, she was returned to surgery on postoperative day 1 for a femoral exploration. No active bleeding sources were noted. BioGlue® (Cryolife, Inc.; Kennesaw, Ga), Surgicel® (Ethicon Inc., a Johnson & Johnson Gateway® company; Somerville, NJ), Gelfoam® (Pharmacia & Upjohn Company, a division of Pfizer Inc.; Kalamazoo, Mich) and Thrombin-JMI® (King Pharmaceuticals®, Inc.; Bristol, Tenn) were placed around the anastomosis site to aid hemostasis. A 10-mm Hemashield Platinum™ Woven Graft (Boston Scientific Corporation; Natick, Mass) was sutured around the initial GORE-TEX graft to stop the “sweating” of blood plasma and to control the bleeding from the LFA anastomosis (Fig. 2). As a supplemental precaution, the patient was administered intravenous recombinant activated Factor VII (rFVIIa). The bleeding from the anastomosis site stopped.
From the start of this surgery through postoperative day 1, the patient received 8 units of packed red blood cells, 6 units of cryoprecipitate, 26 units of fresh frozen plasma, and 11 units of concentrated platelets. Her overall status stabilized under TandemHeart support. In 2 weeks, a MicroMed DeBakey VAD® Child (MicroMed Cardiovascular, Inc.; Houston, Tex) was successfully implanted as a bridge to cardiac transplantation.