Intraoperative Bivalirudin Use in Patient Undergoing Femoral Endarterectomy with Heparin-Induced Thrombocytopenia: Case Report and Review of the Literature.

PURPOSE: To describe the intraoperative use of bivalirudin during lower extremity revascularization in the setting of heparin-induced thrombocytopenia (HIT). CASE SUMMARY: A 65 year-old man presented with left common iliac, external iliac, and femoral artery occlusion necessitating revascularization with left femoral endarterectomy and common and external iliac stent angioplasty. Three months before the femoral endarterectomy, the patient was hospitalized for a coronary artery bypass procedure. During this admission, the patient tested positive for the presence of heparin-PF4 antibody complexes. With the patient's recent history of HIT, bivalirudin was selected as the optimal agent for intraoperative anticoagulation. Bivalirudin was administered as a 50 mg bolus, followed by a continuous infusion initiated at 1.75 mg/kg/hr. Repeated bivalirudin boluses were necessary to maintain an activated clotting time (ACT) necessary for the revascularization procedures and recurrent subacute thrombi despite appropriate ACT values. DISCUSSION: Bivalirudin has been utilized for cardiopulmonary bypass and carotid endarterectomy (CEA), but data for dosing in lower extremity revascularization are lacking. As the risk for thrombosis with HIT continues for months after diagnosis, it is important to elucidate optimal dosing of non-heparin anticoagulant options, such as the direct thrombin inhibitor, bivalirudin. The absence of validated dosing strategies for bivalirudin can result in prolonged operative times, increased risk of bleeding, and inadequate anticoagulation. CONCLUSION: Bivalirudin is an appropriate agent for intraoperative anticoagulation in lower extremity revascularization. However, further investigation into the optimal intraoperative bivalirudin dosing regimen is necessary.

Lateral Axillary Exposure for Antegrade Access during Endovascular Repair of Complex Abdominal Aortic and Thoracoabdominal Aneurysms.

BACKGROUND: During endovascular treatment of pararenal aortic aneurysms (PAA) and thoracoabdominal aortic aneurysms (TAAA), our antegrade vascular access of choice is a lateral axillary exposure (LAE). We directly access the axillary artery with multiple sheaths followed by primary closure of the axillary artery at case completion. The aim of this study is to describe our technique and to report our results with this approach. METHODS: This study is a single-institution, retrospective review of 53 patients who were treated with parallel grafts for endovascular repair of PAA and TAAA from 2006 to 2018. The aortic repairs requiring LAE included: 9 cases of endo-leaks from prior endovascular repair, 20 TAAAs, and 24 PAAs. The axillary artery was exposed with a vertical axillary skin incision followed by retraction of the lateral border of the pectoralis major to expose the axillary artery distal to the pectoralis minor. A 5-French (F) through 12F sheaths were used to directly access the axillary artery for delivery of endovascular devices. RESULTS: Two hundred and sixty reno-visceral stents were delivered through 125 axillary sheaths in an antegrade fashion to 114 arteries without intraoperative complications or technical failures. Two postoperative complications included an access-site hematoma managed conservatively (1.9%) and a left brachial vein thrombosis treated with anticoagulation (1.9%). There were no cases of cerebrovascular or peripheral neurologic events, upper extremity ischemia, or reoperation related to LAE. CONCLUSIONS: LAE is a valid approach for upper extremity access during the endovascular repair of complex aortic aneurysms requiring simultaneous delivery of multiple reno-visceral devices. It does not require the use of a prosthetic conduit. There were no neurologic events or upper extremity ischemia in our series.

Professional fee payments by specialty for inpatient open ventral hernia repair: who gets paid for treating comorbidities and complications?

BACKGROUND: The purpose of this study was to determine perioperative professional fee payments to providers from different specialties for the care of patients undergoing inpatient open ventral hernia repair (VHR). METHODS: Perioperative data of patients undergoing VHR at a single center over 3 years were selected from our NSQIP database. 180-day follow-up data were obtained via retrospective review of records and phone calls to patients. Professional fee payments (PFPs) to all providers were obtained from our physician billing system for the VHR hospitalization, the 180 days prior to operation (180Prior) and the 180 days post-discharge (180Post). RESULTS: PFPs for 283 cases were analyzed. Average total 360-day PFPs per patient were $3409 ± SD 3294, with 14.5% ($493 ± 1546) for services in the 180Preop period, 72.5% ($2473 ± 1881) for the VHR hospitalization, and 13.0% ($443 ± 1097) in the 180Postop period. The surgical service received 62% of PFPs followed by anesthesia (18%), medical specialties (9%), radiology (6%), and all other provider services (5%). Medical specialties received increased PFPs for care of patients with COPD and HCT < 38% ($90 and $521, respectively) and for the pulmonary complications ($2471) and sepsis ($2714) that correlated with those patient comorbidities; surgeons did not. Operative duration, mesh size, and separation of components were associated with increased surgeon PFPs (p < .05). At 6 months, wound complications were associated with increased surgeon and radiology payments (p < .01). CONCLUSIONS: Management of acute comorbid conditions and the associated higher postoperative morbidity is not reimbursed to the surgeon under the 90-day global fee. These represent opportunity costs of care that pressure busy surgeons to select against these patients or to delegate more management to their medical specialty colleagues, thereby increasing total system costs. A comorbid risk adjustment of procedural reimbursement is warranted. In negotiating bundled payments, surgeon groups should keep in mind that surgeon reimbursement, unlike medical specialty and hospital reimbursement, have been bundled since the 1990s.

Autologous bone marrow mononuclear cells reduce therapeutic intensity for severe traumatic brain injury in children.

OBJECTIVES: The devastating effect of traumatic brain injury is exacerbated by an acute secondary neuroinflammatory response, clinically manifest as elevated intracranial pressure due to cerebral edema. The treatment effect of cell-based therapies in the acute post-traumatic brain injury period has not been clinically studied although preclinical data demonstrate that bone marrow-derived mononuclear cell infusion down-regulates the inflammatory response. Our study evaluates whether pediatric traumatic brain injury patients receiving IV autologous bone marrow-derived mononuclear cells within 48 hours of injury experienced a reduction in therapeutic intensity directed toward managing elevated intracranial pressure relative to matched controls. DESIGN: The study was a retrospective cohort design comparing pediatric patients in a phase I clinical trial treated with IV autologous bone marrow-derived mononuclear cells (n = 10) to a control group of age- and severity-matched children (n = 19). SETTING: The study setting was at Children's Memorial Hermann Hospital, an American College of Surgeons Level 1 Pediatric Trauma Center and teaching hospital for the University of Texas Health Science Center at Houston from 2000 to 2008. PATIENTS: Study patients were 5-14 years with postresuscitation Glasgow Coma Scale scores of 5-8. INTERVENTIONS: The treatment group received 6 million autologous bone marrow-derived mononuclear cells/kg body weight IV within 48 hours of injury. The control group was treated in an identical fashion, per standard of care, guided by our traumatic brain injury management protocol, derived from American Association of Neurological Surgeons guidelines. MEASUREMENTS AND MAIN RESULTS: The primary measure was the Pediatric Intensity Level of Therapy scale used to quantify treatment of elevated intracranial pressure. Secondary measures included the Pediatric Logistic Organ Dysfunction score and days of intracranial pressure monitoring as a surrogate for length of neurointensive care. A repeated-measure mixed model with marginal linear predictions identified a significant reduction in the Pediatric Intensity Level of Therapy score beginning at 24 hours posttreatment through week 1 (p < 0.05). This divergence was also reflected in the Pediatric Logistic Organ Dysfunction score following the first week. The duration of intracranial pressure monitoring was 8.2 ± 1.3 days in the treated group and 15.6 ± 3.5 days (p = 0.03) in the time-matched control group. CONCLUSIONS: IV autologous bone marrow-derived mononuclear cell therapy is associated with lower treatment intensity required to manage intracranial pressure, associated severity of organ injury, and duration of neurointensive care following severe traumatic brain injury. This may corroborate preclinical data that autologous bone marrow-derived mononuclear cell therapy attenuates the effects of inflammation in the early post-traumatic brain injury period.