James G. Reeves

Chest wall resections and reconstruction: a 25-year experience

BACKGROUND Chest wall defects continue to present a complicated treatment scenario for thoracic and reconstructive surgeons. The purpose of this study is to report our 25-year experience with chest wall resections and reconstructions. METHODS A retrospective review of 200 patients who had chest wall resections from 1975 to 2000 was performed. RESULTS Patient demographics included tobacco abuse, hypertension, diabetes mellitus, alcohol abuse, coronary artery disease, chronic obstructive pulmonary disease, and human immunodeficiency virus. Surgical indications included lung cancer, breast cancer, chest wall tumors, and severe pectus deformities. Twenty-nine patients had radiation necrosis and 31 patients had lung or chest wall infections. The mean number of ribs resected was 4 +/- 2 ribs. Fifty-six patients underwent sternal resections. In addition 14 patients underwent forequarter amputations. Immediate closure was performed in 195 patients whereas delayed closure was performed in 5 patients. Primary repair without the use of reconstructive techniques was possible in 43 patients. Synthetic chest wall reconstruction was performed using Prolene mesh, Marlex mesh, methyl methacrylate sandwich, Vicryl mesh, and polytetrafluoroethylene. Flaps utilized for soft tissue coverage were free flap (17 patients) and pedicled flap (96 patients). Mean postoperative length of stay was 14 +/- 14 days. Mean intensive care unit stay was 5 +/- 9 days. In-hospital and 30-day survival was 93%. CONCLUSIONS Chest wall resection with reconstruction utilizing synthetic mesh or local muscle flaps can be performed as a safe, effective one-stage surgical procedure for a variety of major chest wall defects.

Evidence that cardioprotection by postconditioning involves preservation of myocardial opioid content and selective opioid receptor activation

Opioids introduced at reperfusion (R) following ischemia (I) reduce infarct size much like postconditioning, suggesting the hypothesis that postconditioning increases cardiac opioids and activates local opioid receptors. Anesthetized male rats subjected to 30 min regional I and 3 h R were postconditioned with three cycles of 10 s R and 10 s reocclusion at onset of R. Naloxone (NL), its peripherally restricted analog naloxone methiodide, delta-opioid receptor (DOR) antagonist naltrindole (NTI), kappa-opioid receptor antagonist norbinaltorphimine (NorBNI), and mu-opioid receptor (MOR) antagonist H-D-Phe-Cys-Tyr-D-Trp-Arg-Thr-Pen-Thr-NH2 (CTAP) were administered intravenously 5 min before R. The area at risk (AAR) was comparable among groups, and postconditioning reduced infarct size from 57 +/- 2 to 42 +/- 2% (P < 0.05). None of the antagonists alone altered infarct size. All antagonists abrogated postconditioning protection at higher doses. However, blockade of infarct sparing by postconditioning was lost, since tested doses of NL, NTI, NorBNI, and CTAP were lowered. The efficacy of NorBNI declined first at 3.4 micromol/kg, followed sequentially by NTI (1.1), NL (0.37), and CTAP (0.09), suggesting likely MOR and perhaps DOR participation. Representative small, intermediate, and large enkephalins in the AAR were quantified (fmol/mg protein; mean +/- SE). I/R reduced proenkephalin (58 +/- 9 vs. 33 +/- 4; P < 0.05) and sum total of measured enkephalins, including proenkephalin, peptide B, methionine-enkephalin, and methionine-enkephalin-arginine-phenylalanine (139 +/- 17 vs. 104 +/- 7; P < 0.05) compared with shams. Postconditioning increased total enkephalins (89 +/- 8 vs. 135 +/- 5; P < 0.05) largely by increasing proenkephalin (33 +/- 4 vs. 96 +/- 7; P < 0.05). Thus the infarct-sparing effect of postconditioning appeared to involve endogenously activated MORs and possibly DORs, and preservation of enkephalin precursor synthesis in the AAR.

Inhibition of myocardial apoptosis by postconditioning is associated with attenuation of oxidative stress-mediated nuclear factor-κB translocation and TNFα release

ABSTRACT Oxidative stress-stimulated nuclear factor-κB (NF-κB) activation has been associated with rapid transcription of TNF-α and induction of apoptosis. This study tested the hypothesis that postconditioning (Postcon) reduces myocardial apoptosis and inhibits translocation of NF-κB and release of TNF-α secondary to an attenuation of oxidant generation during reperfusion. Anesthetized rats were subjected to 30 min of ischemia and 3 h of reperfusion and divided randomly to Control or Postcon (three cycles of 10-s reperfusion and 10-s reocclusion applied at the onset of reperfusion) group, respectively. Relative to Control, Postcon reduced the plasma malondialdehyde (1.21 ± 0.08 vs. 0.8 ± 0.06* μM/mL) and decreased the generation of superoxide radical in area at risk myocardium (dihydroethidium staining). Compared with Control, Postcon also inhibited translocation of NF-κB to nuclei (167% ± 21% vs. 142% ± 18%*), decreased the level of plasma TNF-α (1,994 ± 447 vs. 667 ± 130* pg/mL), and inhibited caspase-3 activity (0.57% ± 0.1% vs. 0.21% ± 0.1%*). The number of apoptotic cells (percent total nuclei) in ischemic myocardium was reduced (20% ± 1% vs. 11% ± 2%*), consistent with reduced appearance of DNA fragmentation. To support whether oxidant generation is important in the triggering of cytokine release and apoptosis, N-acetylcysteine (NAC), a potent antioxidant agent, was administered before ischemia and at reperfusion. Treatment with NAC inhibited superoxide radical generation and decreased plasma malondialdehyde to a comparable level to that in Postcon, concomitant with an inhibition of NF-κB expression (42% ± 8%*) and reduction of release of TNF-α (231 ± 72* pg/mL). Caspase-3 activity (0.33% ± 0.1%*) and apoptotic cells (12% ± 1%*) were also comparably reduced by NAC. These data suggest that Postcon attenuates myocardial apoptosis, reduces caspase-3 activity, and is potentially mediated by inhibiting oxidant-activated NF-κB-TNF-α signaling pathway. *P < 0.05 Postcon and NAC vs. Control.

Long-term inhibition of myocardial infarction by postconditioning during reperfusion.

AbstractCardioprotection with postconditioning has been well demonstrated after a short period of reperfusion. This study tested the hypothesis that postconditioning reduces infarct size, vascular dysfunction, and neutrophil accumulation after a long-term reperfusion. Canines undergoing 60 min left anterior descending artery (LAD) occlusion were divided into two control groups of either 3 h or 24 h of full reperfusion and two postconditioning groups with three 30 s cycles of reperfusion and re-occlusion applied at the onset of either 3 h or 24 h of reperfusion. Size of the area at risk (AAR) and collateral blood flow during ischemia were similar among groups. In controls, infarct size as percentage of the AAR (30 ± 3 vs. 39 ± 2* %) by TTC staining, superoxide anion generation from the post-ischemic coronary arteries by lucigenin-enhanced chemiluminescence [(89 ± 5 vs. 236 ± 27* relative light units (RLU/mg)], and neutrophil (PMN) accumulation by immunohistochemical staining in the AAR (52 ± 11 vs. 84 ± 14* cells/mm2 myocardium) significantly increased between 3 and 24 h of reperfusion. Postconditioning reduced infarct size (15 ± 4† and 27 ± 3.6† %), superoxide anion generation (24 ± 4† and 43 ± 11† RLU/mg), and PMN accumulation (19 ± 6† and 45 ± 8† cells/mm2 myocardium) in the 3 and 24 h reperfusion groups relative to time-matched controls. These data suggest that myocardial injury increases with duration of reperfusion; reduction in infarct size and attenuation in inflammatory responses with postconditioning persist after a prolonged reperfusion. * p < 0.05 24 vs. 3 h control; † p < 0.05 postconditioning vs. time-matched control.

The incidence of microemboli to the brain is less with endarterectomy than with percutaneous revascularization with distal filters or flow reversal.

BACKGROUND Current data suggest microembolization to the brain may result in long-term cognitive dysfunction despite the absence of immediate clinically obvious cerebrovascular events. We reviewed a series of patients treated electively with carotid endarterectomy (CEA), carotid artery stenting (CAS) with distal filters, and carotid stenting with flow reversal (FRS) monitored continuously with transcranial Doppler scan (TCD) during the procedure to detect microembolization rates. METHODS TCD insonation of the M1 segment of the middle cerebral artery was conducted during 42 procedures (15 CEA, 20 CAS, and 7 FRS) in 41 patients seen at an academic center. One patient had staged bilateral CEA. Ipsilateral microembolic signals (MESs) were divided into three phases: preprotection phase (until internal carotid artery [ICA] cross-shunted or clamped if no shunt was used, filter deployed, or flow reversal established), protection phase (until clamp/shunt was removed, filter removed, or antegrade flow re-established), and postprotection phase (after clamp/shunt was removed, filter removed, or antegrade flow re-established). Descriptive statistics are reported as mean ± SE for continuous variables and N (%) for categorical variables. Differences in ipsilateral emboli counts based on cerebral protection strategy were assessed using nonparametric methods. RESULTS TCD insonation and procedural success were obtained in 33 procedures (79%; 14 CEA, 14 CAS, and 5 FRS). Highest ipsilateral MESs were observed for CAS (319.3 ± 110.3), followed by FRS (184.2 ± 110.5), and CEA (15.3 ± 22.0). Pairwise comparisons revealed significantly higher ipsilateral MESs with both FRS and CAS when compared to CEA (P = .007 for FRS and P < .001 for CAS vs CEA, respectively), whereas the difference in MESs between FRS and CAS was not significant (P = .053). Periods of maximum embolization were postprotection phase for CEA, protection phase for CAS, and preprotection phase for FRS. Preprotection MESs were frequently observed during both CAS and FRS (20.4% and 63.3% of total MESs across all phases, respectively), and the primary difference between these two methods seemed to be related to lower MESs during the protection phase with FRS. CONCLUSION CEA is associated with lower rates of microembolization compared with carotid stenting. Flow reversal may represent a procedural modification with potential to reduce microembolization during carotid stenting; further investigation is warranted to determine the relationship between cerebral protection strategies and outcomes associated with carotid stenting.

Characterization of resident surgeon participation during carotid endarterectomy and impact on perioperative outcomes

INTRODUCTION The impact of resident surgeon participation during vascular procedures on postoperative outcomes is incompletely understood. We characterized resident physician participation during carotid endarterectomy (CEA) procedures within the 2005-2009 American College of Surgeons National Surgical Quality Improvement Participant Use Datafile and evaluated associations with procedural characteristics and perioperative adverse events. METHODS CEAs were identified using primary current procedural terminology codes; those performed simultaneously with other major procedures or unknown resident participation status were excluded. Group-wise comparisons based on resident participation status were performed using χ(2) or Fishers exact test for categorical variables and t tests or nonparametric methods for continuous variables. Associations with perioperative adverse events (major = stroke, death, myocardial infarction, or cardiac arrest; minor = peripheral nerve injury, bleeding requiring transfusion, surgical site infection, or wound disruption) were assessed using multivariable logistic regression models adjusting for other known risk factors. RESULTS A total of 25,280 CEA procedures were analyzed, of which residents participated in 13,705 (54.2%), while residents were absent in 11,575 (45.8%). Among CEAs with resident physician participation, resident level was categorized as junior (postgraduate year [PGY] 1-2) in 21.9%, senior (PGY 3-5) in 52.7%, and fellow (PGY ≥6) in 25.3%. Major adverse event rates with and without resident participation were 1.9% versus 2.1%, and minor adverse event rates with and without resident participation were 0.9% versus 1.0%, respectively. In multivariable models, resident physician participation was not associated with perioperative risk for major adverse events (odds ratio [OR], 0.90; 95% confidence interval [CI], 0.75-1.08) or minor adverse events (OR, 0.93; 95% CI, 0.72-1.21). CONCLUSIONS Resident surgeon participation during CEA is not associated with risk of adverse perioperative events.

Early outcomes and perioperative risk assessment in elective open thoracoabdominal aortic aneurysm repair: An analysis of national data over a five-year period

Open surgical repair of thoracoabdominal aortic aneurysms remains associated with significant morbidity and mortality. We sought to analyse multicentre national data on early outcomes of open surgical thoracoabdominal aortic aneurysm repair. Patients who underwent open repair of thoracoabdominal aortic aneurysm from 2005 to 2010 were identified from the National Surgical Quality Improvement Program database. The primary endpoint was mortality at 30 days. Patient demographics, clinical variables, and intraoperative parameters were analysed by univariate and multivariate logistic regression methods to identify risk factors for mortality. Of the 682 elective repairs, 30-day outcomes of elective repairs were: 10.0% mortality, 21.6% surgical complications, 42.2% pulmonary complications, 17.2% renal complications, 12.9% cardiovascular complications, 19.2% septic complications, and 6.6% wound complications. Multivariate logistic regression analysis showed that age, ASA-class IV, dependent functional status prior to surgery, and operation time are independent risk factors for mortality. Our study found a higher rate of mortality nationwide, as compared to several previous single center studies.

Endovascular Management of a Ruptured Thoracoabdominal Aneurysm—Damage Control With Superior Mesenteric Artery Snorkel and Thoracic Stent-Graft Exclusion

We report a case of a large ruptured thoracoabdominal aortic aneurysm, which was stabilized with endovascular aortic exclusion and snorkel bypass of the superior mesenteric artery (SMA). An 80-year-old African American woman with multiple medical comorbidities and previous open infrarenal abdominal aortic aneurysm repair presented with a ruptured 10.7 × 7.3 cm thoracoabdominal aortic aneurysm involving the origins of the renal and mesenteric vessels. The patient underwent emergent endovascular aortic repair with placement of a covered stent into the SMA coursing parallel to the aortic endograft. This technique was initially successful in clinically stabilizing the patient; however; 3 weeks after the initial procedure, she presented with recurrent rupture necessitating proximal extension of her snorkeled SMA bypass and aortic endograft into the mid-descending thoracic aorta. The patient stabilized and was successfully discharged home.

Late Gore Excluder endoprosthesis fabric tear leading to abdominal aortic aneurysm rupture 5 years after initial implant

Endoprosthesis fabric tear leading to abdominal aortic aneurysm rupture is a rare event. In this report, we describe a patient who presented with an abdominal aortic aneurysm rupture after a tear in the fabric of the Gore Excluder endoprosthesis (W. L. Gore and Associationes, Flagstaff, Ariz) 5 years after implantation. The reason for the fabric tear was unknown. The complication was successfully treated by relining the endograft with an aortic cuff and two iliac limbs. The patient experienced an uneventful recovery after the intervention.

Anatomic Characteristics of Aortic Transection: Centerline Analysis to Facilitate Graft Selection

BACKGROUND Traumatic transection of the thoracic aorta is a life-threatening complication that most commonly occurs after high-speed motor vehicle collisions. Although such injuries were previously treated with open surgical reconstruction, they are now more commonly being treated with endovascularly placed stent grafts. Unfortunately, most stent grafts are designed for treating aortic aneurysmal disease instead of traumatic injury. Further refinements in stent graft technology depend on a thorough anatomic understanding of the transection injury process. METHODS All patients with computed tomography (CT) evidence of blunt aortic injury (BAI) between 2006 and 2012 at a Level 1 trauma center were queried. Their initial CT scans were imported into the Intuition (Terarecon, Inc.) viewing program, and off-line centerline reconstruction was performed. Standard demographic data were collected in addition to anatomic characteristics, including aortic diameters and the relationship of the injury to the arch vessels. RESULTS Thirty-five patients were identified. Three patients were injured proximal to the left subclavian artery. The average length from the left subclavian artery to the proximal site of injury was 16.2 mm (range 2-31 mm). Most patients had >15 mm of landing zone beyond the left subclavian artery. The range of proximal diameters ranged from 17 to 32 mm, with an average aortic diameter of 23.9 mm. The average length of injured aortic segment was 27 mm. CONCLUSIONS In this contemporary series from a large trauma center, 91% of patients are anatomically able to be treated with a stent graft that does not require coverage of the left common carotid artery. Most patients have an aortic diameter that falls between 21 and 26 mm in diameter, as well as a short segment of injured artery. Centers interested in emergently treating aortic transections are able to do so while maintaining a limited stock of stent grafts that can be used to treat the majority of the population.