Cerebral monitoring with transcranial Doppler ultrasonography improves neurologic outcome during repairs of acute type A aortic dissection

OBJECTIVE: Neurologic complications after repair of acute type A aortic dissection remain significant. The use of power M-mode transcranial Doppler monitoring to verify cerebral blood flow during these repairs might decrease cerebral ischemia by correcting malperfusion. The purpose of this study was to analyze the use of power M-mode transcranial Doppler monitoring during repairs of acute type A dissection with regard to neurologic outcome. METHODS: We performed a prospective study of patients undergoing repairs of acute type A aortic dissection. Repairs included profound hypothermic circulatory arrest and retrograde cerebral perfusion. Patients in whom transcranial Doppler monitoring was used to monitor cerebral blood flow and modify operative technique during repair (study group) were compared with those without monitoring and modification (control group). RESULTS: Between September 2001 and October 2003, we repaired 56 cases of acute type A dissection. Power M-mode transcranial Doppler monitoring was used in 50% (28/56) of cases. Power M-mode transcranial Doppler monitoring altered operative cannulation and guided retrograde cerebral perfusion flow in 28.5% (8/28) and 78.6% (22/28) of cases, respectively. Two patients presented with preoperative stroke, one in each group. One operative death occurred in each group. In-hospital mortality and the occurrence of new stroke were not significantly different between the 2 groups. Temporary neurologic dysfunction occurred less often in the study group (14.8% [4/27] vs 51.8% [14/27], P = .008). CONCLUSIONS: Identification of cerebral malperfusion requires cerebral monitoring. By ensuring cerebral blood flow by using power M-mode transcranial Doppler monitoring and correcting cerebral malperfusion by modifying operative technique, neurologic outcome was improved during repairs of acute type A aortic dissection.     

Anatomic evaluation and relationship between the lumbar pedicle and adjacent neural structures: an anatomic study

OBJECTIVE: Transpedicular spinal fixation has recently been the focus of increased attention in several institutions throughout the world, but its safety and efficacy are still important questions for orthopedic surgeons. Accurate screwing through the pedicle will avoid neurologic complications and increase the stability of the instrumentation. In this study, it was aimed to analyze the anatomic relations quantitatively between the lumbar pedicle and the adjacent dural sac and nerve roots, to determine the risky areas for neural injury during transpedicular screw placement. METHODS: Ten adult cadavers were used for observation of the lumbar pedicle and its relations. After removal of the laminas and facets, the lumbar pedicles, dural sac, and nerve roots were exposed. Interpedicular distance (IPD), pedicle-inferior nerve root distance (PIRD), pedicle-superior nerve root distance (PSRD), and pedicle-dural sac distance (PDSD) were measured. RESULTS: Average distance from the lumbar pedicle to the dural sac medially and to the adjacent nerve roots superiorly and inferiorly through the cranial to caudal lumbar levels ranged from 1.29 to 1.56, from 4.12 to 5.52, and from 1.10 to 1.06 mm, respectively. The mean IPD ranged from 32.77 to 41.24 mm. There were statistically significant differences between the L5 level and other lumbar levels for IPD, PSRD, and PDSD measurements. CONCLUSIONS: These results indicate that although L5 is safer than other lumbar levels for pedicle screw insertion, an improper medial and caudal placement of a pedicular screw will carry a great risk of injury to the dural sac and inferior nerve root.     

Determinants of early and late outcome for reoperations of the proximal aorta

Background

The purpose of this study was to investigate the cause of ascending aorta and aortic arch reoperations and to identify determinants of early and late outcome.

Methods

Between January 1991 and March 2003 we repaired aneurysms of the proximal aorta in 597 patients. Of these patients, 104 had reoperations for replacement of the ascending aorta, aortic root, or transverse aortic arch. Previous surgery was defined as any previous cardiac or proximal aortic repair. Median age was 60 years, and 29 of the patients (28%) were female. Indications for reoperation and replacement of the proximal aorta included acute type A dissection in 6 patients (5.8%), aneurysm with chronic dissection in 60 (57.7%), progression of aneurysm in 23 (22.1%), infection in 12 (1.5%), inflammatory disease in 2 (1.9%), and atheromatous disease in 1 (1.0%). Reoperations included aortic root replacement in 20 patients (19.2%), total arch replacement with elephant trunk in 28 (26.7%), ascending and proximal arch in 39 (37.5%), and ascending aorta in 27 (26.0%). The median interval between operations was 69 months. Retrograde cerebral perfusion was used in 80 (77%) cases.

Results

Chronic dissection was the most common indicator for reoperation in our population, followed by progression of aneurysm and infection. Thirty-day and in-hospital mortality was 13.5% (14 of 104) and 15.4% (16 of 104), respectively. Chronic obstructive pulmonary disease, renal dysfunction, and increased pump time were risk factors for mortality. Median follow-up was 5.02 years. Eight patients died during that period. Estimated survival at 1, 5, and 10 years was 83%, 80%, and 62%, respectively. Freedom from second proximal reoperations was 97.1% (10 of 104). Freedom from subsequent distal thoracic aortic repair was 84.6% (8 of 104).

Conclusions

Reoperations of the ascending aorta and aortic arch can be performed safely with good long-term results. Patients with previous proximal aortic dissection repair need long-term surveillance. Renal dysfunction and chronic obstructive pulmonary disease must be carefully considered before reoperations of the proximal aorta.     

Multi-organ inflammation after hepatic cryoablation in BALB/c mice

BACKGROUND: There is increasing evidence that injury to the liver can precipitate or exaggerate lung injury. We have previously shown that hepatic cryoablation (cryo) causes activation of nuclear factor (NF)-kappaB, cytokinemia (tumor necrosis factor-alpha, Mouse Macrophage Inflammatory Protein-2 [MIP-2]), and lung inflammation in transgenic HLL (5'HIV-LTR-Luciferase gene) mice and in Sprague-Dawley rats. It has been reported that BALB/c mice are susceptible to traumatic injury and are active immune responders. We tested whether activation of NF-kappaB and the development of multiple-organ inflammation in response to hepatic injury from 35% cryo were demonstrable in the BALB/c mouse. METHODS: BALB/c mice (n = 9) were anesthetized, and midline laparotomy was performed. Cryoablation was performed with careful isolation of adjacent structures to avoid inadvertent organ injury to the gastrointestinal tract. A freeze-thaw cycle of the left lobe of the liver was induced, encompassing approximately 35% (by weight). Animals were sacrificed at 1, 2, 4, and 24 h after cryoablation. Serum was collected via IVC puncture and liver, lungs, and kidneys were harvested and freeze-clamped. Two animals were sacrificed without undergoing cryo surgery to serve as a baseline control. NF-kappaB activity was monitored by electrophoretic mobility shift assays. MIP-2 levels and Mouse KC levels from tissue and serum were measured using enzyme-linked immunosorbent assay. Organs were submitted for histological review. We characterized lung inflammation induced by cryosurgery by measuring total and differential cell counts in lung lavage fluid 4 h after hepatic cryoablation. RESULTS: After cryo, NF-kappaB activation was demonstrated in the 1, 2, and 4-h time points by electrophoretic mobility shift assay in the liver and lungs. Mouse KC and MIP-2 levels increased from baseline, peaked at the 4-h time point, and returned to baseline after 24 h in both liver and lung. Lung lavage 4 h after cryoablation showed increased total cells and neutrophilic lung inflammation. CONCLUSIONS: BALB/c mice demonstrate evidence of multi-organ inflammation in response to 35% hepatic cryo. These data demonstrate that this model provides for assessment of liver-mediated multi-system inflammation after direct liver injury.     

Regional hypothermia reduces mucosal NF-kappaB and PMN priming via gut lymph during canine mesenteric ischemia/reperfusion

BACKGROUND: Mesenteric ischemia/reperfusion (I/R) activates pro-inflammatory mediators that exacerbate gut reperfusion injury and prime circulating neutrophils that cause remote organ injury. We have shown that regional intraischemic hypothermia protects the intestinal mucosa during I/R in rats. In this study, we examined the effects of regional hypothermia on I/R-induced transvascular protein clearance, NF-kappaB DNA binding activity, and polymorphonuclear neutrophil (PMN) priming via gut lymph in a canine mesenteric lymphatic fistula model. MATERIALS AND METHODS: Conditioned dogs underwent 60 min of mesenteric ischemia, with or without regional intraischemic hypothermia, and 3 h reperfusion. A mesenteric lymphatic fistula model was used to measure transvascular protein clearance and harvest lymph. Biopsies of distal ileum were obtained at baseline and 0, 180 min of reperfusion for NF-kappaB DNA binding activity using electrophoretic mobility shift assay (EMSA). A kinetic spectrophotometric assay was used to determine fMLP stimulated PMN superoxide production after priming by gut lymph obtained at baseline and 180 min reperfusion. RESULTS: Transvascular protein clearance increased during reperfusion compared to baseline, and hypothermia had no significant effect on this I/R-induced protein clearance. NF-kappaB activity increased three-fold at the end of ischemia and hypothermia prevented this early activation. PMN superoxide production increased 19-fold during I/R (0.06 +/- 0.04 versus 1.14 +/- 0.50 nmol O(2), P < 0.05), but only 2.5-fold during I/R + hypothermia (0.28 +/- 0.09 versus 0.70 +/- 0.32 nmol O(2), P = 0.2). CONCLUSIONS: Regional intraischemic hypothermia prevented early intestinal NF-kappaB activation, partially abrogated PMN priming via gut lymph, but had no significant effect on increased transvascular protein clearance during mesenteric I/R in dogs.     

Preoperative and operative predictors of delayed neurologic deficit following repair of thoracoabdominal aortic aneurysm

PURPOSE: Delayed neurologic deficit has been recognized in recent years as a source of morbidity following thoracic and thoracoabdominal aortic repair. We wanted to find risk factors specifically significant for delayed neurologic deficit. In this initial study we looked at preoperative and operative risk factors. METHODS: We performed 854 thoracoabdominal aortic repairs between February 1991 and May 2001. For this study we excluded 26 patients who died before postoperative neurologic status could be evaluated and 38 who had immediate neurologic deficit on initial postoperative evaluation, leaving 790 consecutive patients. We evaluated a wide range of demographic, preoperative physiological and intraoperative data, using univariate and multivariable statistical analyses. RESULTS: Twenty-one of 790 (2.7%) patients had delayed neurologic deficit. Significant univariate predictors included preoperative renal dysfunction (odds ratio 5.9; P <.006), acute dissection (odds ratio 3.9; P <.05), extent II thoracoabdominal aorta (odds ratio 3.0; P <.03), and use of adjuncts (cerebrospinal fluid drainage and distal aortic perfusion; odds ratio 7.7; P <.03). The use of the adjuncts dropped from the multivariable model but all other factors remained. No other significant risk factors were identified. Twelve of 21 (57%) patients recovered neurologic function with optimization of blood pressure and cerebrospinal fluid drainage. CONCLUSION: Preoperative renal dysfunction, acute dissection, and extent II thoracoabdominal aorta are significant predictors of delayed neurologic deficit. Previous studies have demonstrated that the use of adjuncts protects against immediate neurologic deficit. The findings of this study are consistent with the hypothesis that adjuncts reduce ischemic insult enough to prevent immediate neurologic deficit but that a period of increased spinal cord vulnerability persists several days postoperatively.     

Postoperative risk factors for delayed neurologic deficit after thoracic and thoracoabdominal aortic aneurysm repair: a case-control study

OBJECTIVE: Delayed neurologic deficit after thoracoabdominal or thoracic aortic repair is an unusual complication. We previously examined the preoperative risk factors associated with immediate neurologic deficit to consider their relationship to delayed neurologic deficit. In the current study we wanted to determine whether postoperative events influence the likelihood of delayed neurologic deficit, independent of preoperative risk factors. METHODS: We studied postoperative hemodynamics and cerebrospinal fluid (CSF) drain function in patients who had delayed neurologic deficit (cases) and those who did not (controls). Our database contains data for 854 patients with descending thoracic and thoracoabdominal aortic aneurysm. Cases and controls were identified with a random number generator to select controls in an approximate 4:1 ratio. We identified 18 cases and 67 controls. Further data were obtained from medical records. RESULTS: We found no differences between the groups with regard to oxygen transport abnormalities, eg, pneumothorax, repeat intubation, cardiac arrest, atrial or ventricular dysrhythmia, or dialysis. Significant differences between the groups were present for CSF drain complications (eg, kinks, blood in CSF): 6 of 18 (33%) in the case group versus 3 of 67 (4.5%) in the control group (P <.003). Wide fluctuation in mean arterial pressure (MAP) was significant (P <.02), mainly because of very low MAP in the cases (P <.006). When odds ratio was adjusted for preoperative risk factors of extent II thoracoabdominal aortic aneurysm, acute aortic dissection, and chronic aortic dissection, MAP less than 60 mm Hg and CSF drain complications produced the highest odds of delayed neurologic deficit. CONCLUSION: No single risk factor explained the onset of delayed deficit. Rather, a combination of factors, especially lowest MAP and drain complications, produced the highest odds of deficit. Vigilant optimization of hemodynamics and immediate correction of CSF drain malfunction may prevent development of delayed neurologic deficit.     

Use of high‐frequency vibrational energy in the treatment of peripheral chronic total occlusions

Purpose: Peripheral chronic total occlusions (CTO) are challenging lesions to treat. The CROSSER system (FlowCardia, Sunnyvale, CA) uses high‐frequency low‐amplitude vibrations to break through the cap of the CTO and had been shown to be successful in coronary CTOs. This is a case series demonstrating the use of the CROSSER system with peripheral CTOs. Case Reports: Three patients with peripheral CTO of various lengths, locations, and complexities were treated with the CROSSER system. The device allowed placement of a guidewire across the area of occlusion, thus permitting further percutaneous intervention. The CROSSER system was effective with both ostial and distal lesions, tapered and abrupt lesion morphologies, and was used from both an ipsilateral (antegrade access) and contralateral approach. Conclusion: The CROSSER system is an additional device that may be used to treat peripheral CTOs. © 2009 Wiley‐Liss, Inc.