Complication Of Thoracic Aortic Surgery Research Articles

Expanding perigraft seroma after ascending aorta replacement

BackgroundPerigraft seroma is a persistent and sterile fluid confined within a fibrous pseudomembrane surrounding a graft that develops after graft replacement. Development of perigraft seroma is an uncommon complication that occurs after the surgical repair of the thoracic aorta using woven polyester grafts. mechanism underlying perigraft seroma formation remains unclear.Case presentationHerein, we describe the case of 77-year-old man who underwent repeat sternotomy for the treatment of large perigraft seroma 1 year after ascending aorta replacement for acute type A dissection. After removing a cloudy yellow fluid, we covered the prosthetic graft with fibrin glue and wrapped it with a new graft. Bacterial culture and laboratory examination of the fluid confirmed the final diagnosis of perigraft seroma, and there was no evidence of recurrence. The area in which fluid accumulated around the graft shrunk 1 year after surgery.ConclusionsThe cause of a expanding perigraft after repair of the thoracic aorta remains unknown. Physicians should be aware that chronic expanding mediastinal seroma with Dacron grafts is one of the rare postoperative complications of thoracic aortic surgery. Applying fibrin glue to the graft surface might effectively prevent the recurrence of perigraft seroma.

Management of Aortic Replacement-Induced Chylothorax by Lipiodol Lymphography

Chylothorax is a rare but serious complication of thoracic aortic surgery, leading to malnutrition, respiratory insufficiency, and prolonged hospital stay. In this article, we describe the successful treatment of a case of intractable chylothorax by lipiodol lymphography. The patient was a 39-year-old man who underwent descending aortic replacement for a remaining dissected aneurysm after total arch replacement. Chylothorax developed postoperatively. After complete oral intake cessation, total parenteral nutrition, and plasmatic factor XIII administration, lipiodol lymphography detected the chyle leakage location and subsequently decreased pleural effusion. The patient recovered uneventfully and was discharged on postoperative day 30 without any complications.

Predictors of Outcome in Patients with Spinal Cord Ischemia after Open Aortic Repair

Spinal cord ischemia is a potentially devastating complication of thoracic aortic surgery. However, predictors of outcome have not been well characterized. The study objective was to generate a prognostic score that accurately stratifies patient outcomes, aiding in future management and planning. A retrospective review of 224 consecutive open thoracic aortic surgeries identified patients with spinal cord ischemia, defined as changes on intraoperative somatosensory evoked potentials (SSEP) and/or paraparesis/paraplegia postoperatively. The outcome of interest was poor outcome, defined as death or discharge with a lower extremity motor score ≤40, indicating impaired ambulation. Demographic and clinical characteristics were tested in univariate analyses and significant factors were incorporated in multivariate modeling to determine independent predictors of poor outcome. Seventy-five patients were identified with spinal cord ischemia, of which 43(57 %) had poor outcomes including 28(37 %) that died prior to discharge. Factors associated with poor outcome in univariate analysis included absent lumbar CSF drain (p = 0.03), surgical repair that crossed the diaphragm (p = 0.002), permanent intraoperative SSEP change (p = 0.02), postoperative renal failure (p = 0.004), paraplegia (p = 0.001), and concomitant stroke (p = 0.04). In multivariable analysis, surgical repair crossing the diaphragm (OR 4.8, CI 1.4-16.7, p = 0.02), paraplegia (OR 4.5, CI 1.4-14.0, p = 0.01), and renal failure (OR 6.1, CI 1.7-21.2, p = 0.005) were independently associated with poor outcome. Patients with transient intraoperative neurophysiologic changes were least likely to have poor outcome when compared to patients with no or permanent SSEP changes, and those not monitored (p = 0.03). Development of spinal cord ischemia with thoracic aortic repair often leads to death or disability. Characteristics known at the time of event can accurately predict the likelihood of poor outcome.

The Evolution of Chemokine Release Supports a Bimodal Mechanism of Spinal Cord Ischemia and Reperfusion Injury

Paraplegia remains a devastating complication of thoracic aortic surgery. The mechanism of the antecedent spinal cord ischemia and reperfusion injury (IR) remains poorly described. IR involves 2 injuries, an initial ischemic insult and subsequent inflammatory amplification of the injury. This mechanism is consistent with the clinical phenomenon of delayed onset paraplegia. This study sought to characterize the inflammatory response in the spinal cord after IR and hypothesized that this would support a bimodal mechanism of injury. Male C57Bl/6 mice were subjected to 5 minutes of aortic arch and left subclavian occlusion with subsequent reperfusion to generate spinal cord ischemia. Functional outcomes were scored at 12-hour intervals. Spinal cords were harvested after 0, 6, 12, 18, 24, 36, and 48 hours of reperfusion. Cytokine levels were analyzed using a mouse magnetic bead-based multiplex immunoassay. Inflammatory chemokine concentrations (interleukin [IL]-1β, IL-6, keratinocyte-derived cytokine, macrophage inflammatory protein-1α, monocyte chemotactic protein-1, RANTES, and tumor necrosis factor-α) peaked at 6 hours and 36 to 48 hours after reperfusion. Functional scores reflected initial gain in function with subsequent decline, inversely proportional to cytokine levels. Immunofluorescent staining demonstrated microglia activation at 12 and 48 hours. Spinal cord ischemia and reperfusion injury occurs in 2 phases, correlating to increases in inflammatory chemokines release and microglial activation. These observations chronologically parallel the too-common clinical syndrome of delayed-onset paraplegia. Understanding the molecular pathogenesis of this injury may allow future intervention to prevent this devastating complication.

Regarding “Civilini E, Bertoglio L, Melissano G, Chiesa R. Aortic and Esophageal Endografting for Secondary Aortoenteric Fistula. Eur J Vasc Endovasc Surg 2008;36(3):297–9”

We read with great interest the report of an interesting case of endovascular stent-graft management of a secondary aorto-oesophageal fistula.1Civilini E. Bertoglio L. Melissano G. Chiesa R. Aortic and esophageal endografting for secondary aortoenteric fistula.Eur J Vasc Endovasc Surg. 2008; 36: 297-299Google Scholar In this case, apart from gastrointestinal haemorrhage, the patient presented with systemic signs of sepsis. Because the patient was deemed high risk for open surgical repair, and in the setting of haemodynamic instability, we corroborated his urgent management with the less invasive endovascular treatment. Consequently, as there was evidence of persistent leak from the oesophageal lumen into the peri-aortic structures, deployment of a stent-graft within the oesophagus was undertaken, along with percutaneous drainage of the peri-graft collection. Microbiology of the drained fluid revealed positive cultures. However, scepticism exists regarding the placement of a prosthetic material in an already infected field, and the possibility of persistent/recurrent infection with often devastating consequences remains a concern.2Burks Jr., J.A. Faries P.L. Gravereaux E.C. Hollier L.H. Marin M.L. Endovascular repair of bleeding aortoenteric fistulas: a 5-year experience.J Vasc Surg. 2001; 34: 1055-1059Google Scholar In a systematic review conducted at our institution, aiming to assess the factors associated with poor outcome after endovascular stent-graft treatment of aorto-enteric fistula, it was found that evidence of sepsis preoperatively was a strong factor indicating poor outcome (P<0.05), despite the interruption of the aorto-enteric communication.3Antoniou G.A. Koutsias S. Antoniou S.A. Georgiakakis A. Lazarides M.K. Giannoukas A.D. Outcome after endovascular stent graft repair of aorto-enteric fistula: a systematic review.J Vasc Surg. Nov 21, 2008; https://doi.org/10.1016/j.jvs.2008.08.068Google Scholar Therefore, we strongly advocate that endovascular repair of the aorto-oesophageal fistula should be a bridge to open surgical repair, when optimisation of the patient's condition has been achieved. Aortic and Esophageal Endografting for Secondary Aortoenteric FistulaEuropean Journal of Vascular and Endovascular SurgeryVol. 36Issue 3PreviewThe aorto-esophageal fistula is a well-recognized and potentially fatal complication of thoracic aortic surgery. Several strategies regarding its prevention and subsequent management have been described. We report the management of a large midthoracic fistula complicating redo thoraco-abdominal aortic surgery by the placement of covered stents in the aorta and esophagus to successfully exclude the lesion. While long term durability is uncertain, endografts and long-term antibiotics provide a therapeutic option for palliation in patients unfit for immediate surgery. Full-Text PDF Open ArchiveResponse to Letter to the editor re: ‘Aortic and Oesophageal Endografting for Secondary Aorto-enteric Fistula’European Journal of Vascular and Endovascular SurgeryVol. 37Issue 5PreviewWe appreciate the opportunity to reply to the letter from G.A. Antoniou and A.D. Giannoukas, which raises important issues. We agree that endovascular repair is an emergency bailout procedure to stabilise the patients, improving survival after delayed open surgery. We are pleased to update this case report 16 months after the endoluminal life-saving procedure was performed. At 5 months, the recovery of the patient was satisfactory; however, he stopped the antibiotic therapy 1 month later for reasons that are not clear and soon the fever returned. Full-Text PDF Open Archive

Aortic and Esophageal Endografting for Secondary Aortoenteric Fistula

The aorto-esophageal fistula is a well-recognized and potentially fatal complication of thoracic aortic surgery. Several strategies regarding its prevention and subsequent management have been described. We report the management of a large midthoracic fistula complicating redo thoraco-abdominal aortic surgery by the placement of covered stents in the aorta and esophagus to successfully exclude the lesion. While long term durability is uncertain, endografts and long-term antibiotics provide a therapeutic option for palliation in patients unfit for immediate surgery.

Management of Neurologic Complications of Thoracic Aortic Surgery

Neurologic complications of thoracic aortic surgery are strongly associated with increased morbidity and mortality. Identifying preoperative risk factors for neurologic injury may enable us to refine our perioperative approach, and to lessen or avoid these complications. Methods to identify stroke and spinal ischemia intraoperatively such as neurophysiologic monitoring may enable us to improve outcomes in these patients by immediately instituting measures to improve brain and spine perfusion. The development of both protocols and therapies to treat these complications has allowed us to mitigate and, at times, reverse neurologic injury both intraoperatively and postoperatively.

Comparison of Systemic and Retrograde Delivery of Adenosine A 2A Agonist for Attenuation of Spinal Cord Injury After Thoracic Aortic Cross-Clamping

Paraplegia remains a devastating complication of thoracic aortic surgery, which has been attenuated by retrograde adenosine and systemic adenosine A2A receptor activation. We hypothesized that despite retrograde spinal perfusion of an adenosine A2A agonist (ATL-146e), systemic therapy produces superior spinal cord protection with reduced inflammation. Forty pigs underwent 30-minute thoracic aortic cross-clamping. Pigs received: no therapy (control); retrograde saline (retrograde control); retrograde ATL-146e; systemic ATL-146e; systemic ATL-146e with retrograde saline; or systemic and retrograde ATL-146e. Retrograde therapies were given during ischemia. Systemic ATL-146e (0.06 microg.kg(-1).min(-1)) was given intravenously for 3 hours at reperfusion. At 24 hours, motor function was assessed using the Tarlov scale. Tissue was analyzed for neuronal viability, microtubule-associated protein-2 expression, and neutrophil sequestration (myeloperoxidase activity). Four pigs received retrograde barium showing both radiographic and histologic spinal cord perfusion. Tarlov scores at 24 hours were significantly improved versus both control groups in all ATL groups except the combined ATL-146e group (all p < 0.05). Neuronal viability by hematoxylin and eosin stain was significantly preserved in systemic ATL groups compared with both control groups (all p < 0.05). Microtubule-associated protein-2 expression was significantly preserved compared with both control groups in all systemic ATL groups. Systemic ATL significantly lowered myeloperoxidase activity versus both control groups (p < 0.01). Both retrograde and systemic ATL-146e therapies attenuate ischemic spinal cord injury, but combining the two routes was less effective. Given comparable results between the two routes and the simplicity of systemic delivery, peripheral venous ATL-146e at reperfusion should be preferred for spinal cord protection in thoracic aortic surgery.

Brown-Séquard Syndrome Following Removal of a Cerebrospinal Fluid Drainage Catheter After Thoracic Aortic Surgery

Neurological deficit remains a devastating complication of thoracic aortic surgery despite advances in methods to protect the spinal cord from ischemia. Various techniques have been used, including the combination of cerebrospinal fluid (CSF) drainage and distal aortic perfusion to decrease the incidence of postoperative neurological deficit. These deficits are usually bilateral and result in paraplegia. In this case report we present a patient with Type B aortic dissection and thoracoabdominal aortic aneurysm repair with insertion of a lumbar CSF drainage catheter. Postoperatively, the patient developed unilateral neurological features consistent with Brown-Séquard syndrome after removal of the CSF catheter. The lumbar cerebrospinal fluid catheter was reinserted and the CSF was drained. Medullary T6-7 signal abnormalities were seen on spinal cord magnetic resonance imaging, and we suggest that the spinal cord suffered a direct injury during catheter removal. The patient had an uneventful recovery. We describe a patient who developed unilateral neurologic features suggestive of Brown-Sequard syndrome following removal of a cerebrospinal fluid catheter after thoracic aortic surgery. We suggest that the spinal cord was injured during catheter removal. The catheter was reinserted and the patient had a full neurologic recovery.

Intrathecal gene delivery of glial cell line-derived neurotrophic factor ameliorated paraplegia in rats after spinal ischemia

Paraplegia is a catastrophic complication of thoracic aortic surgery. At present, there is no effective mean to prevent the ischemia-induced spinal cord trauma. Gene delivery of neurotrophic factors may hold promises for prevention of spinal injury. In the present study, we evaluated the effect of glial cell line-derived neurotrophic factor (GDNF) gene delivery on prevention of the pathological changes due to spinal ischemia. Recombinant adenovirus vectors encoding GDNF (Ad-GDNF) and green fluorescent protein (Ad-GFP) were used for gene transfer studies. Treatment with cobalt chloride induced dose-dependent bcl-2 and synaptophysin downregulation in spinal neuronal cells, which could be effectively reversed by GDNF gene transfer. Intrathecal injection of Ad-GDNF led to maximal GDNF expression in spinal cord within 2–7 days. Thus, after intrathecal administration of adenovirus vectors for 3 days, Sprague–Dawley rats received transient aortic occlusion to induce spinal ischemia and were monitored for behavior deficits. The Ad-GDNF-treated rats showed significantly lower paraplegia rate (40%) than that of Ad-GFP- or saline-treated groups (75–85%; P < 0.01). In addition, the Ad-GDNF-treated rats exhibited significantly improved locomotor function comparing with rats of control groups ( P < 0.001). Histological analysis revealed that GDNF gene delivery profoundly attenuated the infiltration of leukocytes in spinal cord after ischemic insults. Furthermore, GDNF gene delivery prominently attenuated the ischemia-induced neuronal loss in dorsal horn lamina VI–VIII and reduction in synaptophysin expression in spinal cords. In conclusion, GDNF gene transfer confers protection to the neuronal cells and synapses networks, thereby alleviated the paraplegia due to spinal ischemia.

Retrograde venous perfusion with hypothermic saline and adenosine for protection of the ischemic spinal cord

Purpose: Spinal cord injury and the resultant postoperative paraplegia are devastating complications of thoracic aortic surgery, for which no widely accepted protective interventions exist. We hypothesized that retrograde venous perfusion-cooling of the spinal cord with a hypothermic saline and adenosine solution would protect it from ischemic injury caused by thoracic aortic occlusion. Methods: Adult domestic swine of either sex (weight range, 20 to 30 kg) were intubated and ventilated. A left thoracotomy was performed. The accessory hemiazygous vein was divided, and a catheter was inserted distally. The aorta was clamped at the left subclavian artery. The venous catheter was not used in the animals in the control group (n = 7); in the animals in the experimental group (n = 7), a cold (4°C) saline and adenosine solution was infused into the accessory hemiazygous vein. After 30 minutes, the clamp and catheter were removed, and the chest was closed. A blinded observer evaluated the animals' hind-leg motor activity 24 hours later. The Tarlov scale was used: 0, complete paralysis; 1, minimal movement; 2, stands with assistance; 3, stands alone; 4, weak walk; 5, normal gait. The animals' rectal temperatures were measured at the end of the experiment, and blood pressure was measured throughout. Two other groups were studied to assess the effect of the intervention on spinal cord temperature. Results: The animals in the control group had a mean Tarlov score of 1.7 ± 0.6; the animals in the experimental group had a mean Tarlov score of 4.9 ± 0.1 (P <.01). The animals in the experimental group had a significantly greater drop in spinal cord temperature than those in the control group (4.05 ± 0.6°C vs 0.58 ± 0.12°C; P <.01). No significant difference in rectal temperatures was found, nor did any arrhythmias or hypotensive episodes occur in either group. Perfusion of the spinal cord was confirmed with angiography by using this approach. Conclusion: Retrograde venous perfusion-cooling of the spinal cord with a hypothermic saline and adenosine solution protects the cord from ischemic injury caused by clamping of the thoracic aorta. (J Vasc Surg 2000;32:171-8.)

Risk factors for acute postoperative renal failure in thoracic or thoracoabdominal aortic surgery: a prospective study.

Acute postoperative renal failure is a common complication of thoracic aorta, thoracoabdominal aorta, or aortic arch surgery. To identify variables associated with acute postoperative renal failure, we prospectively studied 475 consecutive patients undergoing thoracoabdominal aortic surgery over a 12-yr period, including those requiring emergent surgery. One hundred twenty-one (25%) patients developed acute postoperative renal failure, and 39 (8%) required hemodialysis. Using multivariate analysis, acute postoperative renal failure was significantly associated with the following variables: age >50 yr (odds ratio [OR] 2.90 [95% confidence interval 1.52-5.53]), preoperative serum creatinine >120 micromol/L (OR 2.76 [1.70-4.48]), duration of left kidney ischemia >30 min (OR 2.01 [1.27-3.17]), packed red cells administration >5 units (OR 2.04 [1.24-3.37]), and Cell-Saver administration >5 units (OR 2.31 [1.34-1.96]). Reimplantation of visceral, renal arteries and the Adamkievicz artery; duration of visceral, spinal, and right kidney ischemia; requirement for fresh frozen plasma; administration of aprotinin; extracorporeal circulation; and procedures with circulatory arrest and profound hypothermia were not predictive of postoperative renal failure. In addition, age >50 yr (OR 5.59 [1.31-23.91]), requirement for packed red blood cells >5 unit (OR 3.91 [1.58-9.67]), and preoperative serum creatinine concentration >120 micromol/L (OR 2.26 [1.13-4.53]) were independent factors for acute renal failure requiring hemodialysis. In conclusion, acute renal failure is often observed after thoracic aortic surgery. Numerous predictive factors must be considered when evaluating the etiology of this complication. Acute postoperative renal insufficiency is a common complication of thoracic aortic surgery. This study found that age >50 yr, preoperative renal dysfunction, duration of renal ischemia, and amount of blood transfusion are significant predictors of this complication.