Endovascular stent grafts for acute blunt aortic injury.

BACKGROUND: Endovascular stent grafting (EVSG) has emerged as a new treatment for aortic disease and has recently been applied to the treatment of acute blunt aortic injury (BAI). The purpose of this study was to determine the outcome of EVSG for patients with BAI at two tertiary (Level I) trauma centers. METHODS: A retrospective review of patients treated between January 1, 1999, and February 1, 2003, at two centers, Calgary Health Region (Calgary, Alberta) and Harborview Medical Center (Seattle, WA), with EVSG for acute BAI is reported. Variables assessed included age, sex, Injury Severity Score, total length of stay (LOS), intensive care unit LOS, operative technique, complications, technical success, mortality, and follow-up data. RESULTS: Twenty-eight patients treated with EVSG for BAI were identified during this period. Twelve patients were excluded because injuries occurred more than 30 days before grafting (n = 7) or under a different protocol (n = 4), or the procedure was performed in a different center (n = 1). Sixteen patients with acute BAI were reviewed. The mean Injury Severity Score was 36.9 (SD, 17.0), with a median intensive care unit LOS of 7.5 days (interquartile range, 1-17 days) and total LOS of 24.5 days (interquartile range, 7-41 days). Mean follow-up was 10.7 months (range, 3-30 months). Technical success was achieved in all patients, no graft-related complications have been detected during follow-up, and no patient developed postoperative paraplegia. One postoperative mortality occurred secondary to severe comorbid injury. A single patient with a preoperative traumatic carotid dissection demonstrated a postoperative stroke, and one patient required thoracentesis for a pleural effusion. CONCLUSION: Repair of BAI with EVSG can be performed safely in patients with BAI. Mortality, morbidity, and especially paraplegia are reduced. Further long-term studies are required to support the routine use of EVSG technology for BAI.

Life-table analysis of primary and assisted success following endoluminal repair of abdominal aortic aneurysms: the role of supplementary endovascular intervention in improving outcome.

AIM: the aim of this study was to analyse the effect of supplementary endovascular intervention on the outcome of primary endoluminal repair of abdominal aortic aneurysm (AAA). METHODS: between May 1992 and December 1998, 266 patients underwent endoluminal repair of AAA. Minimum period of follow-up was 6 months. Those patients in whom the endoprosthesis could not be deployed were converted to open repair at the primary operation. Patients developing an early endoleak, within 31 days, were treated by a period of observation and secondary endovascular intervention in persistent cases. Patients developing a late endoleak were treated similarly, without a period of observation. Outcome was analysed by the life-table method. Primary success was defined as exclusion of the aneurysm from the circulation resulting from the original operation. Assisted success occurred when aneurysms with endoleaks became excluded from the circulation as a result of supplementary endovascular intervention. RESULTS: endoluminal repair failed in 17 patients requiring conversion to open repair at the original operation. Supplementary endovascular intervention was undertaken in 26 patients, with early endoleaks (n=6) and late endoleaks (n=20). Interventions involved deployment of secondary endoluminal grafts within the primary grafts (n=22), and coil embolisation (n=4). Successful exclusion of the aneurysm sac was achieved in 22 of 26 (85%) patients undergoing supplementary endovascular procedures. Conditional cumulative incidence of primary graft failure and secondary graft failure in the presence of all-cause mortality at 6 years was 47% and 25% respectively. CONCLUSIONS: supplementary endovascular intervention is an important adjunct to endoluminal AAA repair with the potential to improve outcome and avoid conversion to open repair. Successful supplementary endovascular intervention was achieved in 85% of patients in whom it was attempted. Life-table analysis showed these supplementary procedures to be durable in the long term.

Endotension: an explanation for continued AAA growth after successful endoluminal repair.

PURPOSE: To present and analyze several cases that illustrate persistent sac pressurization following endovascular abdominal aortic aneurysm (AAA) repair. METHODS AND RESULTS: Four patients with successful endovascular AAA exclusion presented in follow-up with an expanding aneurysm. Two had initial sac diameter decrease, but by 18 and 24 months, respectively, the AAA had enlarged and become pulsatile. There was no endoleak evident, but the proximal attachment stents had mig rated distally in both cases. One patient developed endoleak with aneurysm expansion at 6 months; contained rupture occurred at 12 months. The last case had slowly evolving aneurysm expansion over 36 months but no endoleak. All endografts were removed and successfully replaced with conventional grafts. Intrasac thrombus was implicated as the means of pressure transmission that precipitated AAA expansion in these cases. CONCLUSIONS: Excluded AAAs can increase in size owing to persistent or recurrent pressurization (endotension) of the sac even when there is no evidence of endoleak. One proposed mechanism is pressure transmission via thrombus that lines the attachment site. Endotension may also represent an indiscernible, very low flow endoleak that allows blood to clot at the source of leakage.

Plasma activation of neutrophil CD18 after skeletal muscle ischemia: a potential mechanism for late systemic injury.

Reperfusion of acutely ischemic skeletal muscle is associated with neutrophil activation, which may augment local injury or cause damage to distant organs. Polymorphonuclear neutrophil glycoprotein CD18 plays a role in this injury, since its blockade substantially reduces damage; however, its mechanisms of control during reperfusion are poorly understood. The purpose of this study was to investigate the importance of circulating plasma factors to CD18-dependent neutrophil function during reperfusion and to relate these to quantitative expression of CD18. Eight rabbits were subjected to hindlimb ischemia for 5 h, followed by 48 h of reperfusion. Plasma collected at seven intervals was incubated with unstimulated neutrophils from uninjured rabbits. CD18-specific neutrophil activation was evaluated by quantifying adherence to protein-coated polystyrene and by measuring oxidant production, detected by chemiluminescence after exposure to complement-opsonized zymosan. CD18 was quantified cytofluorometrically. Plasma collected at end ischemia and during early reperfusion affected no significant alterations of adhesion, oxidant production, or CD18. Late reperfusion plasma (between 8 and 48 h) significantly increased adherence and oxidant production (to 4.11 +/- 0.61 and 2.60 +/- 0.32 times the values of preischemic plasma, P < 0.006). Peak adherence, oxidant production, and CD18 expression were evoked synchronously by 24 h plasma. CD18 expression increased only at 24 h and did not increase proportional to increases in adherence and oxidant production. Control plasma (nonischemic, n = 5) elicited no significant differences of any inflammatory measure during sham ischemia or reperfusion. These results indicate that endogenous mediators may evoke a progressive systemic inflammatory response after ischemia by stimulating CD18-dependent neutrophil function in a delayed but prolonged manner.

Determinants of ischemic injury to skeletal muscle.

PURPOSE: Ischemic injuries to the lower extremity are often graded in severity according to their duration. Other determinants may also influence the extent of an injury, however, and may be equally significant contributors to the final outcome. The purpose of this study was to compare the relative influences of ischemic time, temperature, residual blood flow, muscle location, and fiber type on postischemic necrosis in a rabbit model of skeletal muscle ischemia-reperfusion injury. METHODS: Animals' hindlimbs were rendered ischemic under differing conditions of each determinant and then reperfused for 48 hours. Necrosis in the rectus femoris, semimembranosus, anterior tibial, and soleus muscles was determined by nitroblue tetrazolium staining and computerized planimetry. The severity of each animal's injury was quantified by calculating the cumulative percentage of necrosis by weight of all muscles excised from the ischemic limb. RESULTS: Four hours of ischemia at room temperature resulted in an average of 21% +/- 7% necrosis. Lengthening the ischemic interval to 5 hours increased necrosis to 61% +/- 4% (p < 0.01 vs 4 hours); however injuries were equally or more significantly influenced by changes in ischemic temperature or small changes in ischemic limb residual (collateral) blood flow. The most severe injuries of any encountered were observed when limbs were maintained at body temperature during ischemia (92% +/- 9% necrosis after 5 hours of ischemia, p < 0.01 vs room temperature ischemia), whereas extremely small improvements in ischemic period residual flow (by allowing pelvic collateral cross-flow during ischemia) resulted in significant salvage in all muscles studied. Muscles predominating in fast-twitch fibers had significantly greater necrosis than did those richer in slow-twitch fibers; this difference was apparent only after longer periods (5 hours) of ischemia. Thigh muscles sustained significantly greater injuries than did distal hindlimb muscles, except in animals subjected to body temperature ischemia, where the distribution of necrosis was uniform. CONCLUSIONS: The results of this study indicate that muscle necrosis accompanying an ischemic event can be significantly influenced by numerous determinants in addition to ischemic time, each of which warrants careful clinical scrutiny when appraising the extent of an injury.

A clinically relevant small-animal model of skeletal muscle ischemia-reperfusion injury.

Animal models of skeletal muscle ischemia-reperfusion injury have led to a better understanding of the pathophysiology of this condition and are necessary for the evaluation of potential therapeutics. This study presents a new, well-controlled model of ischemia-reperfusion that more accurately simulates acute arterial occlusions in humans. In rabbits, a whole hindlimb is rendered reversibly ischemic by occlusion of primary and collateral arterial inflow and then reperfused for an extended period of 48 h. Ischemic injuries are standardized by defining and controlling ischemic time, limb temperature, and the extent of collateral circulation. We have characterized this model by measuring anterior tibial and soleus muscle necrosis and edema formation in groups of animals subjected to 4 h of ischemia at either 32 or 36 degrees C, with one of two extents of collateralization and with or without muscle compartment release (fasciotomy). Our results indicate the following: (1) muscle necrosis is significantly worsened by restricting the extent of collateral blood supply or by elevating ischemic temperature; (2) anterior tibial muscle is inherently more sensitive than soleus muscle to ischemic injury; (3) fasciotomy may reduce muscle necrosis by more than 50%; and (4) the amount of edema present in muscles is an unreliable indicator of actual muscle necrosis. We conclude that this new model is a practical, well-controlled, and clinically relevant preparation useful for the investigation of ischemic muscle injury.

Salvage of postischemic skeletal muscle by monoclonal antibody blockade of neutrophil adhesion molecule CD18.

Reperfusion of ischemic skeletal muscle is associated with neutrophil (PMN) adherence to damaged endothelium and PMN-mediated tissue destruction. Neutrophils may attach to endothelium through surface adhesive molecules, such as CD18. The purpose of this study was to determine whether monoclonal antibody blockade of CD18 would reduce skeletal muscle necrosis associated with ischemia and reperfusion. In rabbits, an entire hindlimb was rendered ischemic for 4 hr, followed by 48 hr of in vivo reperfusion. Animals were allocated to one of five treatment groups: ischemia/reperfusion without treatment (I/R controls), I/R plus treatment with the anti-CD18 antibody IB4 (end-ischemic 2 mg/kg dose), I/R plus treatment with an identical dose of isotype-matched control Ig, I/R plus anterior compartment fasciotomy, or I/R plus both IB4 and fasciotomy. After 48 hr of reperfusion anterior tibial muscle necrosis was assessed (by tetrazolium staining and computerized planimetry), wet:dry muscle weights (W:D) were determined, and muscle PMN sequestration was measured by myeloperoxidase (MPO) activity. IB4-treated animals exhibited markedly reduced muscle MPO activity, compared to untreated animals. Although all interventions reduced edema formation (W:D ratios), none did so significantly. IB4 treatment reduced muscle necrosis when used alone (to 28 +/- 7%, vs. 48% +/- 6% in untreated controls), however this was not statistically significant (P = 0.06).2+ Fasciotomy significantly reduced necrosis (to 22 +/- 2%, P < 0.05); however, the addition of IB4 to fasciotomy resulted in necrosis that was significantly lower than that after fasciotomy alone (12 +/- 4%, P < 0.05 vs fasciotomy group) and the least necrosis of any group.(ABSTRACT TRUNCATED AT 250 WORDS)

Sartorius myoplasty in the treatment of exposed arterial grafts.

The long-term success of sartorius myoplasty in 14 of 16 patients who presented with an exposed vascular graft in an infected groin is described. The presenting complications were wound dehiscence (ten patients), hemorrhage (two), skin erosion (two), late bilateral fistulas (one) and false aneurysm (one). Ten grafts were prosthetic and six autogenous. Positive cultures were obtained from 15 wounds; four grew Staphylococcus epidermidis, the remainder mixed or Gram-negative bacteria. Each groin was radically debrided, including the surface of the arterial graft, and, if possible, closed immediately with a sartorius myoplasty applied directly to the graft. Twist, fan and loop myoplasties were equally effective. Grossly infected wounds were debrided initially and obviously infected grafts were replaced in situ before myoplasty. Sartorius myoplasty is recommended as an elegant solution for the infected groin in which there is an exposed arterial graft.

Sartorius myoplasty for deep groin wounds following vascular reconstruction.

Groin wound infections following vascular reconstructive surgery prolong hospital admission and convalescence and may lead to more serious morbidity with prosthetic graft infection, false aneurysm formation, or hemorrhage. Therefore, it is imperative to achieve wound closure as expeditiously as possible. Herein, we describe 11 patients with complicated groin wounds and report our management using sartorius myoplasty. Five of these patients had underlying prosthetic grafts at risk. All patients underwent wound closure with sartorius myoplasty after adequate debridement of necrotic and infected soft tissue. Success of wound closure with complete primary healing was observed in nine patients, while in two, adequate early coverage of femoral vessels was achieved, but extended wound care for superficial skin separation was necessary with eventual complete healing. There was no morbidity or mortality related to the added surgical procedure. One patient underwent late repair of a femoral false aneurysm. There were no other complications seen after an average follow-up of 20 months (range: 6 to 49 months). In summary, we recommend that sartorius myoplasty be considered for wound infections to hasten groin closure, decrease hospital stay, and reduce the chance of infectious complications.