Pediatric splanchnic arterial occlusive disease: clinical relevance and operative treatment.

OBJECTIVE: Splanchnic arterial occlusive disease is rare in childhood. The purpose of this study was to review the clinical relevance and operative treatment of these lesions in a unique experience from a single institution. METHODS: Seventeen children (11 boys and 6 girls) from 2 years to 17 years in age with critical narrowings of the celiac artery (CA) and superior mesenteric artery (SMA) underwent treatment at the University of Michigan from 1974 to 2000. Etiologic factors included embryologic fusion abnormalities of the fetal aortae during formation of the splanchnic arteries (n = 15), inflammatory aortoarteritis (n = 1), and radiation-induced arterial fibrosis (n = 1). Individual lesions included CA occlusions (n = 6) and stenoses (n = 7), SMA occlusions (n = 3) and stenoses (n = 11), and inferior mesenteric artery stenosis (n = 1). Fourteen children had abdominal aortic coarctations, and 15 had renal artery stenoses. Two patients had postprandial abdominal discomfort and food aversion, consistent with intestinal angina. Small stature affected five others, perhaps attributable to severe renovascular hypertension and failure to thrive. Ten children underwent intestinal revascularization, at the time of an aortoplasty or thoracoabdominal bypass for aortic coarctation (n = 7) or at the time of renal artery revascularization (n = 8). Primary splanchnic revascularization procedures included SMA-aortic implantation (n = 3), aorto-SMA and CA bypass with an internal iliac artery graft (n = 3) or a saphenous vein graft (n = 1), CA-aortic implantation at a stenotic SMA origin (n = 2), and CA and SMA intimectomy (n = 1). Secondary operations included SMA-aortic implantation (n = 2). RESULTS: All 10 children who underwent splanchnic revascularization have thrived, gained weight, and are free of abdominal pain, with follow-up periods averaging 9 years. No intestinal ischemic manifestations occurred in the seven children who did not undergo operation. CONCLUSION: Pediatric splanchnic arterial occlusive disease is a rare illness appropriately treated with operation in properly selected children.

Tissue loss, early primary graft occlusion, female gender, and a prohibitive failure rate of secondary infrainguinal arterial reconstruction.

PURPOSE: This study tested the hypothesis that a subset of secondary infrainguinal arterial reconstructions show prohibitive failure rates. METHODS: Records of 79 consecutive patients, 44 men and 35 women, with a mean age of 60 years, who underwent secondary infrainguinal bypass from 1992 to 2000 at the University of Michigan Hospital, were reviewed. Data were analyzed with life-table analysis, logistic regression, and descriptive statistics. RESULTS: Secondary infrainguinal reconstructions were performed in patients who had undergone earlier ipsilateral bypasses once (n = 35) or twice (n = 44). Among the prior procedures, 68% (n = 54) were done at an institution other than the authors'. Comorbidities included coronary artery disease (72%), tobacco use (77%), and diabetes mellitus (34%), but no patient had hemodialysis-dependent renal failure. Disabling claudication, with average ankle brachial index of 0.48, had been the indication for the primary operation in 77% of cases. Femoral-popliteal bypass was the primary procedure in 67%, with a prosthetic graft used in 62%. The mean patency duration of these earlier bypasses was 25 months. The indication for the final bypass was rest pain or tissue loss in 51% of patients, with an average ankle brachial index of 0.37. The most common procedure was a femoral-distal bypass with autologous vein (63%). Mean patency duration of the secondary bypasses was 30 months. Graft failure within 30 days of operation occurred in 22 patients (28%), and amputation was necessitated in 86% of these patients. The presence of rest pain or tissue loss, when accompanied with a history of early prior graft thrombosis in female patients, correlated with worse mean patency rates, recurrent graft failure (P

Cost of routine screening for carotid and lower extremity occlusive disease in patients with abdominal aortic aneurysms.

OBJECTIVE: The burden of clinically relevant noncoronary atherosclerotic occlusive disease in patients with abdominal aortic aneurysms (AAAs) is poorly defined. Furthermore, the cost-effectiveness of routine versus selective preoperative noninvasive examination of the carotid and lower extremity arterial beds has not been established in patients who undergo elective AAA repair. METHODS: Diagnostic vascular laboratory study results were reviewed in 206 patients who underwent evaluation before AAA repair from 1994 to 1998. The patients underwent routine preoperative carotid duplex scan examinations and lower extremity Doppler scan arterial studies with ankle-brachial index (ABI) determinations. The medical records were reviewed for the identification of clinical evidence consistent with cerebrovascular or lower extremity arterial occlusive disease. The costs of routine screening and selective screening were determined with Medicare reimbursement schedules. RESULTS: The prevalence rate of advanced (80% to 100%) carotid artery stenosis (CAS) was 3.4%, and 18% of the patients had CAS between 60% and 100%. Advanced peripheral vascular occlusive disease (PVOD; ABI, <0.3) was found in 3% of the patients, and 12% of the patients had an ABI of less than 0.6. Most patients with advanced CAS (71%) or advanced PVOD (83%) had clinical indications of their disease. The absence of clinical evidence of disease had a negative predictive value of 99% for both advanced CAS and PVOD. The cost of routine screening for all patients for advanced CAS was $5445 per case. Routine screening for severe PVOD costs were $3732 per case discovered. In contrast, the costs for selective screening for advanced CAS or PVOD in patients with appropriate history or symptoms were $1258 and $785 per case found, respectively. CONCLUSION: Routine noninvasive diagnostic testing for the identification of asymptomatic CAS and PVOD in patients with AAA may not be justified. Preoperative screening is more clearly indicated for patients with AAAs who have clinical evidence suggestive of CAS or PVOD.

Variation in death rate after abdominal aortic aneurysmectomy in the United States: impact of hospital volume, gender, and age.

OBJECTIVE: To determine whether high-volume hospitals (HVHs) have lower in-hospital death rates after abdominal aortic aneurysm (AAA) repair compared with low-volume hospitals (LVHs). SUMMARY BACKGROUND DATA: Select statewide studies have shown that HVHs have superior outcomes compared with LVHs for AAA repair, but they may not be representative of the true volume-outcome relationship for the entire United States. METHODS: Patients undergoing repair of intact or ruptured AAAs in the Nationwide Inpatient Sample (NIS) for 1996 and 1997 were included (n = 13,887) for study. The NIS represents a 20% stratified random sample representative of all U.S. hospitals. Unadjusted and case mix-adjusted analyses were performed. RESULTS: The overall death rate was 3.8% for intact AAA repair and 47% for ruptured AAA repair. For repair of intact AAAs, HVHs had a lower death rate than LVHs. The death rate after repair of ruptured AAA was also slightly lower at HVHs. In a multivariate analysis adjusting for case mix, having surgery at an LVH was associated with a 56% increased risk of in-hospital death. Other independent risk factors for in-hospital death included female gender, age older than 65 years, aneurysm rupture, urgent or emergent admission, and comorbid disease. CONCLUSIONS: This study from a representative national database documents that HVHs have a significantly lower death rate than LVHs for repair of both intact and ruptured AAA. These data support the regionalization of patients to HVHs for AAA repair.

Impaired vasoreactivity despite an increase in plasma nitrite in patients with abdominal aortic aneurysms.

OBJECTIVE: This investigation was designed to determine whether differences in vasoreactivity occur in patients with abdominal aortic aneurysms (AAAs) as compared with patients with peripheral arterial occlusive disease (PAOD) or individuals (controls) without known vascular disease. METHODS: Brachial artery vasoreactivity was assessed in a blinded fashion, after endothelium-dependent (ED) and endothelium-independent (EI) flow-mediated vasodilation, in age-matched, male patients with AAAs (n = 11) or PAOD (n = 9) or in controls (n = 10). There were no significant differences in prestudy systolic or diastolic blood pressure, body mass index, or antilipidemic medications among the groups studied. Exclusion criteria included diabetes and tobacco use within 3 months. Quantitative ultrasound scan measurements of brachial artery diameters were performed at rest and after either forearm ischemia (ED) or administration of 0.4 mg sublingual nitroglycerin (EI). Plasma nitric oxide (NO(X) = NO(2) + NO(3)) was measured with the Saville assay. Asymmetric dimethylarginine, an endogenous inhibitor of NO(X) synthase, was measured with liquid chromatography. RESULTS: Initial brachial artery diameters were not significantly different among the groups studied (4.85 +/- 0.18 mm for AAA group, 4.82 +/- 0.17 mm for PAOD group, 4.68 +/- 0.20 mm for controls). ED and EI vasodilation was significantly less (P =.02 and.03, respectively) in the AAA group (-1.71 +/- 1.52 and 8.33 +/- 1.13, respectively) when compared with the controls (2.96 +/- 1.04 and 13.88 +/- 2.16, respectively). However, plasma NO(X) was significantly increased (P =.01) in the AAA group (7.86 +/- 0.85 micromol/L) as compared with both controls (5.13 +/- 0.63 micromol/L) and PAOD (4.85 +/- 0.46 micromol/L). Asymmetric dimethylarginine levels were decreased in the AAA group (0.34 +/- 0.05 micromol/L) as compared with the PAOD group (0.46 +/- 0.09 micromol/L). No correlation existed between aneurysm size and ED or EI vasodilation or plasma NO(X). CONCLUSION: This study is the first to document a divergence between ED and EI vasoreactivity and systemic NO metabolites in patients with AAAs. It is speculated that a dysfunctional vessel wall response, rather than a lack of NO, may be important in the pathogenesis of AAAs.