The real cost of treating venous ulcers in a contemporary vascular practice.

BACKGROUND: Venous leg ulcers (VLUs) are a prevalent and morbid disease that consumes considerable health care resources. Estimates place the total costs for treatment of VLU at 1% of health care budgets in many industrialized countries. Unfortunately, there is little contemporary information on the total cost of treating VLU in the United States, particularly in a wound center staffed by vascular specialists. The purpose of this study was to define the actual cost of treating VLU and to identify factors influencing costs. METHODS: A cohort of 84 patients with active VLU (Clinical, Etiologic, Anatomic, and Pathologic class 6 disease) who were treated in a wound center by five vascular surgeons with a minimum follow-up of 6 months (median, 368 days; range, 336-483 days) was retrospectively studied. Actual costs (not charges) were obtained for outpatient and inpatient facility, visiting nurse services, and our physician practice group to yield true cost. The proportion of healed VLUs and time to complete healing were determined to calculate time to healing as well as ulcer-free intervals. Calculations of cost/ulcer-free days and cost to complete healing for the entire follow-up period were carried out as well as univariate analysis of factors affecting cost. RESULTS: The mean total cost of treating VLU during this follow-up period was $15,732. A total of 50 patients (60%) healed their VLUs without recurrence in a mean time of 122 days (range, 6-379 days) at a cost of $10,563 (range, $430-$50,967). This translated to $86/day of treatment to heal an ulcer, resulting in a cost of $42/ulcer-free day. In comparison, the total cost was threefold higher at $33,907 (range, $390-$132,730) for the patients (n = 17; 20%) who did not heal their VLUs. Significant contributing factors included outpatient facility fees ($10,332) and visiting nurse services ($11,365) related to extended treatment of the open VLU. Patients who had a recurrence of their VLU (n = 17; 20%) during the follow-up period had a total cost of $12,760. Inpatient admission for wound-related issues increased total cost to $33,629. Nearly two thirds of admissions were for treatment of cellulitis with intravenous antibiotics. VLUs treated with surgical intervention did not significantly increase total cost ($12,304 vs $19,503; P > .05) but significantly reduced recurrence rates (34% vs 5%). There were three outliers who experienced complications after treatment of outflow obstruction that dramatically increased the total cost to $71,526. CONCLUSIONS: This economic analysis demonstrates the high true costs associated with modern treatment of VLU by aggressive medical and surgical techniques. Inpatient and outpatient facility fees, physician fees, and visiting nurse payments all contribute to the cumulative tally that results in these staggering direct costs for treatment of VLUs. The daily cost of treatment that accrues for the ongoing care of VLU patients until they are healed provides an economic rationale for initiatives that advance approaches seeking to provide more rapid wound healing. Our analysis also highlights the significant costs associated with treatment of infections and complications encountered in aggressive surgical interventions for patients with extensive chronic central venous occlusive disease. More aggressive early outpatient treatment of infections and refined criteria for selection of outflow stenting candidates may reduce total cost by preventing complications while improving outcomes.

Headache and mitochondrial disorders.

We report on 2 patients who have a mitochondrial myopathy, encephalopathy, lactic acidosis, and recurrent cerebral insults that resemble strokes (MELAS). These 2, and 9 other, reported patients share the following features: ragged red fibers evident on muscle biopsy, normal early development, short stature, seizures, and hemiparesis, hemianopia, or cortical blindness. Lactic acidemia is a common finding. We believe that MELAS represents a distinctive syndrome and that it can be differentiated from 2 other clinical disorders that also are associated with mitochondrial myopathy and cerebral disease: Kearns-Sayre syndrome and the myoclonus epilepsy ragged red fiber syndrome. Existing information suggests that MELAS is transmitted by maternal inheritance. The ragged red fibers suggest an abnormality of the electron transport system, but the precise biochemical disorders in these 3 clinical syndromes remain to be elucidated.

"Unpredictable" late rupture of an abdominal aortic aneurysm after bifurcated Ancure endograft repair.

The goal of endovascular repair of an abdominal aortic aneurysm is to exclude the aneurysm from systemic arterial pressure, thereby preventing rupture. However, the long-term durability of endovascular repair continues to be in question, as aneurysm rupture after endovascular repair continues to be reported. We report the case of an 89-year-old patient who underwent endovascular repair of a 7.1-cm abdominal aortic aneurysm with an Ancure endograft 5 years earlier. Despite close follow-up and a shrinking aneurysm sac on annual contrast-enhanced computed tomography, he presented with aneurysm rupture and a new proximal type I endoleak. The endoleak and rupture were successfully repaired with endovascular placement of a main body extension.

Lactate and oxygen constitute a fundamental regulatory mechanism in wound healing.

For many years, lactate has been known to accelerate collagen deposition in cultured fibroblasts and, without detailed explanation, has been presumed to stimulate angiogenesis. Similarly, hypoxia has been linked to angiogenic effects and collagen deposition from cultured cells. Paradoxically, however, wound angiogenesis and collagen deposition are increased by breathing oxygen and decreased by hypoxia. Lactate accumulates to 4-12 mM in wounds for several reasons, only one of which is the result of hypoxia. Oxygen in wounds is usually low but can be increased by breathing oxygen (without change in lactate). We have reported that lactate elicits vascular endothelial growth factor (VECF) from macrophages, as well as collagen, some heat shock proteins, and VECF from endothelial cells, and collagen from fibroblasts, even in the presence of normal amounts of oxygen. Hypoxia exerts many of these same effects in cultured cells. In this study, we elevated extracellular lactate in wounds by implanting purified solid-state, hydrolysable polyglycolide. A steady-state 2-3 mM additional elevation of lactate resulted. With it, there was a significant short-term elevation of interleukin-1beta, a long-term elevation of VECF (2x) and transforming growth factor-beta1 (2-3x), a 50% elevation in collagen deposition, and a large reduction of insulin-like growth factor-1 (- 90%). We propose that lactate induces a biochemical "perception" of hypoxia and instigates several signals that activate growth factor/cytokine signals while the continued presence of molecular oxygen allows endothelial cells and fibroblasts to reproduce and deposit collagen. The data are consistent with ADP-ribosylation effects and oxidant signaling. (WOUND REP REG 2003;11:504-509)