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Venous thromboembolic disease remains a particularly common source of morbidity in hospitalized patients and is considered one of the most common preventable causes of hospital death, accounting for 50–75,000 of the 200,000 venous thromboembolic (VTE) deaths per year in the USA [1]. The principal determinant of VTE risk seems to be the patient’s indication for hospitalization; hence, all studies of this risk have been based upon comparison of different groups based on a group risk assignment. Moreover, most thrombophylaxis trials have employed venous imaging and invasive venograms as a marker for DVT, rather than symptoms, duplex findings, pulmonary embolism (PE), or fatal PE. The goal of thrombophylaxis in patients undergoing any type of surgery must therefore be to accurately assess DVT risk, understand the types and benefit of therapy, and balance the benefit of prophylaxis with the associated risk of complications, namely, bleeding.

The vascular system is comprised of three major sets of vessels: arteries, veins, and lymphatics. In this chapter, we address disorders of each vascular network. In particular, we discuss peripheral vascular disease, deep vein thrombosis, and lymphedema. We explain the treatment for each disorder, both traditional interventions and surgeries and new, cutting-edge techniques like lymph node transfer and lymphaticovenous anastomosis.

Importance Because of the similarity in clinical outcomes after elective open and endovascular repair of abdominal aortic aneurysm (AAA), cost may be an important factor in choosing a procedure. Objective To compare total and AAA-related use of health care services, costs, and cost-effectiveness between groups randomized to open or endovascular repair. Design, Setting, and Participants This unblinded randomized clinical trial enrolled 881 patients undergoing planned elective repair of AAA who were candidates for open and endovascular repair procedures. Patients were randomized from October 15, 2002, to April 15, 2008, at 42 Veterans Affairs medical centers. Follow-up was completed on October 15, 2011, and data were analyzed from April 15, 2013, to April 15, 2016, based on intention to treat. Main Outcomes and Measures Mean total and AAA-related health care cost per life-year and per quality-adjusted life-year (QALY). Results A total of 881 patients (876 men [99.4%]; 5 women [0.6%]; mean [SD] age, 70 [7.8] years) were included in the analysis. After a mean of 5.2 years of follow-up, mean life-years were 4.89 in the endovascular group and 4.84 in the open repair group ( P = .68), and mean QALYs were 3.72 in the endovascular group and 3.70 in the open repair group ( P = .82). Total mean health care costs did not differ significantly between the 2 groups (endovascular group, $142 745; open repair group, $153 533; difference, −$10 788; 95% CI, −$29 796 to $5825; P = .25). Costs related to AAA, including the initial repair, constituted nearly 40% of total costs and did not differ significantly between the 2 groups (endovascular group, $57 501; open repair group, $57 893; difference, −$393; 95% CI, −$12 071 to $7928; P = .94). Lower costs due to shorter hospitalization for initial endovascular repair were offset by increased costs from AAA-related secondary procedures and imaging studies. The probability of endovascular repair being less costly and more effective was 56.8% when effectiveness was measured in life-years and 55.4% when effectiveness was measured in QALYs for total costs and 31.3% and 34.3%, respectively, for AAA-related costs. Conclusions and Relevance In this multicenter randomized clinical trial with follow-up to 9 years, survival, quality of life, costs, and cost-effectiveness did not differ between elective open and endovascular repair of AAA. Trial Registration clinicaltrials.gov Identifier:NCT00094575

Background/Purpose: If the goal of partial liquid ventilation (PLV) with perfluorocarbons in the management of respiratory failure is to improve dynamic lung compliance (C dyn ) and pulmonary vascular resistance (PVR) while sustaing O 2 delivery, the optimal ventilatory management is unclear. The authors asked if volume-cycled or pressure-limited ventilation had different effects on PVR, cardiac index (CI), and C dyn in uninjured and injured neonatal piglet lungs. Methods: Anesthetized piglets (6 to 8 kg) were ventilated after tracheostomy. C dyn was measured by in-line Fleisch pneumotach/PC data acquisition terminal. Thermodilution instrumentation allowed determination of both Cl and PVR. Volume-control or pressure-limited ventilation was established in uninjured or injured (surfactant deficiency induced by saline lavage at 18 mL/kg) animals. After a stable 30-minute baseline, animals were assigned randomly to one of four groups: group I (n = 9), uninjured animals plus volume-cycled ventilation (intermittent mandatory ventilation [IMV], 10 bpm; tidal volume [TV], 15 mL/kg, positive end-expiratory pressure [PEEP], 5 cm H 2 O; Fio 2 , 1.0; and PLV for 150 minutes); group II (n = 9), uninjured animals plus pressure-limited ventilation (IMV, 10 bpm; peak inspiratory pressure (PIP), 25 cm H 2 O, PEEP, 5 cm H 2 O, Fio 2 , 1.0; and PLV for 150 minutes); group III (n = 7), injured animals plus volume-cycled ventilation (IMV, 10 bpm; TV, 15 mL/kg; PEEP, 5 cm H 2 O; Fio 2 , 1.0 for 30 minutes, followed by saline injury for 30 minutes, followed by PLV rescue for 120 minutes); group IV (n = 7), injured animals plus pressure-limited ventilation (IMV, 10 bpm; PIP, 25 cm H 2 O; PEEP, 5 cm H 2 O; Fio 2 , 1.0 for 30 minutes, followed by saline injury, and PLV rescue). Comparison within and between groups was accomplished by repeated measures analysis of variance (ANOVA) with Tukey correction. Results: There was no significant difference between volumecycled or pressure-limited ventilation in healthy lungs; however, in the setting of lung injury, dynamic compliance was 1.44 ± 0.15 after 180 minutes in the volume-cycled group and 0.91 ± 0.10 in the pressure-limited group after the same interval (mL/cm H 2 O · kg ± SEM). Similarly, PVR was 100 ± 6 in the volume-cycled group and 145 ± 12 in the pressurelimited group after 180 minutes of lung injury (mm Hg/L/kg · min ± SEM). Cardiac index declined significantly in all groups independent of ventilatory mode. Conclusions: These results suggest that in the setting of lung injury, C dyn and PVR improved significantly when volume-cycled, compared with pressure-limited ventilation was used. Although no difference existed between ventilatory modes in healthy lungs, pressure-limited ventilation, when combined with PLV in injured lungs, had adverse effects on lung compliance and pulmonary vascular resistance. Volume-cycled ventilation may optimize the ability of perfluorocarbon to recruit collapsed or atelectatic lung regions.

Objective Prior analysis in the Open vs Endovascular Repair Veterans Affairs (VA) Cooperative Study (CSP #498) demonstrated that survival, quality of life, and total health care costs are not significantly different between the open and endovascular methods of repair of abdominal aortic aneurysm. The device is a major cost of this method of repair, and the objective of this study was to evaluate the costs of the device, abdominal aortic aneurysm repair, and total health care costs when different endograft systems are selected for the endovascular repair (EVR). Within each selected system, EVR costs are compared with open repair costs. Methods The study randomized 881 patients to open (n = 437) or EVR (n = 444). Device selection was recorded before randomization; therefore, open repair controls were matched to each device cohort. Data were excluded for two low-volume devices, implanted in only 13 individuals, leaving 423 control and 431 endovascular patients: 166 Zenith (Cook Medical, Bloomington, Ind), 177 Excluder (W. L. Gore & Associates, Flagstaff, Ariz), and 88 AneuRx (Medtronic, Minneapolis, Minn). Mean device, hospitalization, and total health care costs from randomization to 2 years were compared. Health care utilization data were obtained from patients and national VA and Medicare data sources. VA costs were determined using methods previously developed by the VA Health Economics Resource Center. Non-VA costs were obtained from Medicare claims data and billing data from the patient's health care providers. Results Implant costs were 38% of initial hospitalization costs. Mean device (range, $13,600-$14,400), initial hospitalization (range, $34,800-$38,900), and total health care costs at 2 years in the endovascular (range, $72,400-$78,200) and open repair groups (range, $75,600-$82,100) were not significantly different among device systems. Differences between endovascular and corresponding open repair cohorts showed lower mean costs for EVR (range, $3200-$8300), but these were not statistically different. Conclusions The implant costs of endovascular aneurysm repair are substantial. When evaluating total health care system expenditures, there is large individual variability in costs, and there is no significant difference at 2 years among systems or when an individual system is compared with open repair.

Vascular malformations of the extremities present a difficult therapeutic challenge. Ligation of feeding vessels may lead to tissue necrosis and limb loss and can make subsequent attempts at transcatheter therapy impossible. The purpose of this study was to review our results with transcatheter embolization therapy in symptomatic vascular malformations in the upper and lower extremities in 50 patients. A retrospective review was conducted of a computerized database of all patients undergoing transcatheter therapy of peripheral vascular malformations at our institution. The mean age of the patients was 22 years (range 1-51 years), and 34% were male. The most common presenting symptoms included pain (80%), swelling (68%), ulceration or distal ischemia (18%), and hemorrhage (6%). Previous unsuccessful surgical treatment or embolization had been performed in 24% and 18% of patients, respectively. Predominantly venous lesions were treated by sclerotherapy with injection of ethanol. Arteriovenous and arterial lesions were treated by embolization via the arterial branch feeding vessels with cyanoacrylate. The most common vessels involved and treated were branches of the profunda femoris and tibial arteries (83% of lower extremity lesions), and branches of the brachial and radial arteries (82% of upper extremity lesions). Patients required a mean of 1.6 embolization procedures (range 1-5) over a mean period of 57 months. Sixteen patients (32%) underwent more than one embolization procedure. Of these, one was a planned staged procedure and 15 were performed secondary to residual or recurrent symptoms. Adjunctive surgical procedures were performed subsequent to embolization in three cases (6%). Ninety-two percent of patients remained asymptomatic or improved at a mean follow-up of 56 months. There was one case of limb loss (2%). Diffuse extremity vascular malformations are difficult to eradicate completely and recurrences are common. Although patients may require multiple embolization procedures and occasional adjunctive surgical resection, directed transcatheter embolization should be the treatment of choice for symptomatic extremity vascular malformations.

The natural history and clinical significance of type II or branch vessel endoleaks following endovascular aortic aneurysm (AAA) repair remain unclear. Some investigators have suggested that these endoleaks have a benign course and outcome and that they can be safely observed. The purpose of this study was to document the natural history and outcome of all type II endoleaks that have occurred following endovascular AAA repair at our institution. A review of a prospectively compiled database of all endovascular AAA repairs performed at our institution was performed. From this review, we determined that type II endoleaks appear to have a relatively benign course, with a reasonable chance of spontaneously sealing within a 2-year period. No cases of rupture or aneurysm enlargement were documented in patients with open type II leaks. However, almost one-third of the patients did not manifest a type II leak until after their initial CT scan. The implications of such a "delayed" leak are unclear. Careful follow-up remains mandatory in patients with type II endoleaks to better define outcome.

Background/Purpose: Partial liquid ventilation (PLV) with perfluorocarbons decreases pulmonary vascular resistance (PVR) in injured piglet lungs without supplemental oxygen. These PVR changes may result either from direct mechanical effects or improved arterial oxygenation. In an uninjured hypoxic model of elevated PVR the authors asked the following questions: (1) Does prophylactic or therapeutic PLV ameliorate the PVR response to hypoxia? (2) Do prophylactic and therapeutic PLV have different PVR effects? (3) Does supplemental oxygen modify PVR response to PLV? Methods: Piglet (3 to 4 kg) lungs were isolated in situ without ischemia, hypoxia, or reperfusion injury. Pulmonary artery (PA) and left atrial (LA) cannulae were attached to a bloodprimed extracorporeal membrane oxygenation (ECMO) perfusion circuit with a flow (Q PA ) of 80 mL/kg/min. Pressure-limited, volume-cycled ventilation (PIP v = 15 mL/kg) was initiated. PLV with perfluorodecalin (15 mL/kg) was administered endotracheally. Continuously monitored blood gas parameters allowed airway and extracorporeal adjustment of Fio 2 to produce a Po 2 appropriate to the experimental phase. PVR was calculated as (PPA−PLAQPA). After a stable 30-minute normoxic baseline, animals were assigned randomly to three groups. In group I , control (n = 7), PVR was measured for 150 minutes in hypoxic lungs (Fio 2 = 0.07, P PA o 2 = 40 mm Hg, S PA o 2 = 70%). In group II , prophylactic (n = 8), PLV was administered, followed by 90 minutes of hypoxia, and 60 minutes of oxygen recovery (Fio 2 = 0.21 – 0.30, P PA o 2 > 100 mm Hg, S PA o 2 = 100%). In group III , therapeutic (n = 8), after 30 hypoxic minutes, PLV was administered and maintained for 90 minutes, followed by a 60-minute oxygen recovery phase. Results were expressed as mean ± SEM. Statistical analysis of groups was performed by repeated measures of analysis of variance (ANOVA) and Tukey correction. Results: In group I normoxic gas-ventilated PVR was 174 ± 12 mm Hg/L/kg/min. After 90 hypoxic minutes PVR was 318 ± 37 ( P v baseline). In group II baseline PVR was 183 ± 14. PVR after 30 normoxic minutes of PLV was 199 ± 14 ( P = ns v baseline). After 90 hypoxic minutes, PVR was 350 ± 31 ( P v baseline, and PLV alone) followed by a decrease to 192 ± 19 after 60 minutes of oxygen recovery ( P = ns v baseline or PLV alone). In group III baseline PVR was 160 ± 17 and 325 ± 29 after 30 hypoxic minutes. After 90 hypoxic minutes of PLV, PVR was 366 ± 22 ( P = ns v hypoxia control, P v normoxic baseline). PVR recovered to 189 ± 19 after 60 minutes of oxygen recovery ( P = ns v baseline). Conclusions: Prophylactic/therapeutic PLV had no effect on hypoxia-induced increases in PVR and did not differ from each other. Although PLV alone decreases PVR in the injured lung without supplemental oxygen, elevated PVR associated with hypoxia was ameliorated only by supplemental oxygen in the liquid ventilated lung.

Introduction : Partial liquid ventilation (PLV) with perfluorocarbons can be advantageous in treating lung injury. We studied this phenomenon in isolated piglet lungs devoid of systemic detractors by studying the changes in pulmonary vascular resistance (PVR) after lung injury with and without PLV. The following questions were asked. (1) Does PLV alone affect PVR in the uninjured lung? (2) Does PLV prevent the increase in PVR associated with oleic acid-induced lung injury? (3) Does PLV modify the increase in PVR associated with oleic acid lung injury? (4) Are the prophylactic and therapeutic effects of PLV on the increased PVR associated with oleic acid-induced lung injury different? Methods : Neonatal piglet (3 to 4 kg) lungs were prepared without pulmonary ischemia, hypoxia, or reperfusion injury for in situ study. Before pulmonary vascular isolation (eg, aortic and ductus arteriosus ligation) the pulmonary artery (PA) and left atrium (LA) were cannulated and attached to a blood-primed perfusion circuit (flow, 80 mL/kg/min). Pressure-limited volume-cycled ventilation (FIO 2 , 0.21; TV, 15 mL/kg; PIP, 25 cm H 2 O) was accomplished via occlusive tracheostomy. Blood gas parameters were monitored continuously and maintained within normal range (SpaO 2 , 75%; pH, 7.35 to 7.45; pCO 2 , 35 to 45 torr). Pulmonary artery pressure (P pa ), left atrial pressure (P ia ) and pulmonary blood flow (Q pa ) were recorded and PVR calculated (PVR = Ppa − PiaQpa). After achieving a stable baseline with gas ventilation only, the animal preparations were assigned to one of the following four groups. In group 1 (n = 7) PLV was given alone, using endotracheally administered perfluorodecalin (15 mL/kg). In group 2 (Prophylactic, n=7) PLV was given prophylactically 60 minutes before lung injury induced by injecting oleic acid (OA) at 0.08 mL/kg into the pulmonary artery. In group 3 (Therapeutic, n=8) PLV was given 60 minutes after OA-induced lung injury. P PA , P LA , and Q PA were measured and PVR was calculated. In group 4 (n = 7) OA was given alone. Significance of differences between groups was obtained by repeated measures analysis of variance (ANOVA). Results were expressed as mean ± SEM (mm Hg/L/Kg). Results : Group I showed baseline PVR of the normoxic gas ventilated animals was 127 ± 19 mm Hg/L/kg. PVR 180 minutes after PLV administration was 160 ± 15 mm Hg/L/kg ( P = ns v baseline). In group 2 after OA infusion, PVR increased from 109 ± 13 to 281 ± 26 mm Hg/L/kg ( P v baseline), and 60 minutes later, PVR decreased to 193 ± 22 mm Hg/L/kg ( P v OA). In group 3 PVR on gas ventilation, before lung injury, was 137 ± 28 mm Hg/L/kg. Sixty minutes after OA infusion, PVR increased to 314 ± 23 mm Hg/L/kg ( P v baseline). After 60 additional minutes of PLV, PVR decreased to 201 ± 31 mm Hg/L/kg, ( P v maximum). In group 4 baseline PVR was 96 ± 16 mm Hg/L/kg. After 120 minutes of OA injection, PVR increased to 414 ± 20 mm Hg/L/kg ( P v baseline). Endpoint analysis of PVR at the conclusion of the recording interval showed no difference between group 2 and group 3 (P = not significant [ns]). Conclusions : (1) PLV does not significantly alter PVR in the uninjured lung when given for 2 hours; (2) prophylactic administration of PLV prevents the sustained increase in PVR known to be induced by OA injury; (3) PLV abates OA-induced elevation in PVR when given therapeutically after injury; and (4) Prophylactic and therapeutic PLV have similar effects on PVR in the OA-injured lung.

PARTIAL LIQUID VENTILATION (PLV) AND LUNG INJURY: IS PLV ABLE TO MODIFY PULMONARY VASCULAR RESISTANCE (PVR)? † 1927