Long-term follow-up of Greenfield inferior vena cava filter placement in children.

OBJECTIVE: The long-term results of Greenfield inferior vena cava (IVC) filter placement have been well documented in adults; however, similar data do not exist for pediatric patients. The potential for growth and the increased life expectancy in younger patients may contribute to a difference in the natural history of filters placed in children. The objective of this study was to evaluate the long-term outcome of pediatric patients with IVC filters. METHODS: At the University of Massachusetts Memorial Medical Center, medical records and radiographs of patients 18 years old or younger at the time of IVC filter placement were reviewed. Follow-up data were obtained by interview, physical examination, and venous duplex ultrasound scanning. RESULTS: A total of 15 IVC filters were placed in children 18 years old or younger between 1983 and 1999. In 10 patients the indications for IVC filter placement were lower-extremity deep venous thrombosis (DVT) and/or pulmonary embolism. In five patients, prophylactic filters were placed in the absence of DVT because of a high risk for the development of pulmonary embolism. Surgical exposure of the right internal jugular vein was used to place the first eight filters. The remainder were inserted percutaneously through the right internal jugular vein or the right common femoral vein. There were no complications or mortality related to filter insertion. Follow-up of the surviving 14 patients ranged from 19 months to 16 years. During long-term follow-up, no patient had a pulmonary embolus. Of the nine patients who had lower-extremity DVT, three developed mild common femoral venous reflux documented by duplex scan. Of the five patients who had prophylactic filters, four had no symptoms or duplex evidence of reflux. The other patient, who was paraplegic, had bilateral leg edema but no venous varicosities and no reflux on duplex scan 11 years after filter placement. No patient in either group had chronic venous obstruction. CONCLUSION: In long-term follow-up there were no instances of pulmonary embolism, IVC thrombosis, significant postphlebitic symptoms, or significant filter migration among 14 pediatric patients with Greenfield IVC filters. This suggests a safety profile and efficacy similar to that seen in adults.

Laser scanning cytometry: a novel method for the detection of platelet--endothelial cell adhesion.

BACKGROUND: Adherence of platelets to endothelial cells may be a significant event in the development of vascular thrombosis. Existing models, which examine platelet-endothelial cell interactions, compromise endothelial cell integrity or use radioactivity to identify platelets that adhere to endothelial cells. We report a novel method for in vitro detection of platelet-endothelial cell adhesion that allows endothelial cells to remain as an intact monolayer and for visualization of individual platelets. METHODS: Fluorescently labeled platelets were incubated with a confluent monolayer of endothelial cells. Laser scanning cytometry (LSC) identified platelets bound to endothelial cells based on their fluorescent signals. RESULTS: LSC detection of platelets reliably reproduced well-described findings of thrombin-induced platelet-endothelial cell adhesion. Results demonstrating reduced adhesion with a glycoprotein IIb-IIIa-specific blocking monoclonal antibody confirmed the specificity of the LSC detection of platelet-endothelial cell adhesion. CONCLUSIONS: LSC is a novel method for detecting platelet--endothelial cell adhesion. Its advantages over other methods are: (a) endothelial cells remain undisturbed and adherent throughout; (b) the ability to detect individual bound platelets and subpopulations; (c) the ability to store images and slides and then relocate, revisualize, and reanalyze individual cells or cell populations of interest; and (d) no radioactivity.

Recombinant thrombomodulin inhibits arterial smooth muscle cell proliferation induced by thrombin.

PURPOSE: Restenosis after angioplasty or bypass grafting to restore circulation to ischemic organs is still an unsolved problem. Thrombin generated in high concentrations at the sites of vascular injury plays a central role in thrombosis and hemostasis. alpha-Thrombin has also been implicated as a mitogen for smooth muscle cell (SMC) proliferation that contributes to arterial restenosis. Thrombomodulin has a high affinity of binding with thrombin and converts thrombin from a procoagulant to an anticoagulant. This study was designed to examine whether thrombomodulin could also moderate the thrombin-mediated SMC proliferative response. METHODS: Porcine carotid artery SMCs (passages 4-7) were plated onto 96-well plates and incubated for 3 days. After growth arrest in a defined serum-free medium for 2 to 3 days, SMCs were subjected to the reagents as follows: (1) human alpha-thrombin, (2) recombinant human soluble thrombomodulin containing a chondroitin sulfate moiety, (3) thrombin receptor agonist peptide (SFLLRNPNDKYEPF), and (4) alpha-thrombin or thrombin receptor agonist peptide combined with recombinant thrombomodulin (rTM). The viability and proliferation status of SMCs were quantified with MTT (thiazolyl blue) mitochondrial function and bromodeoxyuridine (BrdU)-DNA incorporation assays. RESULTS: Human alpha-thrombin increased SMC proliferation in a dose dependent manner by more than 25% and 30% with thrombin 1 U/mL to 3 U/mL compared with control groups on day 7 (P <.006). rTM concentrations from 0.5 microg/mL to 3 microg/mL have no significant effect on SMC growth. The stimulation of SMC proliferation induced by alpha-thrombin at 0.5 U/mL, 1 U/mL, and 2 U/mL was significantly inhibited with rTM at 2 microg/mL and 3 microg/mL on days 3, 7, and 10 as evaluated with MTT assay (P <.01 to <.05) and BrdU-DNA incorporation assay on day 3 (P <.008). Thrombin receptor agonist peptide increased SMC BrdU-DNA incorporation at 48 hours (P <.007), and its effect was not altered by rTM. CONCLUSION: rTM containing all of the extracellular domains of thrombomodulin inhibits the effect of thrombin on SMC proliferation in vitro. Because thrombin is a mitogenic mediator of SMC in vascular injury, inhibition of its function in vivo could help to prevent SMC hyperplasia. The success of further studies in vivo may lead to use of rTM for decreasing or preventing arterial restenosis.

Superior vena cava syndrome secondary to an angiotropic large cell lymphoma.

BACKGROUND: Angiotropic large cell lymphoma (ALCL) is characterized by the intravascular proliferation of malignant lymphoid cells in small and medium-sized blood vessels. In the current study, the authors report an unusual case in which the initial presentation of the ALCL was that of superior vena cava (SVC) syndrome. METHODS: The case is presented, followed by a general review of the literature regarding ALCL. RESULTS: Surgical intervention was required for diagnosis in this case. Successful treatment with chemotherapy followed by involved field radiation ensued with a maintained disease remission at 48 months of follow-up. CONCLUSIONS: Although usually presenting in small blood vessels, ALCL can present initially with large blood vessel involvement and should be considered in the differential diagnosis of this condition, even in the absence of extravascular lymph node involvement. Aggressive treatment with antineoplastic therapy is warranted and may result in long term recurrence free survival.

Chronic venous insufficiency is associated with increased platelet and monocyte activation and aggregation.

PURPOSE: This study assessed whether the increased numbers of platelet-monocyte aggregates observed in patients with venous stasis ulceration (VSU) represent a response to dermal ulceration or if it is a condition associated with underlying chronic venous insufficiency (CVI). We also analyzed the expression of CD11b in patients with CVI to determine whether leukocyte activation, known to occur in VSU, is a precursor of or a response to ulceration. METHODS: Patients with varying classes of CVI (n = 24) and healthy control subjects (n = 15), whose status was documented by means of duplex scanning, stood upright and stationary for 10 minutes. Two aliquots of blood, drawn from a distal leg vein and an antecubital fossa vein, were incubated with either buffer or one of three platelet agonists. After fixation, these samples were further incubated with fluorescent-labeled monoclonal antibodies (f-MoAb) specific for CD14 (monocytes) and CD61 (platelets). The activated leukocyte assay was performed by incubating another aliquot of the blood samples with f-MoAb specific for CD11b and CD14. All samples were evaluated by means of flow cytometry. RESULTS: We observed significantly more platelet-monocyte aggregates throughout the circulation in patients with CVI than in control subjects (29% vs. 8%; P <.0002). Furthermore, patients with CVI formed significantly more of these aggregates in response to all platelet agonists than did control subjects. There were no significant differences between baseline numbers of aggregates or response to agonists in patients who had CVI with (n = 10) or without (n = 14) ulceration. Patients with CVI had more circulating platelet-neutrophil aggregates than control subjects (7.2% vs. 3.6%; P =.05). The addition of platelet agonists to the blood of patients with CVI resulted in more platelet-neutrophil aggregates than in control subjects. Monocyte CD11b expression was higher in patients with CVI than in control subjects (7.5 vs. 3.7; P <.01), with no differences noted in CD11b expression between patients with or without ulceration. Neutrophil CD11b expression was low and similar in control subjects and patients with CVI. CONCLUSION: All classes of CVI are associated with significantly increased percentages of platelet-monocyte aggregates and increased percentages of platelet-neutrophil aggregates throughout the circulation. The presence of more of these aggregates and the increased propensity to form aggregates in the presence of platelet agonists in all classes of CVI suggests an underlying state of platelet activation and increased reactivity that is independent of the presence of ulceration. The increased expression of monocyte CD11b throughout the circulation in all classes of CVI suggests that although systemic monocyte activation occurs in CVI, its presence is independent of VSU as well.

The effects of aspirin and hypothermia on platelet function in vivo.

Patients undergoing hypothermic cardiopulmonary bypass are often receiving aspirin therapy. Hypothermia, aspirin and cardiopulmonary bypass can each induce a platelet function defect, but it is not known if the effects of aspirin and hypothermia are additive in this regard. To address this question in humans in vivo, the forearm skin temperature of healthy volunteers was equilibrated and maintained at either normothermia (32 degrees C) or hypothermia (28 degrees C or 22 degrees C) before and 16 h after the ingestion of 650 mg aspirin. A standardized template bleeding time was performed on the forearm and the shed blood emerging from the wound was assayed for platelet surface P-selectin expression by whole blood flow cytometry (reflecting alpha granule secretion) and thromboxane B2 (the stable metabolite of thromboxane A2) by radioimmunoassay. Hypothermia resulted in marked prolongation of the bleeding time. Aspirin resulted in prolongation of the bleeding time under normothermic conditions, but only minimally augmented the hypothermia-induced prolongation of the bleeding time. Platelet surface P-selectin up-regulation in shed blood was abolished by hypothermia. Aspirin had no effect on maximal platelet surface P-selectin expression under normothermic or hypothermic conditions. Both hypothermia and aspirin resulted in markedly reduced shed blood thromboxane B2. Although aspirin slightly augmented the hypothermia-induced reduction in shed blood thromboxane B2, the concentration of thromboxane generated in shed blood under hypothermic conditions in the absence of aspirin had no effect on platelet surface P-selectin or platelet aggregation in whole blood. In conclusion, as determined by three independent parameters of the shed blood emerging from a standardized bleeding time wound (bleeding time, platelet surface P-selectin, and thromboxane B2), aspirin did not significantly augment hypothermia-induced platelet dysfunction in vivo.

Patients with venous stasis ulceration have increased monocyte-platelet aggregation.

PURPOSE: Leukocyte activation has been implicated in the pathogenesis of venous stasis ulceration, but the involvement of activated platelets and leukocyte-platelet aggregates has not been previously investigated. The purpose of this study was to determine whether patients with venous stasis ulceration have increased platelet activation and a propensity toward formation of leukocyte-platelet aggregates. METHODS: Blood was drawn from the superficial veins of the leg just proximal to a venous stasis ulcer and from an antecubital vein in 14 patients with venous stasis ulceration. Blood was also drawn from the antecubital vein of 14 volunteers without evidence of venous disease. Whole-blood flow cytometry was used to analyze the samples before and after activation with a panel of agonists for evidence of platelet activation and the formation of leukocyte-platelet aggregates. RESULTS: Patients with venous stasis ulceration had a greater number of monocyte-platelet aggregates in both the arm and leg samples than did the control subjects (p < 0.01). Furthermore, antecubital blood samples from patients with venous stasis ulceration stimulated with either thrombin-receptor agonist peptide, adenosine diphosphate, or phorbol myristate acetate formed more monocyte-platelet aggregates than did control samples (p < 0.05). No differences in platelet activation or neutrophil-platelet aggregate formation were noted among the three sample groups. CONCLUSIONS: Patients with venous stasis ulceration have an increase in the number of monocyte-platelet aggregates in systemic venous blood as well as in venous blood adjacent to a venous stasis ulcer, implicating the monocyte as the leukocyte involved in the pathogenesis of venous stasis ulceration. No association was identified between the presence of a venous stasis ulcer and either neutrophil-platelet aggregation or the activation of individual platelets. Because platelet activation is necessary for the formation of monocyte-platelet aggregates, these data also suggest that monocyte-platelet aggregation is a more sensitive marker for in vivo platelet activation than is the identification of individual activated platelets.

Is coronary angiography necessary for vascular surgery patients who have positive results of dipyridamole thallium scans?

PURPOSE: Because dipyridamole thallium (DT) scanning is a useful predictor of perioperative cardiac events, a positive results of a DT scan is frequently the basis for performing more invasive cardiac evaluation and for consideration for performing coronary revascularization procedures before performing peripheral vascular surgery. The rationale for this approach has been that the treatment of anatomically significant coronary artery disease would lower the risk of performing a subsequent vascular operation. However, the benefit of performing aggressive diagnostic and therapeutic cardiac procedures in such patients remains unproved. To examine this issue, data from patients who underwent coronary angiography because of thallium redistribution were compared with data from matched control subjects who underwent peripheral vascular operations without further cardiac evaluation. METHODS: The medical records of 70 consecutive patients who underwent coronary angiography because of the presence of two or more segments of redistribution on DT scan were reviewed and compared with 70 other patients matched with respect to age, gender, peripheral vascular operation, and number of segments of redistribution on DT scan who did not undergo additional cardiac evaluation. RESULTS: DT scans were performed on 934 preoperative peripheral vascular surgery patients to help in the assessment of operative risk. Ischemic responses, defined as two or more segments of redistribution, were observed in 297. Of these, 70 underwent cardiac catheterization and 25 underwent coronary revascularization procedures. Adverse outcomes affected 46% of the coronary angiography group and 44% of the control group (p = NS). Patients who underwent coronary angiography and were considered for myocardial revascularization had fewer cardiac events with a subsequent vascular operation than did the control subjects. However, any possible benefit from invasive cardiac evaluation was offset by the three deaths and two myocardial infarctions (MIs) that complicated the cardiac evaluation. There was no significant difference between the angiography group and the matched control subjects with respect to perioperative nonfatal MI (13% vs 9%), fatal MI (4% vs 3%), late nonfatal MI (16% vs 19%), or late cardiac death (10% vs 13%). In long-term follow-up, MIs occurred later in patients who underwent coronary angiography than the control subjects (p = 0.049), but this difference was not associated with an improvement in the overall survival rate. CONCLUSIONS: The risks of extended cardiac evaluation and treatment did not produce any improvement in either the perioperative or the long-term survival rate. For most vascular surgery patients who have a positive result of a DT scan, coronary angiography does not provide any additional useful information.

Heparin and protamine stimulate the production of nitric oxide.

Heparin has been shown to decrease total vascular resistance while protamine stimulates endothelium-dependent vasodilation. This study was undertaken to determine whether heparin and/or protamine could enhance endothelium-derived relaxing factor (EDRF), as determined by nitric oxide (NO) production. Porcine carotid artery endothelial cells (PAECs) were seeded on multiwell plates, grown to confluence, and exposed to heparin (1-20 U/ml) or protamine (50-200 microg/ml) for 24 hours. With the addition of the NO synthase inhibitor, N(G)-monomethyl-L-arginine (NMMA), to heparin and/or protamine, the medium samples were collected in one hour. In a parallel clinical study, plasma samples were collected from patients undergoing cardiopulmonary bypass (CPB). The NO production was measured as reflected by the formation of nitrite (NO2-) and nitrate (NO3-), the stable end-metabolites of NO. NO production by PAECs was significantly increased by heparin > or = 5 U/ml or protamine > or = 50 microg/ml in a concentration-dependent manner. The increase of NO production was prevented by the addition of NMMA. In CPB patients, plasma NO2-/NO3- concentration was significantly increased after heparin administration compared to the preoperative value, at which time the mean plasma heparin level was 4.9+/-0.5 U/ml. Following slow protamine infusion, there was no significant difference in plasma NO2-/NO3- concentration compared to preoperative value. In conclusion NO production increases following exposure of PAECs to heparin and/or protamine. In patients, NO concentration significantly increased after heparin administration by IV bolus, but not with a slow infusion of protamine after CPB.

Effect of heparin on fibrinolytic activity and platelet function in vivo.

Heparin, a polyanionic glycosaminoglycan, is used routinely before the induction of cardiopulmonary bypass. Earlier observations in our laboratory suggested that the postoperative bleeding that occurs, despite neutralization of heparin with protamine, is secondary to hypothermia and dilutional anemia during bypass. An additional, potential mechanism for excessive bleeding following cardiopulmonary bypass is that heparin activates the fibrinolytic system, which may, in turn, adversely affect hemostasis. To understand better the effects of heparin administration on the fibrinolytic system in vivo, we simulated the anticoagulant regimen of cardiopulmonary bypass by administering increasing doses of intravenous heparin to five adult baboons over 60 min. We measured fibrinolytic parameters serially following heparinization and demonstrated that heparin induces activation of the fibrinolytic system. We showed that the fibrinolytic system was activated in vivo as evidenced by an increase in plasmin activity and immunoreactive plasmin light chain, as well as an increase in immunoreactive fibrinogen fragment E in vitro. These results demonstrate that the fibrinolytic system is activated in vivo by the administration of heparin during cardiopulmonary bypass. These data suggest that, despite administration of a neutralizing agent such as protamine, heparin may contribute to postoperative bleeding complications following cardiopulmonary bypass surgery owing principally to its longer lived effects on the fibrinolytic system.

A prospective study of the incidence of deep venous thrombosis in hospitalized children.

PURPOSE: It is commonly believed that the incidence of deep venous thrombosis (DVT) in hospitalized children is less than in adults. However, it is possible that the disease is significantly underdiagnosed in children because the index of suspicion of pediatric practitioners is low, a substantial number of patients may have no symptoms, and DVT screening is not routinely performed. We therefore undertook a prospective study to define the incidence of DVT in hospitalized children with no symptoms. METHODS: Patients included in the study were those younger than 18 years of age who were hospitalized for more than 72 hours and were identified to have two or more risk factors for the development of DVT and had at least one screening duplex scan. Risk factors for the development of DVT considered were a history of DVT or pulmonary embolism, recent operation, immobilization, trauma, stroke or acute neurologic deficit, the presence of cancer, sepsis, greater than 150% ideal body weight, a hypercoagulable state, and the presence of a femoral venous catheter. RESULTS: Over the 9-month period ending December 1994, 1997 patients 17 years of age and younger were admitted to the hospital, and 59 patients including 19 girls and 40 boys were enrolled in the study. The one patient with DVT was a 17-year-old boy hospitalized after a motor vehicle accident with blunt head trauma and a neurologic deficit who underwent multiple orthopedic and neurosurgical procedures. CONCLUSIONS: The development of acute DVT in children is unusual. As a result, DVT prophylaxis and screening is unnecessary in young children with only two risk factors for the development of the disease. Young age appears to be an important protective risk factor for the prevention of DVT.

Surgical exposure of the left subclavian artery by median sternotomy and left supraclavicular extension.

OBJECTIVE: To evaluate the feasibility of surgical exposure of the full length of the left subclavian artery using a median sternotomy and left supraclavicular extension. DESIGN: Anatomic study of five cadavers, and case review of four patients with blunt trauma to the proximal left subclavian artery. MATERIALS AND METHODS: A median sternotomy with left supraclavicular extension was performed on five cadavers and four patients. The depth of various portions of the subclavian artery was measured. Photographs of the dissections were used to document anatomic relationships and to serve as a basis for pen and ink drawings. The hospital records of four patients in which this exposure was used were reviewed for operative details. MEASUREMENTS AND MAIN RESULTS: The left subclavian artery was readily exposed from its origin on the aortic arch to its termination as the axillary artery in all cadaver dissections, including one who was more than 300% ideal body weight. The first portion of the subclavian artery lay at an average wound depth of 6.0 cm, with a mean length of 4.7 cm. The same surgical approach was used for the care of four patients who sustained blunt trauma to the first portion of the left subclavian artery and permitted expeditious control and excellent exposure for placement of a proximal subclavian interposition graft in two, a proximal subclavian to axillary artery graft in the third, and resection and end-to-end anastomosis in the fourth. CONCLUSIONS: Median sternotomy with left supraclavicular extension provides rapid, safe, and reliable exposure of all portions of the left subclavian artery without the morbidity associated with clavicular resection, thoracotomy, or a "trapdoor" incision. Furthermore, the ability to perform this procedure in the supine position allows access to the abdominal cavity, the neck, and the extremities, which often require concomitant operative intervention in a patient with multiple injuries.

Effects of nitric oxide/EDRF on platelet surface glycoproteins.

We examined the effects of nitric oxide (NO)/endothelium-derived relaxing factor (EDRF) on platelet surface glycoproteins (GP). As determined by flow cytometry, in both a washed platelet system and platelet-rich plasma, the EDRF congener (S-nitroso-N-acetylcysteine) markedly inhibited both the thrombin-induced and the (stable thromboxane A2 analogue) U-46619-induced upregulation of P-selectin (alpha-granule protein), CD63 (lysosomal protein), and the GPIIb-IIIa complex (fibrinogen receptor) but minimally inhibited downregulation of the GPIb-IX complex (von Willebrand factor receptor). The inhibitory effects of EDRF were markedly reduced in whole blood or by the addition of washed erythrocytes. Platelets in whole blood were still responsive to guanosine 3',5'-cyclic monophosphate (cGMP), as shown by complete inhibition of P-selectin upregulation by the stable analogue N6,2'-O dibutyryl cGMP. These data suggests that 1) cGMP negatively regulates the platelet surface expression of P-selectin, CD63, and the GPIIb-IIIa complex but not the platelet surface expression of the GPIb-IX complex and 2) hemoglobin within erythrocytes inhibits the effects of EDRF/NO on platelet surface glycoproteins.

Adhesion of activated platelets to venous endothelial cells is mediated via GPIIb/IIIa.

Normal circulating platelets do not adhere to intact, undisturbed endothelium. Studies have shown, however, that platelets will adhere to virally infected or thrombin-stimulated human umbilical vein endothelial cells. Using a novel platelet/endothelial cell adhesion assay we studied the interaction of thrombin-activated platelets to human saphenous vein endothelial cells (HSVEC), and its mechanism(s). Biotinylated platelets were exposed to Hepes-Tyrode buffer, 10E5 or PAC-1 [monoclonal antibodies (Mabs) blocking GPIIb-IIIa], AK4 (Mab blocking P-selectin, 6D1 (Mab blocking vWf binding to GPIb), RGDS (small peptide blocking the fibrinogen binding site), or EDTA (dissociates GPIIb-IIIa complex) and then activated with thrombin. The platelets were subsequently exposed to thrombin-stimulated monolayer HSVEC. Phycoerythrin-streptavidin was added to the wells to fluorescently label the platelets, followed by formaldehyde fixation and washing to remove nonadherent platelets. Adhesion of platelets to HSVEC was assessed using a fluorescent multiwell plate reader. Antibodies which blocked the GPIIb-IIIa receptor and agents which competitively bound the receptor all significantly inhibited activated platelet adhesion to the activated HSVEC. We have found that thrombin significantly increases platelet/HSVEC adhesion, and this event is mediated via the integrin GPIIb-IIIa (fibrinogen receptor). These GPIIb-IIIa receptor blocking Mabs and RGDS may be useful adjuncts for improving patency following angiographic intervention and/or vein grafting in patients with high risk of thrombosis. The assay we have developed is a valuable and relatively simple method for assessing platelet/endothelial cell adhesion and activation.

Successful management of intracardiac extension of tumor thrombus in a patient with advanced nonseminomatous germ cell testicular cancer.

A young patient with testicular germ cell tumor presenting with inferior vena cava thrombus extending into the right heart with free-floating thrombus in the right ventricle and a simultaneous epidural spinal cord compression is presented. Due to the perceived high risk of embolization and the urgent need to begin systemic chemotherapy, he was managed with tumor thrombectomy utilizing cardiopulmonary bypass and hypothermic circulatory arrest followed shortly thereafter by systemic chemotherapy. There were no perioperative complications, and he is alive and without recurrence 24 months following four cycles of systemic chemotherapy.

Ultrasound-guided compression of iatrogenic femoral pseudoaneurysm failure, recurrence, and long-term results.

PURPOSE: Iatrogenic femoral pseudoaneurysms (IFP) have traditionally been treated surgically. Recently, this common problem has been successfully treated without operation by use of ultrasound-guided compression (UGC) to induce thrombosis of the false aneurysm cavity, but the risk factors for failure and the long-term outcome have not been defined. METHODS: All patients referred to the vascular laboratory from June 1992 to November 1994 whose femoral pseudoaneurysms were treated by UGC were included in the study. Data were collected prospectively during the last 18 months of the study. Data regarding the location and morphologic characteristics of the pseudoaneurysms and anticoagulation status were documented. Patients who had successful UGC underwent follow-up duplex scanning and ankle-brachial arterial pressure evaluations. RESULTS: Fifty-seven patients with IFP were treated with UGC over a 30-month period; the last 34 were evaluated prospectively. UGC was successful at obliterating the false aneurysm cavity with the initial attempt in 47 (83%). Thrombosis of seven additional pseudoaneurysms was achieved on subsequent UGC attempts for an overall success rate of 95%. Recurrent false aneurysms were noted in two patients 2 and 10 days after initially successful UGC. Both were treated successfully with repeat UGC. Multivariate analysis of 14 variables revealed heparin anticoagulation (chi-square 9.025, p = 0.001) as the only significant risk factor for failure of UGC. There were no episodes of arterial thrombosis, embolization, or femoral nerve injury associated with UGC. Temporary occlusion of femoral artery during UGC and compression intervals of 20 minutes were well tolerated. Long-term follow-up from 30 to 400 days after UGC was available in 36 patients. There was no late recurrence or significant change in ankle-brachial pressures (p > 0.05). CONCLUSION: UGC is a safe and effective treatment for most catheter-induced femoral pseudoaneurysms with a low complication rate and excellent long-term results at a cost substantially lower than operative treatment. Because the natural history of IFP is unpredictable, UGC appears to be the preferred treatment for all IFPs persisting after cessation of heparin anticoagulation.

Acute peritoneal dialysis following ruptured abdominal aortic aneurysms.

BACKGROUND: Acute renal failure is common after repair of ruptured abdominal aortic aneurysm. Early dialysis has recently been advocated to reduce the mortality associated with multiorgan failure, but hemodialysis (HD) is not well-tolerated in critically ill patients because of hemodynamic instability and risk of bleeding from anticoagulation therapy. Peritoneal dialysis (PD) has the advantage in that it causes minimal cardiopulmonary instability and does not require anticoagulation. The presence of a freshly-closed abdominal wound and an aortic graft, however, have previously been considered to be contraindications to PD. METHODS: Peritoneal dialysis catheters were placed in 69 of the 105 patients who underwent grafting for a ruptured abdominal aortic aneurysm between 1982 and 1993. Criteria for placement included shock, perioperative oliguria, and preoperative renal insufficiency. All charts were reviewed retrospectively to evaluate the safety and efficacy of placing PD catheters and initiating early dialysis in patients at risk for developing acute renal failure. RESULTS: Acute tubular necrosis developed in 31 patients, 19 of whom required dialysis. Peritoneal dialysis alone provided effective dialysis in 8 patients, and it was combined with hemofiltration and/or HD in 9 additional patients for an overall efficacy of 58%. The peritoneal catheter also facilitated the early diagnosis of peritonitis due to colon ischemia in 5 patients, and was helpful in diagnosing intra-abdominal hemorrhage in 4 others. Bacterial peritonitis occurred in 3 (17%) patients undergoing PD with no cause noted for the infection diagnosing other than use of the PD catheter. A single aortic graft infection was diagnosed 4.2 years postoperatively with an enteric organism in a patient with recurrent diverticulitis. Two patients with peritoneal catheters developed abdominal wound dehiscence, but neither had undergone PD (P > 0.2). In a multivariate analysis, placement of a PD catheter did not affect survival. CONCLUSIONS: Placement of a PD catheter at the time of resection of a ruptured abdominal aortic aneurysm in patients at risk for development of acute renal failure is without significant complications and can facilitate early and effective dialysis. The peritoneal dialysis catheter may also be useful in making an early diagnosis of intraperitoneal bleeding and infection.

Neutrophil cathepsin G modulates the platelet surface expression of the glycoprotein (GP) Ib-IX complex by proteolysis of the von Willebrand factor binding site on GPIb alpha and by a cytoskeletal-mediated redistribution of the remainder of the complex.

The effects of neutrophil cathepsin G on the glycoprotein (GP) Ib-IX complex of washed platelets were examined. Cathepsin G resulted in a concentration- and time-dependent decrease in the platelet surface GPIb-IX complex, as determined by flow cytometry, binding of exogenous von Willebrand factor (vWF) in the presence of ristocetin, and ristocetin-induced platelet agglutination. Cathepsin G resulted in proteolysis of the vWF binding site on GPIb alpha (defined by monoclonal antibody [MoAb] 6D1), as determined by increased supernatant glycocalicin fragment (a proteolytic product of GPIb alpha); decreased total platelet content of GPIb; and lack of effect of either cytochalasin B (an inhibitor of actin polymerization), prostaglandin I2 (an inhibitor of platelet activation), or prior fixation of the platelets. However, cathepsin G resulted in minimal decreases in the binding to fixed platelets of MoAbs TM60 (directed against the thrombin binding site on GPIb alpha) and WM23 (directed against the macroglycopeptide portion of GPIb alpha). In contrast to its proteolytic effect on GPIb alpha, the cathepsin G-induced decrease in platelet surface GPIX and the remnant of the GPIb-IX complex (defined by MoAbs FMC25 and AK1) was via a cytoskeletal-mediated redistribution, as determined by lack of change in the total platelet content of GPIX and the GPIb-IX complex; complete inhibition by cytochalasin B, prostaglandin I2, and prior fixation of platelets. Experiments with Serratia protease-treated and Bernard-Soulier platelets showed that neither platelet surface GPIb nor cathepsin G-induced proteolysis of GPIb were required for the cathepsin G-induced redistribution of the remnant of the GPIb-IX complex or the cathepsin G-induced increase in platelet surface P-selectin. In summary, neutrophil cathepsin G modulates the platelet surface expression of the GPIb-IX complex both by proteolysis of the vWF binding site on GPIb alpha and by a cytoskeletal-mediated redistribution of the remainder of the complex. Prior studies show that, although thrombospondin 1, antiserine proteases, and plasma are all inhibitors of cathepsin G, the effects of cathepsin G on platelets, including an increase in surface GPIIb-IIIa, occur during close contact between neutrophils and platelets in a protective microenvironment (eg, thrombosis and local inflammation).(ABSTRACT TRUNCATED AT 400 WORDS)