Percutaneous induced thrombosis of iatrogenic femoral pseudoaneurysms following catheterization.

Femoral pseudoaneurysms are one of the common iatrogenic complications following catheterization procedures done via the femoral approach. Their treatment has evolved over the last decade from operative repair to ultrasound-guided compression (USGC) and more recently to thrombin injection of the pseudoaneurysm. We report our experience with that technique and compare the results of thromboobliteration to those of the compression method. All consecutive iatrogenic femoral pseudoaneurysms diagnosed in the vascular laboratory of two large community hospitals were referred for the study. Under ultrasound guidance, percutaneous thromboobliteration (PTO) of the pseudoaneurysms was done by injecting thrombin solution (500-unit increments) into the pseudoaneurysm. Time to thrombosis, dose of thrombin, patient's discomfort, and ease of procedure were recorded and analyzed. Comparison with results of USGC reported in the literature was made. Percutaneous thromboobliteration may be a simple and very effective treatment of femoral pseudoaneurysms. The high success rate, ease of procedure, and cost benefit over USGC are noteworthy. A larger trial is currently under way. If results are duplicated, PTO will emerge as the preferred treatment for iatrogenic femoral pseudoaneurysms.

A new generation endovascular graft for repair of abdominal aortic aneurysms.

BACKGROUND: Several endovascular grafts are currently being evaluated for repair of abdominal aortic aneurysms (AAA). The goals of our study were twofold. First was to develop a new endovascular graft with several advantages over previous devices: (1) smaller size (16 fr), (2) recapturability (the device can be partially deployed and then recaptured and moved to a new location or entirely removed if needed), and (3) accuracy and ease of placement. Our second goal was to develop an animal model in which a full-scale prototype of the device could be tested. METHODS: Our final endovascular graft prototype was developed after extensive in-vitro testing, and trials of earlier prototypes in dog, pig, and female sheep models. Uncastrated male sheep, 75 to 100 kg, were chosen as the animal model in which to test the device. These animals had infrarenal aortas that were comparable to that of small humans, with diameters of 12 to 15 mm. Two models were used: (1) native infrarenal aorta, and (2) artificial infrarenal aneurysm. Pre-implant and postimplant angiography and intravascular ultrasound were used to evaluate graft placement, and were repeated prior to euthanasia and necropsy. RESULTS: The final prototype was implanted in 22 animals. Sixteen animals had the device placed in their native infrarenal aorta. Three animals were sacrificed immediately after implantation, and 6 more were euthanized after 2 weeks (n = 2), 6 weeks (n = 2), and 3 to 4 months (n = 2). In 7 animals the device is still in place. All procedures were successful. Pathology confirmed complete exclusion of the aorta and thrombosis of all lumbar branches covered by the graft. There was no evidence of graft malposition, migration, or perigraft leak, and no evidence of significant vessel injury on histology. Six animals had artificial aneurysms surgically created and then repaired with the device. A technical error resulted in a failure in 1 case; the remaining aneurysms were all successfully excluded. CONCLUSIONS: We report the development of a new endovascular prosthesis for the repair of AAA. Newer design features provide for smaller delivery size (16 fr), facilitate accurate placement, and provide the option when the device is partially deployed to recapture and reposition the device if necessary. In addition, we have developed an animal model in which this device, and future endovascular aortic devices, can be tested.

Prevention of renal cortical ischemia during aortic clamping with prostaglandin E1.

OBJECTIVES: To investigate the effects of aortic clamping and prostaglandin E1 on systemic hemodynamics and renal cortical and medullary blood flow by means of continuous intraparenchymal laser Doppler fluorometry. DESIGN: Experimental animal study in a porcine model. With the animal under general anesthesia after hemodynamic monitoring was instituted, surgical exposure was obtained through a small left retroperitoneal incision. The kidney was left undisturbed. Intraparenchymal laser Doppler probes (0.44 mm in diameter) were inserted in the renal cortex and medulla. In the first group of six animals, systemic hemodynamic variables, urine output and renal cortical and medullary flow were measured at baseline after 60 minutes of equilibration, and after 15 minutes of aortic clamping and unclamping. Data are given as mean +/- SE. INTERVENTION: In another six animals, prostaglandin E1 (20-micrograms intravenous bolus given over 1 minute) was given before clamping, and the same variables were recorded. RESULTS: In the first group, aortic clamping caused no change in cardiac output or filling pressures. Cortical blood flow decreased from 40.4 +/- 3.7 to 33.3 +/- 2.7 mL/100 g per minute (P < .0004) after clamping, and to 27 +/- 2.3 mL/100 g per minute (P < .0001) after unclamping, and was associated with a decrease in urine output from 3.2 +/- 0.5 to 2 +/- 0.2 mL/min (P < .0013). Medullary flow remained the same at 9.2 +/- 0.8, 10 +/- 0.3, and 9.8 +/- 0.6 mL/100 g per minute, respectively. These adverse effects were prevented when prostaglandin E1 was given before clamping. There was an initial drop in blood pressure (100 +/- 4 to 89 +/- 5 mm Hg, P < .0004), but cardiac output (43.3 +/- 5.8 L/min) and filling pressures (6 +/- 1 mm Hg) were unchanged. Cortical flow was preserved during the entire period of clamping and unclamping (43.3 +/- 5.8 mL/100 g per minute). Medullary flow remained unchanged (10 +/- 0.8 mL/100 g per minute). Urine output increased from 2 +/- 0.3 to 3.4 +/- 0.6 mL/min (P < .006). CONCLUSIONS: In this animal model, infrarenal aortic clamping causes a significant decrease in renal cortical flow and urine output with no significant changes in filling pressures, cardiac output, or medullary blood flow. These adverse effects are prevented by pretreatment with prostaglandin E1, which prevents cortical ischemia and maintains brisk diuresis.

Neurectomy for palliation of primary erythermalgia.

Ankle nerve crushing followed 6 months later by neurectomy was used for relief of a burning sensation and pain in a 32-year-old woman who had symptoms of unilateral primary erythermalgia. The patient continues to experience considerable improvement of the preceding symptoms and no complications from the insensate foot 1 year after neurectomy, although redness and tenseness of the ankle and the foot have persisted.