Cutaneous hyperpigmentation following venous sclerotherapy treated with deferoxamine mesylate.

BACKGROUND: Cutaneous hyperpigmentation after venous sclerotherapy is an adverse sequelae of difficult management. OBJECTIVE: To evaluate the degree of depigmentation with the use of deferoxamine mesylate (DM) in patients with postsclerotherapy hyperpigmentation treated with polydocanol (POL) for telangiectasias and reticular veins (0.2-5 mm diameter) and varicose veins (5-8 mm diameter). METHODS: The experimental group of 36 female patients (mean age 37 years) was divided in two groups. Group I consisted of 30 patients who were treated with POL at 0.25-0.50% concentration for telangiectasias and reticular veins. Group II consisted of six patients with prolonged postsclerotherapy hyperpigmentation (more than 6 months after treatment) in varicose veins that had been treated with POL at 1.5% concentration each week. Groups I and II were injected with DM 500 mg subcutaneously once a week until 81-100% depigmentation was reached. In group I, DM was injected at the time of sclerotherapy. These groups were compared to their respective control groups with similar conditions but allowing spontaneous depigmentation without DM. Evaluation was undertaken clinically and photographically, and the number of days required to reach the desired depigmentation of 81-100% was determined. RESULTS: When DM was used, depigmentation of 81-100% was observed in group I at 27 days, and for group II in 46 days. In each control group, similar depigmentation was seen at 150 +/- 19 and 255 +/- 11 days, respectively. Comparing results, there was a reduction in the time to depigmentation of 82% for each group (P <.0001). CONCLUSION: The weekly subcutaneous administration of DM 500 mg reduces the time to depigmentation by 82% in patients with postsclerotherapy cutaneous hyperpigmentation treated for telangiectasias and reticular veins and prolonged postsclerotherapy hyperpigmentation in varicose veins. In this study we could not explain why such variability exists in the length of time to spontaneous depigmentation.

Patterns of expression of fibrinolytic genes and matrix metalloproteinase-9 in dissecting aortic aneurysms.

Although extensive tissue remodeling occurs during the various phases of aortic dissection, the underlying proteinases remain to be identified. Matrix metalloproteinase-9 (MMP-9) and components of the fibrinolytic system have been implicated in numerous tissue remodeling events and were therefore analyzed in surgical specimens of acute (n = 9), subacute (n = 4), and chronic (n = 7) aortic dissection by in situ hybridization. In the acute phase, intense plasminogen activator inhibitor 1 (PAI-1) gene expression was apparent in areas interfacing the dissecting hematoma, but no tissue-type PA (t-PA), urokinase-type PA (u-PA), or MMP-9 mRNAs were detected. Although PAI-1 mRNA was still present in the subacute phase, t-PA, u-PA, and MMP-9 mRNAs were now obvious, with PA gene expression co-localizing with areas of PAI-1 gene expression. In the chronic phase, PAI-1 mRNA was demonstrated around erythrocyte extravasations and surrounding bands of medial degeneration. However, there was little expression of PAs in these areas, and no MMP-9 was detected. Thus, fibrinolytic genes and MMP-9 are differentially expressed during the progression of aortic dissections. The kinetics of expression are consistent with acute fibrinolytic shutdown in response to the initial injury, a secondary subacute phase with active proteolysis, and finally, a chronic hypofibrinolytic state. Extensive neovascularization in the chronic phase may further reduce the physical stability of the dissected wall.

Infection of a ruptured aortic aneurysm and an aortic graft with bacille Calmette-Guérin after intravesical administration for bladder cancer.

A case of aortic graft infection with bacille Calmette-Guérin (BCG) is described. The graft was placed during urgent repair of a ruptured abdominal aortic aneurysm 2 years after intravesical administration of BCG for grade II transitional cell carcinoma of the bladder with associated carcinoma in situ. At the time of operation, no gross evidence of infection was found and pathologic examination of the aortic wall was unremarkable. Aortic graft infection with BCG was diagnosed 1 year after placement of the graft. Retrospective examination of formalin-fixed, paraffin-embedded aortic wall and thrombus removed at the time of graft placement by the polymerase chain reaction technique demonstrated the presence of mycobacterial DNA. The patient's condition improved with medical therapy during an observation period of 18 months with near total resolution on computed tomography scanning. Ultimately (20 months later), an aortoenteric fistula developed that required graft removal and axillobifemoral bypass.

Expression of fibrinolytic genes in atherosclerotic abdominal aortic aneurysm wall. A possible mechanism for aneurysm expansion.

Expansion of atherosclerotic abdominal aortic aneurysm (AAA) has been attributed to remodeling of the extracellular matrix by active proteolysis. We used in situ hybridization to analyze the expression of fibrinolytic genes in aneurysm wall from eight AAA patients. All specimens exhibited specific areas of inflammatory infiltrates with macrophage-like cells expressing urokinase-type plasminogen activator (u-PA) and tissue-type PA (t-PA) mRNA. Type 1 PA inhibitor (PAI-1) mRNA was expressed at the base of the necrotic atheroma of all specimens and also within some of the inflammatory infiltrates where it frequently colocalized in regions containing u-PA and t-PA mRNA expressing cells. However, in these areas, the cellular distribution of the transcripts for t-PA and u-PA extended far beyond the areas of PAI-1 expression. These observations suggest a local ongoing proteolytic process, one which is only partially counteracted by the more restricted expression of PAI-1 mRNA. An abundance of capillaries was also obvious in all inflammatory infiltrates and may reflect local angiogenesis in response to active pericellular fibrinolysis. The increased fibrinolytic capacity in AAA wall may promote angiogenesis and contribute to local proteolytic degradation of the aortic wall leading to physical weakening and active expansion of the aneurysm.

Changing practice patterns in peripheral arterial disease.

The development of interventional radiologic techniques during the past decade has changed our approach to the treatment of lower extremity peripheral arterial disease (LE-PAD). Balloon and laser-assisted angioplasty, atherectomy (rotary and directional devices), stent implantation, and thrombolysis as well as combinations of all of these approaches, at times with concomitant or secondary surgery, have been used in our institution. A review of our practice patterns during the past 5 years was performed to analyze changing attitudes and results with these newer techniques. All new patients seen in consultation for LE-PAD during three alternate years were reviewed with regard to demographics, initial complaints, initial treatment modality, initial outcome, indications for and results of secondary treatment, and ultimate outcome (at 1 year). The 603 patients were seen during the following three 12-month periods: 1987 to 1988, 1989 to 1990, and 1991 to 1992. An intention-to-treat analysis revealed (1) the number of patients seen for peripheral arterial disease has increased steadily; (2) in the last year more were initially treated with intervention as the primary modality; (3) the results of such catheter-based procedures improved only slightly over this 5-year period, despite our learning curve and the fact that we discarded several ineffective interventional approaches; (4) the fraction of patients primarily operated on and the excellent results of surgery have not changed; and (5) the number of operations for proximal (aortoiliac) disease has decreased markedly, with a corresponding increase in distal reconstructions. The evolution of our current approach to the treatment of LE-PAD is based on this continuing experience.

Initial experience with the Palmaz stent for aortoiliac stenoses.

The initial 37 consecutive patients to be treated at our institution with the Palmaz stent placed in the aortoiliac arteries were retrospectively reviewed. In these patients, 50 stenoses and six occlusions were treated with 128 stents. Nine patients with combined iliac and common femoral obstruction underwent common femoral endarterectomy and profoundaplasty with intraoperative iliac artery angioplasty and stent application. Stenoses were reduced from 57 +/- 17% to 1 +/- 5% (p < 0.01), and peak systolic pressure gradients across the lesions were reduced from 45 +/- 30 mm Hg to 1.3 +/- 3.4 mm Hg (p < 0.01). Symptoms resolved in 27 patients and improved in eight patients. One patient died and four patients were treated nonoperatively for complications. During a mean follow-up of 12 months (6 to 21 months), six patients had recurrence of symptoms (16%) and four patients died of other diseases. Routine arteriograms after 6 months in 19 patients demonstrated recurrent mild to moderate stenoses (9% to 43%) in six patients (32%), but only two were symptomatic (11%). Secondary procedures included reexpansion of aortic and iliac stents in two patients and aortofemoral bypass in two patients. Early results suggest the efficacy of the Palmaz stent in the management of aortoiliac stenoses and its use intraoperatively in conjunction with surgical correction of outflow. Close follow-up of these patients by multidisciplinary groups is warranted.

CHAT analysis of the influence of specific risk factors on late results after carotid endarterectomy.

The CHAT classification separates various current and historical presentations of cerebrovascular disease in an effort to determine important prognostic clues for management and prognosis. To evaluate known risk factors for late stroke and death, we followed up for an average of 44 months 633 patients who had undergone 714 carotid operations. We analyzed the indication for surgery (by CHAT) and the effect of preoperative risk factors (age, hypertension, cardiac disease, tobacco use, diabetes, hyperlipidemia, renal disease, pulmonary disease, and total risk factor score) on the end points of late stroke and death. Ipsilateral stroke was uncommon after carotid endarterectomy: with life-table analysis, the probability of late stroke at 5 years after carotid endarterectomy was 3%. Among the 127 patients with amaurosis fugax, the incidence of late stroke and of mortality was a combined total of 1% per year, and the 17 patients who had been first seen with permanent ocular stroke (blindness) fared equally well. The 28 patients who were first seen with vertebrobasilar symptoms and were treated by carotid endarterectomy also fared particularly well, with no late strokes or deaths within the first 5 years. Logistic regression analyses revealed that the various indications for carotid endarterectomy were associated with differing patterns of risk factors as significant predictors of late stroke or death. For patients first seen with asymptomatic lesions, only diabetes was an important predictor for late stroke (p = 0.05) and renal disease was the only marker for early death (p = 0.05). On the other hand, those factors were not significant risk factors for patients first seen with amaurosis fugax, for whom tobacco use was a negative predictor for stroke (p = 0.06) and male gender a negative predictor for early death (p = 0.03). After cortical transient ischemic attacks and carotid endarterectomy, there were no risk factors predictive of late stroke or of death. For patients with prior stroke, age was a very strong predictor of stroke (p = 0.01) and both age and a history of cardiac disease were significant risk factors for early death (p = 0.007). In contrast to the results in reports of patients treated medically for transient ischemic attacks and stroke, we found that several risk factors appeared to play relatively minor roles. In conclusion, stroke after carotid endarterectomy was uncommon, least common after ocular symptoms, and most likely after permanent cortical stroke. Specific risk factors were less important for patients after carotid endarterectomy than for the medically treated stroke patient.

Increased type 1 plasminogen activator inhibitor gene expression in atherosclerotic human arteries.

Decreased fibrinolytic capacity has been suggested to accelerate the process of arterial atherogenesis by facilitating thrombosis and fibrin deposition within developing atherosclerotic lesions. Type 1 plasminogen activator inhibitor (PAI-1) is the primary inhibitor of tissue-type plasminogen activator and has been found to be increased in a number of clinical conditions generally defined as prothrombotic. To investigate the potential role of this inhibitor in atherosclerosis, we examined the expression of PAI-1 mRNA in segments of 11 severely diseased and 5 relatively normal human arteries obtained from 16 different patients undergoing reconstructive surgery for aortic occlusive or aneurysmal disease. Densitometric scanning of RNA (Northern) blot autoradiograms revealed significantly increased levels of PAI-1 mRNA in severely atherosclerotic vessels (mean densitometric value, 1.7 +/- 0.28 SEM) compared with normal or mildly affected arteries (mean densitometric value, 0.63 +/- 0.09 SEM; P less than 0.05). In most instances, the level of PAI-1 mRNA was correlated with the degree of atherosclerosis. Analysis of adjacent tissue sections from the same patients by in situ hybridization demonstrated an abundance of PAI-1 mRNA-positive cells within the thickened intima of atherosclerotic arteries, mainly around the base of the plaque. PAI-1 mRNA could also be detected in cells scattered within the necrotic material and in endothelial cells of adventitial vessels. In contrast to these results, PAI-1 mRNA was visualized primarily within luminal endothelial cells of normal-appearing aortic tissue. Our data provide initial evidence for the increased expression of PAI-1 mRNA in severely atherosclerotic human arteries and suggest a role for PAI-1 in the progression of human atherosclerotic disease.

Failure of aspirin plus dipyridamole to prevent restenosis after carotid endarterectomy.

OBJECTIVE: To evaluate therapy with aspirin plus dipyridamole in reducing restenosis after carotid endarterectomy. PATIENTS: A total of 163 patients having 175 surgical carotid endarterectomies. INTERVENTION: Eighty-three patients (90 endarterectomies) were randomly assigned to receive oral aspirin, 325 mg, plus dipyridamole, 75 mg, beginning 12 hours preoperatively, followed by a second dose administered within 8 hours after the operation, and given three times daily thereafter for 1 year. Eighty patients (85 endarterectomies) received placebo medication that was identical in appearance to the study drugs. MEASUREMENTS: After the adequacy of the surgical procedure was confirmed by intraoperative angiography, restenosis at the endarterectomy sites was evaluated using serial duplex ultrasound studies before hospital discharge and at 3-month intervals postoperatively for 1 year. RESULTS: Based on the time for developing identifiable restenosis and on efficacy analysis, greater than 50% restenosis developed in 11 operated vessels (16%) in the treated group and in 10 arteries (14%) in the placebo group, yielding an observed risk increase of 14% (95% CI, -52% to 167%; P greater than 0.2). By intention-to-treat analysis, greater than 50% restenosis developed in 16 of 90 operated vessels in treated patients and in 10 of 85 arteries in patients receiving placebo (26% for the treated group and 12% for the placebo group; P = 0.18, Mantel-Haenszel statistic), representing an observed risk increase of 110% (CI, -5% to 365%). Similar differences were observed for greater than 20% restenosis and for the comparison of patients rather than operated vessels by either intention-to-treat or efficacy analyses. CONCLUSIONS: Because therapy not only failed to reduce carotid restenosis but may have actually increased its frequency, treatment with aspirin plus dipyridamole probably has no clinically important benefit on restenosis in patients having carotid endarterectomy.

Combined carotid endarterectomy and coronary artery revascularization: a sobering review.

The clinical outcome of 99 patients who underwent combined single-stage carotid thromboendarterectomy and coronary artery bypass grafts in three different hospitals over a 15-year period was analyzed. Coronary revascularization was elective in 16 patients, urgent in 46 and emergent in 37 patients. Asymptomatic carotid artery stenosis of greater than or equal to 80% was detected in 79% of patients. Sequential reconstruction of the carotid artery circulation followed by restoration of the coronary circulation was performed in all patients by two separate surgical teams. The population included 79 men and 20 women, with a mean age of 67 +/- 6 years, of whom 53% had a previous myocardial infarction, 59% had hypertension and 49% had a history of smoking. Three or more coronary arteries were revascularized in 90% of patients. The overall major neurological complication rate was 25%, with an 11% stroke rate ipsilateral to the operated carotid. Other major complications included respiratory failure (5%), multisystem failure (8%), and myocardial infarction (8%). The overall mortality was 12%. Ten of the 12 deaths were directly related to the cardiac operation, and 2 died as a result of stroke. We conclude that a combined carotid and coronary artery operation results in a high morbidity and mortality in institutions with excellent records for each operation when performed separately. Whenever possible, these high risk patients should be carefully assessed regarding the need for both procedures, since prophylactic carotid endarterectomy has not been shown to significantly reduce the neurologic risk of coronary bypass.

Real-time color duplex scanning after sclerotherapy of the greater saphenous vein.

A color real-time duplex scanner was used to scan the greater saphenous vein in 89 limbs of 55 patients to study the efficacy of prior greater saphenous vein sclerotherapy. The greater saphenous vein was insonated from the saphenofemoral junction to the knee to evaluate both reflux to a standardized 30 mm Hg Valsalva maneuver and evidence of greater saphenous vein obliteration by sclerotherapy. These data were correlated with the number of sclerosing injections used (mean, 1.8; range, 1 to 6), time from the last injection (mean, 27.5 mo.; range, 3 to 55 mo), and concentration of injectant used (0.5% to 3% sodium tetradecyl sulfate). Fifty-one of 89 injected limbs (57%) demonstrated reflux through the saphenofemoral junction, and reflux down the more distal greater saphenous vein was found in 67 of 89 injected limbs (75%). Greater saphenous vein obliteration was noted in only 18 of 89 injected limbs (20%); two were totally obliterated, and 16 were partially obliterated. The greater saphenous vein was obliterated in 6% below a refluxing saphenofemoral junction and in 40% below a nonrefluxing junction. A greater saphenous vein obliteration rate of 9% was found with a refluxing greater saphenous vein, and 50% in a nonrefluxing greater saphenous vein. Femoral vein reflux was identified in 11 of the 110 limbs (10%) and in every case was associated with both saphenofemoral junction and greater saphenous vein reflux. We noted a trend toward more successful results with more concentrated injectate (3% sodium tetradecyl sulfate). Fifty percent of patients reported improvement in symptoms.(ABSTRACT TRUNCATED AT 250 WORDS)

Comparison of transcranial and cervical continuous-wave Doppler in the evaluation of intracranial collateral circulation.

Adequate intracranial collateral circulation reduces risk of stroke in carotid artery surgery. To evaluate their relative accuracies in assessing intracranial collateral blood flow, we prospectively compared transcranial Doppler and continuous-wave Doppler of the cervical carotid arteries combined with compression of the common carotid artery in 28 consecutive patients before carotid endarterectomy. Ten healthy volunteers served as controls. Three patients (11%) were excluded from compression of arteries because of diffuse disease in the common carotid artery. A total of 199 compressions were performed without complications. Lack of a suitable transtemporal window precluded the performance of transcranial Doppler in three patients (12%). The anterior communicating artery was identified in all the normal volunteers and 80% of patients by both methods. The posterior communicating artery was identified by both methods in 16 of 20 attempts in controls. Continuous-wave Doppler identified the posterior communicating artery in 30 of 50 attempts in patients; transcranial Doppler identified the posterior communicating artery in 20 of 44 attempts in patients (p greater than 0.5). Detection of intracranial collaterals correlated with intraoperative carotid artery back pressure measurements in 23 of 25 patients (92%). We conclude that continuous-wave Doppler of the extracranial arteries combined with common carotid artery compression is a safe and easy way to detect intracranial collaterals, with an accuracy equivalent to transcranial Doppler.

Does carotid restenosis predict an increased risk of late symptoms, stroke, or death?

The identification of carotid restenosis as an unexpected late complication of carotid endarterectomy has prompted concerns regarding its importance as a source of new cerebral symptoms, stroke, and death. To investigate these concerns, we analyzed a consecutive series of 507 patients undergoing 566 carotid endarterectomies, each documented as technically satisfactory. Post-operative duplex Doppler examination data at 3 days, 1, 3, 6, 12 months, and annually thereafter in 484 arteries (85.5%) permitted classification of these arteries according to the most severe degree of postoperative stenosis: normal (n = 306); 1% to 19% (n = 89); 20% to 50% (n = 40); more than 50% (n = 49, including 8 occluded). The incidence of more than 50% restenosis was 14.5% in female and 7.7% in male patients (p = 0.003). Life table analyses to 10 years revealed a significantly greater life expectancy among those with restenosis (p = 0.05). Stroke was also less likely in patients with restenosis, although this difference did not reach statistical significance. When survival and stroke were both endpoints, the likelihood of patients with more than 50% restenosis remaining alive and stroke free was also greater than the less than 20% stenotic group (p = 0.03). Thus patients with carotid restenosis were less likely than patients with normal postoperative scans to have late symptoms, stroke, or early death.

Utility of computed tomography for surveillance of small abdominal aortic aneurysms. Preliminary report.

To assess the ability of computed tomography to predict the potential for expansion of small abdominal aortic aneurysms, we analyzed the computed tomographic scans of 30 patients who had two or more abdominal computed tomographic scans at least 6 months apart between 1979 and 1989. Clinical variables and 10 defined objective characteristics of computed tomography were evaluated. Twenty-five men and five women with abdominal aortic aneurysms ranging from 30 to 64 mm (mean, 45 mm) were followed up with serial computed tomographic scans for a mean (+/- SE) of 26 +/- 3 months. In 19 patients, enlargement of aneurysm diameter of 3 mm or more on serial computed tomographic scans was noted, whereas in 11, there was little or no expansion. Of the clinical variables studied, only serum cholesterol correlated with an increased risk of expansion. Thrombus area, measured by computed tomography, was 7.3 +/- 0.9 cm2 in enlarging aneurysms vs 4.3 +/- 0.9 cm2 in stable aneurysms. Based on these preliminary data, we conclude that computed tomography may provide valuable information about the likelihood of future expansion of small abdominal aortic aneurysms.

Propagation of deep venous thrombosis identified by duplex ultrasonography.

To investigate the efficacy of anticoagulation in preventing continuing thrombosis, we prospectively evaluated 24 patients with acute deep venous thrombosis using duplex ultrasonography. All patients were hospitalized with conclusive ultrasonic evidence of deep venous thrombosis identified in one of four levels: I, calf only; II, calf-popliteal; III, calf-popliteal-femoral; or IV, calf-popliteal-femoral-iliac. Duplex scans were obtained on admission and on three subsequent occasions during therapy. Progression of thrombosis was defined as advancement of thrombus to the more proximal venous level. Demographic data, symptoms, risk factors for deep venous thrombosis, physical findings, anticoagulation regimens, and hematologic variables were ascertained. Adequacy of anticoagulation was defined as elevation of baseline activated partial thromboplastin time by 150%. Nine patients (38%) had progression of thrombosis, and 15 (62%) had stable or improving duplex scans. Progression occurred as follows: I----II (2), I----III (2), II----III (1), and III----IV (4). Of the demographic and clinical variables examined, only smoking correlated with progression of thrombus (p = 0.04). Average heparin dose in the stable group was 1214 +/- 294 units/hr and 1122 +/- 248 units/hr in the group that progressed (p = 0.8): activated partial thromboplastin time was 45.6 +/- 7 seconds in the stable group and 49.8 +/- 9 seconds in the progression group (p = 0.7). Nine patients in the stable group had consistently adequate anticoagulation, whereas six did not; six in the progression group were consistently anticoagulated, and three were not. Two patients (one with stable thrombus and one with progressive thrombus) suffered nonfatal pulmonary emboli. Clot progression as determined by duplex scanning did not predict acute complications of deep venous thrombosis.

The natural history of amaurosis fugax with minor degrees of internal carotid artery stenosis.

The natural history of amaurosis fugax with hemodynamically insignificant degrees of internal carotid artery stenosis is uncertain. Seventy-three patients over age 40 who presented with amaurosis fugax without obvious cause and had ipsilateral stenoses of 50% or less with carotid duplex scanning were followed for a mean period of 35.5 months (range 3-110) without surgical intervention. At the initial vascular laboratory duplex evaluation, 35 patients had normal arteries (47.9%), 29 had minor (0-19%) stenoses of the ipsilateral internal carotid arteries (39.7%), and 11 had 20-50% stenosis (15.1%). Four patients with 0-19% stenosis and one patient with 20-50% stenosis experienced a subsequent stroke or permanent ipsilateral blindness. When analyzed by life-table format, stroke, blindness, and early death were more frequent in patients with minor degrees of stenosis than in those with normal arteries. Investigations in all patients with amaurosis fugax should be aimed at identifying whether the symptoms are explained by arteriosclerotic, systemic, collagen, cardiac, hematologic, or ophthalmologic disease. When no other etiology is found, and localized carotid bifurcation atherosclerosis of even modest degrees is identified, an atheroembolic etiology should be considered.

Intraoperative transcranial Doppler: limitations of the method.

To test the hypothesis that the transcranial Doppler is a useful technique for intraoperative neuromonitoring, we prospectively used it to study 83 patients undergoing carotid end-arterectomy. A 2 MHz pulsed-wave, range-gated transcranial Doppler was positioned at the transtemporal window after induction of general anesthesia. Mean middle cerebral artery velocity, intraarterial blood pressure, end-tidal PCO2, heart rate, and a spectral array of electroencephalographic activity were recorded continuously throughout the operation. Internal carotid artery back pressure was measured routinely. On completion of the endarterectomy, duplex ultrasound examinations and arteriograms were uniformly obtained to assess technical adequacy. Forty-nine of the 83 patients (60%) had complete preoperative and intraoperative transcranial Doppler examinations. Eleven (13%) had incomplete assessments because of small or absent transtemporal windows. Twenty-three (27%) had unsuccessful monitoring because of technical difficulties, primarily because of inability to maintain probe position--with loss of mean middle cerebral artery velocity recording. In the patients with complete studies, transcranial Doppler failed to provide information that altered surgical therapy. All monitoring modalities were normal in the one patient (1.2%) who sustained an operative stroke. We conclude that at this time, transcranial Doppler has not been useful to routinely monitor the intraoperative events during carotid endarterectomy.

The elusive isolated hypogastric artery aneurysm: novel presentations.

Isolated aneurysms of the internal iliac artery are rare. Their anatomic location makes them true pelvic aneurysms and they may grow to a large size undetected. Their late recognition may be prompted by rupture or symptoms related to compression of neurologic, gastrointestinal, genitourinary, or venous structures. We have encountered three isolated hypogastric artery aneurysms with unique presentations. In one patient with bilateral isolated hypogastric artery aneurysms, one ruptured into the bladder, and at a later time the other caused ureteral obstruction. Another patient had obturator neuropathy as a result of his aneurysm. In the patient with large bilateral aneurysms, one was detected by rectal examination, and the other was found by palpation of the abdomen. The second patient with a smaller aneurysm required examination of the pelvis by CT scanning to establish the diagnosis. Awareness of the existence of these lesions is required to identify such patients who describe symptoms uncommonly associated with abdominal aneurysms. Operative management consisted of exclusion of the aneurysm and partial or complete aneurysmorrhaphy with preservation of iliac arterial flow to maintain extremity perfusion. Recovery was complete in each instance. A review of published cases is presented.