Management of splenic artery aneurysms: the significance of portal and essential hypertension.

BACKGROUND: Splenic artery aneurysm(s) (SAA) are rare. But the incidence and significance of SAA among patients with portal hypertension (PHTN), especially among those who undergo orthotopic liver transplantation (OLT), have not been clearly delineated. STUDY DESIGN: An 11-year (February 1987 to June 1998) retrospective review of our experience with treated SAA was performed. Patient characteristics, risk factors, clinical presentation, surgical management, aneurysm characteristics, and patient outcomes were assessed. Patients were separated according to a history of PHTN for analysis. Patients were also subdivided into ruptured versus elective presentations. RESULTS: Thirty-four patients (22 in the PHTN group) were treated for SAA during the study period. Sixty-two percent (21 of 34) were women; the average age was 50.6 years. In patients without a history of PHTN (n = 12), essential hypertension was a significant risk factor (p < 0.001) for development of SAA. All patients underwent surgical treatment for SAA: resection with splenectomy (n = 23), ligation with splenectomy (n = 5), ligation of SAA only (n = 4), and vascular reconstruction (n = 2). The average size of all treated SAA was 4.8 +/- 2.6 cm, ranging from 1.5 to 12cm. Operative mortality after SAA rupture (n = 15) was 40%, compared with zero mortality for elective SAA repair (n = 19, p < 0.005). Rupture of SAA was associated with a higher mortality in patients with PHTN compared with patients without such history (56% versus 17%, respectively). After a mean followup period of 46 months, survival after rupture was 60% in contrast to 84% after elective repair. The majority of our patients with a history of PHTN (20 of 22) has undergone OLT, representing 0.46% of all OLT recipients (n = 4,374) during the study period. In four patients, SAA were repaired concurrently during transplantation. Of the 7 patients presented with rupture of SAA after OLT, 6 patients presented within 3 to 16 days postoperatively, with a median of 6 days and an overall mortality of 57%. CONCLUSIONS: Essential hypertension and PHTN appear to be significant risk factors for development of SAA. Rupture of SAA is associated with a significant mortality, highest among patients with PHTN. Elective repair remains a safe and effective method of treatment. The significance of SAA is recognized among patients undergoing liver transplantation. A decision should be made to screen and electively treat SAA found in liver transplant patients, especially if the aneurysm is larger than 1.5 cm. Awareness of the increased rupture risk is crucial in management during the immediate posttransplant period.

Iliocaval complications of retroperitoneal fibrosis.

BACKGROUND: Retroperitoneal fibrosis can compress ureters, nerves, and blood vessels in the abdomen. However, clinically significant large-vein obstruction secondary to this process is rare. METHODS: Three hundred forty patients with retroperitoneal fibrosis were treated at our institution between 1976 and 1993. The clinical data from seven of these patients, who were treated for iliocaval complications of retroperitoneal fibrosis, were reviewed. RESULTS: Six patients had signs and symptoms of chronic obstruction, and one patient presented with acute iliocaval thrombosis and underwent attempt at venous thrombectomy in the referring hospital. All patients exhibited extremity edema and three had venous claudication. Iliocaval occlusion was confirmed in all patients by venography, computed tomography, or magnetic resonance imaging. The obstructive process involved the iliocaval tree (four patients), the inferior vena cava alone (two patients), and the iliac vein alone (one patient). Five patients were managed conservatively with leg elevation, compression stockings, and anticoagulation. Two patients received prednisone. One patient underwent an iliocaval bypass from the external iliac vein to the juxtarenal cava using a ringed polytetrafluoroethylene graft with a femoral arteriovenous fistula. A second patient with an isolated left common iliac vein obstruction underwent a left-to-right femorofemoral saphenous vein bypass. Four patients treated conservatively continued to have extremity edema. The two patients managed surgically remain asymptomatic from venous insufficiency, with patent grafts at 25 and 12 months after surgery, respectively. CONCLUSION: Iliocaval obstruction is an unusual complication of retroperitoneal fibrosis. Although most cases can be managed conservatively, reconstruction is an option for patients who have failed medical treatment and are symptomatic secondary to chronic venous obstruction. Lifelong anticoagulation should be considered for all patients with progressive iliocaval obstruction secondary to retroperitoneal fibrosis.

Oxygen-dependent chronic obstructive pulmonary disease does not prohibit aortic aneurysm repair.

BACKGROUND: Severe oxygen-dependent chronic obstructive pulmonary disease (COPD) is considered by many to be a contraindication to open abdominal aortic aneurysm (AAA) repair. We reviewed our own experience with this patient population. METHODS: From July 1995 to March 1999, 14 consecutive patients limited by home oxygen-dependent COPD underwent elective open infrarenal AAA repair. Their medical records were reviewed. RESULTS: The mean aortic aneurysm size was 6.3 cm. The mean PaO2 = 70 mm Hg, PaCO2 = 45 mm Hg, forced expiratory volume in 1 second (FEV1) = 34% of predicted, and forced vital capacity (FVC) = 67% of predicted. All 14 patients were extubated within 24 hours, mean length of hospital stay was 5.9 days, and there were no perioperative deaths. CONCLUSIONS: Severe home oxygen-dependent COPD is not a contraindication to safe elective open AAA repair.

Mesenteric venous thrombosis.

MVT is an uncommon form of visceral ischemia. Symptoms and signs of MVT are usually nonspecific and should not be relied on for accurate diagnosis. A simple, logical diagnostic algorithm can be used to manage most of these patients (Fig. 6). CT or MRI appears to be the most sensitive diagnostic test and should be obtained early for any patient suspected of harboring MVT. Patients with peritonitis require prompt abdominal exploratory laparotomy to rule out ischemic bowel. Once the diagnosis of acute MVT is confirmed, the patient should be anticoagulated with heparin. During operation, all nonviable bowel should be resected with intent for a second-look laparotomy after 24 hours if there is any question of ongoing ischemia. We recommend using fluorescein-assisted evaluation of marginally viable bowel intraoperatively. After the operation, anticoagulation is continued with heparin and then oral warfarin sodium when the patient's bowel function returns. For those patients without peritonitis, we recommend prompt anticoagulation followed by at least a 48- to 72-hour period of close observation. All patients who have had an episode of acute MVT and do not have a contraindication to anticoagulation should be anticoagulated on a life-long basis with warfarin sodium. Despite our increased awareness of acute MVT, the 30-day mortality rate remains high. Acute MVT typically has a more insidious and unpredictable course than do other forms of visceral ischemic syndromes, with a mortality rate as high as that of its arterial counterpart. Although there has been a slight improvement in survival during the last 20 years, the recurrence rate remains high and the long-term prognosis is poor in this group of patients. Survival of patients with chronic MVT is better than that of those with acute MVT and appears to be determined by the underlying disease.

Heparin-induced thrombocytopenia: pathophysiology.

HIT is a procoagulant disorder that is associated with significant morbidity and mortality if undetected and untreated. It occurs in approximately 5% of all patients receiving heparin therapy. HIT can be separated into two different types based on the clinical presentation and the pathophysiological mechanism. Type I HIT is an early, mild form of thrombocytopenia that is thought to be non-immune-mediated. No therapy is necessary for this type of HIT. Type II HIT has a delayed onset and is immunologically mediated. It is the more severe form and is associated with the development of HITT. Once suspected or diagnosed, all heparin therapy must be withdrawn. The thrombocytopenia will generally resolve within several days to a week. Minimizing the risk to the patient for developing HIT is the best form of prevention currently available.

The effects of nimodipine on ischemic injury of the spinal cord during thoracic aortic cross-clamping.

BACKGROUND: The purpose of this study was to evaluate the protective effects of a neuroselective calcium antagonist, nimodipine on spinal cord ischemia during and after thoracic aortic cross-clamping. METHODS: Thirty adult dogs underwent 60 minutes of thoracic aortic cross-clamping via a left thoracotomy. The dogs were randomized into 3 groups (n = 10) and received either intravenous control (normal saline), sham (polyethylene glycol) or nimodipine solution during a period of 150 minutes. Spinal cord perfusion (SCP) was directly monitored using a laser doppler flowmeter. After 48 hours, neurologic status was assessed using Tarlov scores and the spinal cords evaluated histologically for evidence of ischemia (grades 1-4: severe to mild ischemia). RESULTS: Twenty-six dogs survived the operation. Proximal (carotid) blood pressure increased 30-40% and cerebrospinal fluid (CSF) pressure increased 50% during cross-clamping for all 3 groups. The SCP decreased predictably during cross-clamping in all dogs but after unclamping, the nimodipine group had significantly less hyperperfusion than the saline and sham control groups (30 min after unclamping, control: 74.1 +/- 12.6 ml/min, sham: 51.8 +/- 4.15 ml/min, nimodipine: 33.1 +/- 3.9 ml/min, p = 0.04). This hyperperfusion phenomenon correlated with adverse neurologic (Tarlov score) outcome (p = 0.01). Paraplegia rates were 78% (control), 70% (sham) and 71% (nimodipine) (p = NS). The histologic grades of the spinal cords from those dogs which received nimodipine tended to correspond to better tissue preservation (control: 1.72 +/- 0.49, sham: 1.75 +/- 0.46, nimodipine: 2.14 +/- 0.56, p = NS). CONCLUSIONS: Nimodipine used as single agent therapy failed to show a statistically significant clinical neurologic benefit. However, nimodipine significantly decreased postischemic reperfusion hyperemia in the spinal cord as measured by laser doppler flowmetry. This reduced hyperperfusion, which significantly correlated with functional outcome, may be responsible for dampening neural cell damage. Thus, nimodipine should be considered as an adjunct to a multimodality approach in the prevention of spinal cord ischemia during thoracic and thoracoabdominal aortic reconstructions.

An arginine analog inhibits responses of both the endothelium and smooth muscle of canine in situ vein grafts.

Increased shear, pressure, and oxygen tension in vein grafts may alter production of endothelium-derived vasoactive and anti-mitogenic factors such as nitric oxide which subsequently affect development of neointimal hyperplasia. This study was designed to determine whether or not nitric oxide mediates endothelium-dependent responses in femoral in situ vein grafts. Non-reversed, canine femoral vein grafts were placed bilaterally to bypass a ligated segment of the femoral artery in dogs. After 6 weeks, the grafts were removed, cut into rings, and suspended in organ chambers for measurement of isometric force. In some rings the endothelium was removed deliberately. In the presence of indomethacin, the synthetic analog of L-arginine, L-N(G)-monomethyl-arginine (10(-4) M; L-NMMA) did not cause a significant change in baseline tension of rings with endothelium. L-NMMA reduced only contractions of rings with endothelium to the alpha-adrenergic agonist UK 14,304. The analog also reduced maximal relaxations to the calcium-ionophore, A23187 in rings with endothelium. In addition, L-NMMA reduced relaxations of rings without endothelium to adenosine diphosphate by 35%. Positive immunostaining for nitric oxide synthase was present in both the myointima and media of histological sections of grafts. In conclusion, these results suggest that in situ vein grafts exhibit two unique properties which are unlike unoperated arteries or veins: (i) alpha2-adrenergic receptors may be coupled to the release of contractile endothelium-derived factors associated with production of nitric oxide: and (ii) nitric oxide may be released by the smooth muscle in response to purinergic stimulation. The presence of nitric oxide synthase throughout the wall of the graft may result in production of nitric oxide in response to adenosine diphosphate released by platelets and to circulating catecholamines.

A biomechanical study of the collateral ligaments of the proximal interphalangeal joint.

Collateral ligament injuries of the proximal interphalangeal joint are common. A significant number of these injuries result in complete rupture of the ligament. The forces that damage the ligaments are abduction and adduction stresses. Previous studies have investigated laxity, angulation, and patterns of failure, but detailed biomechanical rupture studies are scant. Sixty-eight proximal interphalangeal joints from fresh human cadaver fingers (average age, 67 years) were stressed at velocities of 1 mm/sec, 4 mm/sec, and 10 mm/sec. Sectioning studies were also done. Four distinct rupture patterns were noted: midsubstance tear, proximal detachment, distal detachment, and distal avulsion fracture. The prevalence of these patterns differed with the rate at which the ligaments were stressed. Lower speeds tended to produce midsubstance tears, while higher speeds yielded distal damage. The study confirmed that the lateral collateral ligament is the primary restraint against medial-lateral stress and that other supporting structures (the extensor hood and the palmar plate) did not contribute significantly to side-to-side stability.

Two unusual variants of internal carotid artery aneurysms due to fibromuscular dysplasia.

Aneurysms of the internal carotid artery (ICA) secondary to fibromuscular dysplasia (FMD) are extremely rare. We report two unique variants of extracranial ICA aneurysms due to FMD. The first patient was a hypertensive 51-year-old woman who was found to have a nontraumatic, nonmycotic saccular pseudoaneurysm of the right ICA. The second patient was a 46-year-old woman who presented with 90% stenosis and a focal dissecting aneurysm of the right ICA. Both underwent successful aneurysm resection with interposition saphenous vein grafting after anterior subluxation of the mandible. A review of the literature revealed only 21 other reported cases of aneurysms of the extracranial ICA due to FMD; all were managed successfully with surgical repair. Surgery can be performed with minimal or no morbidity, even in the distal ICA, if the exposure is adequate.

Experimental evaluation of bleeding complications, thrombogenicity and neointimal characteristics of prosthetic patch materials used for carotid angioplasty.

Experiments were designed to compare perioperative blood loss, early thrombogenicity and morphologic and functional characteristics of the neointima of three types of prosthetic materials used for carotid artery patch angioplasty. Bilateral carotid patch angioplasties were performed in 20 dogs, using 20 gelatin-impregnated fluoropassivated Dacron (GIF), 10 untreated knitted Dacron and 10 expanded polytetrafluoroethylene (PTFE) patches (5 cm2). Intraoperative blood loss, platelet deposition at 24 h and neointimal morphology at 6 weeks after the operation were assessed. Bioassay of the neointima was performed at 6 weeks in 16 patches. Mean (s.e.m.) blood loss was significantly less in GIF patches (14.7 (2.7) ml) compared with either PTFE (75.6 (24) ml) or untreated Dacron (64.3 (9.5)) (P < 0.005). Mean (s.e.m.) platelet deposition in GIF patches (1380 (328) platelets/cm2) was approximately 50% less at 24 h than in untreated Dacron (2562 (1035) platelets/cm2) or PTFE (2140 (998( platelets/cm2) patches (P < 0.05). Neointimal coverage was greater in PTFE (94 (1.3%)) compared with GIF (79 (2.7%)) or untreated Dacron (86 (2.4%)) patches (P < 0.05). The thickness of the neointimal layer of PTFE (0.5 (0.01) mm) patches was greater than other patch types; GIF (0.2 (0.01) mm) or untreated Dacron (0.3 (0.01) mm) (P < 0.50). Under bioassay conditions, acetylcholine caused release of vasoactive relaxing factor(s) from all patches. However, relaxations from baseline were less with GIF patches (-37.9 (11.7)% versus -54.5(9.6( for untreated Dacron; -50.2 (15.2)% for PTFE) (P = n.s.). Endothelin-1 release occurred from all patches and was increased with the extent of neointimal coverage. These data demonstrate that GIF patches caused the least perioperative bleeding, were the least thrombogenic at 24 h and developed the thinnest neointima at 6 weeks. All patch materials developed a functioning neointima.

Low dose heparin therapy: in vitro verification of antithrombotic effect.

Low dose heparin therapy has been used routinely for prophylaxis of deep venous thrombosis, yet in vitro data regarding its antithrombotic effects are sparse. The effects of heparin on venous thrombus formation were studied in an in vitro perfusion system. Fresh blood collected from human volunteers was treated with varying heparin doses and perfused at a shear rate of 100 sec-1 over everted, injured porcine vein segments, simulating conditions in the venous circulation. Platelet and fibrin deposition were measured by use of indium 111 and iodine 125 radiolabels, respectively. The effects of heparin on the intrinsic coagulation cascade were monitored by the activated clotting time. Increasing doses of heparin resulted in significant reductions in fibrin and platelet deposition (ANOVA F = 2.67 and 3.17, respectively, p less than 0.05). At a dose of only 0.19 USP units/ml blood, equivalent to a 1000 unit bolus of heparin in a 70 kg man, a noticeable reduction in both fibrin and platelet deposition was observed without an increase in the activated clotting time. These data confirm the antithrombotic effects of heparin at low dose ranges and may explain the clinically observed phenomenon of deep venous prophylaxis without an appreciable alteration in the conventional coagulation assays.

Future alternatives to heparin: low-molecular-weight heparin and hirudin.

The antithrombotic effects of standard heparin were compared with those of low-molecular-weight heparin (LMWH) and hirudin by use of an in vitro perfusion system. Fresh blood collected from human volunteers was treated with varying doses of these three agents and perfused in a recirculating system over everted porcine vein segments. A low shear rate (100/sec) was selected to simulate conditions in large arteries and veins. Platelet and fibrinogen deposition were evaluated with indium 111 and iodine 125 radiolabels, respectively. Anticoagulant activity was assessed by measuring the activated clotting time (ACT). Anti-Xa activity was assayed to determine the degree to which these agents used antithrombin III pathways. Low-molecular-weight heparin was the weakest anticoagulant, requiring 32 micrograms/ml blood to double the ACT. By contrast, the ACT doubled with only 0.75 and 1.10 micrograms/ml blood of heparin and hirudin, respectively. Heparin and hirudin inhibited platelet and fibrin deposition at equivalent doses. Low-molecular-weight heparin was a less potent inhibitor of fibrin than heparin or hirudin. Hirudin, a direct thrombin inhibitor, exhibited minimal anti-Xa activity, contrasted with 0.14 anti-Xa units/micrograms for LMWH and 0.13 anti-Xa units/mg for heparin. These data suggest that heparin and hirudin are more potent anticoagulants and antiplatelet agents than LMWH.

Left atrial myxoma with embolization presenting as an acute infrarenal aortic occlusion.

We present the case of a 42-year-old woman who had acute total infrarenal aortic occlusion resulting from embolic implantation from a left atrial myxoma. We propose that the small aortic aneurysm that was discovered and repaired in this case may be a direct result of invasion and destruction of the aortic elastic laminae by implanted myxomatous tissue originating in the primary atrial tumor. This behavior has been noted in small vessels of the cerebrum and upper extremities with this lesion, but no prior reports of this occurrence in the aorta has been noted after extensive review of the literature.

Long-term fate of the aneurysmal sac after endoluminal exclusion of abdominal aortic aneurysms.

PURPOSE: Shrinkage of an abdominal aortic aneurysm (AAA) is the hallmark of successful endoluminal treatment. Our goal was to prospectively assess the midterm to long-term shrinkage of the AAA sac after endovascular repair. METHODS: A total of 123 patients with AAA underwent endoluminal treatment with the Ancure device at our institution between February 1996 and February 2000. At least a 1-year follow-up was available for 70 of the 123 patients. AAA sac size, presence of endoleaks, calcifications, and outcome data were collected on these patients at 6, 12, 24, and 36 months after repair and compared with the preoperative AAA size and characteristics. All endoleaks found at the 6-month follow-up visit were treated aggressively with embolotherapy. An AAA sac regression of 0.5 cm or more was considered the minimum measurable decrease. Regression of the sac diameter to 3.5 cm or less was considered a complete collapse of the sac. RESULTS: Successful endoluminal repair was accomplished in 119 of 123 patients. The mortality rate was 0.8% (1/123). There was a steady decrease in AAA sac size from baseline (5.56 +/- 0.1 cm), to 6 months (5.0 +/- 0.14 cm, P =.0006), to 12 months (4.65 +/- 0.13 cm, P =.04), and to 24 months (4.26 +/- 0.16 cm, P =.03). At 24 months, 74% (29/39) had a decrease in sac size of 0.5 cm or more, with 28% (11/39) complete collapse. Patients with initial endoleaks had the same likelihood of regression of sac size (> or = 0.5 cm) when compared with the group of patients with no endoleaks at the 24-month evaluation (64% vs 76%, P =.09). CONCLUSION: Endoluminal AAA repair resulted in a significant reduction in sac size that continues up to 2 years. Significant shrinkage occurs as early as 6 months after placement. The initial presence of endoleaks does not predict the lack of sac regression.

Surgical technique and preliminary results of endoscopic subfascial division of perforating veins.

PURPOSE: Direct surgical ligation of incompetent perforating veins has been reported to effectively treat severe chronic venous insufficiency. It is associated, however, with significant wound complications. We evaluate our early experience with endoscopic subfascial division of the perforating veins. METHODS: From August 5, 1993, to December 31, 1994, 11 legs in nine patients (five male and for female) were treated with endoscopic subfascial division of perforating veins. Nine of the 11 legs had active or recently healed venous ulcers. Mean duration of the ulcerations was 5.6% years. Standard laparoscopic equipment with 10-mm ports was used to perform clipping and division of medial perforating veins through two small incisions made just below the knee, avoiding the area of ulcer and lipodermatosclerosis. Carbon dioxide was insufflated at a pressure of 30 mm Hg into the subfascial space to facilitate dissection, and a pneumatic thigh tourniquet was used to obtain a bloodless operating field. Concomitant removal of superficial veins was performed in eight limbs. Mean follow-up was 9.7 months (range, 2 to 13 months). RESULTS: A mean of 4.4 perforating veins (range, 2 to 7) were divided; tourniquet time averaged 58 minutes (range, 30 to 72). Wound infection of a groin incision and superficial thrombophlebitis were early complications; each occurred in one patient. In seven legs the ulcer healed or did not recur and symptoms resolved. In three legs, the ulceration improved, and in one it was unchanged. CONCLUSIONS: Endoscopic subfascial division of perforating veins seems to be a safe technique, with favorable early results obtained in a small number of patients. This preliminary experience supports further clinical trials to evaluate this technique.

Exclusion of accessory renal arteries during endovascular repair of abdominal aortic aneurysms.

OBJECTIVE: Adequate proximal neck length is important for proper endovascular treatment of abdominal aortic aneurysms (AAAs). Placement of endografts in AAAs with relatively short proximal necks may require covering the origin of accessory renal arteries. Exclusion of these arteries carries the theoretical concern of regional renal ischemia associated with loss of parenchyma or worsening hypertension. We reviewed our experience with accessory renal exclusions during endovascular AAA repair to determine the frequency and severity of complications. METHODS: Complete records were available for review on 311 of 325 consecutive patients treated with endovascular grafts for AAAs from February 6, 1996, to March 15, 2001. The presence of accessory renal arteries was ascertained from preoperative/intraoperative aortography or from computed tomographic scanning. Sizes of the accessories were measured by using the main renal arteries as a reference. Considerations for excluding the accessory renal arteries were based on the likelihood of successful proximal attachment to healthy aorta, an accessory vessel whose size does not exceed the diameter of the main renal artery, and the absence of renal disease. RESULTS: The mean follow-up was 11.5 months. Fifty-two accessory renal arteries were documented in 37 patients (12%), ranging from 1 to > or =3 per patient. Of these, 26 accessory renal arteries were covered in 24 patients. Patients ranged in age from 57 to 85 years (mean, 74.1 years), with 20 men and 4 women. The Ancure device was used in 23 patients and the Excluder device in one. Of the accessories excluded, 22 originated above the aneurysm and 4 originated directly from the aneurysm itself. There were no perioperative mortalities. One patient died 5 months after surgery from an unrelated condition. There was one type I (distal) endoleak and no type II endoleaks. Five patients (21%) had segmental renal infarction associated with the side of accessory renal artery exclusion. Only one patient with segmental infarction had significant postoperative hypertension that resulted in changes in blood pressure medication. The blood pressure reverted to normal 3 months later. One patient with a stenotic left main renal artery required exclusion of the accessory renal artery for successful proximal attachment. Serum creatinine levels remained unchanged throughout follow-up in all but one patient, in whom progressive postoperative renal failure developed despite normal renal flow scan, presumably from intraoperative manipulation and contrast nephropathy. CONCLUSION: Exclusion of accessory renal arteries to facilitate endovascular AAA repair appears to be well tolerated. Long-term sequelae seem infrequent and mild.

Thrombin injection versus compression of femoral artery pseudoaneurysms.

OBJECTIVE: The compression of femoral artery pseudoaneurysms is a time consuming, painful, and sometimes unsuccessful procedure. Thrombin injection has been advocated as a superior alternative. In this study, we compare our experiences with both techniques. METHODS: All the records of femoral artery false aneurysms that were treated in the vascular laboratory from January 1996 to April 1999 were retrospectively reviewed. Treatment with ultrasound scan-guided compression was compared with treatment with dilute thrombin injection (100 U/mL). RESULTS: Both groups had similar demographics and aneurysm sizes (P >.2). Of the pseudoaneursyms, 88% were caused by cardiac catheterization and the others were the results of femoral artery access for cardiac surgery (6%), arteriography (5%), and renal dialysis (1%). Compression was successful in 25 of 40 patients (63%). Nine persistent aneurysms necessitated operation, and six were treated successfully with thrombin injection. Primary thrombin injection successfully obliterated 21 pseudoaneurysms in 23 patients. Overall, 27 of 29 pseudoaneurysms were treated successfully with thrombin injection (93%). Thrombosis occurred within seconds of the thrombin injection and required, on average, 300 units of thrombin (100 to 600 units). The patients who underwent successful compression required an average of 37 minutes of compression (range, 5 to 70 minutes) and required analgesia on several occasions. No patients in the thrombin group required analgesia or sedation. Neither group had complications. A cost analysis shows that thrombin treatment results in considerable savings in vascular laboratory resource use but not in overall hospital expenditures. CONCLUSION: Ultrasound scan-guided thrombin injection is a safe, fast, and painless procedure that completely obliterates femoral artery pseudoaneurysms. The shift from compressive therapy to thrombin injection reduces vascular laboratory use and is less expensive, although it does not significantly impact hospital costs.

Utility of clinical pathway and prospective case management to achieve cost and hospital stay reduction for aortic aneurysm surgery at a tertiary care hospital.

PURPOSE: We reviewed our experience with a clinical pathway instituted in December 1993 for all nonurgent abdominal aortic aneurysm (AAA) surgery. METHODS: We analyzed a reference group of 49 consecutive pre-pathway AAA patients (group I) and the 44 patients enrolled in the first year of the pathway (group II). On the basis of the interim review of data collected during the first year, pathway modifications were made, and 34 patients enrolled after these modifications (group III) were also analyzed. RESULTS: Comparison of groups I and II showed that institution of the pathway resulted in a marginally significant reduction in mean charges of 14.7% (p = 0.09), and a slight fall in mean length of stay (LOS) (13.8 vs 13.1 days, NS) and mortality rate (4.1% vs 2.3%, NS). For group II, a significant correlate (p < 0.05) of increased charges was fluid overload as diagnosed by chest radiograph. This recognition led to active efforts to reduce perioperative fluid administration. Comparison of groups II and III revealed that the practice modifications led to marked reduction in the incidence of fluid overload (73% vs 24%; p < 0.01), mean charges (30.4% reduction; p < 0.05), mean LOS (13.1 vs 10.2 days; p < 0.05), and median LOS (11 vs 8 days). Multiple regression analysis of all pathway patients showed that preoperative renal insufficiency is a significant predictor of both increased LOS (p < 0.01) and charges (p < 0.01), but that age, sex, and coronary disease were not predictive. Of the postoperative parameters analyzed, important correlates of increased charges were acute renal failure (p < 0.01) and fluid overload (p < 0.01). CONCLUSIONS: Institution of a clinical pathway for AAA repair resulted in significant charge reduction and a slight reduction in stay. Practice modifications based on interim data analysis yielded further significant reductions in charges and LOS, with overall per-patient charge savings (group I vs III) of 40.6% (p < 0.05) and overall LOS reduction of 3.5 days (p < 0.05). The reduction in actual charges was seen despite an overall increase in the hospital rate structure. Comparing groups I, II, and III, we found no indication of increasing mortality rate. Ongoing analysis has identified correlates of increased charges, potentially permitting identification of high-cost subgroups and more focused cost-control efforts. Rather than restricting management, clinical pathways with periodic data analysis may improve quality of care.