Accreditation of vascular laboratories.
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Biomedical subjects
Publications and source records attributed to D F Bandyk.
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Slime-producing coagulase-negative staphylococci are pathogens in vascular surgery by virtue of their ability to adhere to and persist on prosthetic graft material. Inguinal and abdominal skin sites were cultured in 41 patients upon hospitalization, and slime production and antimicrobial susceptibility were assessed in all recovered staphylococcal isolates. Twenty-one patients eventually underwent lower-extremity revascularization. In the operative population, cultures were also obtained on the day of surgery and fifth postoperative day. All 21 patients received perioperative cefazolin. Of 327 coagulase-negative staphylococci recovered, Staphylococcus epidermidis (47%), S. haemolyticus (21%), and S. hominis (10%) were the predominant isolates. Slime-producing coagulase-negative staphylococci were recovered from 17 of 21 patients at admission but only from 8 of 21 patients on day 5 postoperation (P less than 0.05). S. epidermidis isolates demonstrated increasing multiple resistance from admission to 5 days postoperation to methicillin, gentamicin, clindamycin, erythromycin, and trimethoprim-sulfamethoxazole (P less than 0.05). All coagulase-negative staphylococcal isolates were susceptible to ciprofloxacin and vancomycin. Slime-producing capability was not associated with increased methicillin resistance for the recovered isolates. The data demonstrate that patients enter the hospital colonized with slime-producing strains of coagulase-negative staphylococci and that during hospitalization the staphylococcal skin burden shifts from a predominately susceptible to a resistant microbial population, which may enhance the importance of slime production as a risk factor in lower-extremity revascularization.
Abnormalities of the conduit, outflow tract, and graft hemodynamics are important elements in the mechanism of vein graft thrombosis, and their role must be defined when planning reoperation. In a consecutive series of 353 in situ saphenous vein bypass graftings performed for occlusive or aneurysmal disease, graft thrombosis occurred in 18 (5%) patients during the perioperative period and unexpectedly in 14 (4%) patients after discharge from the hospital. Assessment of graft hemodynamics (calculation of blood flow velocity) before thrombosis was helpful in predicting success after graft revision. Five grafts with known low flow (systolic flow velocity less than 40 cm/sec) that thrombosed in the perioperative period did not have patency restored by thrombectomy or graft replacement unless the outflow tract was also modified. If poor quality vein or technical error was the mechanism of thrombosis, translocation of the distal anastomosis to a proximal arterial segment (n = 4), and graft replacement with normal autologous vein (n = 5) or prosthetic graft (n = 1) were successful in relieving limb ischemia. After discharge from the hospital, unexpected graft thrombosis was successfully treated by a variety of secondary procedures (thrombolysis/thrombectomy, autologous or prosthetic replacement) if prior surveillance with duplex scanning demonstrated low flow as a result of graft stenosis (n = 7) or normal graft hemodynamics (n = 5). Prosthetic replacement of two failed bypass grafts with low flow caused by diseased outflow did not remain patent. Scrutiny of graft hemodynamics and limb arterial anatomy for alternative outflow sites can identify patients likely to benefit from reoperation after in situ bypass thrombosis.
The mechanisms involved in bacterial adherence to vascular grafts are important in understanding prosthetic infections. Albumin-coated Dacron (ACD) is a new development in vascular graft fabrication. However, albumin acts as a receptor for certain gram-positive bacterial adhesions. Five pathogenic, coagulase-negative Staphylococcus epidermidis strains were used to measure the differential microbial adherence to ACD versus untreated velour-knitted Dacron (VKD) vascular prostheses. Specimens of VKD, preclotted VKD, and ACD were inoculated with each of the five strains (10(7) colony-forming units/ml) for 2, 4, 8, 12, and 24 hours. After incubation, graft specimens were washed to remove nonadherent organisms and oscillated ultrasonically to remove adherent organisms. The sonication effluent was plated to trypticase soy agar to quantitate the adherent organisms. Adherence was significantly greater (p less than 0.01) to VKD compared with preclotted VKD and ACD at 2, 4, 8, and 24 hours. Four of the five study strains demonstrated significantly greater adherence to VKD than to either ACD or preclotted VKD. Adherence of S. epidermidis increased with exposure time. Albumin bonded to velour-knitted Dacron does not increase coagulase-negative staphylococcal adherence compared with the noncoated vascular prostheses. Binding albumin to vascular prostheses does not increase the risk of staphylococcal colonization.
The tensile strength and histologic features of anastomotic bonding were studied prior to and following in situ replacement of aortic vascular prostheses infected by Staphylococcus epidermidis. Sterile (n = 6) and infected (n = 19) Dacron grafts were used to replace the abdominal aorta of 25 dogs. After five weeks, grafts were explanted, and peak tensile force (measured in kilograms) required for anastomotic disruption was measured using a linear gain tensiometer. Anastomotic tensile strength (mean +/- SEM) of infected grafts (5.4 +/- 0.5 kg) was decreased when compared with that of sterile, control grafts (9.0 +/- 0.9 kg). The decreased anastomotic tensile strength of infected grafts was the result of an inflammatory aortitis adjacent to the suture line. Only grafts infected with the study strain of bacteria demonstrated signs of infection. In 19 dogs, the graft infection was treated by graft excision, antibiotic administration, and in situ graft replacement (Dacron or polytetrafluoroethylene prostheses). After five weeks and 12 weeks, anastomotic tensile strength of polytetrafluoroethylene (10.6 +/- 0.6 kg) and Dacron (10.8 +/- 0.5 kg) replacement grafts was similar to that of uninfected control grafts. In situ replacement of vascular prostheses infected by S epidermidis can result in graft healing with normal anastomotic bonding.
The influence of venous patching on luminal prostacyclin (PGI2) and thromboxane A2 (TBX) production of endarterectomized arteries was studied in a canine model. Fifteen dogs underwent bilateral common carotid endarterectomies. In each dog, one artery was closed primarily and the contralateral artery was closed by vein-patch angioplasty. At six and 12 weeks after operation, luminal prostanoid production from the venous patch, adjacent endarterectomized artery, and control artery and vein was measured by radioimmunoassay for 6-keto-prostaglandin F1 alpha and thromboxane B2. Venous patches underwent "incomplete" biochemical adaptation with decreased luminal production of PGI2 compared with control and endarterectomized arteries. Thromboxane production from venous patches was increased compared with normal vein but similar to control and endarterectomized arteries. At six weeks, PGI2 production of vein-patched arterial segments was increased compared with arteries closed primarily. These data indicate that vein-patch angioplasty favorably influences surface thrombogenicity of healing, endarterectomized arteries and support its use in reparative carotid surgery.
Aneurysm imaging is important in deciding on the timing of and operative approach for aneurysmorrhaphy. Various noninvasive and invasive imaging techniques are available for the anatomic definition of abdominal aortic aneurysms, involvement of adjacent structures, and intra-abdominal pathology. Careful preoperative evaluation can avert hemorrhagic, embolic, and ischemic complications of elective aneurysm repair.
Culture of prosthetic material is routinely used to exclude or implicate infection in the pathogenesis of late-appearing graft complications. In a canine model of aortic graft infection caused by a bacterial biofilm, the influence of culture media (blood agar and tryptic soy broth) and mechanical surface biofilm disruption (tissue grinding and ultrasonic oscillation) on microorganism recovery was determined. Dacron prostheses colonized in vitro with Staphylococcus epidermidis were implanted in the infrarenal aortas of 36 dogs. After 3 weeks an infection with anatomic characteristics of late graft infection in humans was present. Explantation (+/- surface biofilm disruption) of infected grafts showed broth culture was superior (p less than 0.001) to agar media in confirming infection. The recovery rate of S. epidermidis was 30% with agar media, was 72% with broth media alone, and was 83% with broth media plus biofilm disruption. In situ replacement of infected grafts plus parenteral antibiotics resulted in early (1 month) healing of 31 grafts without signs of infection. All replacement grafts were sterile when cultured in broth media alone, but the addition of biofilm disruption isolated the study strain from eight (22%) of 36 grafts (p less than 0.01). Biofilm disruption by tissue grinding or sonication increased bacteria recovery equally. When biofilm bacterial concentration was less than 100 colony-forming units/cm2 of graft, only culture in broth media reliably recovered microorganisms. In the absence of perigraft inflammation, microbiologic recovery techniques that identify bacterial biofilms are necessary to exclude infection in studies concerning the pathogenesis of late graft complications or the treatment of S. epidermidis prosthetic infections.
Compartment syndromes occur following lower extremity injuries and have been associated with the use of pneumatic or "medical" antishock trousers (MAST). Review of 12 previously reported cases and 15 new cases suggests that lower extremity trauma and systemic hypotension are cofactors responsible for the development of compartment syndrome but MAST use also contributes to the process by prolonging muscle ischemia. Complications of lower limb compartment hypertension may be averted by early recognition and fasciotomy. Associated amputations and mortality are directly related to the severity of injury, or indirectly to delay in diagnosis and treatment of the compartment syndrome and its complications.
Implementation of a protocol that monitored in situ saphenous vein bypass hemodynamics for low-flow states provided insight into the pathophysiologic characteristics and time course of graft failure. From 1981 to 1988, 250 in situ bypasses to popliteal (n = 83) or tibial (n = 167) arteries were performed in 231 patients. Indications for operation included critical limb ischemia in 232 cases (93%), popliteal aneurysm in 11 cases (4%), and disabling claudication in seven cases (3%). Arterial pressure measurements, continuous-wave Doppler spectral analysis, and duplex ultrasonography were used to assess patency, detect hemodynamic changes indicative of graft stenosis, and localize anatomic hemodynamic changes indicative of graft stenosis. Seventy grafts with correctable anatomic lesions (retained venous valves, graft stenosis, arteriovenous fistula, native vessel atherosclerosis) that decreased graft blood flow or ankle arterial pressure or both were identified. Correction of vein conduit or anastomotic lesions comprised 73 (77%) of the 95 revisions performed. Vein-patch angioplasty of a stenosis was the most common secondary operation performed. Graft revision was highest in the perioperative period (10% at 30 days), decreased to 7% per 6-month interval until 18 months, and was 3% per year thereafter. The primary patency rate of grafts not identified to have a correctable lesion was 86% at 4 years, a level similar to the secondary patency of 81% for grafts requiring one or multiple revisions. The surveillance protocol identified grafts with correctable lesions before thrombosis thereby permitting elective revision of patent grafts. Hemodynamic studies confirmed that a frequent mechanism of late failure of grafts was the development of a low-flow state produced by lesions not amenable to revision.
Patients suffering blunt leg trauma resulting in below-knee fracture, tibial artery injury, and soft-tissue damage are at major risk for amputation. In an attempt to identify the factors which may forecast limb loss despite vascular surgical repair, all patients with tibial fractures admitted between 1980-1988 were reviewed. Forty-four of 366 (12%) patients presented with clinical evidence of tibial artery injury. Twenty-seven of these 44 patients had angiographic evidence of at least one patent tibial vessel providing adequate distal flow. The remaining 17 patients required operative repair of injured tibial arteries because of persistent distal ischemia. The amputation rate was 35% (6/17--4 BKA, 2 AKA), three of these having patent vascular repairs at the time of the amputation. Operative indications for amputation were ischemic nonviable muscle in three patients, and severe soft-tissue wound infection in three. Patients who required amputation had a significantly greater incidence (Fisher's exact test) of three or more fascial compartments involved in muscular injury (p = 0.005), two or more injured tibial vessels (p = 0.01), failed vascular reconstruction (p = 0.03), a cadaveric foot at initial exam (p = 0.03), and severe muscle crush injury or muscle tissue loss (p = 0.03). No extremity was salvaged when more than two of these factors was present, and a failed vascular reconstruction led to limb amputation in all cases. These factors will predict an irretrievable extremity following blunt tibial artery trauma, allowing amputation before life-threatening wound sepsis develops.
The internal jugular vein is an excellent source of autogenous tissue for carotid artery reconstruction because of its availability in the operative incision, adequate size, and ability to be harvested without morbidity. For 153 of 453 consecutive carotid reconstructions, the durability of the internal jugular vein (n = 76) and the greater saphenous vein (n = 77) as a patch angioplasty was compared. Mean postoperative follow-up was 17 months (1 to 52 months). The vein-patched carotid-bifurcation was studied by means of duplex ultrasonography to assess patency, detect restenosis, and measure cross-sectional diameter during systole. No carotid bifurcation occluded after operation. No ruptures or aneurysmal dilatations of the vein patches were observed. The maximum diameter (mean +/- SD) of the carotid patch angioplasties constructed with internal jugular vein (9.4 +/- 1.9 mm) was similar to patches made with greater saphenous vein (9.6 +/- 1.7 mm). In 95 patients serial duplex examinations demonstrated maximum diameter changes of the vein-patched internal carotid artery ranging from an increase of 3.5 mm to a decrease of 3.0 mm. Asymptomatic restenosis (greater than 50% diameter reduction) was detected in 2/95 (2.1%) patients. Because of the premium placed on the saphenous vein for peripheral arterial reconstruction and coronary artery bypass grafting, the ipsilateral internal jugular vein should be used more frequently for carotid patch angioplasty.
Doppler-derived blood flow velocity and limb blood pressure measurements were used to characterize the hemodynamics of 128 in situ saphenous vein arterial bypasses. The magnitude and configuration of the graft velocity waveform was the best predictor of clinical outcome. Successful bypasses had antegrade flow throughout the pulse cycle and a blood flow velocity above 40 cm/s. A low graft blood flow velocity (less than 40 cm/s) was associated with technical error or early graft failure due to poor runoff. The return of normal limb blood pressure correlated with a technically satisfactory bypass but was measured in only 50% of limbs on the first day after surgery. In 28 bypasses with high blood flow velocity (mean +/- SD) in systole (102 +/- 20 cm/s) and diastole (35 +/- 11 cm/s), postoperative limb blood pressure was initially low (mean ankle-brachial pressure index = 0.68) due to restriction of blood flow through small-diameter (less than 4-mm) venous conduits. As revascularization hyperemia abated, diastolic blood flow velocity decreased and limb blood pressure normalized. Despite the high blood flow velocity and pressure gradient associated with flow-restrictive venous conduits, limb ischemic symptoms resolved, and graft patency was not decreased. An understanding of graft and limb hemodynamics after in situ bypass grafting is critical when noninvasive diagnostic techniques are used to document technical adequacy and for postoperative surveillance.
Familial hypercoagulable states are a collection of syndromes characterized by an inherited deficiency of various proteins involved in the control of coagulation and include antithrombin III, plasminogen, protein C, and protein S. Affected patients usually develop venous thrombosis as adults. During a 15-month interval, we identified five patients with venous thrombosis accompanied by protein C deficiency. Four patients presented with deep venous thrombosis, which was recurrent in two, and one patient developed mesenteric venous thrombosis. The kindred of this last patient suggested an autosomal dominant genetic transmission of protein C deficiency. Patients' ages at the time of diagnosis of disease ranged from 28 to 41 years. All patients had low levels of protein C (range, 34 to 67 U/dL; normal, 70 to 130 U/dL). All patients were treated with heparin sodium immediately and then given long-term oral anticoagulation therapy with warfarin sodium. Protein C deficiency is a predisposing factor to the development of venous thrombosis that has only recently been recognized. Treatment of symptomatic protein C deficiency requires short-term heparin therapy followed by long-term oral anticoagulation therapy with warfarin. Oral anticoagulation treatment must be initiated slowly with no loading dose to avoid warfarin-associated skin necrosis. Patients with unexplained or unusual thrombosis, especially if it occurs at an early age, and patients with recurrent episodes of lower limb venous thrombosis should have their protein C levels measured. If a deficiency is documented, long-term warfarin anticoagulation therapy is recommended.
Doppler-derived blood flow velocity measurements were used to characterize the hemodynamics of 66 internal mammary artery grafts and 60 saphenous vein grafts to the coronary arteries at operation. Pulsed Doppler spectral analysis of centerstream graft flow demonstrated predominantly diastolic flow with a variable, multiphasic flow pattern in systole. The magnitude and configuration of the graft flow velocity waveform varied with graft type and whether the runoff was to single or multiple arteries. At operation, peak diastolic flow velocity was greater (P less than 0.0001) in internal mammary artery grafts to a single outflow artery (71 +/- 2 cm/sec) compared with single vein grafts (31 +/- 4 cm/sec). Sequential grafts demonstrated increased flow velocity and forward flow throughout the pulse cycle, indicative of low outflow resistance. Analysis of the phasic flow patterns permitted an assessment of functional graft patency. Technical errors (anastomotic stricture, internal mammary pedicle torsion) were identified in three grafts with low or absent diastolic flow. Vasospasm of the internal mammary artery was associated with high flow velocity throughout the pulse cycle. Observed differences in patency and the development of intimal hyperplasia between internal mammary artery and saphenous vein grafts may be related to graft hemodynamics.
The goal of carotid endarterectomy is to remove an obstructing or embologenic lesion and reconstruct a durable arterial segment free of flow abnormality. The technical adequacy of 250 endarterectomy sites in 235 patients was assessed at operation by pulsed Doppler spectral analysis and arteriography and was correlated with postoperative patency, the incidence of residual and recurrent stenosis, and clinical outcome. Duplex scanning was used after operation to categorize disease severity. At operation, 10 patients (4%) had angiographic and Doppler flow abnormalities identified in the internal carotid artery. Vessel exploration identified intimal flaps, platelet aggregation, or stricture. Residual flow disturbances at the endarterectomy site correlated with perioperative thrombosis and stroke, angiographic abnormalities, primary closure of the arteriotomy, and a postoperative duplex scan consistent with stenosis. In 175 patients (182 sites) with normal arterial flow after carotid bifurcation endarterectomy, no thrombotic events occurred and the incidence of recurrent stenosis (life-table analysis) was zero at 3 months, 5% at 1 year, and 9% at 2 years. The incidence of occlusion and recurrent stenosis was increased (8% at 3 months, 18% at 1 year, and 21% at 2 years) in 68 arteries with residual flow disturbance identified at operation. Assessment of endarterectomy sites for turbulence identifies anatomic lesions that threaten patency and increase the incidence of residual and recurrent stenosis.
Abnormalities of the fibrinolytic system can result in unusual or unexplained clotting that occurs spontaneously or after minor trauma. We identified five patients with limb-threatening arterial thrombosis of the upper extremity associated with either a low level of plasminogen or an abnormal immunoreactive plasminogen. All patients had extensive thrombosis of the brachial, radial, and ulnar arteries. Two patients had concomitant thrombus of the subclavian artery, which in one patient was associated with distal embolization to the hand. There was no evidence of atherosclerosis in any patient. Detection of an abnormal plasminogen level was done by immunoelectrophoresis of the patient's serum with antiplasminogen sera. In these patients a separate immunoreactive band located near the anode and distinct from the normal single plasminogen band was detected. Because of extensive thrombosis of the arterial system, exploration of the brachial artery, as well as the origin of all the forearm vessels, was necessary for complete balloon catheter thrombectomy. Prompt diagnosis and treatment are necessary to prevent the catastrophic complication of arm or hand amputation. Patients with an abnormal plasminogen level should receive perioperative heparin therapy and long-term warfarin to prevent recurrent thrombotic episodes.
A canine model was developed to study the efficacy of graft replacement as treatment for vascular prosthesis infections from Staphylococcus epidermidis. Infrarenal aortic graft infections were established in 18 dogs by implantation of Dacron prostheses colonized in vitro with a slime-producing strain of S. epidermidis to form an adherent bacteria-laden biofilm (5 X 10(6) colony-forming units/cm2 graft). Study animals developed a graft infection with anatomic and microbiologic characteristics typical of late prosthetic graft infections in humans (sterile perigraft exudate, absent graft incorporation, and normal serum leukocyte count and sedimentation rate). The S. epidermidis study strain was isolated from 14 of 18 explanted grafts (78%) by mechanical disruption of the graft surface biofilm and culture in broth media. Four dogs with sterile graft cultures had histologic evidence of bacterial infection. The established prosthetic surface biofilm infection was treated by graft excision, parenteral cefazolin, and graft replacement with a Dacron or polytetrafluoroethylene (PTFE) vascular prosthesis. One month after graft replacement, no PTFE graft had signs of infection, but perigraft exudate and inflammation involved three of nine Dacron grafts (33%). The study strain was recovered from four of nine PTFE grafts (44%) and two of nine Dacron (22%) replacement grafts (p greater than 0.05). Prosthetic replacement of Dacron prostheses infected by S. epidermidis as a bacteria-laden surface biofilm can result in early graft healing, but persistent colonization of one third of replacement grafts signify that recurrent clinical infection remains a risk.