Understanding the dialysis access steal syndrome. A review of the etiologies, diagnosis, prevention and treatment strategies.

Distal hypoperfusion ischemic syndrome (DHIS), commonly referred to as hand ischemia or 'steal' after dialysis access placement, occurs in 5-10% of cases when the brachial artery is used, or 10 times that of wrist arteriovenous fistulas (AVFs) using the radial artery. It is typically seen in elderly women with diabetes, and may carry severe morbidity including tissue or limb loss if not recognized and treated. Three distinct etiologies include (1) blood flow restriction to the hand from arterial occlusive disease either proximal or distal to the AV access anastomosis, (2) excess blood flow through the AV fistula conduit (true steal), and (3) lack of vascular (arterial) adaptation or collateral flow reserve (ie atherosclerosis) to the increased flow demand from the AV conduit. These three causes of steal may occur alone or in concert. The diagnosis of steal is based on an accurate history and physical examination and confirmed with tests including an arteriogram, duplex Doppler ultrasound (DDU) evaluation with finger pressures and waveform analysis. Treatment of steal includes observation of developing symptoms in mild cases. Balloon angioplasty is the appropriate intervention for an arterial stenosis. At least three distinct surgical corrective procedures exist to counteract the pathophysiology of steal. The ultimate treatment strategy depends on severity of symptoms, the extent of patient co-morbidity, and the local dialysis access technical team support and skills available.

Incidental splenic injury during abdominal vascular surgery: a case-controlled analysis.

BACKGROUND: The small but finite risk of postsplenectomy sepsis is generally regarded as a firm indication for splenic preservation after iatrogenic injury, especially in the young. But splenectomy may be preferable in patients who sustain splenic injuries during vascular operations because of the potential for continued bleeding associated with anticoagulation. The purpose of this study was to determine the perioperative morbidity of incidental splenectomy among patients undergoing abdominal vascular operations. STUDY DESIGN: We studied 17 patients who underwent incidental splenectomy at the time of abdominal vascular operations. Complete data collected on each subject included preoperative and postoperative blood counts, operative indications and details, transfusion requirements, length of hospital stay, and outcomes. Using age- and gender-matched case controls undergoing identical vascular operations from the same period, we evaluated the complication rate and outcomes of patients who underwent splenectomy for iatrogenic injuries of the spleen, versus those who did not sustain splenic injuries. RESULTS: The estimated prevalence of iatrogenic splenic injury during the study period was 0.5%. Mean operative time, estimated blood loss, and duration of mechanical ventilation tended to be greater in the splenectomy patients, but the differences did not achieve statistical significance. Splenorrhaphy was attempted in seven patients, but continued bleeding mandated spleen removal in all cases. Splenectomy patients had a higher transfusion requirement (p = 0.03) and a longer mean length of stay (p = 0.03) than controls. Compared with controls, there was a higher prevalence of infectious complications in the splenectomy patients (p = 0.015), but there was no difference in the prevalence of thromboembolic complications between groups. Two of the splenectomy patients died in the postoperative period from multisystem organ failure, and one died of a missed splenic injury. CONCLUSIONS: These data suggest that incidental splenectomy during abdominal vascular operations is associated with increased postoperative infectious complications and prolonged hospitalization.

Early normalization of platelet survival by endothelial seeding of Dacron arterial prostheses in dogs.

Current synthetic vascular prostheses do not acquire a complete lining of vascular endothelium in humans or dogs. Seeding of autogenous venous endothelium has bee reported to remedy this defect, but previous studies have been primarily morphologic. To see if venous endothelial seeding caused a measurable decrease in platelet-prosthetic interaction in vivo, serial 111In-labeled platelet survival studies were done in dogs with seeded (N = 8) and unseeded (n = 9) thoracoabdominal Dacron bypass prostheses.l Changes in platelet survival time (PST) were compared with endothelial coverage scores, which were determined by blinded survey of removed prostheses by scanning electron microscopy (SEM). The PSTs before surgery (+/- SD) were 5.02 +/- 0.79 days (seeded) and 5.31 +/- 0.99 days (control) (P = 0.51). Seven weeks after surgery the PSTs were 4.01 +/- 1.10 days (seeded) and 2.67 +/- 0.88 days (control) (P = 0.013). The subgroup of four dogs with seeded prostheses that had complete endothelial coverage showed restoration of the platelet survival pattern to that of the linear decay seen before surgery, SEM studies showed that this normalization of PST occurred despite the presence of small nidi of platelet adhesion on exposed Dacron fibers and irregularities of the endothelial pattern consistent with flow disturbances and venous jet lesions near anastomoses. Endothelial seeding, when technically successful, appears to sharply curtail the degree of platelet interaction with vascular prostheses and restores a normal platelet survival pattern. Longer studies of seeded prostheses are needed to determine if seeding protects against the late complications of intimal hyperplasia and thrombotic occlusion.

Reduction of venous thrombosis complicating phlebography.

Patients who underwent radiographic phlebography were studied to determine the frequency of postphlebographic venous thrombosis. In a group of 23 patients who had negative phlebograms performed with standard contrast agent (60% sodium methylglucamine diatrizoate), nine had positive 125I-fibrinogen leg scans. On repeat phlebography, three had confirmed deep vein thrombosis, six overall developed deep or superficial thrombosis, and three had positive scans without demonstrable thrombi. In a second group of 34 patients studied with the contrast material diluted to 45%, only three developed positive scans, one due to deep venous thrombosis and two to superficial thrombosis. There was also a reduction in the incidence of postphlebographic symptoms of pain, tenderness, and erythema, but no apparent sacrifice in diagnostic accuracy.

Deep venous thrombosis and postsplenectomy thrombocytosis.

Eighty-six patients undergoing elective splenectomy have been investigated preoperatively and postoperatively by serial platelet counts and leg scanning using iodine 125-labeled fibrinogen. The presence of deep leg vein thromboses detected by labeled fibrinogen was confirmed by dye phlebography. In only five patients (6%) did deep venous thrombosis develop. In none of these five patients did an elevation in platelet count to 600,000/cu mm develop before or at the time of development of the thrombosis. None of 21 other patients who did have a rise in platelet count greater than 1,000,000/cu mm had evidenced of venous thrombosis. These data do not substantiate the need for routine prophylactic antithrombotic therapy in patients in whom postsplenectomy thrombocytosis develops.