Spontaneously ruptured splenic aneurysm in a young patient with Ehlers-Danlos syndrome.

The authors describe a young patient with a history of type IV vascular Ehlers-Danlos syndrome (EDS) who underwent successful treatment for a spontaneous haemorrhage from a splenic artery aneurysm, and the authors would like to remind clinicians of the mortality and morbidity associated with vascular-type EDS.

Transcranial Doppler ultrasonography-directed intravenous glycoprotein IIb/IIIa receptor antagonist therapy to control transient cerebral microemboli before and after carotid endarterectomy.

BACKGROUND: Patients with a transient focal neurological deficit, critical carotid stenosis and/or microemboli detected by transcranial Doppler ultrasonography (TCD) have a significant risk of stroke. The effect of tirofiban, a selective glycoprotein IIb/IIIa inhibitor, was assessed in patients with microembolic signals on TCD after transient ischaemic attacks or carotid endarterectomy (CEA). METHODS: Thirty-three patients with microemboli on TCD (13 symptomatic preoperative, 19 postoperative, one both) were treated with tirofiban between 2002 and 2007. All patients had carotid stenosis greater than 70 per cent. TCD monitoring was used during and after tirofiban therapy. RESULTS: The median (range) rate of microemboli decreased from 22 (4-260) per h before surgery and 81 (44-216) per h after surgery to 0 (0-9) per h in both groups (P < 0.001, Mann-Whitney U test). This occurred rapidly (preoperative median 30 min; postoperative median 45 min) and was well tolerated in all patients, with no serious adverse effects. CONCLUSION: Cerebral microemboli were controlled by tirofiban both before and after CEA. Further study is required to compare the relative efficacy of tirofiban and dextran.

Control of emboli in patients with recurrent or crescendo transient ischaemic attacks using preoperative transcranial Doppler-directed Dextran therapy.

BACKGROUND: Transcranial Doppler (TCD)-directed Dextran 40 treatment after carotid endarterectomy reduces the rate of early postoperative thrombosis. This study assessed the efficacy of intravenous Dextran 40 at controlling symptoms and emboli before elective carotid endarterectomy in patients with recurrent or crescendo transient ischaemic attacks (TIAs). METHODS: In a prospective study, patients with more than 70 per cent internal carotid artery stenosis who had two or more symptomatic episodes within 30 days and TCD-detected microemboli were studied. Dextran 40 was commenced at 20 ml/h and TCD was repeated to reassess the rate of embolization. The infusion was increased in 20-ml/h increments until symptoms and emboli were controlled. The patient then had carotid surgery on the next elective list. RESULTS: Nineteen patients with internal carotid stenosis greater than 70 per cent, recurrent symptoms and TCD-detected emboli were studied. All patients had symptoms and emboli controlled with Dextran 40. One patient with both unstable angina (awaiting urgent operation) and crescendo TIAs died from a myocardial infarct before undergoing operation. Of the 18 patients who had an operation, one suffered a non-disabling stroke on the third postoperative day. CONCLUSION: TCD-directed Dextran 40 offers a safe approach to high-risk patients before elective carotid endarterectomy, and warrants further study.

The influence of diabetes on the vasomotor responses of saphenous vein and the development of infra-inguinal vein graft stenosis.

There has been a prejudice that diabetes modulates the function of saphenous vein in a manner that predisposes to bypass graft failure, although most of the evidence accrues from animal studies. We have investigated the effect of diabetes on the vasodilator responses and ultrastructure of saphenous vein harvested from patients undergoing infrainguinal bypass surgery for limb salvage and the development of stenoses within the vein grafts. Of 55 consecutive patients undergoing vein bypass surgery for critical ischemia, 16 (29%) were diabetic: diabetes was not a risk factor for graft stenosis, which occurred in 17 of 56 (30%) grafts. Endothelium-dependent relaxation by nitric oxide pathways stimulated after receptor activation (bradykinin and thrombin) was not different in vein rings from diabetic (n = 12) and nondiabetic patients (n = 12). Prostarioid-mediated vasorelaxation was absent in vein rings from diabetic patients, and the production of 6-keto prostaglandin F(1alpha) (PGF(1alpha)) from diabetic vein was only 66 +/- 27 pg x cm-2 x min-1 compared with 112 +/- 20 pg x cm-2 x min-1 from control vein (P = 0.011). Fibrinogen-mediated vasorelaxation, normally inhibited by K+ channel blockers, was negligible in vein from diabetic patients. No ultrastructural differences were observed between the endothelium of saphenous vein harvested from diabetic and nondiabetic patients. However, diabetes was associated significantly with the presence of spiraled collagen in media. The maintenance of receptor-activated stimulation of nitric oxide pathways and the damping of the response to fibrinogen in saphenous vein endothelium may provide, in part, for the good prognosis of vein graft surgery in diabetic patients: diabetes is not a risk factor for early (12 months) infrainguinal vein graft stenosis.

Influence of hypercholesterolemia and adventitial inflammation on the development of aortic aneurysm in rabbits.

Abdominal aortic aneurysms are characterized by intimal atherosclerosis, disruption and attenuation of the elastic media, and a variable adventitial inflammatory infiltrate. We have developed an animal model of this disorder to evaluate the contribution of hypercholesterolemia, medial injury, and adventitial inflammation to aneurysmal dilatation. To accomplish this, we used periaortic application of calcium chloride, which induced both medial injury with calcification and endothelial injury. Ultrasonography was used to demonstrate the dilatation and thickening of the aortic wall. Over the first 3 weeks after periaortic application of 0.25 mol/L CaCl2, the external aortic diameter increased from 3.5 +/- 0.5 to 4.2 +/- 0.8 mm, but the ID remained unchanged. This apparent wall thickening was accompanied by vascular remodeling, and biochemical changes included approximately 50% reduction in tissue hydroxyproline concentration and increased activity of gelatinases (matrix metalloproteinase [MMP]-2 and MMP-9). Independently, cholesterol feeding to induce hypercholesterolemia or the concomitant periaortic application of thioglycollate had little effect on the histological, biochemical, or diameter changes. Together, hypercholesterolemia and thioglycollate were associated with rapid aortic dilatation in CaCl2, treated animals but not controls: after 3 weeks, the ID and OD had doubled, the OD increasing from 3.5 +/- 0.4 to 7.1 +/- 0.4 mm, P = .005. The remarkable feature that accompanied this dilatation was the infiltration of cells, mostly foamy macrophages, into the adventitia, with a further reduction in hydroxyproline concentration. Adventitial inflammation may provide the critical stimulus to dilatation of an aorta with preexisting intimal and medial injury.

Smoking impairs the activity of endothelial nitric oxide synthase in saphenous vein.

Smoking impairs the endothelium-dependent relaxation of arteries and veins, with the maximum relaxation in response to the calcium ionophore A23187 of saphenous vein rings being reduced from 53 +/- 4% in nonsmokers to 27 +/- 5% in smokers. We have investigated whether this endothelial dysfunction was attributable to altered activity or concentration of nitric oxide synthase (NOS). The concentration of NOS in saphenous vein endothelium, determined by Western blotting and immunohistochemistry, was not different in nonsmokers and smokers. Nitrite production from vein strips stimulated with A23187 was higher in nonsmokers (median 23.6 nmol.cm-2.h-1) than smokers (median 3.3 nmol.cm-2.h-1), P=.001, this difference being abolished when vein strips were preincubated in the presence of NG-monomethyl-L-arginine. Organ chamber studies to monitor the endothelium-dependent relaxation of vein rings in response to A23187 showed that preincubation of rings from smokers with either L-arginine (3mmol/L) or superoxide dismutase (250 U/mL) did not improve the maximum relaxation. In contrast, preincubation of vein rings from smokers with 20 micromol/L tetrahydrobiopterin increased the maximum relaxation from 27 +/- 5% to 51 +/- 6%, P=.01. Preincubation of vein from smokers with tetrahydrobiopterin also significantly increased nitrite and cGMP production in response to stimulation with A23187. The impaired endothelium-dependent relaxation of saphenous vein rings from smokers appears to be caused by a reduction in the activity of endothelial NOS that is attributable to an inadequate supply of the coenzyme tetrahydrobiopterin.

Inflammation and matrix metalloproteinases in the enlarging abdominal aortic aneurysm.

The risk of rupture of an abdominal aortic aneurysm increases with aortic diameter. To obtain insight into the pathological processes associated with the vascular remodeling that accompanies aortic dilatation, we compared the histological features and the activity of matrix metalloproteinases (MMPs) in biopsies from 21 small (4.0 to 5.5 cm in diameter) and 45 larger abdominal aortic aneurysms. The histological feature most clearly associated with enlarging aneurysm diameter was a higher density of inflammatory cells in the adventitia, P = .018. This inflammation was nonspecific, principally macrophages and B lymphocytes. Fibrosis of the adventitia provided compensatory thickening of the aortic wall as the aneurysm diameter increased. A combination of zymography and immunoblotting identified gelatinase A (MMP-2) as the principal metallogelatinase in small aneurysms, whereas zymography indicated an increasing activity of gelatinase B (MMP-9) in large aneurysms. Homogenates prepared from both small and large aneurysms had similar total activity against gelatin or type IV collagen. However, the concentration of gelatinase A, determined by immunoassay, was highest for small aneurysms: median concentrations, 385, 244, and 166 ng/mg protein for small aneurysms, large aneurysms, and atherosclerotic aorta, respectively. Immunolocalization studies indicated that gelatinase A was concentrated along fibrous tissue of both the acellular media and the atherosclerotic plaque. The recruitment of inflammatory cells into the adventitia, with subsequent elaboration of metalloproteinases, including gelatinase B, may contribute to the rapid growth and rupture of larger aneurysms.

The influence of fibrinogen concentration on the development of vein graft stenoses.

OBJECTIVE: The aim of this study was to identify factors associated with the development of graft stenoses in the first year after bypass. DESIGN AND SETTING: Between January 1992 and April 1993, 75 consecutive patients undergoing distal vein bypass surgery were entered into a graft surveillance programme at Charing Cross Hospital. The grafts (n = 79) were surveyed by colour flow Doppler ultrasonography at 7 days, 3, 6, 9 and 12 months and the site of stenoses (> 50%) recorded. Position of the distal anastomosis, graft type (in situ or reverse) and clinical history were recorded. At the 3-month surveillance a blood sample was taken for the estimation of smoking markers, lipids and fibrinogen. RESULTS: The site of the distal anastomosis was to the suprageniculate popliteal in nine, infrageniculate popliteal in 32 and tibio/peroneal vessels in 38 cases. In the first month following bypass there were six deaths, giving a 30 day mortality of 7.5%, three patients were lost to follow up, seven grafts occluded, three were replaced by PTFE, four patients underwent amputation and one patient had a redo vein graft. In the remaining grafts 20/63 (32%) developed stenoses within the first year after bypass. The development of a graft stenosis was not associated with sex, diabetic status, site of distal anastomosis, graft type or serum lipids. Multiple regression analysis identified only one factor associated significantly with the development of vein graft stenosis: fibrinogen concentration (p = 0.003). Life table analysis showed that after 1 year only 46% of grafts remained free of stenoses in patients with above median fibrinogen concentrations compared with 84% of grafts in patients with below median fibrinogen concentrations, p = 0.009. CONCLUSIONS: Increased plasma fibrinogen concentration is a potent risk factor for the development of vein graft stenosis. These results prompt consideration of the role of fibrinogen in stimulating smooth muscle cell proliferation in the stenotic lesion.

Consultants: when to look outside for help.

Consultants not only provide an objective opinion, but they also bring complementary expertise to a nursing organization. If used appropriately, they can be both productive and cost-effective to the nursing organization. Nurse managers need to address the following issues: when to look for outside assistance; how to select the appropriate nursing consultant; what to expect from a consulting engagement; and how to evaluate the performance of a consultant.

Is thickening of the basal lamina in the saphenous vein a hallmark of smoking?

OBJECTIVE: To investigate whether smoking causes ultrastructural changes in the intima of the proximal saphenous vein. DESIGN: Proximal saphenous veins from heavy smokers and non-smokers were examined with scanning and transmission electron microscopy to determine changes in surface ultrastructure, in the intercellular junction, and in the thickness of the basal lamina. Immunogold labelling was used to identify specific components of the endothelial basal lamina. MATERIAL: Vein specimens were obtained from patients undergoing varicose vein surgery (12 patients) or distal bypass surgery (eight patients). MAIN RESULTS: The only ultrastructural change that discriminated between specimens was thickening of the endothelial basal lamina. All specimens with a thickened basal lamina were from heavy smokers. Immunogold labelling studies showed that the thickened basal lamina contained specific accumulations of fibronectin but not heparan sulphate proteoglycans, type IV collagen, or laminin. CONCLUSIONS: Two ultrastructural characteristics are associated with smoking: thickening of the endothelial basal lamina and a specific accumulation of fibronectin in the thickened basal lamina. Such abnormalities in the saphenous veins from smokers may contribute to the poorer performance of these veins as bypass conduits.

Smoking impairs endothelium-dependent relaxation of saphenous vein.

Samples of proximal saphenous vein were obtained from heavy smokers and non-smokers: 28 were obtained at varicose vein surgery and eight at infrainguinal bypass surgery. The veins were prepared for histological examination and for mounting in an organ bath to measure changes in isometric tension. Vein rings from both smokers and non-smokers responded equally to sodium nitroprusside, a reagent that acts directly on smooth muscle cells, undergoing 90-100 per cent relaxation. The mean(s.e.m.) maximum relaxation in response to bradykinin of rings obtained at varicose vein surgery was 50.0(5.3) per cent in non-smokers compared with only 31.6(2.2) per cent in smokers (P = 0.03). Similarly, in specimens obtained at bypass surgery the mean(s.e.m.) maximum relaxation in smokers was only 25.1(6.3) per cent compared with 48.4(4.1) per cent in smokers (P = 0.04). Relaxation in response to the bradykinin stimulus was abolished in the presence of L-nitroarginine methyl ester, a specific inhibitor of the synthesis of endothelium-derived relaxing factor (EDRF). Preincubation of the vein rings with L-arginine, the precursor of EDRF, did not increase the vasorelaxation in smokers. The mean(s.e.m.) maximum relaxation in response to the calcium ionophore A23187 was 53.5(3.8) per cent in non-smokers compared with only 27.0(4.9) per cent in smokers (P = 0.01). The results indicate that heavy smokers have impaired release of EDRF in response to both bradykinin and calcium ionophore. This impairment may increase vasomotor tone, platelet aggregation and smooth muscle proliferation, thereby resulting in an increased risk of graft occlusion.

Familial hollow visceral myopathy with varying urological manifestations.

A family with hereditary hollow visceral myopathy is described, with characteristic variation in expression between affected members. Very severe and widespread involvement of the gastrointestinal and urinary tracts in 1 patient contrasted with isolated urinary tract involvement in 2 others, and it is suggested that hollow visceral myopathy should be considered in the differential diagnosis of primary detrusor failure. The management of urinary tract involvement is discussed and a conservative approach is recommended.

So, your nursing management system doesn't work.

NMIS systems can be of great assistance to the nursing department. Unless the patient acuity/classification portion of your NMIS is meeting your needs, the efforts needed to maintain and run the system will be useless. If your hospital is experiencing difficulties with its NMIS, studying potential problem areas might help to clarify the problem. If your hospital has purchased and is planning to implement a NMIS, you should actively involve all levels of nursing management and staff. To assure the system will meet your needs, ask questions and discover the answers throughout the implementation process. If you are planning to purchase a NMIS, a requirements definition study would be worth your time and effort. Your requirements for the system should be in writing to the potential vendor, thus allowing the vendor to respond to each of the requirements in a written proposal.