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Vascular Occlusion (vascular + occlusion)
Selected AbstractsSystematic review of randomized controlled trials of pharmacological interventions to reduce ischaemia-reperfusion injury in elective liver resection with vascular occlusionHPB, Issue 1 2010Mahmoud Abu-Amara Abstract Background:, Vascular occlusion during liver resection results in ischaemia-reperfusion (IR) injury, which can lead to liver dysfunction. We performed a systematic review and meta-analysis to assess the benefits and harms of using various pharmacological agents to decrease IR injury during liver resection with vascular occlusion. Methods:, Randomized clinical trials (RCTs) evaluating pharmacological agents in liver resections conducted under vascular occlusion were identified. Two independent reviewers extracted data on population characteristics and risk of bias in the trials, and on outcomes such as postoperative morbidity, hospital stay and liver function. Results:, A total of 18 RCTs evaluating 17 different pharmacological interventions were identified. There was no significant difference in perioperative mortality, liver failure or postoperative morbidity between the intervention and control groups in any of the comparisons. A significant improvement in liver function was seen with methylprednisolone use. Hospital and intensive therapy unit stay were significantly shortened with trimetazidine and vitamin E use, respectively. Markers of liver parenchymal injury were significantly lower in the methylprednisolone, trimetazidine, dextrose and ulinastatin groups compared with their respective controls (placebo or no intervention). Discussion:, Methylprednisolone, trimetazidine, dextrose and ulinastatin may have protective roles against IR injury in liver resection. However, based on the current evidence, they cannot be recommended for routine use and their application should be restricted to RCTs. [source] The safety and efficacy of ablative techniques adjacent to the hepatic vasculature and biliary systemANZ JOURNAL OF SURGERY, Issue 1-2 2010Christopher D. Mann Abstract Ablative techniques may provide an alternative to resection in treating awkwardly placed hepatic malignancy adjacent to major vascular and biliary structures. The heat-sink effect may reduce efficacy adjacent to major vascular structures. Vascular occlusion improves efficacy but is associated with increased vascular and biliary complications. The safety and efficacy of ablation in these situations remain to be defined. Further studies comparing both safety and efficacy are needed. [source] Cardiovascular risk factors and collateral artery formationEUROPEAN JOURNAL OF CLINICAL INVESTIGATION, Issue 12 2009D. De Groot Abstract Arterial lumen narrowing and vascular occlusion is the actual cause of morbidity and mortality in atherosclerotic disease. Collateral artery formation (arteriogenesis) refers to an active remodelling of non-functional vascular anastomoses to functional collateral arteries, capable to bypass the site of obstruction and preserve the tissue that is jeopardized by ischaemia. Hemodynamic forces such as shear stress and wall stress play a pivotal role in collateral artery formation, accompanied by the expression of various cytokines and invasion of circulating leucocytes. Arteriogenesis hence represents an important compensatory mechanism for atherosclerotic vessel occlusion. As arteriogenesis mostly occurs when lumen narrowing by atherosclerotic plaques takes place, presence of cardiovascular risk factors (e.g. hypertension, hypercholesterolaemia and diabetes) is highly likely. Risk factors for atherosclerotic disease affect collateral artery growth directly and indirectly by altering hemodynamic forces or influencing cellular function and proliferation. Adequate collateralization varies significantly among atherosclerotic patients, some profit from the presence of extensive collateral networks, whereas others do not. Cardiovascular risk factors could increase the risk of adverse cardiovascular events in certain patients because of the reduced protection through an alternative vascular network. Likewise, drugs primarily thought to control cardiovascular risk factors might contribute or counteract collateral artery growth. This review summarizes current knowledge on the influence of cardiovascular risk factors and the effects of cardiovascular medication on the development of collateral vessels in experimental and clinical studies. [source] Systematic review of randomized controlled trials of pharmacological interventions to reduce ischaemia-reperfusion injury in elective liver resection with vascular occlusionHPB, Issue 1 2010Mahmoud Abu-Amara Abstract Background:, Vascular occlusion during liver resection results in ischaemia-reperfusion (IR) injury, which can lead to liver dysfunction. We performed a systematic review and meta-analysis to assess the benefits and harms of using various pharmacological agents to decrease IR injury during liver resection with vascular occlusion. Methods:, Randomized clinical trials (RCTs) evaluating pharmacological agents in liver resections conducted under vascular occlusion were identified. Two independent reviewers extracted data on population characteristics and risk of bias in the trials, and on outcomes such as postoperative morbidity, hospital stay and liver function. Results:, A total of 18 RCTs evaluating 17 different pharmacological interventions were identified. There was no significant difference in perioperative mortality, liver failure or postoperative morbidity between the intervention and control groups in any of the comparisons. A significant improvement in liver function was seen with methylprednisolone use. Hospital and intensive therapy unit stay were significantly shortened with trimetazidine and vitamin E use, respectively. Markers of liver parenchymal injury were significantly lower in the methylprednisolone, trimetazidine, dextrose and ulinastatin groups compared with their respective controls (placebo or no intervention). Discussion:, Methylprednisolone, trimetazidine, dextrose and ulinastatin may have protective roles against IR injury in liver resection. However, based on the current evidence, they cannot be recommended for routine use and their application should be restricted to RCTs. [source] Transfemoral Snaring and Stabilization of Pacemaker and Defibrillator Leads to Maintain Vascular Access During Lead ExtractionPACING AND CLINICAL ELECTROPHYSIOLOGY, Issue 3 2009AVI FISCHER M.D. Background: Lead extraction is an effective method for removing pacemaker and defibrillator leads and to obtain venous access when central veins are occluded. Objective: We report a series of patients who required lead extraction and preservation of vascular access requiring a vascular snare introduced from the femoral vein to provide traction on the lead. This technique allowed advancement of the extraction sheath beyond the level of vascular occlusion, preserving vascular access in all patients. Methods: All patients had peripheral contrast venography performed immediately prior to the procedure to identify the site(s) of venous occlusion. An extraction sheath was employed and with direct manual traction, the lead tip pulled free from the myocardial surface prior to advancement of the sheath beyond the occlusion. A transfemoral snare was used to grasp the distal portion of the lead and traction was used to immobilize the lead. Results: In all patients, transfemoral snaring of the leads was necessary to allow safe advancement of a sheath to open the occluded venous system. There were no complications in any of the patients. Conclusion: Our series demonstrates the simple and safe technique of transfemoral lead snaring to assist lead extraction and maintain vascular access in the setting of venous occlusion, when the distal lead tip pulls free of the myocardium before an extraction sheath is passed beyond the point of venous obstruction. [source] Successful management of bleeding with recombinant factor VIIa (NovoSeven®) in a patient with Burkitt lymphoma and thrombosis of the left femoral and left common iliac veinsPEDIATRIC BLOOD & CANCER, Issue 3 2007Abstract We present the case of an 18-year-old female with Burkitt lymphoma involving the intra-abdominal and inguinal lymph nodes. The tumor had invaded the left femoral and common iliac veins causing secondary thrombosis and vessel occlusion. Chemotherapy and anticoagulant treatment resulted in mild thrombocytopenia and a prolonged prothrombin time, respectively, which exacerbated postoperative bleeding following surgical removal of a deep inguinal necrosis. After 6 days, bleeding combined with epistaxis was considered to be life threatening and anticoagulant reversal with recombinant factor VIIa was successfully performed. The patient has since achieved complete remission and subsequent antithrombotic therapy has resolved the vascular occlusion. Pediatr Blood Cancer 2007;49:332,335. © 2006 Wiley-Liss, Inc. [source] Rate-sensitive contractile responses of lymphatic vessels to circumferential stretchTHE JOURNAL OF PHYSIOLOGY, Issue 1 2009Michael J. Davis Phasic contractile activity in rat portal vein is more sensitive to the rate of change in length than to absolute length and this response is widely assumed to be a general characteristic of myogenic behaviour for vascular smooth muscle. Previously, we found that rat lymphatic vessels exhibit phasic contractile behaviour similar to that of portal vein. In the present study, we hypothesized that lymphatic muscle would exhibit rate-sensitive contractile responses to stretch. The hypothesis was tested on rat mesenteric lymphatics (90,220 ,m, i.d.) using servo-controlled wire- and pressure-myograph systems to enable ramp increases in force or pressure at different rates. Under isometric conditions in wire-myograph preparations, both the amplitude and the frequency of phasic activity were enhanced at more optimal preloads, but superimposed upon this effect were bursts of contractions that occurred only during fast preload ramps. In such cases, the ratio of contraction frequency during the ramp to that at the subsequent plateau (at optimal preload) was > 1. Further, the frequency ratio increased as a function of the preload ramp speed, consistent with a rate-sensitive mechanism. In contrast, the amplitude ratio was < 1 and declined further with higher ramp speeds. Downward preload ramps produced corresponding rate-sensitive inhibition of contraction frequency but not amplitude. Similar findings were obtained in pressurized lymphatics in response to pressure ramps and steps. Our results suggest that lymphatics are sensitive to the rate of change in preload/pressure in a way that is different from portal vein, possibly because the pacemaker for generating electrical activity is rate sensitive but lymphatic muscle is not. The behaviour may be widely present in collecting lymphatic vessels and is probably an important mechanism for rapid adaptation of the lymphatic pump to local vascular occlusion. [source] Connective Tissue Growth Factor Promotes Fibrosis Downstream of TGF, and IL-6 in Chronic Cardiac Allograft RejectionAMERICAN JOURNAL OF TRANSPLANTATION, Issue 2 2010A. J. Booth Cardiac transplantation is an effective treatment for multiple types of heart failure refractive to therapy. Although immunosuppressive therapeutics have increased survival rates within the first year posttransplant, chronic rejection (CR) remains a significant barrier to long-term graft survival. Indicators of CR include patchy interstitial fibrosis, vascular occlusion and progressive loss of graft function. Multiple factors have been implicated in the onset and progression of CR, including TGF,, IL-6 and connective tissue growth factor (CTGF). While associated with CR, the role of CTGF in CR and the factors necessary for CTGF induction in vivo are not understood. To this end, we utilized forced expression and neutralizing antibody approaches. Transduction of allografts with CTGF significantly increased fibrotic tissue development, though not to levels observed with TGF, transduction. Further, intragraft CTGF expression was inhibited by IL-6 neutralization whereas TGF, expression remained unchanged, indicating that IL-6 effects may potentiate TGF,-mediated induction of CTGF. Finally, neutralizing CTGF significantly reduced graft fibrosis without reducing TGF, and IL-6 expression levels. These findings indicate that CTGF functions as a downstream mediator of fibrosis in CR, and that CTGF neutralization may ameliorate fibrosis and hypertrophy associated with CR. [source] Imaging the future of stroke: I. Ischemia,ANNALS OF NEUROLOGY, Issue 5 2009David S. Liebeskind MD Envisioning the future of stroke appears daunting considering the milestones already achieved in stroke imaging. A historical perspective on the developments in stroke care provides a striking narrative of how imaging has transformed diagnosis, therapy, and prognosis of cerebrovascular disorders. Multimodal imaging techniques such as CT and MRI, incorporating parenchymal depictions, illustration of the vasculature, and perfusion data, can provide a wealth of information regarding ischemic pathophysiology. Key elements of ischemic pathophysiology depicted with imaging include vascular occlusion, compensatory collateral flow, resultant hemodynamic conditions that reflect these sources of blood flow, and the neurovascular injury that ensues. The mantra of "time is brain" has been perpetuated, but this does not provide an entirely accurate reflection of ischemic pathophysiology and imaging insight shows far more than time alone. Maximizing the potential of perfusion imaging will continue to expand the nascent concept that cerebral ischemia may be completely reversible in certain scenarios. Novel modalities provide a fertile ground for discovery of therapeutic targets and the potential to assess effects of promising strategies. Beyond clinical trials, imaging has become a requisite component of the neurological examination enabling tailored stroke therapy with the use of detailed neuroimaging modalities. In this first article on ischemia, the focus is on the most recent imaging advances and exploring aspects of cerebral ischemia where imaging may yield additional therapeutic strategies. A subsequent article will review recent and anticipated imaging advances in hemorrhage. These thematic overviews underscore that imaging will undoubtedly continue to dramatically shape the future of stroke. Ann Neurol 2009;66:574,590 [source] In situ hypothermic liver preservation during radical liver resection with major vascular reconstructionBRITISH JOURNAL OF SURGERY (NOW INCLUDES EUROPEAN JOURNAL OF SURGERY), Issue 12 2009D. DuBay Background: The in situ hypothermic liver preservation technique may allow a more aggressive approach to tumours of the caval confluence and/or all three hepatic veins, which would otherwise be deemed irresectable. Methods: All descriptive data regarding patient demographics, operative characteristics, perioperative complications and outcomes of nine patients in whom this technique was used were collected prospectively. Results: Seven patients underwent liver trisegmentectomy and two had primary retrohepatic venal caval resection. Total hepatic vascular occlusion with in situ hypothermic liver preservation was used for venous reconstruction in all patients. The vena cava was reconstructed with prosthetic graft in seven patients. All main hepatic veins were reconstructed in the seven liver resections. In situ hypothermic liver preservation was well tolerated as evidenced by preserved hepatic synthetic function early after operation. One patient died 66 days after surgery. There were two recurrences after a median follow-up of 14 (range 2,33) months; local recurrence was identified in one patient after 4 months and distant metastasis in another after 8 months. Conclusion: The in situ hypothermic liver preservation technique appears to be a useful adjunct to radical hepatobiliary tumour excision procedures that require total hepatic vascular exclusion and major vascular reconstruction. Copyright © 2009 British Journal of Surgery Society Ltd. Published by John Wiley & Sons, Ltd. [source] Ischaemic preconditioning improves microvascular perfusion and oxygenation following reperfusion injury of the intestine,BRITISH JOURNAL OF SURGERY (NOW INCLUDES EUROPEAN JOURNAL OF SURGERY), Issue 9 2005I. H. Mallick Background: Ischaemia,reperfusion (IR) injury of the intestine occurs commonly during abdominal surgery. Ischaemic preconditioning (IPC) provides a way of protecting the organ from damage inflicted by IR. This study was designed to evaluate the beneficial effect of IPC, focusing on the intestinal microcirculation and oxygenation in intestinal IR injury. Methods: Rats were allocated to three groups. Animals in the IR and IPC groups underwent 30 min of intestinal ischaemia followed by 2 h of reperfusion. In the IPC group this was preceded by 10 min of ischaemia and 10 min of reperfusion. Animals in the third group underwent laparotomy but no vascular occlusion. Intestinal microvascular perfusion, oxygenation and portal venous blood flow (PVF) were monitored continuously. At the end of the reperfusion period, blood samples were obtained for measurement of lactate dehydrogenase (LDH) and biopsies of ileum for histological evaluation. Results: IPC improved intestinal microvascular perfusion and tissue oxygenation significantly at the end of the reperfusion period (P < 0·001). PVF improved significantly in the IPC compared with the IR group (P = 0·005). The serum LDH concentration was significantly lower in the IPC than the IR group (mean(s.e.m.) 667·1(86·8) versus 1973·8(306·5) U/l; P < 0·001) Histological examination showed that ileal mucosa was significantly less injured in the IPC group. Conclusions: This study demonstrated that IPC improves intestinal microvascular perfusion and oxygenation. Copyright © 2005 British Journal of Surgery Society Ltd. Published by John Wiley & Sons, Ltd. [source] 1263: Symptoms and signs of posterior uveitisACTA OPHTHALMOLOGICA, Issue 2010M KHAIRALLAH Purpose Posterior uveitis (PU) is an important anatomic form of uveitis in which the primary site of inflammation is the choroid or retina, with or without subsequent vitreous involvement. Methods Review of symptoms and signs of PU. Results The onset of PU can be sudden or less frequently insidious. Most common ocular symptoms include blurred vision, loss of vision, and floaters. Some patients with PU may have no symptoms, especially if inflammatory process is asymmetric. PU is usually associated with vitritis that can vary from mild to severe. Vitritis should be graded according to standardized grading systems. Other vitreous changes may include vitreous strands, vitreous hemorrhage, vitreous traction, and posterior vitreous detachment. Retinal and/or choroidal inflammation can be focal, multifocal, or more diffuse. It is important to distinguish between active and inactive chorioretinal disease. Retinal vasculitis can occur in the setting of several PU entities. It can involve retinal veins or arteries. It appears as focal, multifocal, or diffuse vascular cuffing or sheathing. Other retinal vasculitic changes include retinal hemorrhages, retinal vascular occlusion, retinal/optic disc neovascularization, and aneurysms. Maculopathy is common patients with PU. It may result from direct inflammatory infiltration, macular edema, serous retinal detachment, retinal ischemia, epiretinal membrane, or macular hole. Optic nerve involvement that can occur in association with PU include optic disc hyperemia/edema, optic neuritis, neuroretinitis, optic disc exudate, and optic disc granuloma. Conclusion Clinical examination is a key step in the diagnostic approach to PU. Clinician should be aware of the array of ocular symptoms of signs and their importance in orienting the differential diagnosis. [source] AML with bilateral retinal detachmentACTA OPHTHALMOLOGICA, Issue 2007E SARKADY Purpose: To present a case of thrombotic ocular and CNS involvement complicating acute myeloid leukaemia (AML). Methods: A 42 year old woman developed blurred vision shortly after diagnosis and treatment of M6 AML. Investigations showed anterior orbital infiltration, retinal detachment and panuveitis. Iris biopsy and vitreous aspirate were negative. She developed right temporal lobe infarction and died following further CNS infarction two months after initial diagnosis. Results: Post mortem examination showed cerebral oedema, multiple cerebral infarctions and hepatosplenomegaly; both eyes contained vitreous exudates, retinal detachment and uveal thickening. Microscopy showed exudative and haemorrhagic retinal detachment, without inflammatory or neoplastic infiltrate, and bilateral uveal leukaemic infiltration with infarction. Neoplastic cells infiltrated the leptomeninges and brain parenchyma with focal vascular occlusion. Lung vessels were occluded by neoplastic cells. The spleen and bone marrow were heavily infiltrated. Partial immunophenotyping suggested a diagnosis of acute promyelocytic leukaemia (APL). Conclusions: Acute leukaemia involves the eye occurs in 39-53% cases. Visual loss is uncommon. Retinal involvement most frequently occurs in the form of superficial haemorrhages, detachment is uncommon. Acute lymphoblastic leukaemia (ALL) treated with L-asparaginase, acute promyelocytic leukaemia (APL) and non-M3 AML may present with a prothrombotic state which may be catastrophic, as occurred in this fatal case. [source] Prospective Study of the Clinical Features and Outcomes of Emergency Department Patients with Delayed Diagnosis of Pulmonary EmbolismACADEMIC EMERGENCY MEDICINE, Issue 7 2007Jeffrey A. Kline MD Objectives:The authors hypothesized that emergency department (ED) patients with a delayed diagnosis of pulmonary embolism (PE) will have a higher frequency of altered mental status, older age, comorbidity, and worsened outcomes compared with patients who have PE diagnosed by tests ordered in the ED. Methods:For 144 weeks, all patients with PE diagnosed by computed tomographic angiography were prospectively screened to identify ED diagnosis (testing ordered from the ED) versus delayed diagnosis (less than 48 hours postadmission). Serum troponin I level, right ventricular hypokinesis on echocardiography, and percentage pulmonary vascular occlusion were measured at diagnosis; patients were prospectively followed up for adverse events (death, intubation, or circulatory shock). Results:Among 161 patients with PE, 141 (88%) were ED diagnosed and 20 (12%) had a delayed diagnosis. Patients with a delayed diagnosis were older than ED-diagnosed patients (61 [±15] vs. 51 [±17] years; p < 0.001), had a longer median time to heparin administration (33 vs. 8 hours; p < 0.001), and had a higher frequency of altered mental status (30% vs. 8%; p = 0.01) but did not have a higher frequency of prior cardiopulmonary disease (25% vs. 23%). Patients with a delayed diagnosis had equal or worse measures of PE severity (right ventricular hypokinesis on echocardiography, 60% vs. 58%; abnormal troponin I level, 55% vs. 24%); on computed tomographic angiography, ten of 20 patients with a delayed diagnosis had PE in lobar or larger arteries and >50% vascular obstruction. Patients with a delayed diagnosis had a higher rate of in-hospital adverse events (9% vs. 30%; p = 0.01). Conclusions:In this single-center study, the diagnosis of PE was frequently delayed and outcomes of patients with delayed diagnosis were worse than those of patients with PE diagnosed in the ED. [source] Heel skin hyperaemia: direct compression versus vascular occlusionCLINICAL PHYSIOLOGY AND FUNCTIONAL IMAGING, Issue 6 2003Harvey N. Mayrovitz Summary Vulnerability of the heel to ulceration in bed-bound persons is related to direct pressure-induced blood flow decreases. Periodic pressure reduction is a clinical strategy to help prevent ulcers by allowing flow-repayment hyperaemia that has a magnitude and duration thought to be related to the duration of the prior interval of ischaemia. However, there are reasons to question whether effects of flow stoppages caused by direct tissue loading are similar to those because of ischaemia without superimposed direct pressure. This question was investigated by comparing posterior heel skin blood flow responses via laser-Doppler perfusion monitoring of 27 supine-lying subjects in whom blood flow was reduced by 5-min of direct heel loading on a support surface and by 5-min of ankle-cuff compression. Results showed that blood flow reductions were the same for both methods but the hyperaemia was significantly greater when flow reduction was produced by direct heel loading. This was true for ratio of peak hyperaemic flow to baseline (8·20 ± 1·32 s versus 4·68 ± 0·80 s, P,0·001), hyperaemic to baseline 3-min flow-time area ratios (4·70 ± 0·65 s versus 1·95 ± 0·29 s, P,0·001) and for total hyperaemia durations (352 ± 39 s versus 181 ± 14 s, P<0·001). These findings raise new questions regarding the precise physiological effects of heel and tissue loading in general, the factors that contribute to the hyperaemic response and their clinical impact and interpretation. Possible sources of the observed greater post-loading hyperaemia responses are discussed. [source] |