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The Cochrane Database of Systematic... Nov 2016Drains are often used in leg wounds after vascular surgery procedures despite uncertainty regarding their benefits. Drains are placed with the aim of reducing the... (Review)
Review
BACKGROUND
Drains are often used in leg wounds after vascular surgery procedures despite uncertainty regarding their benefits. Drains are placed with the aim of reducing the incidence and size of blood or fluid collections. Conversely, drains may predispose patients to infection and may prolong hospitalisation. Surgeons need robust data regarding the effects of drains on complications following lower limb arterial surgery.
OBJECTIVES
To determine whether routine placement of wound drains results in fewer complications following lower limb arterial surgery than no drains.
SEARCH METHODS
In June 2016 we searched: the Cochrane Wounds Specialised Register; the Cochrane Central Register of Controlled Trials (CENTRAL; the Cochrane Library); Ovid MEDLINE; Ovid MEDLINE (In-Process & Other Non-Indexed Citations); Ovid EMBASE and EBSCO CINAHL. We also searched clinical trial registries for ongoing studies.There were no restrictions with respect to language, date of publication or study setting.
SELECTION CRITERIA
We considered randomized controlled trials (RCTs) that evaluated the use of any type of drain in lower limb arterial surgery.
DATA COLLECTION AND ANALYSIS
Two authors independently determined study eligibility, extracted data and performed an assessment of bias. An effort was made to contact authors for missing data. The methods and results of each eligible study were summarised and we planned to pool data in meta-analyses when it was considered appropriate, based upon clinical and statistical homogeneity.
MAIN RESULTS
We identified three eligible trials involving a total of 222 participants with 333 groin wounds. Suction drainage was compared with no drainage in all studies. Two studies were parallel-group, randomized controlled trials, and one was a split-body, randomized controlled trial. Trial settings were not clearly described. Patients undergoing bypass and endarterectomy procedures were included, but none of the studies provided details on the severity of the underlying arterial disease.We deemed all of the studies to be at a high risk of bias in three or more domains of the 'Risk of bias' assessment and overall the evidence was of very low quality. Two out of three studies had unit of analysis errors (with multiple wounds within patients analysed as independent) and it was not possible to judge the appropriateness of the analysis of the third. Meta-analysis was not appropriate, firstly because of clinical heterogeneity, and secondly because we were not able to adjust for the analysis errors in the individual trials. One trial yielded data on surgical site infections (SSI; the primary outcome of the review): there was no clear difference between drained and non-drained wounds for SSI (risk ratio 1.33; 95% confidence interval 0.30 to 5.94; 50 participants with bilateral groin wounds; very low quality evidence). It was not possible to evaluate any other outcomes from this trial. The results from the other two studies are unreliable because of analysis errors and reporting omissions.
AUTHORS' CONCLUSIONS
The data upon which to base practice in this area are limited and prone to biases. Complete uncertainty remains regarding the potential benefits and harms associated with the use of wound drains in lower limb arterial surgery due to the small number of completed studies and weaknesses in their design and conduct. Higher quality evidence is needed to inform clinical decision making. To our knowledge, no trials on this topic are currently active.
Topics: Aged; Drainage; Female; Groin; Hematoma; Humans; Lower Extremity; Male; Peripheral Arterial Disease; Randomized Controlled Trials as Topic; Reoperation; Suction; Surgical Wound Infection; Vascular Surgical Procedures
PubMed: 27841438
DOI: 10.1002/14651858.CD011111.pub2 -
Medicine Oct 2023Our aim was to determine the laboratory parameters that distinguish pseudothrombocytopenia from true thrombocytopenia. A total of 107 patients who were referred to the...
Our aim was to determine the laboratory parameters that distinguish pseudothrombocytopenia from true thrombocytopenia. A total of 107 patients who were referred to the adult hematology outpatient clinic with thrombocytopenia and subsequently diagnosed with acute myeloid leukaemia, immune thrombocytopenia and pseudothrombocytopenia were included in our study. Hemogram parameters on admission, platelet value in the control hemogram and peripheral smear findings were recorded. Forty three (40.2%) males and 64 (59.8%) females, were included in our study. There were 25 patients in the leukaemia group, 39 in the immune thrombocytopenia group and 43 in the pseudothrombocytopenia group. Control platelet value and red cell distribution width/platelet ratio were found to be statistically significantly different between the 3 groups. Receiver operating characteristic analysis based on platelet values showed that platelet value ≤ 38,000/µL (86% sensitivity, 78.1% specificity, P < .001), difference between 2 consecutively measured platelet levels ≤ 11. 000/µL (79.1% sensitivity, 79.7% specificity, P < .001), red cell distribution width/platelet ratio ≥ 0.413 (90.7% sensitivity, 78.1% specificity, P < .001) were found to be in favor of true thrombocytopenia. In the differentiation of pseudothrombocytopenia and true thrombocytopenia, the difference between the hemogram parameters at the time of admission and the platelet count in the control blood count may be guiding. This result may reduce patient and physician anxiety and prevent patient referral.
Topics: Adult; Male; Female; Humans; Purpura, Thrombocytopenic, Idiopathic; Thrombocytopenia; Platelet Count; Blood Platelets; Blood Cell Count; Edetic Acid; Platelet Aggregation
PubMed: 37832120
DOI: 10.1097/MD.0000000000035395 -
Journal of Thrombosis and Haemostasis :... Jan 2017The recent discovery that von Willebrand factor (VWF) regulates blood vessel formation has opened a novel perspective on the function of this complex protein. VWF was... (Review)
Review
The recent discovery that von Willebrand factor (VWF) regulates blood vessel formation has opened a novel perspective on the function of this complex protein. VWF was discovered as a key component of hemostasis, capturing platelets at sites of endothelial damage and synthesized in megakaryocytes and endothelial cells (EC). In recent years, novel functions and binding partners have been identified for VWF. The finding that loss of VWF in EC results in enhanced, possibly dysfunctional, angiogenesis is consistent with the clinical observations that in some patients with von Willebrand disease (VWD), vascular malformations can cause severe gastrointestinal (GI) bleeding. In vitro and in vivo studies indicate that VWF can regulate angiogenesis through multiple pathways, both intracellular and extracellular, although their relative importance is still unclear. Investigation of these pathways has been greatly facilitated by the ability to isolate EC from progenitors circulating in the peripheral blood of normal controls and patients with VWD. In the next few years, these will yield further evidence on the molecular pathways controlled by VWF and shed light on this novel and fascinating area of vascular biology. In this article, we will review the evidence supporting a role for VWF in blood vessel formation, the link between VWF dysfunction and vascular malformations causing GI bleeding and how they may be causally related. Finally, we will discuss how these findings point to novel therapeutic approaches to bleeding refractory to VWF replacement therapy in VWD.
Topics: Angiodysplasia; Animals; Blood Coagulation; Blood Platelets; Endothelial Cells; Gastrointestinal Hemorrhage; Glycoproteins; Hemorrhage; Hemostasis; Humans; Megakaryocytes; Mice; Neovascularization, Pathologic; Neovascularization, Physiologic; Signal Transduction; Stem Cells; Vascular Endothelial Growth Factor Receptor-2; von Willebrand Diseases; von Willebrand Factor
PubMed: 27778439
DOI: 10.1111/jth.13551 -
Seminars in Immunopathology May 2023Acute ischaemic and haemorrhagic stroke account for significant disability and morbidity burdens worldwide. The myeloid arm of the peripheral innate immune system is... (Review)
Review
Acute ischaemic and haemorrhagic stroke account for significant disability and morbidity burdens worldwide. The myeloid arm of the peripheral innate immune system is critical in the immunological response to acute ischaemic and haemorrhagic stroke. Neutrophils, monocytes, and dendritic cells (DC) contribute to the evolution of pathogenic local and systemic inflammation, whilst maintaining a critical role in ongoing immunity protecting against secondary infections. This review aims to summarise the key alterations to myeloid immunity in acute ischaemic stroke, intracerebral haemorrhage (ICH), and subarachnoid haemorrhage (SAH). By integrating clinical and preclinical research, we discover how myeloid immunity is affected across multiple organ systems including the brain, blood, bone marrow, spleen, and lung, and evaluate how these perturbations associate with real-world outcomes including infection. These findings are placed in the context of the rapidly developing field of human immunology, which offers a wealth of opportunity for further research.
Topics: Humans; Stroke; Brain Ischemia; Hemorrhagic Stroke; Subarachnoid Hemorrhage
PubMed: 36346451
DOI: 10.1007/s00281-022-00968-y -
Stroke Jun 2018Rho-kinase, an effector of RhoA, is associated with various cardiovascular diseases in circulating blood cells. However, the role of RhoA/Rho-kinase in peripheral blood...
BACKGROUND AND PURPOSE
Rho-kinase, an effector of RhoA, is associated with various cardiovascular diseases in circulating blood cells. However, the role of RhoA/Rho-kinase in peripheral blood mononuclear cells from patients with spontaneous aneurysmal subarachnoid hemorrhage (aSAH) has not yet been studied in relation to the severity of this disease. Therefore, we analyzed the expression and activity of RhoA as a possible biomarker in aSAH.
METHODS
Twenty-four patients with aSAH and 15 healthy subjects were examined. Peripheral blood mononuclear cells were collected, and RhoA activity and expression were determined by RhoA activation assay kit (G-LISA) and enzyme-linked immunosorbent assay tests, respectively. The severity of aSAH was determined from the World Federation of Neurological Surgeon scale, and vasospasm was evaluated using clinical symptoms, arteriography, and sonography.
RESULTS
RhoA expression was significantly increased in peripheral blood mononuclear cells from patients on days 0, 2, and 4 after aSAH versus healthy subjects (=0.036, 0.010, and 0.018, respectively, by Mann-Whitney analysis). There was a significant correlation between RhoA expression and injury severity on days 2 and 4 (Spearman test, day 2: =0.682, n=14, =0.007; day 4: =0.721, n=14, =0.004). No significant correlation was observed on day 0 (day 0: =0.131, n=6, =0.805). Active RhoA was not significantly different in patients and healthy subjects on days 0, 2, and 4 (=0.243, 0.222, and 0.600, respectively) nor did it increase significantly on days 0 and 2 in patients with vasospasm versus patients without vasospasm (=0.064 and 0.519, respectively). In contrast, active RhoA was significantly higher on day 4 in patients who developed vasospasm versus patients without vasospasm (=0.028).
CONCLUSIONS
Our preliminary results indicate that RhoA expression and activity in peripheral blood mononuclear cells might be related with aSAH severity and cerebral vasospasm. RhoA is a potential biomarker of the risks associated with aSAH.
Topics: Biomarkers; Cerebral Angiography; Female; Humans; Leukocytes, Mononuclear; Male; Middle Aged; Risk Factors; Subarachnoid Hemorrhage; Vasospasm, Intracranial; rhoA GTP-Binding Protein
PubMed: 29735721
DOI: 10.1161/STROKEAHA.117.020311 -
Chinese Journal of Traumatology =... Feb 2020Traumatic peripheral vascular injury is a significant cause of disability and death either in civilian environments or on the battlefield. Penetrating trauma and blunt... (Review)
Review
Traumatic peripheral vascular injury is a significant cause of disability and death either in civilian environments or on the battlefield. Penetrating trauma and blunt trauma are the most common forms of vascular injuries. Besides, iatrogenic arterial injury (IAI) is another pattern of vascular trauma. The management of peripheral vascular injuries has been improved in different environments and wars. There are different types of vascular injuries, such as vasospasm, contusion, intimal flaps, intimal disruption or hematoma, external compression, laceration, transection and focal wall defects, etc. The main clinical manifestations of vascular injuries are shock following massive hemorrhage and limb necrosis due to tissue and organ ischemia. Ultrasound, computed tomography angiography (CTA) and magnetic resonance angiography (MRA) are most valuable for assessment of peripheral vascular injuries. Angiography remains the gold standard for diagnosing vascular trauma. Immediate hemorrhage control and rapid restoration of blood flow are the primary goals of vascular trauma treatment. There are many operative treatment methods for vascular injuries, such as vascular suture or ligation, vascular wall repair and vascular reconstruction with blood vessel prostheses or vascular grafts. Embolization, balloon dilation and covered stent implantation are the main endovascular techniques. Surgical operation is still the primary treatment for vascular injuries. Endovascular treatment is a promising alternative, proved to be safe and effective, and preferred selection for patients. In summary, rapid diagnosis and timely surgical intervention remain the mainstays of the treatment. However, many issues need to be resolved by further studies.
Topics: Blood Vessel Prosthesis Implantation; Computed Tomography Angiography; Early Diagnosis; Endovascular Procedures; Hemorrhage; Humans; Iatrogenic Disease; Magnetic Resonance Angiography; Plastic Surgery Procedures; Vascular Surgical Procedures; Vascular System Injuries; Wounds, Nonpenetrating; Wounds, Penetrating
PubMed: 32014343
DOI: 10.1016/j.cjtee.2019.11.003 -
Neurology India 2022Malignant atrophic papulosis (MAP), or systemic Degos disease, is an obliterative vasculopathy of unknown origin, characterized by erythematous papules found on the... (Review)
Review
Malignant atrophic papulosis (MAP), or systemic Degos disease, is an obliterative vasculopathy of unknown origin, characterized by erythematous papules found on the skin, central nervous system (Neuro-MAP) and gastrointestinal tract. Neurological involvement occurs in approximately 20% of systemic cases, is progressive and largely fatal. It can be described in two forms: 1) the parenchymal presenting with meningoencephalitis and meningomyelitis and 2) the neurovascular presenting with large cerebral infarcts, intracranial and subarachnoid hemorrhage, subdural hematoma and venous sinus thrombosis. Predilection to subdural hematoma or hygroma is characteristic for neurological involvement in MAP in comparison to other vasculpathies and vasculitides. Peripheral nervous system manifestations are less common and include polyradiculopathy, neuropathy, and myopathy. CSF analysis usually shows mild to moderate pleocytosis, increased protein content, and normal glucose. Brain MRI may reveal cortical, subcortical and deep white matter ischemic lesions with possible nodular, leptomeningeal, dural, or ependymal enhancement. Spinal cord MRI may reveal patchy lesions from the periphery to the center or cord atrophy in progressive course. Neurological involvement in MAP has a grave prognosis. The interval from onset of papulosis to death averages two years in patients with neurological involvement. There is no confirmed treatment for MAP but there are promising reports with eculizumab and treprostinil.
Topics: Atrophy; Hematoma, Subdural; Humans; Malignant Atrophic Papulosis; Prognosis; Skin
PubMed: 35263846
DOI: 10.4103/0028-3886.338719 -
Journal of Internal Medicine Apr 2006The increase of plasma and blood viscosity is usually associated with pathological conditions; however, elevation of both parameters often results in increased perfusion... (Review)
Review
The increase of plasma and blood viscosity is usually associated with pathological conditions; however, elevation of both parameters often results in increased perfusion and the lowering of peripheral vascular resistance. In extreme haemodilution, blood viscosity is too low and insufficient to maintain functional capillary density, a problem that in experimental studies is shown to be corrected by increasing plasma viscosity up to 2.2 cP. This effect is mediated by mechanotransduction-induced nitric oxide (NO) production via shear stress in the endothelium as shown by microelectrode perivascular measurements of NO concentration. Moderate elevations of blood viscosity by increasing haematocrit ( approximately 10%) result in comparable reductions of blood pressure and peripheral vascular resistance, an effect also NO-mediated as it is absent after Nomega-nitro-L-arginine methyl ester treatment and in endothelial nitric oxide synthase-deficient mice. These findings show that the rheological properties of plasma affect vessel diameter in the microcirculation leading to counterintuitive responses to the changes in blood and plasma viscosity. Application of these findings to haemorrhagic shock resuscitation leads to the concept of hyperosmotic-hyperviscous resuscitation as a modality for maintaining the recovery of microvascular function.
Topics: Animals; Blood Viscosity; Hemorheology; Hemorrhage; Homeostasis; Humans; Hypertension; Hypotension; Mechanotransduction, Cellular; Nitric Oxide; Resuscitation
PubMed: 16594904
DOI: 10.1111/j.1365-2796.2006.01622.x -
Experimental Biology and Medicine... Apr 2017The ability to quickly diagnose hemorrhagic shock is critical for favorable patient outcomes. Therefore, it is important to understand the time course and involvement of... (Review)
Review
The ability to quickly diagnose hemorrhagic shock is critical for favorable patient outcomes. Therefore, it is important to understand the time course and involvement of the various physiological mechanisms that are active during volume loss and that have the ability to stave off hemodynamic collapse. This review provides new insights about the physiology that underlies blood loss and shock in humans through the development of a simulated model of hemorrhage using lower body negative pressure. In this review, we present controlled experimental results through utilization of the lower body negative pressure human hemorrhage model that provide novel insights on the integration of physiological mechanisms critical to the compensation for volume loss. We provide data obtained from more than 250 human experiments to classify human subjects into two distinct groups: those who have a high tolerance and can compensate well for reduced central blood volume (e.g. hemorrhage) and those with low tolerance with poor capacity to compensate.We include the conceptual introduction of arterial pressure and cerebral blood flow oscillations, reflex-mediated autonomic and neuroendocrine responses, and respiration that function to protect adequate tissue oxygenation through adjustments in cardiac output and peripheral vascular resistance. Finally, unique time course data are presented that describe mechanistic events associated with the rapid onset of hemodynamic failure (i.e. decompensatory shock). Impact Statement Hemorrhage is the leading cause of death in both civilian and military trauma. The work submitted in this review is important because it advances the understanding of mechanisms that contribute to the total integrated physiological compensations for inadequate tissue oxygenation (i.e. shock) that arise from hemorrhage. Unlike an animal model, we introduce the utilization of lower body negative pressure as a noninvasive model that allows for the study of progressive reductions in central blood volume similar to those reported during actual hemorrhage in conscious humans to the onset of hemodynamic decompensation (i.e. early phase of decompensatory shock), and is repeatable in the same subject. Understanding the fundamental underlying physiology of human hemorrhage helps to test paradigms of critical care medicine, and identify and develop novel clinical practices and technologies for advanced diagnostics and therapeutics in patients with life-threatening blood loss.
Topics: Arterial Pressure; Blood Volume; Hemodynamics; Humans; Models, Cardiovascular; Oxygen; Shock, Hemorrhagic
PubMed: 28346013
DOI: 10.1177/1535370217694099 -
Aging Sep 2023Intracerebral hemorrhage (ICH) is a stroke subtype with high mortality and disability rate, and neuroinflammation is involved in secondary brain injury. Galectin-3...
BACKGROUND
Intracerebral hemorrhage (ICH) is a stroke subtype with high mortality and disability rate, and neuroinflammation is involved in secondary brain injury. Galectin-3 (Gal-3) is one of the scaffold proteins of Galectins. Studies have indicated that Gal-3 plays an important role in the physiological and pathological state of the nervous system. Here we focus on the role of Gal-3 in ICH, especially in neuroinflammation.
METHODS
Injection of autologous blood into the right basal ganglia was used to simulate ICH injury, and the level of Gal-3 in brain was regulated by related means. The changes of Gal-3 were detected by western blot and immunofluorescence, the level of neuroinflammation by immunofluorescence staining and ELISA. Apoptosis and neuron loss were detected by TUNEL staining FJB staining and Nissl staining, and neurological deficits were judged by neurobehavioral tests.
RESULTS
The protein level of Gal-3 increased at 24 h after ICH. Downregulation of Gal-3 level can reduce the infiltration of M1-type microglia and peripheral inflammatory cells, thus alleviating post-ICH neuroinflammation, and reducing cell apoptosis and neuron loss in brain tissue. ICH-induced neurological damage was rescued. Meanwhile, the promotion in the expression level of Gal-3 increased neuroinflammatory activation and nerve cell death, aggravating ICH-induced brain injury.
CONCLUSIONS
This study proves that Gal-3 is involved in neuroinflammation and nerve damage after ICH. Gal-3 expression should not be encouraged early on to prevent neuroinflammation. which provides a new possibility for clinical treatment for ICH patients.
Topics: Humans; Galectin 3; Toll-Like Receptor 4; Microglia; Neuroinflammatory Diseases; Galectins; Cerebral Hemorrhage; Brain Injuries; Phenotype; Intracranial Hemorrhages
PubMed: 37698533
DOI: 10.18632/aging.205014