Pneumatic Compression (pneumatic + compression)

Distribution by Scientific Domains


Selected Abstracts


Antiplatelet drug use preceding the onset of intracerebral hemorrhage is associated with increased mortality

FUNDAMENTAL & CLINICAL PHARMACOLOGY, Issue 3 2007
Karine Lacut
Abstract Recent studies highlight the contribution of antiplatelet therapy to clinical severity and increased mortality of intracerebral hemorrhage (ICH) but results are discrepant. The aim of this report was to evaluate the association between antiplatelet drug use preceding the onset of ICH and the mortality, assessed at regular intervals, among patients with acute ICH. We analyzed data from a randomized study which enrolled consecutive patients with a documented acute ICH to evaluate the efficacy of intermittent pneumatic compression of the legs in venous thrombosis prevention. Clinical characteristics and treatment used before the onset of ICH were checked at the time of inclusion. Mortality was assessed at regular intervals until 3 months after ICH diagnosis. Among 138 patients included in this report, 30 were current users of antiplatelet therapy at the time of ICH; they were significantly older and less frequently heavy drinkers than non-users of antiplatelet drugs. Mortality rates were 20% at 8 days, 40% at 1 month, and 47% at 3 months among antiplatelet drug users compared with 6.5%, 13% and 19% among non-users. The corresponding estimated risks for mortality related to antiplatelet drug use were 3.6 (95% CI 1.1,12), 4.5 (95% CI 1.8,11), and 3.6 (95% CI 1.5,8.6). Adjusted for age, hypertension and alcohol over use, antiplatelet therapy remained significantly associated with an increased mortality rate of acute ICH. Current antiplatelet drug use preceding the onset of ICH is associated with increased short-term ICH mortality, independently of age. [source]


Should we give thromboprophylaxis to patients with liver cirrhosis and coagulopathy?

HPB, Issue 6 2009
Marco Senzolo
Abstract Patients with liver cirrhosis are characterized by decreased synthesis of both pro- and anticoagulant factors, and recently there has been evidence of normal generation of thrombin resulting in a near normal haemostatic balance. Although it is generally recognized that bleeding is the most common clinical manifestation as a result of decreased platelet function and number, diminished clotting factors and excessive fibrinolysis, hypercoagulability may play an under recognized but important role in many aspects of chronic liver disease. In fact, they can encounter thrombotic complications such as portal vein thrombosis, occlusion of small intrahepatic vein branches and deep vein thrombosis (DVT). In particular, patients with cirrhosis appear to have a higher incidence of unprovoked DVT and pulmonary embolism (PE) compared with the general population. In dedicated studies, the incidence of DVT/PE ranges from 0.5% to 1.9%, similar to patients without comorbidities, but lower than patients with other chronic diseases (i.e, renal or heart disease). Surprisingly, standard coagulation laboratory parameters are not associated with a risk of developing DVT/PE; however, with multivariate analysis, serum albumin level was independently associated with the occurrence of thrombosis. Moreover, patients with chronic liver disease share the same risk factors as the general population for DVT/PE, and specifically, liver resection can unbalance the haemostatic equilibrium towards a hypercoagulable state. Current guidelines on antithrombotic prophylaxis do not specifically comment on the cirrhotic population as a result of the perceived risk of bleeding complications but the cirrhotic patient should not be considered as an auto-anticoagulated patient. Therefore, thromboprophylaxis should be recommended in patients with liver cirrhosis at least when exposed to high-risk conditions for thrombotic complications. Low molecular weight heparins (LWMHs) seem to be relatively safe in this group of patients; however, when important risk factors for bleeding are present, graduated compression stockings or intermittent pneumatic compression should be considered. [source]


Compression therapy promotes proliferative repair during rat Achilles tendon immobilization

JOURNAL OF ORTHOPAEDIC RESEARCH, Issue 7 2010
Nikos Schizas
Abstract Achilles tendon ruptures are treated with an initial period of immobilization, which obstructs the healing process partly by a reduction of blood circulation. Intermittent pneumatic compression (IPC) has been proposed to enhance tendon repair by stimulation of blood flow. We hypothesized that daily IPC treatment can counteract the deficits caused by 2 weeks of immobilization post tendon rupture. Forty-eight Sprague-Dawley SD) rats, all subjected to blunt Achilles tendon transection, were divided in three equal groups. Group A was allowed free cage activity, whereas groups B,C were immobilized at the operated hindleg. Group C received daily IPC treatment. Two weeks postrupture the rats were euthanatized and the tendons analyzed with tensile testing and histological assessments of collagen organization and collagen III-LI occurrence. Immobilization significantly reduced maximum force, energy uptake, stiffness, tendon length, transverse area, stress, organized collagen diameter and collagen III-LI occurrence by respectively 80, 75, 77, 22, 47, 65, 49, and 83% compared to free mobilization. IPC treatment improved maximum force 65%, energy 168%, organized collagen diameter 50%, tendon length 25%, and collagen III-LI occurrence 150% compared to immobilization only. The results confirm that immobilization impairs healing after tendon rupture and furthermore demonstrate that IPC-treatment can enhance proliferative tendon repair by counteracting biomechanical and morphological deficits caused by immobilization. © 2010 Orthopaedic Research Society. Published by Wiley Periodicals, Inc. J Orthop Res 28:852,858, 2010 [source]


Design of an Artificial Left Ventricular Muscle: An Innovative Way to Actuate Blood Pumps?

ARTIFICIAL ORGANS, Issue 6 2009
Benjamin Van Der Smissen
Abstract Blood pumps assist or take over the pump function of a failing heart. They are essentially activated by a pusher plate, a pneumatic compression of collapsible sacs, or they are driven by centrifugal pumps. Blood pumps relying upon one of these actuator mechanisms do not account for realistic wall deformation. In this study, we propose an innovative design of a blood pump actuator device which should be able to mimic fairly well global left ventricular (LV) wall deformation patterns in terms of circumferential and longitudinal contraction, as well as torsion. In order to reproduce these basic wall deformation patterns in our actuator device, we designed a novel kind of artificial LV "muscle" composed of multiple actively contracting cells. Its contraction is based on a mechanism by which pressurized air, inside such a cell, causes contraction in one direction and expansion perpendicular to this direction. The organization and geometry of the contractile cells within one artificial LV muscle, the applied pressure in the cells, and the governing LV loading conditions (preload and afterload) together determine the global deformation of the LV wall. Starting from a simple plastic bag, an experimental model based on the abovementioned principle was built and connected to a lumped hydraulic model of the vascular system (including compliance and resistance). The wall deformation pattern of this device was validated visually and its pump performance was studied in terms of LV volume and pressure and heart rate. Our experimental results revealed (i) a global LV motion resembling a real LV, and (ii) a close correlation between our model and a real LV in terms of end-systolic volume and pressure, end-diastolic volume and pressure, stroke volume, ejection fraction and pressure-volume relationship. Our proposed model appears promising and it can be considered as a step forward when compared to currently applied actuator mechanisms, as it will likely result in more physiological intracavity blood flow patterns. [source]