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Query: UMLS:C0022116 (ischemia)
 91,303 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Deep pressure sores (DPS) are associated with inadequate soft tissue perfusion and excessive tissue deformation over critical time durations, as well as with ischemia-reperfusion cycles and deficiency of the lymphatic system. Muscle tissue shows the lowest tolerance to pressure injuries, compared with more superficial tissues. In this communication, we present new histopathology data for muscle tissue of albino (Sprague-Dawley) rats exposed to pressures for 15 or 30 min. These data are superimposed with an extensive literature review of all previous histopathology reported for albino rat skeletal muscles subjected to pressure. The pooled data enabled a new mathematical characterization of the pressure-time threshold for cell death in striated muscle of rats, in the form of a sigmoid pressure-time relation, which extends the previous pressure-time relation to the shorter exposure periods. We found that for pressure exposures shorter than 1 h, the magnitude of pressure is the important factor for causing cell death and the exposure time has little or no effect: even relatively short exposures (15 min - 1 h) to pressures greater than 32 kPa (240 mmHg) cause cell death in rat muscle tissue. For exposures of 2 h or over, again the magnitude of pressure is the important factor for causing cell death: pressures greater than 9 kPa (67 mmHg) applied for over 2 h consistently cause muscle cell death. For the intermediate exposures (between 1 and 2 h), the magnitude of cell-death-causing pressure strongly depends on the time of exposure, i.e., critical pressure levels drop from 32 to 9 kPa. The present sigmoidal pressure-time cell death threshold is useful for design of studies in albino rat models of DPS, and may also be helpful in numerical simulations of DPS development, where there is often a need to extrapolate from tissue pressures to biological damage.
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PMID:Pressure-time cell death threshold for albino rat skeletal muscles as related to pressure sore biomechanics. 1619 45

A 75-year-old man with a past history of bilateral thalamic hemorrhage was scheduled for cholecystectomy and cholelithotomy under general anesthesia. Although the preoperative ECG showed a complete right bundle branch block, the echocardiogram revealed no abnormality. Anesthesia was induced with thiopental and vecuronium, and maintained with sevoflurane in oxygen. Soon after changing to the left decubitus position for the insertion of an epidural catheter, ECG showed complete atrioventricular block, which did not respond to atropine. Adrenalin was transiently effective, but arrhythmia continued. After administration of dopamine, norepinephrine and isoproterenol, we inserted a temporary transvenous pacemaker catheter, and the hemodynamics became stable by ventricular pacing. The operation was postponed. Subsequent cardiologic examination showed no ischemia. The atrioventricular block disappeared 7 hours after the induction of general anesthesia. We should be very careful with the anesthetic management of a patient with a complete right bundle branch block.
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PMID:[A case of complete atrioventricular block after induction of general anesthesia]. 1629 74

Despite improved awareness and quality of care among health care personnel, pressure ulcers prevalence remains high especially in the inpatient setting. Pressure ulcers are associated with increased morbidity and mortality, affecting the quality of life of patients and their caregivers, and significantly increasing direct and indirect healthcare costs. Early risk assessment for developing a pressure ulcer is essential to decide on the appropriate preventive measures and for initiation of a tailored therapeutic approach. Interventions include strategies to reduce extrinsic and intrinsic risk factors associated with tissue ischemia, optimization of patient's nutritional status, and local wound care. This revision intends to review current evidence-based therapeutic interventions in pressure ulcer care, and support implementation of management protocols in an inpatient ward.
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PMID:[Pressure ulcer management--Evidence-based interventions]. 1698 41

Decubitus ulcers appear to be associated with insidious trauma. Differential diagnosis can be tricky, and etiology is controversial with sustained localized pressure which plays a significant role. Sustained pressure can stretch soft tissues and blood vessels, causing multiple microthrombi around the point of maximum compression. This leads to prolonged ischemia and produces a plaque of dead tissue surrounded by microthrombi. Prevention often includes regular movement or supports that move the patient. Good nutrition is important, but the adverse effects of fever should not be overlooked. Anti-thrombotic agents should be considered. Occlusive dressings can be used for existing ulcers, while traditional treatments are less appropriate. Pressure and other stresses theoretically should be relieved.
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PMID:The decubitus ulcer: many questions but few definitive answers. 1727 7

Chronic wounds are major health problems that affect millions of people in the United States every year. Management of these wounds costs billions of dollars annually in the United States. Despite their clinical importance, the molecular mechanisms underlying these clinical conditions remain elusive. Repetitive ischemia-reperfusion (I-R) may play a pivotal role in chronic wound formation. The development of therapies for these wounds is hindered by the lack of animal models that allow identification of the molecular mechanisms underlying chronic wound formation. In the first study of its kind, we adapted our rat pressure sore model by imposing two cycles of ischemia (2 hours) and two cycles of reperfusion (24 hours), and we examined gene expression to better understand the molecular events that occur at the very early stages of cutaneous I-R injury with a goal of devising preventing strategies. We successfully tested our hypothesis and demonstrated that while cytoprotective genes, such as heat shock protein 70, heat shock protein 90, hypoxia-inducible factor-1alpha, vascular endothelial growth factor, and heme oxygenase-1, were initially up-regulated during the first cycle of I-R, their up-regulation was subsequently reduced or completely abolished during the second cycle of I-R. These findings raise the possibility that reduced up-regulation of these cytoprotective genes may be causally linked to cutaneous I-R injury.
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PMID:Reduced up-regulation of cytoprotective genes in rat cutaneous tissue during the second cycle of ischemia-reperfusion. 1735 52

Pressure ulcers are areas of tissue damage caused by unrelieved pressure that results in ischemia. About 70% of pressure ulcers occur in adults who are older than 65 years of age; the most common sites are the sacrum and heels. The rate at which new ulcers develop in acute care settings varies from 0.4% to 38%, with a mean incidence of about 7%. Recovery in patients who have pressure ulcers is delayed, as demonstrated by an increased length of hospitalization and increased health care costs. This article addresses recovery in older adults who are at risk for the development of a pressure ulcer.
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PMID:Hospital recovery is facilitated by prevention of pressure ulcers in older adults. 1769 48

Deep tissue injury (DTI) is a severe pressure ulcer, which initiates in muscle tissue under a bony prominence, and progresses outwards. It is associated with mechanical pressure and shear that may cause capillaries to collapse and thus, induce ischemic conditions. Recently, some investigators stipulated that ischemia alone cannot explain the etiology of DTI, and other mechanisms, particularly excessive cellular deformations may be involved. The goal of this study was to evaluate the functioning of capillaries in loaded muscle tissue, using animal and finite element (FE) models. Pressures of 12, 37, and 78 kPa were applied directly to one gracilis muscle of 11 rats for 2 h. Temperatures of the loaded and contralateral muscles were recorded with time using infrared thermography (IRT) as a measure of the ischemic level. In addition, a non-linear large deformation muscle-fascicle-level FE model was developed and subjected to pressures of 12-120 kPa without and with simultaneous shear strain of up to 8%. For each simulation case, the accumulative percentage of open capillary cross-sectional area and the number of completely closed capillaries were determined. After 2 h, temperature of the loaded muscles was 2.4 +/- 0.3 degrees C (mean +/- standard deviation) lower than that of the unloaded contralateral limbs (mean of plateau temperature values across all pressure groups). Temperature of the loaded muscles dropped within 10 min but then remained stable and significantly higher than room temperature for at least 30 additional minutes in all pressure groups, indicating that limbs were not completely ischemic within the first 40 min of the trials. Our FE model showed that in response to pressures of 12-120 kPa and no shear, the accumulative percentage of open capillary cross-sectional area decreased by up to 71%. When shear strains were added, the open capillary cross-sectional area decreased more rapidly, but even for maximal loading, only 46% of the capillaries were completely closed. Taken together, the animal and FE model results suggest that acute ischemia does not develop in skeletal muscles under physiological load levels within a timeframe of 40 min. Since there is evidence that DTI develops within a shorter time, ischemia is unlikely to be the only factor causing DTI.
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PMID:The effects of pressure and shear on capillary closure in the microstructure of skeletal muscles. 1789 78

Pressure-related deep tissue injury (DTI) represents a severe pressure ulcer, which initiates in compressed muscle tissue overlying a bony prominence and progresses to more superficial tissues until penetrating the skin. Individual subjects with impaired motor and/or sensory capacities are at high risk of developing DTI. Impaired diffusion of critical metabolites in compressed muscle tissue may contribute to DTI, and impaired diffusion of tissue damage biomarkers may further impose a problem in developing early detection blood tests. We hypothesize that compression of muscle tissue between a bony prominence and a supporting surface locally influences the diffusion capacity of muscle. The objective of this study was therefore, to determine the effects of large compression strains on free diffusion in a tissue-engineered skeletal muscle model. Diffusion was measured with a range of fluorescently labeled dextran molecules (10, 20, 150kDa) whose sizes were representative of both hormones and damage biomarkers. We used fluorescence recovery after photobleaching (FRAP) to compare diffusion coefficients (D) of the different dextrans between the uncompressed and compressed (48-60% strain) states. In a separate experiment, we simulated the effects of local partial muscle ischemia in vivo, by reducing the temperature of compressed specimens from 37 to 34 degrees C. Compared to the D in the uncompressed model system, values in the compressed state were significantly reduced by 47+/-22% (p<0.02). A 3 degrees C temperature decrease further reduced D in the compressed specimens by 10+/-6% (p<0.05). In vivo, the effects of large strains and ischemia are likely to be summative, and hence, the present findings suggest an important role of impaired diffusion in the etiology of DTI, and should also be considered when developing biochemical screening methods for early detection of DTI.
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PMID:The free diffusion of macromolecules in tissue-engineered skeletal muscle subjected to large compression strains. 1806 75

The formation of pressure ulcers is dependent on multiple factors including ischemia-reperfusion (IR). This study assessed the mechanism of a previously reported murine model of cutaneous IR injury. Three cycles of IR (days 1-3) by external application of two magnetic plates were performed to induce pressure ulcer formation. Increased infiltration of neutrophils and macrophages, and augmented expression of proinflammatory cytokines and inducible nitric oxide synthase (iNOS), were observed during IR cycles. In this model, monocyte chemoattractant protein-1 (MCP-1) was remarkably increased at day 1 in the skin followed by inflammatory cell infiltration. Therefore, IR cycles were performed in MCP-1-deficient (MCP-1(-/-)) mice to evaluate the role of this chemokine in pressure ulcer development. MCP-1(-/-) mice showed reduced macrophage infiltration and expression of tumor-necrosis factor-alpha (TNF)-alpha and iNOS during IR cycles leading to attenuated apoptosis and skin injury. Importantly, MCP-1 played a role in apoptosis and injury via inducing iNOS during the reperfusion rather than the ischemic period. These findings indicate that MCP-1 may be a critical factor for macrophage recruitment and subsequent skin inflammation and injury during IR cycles. We propose that this is a useful model for investigating the mechanism of pressure ulcer formation using various transgenic mice.
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PMID:The loss of MCP-1 attenuates cutaneous ischemia-reperfusion injury in a mouse model of pressure ulcer. 1821 77

Small-bowel volvulus around the superior mesenteric artery is a very unusual cause of small-intestinal obstruction, which may result in intestinal ischemia and necrosis. A 45-year-old woman, who had received a living-donor liver transplant with a right lobe graft for fulminant hepatic failure 5 years earlier, underwent a liver biopsy and was placed in the right decubitus position. Abdominal pain, high fever, tachycardia, and altered mental status developed quickly, suggesting abdominal sepsis. Computed tomography (CT) showed a "target sign," representing a counter-clockwise rotation of the mesenteric pedicle. However, without laparotomy, the symptoms subsided completely within 12 h by her lying strictly in the left decubitus position. A second CT scan showed an orthotopic untwisted jejunum. Although many complications associated with percutaneous liver biopsy have been described, to our knowledge this is the first report of positioning-associated intestinal volvulus after a liver biopsy.
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PMID:Small-intestinal volvulus around the superior mesenteric artery as an extremely rare positioning-associated complication after percutaneous liver biopsy. 1851 44


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