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

Dysbaric osteonecrosis appears to be independent of decompression sickness. The 2 conditions, however, may share etiologic and pathogenetic factors. The incidence of osteonecrosis is influenced by the number of hyperbaric exposures, extent of pressure, decompression profile and possibly by the rate of compression and degree of obesity. Though etiology and pathogenesis are unclear, osteonecrosis is probably due to ischemia, with gas bubbles causing direct or indirect circulatory impairment. In vitro experiments, as well as human and animal studies, suggest multiple pathogenetic mechanisms: intraosseous vessel compression by extravascular bubbles; vessel obstruction by bubbles, fibrin thrombi, platelet aggregates, clumped erythrocytes or coalesced lipids; and narrowing of arterial lumina by bubble-induced myointimal thickening. Obstructing materials, whether autochthonous or embolic, may result from blood-bubble interface reactions. Rheologic changes and blood flow redistribution could play contributing roles. It seems likely that multiple pathogenetic factors act in concert or sequentially. Proposed nonischemic changes, such as hyperoxic injury gas-induced osmosis, or autoimmunity, lack sufficient supporting evidence. The peculiar vulnerability of bone may be related to gas supersaturation of the fatty marrow; sensitivity to extravascular gas pressure because of tissue rigidity; poor vascularization; and the presence of uranium 238 which promotes nucleation and subsequent gas bubble formation.
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PMID:Dysbaric osteonecrosis. Etiological and pathogenetic concepts. 63 12

Ischaemia is a major mechanism underlying central nervous system (c.n.s.) damage in decompression sickness. Some recent experimental observations on the effect of bubble-induced ischaemia on c.n.s. tissue sharpen and extend our understanding of the pathophysiology of decompression sickness. After bubble-induced brain ischaemia, a measurable increase in 111In-labelled leucocytes occurs in the injured hemisphere. By 4 h into the recovery period the cells are concentrated in zones of low blood flow, as measured by the [14C]iodoantipyrine technique. The presence of these cells during the critical early hours of c.n.s. ischaemia suggests that they may contribute to the evolution of neuronal damage. Oedema is often cited as the cause of clinical deterioration after c.n.s. ischaemia or trauma. Recent evidence indicates that the presence and degree of circumscribed brain oedema is not a good predictor of the amount of nerve cell recovery (by using cortical sensory evoked response) after bubble-induced brain ischaemia. This brings into question the role of circumscribed oedema of the c.n.s. in dysfunction of post-ischemic nerve cells.
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PMID:Several new aspects of bubble-induced central nervous system injury. 614 76

Using the spinal cord decompression sickness model described in Part I, we explored the effects of delay to treatment on the recovery of spinal evoked potentials (SEP). The primary treatments of oxygen at 60 fsw (2.8 bar) and air at 165 fsw (6.0 bar) were studied. In this exploratory study the results were surprisingly poor in all treatments applied. There is evidence that in this model a delay of 15-18 min between diagnosis and start of therapy would generally allow some recovery of SEP, which would rarely be complete. Supporting experiments involving cord ischemia are described. The results from this study enabled us to design a set of practicable experimental criteria for the purpose of discovering the optimal combinations of oxygen and pressure for the treatment of spinal cord decompression sickness.
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PMID:A model of spinal cord dysbarism to study delayed treatment: II. Effects of treatment. 648 1

The microsphere technique was used to determine whether blood flow to the central nervous system and various organs is impaired in rats with spinal cord injury induced by decompression sickness. For this purpose cannulas were placed in the left ventricle of the rats for the injection of microspheres and in the tail artery as the reference site for withdrawal of blood for the calculation of cardiac output (CO) and blood flow (BF) and for measurement of blood pressure (BP) and heart rate (HR). The rats were then subjected to a simulated dive that by electrophysiologic criteria rapidly (within 60 min after diving) induces severe neurologic deficits in the cord. Microspheres were used to determine CO and BF before and at 10, 60, and 180 min after diving. CO, BP, and HR were not affected by diving. BF to various regions of the brain, heart, bone, and fat was also not affected by diving. BF decreased in the lung (40%) and skeletal muscle (50%) and increased in spinal cord (20%) at 10 min after diving. At 60 and 180 min after diving the only alterations seen were increases in hepatic arterial and portal BF. Analysis of the distribution of cardiac output showed that diving induced changes that essentially paralleled the BF changes described above. We conclude that perfusion in the central nervous system is maintained in rats with spinal cord injury induced by decompression sickness. These results indicate that ischemia does not play a role in the pathophysiology of neuronal injury in this model of decompression sickness.
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PMID:Role of ischemia in rats with spinal cord injury induced by decompression sickness. 755 88

We reviewed 44 cases of ischemia and infarction of the spinal cord at two university hospitals. Three patients experienced transient ischemic attacks. Etiologies of completed strokes were diverse and included rupture and surgical repair of aortic aneurysms, aortic dissection, aortic rupture and thrombosis, global ischemia, anterior spinal artery embolism, repair and thrombosis of spinal arteriovenous malformations, hematomyelia, epidural hematoma, cervical osteophytosis, celiac plexus block, systemic lupus erythematosus, coagulopathy, and decompression sickness. Motor function improved in 12 patients, was substantial in only one, and occurred largely within the first 2 to 4 weeks. Favorable ambulatory outcome correlated with improving neurologic examinations and relatively preserved strength in hip abductors and knee extensors. More extensive deficits without initial improvement portended a more severe prognosis. Autonomic dysfunction, pain, paresthesia, and depression were common and impeded recovery in some patients. The mean level of deficit was at T-8 and in cases of global ischemia was at T-9, which leads us to dispute the classical view of a midthoracic watershed zone of ischemic vulnerability near T-4.
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PMID:Spinal cord infarction: etiology and outcome. 915 13

Pathophysiologic mechanisms involved in the application of HBO therapy are poorly understood that may limit its clinical use. However, useful indications are well standardized in the setting of critical care medicine, CO poisoning, decompression sickness, gas gangrene and soft tissue anaerobic infections, crush syndrome, burns, sudden deafness... HBO therapy is also indicated in the management of chronic limb ischemia, diabetic foot lesion, osteomyelitis, osteoradionecrosis. These clinical indications have been evaluated in a Consensus Conference on Hyperbaric Medicine that has classified its application according to its efficiency. Indications were classified as strongly recommended (positively affects the patient's survival), recommended (does not influence the patient's survival but is important for the prevention of serious disorders) and optional (regarded as a additional treatment modality). Clinical application of HBO therapy requires specific equipment including a multiplace hyperbaric chamber and specific educational program and training for personnel employed in the clinical hyperbaric center. Lastly, HBO therapy is related to accurate rules defining its indications as well as its evaluation that are minimal prerequisites for safety and clinical results.
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PMID:[Indications for hyperbaric oxygen therapy. Organization of the treatment unit. Training of personnel]. 896 13

To examine the changes in blood-brain barrier (BBB), cerebral microcirculation, and histology from 15 min to 72 h after decompression, 90 rats were exposed to experimental compression to 6 atm abs air for 90 min and subsequent rapid decompression. The disruption of BBB was examined by Evans blue extravasation. The cerebral microcirculation was demonstrated by perfusion with India ink. The area stained with Evans blue and the regions of defective filling with India ink, observed immediately after decompression decreased in size with time and were undetectable 3-24 h after decompression. The edematous brain tissue with enlarged perivascular space and darkly stained nerve cells also decreased to the uncompressed control level 1-24 h after decompression. These reversible dysbaric changes, however, reappeared 48-72 h after decompression. The different mechanisms, the physicochemical effects of microbubbles, and the maturation phenomenon after temporary brain ischemia induced by dysbaric microbubbles may be involved in the brain damage after decompression sickness.
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PMID:Reversibility in blood-brain barrier, microcirculation, and histology in rat brain after decompression. 906 51

Medical issues in sport diving include illnesses that are caused by diving, and medical disorders that compromise safety. Cerebral air embolism and decompression sickness of the brain and spinal cord can result from diving. Sport divers may manifest a spectrum of symptoms from air embolism, which can range from unconsciousness to minimal symptoms, which include fatigue, personality change, poor concentration, irritability, and changes in vision. The physician must search for these minor symptoms in divers who are suspected of pulmonary barotrauma. Medical disorders of concern in diving include diseases of the lungs, the heart, the brain, and the endocrine system, particularly diabetes. Other factors involved in diving safety are exercise capacity and training. Clinical practice standards usually prohibit diving by individuals who have a seizure disorder that requires continuous medication. In the United States, we will not approve diving for individuals who have insulin-dependent diabetes or severe asthma. Some divers can return to diving after myocardial infarction or bypass surgery if they demonstrate good exercise tolerance and no ischemia on a graded exercise test, which simulates the physical activity needed for safe diving.
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PMID:Medical aspects of sport diving. 914 89

Therapy for acute ischemic stroke can be approached in two basic ways: first, by an attempt to restore or improve blood flow in an occluded vascular territory and, second, via therapy directed at the cellular and metabolic targets. As local anoxia and energy failure are the initiating cellular stage in ischemia, the inhalation of oxygen at increased atmospheric pressures might be effective. Treatment of acute focal cerebral ischemia with hyperbaric oxygen (HBO) has been reported in animals and humans. In general, the results of research in animals have suggested a promising role for the use of HBO. More than 400 cases of human ischemic stroke treated with HBO have been reported. In about half of the cases, improvement in status has been claimed on clinical or electroencephalographic grounds. In fact, the effectiveness of HBO in most disease processes other than carbon monoxide poisoning and decompression sickness is a subject of major ongoing debate. This short review will attempt: (1) to recall some early experiments involving HBO in the treatment of acute ischemia: (2) to point out some conflicting results regarding the role of HBO on cellular and metabolic disorders; and (3) to determine the possibility of a future role for HBO therapy in acute ischemic stroke.
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PMID:Hyperbaric oxygen in the treatment of acute ischemic stroke: an unsettled issue. 926 Aug 51

Dysbaric osteonecrosis was induced successfully in adult sheep after 12 to 13, 24-hour exposures to compressed air (2.6-2.9 atmospheres absolute) during a 2-month period. All exposed sheep had decompression sickness and extensive bone and marrow necrosis in their long bones. Radiographic analysis of these progressive lesions showed mottled to distinct medullary opacities and endosteal thickening characteristic of dysbaric osteonecrosis. Six months after the last hyperbaric exposure, neovascularization of once ischemic fatty marrow was centripetal from the diaphyseal cortex. Proliferating endosteal new bone, fatty marrow calcification, and appositional new bone formation were widespread. Juxtaarticular osteonecrosis involved marrow fibrosis and loss of osteocytes in subchondral cortical bone. Tidemark reduplication in juxtaarticular bone and cartilage thinning suggested possible early osteoarthritis induction by recurrent episodes of transient ischemia after multiple hyperbaric exposures. Dysbaric osteonecrosis appears to involve a bone compartment syndrome of elevated intramedullary pressure initiated by decompression induced N2 bubble formation in the fatty marrow of the long bones. An animal model that can be used to investigate the pathogenesis, diagnosis, and treatment of dysbaric osteonecrosis is discussed.
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PMID:Dysbaric osteonecrosis in divers and caisson workers. An animal model. 937 84


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