Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0022116 (ischemia)
 91,303 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Dysbaric osteonecrosis is associated with exposure to large ambient pressure changes, and comprises necrotic lesions in the fatty marrow-containing shafts of the long bones, and the ball and socket joints (hips and shoulders). The fundamental causes are still in question and the illness remains a significant health hazard. Radiological and pathological features of both dysbaric and non-dysbaric osteonecrosis are indistinguishable and both are characterized by intramedullary venous stasis, ischemia and necrosis of bone. It has been generally accepted that gas bubbles (probably by initiating intramedullary venous stasis) are the prime cause of dysbaric osteonecrosis, as well as being responsible for Type 1 Decompression Sickness or 'the bends'. Importantly, however, not all series have found a correlation between dysbaric osteonecrosis and 'the bends'. Thus even though it is likely that gas bubbles remain the prime cause of dysbaric osteonecrosis, workers have proposed that in some cases there is another etiological factor which may exaggerate the pathologic effects of gas bubbles, making the bone more susceptible to necrosis. It is proposed that rapid compression by impeding venous drainage from bone initiates intramedullary venous stasis. In the presence of intramedullary gas bubbles, this may progress to thrombosis, ischemia and bone necrosis. The review offers an explanation for total sparing of the knee joint in dysbaric osteonecrosis, and sole involvement of the hip and shoulder (in terms of sub-articular lesions and subsequent joint collapse). In addition to continued observance of proper decompression procedures, a slower rate of compression may further reduce the incidence of dysbaric osteonecrosis. Bone death or osteonecrosis is a concept which Hippocrates put forward in antiquity (1), but it was not until 1794 that James Russell of Edinburgh wrote the first modern-day descriptions. In these cases infection was the predominant etiology (1,2). In 1888 Konig described necrosis of the adult femoral head without infection (3) (aseptic necrosis of bone) and in the same year Twynam reported a case of osteonecrosis in a caisson worker (4) in which there was still a significant infective component. In 1911 Bornstein and Plate, followed later and independently by Bassoe in 1913, presented radiological confirmation of aseptic necrosis of bone in compressed air workers (5). The first report of aseptic necrosis in an underwater diver subsequently appeared in 1936 (6). The condition of aseptic necrosis of bone in association with exposure to raised ambient pressure (previously referred to as caisson disease, pressure-induced osteoarthropathy (7), 'bone rot' (8) and other synonyms (6)) is now generally known as dysbaric osteonecrosis (6). Despite detailed examination of this problem by many authorities, dysbaric osteonecrosis still remains a significant occupational hazard with serious medico-legal consequences (5-13). This suggests that preventative measures are being based upon an incomplete understanding of the pathophysiology of the disease, and that other etiological factors are perhaps being overlooked.
 ...
PMID:Dysbaric osteonecrosis: a reassessment and hypothesis. 1085 44

Pulmonary barotrauma-induced cerebral arterial gas embolism (CAGE) continues to complicate compressed gas diving activities. Inadequate lung ventilation secondary to inadvertent breath holding or rapid buoyant ascent can quickly generate a critical state of lung over-pressure. Pulmonary over-pressurization may also occur as a consequence of acute and chronic pulmonary pathologies. Resulting barotrauma frequently causes structural failure within the terminal distal airway. Respiratory gases are then free to embolize the systemic circulation via the pulmonary vasculature and the left heart. The brain is a common target organ. Bubbles that enter the cerebral arteries coalesce to form columns of gas as the vascular network narrows. Small amounts of gas frequently pass directly through the cerebral circulation without occlusion. Larger columns of gas occlude regional brain blood flow, either transiently or permanently, producing a stroke-like clinical picture. In cases of spontaneous redistribution, a period of apparent recovery is frequently followed by relapse. The etiology of relapse appears to be multifactoral, and chiefly the consequence of a failure of reperfusion. Prediction of who will relapse is not possible, and any such relapse is of ominous prognostic significance. It is advisable, therefore, that CAGE patients who undergo spontaneous recovery be promptly recompressed while breathing oxygen. Therapeutic compression will serve to antagonize leukocyte-mediated ischemia-reperfusion injury; limit potential re-embolization of brain blood flow, secondary to further leakage from the original pulmonary lesion or recirculation of gas from the initial occlusive event; protect against embolic injury to other organs; aid in the resolution of component cerebral edema; reduce the likelihood of late brain infarction reported in patients who have undergone spontaneous clinical recovery; and prophylax against decompression sickness in high gas loading dives that precede accelerated ascents and omitted stage decompression.
 ...
PMID:Pulmonary barotrauma-induced cerebral arterial gas embolism with spontaneous recovery: commentary on the rationale for therapeutic compression. 1184 83

Arterial gas embolism may occur as a consequence of lung rupture, decompression sickness, following operative procedures or as accidental infusion of gas during various diagnostic procedures. It can lead to severe morbidity or even death. Microdialysis is a technique that has been extensively used for evaluating localized changes in the brain. The microdialysis probe is only capable of measuring changes in the immediate adjacent tissue. In arterial gas embolism the changes are multifocal. Thus a probe located in the cerebral cortex will not detect the total amount of damage. We used microdialysis in the cisterna magna of 9 anaesthetized pigs to study the diffuse injury following arterial gas embolism. After injection of 5.0 mL of air in the internal carotid artery, we found a significantly increased lactate-pyruvate ratio in the cerebrospinal fluid, lasting for 2 hours. This indicates anaerobic metabolism. Mean levels of glycerol were significantly increased, indicating membrane disruption. Glutamate levels were also elevated, although not significantly. The injection of air affected carotid flow. Flow in the carotid artery of the side of injection decreased significantly, but returned to baseline in 1 hour. Flow in the contralateral carotid was increased, but not significantly. We conclude that massive air embolism causes ischemia and reduced blood flow in the brain that can be detected in the cisterna magna.
 ...
PMID:Microdialysis in cisterna magna during cerebral air embolism in swine. 1267 Jan 24

Gas embolism is a known complication of various invasive procedures, and its management is well established. The consequence of gas microemboli, microbubbles, is underrecognized and usually overlooked in daily practice. We present the current data regarding the pathophysiology of microemboli and their clinical consequences. Microbubbles originate mainly in extracorporeal lines and devices, such as cardiopulmonary bypass and dialysis machines, but may be endogenous in cases of decompression sickness or mechanical heart valves. Circulating in the blood stream, microbubbles lodge in the capillary bed of various organs, mainly the lungs. The microbubble obstructs blood flow in the capillary, thus causing tissue ischemia, followed by inflammatory response and complement activation. Aggregation of platelets and clot formation occurs as well, leading to further obstruction of microcirculation and tissue damage. In this review, we present evidence of the biological and clinical detrimental effects of microbubbles as demonstrated by studies in animal models and humans, and discuss management of the microbubble problem with regard to detection, prevention, and treatment.
 ...
PMID:Microbubbles: pathophysiology and clinical implications. 1623 69

Avascular necrosis of bone (AVN) occurs as two main variants, local and systemic. Local AVN is usually caused by trauma or microtrauma; examples include primary osteonecrosis of the medial condyle, vertebral osteonecrosis, necrosis after meniscectomy, and osteonecrosis of the mandible or small bones. Systemic AVN manifests as epiphyseal necrosis or bone infarction, which is often multifocal. Little is known about the factors that trigger AVN. One possible mechanism is intraluminal obliteration of blood vessels by microscopic fat emboli, sickle cells, nitrogen bubbles (caisson disease), or focal clotting due to procoagulant abnormalities. Extraluminal obliteration may result from elevated marrow pressure or increased marrow fat. Cytotoxicity and genetic factors may be involved also. Many factors are probably capable of inducing AVN, and combinations of factors may be required, although the final mechanism is always critical ischemia. The natural history of AVN is better understood than the early triggering factors. AVN becomes detectable 1-6 months after exposure to an easily identifiable risk factor such as high-dose glucocorticoid therapy or femoral neck fracture. Later on, AVN is uncommon even when the patient remains exposed to the risk factor. The turning point in the natural history of AVN is subchondral plate fracture, which leads to collapse of the necrotic segment of the epiphysis, usually within the first 2 years. The risk of collapse depends chiefly on the initial size and location of the necrotic segment, which can be determined accurately by magnetic resonance imaging (MRI). This natural history has obvious clinical implications.
 ...
PMID:Pathophysiology and natural history of avascular necrosis of bone. 1693 Oct 94

Understanding the biochemical mechanisms influencing bubble pathophysiology may foster novel pharmacologic non-recompressive strategies that may prevent, ameliorate, and treat decompression sickness (DCS), and the injury sustained from arterial gas emboli (AGE) encountered in hyperbaric and hypobaric exposures, as well as in surgery and trauma. This review explores the biochemical effects of nitric oxide (NO) release agents, their potential impact on bubble pathophysiology, and possible use as a pharmacological intervention to reduce DCS risk and AGE injury. The hypotheses discussed contend that exogenous NO administration or mediators of endogenous NO up-regulation may reduce DCS risk and severity by mediating; (1) decreased populations of gaseous nuclei, (2) decreased bubble nuclei adherence, (3) depression of the deleterious bubble-mediated inflammatory and coagulation cascades and (4) preservation of endothelial integrity, which may defend against bubble-mediated injury. Statin medications alter numerous biochemical, and biophysical processes, which may influence bubble formation. Statins preserve endothelial integrity, reduce ischemia/reperfusion injury, and depress the interdependent inflammatory and coagulation cascades via pleiotropic properties involving up-regulation of endothelial nitric oxide synthase (eNOS) and NO. Numerous studies are researching statins, for their potential efficacy in reducing primary and secondary morbidity and mortality from cardiocerebrovascular, inflammatory (autoimmune), and infectious (sepsis) disease. Additionally, statin-mediated lipid reduction may reduce bubble generation via alterations in plasma "rheology", and surface tension. The statins are attractive potential NO release with minimal adverse side effects, and proven long-term safety, that may potentially mitigate the risk and severity of DCS. We will elaborate on the insight gained into the mechanisms proven and hypothesized for NO-mediated reductions in bubble formation, and DCS incidence and severity, with a focus on the potential for statin medications, in addition to the direct NO-donor medications such as isosorbide mononitrate and nitroglycerine.
 ...
PMID:Investigating the potential of statin medications as a nitric oxide (NO) release agent to decrease decompression sickness: a review article. 1785 2

The presentation of clinical symptoms due to decompression during diving, varies significantly, as mainly minor disturbances for the gastrointestinal tract in particular have been reported. The following case debates whether diving can cause severe symptoms from the gastrointestinal system. We describe a clinical case of ischemic colitis presented in a 27-year-old male, who manifested abdominal pain while in the process of scuba diving 20 meters undersea, followed by bloody diarrhoea as soon as he ascended to sea level. Taking into account his past medical history, the thorough, impeccable clinical and laboratory examinations and presence of no other factors predisposing to ischemia of the colon, we assume that a possible relationship between diving conditions and the pathogenesis of ischemic colitis may exist. This unusual case might represent a hematologic manifestation of decompression sickness, due to increased coagulability and/or transient air emboli, occurring during a routine scuba diving ascent to sea level.
 ...
PMID:Acute ischemic colitis during scuba diving: report of a unique case. 1850 37

Hyperbaric oxygen therapy (HBOT) is a primary or adjunctive therapy for a variety of medical disorders including some involving the eye. This paper is the first comprehensive review of HBOT for ocular indications. The authors recommend the following as ocular indications for HBOT: decompression sickness or arterial gas embolism with visual signs or symptoms, central retinal artery occlusion, ocular and periocular gas gangrene, cerebro-rhino-orbital mucormycosis, periocular necrotizing fasciitis, carbon monoxide poisoning with visual sequelae, radiation optic neuropathy, radiation or mitomycin C-induced scleral necrosis, and periorbital reconstructive surgery. Other ocular disorders that may benefit from HBOT include selected cases of ischemic optic neuropathy, ischemic central retinal vein occlusion, branch retinal artery occlusion with central vision loss, ischemic branch retinal vein occlusion, cystoid macular edema associated with retinal venous occlusion, post-surgical inflammation, or intrinsic inflammatory disorders, periocular brown recluse spider envenomation, ocular quinine toxicity, Purtscher's retinopathy, radiation retinopathy, anterior segment ischemia, retinal detachment in sickle cell disease, refractory actinomycotiC lacrimal canaliculitis, pyoderma gangrenosum of the orbit and refractory pseudomonas keratitis. Visual function should be monitored as clinically indicated before, during, and after therapy when HBOT is undertaken to treat vision loss. Visual acuity alone is not an adequate measure of visual function to monitor the efficacy of HBOT in this setting. Ocular examinations should also include automated perimetry to evaluate the central 30 degrees of visual field at appropriate intervals. Interpretation of the literature on the efficacy of HBOT in treating ocular disorders is complicated by several factors: frequent failure to include visual field examination as an outcome measure, failure to adequately address the interval from symptom onset to initiation of HBOT, and lack of evidence for optimal treatment regimens for essentially all ocular indications. Because some ocular disorders require rapid administration of HBOT to restore vision, patients with acute vision loss should be considered emergent when they present. Visual acuity should be checked immediately, including vision with pinhole correction. If the patient meets the criteria for emergent HBOT outlined in the paper, normobaric oxygen should be started at the highest inspired oxygen fraction possible until arrangements can be made for HBOT.
 ...
PMID:Hyperbaric oxygen therapy and the eye. 1902 63

Optic disc swelling occurs when there is an obstruction to axonal transport at the level of the lamina cribrosa. This may result from compression, ischemia, inflammation, or metabolic and toxic etiologies. Some of these etiologies may be life threatening and others may be self-limited. Thus, differentiating the different etiologies is important, albeit often difficult. We present a case of a 25-yr-old high-performance fighter aviator who presented with unilateral optic disc swelling 2 d after an F-16 flight, in which decompression was suspected. Visual acuity of the affected eye was decreased to 20/25, with enlarged blind spot and shallow arcuate scotomata on visual field testing. Pupil function, brightness intensity, and color vision were normal. Marked swelling of the entire optic disc, retinal flame-shaped hemorrhages, and engorgement of the retinal veins were seen. Since decompression sickness with nitrogen bubbles obstructing the optic nerve head vasculature was suspected, he was treated with hyperbaric oxygen. He rapidly improved, recovering full vision function within 6 d. No concurrent disease was found on extensive investigation. He returned to high-performance aviation 3 mo after onset of symptoms. No recurrence was seen during 3 yr of follow-up.
 ...
PMID:Unilateral optic disc swelling in a fighter pilot. 1981 43

Nitrogen supersaturation and bubble formation can occur in the vascular system after diving, leading to death and nervous disorders from decompression sickness (DCS). Bubbles alter the vascular endothelium, activate platelets, and lead to focal ischemia with neurological damage mediated by the mechanosensitive TREK-1 neuronal potassium ion channel that sets pre- and postsynaptic resting membrane potentials. We report a neuroprotective effect associated with TREK-1. C57Bl6 mice were subjected to decompression from a simulated 90 msw dive. Of 143 mice that were wild type (WT) for TREK-1, 51.7% showed no DCS, 27.3% failed a grip test, and 21.0% died. Of 88 TREK-1 knockouts (KO), 26.1% showed no DCS, 42.0% failed a grip test, and 31.8% died. Mice that did not express TREK-1 had lower DCS resistance and were more likely to develop neurological symptoms. We conclude that the TREK-1 potassium channel was neuroprotective for DCS.
 ...
PMID:Neuroprotective role of the TREK-1 channel in decompression sickness. 2232 54


<< Previous 1 2 3 4 Next >>