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

Five high-risk patients received nonresective treatment of abdominal aortic aneurysms (AAAs). This treatment included ligation of the iliac arteries to induce acute thrombosis of AAA and a simultaneous axillobifemoral bypass for restoration of arterial flow to the lower extremities. Of these five patients, lethal complications associated with this procedure developed in four. The complications included rupture, infection of the thrombotic aortic aneurysm, visceral ischemia, and consumptive coagulopathy. This high incidence of lethal complications and the unacceptably high patient mortality in these five patients indicates extreme precaution in the application of nonresective treatment for AAA.
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PMID:Lethal complications associated with nonrestrictive treatment of abdominal aortic aneurysms. 711 68

Multiple extremity gangrene developed in five patients as a complication of dopamine therapy. The clinical conditions were (1) penetrating chest trauma requiring pneumonectomy with postoperative sepsis, (2) cardiac arrest with aspiration pneumonia, (3) lymphoma with sepsis, (4) Klebsiella pneumonia, and (5) myocardial infarction. The development of acrocyanosis leading to gangrene occurred at dopamine dosages of 5.1 to 10.2 micrograms/kg/min. The alpha-adrenergic vasoconstriction effects of dopamine would not be expected from the doses employed in these patients. Thus, other factors beside pure alpha vasoconstriction are responsible for tissue necrosis after the use of dopamine. We believe that the embolic complications of disseminated intravascular coagulation and hypovolemia are serious risk factors in the development of dopamine gangrene. Peripheral vasoconstriction from dopamine, even at low doses, may set the stage for thrombotic complications of disseminated intravascular coagulation and lead to tissue damage. In laboratory models of disseminated intravascular coagulation, an alpha-adrenergic drug is required to produce peripheral ischemic tissue damage. Treatment of tissue ischemia related to dopamine depends on early recognition of acrocyanosis. Phentolamine, an alpha blocker, has been recommended for treating dopamine ischemia, either through local instillation into ischemic tissues or intravenous infusion. We recommend a high index of suspicion for, and early treatment of, underlying consumptive coagulopathy in all patients requiring dopamine.
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PMID:Dopamine gangrene. Association with disseminated intravascular coagulation. 730 16

The case of an obese patient who developed massive centrilobular liver cell necrosis, severe coagulopathy, acute renal failure, and encephalopathy is presented. Hypovolemia and heart failure were absent, but the acute liver disease was associated with severe arterial hypoxemia due to obstructive sleep apnea that was shown by the nocturnal blood oxygen desaturation, the results of the polysomnographic study, and normal baseline pulmonary function tests. In this obese patient, liver cell necrosis was caused by severe liver cell hypoxia secondary to severe arterial hypoxemia as a consequence of obstructive sleep apnea associated with a Pickwickian syndrome. This observation is consistent with the hypothesis that liver ischemia was directly related to severe arterial hypoxemia.
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PMID:Ischemic hepatitis due to obstructive sleep apnea. 755 54

Present study is designed to examine an effect of Stobadine, a new cell-protective agent with antiarrhythmic properties, on survival, electron microscopic changes in microvasculatory bed of selected brain areas and acid-base parameters of arterial blood after global brain ischemia and reperfusion. Forty dogs (weighting 6 to 15 kg) were anesthetized using pentobarbital i.v. (5%, 35 mg/kg). An intubation and controlled ventilation was performed. One catheter was placed into v. femoralis (for drug administration), another to a. femoralis (for blood samples) and third one into the left common carotid artery (continuous brain blood feeding pressure measurement). Each dog underwent an surgical obstruction of principal brain-supplying arteries and immediate administration of hypotensive agent (Arfonad, 0.062%) resulting in 7 minutes lasting global brain ischemia (brain feeding pressure 1.0-1.5 kPa). If survived, animals were killed at one (perfusion-fixed for electron microscopy) or three days after ischemia. Ultrastructural changes were evaluated at 24 hour of recirculation (control and S2 groups only). Vehicle or 1, 2 or 5 mg/kg of Stobadine (group S1, S2, S5 resp.) i.v. was given 30 minutes prior to ischemia. Significantly longer survival was observed in group S2 (8 of 11 until 72 hour) as compared to control group (none of 7, p < 0.005 by Student's t-test). The ultrastructural changes of blood-brain barrier structures were none or minimal in S2 (single damage type), but in control group three major types of capillary damages has appeared at 24 hour after insult. They include intravascular coagulopathy (type I), no-reflow (type II) phenomenon with astrocyte edema, and capillary necrosis (type III) finally. Stobadine pretreated animals experienced hypercapnia, elevated arterial O2 and slight deeper acidemia (depending on dosage) as compared to control group. Respiratory compensation of metabolic acidosis was present in control group, but lacking in all stobadine pretreated animals. Stobadine at 2 mg/kg improves survival (Student p < 0.005, Mantel-Cox p < 0.05, Fischer p = 0.004). Stobadine has a protective effect on neurons and structures of blood-brain barrier (endothel, astrocytes, basement membrane) seen in electron microscope.
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PMID:Effects of stobadine on survival, histopathologic outcome and acid-base status after global brain ischemia in dogs. 756 Sep 9

Acute dysvascular limb in young adults is a rare entity. Diagnosis is often difficult because symptoms are not recognized as ischemic. The most common causes of this condition are premature atherosclerosis, thromboangiitis obliterans, microemboli, popliteal entrapment syndrome, collagen vascular disease, Takaysu's arteritis, and coagulopathy. A case study is presented to illustrate the disease process. A systematic approach to diagnosis, consisting of history and physical examination, palpation and auscultation of peripheral pulses at rest and following exercise, and noninvasive vascular examination at rest and following exercise, is recommended. Suggestion of an ischemic condition following noninvasive studies should be followed up with an arteriogram. The prognosis is dependent on the underlying etiology of the ischemia, early detection, and appropriate treatment.
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PMID:Acute dysvascular limb in a young adult. A case study. 785 53

We describe 4 patients with coagulopathy and vasculitis that demonstrated marked tissue ischemia and necrosis. In the clinical setting of rapid evolution of vascular insufficiency, the possibility of combined vasculopathic processes should be considered. This is especially so in patients with underlying connective tissue disease such as systemic lupus erythematosus or rheumatoid arthritis, in which both vasculitis and antiphospholipid antibodies are frequently present. Treatment of both pathologic processes may be required to prevent progressive tissue ischemia and necrosis. The use of antiplatelet and/or anticoagulation should be given consideration in addition to immunosuppressive agents.
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PMID:The concomitant expression of vasculitis and coagulopathy: synergy for marked tissue ischemia. 800 3

Twenty five cases of severe or persistent bleeding in obstetric and gynecologic patients treated with internal iliac arterial ligation are analyzed. A short history of every patient is described. There was no complication of the procedure neither ischemia after several years of control. Four pregnancies in two cases observed in seven years. The procedure failed in three cases, but was successful in the others. It is concluded that the coagulopathy when it is present must be corrected and the internal iliac arterial ligation is certainly it is a useful alternative as extreme solution in some cases of severe or persistent hemorrhage.
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PMID:[Ligation of internal iliac artery as treatment of hemorrhage in obstetrics and gynecology]. 820 38

Recovery without residual neurological damage after cardiac arrest with global cerebral ischemia is still a rare event. Severe impairment of bodily or cognitive functions is often the result. The individual, emotional, and social aspects of brain damage and rehabilitation are seldom taken into account. Efforts to improve the prevention of brain damage immediately after successful resuscitation of patients are missing. The efficacy of hypothermia in preserving neurologic function when instituted before and during certain no-flow cardiovascular states has been well documented both clinically and experimentally since the 1950s. Most studies have used moderate (28-33 degrees C) to deep (20-28 degrees C) hypothermia to demonstrate these protective effects. Considering the use of hypothermia for preservation and resuscitation, the lack of controlled outcome trials, the long period of time required to reach therapeutic hypothermia, and the incidence of rewarming complications such as infection, arrhythmia, and coagulopathy have made it difficult to apply these methods to emergency situations such as cardiac arrest. Recent experimental evidence in dogs has shown that hypothermia induced after cardiac arrest does indeed mitigate the effects of the postresuscitation syndrome and improves neurologic function and reduces histologic brain damage. More importantly, such benefits can be demonstrated with mild (34-36 degrees C) hypothermia, thus minimizing complications and requiring less time for induction of hypothermia. Ice water nasal lavage, direct carotid infusion of cold fluids, use of a cooling helmet, and peritoneal cooling are promising techniques for clinical cerebral cooling. External auditory canal temperature (e.g., tympanic membrane temperature changes) could provide an approximation to brain temperatures. For accurate temperature monitoring, however, a central pulmonary artery thermistor probe should be inserted. Temperature monitoring is needed to avoid temperature < 30 degrees C. Mild hypothermia may prove to be an important and secure component for cerebral preservation and resuscitation during and after global ischemia; it may also prove to be a useful method of cerebral resuscitation after global ischemic states, thereby promoting the prevention of neuromental diseases.
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PMID:Mild resuscitative hypothermia and outcome after cardiopulmonary resuscitation. 871 99

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

We report a 10-month-old boy with heat stroke because he was left in a car. He showed hyperthermia, coma and convulsions at the time of his admission. Liver dysfunction and coagulopathy were observed, but they were improved after several days. Consciousness was gradually recovered, but currently he shows neurological sequelae. Cranial CT showed brain edema until the 7th hospital day. Cranial MRI on the fortieth hospital day showed the finding of cortical laminar necrosis in the vascular boundary zones. This finding suggest that brain ischemia was related with the neurological involvement of heat stroke.
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PMID:[A case of heat stroke with cortical laminar necrosis on vascular boundary zones]. 883 Dec 47


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