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

Dissection of the cervicocranial arteries is becoming more frequently recognized as a cause of neurological disorders. Typical clinical features seen with dissection include unilateral headache, oculosympathetic palsy, amaurosis fugax, and symptoms of focal brain ischemia. The diagnosis of carotid or intracranial dissection is usually best confirmed by angiography, although magnetic resonance imaging and computed tomography have been shown to visualize intimal dissection. The prognosis in cases of spontaneous dissection is generally benign unless the initial manifestation involves infarction with substantial deficit. The best approach to treatment appears to be the administration of the anticoagulant, heparin, followed by warfarin or antiplatelet therapy. Surgical intervention is reserved for cases of progressive or recurrent ischemic complication that occurs despite the administration of adequate doses of anticoagulants.
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PMID:Cervicocranial arterial dissection. 187 Jun 93

The definition, pathogenesis, incidence and characteristics, detection, treatment, and prognosis of silent myocardial ischemia (SMI) are reviewed. SMI is the occurrence of myocardial ischemia for which there is objective evidence (electrophysiological, hemodynamic, and metabolic changes) but no angina. Patients with SMI are classified as type 1 (completely asymptomatic), type 2 (SMI after myocardial infarction), and type 3 (both symptomatic and silent ischemia). Episodes of SMI are true ischemic events. The absence of pain may be due to defects in pain perception, an altered physiological response to ischemia, or a lesser degree of ischemia. The incidence of SMI is 2-5% in totally asymptomatic patients, 20-30% in patients who have suffered myocardial infarction, and 44-84% in patients who have symptomatic ischemia. SMI can be detected by exercise testing, portable electrocardiographic monitoring, or imaging techniques. Patients with SMI have more frequent adverse cardiac events (except death) than patients without SMI. The frequency of adverse cardiac events is similar in patients with angina and patients with SMI. SMI has been treated with nitrates, calcium-channel blockers, and beta blockers. Beta blockers appear to be the most consistent in reducing the number and duration of episodes. Combination therapy with beta blockers and nifedipine may be more effective than therapy with either agent alone. Because of the limited number of studies and the possible contribution to the results of spontaneous variability in the occurrence of SMI, no definite conclusions can be drawn about drug efficacy. There is no evidence that the prognosis of patients with SMI is altered by drug therapy; routine treatment with anti-ischemic drugs cannot be recommended. Patients must be evaluated individually, with aggressive management being reserved for those at high risk for myocardial infarction or other serious cardiac events.
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PMID:Current concepts of silent myocardial ischemia. 197 45

The authors show that the variations of intraocular hyper- and hypotension stand for a reserved prognosis in the evolution of the operated retina detachment. Likewise, they consider that the repeated operations in the retina detachment may lead to the syndrome of anterior ischemia, unfavourable to the visual function.
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PMID:[Variable pressure changes (+/-) in the anterior ischemia syndrome--the elements of a reserved prognosis in the surgery of retinal detachment]. 210 Oct 30

The empiric administration of 50% dextrose to all patients presenting to the ED with altered mental status is a standard of care predicated on the assumption that glucose administration is harmless to nonhypoglycemic patients. Considerable evidence now disputes this assumption. Glucose administration before complete cerebral ischemia in experimental animals worsens neurologic and histologic outcome. Administration of glucose during severe incomplete ischemia has a similar detrimental effect. The translation of these experimental findings into clinical practice has been slow, perhaps hindered by the frequent use of rodent models and large bolus doses of glucose. However, evidence is now provided by primate and human studies and by experimental designs using clinically relevant doses of glucose. These clinical and experimental findings in conjunction with the wide availability of a rapid bedside screen for hypoglycemia provide the rationale for an alteration in the standard of care. The empiric administration of glucose should be avoided in patients at risk of cerebral ischemia, such as those with acute stroke, impending cardiac arrest, or severe hypotension or receiving CPR. A bedside fingerstick blood glucose estimation should be performed immediately on all patients presenting with altered mental status. The administration of 50% dextrose should be reserved for those patients in whom hypoglycemia is demonstrated; this practice will uphold Hippocrates' most basic principle of clinical medicine, "The physician must...do no harm."
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PMID:50% dextrose: antidote or toxin? 212 May 1

The empiric administration of 50% dextrose to all patients presenting to the ED with altered mental status is a standard of care predicated on the assumption that glucose administration is harmless to non-hypoglycemic patients. Considerable evidence now disputes this assumption. Glucose administration before complete cerebral ischemia in experimental animals worsens neurologic and histologic outcome. Administration of glucose during severe incomplete ischemia has a similar detrimental effect. The translation of these experimental findings into clinical practice has been slow, perhaps hindered by the frequent use of rodent models and large bolus doses of glucose. However, evidence is now provided by primate and human studies and by experimental designs using clinically relevant doses of glucose. These clinical and experimental findings in conjunction with the wide availability of a rapid bedside screen for hypoglycemia provide the rationale for an alteration in the standard of care. The empiric administration of glucose should be avoided in patients at risk for cerebral ischemia, such as those with acute stroke, impending cardiac arrest, or severe hypotension or receiving CPR. A bedside fingerstick blood glucose estimation should be performed immediately on all patients presenting with altered mental status. The administration of 50% dextrose should be reserved for those patients in whom hypoglycemia is demonstrated; this practice will uphold Hippocrates' most basic principle of clinical medicine, "The physician must ... do no harm."
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PMID:50% dextrose: antidote or toxin? 218 38

PTCA is a widely used technique in patients post-acute myocardial infarction (AMI) as well as in unstable angina (UA). The precise timing of its application and some aspects of the indication nowadays remains a matter of controversy. Primary PTCA is not generally considered to be the initial treatment of AMI. In contrast, immediate PTCA after thrombolysis has been proposed attempting to decrease the incidence of early reocclusion, improve myocardial salvage, decrease the incidence of postinfarction angina and improve survival. Nevertheless, three recent controlled studies (TAMI, TIMI II and ECSG) have demonstrated that an "aggressive" strategy with obligatory, invasive intervention following thrombolysis does not provide any advantage in terms of survival, rate of reocclusion or improved ventricular function and is, in fact, likely to be harmful. Emergent coronary arteriography after AMI should be reserved for unstable patients with continued or recurrent ischemia in the CCU. In elective basis it should be indicated in all patients with spontaneous or provocable ischemia prior to hospital discharge. If high grade coronary stenoses are identified, the patient should be considered for PTCA or surgical revascularization. In our own experience with coronary arteriography 24 hours to 15 days after intravenous thrombolysis with SK, PTCA is anatomically feasible in 44% of all the patients and in 60% of those showing a patent vessel. However, when indicated because of postinfarction angina or a positive stress test, PTCA was performed only in 22%, some of them presenting with a totally occluded vessel. In case of stenosis lesser than 100% the dilation success rate is slightly lower than that of out entire series (84% vs 88%), but the incidence of acute occlusion is significantly higher (10% vs 6%), particularly in patients with angiographic evidence of intracoronary thrombi. The incidence of "non-significant" (less than 70%) stenosis spontaneously increases when the coronary arteriography is performed late during hospitalization (34% vs 17% when the patient is studied in the first 24-48 hours).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Coronary angioplasty in acute coronary syndrome]. 220 92

In this three year prospective study of 177 patients with acute peripheral arterial ischemia those subjects with acute iliofemoral emboli or ischemia with a neurosensory deficit had urgent operations. The remainder included patients less likely to have limb salvage after surgery and who therefore were treated with thrombolytic therapy. This was done in three open studies of intravenous, acylated, plasminogen-streptokinase activator complex, low dose intraarterial streptokinase and intraarterial tissue-plasminogen activator (t-PA). The overall outcome after 30 days of thrombolytic therapy was limb salvage (55%), amputation (15%), and death (30%). The severity of the presenting ischemia was the most important prognostic indicator. In patients with a neurosensory deficit, limb salvage after either embolectomy or surgical reconstruction (59%) was more likely than after thrombolysis (31%). In patients without a neurosensory deficit, limb salvage after thrombolysis (68%) was better, though not significantly, than after surgery (53%). Local intraarterial thrombolysis with either streptokinase or t-PA produced an encouraging 66% limb salvage in 59 cases. In management of acute peripheral arterial occlusions an approach based on the severity of ischemia is optimal, with urgent surgery for patients with a neurosensory deficit and intraarterial thrombolytic therapy reserved as an alternative in selected cases with stable ischemia.
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PMID:Acute peripheral arterial ischemia: a prospective evaluation of differential management with surgery or thrombolysis. 251 79

Potent pharmacological agents that rapidly induce coronary thrombolysis reduce morbidity and mortality from evolving myocardial infarction especially when administered early after the onset of ischemia. However, recanalization frequently unmasks residual, high-grade stenoses that can impair reflow, predispose to reocclusion, and limit salvage of myocardium. Coronary angioplasty performed immediately after recanalization induced by thrombolysis reduces the severity of stenosis and can enhance salvage. Unfortunately, complication rates are higher with emergency compared with delayed angioplasty. Thus, mechanical recanalization early after thrombolysis should be reserved for patients with signs or symptoms of recurrent ischemia or for those in whom pharmacological recanalization has failed but a large amount of myocardium remains at risk.
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PMID:Angioplasty after thrombolysis in the treatment of evolving myocardial infarction. 252 6

From 1975 to 1988, 25 patients with a vertebral artery (VA) injury were treated. Admission neurologic status was intact in 14 patients (56 percent). Eight patients had deficits due to direct nerve or spinal cord injury, two patients had symptoms referable to vertebrobasilar ischemia, and one patient had a contralateral deficit due to an associated carotid artery injury. Twenty-two of 25 patients (88 percent) underwent diagnostic arteriography. Twelve patients (48 percent) with 9 occlusive and 3 minimal injuries were observed. Seven patients (28 percent), three with exsanguinating hemorrhage, were treated by operative exploration and VA ligation. Six patients (24 percent), two with a VA pseudoaneurysm and four with an arteriovenous fistula, were managed by percutaneous transcatheter embolization. The neurologic status was unchanged or improved in 22 patients (88 percent) at discharge. Two patients developed Horner's syndrome after VA ligation. Transient posterior circulation ischemia occurred in a single patient after percutaneous transcatheter embolization. There was no mortality. The majority of VA injuries are best managed by nonoperative methods. Untoward neurologic sequelae are rare. Operative intervention and VA ligation should be reserved for patients with active hemorrhage or large pseudoaneurysms and arteriovenous fistulas which cannot be embolized.
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PMID:Trends in the management of traumatic vertebral artery injuries. 275 37

In conclusion, the PIA patient is at high risk, with higher early as well as late mortality. The pathophysiology of PIA is complex and may vary from patient to patient. The concepts of ischemia at a distance and ischemia in the infarct zone have led to a better understanding of early PIA. Coronary spasm may play an important role in most PIA patients as in the general population of patients with angina pectoris. Medical therapy is efficacious in many, although it may on rare occasion aggravate myocardial ischemia. Urgent coronary arteriography is generally safe and should be performed as soon as possible for medically refractory PIA. CABG appears to be safe in experienced hands, but its timing must be individualized. The IABP should be reserved for more unstable patients for fear of vascular complications. Randomized controlled trials such as the BARI Trial will further compare PTCA with CABG.
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PMID:Postinfarction angina. 288 57


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