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

Between January 1975 and December 1980, 104 extra-anatomic bypasses were performed on 102 patients. Of these, there were 81 femorofemoral bypasses on 80 patients and 23 axillofemoral bypasses on 22 patients. Those who underwent femorofemoral grafting were divided into three groups: group 1 - 18 patients who had undergone previous aortofemoral bypass grafting with occlusion of one limb of the graft, group 2 - 17 patients who were considered to be at high risk and group 3 - 45 patients who could have tolerated a conventional reconstructive procedure. Our results indicate that the cumulative patency rate of the femorofemoral bypass at the end of 1 year and 5 years is good and that this operation is an excellent first choice procedure in cases of unilateral iliac disease, to relieve severe ischemia or disabling claudication, whether the patient is a poor or good operative risk. On the other hand, axillofemoral grafting has a lower patency rate and should be reserved for high-risk patients and for the relief of severe ischemia only.
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PMID:Extra-anatomic bypass grafting in the lower extremity. 686 Oct 25

During a 20 year period, the outcome of 719 amputations in 552 patients demonstrates that, in a majority of patients, conservation of the foot or knee can be achieved. Two hundred and eighty-seven local amputations of the foot performed upon 249 patients resulted in satisfactory healing in 167 of the 237 surviving patients, with a hospital mortality of 4.8 per cent. In 246 patients, 277 below knee amputations were performed with healing in 192 of 220 survivors but with a 10.5 per cent hospital mortality. Midthigh amputations were reserved for those patients with quite extensive gangrene and gross ischemia. In 155 such patients, the hospital mortality was almost 30 per cent.
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PMID:Management of ischemia of the foot beyond arterial reconstruction. 705 81

From 1973 to 1979, 49 patients with internal carotid occlusion were evaluated and treated. Eighteen of 49 (37%) presented with transient ischemic attack/prolonged reversible ischemic neurological deficit, 14 of 49 (29%) presented with mild completed stroke, 13 of 49 (27%) presented with severe completed stroke, and 4 of 49 (8%) were asymptomatic. Surgical treatment consisting of extracranial-intracranial (EC-IC) bypass, internal carotid stump reconstruction and endarterectomy to open the occlusion, contralateral endarterectomy for carotid stenosis opposite the occlusion, and iatrogenic carotid occlusion with EC-IC bypass was carried out on 22 (45%) patients considered at risk for ischemia based on angiographic evidence of poor collateral circulation and potential sources of emboli. Medical treatment consisting of anticoagulants or anti-platelet aggregation agents was used in 27 (55%) patients with good collateral circulation. By 6 weeks after the initiation of treatment, 10 of 49 (20%) reached end points of new strokes and death. By an average of 3 years after treatment began, 30 of 49 (61%) reached the same end points. The results suggest that new ischemic events in the distribution of the occluded carotid artery occur infrequently if the angiographic study shows adequate collateral circulation to the ischemic territory at risk. Surgical revascularization should be reserved for patients with (a) recurrent ischemic events after the diagnosis of carotid occlusion or (b) poor collateral circulation.
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PMID:Overall management of vascular lesions considered treatable with extracranial-intracranial bypass: part 1. Internal carotid occlusion. 712 79

Fibrotic contracture of skeletal muscle can follow weeks or months after the severe ischemic insult of compartment syndrome. Commonly known as Volkmann's ischemic contracture, the affected limb often becomes dysfunctional and painful, and may lose sensibility. The pathogenesis of the muscle contracture includes prolonged ischemia, myonecrosis, fibroblastic proliferation, contraction of the cicatrix, and myotendinous adhesion formation. Resultant shortening or overpull of involved muscles leads to stiffness and deformity. Simultaneously, nerve injury from initial ischemia or subsequent soft tissue fibrotic compression leads to muscle paresis or paralysis of the involved compartment and of those muscles more distally innervated. The resultant deformity is thus a combination of varying degrees of contracture and weakness depending on which muscles and nerves are affected. Deformity and functional impairment in the foot and ankle secondary to ischemia are determined by many factors, including: (1) which leg compartment, if any, has been affected and to what degree extrinsic flexor or extensor overpull is exhibited, (2) degree of nerve injury sustained causing weakness or paralysis of extrinsic or intrinsic foot and ankle muscles (3) which foot compartment, if any, has been affected and to what degree intrinsic overpull is exhibited, and (4) degree of sensory nerve injury leading to anesthesia, hypoesthesia, or hyperesthesia of the foot. Therefore, a variety of clinical presentations can be encountered following compartment syndrome of the leg and foot. Treatment is based on an appreciation of the pathoanatomy of the deformity. Nonoperative therapy is aimed at obtaining or preserving joint mobility, increasing strength, and providing corrective bracing and accommodative footwear. Operative management is usually reserved for treatment of residual nerve compression or severe and problematic deformities. Established surgical protocols are performed in a stepwise fashion, to include: (1) release of residual or secondary nerve compression, (2) release of fixed contractures, using infarct excision, myotendinous lengthening, muscle recession, or tenotomy, (3) tendon transfers or arthrodesis to increase function, and (4) ostectomy or amputation for severe, refractory deformities.
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PMID:Volkmann's ischemic contracture of the foot and ankle: evaluation and treatment of established deformity. 755 Sep 46

Idiopathic dilated cardiomyopathy (IDC) accounts for 25% of cases of heart failure in the United States. Understanding the relationship between an inciting event or agent and the development of IDC has progressed only recently. Once IDC has developed, treatment is palliative and little can be done to alter the natural course of the disease. Active myocarditis, a suspected precursor of IDC, is myocardial inflammation and injury without ischemia. The disease ranges from a self-limited flulike illness to one of serious consequence with arrhythmias, heart failure, or death. Many agents have been associated with myocarditis, and the clinical manifestations depend on an interplay between the inciting agent and the host response. The development of a murine model and the expanded use of endomyocardial biopsy using the Dallas criteria have increased our understanding of myocarditis and its sequelae. Therapy consists of managing symptoms using conventional medical regimens for heart failure. Immunosuppressive therapy should be reserved for patients with biopsy-proven disease who have failed conventional therapy. Continued deterioration warrants ventricular assistance and consideration of cardiac transplantation.
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PMID:Myocarditis and idiopathic dilated cardiomyopathy. 765 92

Adjunctive therapy for acute myocardial infarction should include aspirin, beta-adrenergic blocking agents, and, in most patients, consideration of the use of angiotensin-converting enzyme inhibitors, especially if left ventricular function is reduced. Heparin has an important adjunctive role in enhancing early vessel patency in patients who receive tissue-type plasminogen activator and in decreasing the frequency of reocclusion of an infarct-related artery during any thrombolytic therapy. Heparin must also be administered to all patients who undergo primary angioplasty. Intravenously administered nitroglycerin and orally administered nitrates are probably most effective in patients with symptomatic ischemia. Calcium channel blockers and prophylactic antiarrhythmic agents are not indicated for most patients with acute myocardial infarction. Currently, insufficient evidence is available to recommend the widespread use of intravenously administered magnesium sulfate in the setting of acute myocardial infarction. In patients with ischemic pain, judicious intravenous administration of morphine can provide relief. Use of warfarin sodium should be reserved for patients at risk for left ventricular mural thrombus. Although the use of lipid-lowering agents after myocardial infarction has been controversial, recent studies have demonstrated the importance of such therapy for secondary prevention of death and morbidity.
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PMID:Adjunctive therapy in the management of patients with acute myocardial infarction. 773 Dec 56

Ten patients (six men and four women; mean age, 40 yr) with spontaneous dissection of the basilar artery are reported. Clinically, six were admitted with subarachnoid hemorrhage (SAH) and four were admitted with brain stem ischemia. Angiography demonstrated string sign in four patients, pearl reaction in four, double lumen in one, and arterial ectasia with mural retention of contrast medium in one. Magnetic resonance imaging was performed in two patients. Follow-up angiograms or magnetic resonance angiography in six patients showed spontaneous healing in two patients, improvement in two, progression in one, and no change in one. Nine patients were treated medically, and one underwent selective intravascular occlusion of the dissecting aneurysm. One patient died after further SAH, two remain severely disabled, three have residual neurological deficit, and four are in good clinical condition. The most interesting observations in this series include a relatively good course in a substantial number of patients and low further bleeding potential after SAH, the late "globular" evolution, which may be favorable for reconstructive treatment, and the diagnostic value of associated computed tomographic/angiographic findings. Surgical options in basilar dissection are very poor; in some reported cases, wrapping has been tried with disappointing results. In light of the possibility of spontaneous healing or improvement, wrapping should be reserved for only those patients with recurrent SAH or angiographic progression of the dissection.
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PMID:Dissecting aneurysms of the basilar artery. 773 4

Between 1978 and 1992, 70 patients were operated for type B aortic dissection (tear in the descending aorta without involvement of the ascending aorta). 15/70 (21%) patients had an acute dissection (onset of symptoms < 24 h), 19/70 (27%) a subacute dissection (onset of symptoms < 14 days), and 36/70 (51) a chronic dissection (onset of symptoms > 14 days). The indications for surgery in cases of acute dissection were: hematothorax, oliguria, leg ischemia and persistent pain. Persistent hypertension was an additional indication in cases of subacute dissection. In large majority (93%) of chronic dissections the indication for surgery was enlarged aortic diameter. In 86% (60/70) graft replacement of the aorta was performed, in 6% (4/70) extra-anatomic bypass, in 3% (2/70) fenestration, in 3% (2/70) thrombendarterectomy, in 3% (2/70). The overall mortality was 17% (12/70); 27% of acute dissection, 26% for subacute dissection, and 8% for chronic dissection. The morbidity for acute dissection was 73%, of subacute dissection 43%, and of chronic dissection 12%. The most frequent complications were: leg ischemia (8 patients), renal failure (4 patients), paraparesis (4 patients) and sepsis (2 patients). No paraparesis was encountered in surgery of the chronic dissection. Conservative treatment was tried in all acute B-dissections, with surgical therapy being reserved for complications of the dissection, such as rupture, such as rupture, risk of rupture (hematothorax, large aortic diameter resp. expansion, persistent hypertension, persistent pain) or ischemia of distal vascular beds. Long-term survival for chronic type B dissections is good. Strong control of risk factors (hypertension) is essential.
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PMID:[Type B aortic dissections: surgical technique and results]. 787 97

Acute mesenteric ischemia represents one to two percent of all gastrointestinal illnesses. There are three possible causes of acute arterial mesenteric ischemia: embolism, thrombosis, and nonocclusive mesenteric insufficiency. The key to early diagnosis is a high index of suspicion. The classic clinical picture of obvious cardiac disease, sudden onset of severe abdominal pain and gastrointestinal emptying, is not always present. Serum markers and plain films are often nondiagnostic but may suggest acute arterial mesenteric ischemia. Angiography establishes the diagnosis and allows for planning of aortomesenteric bypass, if indicated. Papaverine is immediately instilled to decrease splanchnic vasoconstriction. Embolic and thrombotic disease is treated by laparotomy with re-establishment of visceral perfusion. Only after blood flow is restored is nonviable bowel resected. Clinical methods of assessing intestinal viability include Doppler scanning, intravascular dyes, and tissue oximetry. The decision to perform a second-look laparotomy is made prior to closure of the abdomen. Pharmacologic treatment is the mainstay of nonocclusive ischemia. Surgery is reserved for clinical deterioration. Survival is dependent on the cause and extent of occlusion as well as the rapidity of diagnosis and therapy. Bowel necrosis results in mortality rates between 80 percent and 95 percent.
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PMID:Mesenteric ischemia. Acute arterial syndromes. 760 44

The application of coronary angioplasty (PTCA) for early mechanical reperfusion in patients with evolving acute myocardial infarction (AMI) was introduced at the beginning of the '80s. There are 5 distinct approaches to PTCA for AMI mainly based on the timing of the intervention: primary or direct PTCA refers to emergency recanalization (as soon as possible) of the "culprit" vessel by the interventional procedure without the use of thrombolytic agents; immediate or sequential PTCA is the combination of administration of intravenous thrombolytic therapy followed very closely by PTCA; rescue PTCA refers to the use of PTCA as a mechanical approach for reperfusion when thrombolytic therapy has failed (60 to 120 min after such therapy has been initiated); deferred or adjunctive PTCA implies coronary angiography and PTCA delayed by at least several days after thrombolytic therapy and reserved for patients with residual ischemia; elective PTCA refers to a delayed symptom-derived procedure after thrombolytic therapy. Immediate PTCA, in which the procedure urgently follows the thrombolytic therapy has been studied in 3 randomized trials (TAMI 1, ECoS, TIMI 2A). All 3 trials have shown that immediate PTCA does not affect positively, but can worsen, the outcome of thrombolytic therapy since it increases mortality and bleeding complication with no improvement in reocclusion rate. Rescue PTCA was evaluated by several Authors who were able to demonstrate that mechanical reperfusion after failed thrombolytic therapy improves prognosis and reduces in-hospital and long-term mortality in this subgroup of patients with AMI. Deferred or adjunctive and elective PTCA represent therapeutic approaches in patients with residual ischemia following a successful thrombolysis able, when residual or recurrent ischemia are present, to prevent major cardiac events and to improve clinical outcome. The major interest was addressed to the role of primary PTCA in evolving AMI, as alternative therapy to thrombolysis. Randomized trials have been able to demonstrate that primary PTCA could dramatically improve the clinical outcome in AMI complicated by cardiogenic shock. Moreover, this approach can be safely performed in patients with contraindications for thrombolytic therapy with excellent results. Despite other advantages, primary or direct PTCA for evolving AMI is still presenting few points which have to be furtherly evaluated: acute or subacute reocclusion rates, restenosis rates, costs and availability to majority of population. The on-going clinical evaluation of other devices for mechanical reperfusion (transluminal extraction catheter-TEC, directional atherectomy, coronary stents, thermal PTCA, prolonged autoperfusion), in order to improve acute and subacute results, could furtherly expand the use of this approach in AMI-patients.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:[Role of direct coronary angioplasty in the course of acute myocardial infarction]. 802 10


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