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

31 patients with coronary artery disease (11 patients with diabetes mellitus and autonomic neuropathy. 10 patients with diabetes without neuropathy, and 10 patients with asymptomatic myocardial ischemia) participated in a study designed to investigate whether there is a difference in forearm skeletal muscle ischemia and pain threshold. The degree of ischemia was determined by plethysmographically measured reactive hyperemia. There was no difference in maximum reactive hyperemia after passive forearm ischemia of 5-min duration in the three groups. After symptom-limited ischemic work, there was significantly more reactive hyperemia in patients with silent myocardial ischemia as compared to diabetic patients. Exercise time was longer in patients with silent myocardial ischemia (153 +/- 51 s) than in patients with diabetic neuropathy (139 +/- 45 s) and diabetics without neuropathy (120 +/- 45 s). Pain as a cause of termination of symptom-limited ischemic forearm exercise occurred less frequently in patients with diabetic neuropathy (2/11) and patients with silent myocardial ischemia (3/10) as compared to patients with diabetes without neuropathy. Patients with silent myocardial ischemia had a higher ischemic tolerance in the ischemic working forearm than did diabetic patients with and without neuropathy. In patients with neuropathy, however, ischemic pain occurred less frequently at the same ischemic work level compared to diabetics without neuropathy. Therefore, diabetic neuropathy appears to facilitate the occurrence of silent myocardial ischemia. The data presented here suggest that there is a qualitative difference in ischemic tolerance between patients with silent myocardial ischemia and patients with diabetic neuropathy.
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PMID:[Comparison of ischemic pain threshold and reactive hyperemia in autonomic diabetic neuropathy and silent myocardial ischemia]. 205 51

Ischemia plays an important role in the development of neuropathies associated with various disorders, such as peripheral vascular occlusive diseases, necrotizing vasculitides, diabetes mellitus and nerve compression or trauma. Although a multiple mononeuropathy or an asymmetrical polyneuropathy is the usual clinical presentation of ischemic neuropathy, some patients present with a neuropathy that is mainly distal and symmetrical. Pathologically, nerve ischemia results in focal or multifocal central fascicular or sector fiber degeneration. These ischemic lesions tend to begin at mid-upper arm or midthigh level, which is the watershed zone of poor perfusion, and become more diffuse distally. Nerve ischemia at the level of distal small fascicles often induces sub-perineurial crescent lesion rather than central fascicular fiber degeneration. Physiologically, reduced nerve blood flow with endoneurial hypoxia has been demonstrated in experimental diabetic and galactose neuropathies. Endoneurial ischemia/hypoxia in galactose neuropathy appears to be due to increased intercapillary distances and constriction of trans-perineurial vessels resulting from endoneurial edema. Although acute ischemic neuropathy has been well investigated, little is known about functional or structural responses of peripheral nerve to chronic ischemia.
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PMID:[Ischemic neuropathy]. 209 82

To elucidate the prevalence and features of painless myocardial ischemia among diabetic patients, 44 consecutive patients with angiographically-documented coronary artery disease and positive treadmill tests were examined. They were 26 with diabetes and 18 without it. Painless myocardial ischemia was defined as the absence of chest pain with 1 mm or more ST segment depression during the exercise stress tests. The severity of ischemia was determined by the magnitude of the ST segment depression. Painless myocardial ischemia was observed in 18 of the 26 (69%) diabetics, and in three of the 18 (17%) non-diabetics (p less than 0.005). The frequency of painless ischemia in the diabetics was relatively high regardless of the severity of ischemia, while painless ischemia was less frequent in the non-diabetics with severe ischemia. With a level of 2.5 mm ST depression, 11 of 12 (92%) diabetics were free of pain compared to four of 11 (36%) non-diabetics (p less than 0.01). Absence of chest pain during the exercise tests was not concordant with prior angina in diabetics, as opposed to non-diabetics in whom both clinical and exercise-induced angina developed concordantly. The diabetic patients without chest pain had a higher prevalence of three major diabetic complications such as neuropathy, nephropathy and retinopathy compared to those developing chest pain (p less than 0.025). It was concluded that in diabetics, painless myocardial ischemia is frequently observed during exercise stress tests and its prevalence is relatively high regardless of the severity of ischemia.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Painless myocardial ischemia in diabetic patients with coronary artery disease: evaluations by treadmill exercise tests]. 210 4

A patient presented with a neuropathy originally ascribed to prolonged effect of epidural anesthesia following major intraabdominal surgery. Subsequent investigation revealed the cause of the neuropathy to be an arterial thrombosis. Two percent lidocaine and 0.5% bupivicaine were used intraoperatively and epidural morphine was administered at the end of the operation. The causes of prolonged neural blockade from epidural anesthesia are reviewed. Ischemia is a well known cause of neuropathy, and when ischemic pain is masked with the use of epidural narcotics, the neurologic deficit produced can be similar to that of prolonged action of epidurally administered local anesthesia. Ischemia should be included in the differential diagnosis of prolonged neurologic deficit in this situation. If examination reveals ischemia as a possible cause of neurologic deficit (e.g., asymmetrical or absent pulses), an angiogram should be obtained quickly to provide the best opportunity for rapid surgical treatment.
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PMID:Ischemic neuropathy presenting as prolonged epidural anesthesia. 217 16

Five cases of exertional disruption of the axillary anastomosis occurred at intervals of 13 to 30 days after axillofemoral polytef (polytetrafluoroethylene [PTFE]) graft insertion. Graft evulsion was preceded by effort and heralded by axillary pain, an expanding hematoma, and a pseudoaneurysm formation. Proximal control of the subclavian artery by a supraclavicular approach or balloon allowed safe wound exploration. Successful reconstruction required lengthening of the graft or replacement. Secondary disruption occurred with simple repair. Although temporary postoperative brachial plexus neuropathy was common, no significant hand ischemia was noted. Twenty-two reports of axillary anastomotic disruption were made to the Food and Drug Administration, Washington, DC, during a 2-year period, and one manufacturer of polytef grafts provided data on 10 reports received throughout 7 years. Surface anatomy measurements in 20 control patients demonstrated that arm abduction and lateral flexion of the body increased the distance between the axillary and femoral arteries by a mean of 15.5%. Similar measurements taken from the proximal axillary artery showed a mean length increase of less than 10%. This complication may be avoided by inserting the polytef graft with several centimeters of excess length and positioning the axillary anastomosis medial to the pectoralis minor muscle.
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PMID:Exertional disruption of axillofemoral graft anastomosis. 'The axillary pullout syndrome'. 233 Dec 21

We defined the causal pathways responsible for 80 consecutive initial lower-extremity amputations to an extremity in diabetic patients at the Seattle Veterans Affairs Medical Center over a 30-mo interval from 1984 to 1987. Causal pathways, either unitary or composed of various combinations of seven potential causes (i.e., ischemia, infection, neuropathy, faulty wound healing, minor trauma, cutaneous ulceration, gangrene), were determined empirically after a synthesis by the investigators of various objective and subjective data. Estimates of the proportion of amputations that could be ascribed to each component cause were calculated. Twenty-three unique causal pathways to diabetic limb amputation were identified. Eight frequent constellations of component causes resulted in 73% of the amputations. Most pathways were composed of multiple causes, with only critical ischemia from acute arterial occlusions responsible for amputations as a singular cause. The causal sequence of minor trauma, cutaneous ulceration, and wound-healing failure applied to 72% of the amputations, often with the additional association of infection and gangrene. We specified precise criteria in the definition of causal pathway to permit estimation of the cumulative proportion of amputations due to various causes. Forty-six percent of the amputations were attributed to ischemia, 59% to infection, 61% to neuropathy, 81% to faulty wound healing, 84% to ulceration, 55% to gangrene, and 81% to initial minor trauma. An identifiable and potentially preventable pivotal event, in most cases an episode involving minor trauma that caused cutaneous injury, preceded 69 to 80 amputations. Defining causal pathways that predispose to diabetic limb amputation suggests practical interventions that may be effective in preventing diabetic limb loss.
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PMID:Pathways to diabetic limb amputation. Basis for prevention. 235 Oct 29

Dissecting aneurysm of the aorta keeps on being nowadays a diagnostic problem, although it is a well known entity. Dissecting aneurysms may be classified into type A, dissection involving the ascending aorta, and type B, dissection involving descending aorta. The frequency of neurologic manifestations oscillates from 18 to 30%. From the 133 cases of dissecting aneurysm attended at our hospital, 30 (22.5%) presented neurologic manifestations. Nine patients (30%) had symptoms of ischemic neuropathy; 13 (43.3%) presented symptoms compatible with spinal ischemia and 14 (46.7%) presented manifestations of brain ischemia, with involvement of supraaortic trunks proven at autopsy in eight cases. The neurologic complications of type A and B dissecting aneurysms were similar (28 and 26%); in up to 30% of patients, it was the initial symptom. In type A dissecting aneurysm, the most frequent neurologic manifestation was brain ischemia (57.1%) whereas ischemic neuropathy and spinal ischemia predominated in type B dissecting aneurysm. The overall mortality rate reached 76.7% (85.7% for type A and 55.5% for type B). The modality of treatment had no clear influence on the survival. In the presence of brain complications, the mortality was 100%.
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PMID:[Neurologic manifestations of dissecting aneurysms of the aorta]. 273 70

A retrospective review was undertaken of 127 lower extremity fasciotomies performed for compartment syndrome after acute ischemia and revascularization in 73 patients with vascular trauma and 49 patients with arterial occlusive disease. One hundred twelve (88%) fasciotomies were performed early (at the time revascularization); 15 (12%) were delayed because of late compartment syndrome diagnosis. Ninety-four (77%) patients had more than one accepted indication for fasciotomy. Double-incision fasciotomy was used in 98 (77%) extremities, single-incision fasciotomy was used in 19 (15%), and fasciotomy-fibulectomy was used in 10 (8%). Fasciotomies were closed in 88 (69%) patients an average of 14 days after surgery. Seven patients needed multiple skin grafting procedures or myocutaneous flaps to close the wound; none compromised limb salvage. Five other patients had minor wound infections that resolved. Functional status returned to preoperative levels by the time of discharge from the hospital in 59 (48%) patients. Thirty-one (24%) patients had residual lower extremity disability related to delayed union of the fracture (five), chronic neuropathy (20), leg swelling (one), or ischemic nonhealing fasciotomy wounds (three); two patients had unrelated disabilities. Fourteen (11%) amputations were required for refractory limb ischemia; two (1.6%) were required for wet gangrene of the foot, which infected the fasciotomy site; the others had open noninfected incisions. Eighteen (15%) patients died of cardiopulmonary failure or multisystem failure or both, without fasciotomy-related problems. Open fasciotomy for compartment syndrome after acute lower extremity ischemia and revascularization was associated with an increased risk of minor wound morbidity. However, limb loss and death resulted from persistent ischemia and underlying systemic disease processes or injuries, but not from open fasciotomy wound complications.
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PMID:Does open fasciotomy contribute to morbidity and mortality after acute lower extremity ischemia and revascularization? 277 98

We describe a patient with chronic multifocal demyelinating neuropathy associated with persistent conduction block. Multifascicular lesions in sural nerve included a complete loss of myelinated fibers, demyelination, remyelination, onion bulb formation, and axonal attenuation. On the basis of these morphometric results we hypothesize that nerve ischemia may be involved in the pathogenesis of chronic multifocal demyelinating neuropathy.
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PMID:Is ischemia implicated in chronic multifocal demyelinating neuropathy? 277 Oct 81

Two adult diabetic patients with chronic asymptomatic optic neuropathy attributed to an ischemic etiology are reported. In one case the typical syndrome of ischemic optic neuropathy occurred in one eye, while the fellow eye had asymptomatic hyperemic optic disc edema that persisted for 6 months without optic atrophy. A minor visual field defect initially detected in that eye resolved spontaneously in 1 month. In the second case, a recent onset, middle-aged diabetic developed bilateral optic neuropathy and optic disc edema that persisted for 12 months, with minimal signs of visual dysfunction. Axoplasmic transport blockage from low-grade ischemia to the optic nerve may cause acute or chronic optic disc edema with minimal or no visual symptoms.
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PMID:Chronic asymptomatic ischemic optic neuropathy. A report of two cases in adults with diabetes mellitus. 296 25


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