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

A purine degradation study, thermography and near infrared spectroscopy of the extremities were performed on 2 young males with Fabry disease and 2 healthy controls. Two-minute semi-ischemic forearm exercise caused a distinct increase in lactate in all subjects, but venous hypoxanthine and ammonia were greatly increased only in the Fabry patients, suggesting a relatively hypoxic state of the extremities. Limb thermograms of the patients revealed glove and stocking type disturbance at rest. Poor recovery of the skin temperature of the hands and forearms after exercise was observed in the patients, but the sharp increase in oxygenated hemoglobin after total ischemia was found to be normal or near infrared spectroscopy. Neurotropin showed an analgesic effect, i.e. a strong and selective heat-productive action on the painful lesions, and suppressed the hypoxanthine level after exercise in 1 patient. Although the pathophysiology of the pain in Fabry disease has not been clearly elucidated, a relatively hypoxic state with peripheral hypothermia might play an important role in triggering of a painful attack or chronic burning paresthesia.
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PMID:Relative hypoxia of the extremities in Fabry disease. 145 89

Acute embolic occlusion of a peripheral artery requires rapid and precise diagnosis in order to provide the appropriate treatment without delay. The symptoms and findings of acute arterial occlusion are characterized by "the six Ps": pain of sudden onset in the hypoperfused extremity, paleness, pulselessness, paresthesias, paralysis and, in the extreme case, prostration with the symptoms of shock. With embolization in arterial segments with only minimal residual perfusion via collaterals (for example, the femoral bifurcation), a complete ischemic syndrome is usually incurred manifesting the six Ps as delineated. If preformed collateral systems provide some perfusion distal to an arterial occlusion (for example, in the common iliac artery), there is frequently an incomplete ischemic syndrome observed which is characterized by pain, paleness and pulselessness. Peripheral arterial embolism has a predilection for the femoral bifurcation, the superficial femoral artery and the popliteal artery. In principle, however, embolization can occur in every arterial segment. The diagnosis of the acute ischemic syndrome can generally be established on the basis of the history and physical examination. Diagnostic aid can be provided by electronic segmental oscillography to demonstrate diminished or absent oscillations and with the Doppler sonographically-determined systolic arterial pressure at the ankle which, in the case of severe ischemia, is less than 50 mmHg. Arteriography provides the most accurate morphological information. Abrupt occlusion of the vessel and no collateral perfusion especially in the absence of arteriosclerotic changes are strongly indicative of embolism but not conclusive. If the clinical diagnosis is unequivocal, arteriography need not be performed prior to embolectomy with a Fogarty catheter.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[The diagnosis of peripheral arterial embolism]. 176 45

Acute arterial occlusion in an extremity must be treated as a medical-surgical emergency since not only the affected limb is endangered, but the life of the patient as well. The cause of the acute occlusion is an embolism or in situ thrombosis. The most common source of embolism is the heart from which about 30% of the cardiac emboli obliterate the bifurcation of the femoral artery and about 4/5 of all emboli involve the extremities. Arterio-arterial emboli arise from aneurysms or from nonocclusive, ulcerated atheromatous plaques. Acute in situ thrombosis occurs mostly at the site of stenotic arteriosclerotic lesions. Aneurysms and dilated forms of atherosclerosis can be both the cause of in situ thrombosis as well as the source of an embolism. Differentiation between thrombosis and embolism can be extremely difficult but for acute treatment, however, it is of little relevance. There is a peak of both events in the seventh and eighth decades. On complete occlusion without adequate collaterals, the presentation is characterized by "the six Ps": pain, pallor, pulselessness, paresthesia, paralysis and prostration. With acute occlusion of central points such as the aortic bifurcation or the femoral artery bifurcation, there is complete ischemia with onset of rhabdomyolysis after four to six hours which can lead to severe local and generalized symptoms due to the dangerous metabolites released. In contrast, occlusion of isolated lower leg arteries usually only lead to transient symptoms. If arterial occlusion is suspected, prior to transportation to the hospital, 5000 I.E. heparin should be given intravenously. Acute thrombotic occlusion of large arteries is the surgical domain.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Therapy of acute peripheral arterial occlusion]. 183 82

Medical personnel should be able to recognize vascular injuries. Knowing the key signs of ischemia, namely pallor, pulselessness, pain, paresis, and paresthesia and the soft signs of vascular injury will help to prevent limb loss.
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PMID:Recognition of vascular injury in the trauma patient. 211 86

This case report documents an acute rupture of the lateral head of the gastrocnemius muscle at the myotendinous junction and a lateral dislocation of the tibialis anterior tendon with a clinical presentation consistent with a compartment syndrome, despite the intraoperative finding of a rupture of the posterior and lateral compartments. Extensive hematoma formation led to marked edema, paresthesias, muscle weakness, and severe pain in the involved leg. Surgical repair of the torn muscle and dislocated tendon and evacuation of the dissecting hematoma resulted in a well-functioning extremity. The authors emphasize the importance of prompt diagnosis of soft tissue injuries, which may place a patient at risk for a compartment syndrome. A compartment syndrome may lead to severe ischemia and irreversible tissue necrosis if intracompartmental hemorrhage of a torn muscle persists, and may require a surgical decompression. The clinical presentation, as well as adjunctive techniques in the diagnosis of a patient with a partial rupture of the gastrocnemius muscle, and a compartment syndrome, were presented.
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PMID:Rupture of the lateral head of the gastrocnemius muscle at the musculotendinous junction mimicking a compartment syndrome. 258 26

We review our recent experience with occlusion of the cervical internal carotid artery (ICA) in 15 patients with symptomatic aneurysms of the cavernous segment. All the patients were women and ranged in age from 38 to 74 years. Ten patients sought treatment initially for ophthalmoplegia, 9 for retro-orbital pain, 8 for facial paresthesia, and 3 for loss of vision. Two patients had symptoms of transient ocular or brain ischemia. The diameter of the aneurysm was greater than 3 cm in 10 patients. Ten patients underwent gradual occlusion of the ICA by Selverstone clamp under anticoagulation and monitoring of neurological status. One patient underwent ligation of a severely stenotic ICA under general anesthesia and electroencephalographic monitoring. Four patients underwent trapping of the aneurysm (after attempts at direct obliteration) under electroencephalographic and cerebral blood flow monitoring. Two patients with incompetent circle of Willis collaterals underwent prophylactic superficial temporal artery to middle cerebral artery bypass surgery prior to ICA occlusion. There was no postoperative clinical change in 9 patients. Ophthalmoplegia improved in 2 patients, and facial pain improved in 3. Three patients developed new extraocular muscle palsies within hours of ICA occlusion; these resolved in all patients by 1 week postoperatively. No change in aneurysm size was documented by serial postoperative computed tomographic or magnetic resonance imaging scans. After a follow-up of 5 to 6 years (range, 6 months-9 years), 11 patients have remained neurologically stable. Two patients experienced delayed transient worsening of visual or facial symptoms.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Internal carotid artery occlusion for cavernous segment aneurysm. 277 Oct 11

Transcatheter arterial chemoinfusion and/or chemoembolization of the internal iliac artery have been used for the treatment of pelvic malignancies. Intraarterial chemoinfusion is expected to deliver a higher concentration of chemotherapeutic agents directly to the neoplasm, reducing the problems of systemic side effects. In 35 cases of pelvic malignancies, 61 procedures of intraarterial chemoinfusion and/or chemoembolization of cisplatin (CDDP) and/or adriamycin (ADR) were performed in combination with or without occlusion of the superior and/or inferior gluteal arteries by the use of steel coils. For chemoinfusion and chemoembolization, the anterior division of the internal iliac artery was selected. In 19 procedures of 14 cases, pain of the lower extremities and the hips developed soon after chemoinfusion and chemoembolization, and gradually followed by paresthesia. Each patient was complicated with numbness, dysesthesia and/or weariness of the lower extremities, thighs and the plantar and dorsal of the foot. These symptoms continued long without recovery. Additionally, the most severe complication such as paralysis and muscular atrophy of the unilateral lower limb occurred in one patient, and at the 14 months follow-up the patient was still suffering from paralysis and gait disturbance. A neurologic examination revealed damage of the sciatic nerve at the level of L5, S1 and S2. It was suggested that the cause of the neurologic complications was attributed to ischemia and/or to deliver a higher concentration of chemotherapeutic agents of the sciatic nerves, and that any previous surgery, radiotherapy or intraarterial chemoinfusion combined with embolization was not related to the symptoms under discussion.
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PMID:[Neurologic complications following intraarterial chemoinfusion and/or chemoembolization of pelvic malignancies]. 279 64

The effects of inflation of a 7-cm tourniquet applied to the upper arm of eight volunteers on venous lactate, venous blood gases, and ulnar nerve somatosensory evoked potentials (SSEPs) were investigated. The inflation pressure was 100 mmHg over the systolic pressure. Venous blood samples for lactate and blood gas determinations were withdrawn before tourniquet inflation; immediately and at 2, 5, 10, 15 min after tourniquet deflation; and additionally at 30, 45, and 60 min after deflation in the last four volunteers. SSEP stimulating surface electrodes were placed over the ulnar nerve at the wrist. Recording electrodes were placed over the ipsilateral ulnar groove of the elbow, Erb's point, and on the contralateral cortex. Averaged responses were acquired before inflation of the tourniquet, every 5-10 min during tourniquet inflation, and every 5-10 min for 45-60 min after tourniquet deflation. The tourniquet was inflated for 36 +/- 11 min. After deflation of the tourniquet, postdeflation pain and paresthesias were felt by five volunteers; these occurred at 30-120 s after deflation and lasted for 75-120 s. The postdeflation pains were characterized as burning, cramping, paresthesias, buzzing, or severe expansion of the hand. The venous blood lactate levels were significantly elevated for 10 min, and the time course of its change did not correlate with reperfusion pain. The PO2 and O2Hb saturation in venous blood were significantly elevated for 10-15 min after deflation. The elevated lactate and PO2 levels in the presence of a restored blood flow probably result from continued anaerobic muscle metabolism secondary to capillary closure from the tourniquet-induced ischemia.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Changes in venous blood lactate, venous blood gases, and somatosensory evoked potentials after tourniquet application. 314 9

In 1980, 120 cases with late-life migrainous accompaniments resembling transient ischemic attacks were presented. In the present paper, 85 further cases examined in the past five years are analyzed. The findings support the concept advanced previously. In general, the cases are divided into the same categories: visual--21 cases, visual and paresthesias--6, visual and speech disturbance--2, visual, paresthesias and speech disturbance--3, visual, paresthesias, speech disturbance, and weakness--20, visual and brainstem symptoms--3, and cases without visual symptoms--32. The ages ranged from 40 to 73 years. Headache occurred in association with the episodes in only 40% of cases. There was a history of recurrent headache in 65%. The condition can justifiably be regarded as benign. Migrainous accompaniments account for some of the cases of transient ischemia with normal angiograms. Knowledge of the condition helps in the planning of rational management.
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PMID:Late-life migraine accompaniments--further experience. 353 32

Arterial embolism is usually caused by cardiac disease, and atherosclerotic coronary vascular disease is the primary precursor. Other cardiac states, as well as several uncommon causes, are part of the etiologic spectrum. The earliest signs are pain, paresthesias, pallor, and pulselessness. Severe ischemia is indicated by paralysis, a late feature. Arterial embolism and acute thrombosis can be difficult to distinguish, and deep venous thrombosis may also be suspected in the differential diagnosis. To restore arterial flow, anticoagulation treatment with heparin (Lipo-Hepin, Liquaemin) is given and surgical embolectomy is performed. Heparin infusion is continued until the patient is ambulatory, and then warfarin sodium (Coumadin, Panwarfin) is given over the long term. Fibrinolysis has also been used to treat acute arterial occlusion. Complications of embolism must be carefully guarded against, and additional procedures are sometimes necessary.
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PMID:Management of arterial emboli. Gleanings from 20 years of experience. 357 97


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