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

The use and safety of the esophageal electrocardiogram for detection and diagnosis of dysrhythmias or ischemia during anesthesia was compared with the conventional electrocardiogram using leads II and V5 in 20 patients undergoing coronary artery bypass graft surgery. Using an intra-atrial electrocardiogram as the standard to provide detection and definitive diagnosis of dysrhythmias, the correct diagnosis from leads II and V5 was made in 53.8% and 42.3% of cases, respectively, whereas 100% of the dysrhythmias were properly diagnosed from the esophageal electrocardiogram (p less than 0.05). In two patients, the presence of a significant dysrhythmia was not detected using standard leads II and V5 alone. Large, distinct P waves, resulting from the proximity of the esophageal lead to the left atrium, clearly established the temporal relationship between atrial and ventricular depolarization. Posterior myocardial ischemia was diagnosed in one patient by ST-segment elevation in the esophageal electrocardiogram, whereas leads II and V5 did not demonstrate ischemic changes. No complications were encountered during the study. The esophageal lead is safe, simple to use, and provides valuable information for detection or diagnosis of dysrhythmias and myocardial ischemia during anesthesia.
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PMID:Esophageal lead for intraoperative electrocardiographic monitoring. 698 Jun 6

Ischemia-reperfusion-induced injury of the coronary vasculature could result in an attenuated vasodilator or increased vasoconstrictor tone that might impact on myocardial recovery and viability. In 30 open-chest dogs the left circumflex coronary artery was occluded for 15 or 60 min and then reperfused, and responses to intracoronary acetylcholine, the alpha 1-adrenergic agonist methoxamine, and the alpha 2-adrenergic agonist BHT-933 (n = 10 each) were measured. In the experiments with 60 min of occlusion, triphenyltetrazolium chloride (TTC) staining was used to distinguish reversibly (TTC+) and irreversibly (TTC-) injured myocardium. After 15 min of occlusion, the vasodilator response to acetylcholine was not altered but was significantly reduced in TTC+ subendocardium and midmyocardium after 60 min of occlusion and was further reduced in TTC- subendocardium, midmyocardium, and also in subepicardium. The vasoconstrictor responses to methoxamine and BHT-933 were not altered after 15 or 60 min of occlusion in both TTC+ and TTC- myocardium. Posterior wall thickening was not affected by acetylcholine, methoxamine, or BHT-933. Thus, in reversibly injured myocardium after 15 min of occlusion, cholinergic and alpha-adrenergic coronary vasomotor responses are unchanged. With increasing duration of ischemia, reversibly and even more so irreversibly injured reperfused myocardium are characterized by an impaired cholinergic coronary vasodilation but not an enhanced alpha-adrenergic coronary vaso-constriction.
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PMID:Cholinergic and alpha-adrenergic coronary vasomotion [corrected] with increasing ischemia-reperfusion injury. 786 16

Proximal fibulotibial dislocation may remain escape detection in leg injuries. Posterior dislocations are unusual and are associated with shortening of the limb due to the tibial fracture. Two cases of such dislocation are reported, associated with lower limb ischemia due to an injury of the arterial popliteal trifurcation. An anatomical model indicates the mechanism of this lesion. Such an unusual association has not be found elsewhere in literature.
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PMID:[Proximal fibulo-tibial dislocation and ischemia associated with a leg fracture. Apropos of 2 cases]. 823 41

We studied 75 patients with severe intracranial vertebral artery (ICVA) occlusive disease from the New England Medical Center Posterior Circulation Registry to learn the etiologies and locations of the vascular lesions, the location and patterns of related ischemia and infarctions, and the outcomes. All patients had neuroimaging and vascular studies. Thirty-nine percent of patients had bilateral ICVA lesions. Twenty-four percent also had basilar artery disease and 36% had associated extracranial disease. The most common site of lesions was the distal ICVA after the origin of the posterior inferior cerebellar artery (PICA). Twenty-five percent of patients had only proximal intracranial posterior circulation territory infarcts (medullary and PICA cerebellar); 32% had infarcts that involved other intracranial territories in addition to the proximal territory. We found more distal intracranial territory infarcts resulting mainly from embolism from ICVA lesions than reported previously; this occurred in 17% of all patients. The ICVA was a recipient site for emboli in 8% of patients. Thirteen percent of patients died during follow-up. The outcome was favorable in most surviving patients. Three-fourths of them had no deficit or only slight disability. The patients with distal territory infarcts due to emboli from the ICVA had the worst outcome.
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PMID:Intracranial vertebral artery disease in the New England Medical Center Posterior Circulation Registry. 913 25

We studied 91 patients with proximal intracranial territory posterior circulation ischemia from the New England Medical Center Posterior Circulation Registry to learn their distribution, underlying cardiovascular causes and longterm outcome. All patients had imaging and vascular studies. Six patients had proximal territory TIAs. Among 85 stroke patients, 52% had infarcts limited to the proximal territory, while 48% also had infarcts in other intracranial posterior circulation territories. Eighty-five percent of proximal territory infarcts were posterior inferior cerebellar artery (PICA) territory cerebellar infarcts and 30% were lateral medullary infarcts. One patient had a hemimedullary syndrome. Six patients had PICA territory cerebellar and lateral medullary infarcts. The most common vascular lesion in lateral medullary infarct patients was ipsilateral intracranial vertebral artery (ICVA) disease (38% isolated ICVA disease) and in PICA territory cerebellar infarcts, extracranial vertebral artery (ECVA) disease (29% isolated ECVA disease). Half of all lateral medullary infarcts were due to a hemodynamic mechanism, most often in situ thrombosis of an ICVA occlusive lesion. Half of all PICA territory cerebellar infarcts were due to intra-arterial embolism and one-fifth to cardiac origin embolism. Embolism was a more frequent cause of proximal territory posterior circulation infarcts than intrinsic ICVA disease. The etiological profiles of lateral medullary and PICA cerebellar infarcts were different. Seventeen percent of all patients died during follow-up (41 months) but mortality related to the acute stroke or new strokes was only 6 percent. The outcome was favorable in the surviving patients; 89% had no or only slight disability.
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PMID:Proximal intracranial territory posterior circulation infarcts in the New England Medical Center Posterior Circulation Registry. 913 26

A 30-year-old healthy woman was involved in a road traffic accident. She sustained a fracture dislocation of T11/12 with a complete Frankel A paraplegia below T11. She had no associated injuries. High Dose Methylprednisolone was administered according to the NASCIS III protocol (48 h) together with low molecular weight Heparin and gastroprotected medication. Complete transection of the spinal cord and an anterior haematoma from T11 to T12 were confirmed on X rays, CT's and MRI scans. Posterior surgical stabilisation was performed using Isola instrumentation, starting 8 h post injury. Her post surgical period was uneventful except for some episodes of low blood pressure (85/60 mmHg) from which she had no symptoms. On the 12th post operative day, while in the physiotherapy department, she complained of right scapular pain. This occurred every time she was sat up and was associated with paraesthesia of both upper limbs. Two days later she deteriorated neurologically and her level ascended initially to T8 and then to T3. MRI of the spine with and without gadolinium showed spinal cord oedema between C3 and T1. There was no evidence of haemorrhage or syringomyelia. The authors discussed this case making different hypotheses. They are mainly the following: (1) Gradually ascending ischaemia due to a vascular disorder; (2) Double spinal trauma; (3) Ischaemia related to repeated hypotensive episodes; (4) Low grade intramedullary tumour; and (5) Thrombus of the Radicularis Magna artery. The case has been recognised as being very rare and interesting. In the conclusions, the presenting author stresses the importance of adopting MRI-compatible instrumentation for the surgical stabilisation of the spine, and careful monitoring of blood pressure during the acute phase of spinal cord injury. Dr Aito agrees with Mr El Masry about the opportunity of forming a group of clinicians in order to discuss protocols to cope with this devastating complication.
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PMID:Ascending myelopathy in the early stage of spinal cord injury. 1049 Aug 52

Acute symptomatic groin hernias with potential or definite ischemia represent a special group of all the groin hernias. The method of choice to treat these hernias has to fulfill the following criteria: 1. Easy reduction of the hernia sac and its contents without causing damage. 2. Good exposure and easy access for possible resection. 3. Safe hernia repair through the same access. According to our experience with 44 incarcerated and strangulated groin hernias operated between 1993 and 1997 and after a literature review, we took the following procedure as our routine: Posterior approach and mesh repair. We do not use a meshgraft only in the presence of colonic necrosis or peritonitis.
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PMID:[Incarcerated and strangulated hernias--surgical approach and management]. 1070 34

Posterior circulation revascularization has evolved as a method to treat selected patients with vertebrobasilar ischemia who have inaccessible atherosclerotic occlusive disease and who have failed maximal medical therapy. In addition, complex unclippable aneurysms of the posterior circulation are another indication for revascularization of the vertebrobasilar territory. Careful preoperative evaluation and meticulous attention to detail intraoperatively yield good patient outcomes with minimal morbidity and mortality. This article reviews the vascular anatomy of the posterior circulation and the indications, preoperative evaluation, operative techniques, clinical outcomes, and alternative treatments for patients requiring posterior circulation revascularization procedures.
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PMID:Posterior cerebral circulation revascularization. 1139 Mar 12

Posterior encephalopathy is characterised by headache, impairment of consciousness, seizures and progressive visual loss. MRI shows bilateral, predominantly posterior, cortical and subcortical lesions with a distribution. Our aim was to analyse the MRI lesion pattern and angiographic findings because the pathophysiology of posterior encephalopathy is incompletely understood. We report three patients with clinical and imaging findings consistent with posterior encephalopathy who underwent serial MRI including diffusion-weighted imaging (DWI) and construction of apparent diffusion coefficient (ADC) maps, and four-vessel digital subtraction angiography (DSA). DWI revealed symmetrical subcortical and cortical parieto-occipital high signal. High and also low ADCs indicated probable vasogenic and cytotoxic oedema. On follow-up there was focal cortical laminar necrosis, while the white-matter lesions resolved almost completely, except in the arterial border zones. DSA revealed diffuse arterial narrowing, slightly more marked in the posterior circulation. These findings suggest that posterior encephalopathy may in some cases be due to diffuse, severe vasospasm affecting especially in the parieto-occipital grey matter, with its higher vulnerability to ischemia. Cerebral vasospasm due to digitoxin intoxication, resulting in posterior encephalopathy, has not yet been described previously.
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PMID:Posterior encephalopathy with vasospasm: MRI and angiography. 1457 25

Among 407 New England Medical Center Posterior Circulation registry patients, 59% had strokes without transient ischemic attacks (TIAs), 24% had TIAs then strokes, and 16% had only TIAs. Embolism was the commonest stroke mechanism (40% of patients including 24% cardiac origin, 14% intraarterial, 2% cardiac and arterial sources). In 32% large artery occlusive lesions caused hemodynamic brain ischemia. Infarcts most often included the distal posterior circulation territory (rostral brainstem, superior cerebellum and occipital and temporal lobes); the proximal (medulla and posterior inferior cerebellum) and middle (pons and anterior inferior cerebellum) territories were equally involved. Severe occlusive lesions (>50% stenosis) involved more than one large artery in 148 patients; 134 had one artery site involved unilaterally or bilaterally. The commonest occlusive sites were: extracranial vertebral artery (52 patients, 15 bilateral) intracranial vertebral artery (40 patients, 12 bilateral), basilar artery (46 patients). Intraarterial embolism was the commonest mechanism of brain infarction in patients with vertebral artery occlusive disease. Thirty-day mortality was 3.6%. Embolic mechanism, distal territory location, and basilar artery occlusive disease carried the poorest prognosis. The best outcome was in patients who had multiple arterial occlusive sites; they had position-sensitive TIAs during months to years.
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PMID:New England Medical Center Posterior Circulation registry. 1534 66


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