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Query: UMLS:C0030193 (pain)
 261,466 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Upper extremity venous thrombosis is a clinical entity with numerous etiologic factors. Only 2% of all cases of deep venous thrombosis involve the upper extremity, and the incidence of pulmonary embolism related to thrombosis in this location is approximately 12%. Primary or "effort" thrombosis of the upper limb is related to the inherent anatomical structure of the thoracic outlet and axillary region. Secondary thrombosis may have such diverse origins as trauma, infection, congestive heart failure, central venous catheters, neoplasms, septic phlebitis, intravenous drug use, and hypercoagulable states. Patients present with peripheral edema and prominent superficial veins, and neurologic symptoms (pain and paresthesias) are usually present as well. Clinical diagnosis is confirmed by venography or sonography. Treatment regimens include conservative measures, thrombolysis with fibrinolytic agents, and surgical correction of indicated thoracic outlet and axillary structures. We present an unusual case in which upper extremity venous thrombosis in a young healthy female athlete was associated with the presence of cervical ribs. The patient was successfully treated with focal thrombolysis and surgical resection of her ipsilateral cervical rib.
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PMID:Upper extremity venous thrombosis. Case report and literature review. 218 88

The authors describe the case of a 57-year-old male patient with severe left ventricular dysfunction (ejection fraction of left ventricle--37%, left ventricular end diastolic pressure 32 mm Hg) as a result of an extensive anterior Q infarction of the heart muscle. The patient did not have signs of congestive heart failure. He was treated on account of angina pectoris on exertion, grade III according to NYHA, hypertension and diabetes. Nifedipine and diltiazem administration led to repeated attacks of cardiac asthma. Calcium channel blockers should be administered to patients with angina pectoris and severe left ventricular dysfunction only when nitrates alone do not eliminate ischaemia and pain. They should be administered carefully and with the knowledge that they may in rare instances cause clinical deterioration of left ventricular function.
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PMID:[Cardiac asthma after nifedipine and diltiazem]. 227 77

We describe 3 patients with painful intraarticular knee effusions composed of a viscous milky white suspension of monosodium urate crystals, in the absence of any cellular component. Two patients presented with acute bilateral knee pain. One patient presented with unilateral knee pain of gradual onset. All 3 patients had a history of ethanol abuse. Two patients had a history of gout. Two patients had chronic renal insufficiency, hypertension, and congestive heart failure. One patient had alcoholic cirrhosis. Two patients' pain responded to colchicine. One patient's discomfort was relieved only by repeated arthrocentesis. We conclude that intraarticular free urate can cause painful joints in the absence of an apparent inflammatory response.
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PMID:Intraarticular noninflammatory free urate suspension (urate milk) in 3 patients with painful joints. 235 87

To compare the natural history of patients with new onset ischemic heart disease with that of patients with exacerbations of chronic ischemic heart disease, short- and long-term outcomes of 3,465 emergency room patients with acute ischemic heart disease at four community and three university hospitals were evaluated. Acute myocardial infarction was diagnosed in 598 (33%) of the 1,835 patients with a prior history of infarction or angina and 934 (57%) of the 1,630 without such a history (p less than 0.001). Patients with new onset ischemic heart disease with acute myocardial infarction were more likely than patients with infarction and exacerbated chronic ischemic heart disease to have Q wave infarction (57% versus 36%) and to receive thrombolytic therapy (11% versus 5%); they also had higher maximal creatine kinase levels (1,088 +/- 1,299 versus 733 +/- 906 U/liter) (p less than 0.0001 for all three). After adjustment for differences in clinical presentation and initial triage, patients with new onset ischemic heart disease with acute myocardial infarction were less likely than the comparison group to have congestive complications (odds ratio 0.63, 95% confidence interval 0.47 to 0.84, p less than 0.01) but not less likely to have arrhythmic, ischemic or overall complications. Among patients with angina without acute myocardial infarction, patients with new onset ischemic heart disease were less likely to have recurrent ischemic pain and congestive heart failure. In multivariate analysis of long-term follow-up data on 457 patients from one hospital, patients with new onset ischemic heart disease had better cardiovascular survival rates.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Comparison of the natural history of new onset and exacerbated chronic ischemic heart disease. The Chest Pain Study Group. 219 11

The regulation of the peripheral-limb circulation was investigated in 21 patients suffering from chronic cardiac failure (NYHA stage II and III). In 11 patients the extremital circulation was intact, while 10 patients suffered from peripheral obliterative arterial disease, too (intermittent claudication or rest pain). The control group consisted of 75 subjects with normal cardiac condition. In 35 of the control subjects the peripheral circulation was intact, the remaining 40 suffered from extremital venous isotope dilution technique. In congestive heart failure the limb blood flow and the limb oxygen consumption slightly diminished, but remained in the normal range. The limb vascular resistance significantly increased. In patients suffering from intermittent claudication or rest pain, the marked diminution of the limb blood flow and elevation of the vascular resistance was more pronounced in congestive heart failure than in healthy subjects. The pathologically elevated limb vascular resistance decreased and the limb blood flow significantly increased in congestive heart failure on administration of vasodilator drugs. A pathological and mostly reversible increase in extremital vascular resistance is the most characteristic sign of the peripheral circulation in congestive heart failure.
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PMID:The characteristics of the peripheral-limb-circulation in congestive heart failure. 277 85

Parenterally administered narcotic analgesics are a critically important part of therapy for the patient with acute myocardial ischemic syndromes. These agents are very effective and, when used with appropriate caution and monitoring, are also generally safe. They not only relieve the sensation of severe pain but also reduce the effective and physiologic reaction to pain and thus reduce patient anxiety. Because these agents all depress respiratory drive to some degree in the doses used for adequate analgesia, close attention to respiratory status is mandatory. In patients with underlying pulmonary disease or significant congestive heart failure, this monitoring should be even more intensive and include arterial blood gas measurements and preparations for possible narcotic antagonist administration and ventilatory assistance. With regard to the hemodynamic changes produced by these agents, several important points are worth noting. It must be remembered that the conclusions regarding hemodynamic effects of these agents are derived from studies involving patient groups that were generally hemodynamically stable, usually pain-free, and almost always at least several hours following acute presentation. Thus, the hemodynamic effects of these agents may be quite different in patients with active pain during a period of acute ischemia, or in patients that are hemodynamically unstable. Hemodynamic studies during these acute settings, however, are extremely difficult to perform because the patient's acute distress mandates rapid administration of an analgesic agent prior to the institution of invasive monitoring. With these cautions relating to data interpretation in mind, it is still possible to make certain recommendations regarding the use of analgesic therapy in acute MI.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Analgesic therapy in acute myocardial infarction. 290 10

Previous clinical studies with intravenous enoximone have used cumulative dosing to quantify enoximone's hemodynamic effects. The magnitude and duration of the hemodynamic effects of single intravenous doses of enoximone were evaluated in patients with congestive heart failure. Sixty patients, who were in New York Heart Association functional classes III and IV, received single intravenous doses of enoximone, either 0.25 (12 patients), 0.5 (13 patients), 1 (14 patients), 1.5 (10 patients) or 2 mg/kg (11 patients). Cardiac index was increased by 20% with the 0.25 mg/kg dose and by 48% and 42% with the 1.5 and 2 mg/kg doses, respectively. These increases were statistically significant (Student's paired t test with Bonferroni's correction, p less than 0.007) for 1 hour after 0.25 and 0.5 mg/kg, for 2 hours after 1 mg/kg and for 4 hours after 1.5 and 2 mg/kg. Enoximone also reduced pulmonary artery diastolic pressure by 19% with 0.25 mg/kg and by 29% with 2 mg/kg. The duration of effect varied from 1 hour with 0.25 mg/kg to 4 hours with 2 mg/kg. Enoximone produced no consistent or dose-related effects on heart rate or blood pressure. Eighteen adverse reactions were reported by 15 patients, of which 11 were minor and transient (vein pain, flushes, nausea). In 5 patients ventricular or supraventricular arrhythmias were observed, including nonsustained ventricular tachycardia and extrasystoles; 3 of these patients had evidence of arrhythmias before enoximone. Laboratory studies before and after treatment showed no drug-related effects. Dose-related effects on the magnitude and duration of hemodynamic responses to intravenous enoximone were evident within the dose range of 0.25 to 2 mg/kg.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:A dose-response study of intravenous enoximone in congestive heart failure. 295 65

The effect of intravenous enoximone on forearm venous circulation was studied in ten healthy volunteers (group A) and in ten patients with NYHA class III-IV congestive heart failure (group B). Distensibility of the forearm capacitance vessels was assessed from pressure-volume curves by venous occlusion plethysmography using a mercury-in-rubber strain gauge. Three recordings each at 3-min intervals were obtained before the infusion and again 20 min after completion of the infusion. Venous volume changes (VV) at congesting pressures of 10, 20, and 30 mmHg before and after enoximone were compared. Forearm muscle blood flow was also measured by venous occlusion plethysmography; electrocardiogram, heart rate, and cuff blood pressure were recorded throughout. Enoximone at a dose of 1 mg/kg body weight was infused over 10 min through a peripheral vein in group A and via a central line in group B. In group A, the effect of the injection vehicle was also assessed. VV10, VV20, and VV30 did not differ from baseline values after enoximone in both groups A and B. The vehicle caused a small but significant degree of venoconstriction in group A (VV20, 2.64 +/- 0.9 to 2.48 +/- 0.83 ml/100 ml, P less than 0.05; VV30, 3.47 +/- 1.27 to 3.33 +/- 1.20 ml/100 ml, P less than 0.05), which could be explained by an acute response to local pain from the infusion. This effect was not evident following enoximone, perhaps as a result of its counterbalancing vasodilating action to venoconstriction induced by acute pain.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:The effects of enoximone (MDL-17043) on forearm venous circulation in healthy volunteers and patients with heart failure. 296 30

Intravenous nitroglycerin is frequently used in the treatment of acute myocardial infarction for its vasodilating effect on lowering both preload and afterload and in the control of ischemic heart pain. The end point for doses of nitroglycerin infusion is either relief of persistent or recurrent angina or controlling congestive heart failure by lowering left ventricular end diastolic pressure and volume. Nitroglycerin accomplishes these end points primarily through its venodilating property. Intolerable headaches or symptomatic hypotension may prevent achieving the clinical end point. Nevertheless, high doses of intravenous nitroglycerin may need to be administered to achieve a desired hemodynamic and therapeutic effect. Changes in mental status, i.e., lethargy and confusion, should be a warning sign of possible ethanol intoxication. An alcohol blood level verifies the clinical impression and gradually withdrawing the intravenous nitroglycerin is all that is necessary to effect a total recovery from this reaction.
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PMID:An unusual complication of intravenous nitroglycerin. 309 6

We tested the hypothesis that preservation of left ventricular function results from treatment with intravenous streptokinase given in the first 2 hours from onset of acute transmural myocardial infarction together with nitroglycerine and verapamil. Thirty-three consecutive patients with onset of pain less than 2 hours prior to admission, received intravenous streptokinase 1.5 x 10(6) units with intravenous nitroglycerine and verapamil; 23 concurrently admitted "control" patients with pain onset 2-4 hours received intravenous nitroglycerine and verapamil only. Radionuclide ventriculographic assessment at 2 days revealed a significantly greater left ventricular ejection fraction in the streptokinase-treated patients (54.5 +/- 2.8 vs 46.1 +/- 2.9; P less than 0.05), which persisted at 28-35 days (50.1 +/- 2.3 vs 41.2 +/- 2.9; P less than 0.05). Streptokinase-treated patients had a significantly increased incidence of ischaemic events in the 35 days following infarction, but a lower incidence of death, congestive cardiac failure and non-fatal ventricular tachycardia than control group patients. Infarct-related artery patency assessed at 3-5 days was 94% in streptokinase-treated patients. We conclude that early presentation and treatment with intravenous streptokinase, nitroglycerine and verapamil is associated with a high incidence of successful thrombolysis and significant preservation of left ventricular function. Nitroglycerine and verapamil may augment the efficacy of streptokinase in this group of patients.
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PMID:Myocardial salvage with streptokinase combined with nitroglycerine and verapamil in acute myocardial infarction. 314 49


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