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Query: UMLS:C0149871 (deep vein thrombosis)
 12,364 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A case of reversible vasospasm is reported in a 54-year-old man with a closed bimalleolar ankle fracture. On admission the patient had normal distal pulses and laboratory studies. He was a heavy smoker who continued to smoke in the hospital. Deep venous thrombosis (DVT) prophylaxis included dihydroergotamine and heparin (DHE-H). In the early postoperative period, marked spasm of all three arteries developed on the operative side. Smoking privileges and DHE-H were discontinued. The vasospasm resolved after intraarterial nitroglycerin. This case suggests an infrequent but potentially limb-threatening complication of DHE-H.
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PMID:Reversible vasospasm in association with the use of heparin and dihydroergotamine. 139 56

Prolonged arterial spasm as a complication of ergot-containing medications has been reported since antiquity. This article describes our experience with a patient who had severe bilateral arterial spasm in the upper extremities 6 days after the initiation of a regimen of dihydroergotamine and heparin for prophylaxis against deep venous thrombosis. The spasm was refractory to oral calcium channel blocking agents and direct intraarterial infusion of tolazoline (Priscoline). However, intraarterial nitroglycerin produced a prompt and dramatic improvement in symptoms and in physical and arteriographic findings. This experience suggests that intraarterial nitroglycerin may be an appropriate first choice for ergot-induced arterial spasm.
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PMID:Bilateral upper extremity ischemia after administration of dihydroergotamine-heparin for prophylaxis of deep venous thrombosis. 313 97

Sudden cardiac death (SCD) due to acute myocardial infarction (AMI) is mostly the result of ventricular fibrillation (VP) which is an electrical accident appearing on the basis of electrical instability of the myocardium. In addition to the chronic electrical instability predisposing to ventricular arrhythmias the trigger effect of a precipitating factor also seems necessary which may disrupt the normal sequence of cardiac contractions. In view of this hypothesis the following strategy of therapeutic interventions aimed at preventing SCD from AMI seems to be logical: Prophylactic measures to prevent pathological processes underlying chronic electrical instability of the heart i.e. elimination of identified risk factors of ischemic heart disease. Protection from SCD due to AMI: by using drugs which could, prevent further electrical destabilization as shifts in myocardial and plasma ionic balance, in pH, in pCO2, accumulation of potentially arrhythmogenic metabolites: Inhibit the trigger effect of sudden changes: in hemodynamics, in the autonomic nervous outflow and balance. The general supportive measures include therapeutic interventions which are not directly connected with appearance of lethal arrhythmias but may indirectly contribute to their development as pain, arterial Hb desaturation, deep vein thrombosis. Some of the measures listed above are capable of limiting the size of the developing infarct, a major determinant of the future conditions of life and prognosis of the patient. In the prehospital phase of AMI when two thirds of all coronary deaths occur general supportive measures and drug treatment of life threatening arrhythmias should be applied simultaneously. Sedatives and anxiolytics, furthermore analgetics are widely used. They are however often associated with bradycardia and sometimes with hypotension. This latter is dominant in patients with inferior infarction, showing a parasympathetic hyperactivity, when atropine treatment is needed. Sympathetic hyperactivity responds to analgesia and sedation but beta blockers may be required to reduce increased MVO2. These agents belong to the group of anti-ischemic drugs. The beneficial anti-ischemic action of beta-blockers is mostly due to their negative chronotropic and inotropic effect. A direct metabolic action was shown by use as well as the presence of a positive steal phenomenon in the experimental angina model in dogs. Anti-ischemic action of coronary vasodilators. The most reliable drug for preventing or abolishing anginal attack is still the classic nitroglycerin. On the other hand persantine a potent coronary dilator failed to protect against anginal attack in man.
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PMID:[Pharmacological possibilities for the prevention of complications following myocardial infarction]. 382 Nov 31

Noninvasive investigative methods are valuable for the practical diagnosis of several peripheral vascular disorders. Doppler ultrasound is very useful for the detection of incompetent saphenous and perforating veins and for the measurement of systolic ankle pressure, which today is the best screening method for arterial stenoses or occlusions. Acral oscillography, photoplethysmography and thermography, combined with vasodilator (nitroglycerin) or vasoconstrictor (cold) stress tests, may disclose small vessel disease and vasospastic disorders (Raynaud phenomenon). To answer the question of whether varicosities should be eliminated by surgery or sclerotherapy in patients with severe stages of chronic venous insufficiency (e.g. crural ulcers), investigations of the venous pump by venous pressure measurement or (photo-)plethysmography with and without digital occlusion of the suspected leakage points are recommended. Doppler probe, plethysmography and thermography are valuable screening methods for deep vein thrombosis and help to restrict phlebography to patients on whom fibrinolysis or thrombectomy is carried out. For the majority of patients undergoing conservative treatment, these noninvasive diagnostic procedures are usually sufficient.
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PMID:[Supplementary instrumental examinations in the most frequently occurring peripheral vascular diseases in general practice]. 388 24

A 77-year-old man was referred with a 5-year history of an intermittently painful, nonhealing right medial ankle ulcer. The ulcer had not responded to multiple treatment modalities, including Unna boots, compression therapy, sclerotherapy, and split-thickness skin grafting. The past medical history was significant for a deep venous thrombosis in the right leg 30 years earlier (treated with warfarin for 3 months) and a history of greater saphenous vein harvesting for coronary bypass grafting 28 years previously. After the vein stripping, the patient had suffered from increasing right leg edema and stasis changes in the right leg. His history was also remarkable for coronary artery disease, dyslipidemia, and lymphoma treated with chemotherapy 8 years before presentation, with no evidence of recurrence. He had stopped smoking approximately 20 years earlier. Medications included atenolol, simvastatin, nicardipine, nitroglycerin, and aspirin. Skin examination revealed a 3.0 x 3.5-cm ulcer adjacent to the medial malleolus. The edges of the ulcer appeared raised and rolled (Fig. 1). Centrally, there was granulation tissue, which appeared healthy. There were surrounding dermatitic changes. Dorsalis pedis and the posterior tibial pulses were normal. Noninvasive vascular studies revealed severe venous incompetence of the right popliteal and superficial veins. Arterial studies and transcutaneous oximetry were normal. Computed tomographic scan of the pelvis did not reveal any adenopathy, and radiographic imaging did not reveal any bony changes suggestive of osteomyelitis. Biopsy of the ulcer edge and base showed infiltrating basal cell carcinoma (Fig. 2). Mohs' micrographic surgery required three layers; the final extent of the ulcer was 7.8 x 6.9 cm. A split-thickness skin graft was placed.
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PMID:Infiltrating basal cell carcinoma in the setting of a venous ulcer. 1094 Jan 16

Superficial vein thrombosis is characterized by clotting of superficial veins (ie, following direct trauma) with minimal inflammatory components. Superficial thrombophlebitis is a minimally thrombotic process of superficial veins associated with inflammatory changes and/or infection. Treatments generally include analgesics, elastic compression, anti-inflammatory agents, exercise and ambulation, and, in some cases, local or systemic anticoagulants. It is better to avoid bed rest and reduced mobility. Topical analgesia with nonsteroidal, anti-inflammatory creams applied locally to the superficial vein thrombosis/superficial thrombophlebitis area controls symptoms. Hirudoid cream (heparinoid) shortens the duration of signs/symptoms. Locally acting anticoagulants/antithrombotics (Viatromb, Lipohep, spray Na-heparin) have positive effects on pain and on the reduction in thrombus size. Intravenous catheters should be changed every 24 to 48 hours (depending on venous flow and clinical parameters) to prevent superficial vein thrombosis/superficial thrombophlebitis and removed in case of events. Low molecular weight heparin prophylaxis and nitroglycerin patches distal to peripheral lines may reduce the incidence of superficial vein thrombosis/superficial thrombophlebitis in patients with vein catheters. In case of superficial vein thrombosis/superficial thrombophlebitis, vein lines should be removed. In neoplastic diseases and hematological disorders, anticoagulants may be necessary. Exercise reduces pain and the possibility of deep vein thrombosis. Only in cases in which pain is very severe is bed rest necessary. Deep vein thrombosis prophylaxis should be established in patients with reduced mobility. Antibiotics usually do not have a place in superficial vein thrombosis/superficial thrombophlebitis unless there are documented infections. Prevention of superficial vein thrombosis should be considered on the basis of patient's history and clinical evaluation.
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PMID:Management of superficial vein thrombosis and thrombophlebitis: status and expert opinion document. 1747 77