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Query: UMLS:C0034063 (pulmonary edema)
 10,665 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

11 patients with atheromatous renovascular hypertension had a history of multiple episodes of pulmonary oedema. 7 had stenosis of both renal arteries, 2 had stenosis of the artery to a solitary kidney, and 2 had unilateral stenosis with an intact contralateral kidney. Successful revascularisation (by angioplasty in 8, and surgery in 3) improved blood pressure and renal function, and virtually eliminated pulmonary oedema. In a second series of 55 consecutive patients with azotaemia and renovascular hypertension, pulmonary oedema occurred in 13 (23%). Blood pressure and renal function were not significant predictors of pulmonary oedema, but coronary heart disease and bilateral (vs unilateral) renal artery stenosis were. Bilateral renal artery stenosis may be a specific and treatable predisposing factor to pulmonary oedema in azotaemic hypertensive patients.
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PMID:Recurrent pulmonary oedema in hypertension due to bilateral renal artery stenosis: treatment by angioplasty or surgical revascularisation. 290 Sep 30

Renal artery stenosis of the transplant kidney occurs in approximately 6% of renal allograft recipients. Severe bilateral renal artery stenosis and unilateral renal artery stenosis to a single functioning kidney have been described as causes of recurrent pulmonary edema in nontransplant patients with normal cardiac function. We report 2 patients with severe transplant renal artery stenosis who presented with recurrent episodes of acute pulmonary edema. Successful revascularization in 1 patient prevented the recurrence of pulmonary edema. In renal allograft recipients who present with unexplained recurrent episodes of acute pulmonary edema, who do not have an obvious cardiac cause, transplant renal artery stenosis should be considered as a possible etiology.
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PMID:Transplant renal artery stenosis presenting with recurrent acute pulmonary edema. 868 44

The sudden onset of pulmonary edema in patients with renal artery stenosis is an increasingly recognized entity. Some data also support an association between renal artery stenosis and chronic cardiac failure. We report a 60-year-old man with chronic renal failure who had most normal arterial blood pressure despite highly severe chronic congestive heart failure. Renovascular disease was suspected and an arteriography revealed very tight bilateral artery stenosis. Removal of stenosis led to both renal and cardiac functions improvement.
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PMID:Chronic congestive heart failure associated with bilateral renal artery stenosis. 924 81

Pulsus alternans is usually found in patients with reduced systolic ventricular function. We describe a patient with recurrent pulmonary edema, hypertension, bilateral renal artery stenosis, but with normal systolic function. Pulsus alternans was demonstrated in both pulmonary artery, right ventricle, and left ventricle pressures. After successful renal artery revascularization, the pulsus alternans disappeared. This case illustrates that pulsus alternans can be present with diastolic dysfunction of the left ventricle in the absence of systolic dysfunction.
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PMID:Pulsus alternans in diastolic left ventricular dysfunction--a case report. 940 36

Abrupt onset pulmonary edema, that rapidly resolves (flash edema) may be due to renal artery stenosis. We describe two patients with renal artery stenosis who experienced a life-threatening episode of flash edema. Relief of the stenosis prevented recurrence of the flash edema.
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PMID:Rapid onset pulmonary edema (flash edema) in renal artery stenosis. 959 69

Hypertensive crisis is defined as a severe elevation in BP and is classified as either urgency or emergency. In hypertensive urgency there is no end-organ injury and no evidence that acute BP lowering is beneficial. Indeed, rapid uncontrolled pressure reduction may be harmful. Therefore, in hypertensive urgencies BP should be lowered gradually over 24 to 48 hours using oral antihypertensives. When the cause of transient BP elevations is easily identified, appropriate treatment should be given. When the cause is unknown, an oral antihypertensive should be given. The efficacy of available treatments appear similar; however, the underlying pathophysiological and clinical findings, mechanism of action and potential for adverse effects should guide choice. Captopril should be avoided in patients with bilateral renal artery stenosis or unilateral renal artery stenosis in patients with a solitary kidney. Nifedipine and other dihydropyridines increase heart rate whereas clonidine, beta-blockers and labetalol tend to decrease it. This is particularly important in patients with ischaemic heart disease. Labetalol and beta-blockers are contraindicated in patients with bronchospasm and bradycardia or heart blocks. Clonidine should be avoided if mental acuity is desired. In hypertensive emergency there is an immediate threat to the integrity of the cardiovascular system. BP should be immediately reduced to avoid further end organ damage. Sodium nitroprusside is the most popular agent. Nitroglycerin (glyceryl trinitrate) is preferred when there is acute coronary insufficiency. A beta-blocker may be added in some patients. Loop diuretics, nitroglycerin and sodium nitroprusside are effective in patients with concomitant pulmonary oedema. Enalaprilat is also theoretically helpful, especially when the renin system might be activated. Initial treatment of aortic dissection involves rapid, controlled titration of arterial pressure to normal levels using intravenous sodium nitroprusside and a beta-blocker. If beta-blockers are contraindicated, urapidil or trimetaphan camsilate are alternatives. Hydralazine is the drug of choice for patients with eclampsia. Labetalol, urapidil or calcium antagonists are possible alternatives if hydralazine fails or is contraindicated. For patients with catecholamine-induced crises, an alpha-blocker such as phentolamine should be given; labetalol or sodium nitroprusside with beta-blockers are alternatives. There are few, if any, comparative or randomised trials providing definitive conclusions about the efficacy and safety of comparative agents. Some investigators recommend decreasing the diastolic BP to no less than 100 to 110 mm Hg. A reasonable approach for most patients with hypertensive emergencies is to lower the mean arterial pressure by 25% over the initial 2 to 4 hours with the most specific antihypertensive regimen.
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PMID:Comparative tolerability profile of hypertensive crisis treatments. 970 48

Revascularization cures or attenuates the clinical manifestations of renal artery stenosis (hypertension, ischemic nephropathy, pulmonary edema, angina, and congestive heart failure). Traditional approaches have been sub-optimal due to low rates of success and long-term patency after angioplasty, and to relatively high rates of perioperative morbidity and mortality. Endovascular stent placement is an alternative interventional method for renal artery revascularization. Technical success rates are excellent, and the impact on clinical outcomes (blood pressure, renal function, and cardiac complications) is promising.
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PMID:Endovascular stents for renal artery revascularization. 986 68

Pulmonary edema and congestive heart failure (both referred to here as PE) have been reported to be complications of bilateral renal artery stenosis or unilateral stenosis in a solitary functioning kidney (both referred to as BRAS). The goals of this study were to determine whether a history of PE was more common in patients with BRAS than in those with unilateral stenosis and a normal contralateral kidney (URAS), and whether recurrent PE could be prevented by renal artery stent placement. We evaluated 90 consecutive patients with renovascular disease who were treated with percutaneous renal artery stent placement. History and clinical follow-up were obtained through chart review and phone contact with referring physicians. Mean follow-up was 18.4 months after stent placement. Twenty-three of 56 (41%) subjects with BRAS had a history of PE before revascularization, compared with four of 34 (12%) subjects with URAS (P = .05). Twenty-five of the 27 patients with history of PE had adequate clinical follow-up. Seventeen of the 22 (77%) subjects with BRAS and history of PE had no further PE after stent placement in one or both renal arteries. The five BRAS subjects with recurrent PE after stent placement had evidence of stent thrombosis or restenosis. In contrast, only one of three (33%) URAS subjects with a history of PE remained free of PE after stent placement. We conclude that PE is a common complication of BRAS, but not of URAS. In patients with BRAS, recurrent PE can be prevented by successful stent placement in one or both renal arteries.
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PMID:Prevention of recurrent pulmonary edema in patients with bilateral renovascular disease through renal artery stent placement. 1007 77

Disseminated cholesterol crystal embolism (CCE) is a devastating complication of atherosclerosis that is often considered beyond therapeutic resources. We designed and implemented a treatment protocol based on an analysis of the main causes of death in disseminated CCE with renal involvement. From 1985 to 1996, we applied this protocol in 67 consecutive atherosclerotic patients admitted to our renal intensive care unit for acute renal failure (serum creatinine level, 6 +/- 2.5 mg/dL) accompanied by signs and symptoms of CCE. The other principal clinical features in these patients were cardiac failure with pulmonary edema (61%), gastrointestinal ischemia (33%), cutaneous ischemia (90%), and retinal cholesterol embolism (22%). Disseminated CCE followed one or several precipitating factors, including angiographic procedure(s) (85%), anticoagulant treatment (76%), and cardiovascular surgery (33%). Our treatment schedule systematically addressed the identified causes of death in these patients. (1) To avoid CCE recurrence, any form of anticoagulant treatment was withdrawn, and aortic catheterization and surgery were proscribed. (2) To treat or prevent cardiac failure, a high-dose vasodilator regimen was instituted, including angiotensin-converting enzyme (ACE) inhibitors. In case of cardiac failure refractory to vasodilators, loop diuretics were added and, if necessary, overhydration was corrected by ultrafiltration/hemodialysis (11 patients). (3) To avoid cachexia, severe metabolic disorders were treated by hemodialysis (41 patients), and special attention was given to providing enteral or parenteral nutritional support. Patients with declining general status and laboratory evidence of inflammation, as well as those with new episodes of CCE, were treated with corticosteroids. Statistical analysis found a significant correlation between the requirement for hemodialysis and previous anticoagulation, degree of renal insufficiency, and severity of cardiac failure. Conversely, there was no correlation between requirement for hemodialysis and ACE inhibitor treatment or presence of atherosclerotic renal artery stenosis/thrombosis. The inhospital mortality rate was 16%. There were no clinical or laboratory elements found on admission that were predictive of inhospital mortality. Among survivors, 32% had to remain on maintenance hemodialysis therapy for irreversible chronic renal failure. Including initial hospitalization, the 1-year survival rate was 87%, which compares favorably with reports in the literature indicating a first-year mortality rate of 64% to 81%. Overall follow-up was 19 +/- 20 months, ranging from 1 to 74 months. The 4-year survival rate was 52%. We conclude that an intensive-care, specific-treatment schedule reduces mortality in multivisceral cholesterol embolism.
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PMID:Supportive treatment improves survival in multivisceral cholesterol crystal embolism. 1067 43

Renovascular disease appears to be increasing in prevalence, particularly in older subjects with atherosclerotic disease elsewhere. Its clinical manifestations and presentation are changing because of rapid advances in medical therapy and other comorbid events. Although fibromuscular dysplasia and other diseases affecting the renal artery can produce the syndrome of renovascular hypertension, atherosclerotic renal artery stenosis is the most common clinical entity. It can produce a spectrum of manifestations, ranging from asymptomatic ("incidental"), identified during angiographic evaluation of other conditions, to progressive hypertension to accelerated cardiovascular disease with pulmonary edema and advanced renal failure. With the widespread application of drugs which block the renin-angiotensin system, including angiotensin-converting enzyme inhibitors and angiotensin antagonists, many cases of renovascular hypertension remain unsuspected and never produce adverse effects. Clinicians need to be alert to the potential for disease progression, with the potential for total renal artery occlusion and/or loss of viable renal tissue. Selection of patients for renal revascularization depends on individual balance of risks and benefits regarding the likely outcomes regarding both improvements in blood pressure control and preservation of renal function.
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PMID:Epidemiology and clinical presentation. 1102 94


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