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Query: UMLS:C0235886 (leg edema)
 674 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Bronchiolitis obliterans organizing pneumonia (BOOP) has been described after bone marrow, lung, heart-lung, and renal transplantation, but rarely after orthotopic liver transplantation (OLT). We report a case of BOOP after OLT to emphasize BOOP as an under diagnosed and treatable cause of nonresolving pneumonia, which may not be preventable by maintenance low-dose prednisone. A 48-year-old man was hospitalized for dyspnea and cough one month after OLT. Among his medications were tacrolimus and prednisone. Physical examination was significant for lung crepitations and bilateral leg edema. Chest x-ray revealed bilateral infiltrates. Computed tomography (CT) of the chest demonstrated bilateral diffuse infiltrates with areas of sparing and nodularities. Bronchoscopy was normal and bronchoalveolar lavage was negative. Lung biopsy was performed and demonstrated serpiginous plugs of fibroblastic tissue filling the alveolar spaces, focal fibrosis of some alveolar septa, and reactive pneumocytic hyperplasia consistent with BOOP. Methylprednisolone was continued with clinical improvement and weaning from the ventilator, but subsequent sepsis and multisystem organ failure finally led to the patient's death.
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PMID:Bronchiolitis obliterans organizing pneumonia after orthotopic liver transplantation. 1500 77

Aortocaval fistula (ACF) represents a rare complication of abdominal aortic aneurysm (AAA) that may lead to hyperdynamic heart failure. We briefly describe a 58-year-old man with an old myocardial infarction, who developed leg oedema and worsening exertional dyspnea due to ACF complicating an AAA. This uncommon case highlights that an appropriate investigation for AAA and ACF should be performed in high-risk patients presenting with a history of worsening leg oedema and dyspnea in the absence of an obvious precipitating factor.
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PMID:Leg oedema and exertional dyspnea due to aortocaval fistula complicating an abdominal aortic aneurysm. 1509 7

We report a case of non-Hodgkin lymphoma (NHL) with acute renal failure. A 62-year-old man was admitted to our hospital on March 8, 2002 with leg edema and dyspnea on effort. About 3 weeks before admission, he was found to have slightly high serum creatinine (Cr) and high lactate dehydrogenase (LDH) levels by another home doctor. Physical examination revealed anemic conjunctivae and leg edema, but the urinary volume was preserved. Blood examination showed high BUN (64 mg/dl) and Cr levels (3.91 mg/dl). Urinary analysis showed proteinuria (1.05 g/day) and high BMG (14,434/microg/day) and NAG (4.55 U/day) levels, suggesting severe tubulointerstitial injury. On ultrasonography of the kidney, the bilateral kidneys showed marked swelling without hydronephrosis. To investigate the genesis of renal failure, we performed a renal biopsy. The specimen showed normal glomeruli, but a large number of cells infiltrated in the tubulointerstitial area with normal tubulointerstitial structure. The cells stained positively with anti-leukocyte antigen and L26 (B cell marker), and negatively with cytokeratin and UCHL-1 (T cell marker). These findings indicate that the interstitial cells were non-Hodgkin lymphoma with B cell diffuse large cells. Chemotherapy was performed with VAD (vincristine sulfate, doxorubicin hydrochloride, dexamethasone) considering his renal dysfunction. To avoid tumor lysis syndrome after chemotherapy, hemodialysis was performed on days 1-4 after the initiation of chemotherapy. After a series of chemotherapy, the urinary volume increased and serum Cr levels decreased to 2 mg/dl. After additional therapy with 4 courses of CHOP, he improved and was discharged on day 180 after admission.
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PMID:[Case of non-Hodgkin lymphoma with acute renal failure successfully treated with chemotherapy]. 1564 40

Yellow nail syndrome is a type of lymphatic dysplasia syndrome characterised by the triad of yellow nails, lymphoedema, and pleural effusions. The case history is presented of a 70 year old patient with yellow nail syndrome who complained of dyspnoea caused by massive chylothorax. The patient underwent insertion of a pleuroperitoneal shunt which resulted in abdominal distension and deterioration of leg oedema. The pleuroperitoneal shunt was replaced by a pleurovenous shunt on the right side which led to an improvement in the bilateral pleural effusions, abdominal distension, and leg oedema. A pleurovenous shunt may be an alternative rescue therapy for yellow nail syndrome.
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PMID:Implantation of a pleurovenous shunt for massive chylothorax in a patient with yellow nail syndrome. 1574 46

A 69-year-old woman caught a cold resulting in nausea, vomiting, diarrhea and severe anorexia. Then she suffered progressively from dyspnea and leg edema, and finally became delirious. On admission severe hypoglycemia, hypothermia, marked tachycardia, generalized edema, mild jaundice and cachexy were noted. EKG showed atrial fibrillation. A chest X-ray, chest CT and echocardiography showed congestive heart failure. Therapeutic use of diuretics induced shock leading to serious liver dysfunction and disseminated intravascular coagulation. However, combined therapy by intravenous glucose, digitalis, diuretics, anti-fibrinolytic drug and hydrocortisone were effective. Addition of antithyroid therapy brought a further favorable outcome.
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PMID:Severe starvation hypoglycemia and congestive heart failure induced by thyroid crisis, with accidentally induced severe liver dysfunction and disseminated intravascular coagulation. 1580 13

Ergot derivative dopamine agonists, e.g. pergolide, bromocriptine, dihydroergocriptine used in treatment of Parkinson's disease can cause pleural, pericardial, retroperitoneal and valvular fibrotic changes. Case No 1: A 56-year-old woman with PD was treated with pergolide 3mg/24h since July 2002. In June 2003, edema of lower extremities was first noticed and echocardiography found a minor mitral regurgitation without any morphological changes of the valve. In January 2004, left- sided cardiac failure rapidly developed and echocardiography revealed multivalvular insufficiency with predominating severe mitral regurgitation. Mitral valve replacement was performed and pergolide was changed to ropinirole. Until now, neither cardiac functions nor motor status are sufficiently compensated. Case No 2: A 66-year-old-man with PD since 1996 was treated with pergolide 3 mg/day since 1999. In the beginning of 2004, leg edema appeared. On examination, bilateral hydronephrosis with ureteric strictures and incipient renal insufficiency was found. Bilateral ureteroplasty was performed and the histology showed periureteric fibrosis. Treatment with steroids was initiated and pergolide was changed to pramipexole. Despite the treatment, the fibrosis progressed, requiring ureteral stenting. Based on the literature review and on our own experience, we propose following guidelines to minimize the risk of complications: A. Not to use EAD as the first-line dopamine agonists. B. Regularly follow all patients treated with EAD, especially monitor the majorsymptoms: dyspnea, cough, fatigue, leg edema (also asymmetric), symptoms of urinary outflow obstruction, cardiac insufficiency, chest pain, heart murmur. An elevated ESR, C-reactive protein or anemia support the diagnosis. C. All symptomatic patients should undergo workup for serosal fibrosis (according to type of complication): chest X-ray or CT scan, spirometry, renal functions, renal ultrasound, CT of retroperitoneum. D. Before the introduction of EAD therapy, examine the renal functions, perform chest X-ray and echocardiography. Screening echocardiography should be performed in 3-6 months and subsequently in every 6-12 months.
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PMID:[Organ changes induced by ergot derivative dopamine agonist drugs: time to change treatment guidelines in Parkinson's disease?]. 1580

A 76-year-old woman was admitted to our hospital with a 2-month history of increasing abdominal distension, leg edema, and dyspnea. The serum transaminase level was about twice the upper limit of normal. The CT showed no tumor. Fluorine-18 2-deoxy-2-fluoro-D-glucose (FDG)-positron emission tomography (PET) showed diffuse abnormal accumulation throughout the entire liver. She was diagnosed by histopathological examination as having hepatic angiosarcoma causing veno-occlusive disease (VOD). This is the first report of hepatic angiosarcoma with FDG-PET.
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PMID:A case of diffuse hepatic angiosarcoma diagnosed by FDG-PET. 1624 91

A common challenge for primary care physicians is to determine the cause and find an effective treatment for leg edema of unclear etiology. We were unable to find existing practice guidelines that address this problem in a comprehensive manner. This article provides clinically oriented recommendations for the management of leg edema in adults. We searched on-line resources, textbooks, and MEDLINE (using the MeSH term, "edema") to find clinically relevant articles on leg edema. We then expanded the search by reviewing articles cited in the initial sources. Our goal was to write a brief, focused review that would answer questions about the management of leg edema. We organized the information to make it rapidly accessible to busy clinicians. The most common cause of leg edema in older adults is venous insufficiency. The most common cause in women between menarche and menopause is idiopathic edema, formerly known as "cyclic" edema. A common but under-recognized cause of edema is pulmonary hypertension, which is often associated with sleep apnea. Venous insufficiency is treated with leg elevation, compressive stockings, and sometimes diuretics. The initial treatment of idiopathic edema is spironolactone. Patients who have findings consistent with sleep apnea, such as daytime somnolence, loud [corrected] snoring, or neck circumference >17 inches, should be evaluated for pulmonary hypertension with an echocardiogram. If time is limited, the physician must decide whether the evaluation can be delayed until a later appointment (eg, an asymptomatic patient with chronic bilateral edema) or must be completed at the current visit (eg, a patient with dyspnea or a patient with acute edema [<72 hours]). If the evaluation should be conducted at the current visit, the algorithm shown in Figure 1 could be used as a guide. If the full evaluation could wait for a subsequent visit, the patient should be examined briefly to rule out an obvious systemic cause and basic laboratory tests should be ordered for later review (complete blood count, urinalysis, electrolytes, creatinine, blood sugar, thyroid stimulating hormone, and albumin).
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PMID:Approach to leg edema of unclear etiology. 1651 3

Physical examination demonstrated petechiae, leg oedema and mild dyspnoea. Chest radiograph showed minimal bilateral hazy increased opacification, mainly on the right side, and small bilateral pleural effusions. High-resolution CT demonstrated extensive bilateral ground-glass opacities most severe in the middle and lower lung zones. Also noted were a few slightly thickened interlobular septa, a few poorly defined small nodules, bronchial wall thickening and small bilateral pleural effusions. Blood tests revealed high leukocyte and low platelet counts. Renal function was normal. Serological test (ELISA) for hantavirus using SNV (Sin Nombre virus) antigen was positive. The patient received supportive treatment, gradually improved, and was discharged 10 days after hospital admission. His symptoms completely resolved and follow-up radiographs returned to normal.
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PMID:Hantavirus pulmonary syndrome: high-resolution CT findings in one patient. 1726 65

We report a patient with adenocarcinoma of the prostate, who eventually developed Cushing syndrome due to ectopic adrenocorticotropic hormone (ACTH) secretion from the tumor. At first, maximal androgen blockade (MAB) therapy was effective for the prostate carcinoma, which was positive for prostate-specific antigen (PSA) and negative for ACTH on the biopsy specimen. However, 3 years later, the patient complained of bilateral leg edema. A chest computed tomographic (CT) scan showed bilateral pleural effusion and inflammatory changes, focused on the right upper-lobe. While his PSA was not elevated, and there were no obvious tumor metastases, his serum cortisol and ACTH levels were elevated, without any evidence of lesions that could release ectopic ACTH. Two weeks later, the patient complained of dyspnea and bilateral pleural effusion, and inflammatory changes were worse. Although the patient was administered inhibitors of adrenocorticoid synthesis-metyrapone, they did not have enough clinical efficiency. Steroid pulse therapy was also administered but the patient's severe pneumonia and pleural effusion did not improve and he finally died of respiratory failure. In contrast to the initial biopsy specimen findings, on autopsy, the tumor was negative for PSA but positive for ACTH. Thus, it would appear that the tumor began to produce and release ectopic ACTH after therapy, which resulted in the development of Cushing syndrome in this patient with prostate carcinoma.
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PMID:Cushing syndrome associated with prostatic tumor adrenocorticotropic hormone (ACTH) expression after maximal androgen blockade therapy. 1751 28


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