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

Although revascularization of renal artery stenosis (RAS) from fibromuscular dysplasia (FMD) generally yields satisfying outcomes, traditional approaches to revascularization for atherosclerotic renal artery stenosis (ARAS) have been suboptimal because of the invasiveness, relatively high perioperative morbidity and mortality rates of surgery, and the low rates of technical success and long-term patency with percutaneous renal balloon angioplasty (PTA). Endovascular stents have been deployed for failed PTA (unsatisfactory results or complications) and treatment of restenotic lesions. Compared to PTA, primary stenting of ostial ARAS gives superior technical success rates greater than 95% and improved long-term patency. Curing hypertension after RAS revascularization is rare (< 10%). Improved control with fewer medications is a more realistic goal. Renal function as judged by serum creatinine improves in 20% to 30%, stabilizes in 40% to 60%, and deteriorates in 20% to 30% of patients whose renal function is impaired initially. One study demonstrated successful stenting slowed the rate of progression of renal failure in 89% of patients whose serum creatinine was less than 400 mol/L. Complications of renal artery stenting may be substantial, though procedure-related mortality is low. Patient selection for renal revascularization remains controversial. Those with renovascular disease and uncontrolled hypertension, progressive renal failure, or recurrent flash pulmonary edema should be carefully considered for renal artery stenting in experienced centers.
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PMID:Renal Artery Stent Placement: Indications and Results. 1109 60

The objective of this study was to determine prospectively which risk factors require cardiac monitoring for blunt cardiac injury (BCI) following blunt chest trauma. All patients who sustained blunt chest trauma had an electrocardiogram (ECG) on admission to our urban level I trauma center. Those with ST segment changes, dysrhythmias, hemodynamic instability, history of cardiac disease, age > 55 years, or a need for general anesthesia within 24 hours (group 1) were admitted to the intensive care unit (ICU) for 24 hours where they were subjected to serial ECGs, creatinine phosphokinase (CPK) assays, and echocardiography (ECHO). Those with only mechanism for BCI, i.e., none of the above risk factors (group 2), were admitted to a nonmonitored bed and had a follow-up ECG 24 hours later. A series of 315 patients were admitted with blunt chest trauma during a 17-month period; 144 patients were in group 1 and 171 in group 2. Overall, 22 patients were diagnosed as BCI (+BCI), defined as evolving ST segment changes, dysrhythmias, a CPK-MB index of > 2.5, or hemodynamic instability. Of the 18 +BCI patients in group 1, all were symptomatic (i.e., none was included solely for a cardiac history, age, or need for general anesthesia). Six of these patients required treatment for dysrhythmias, hypotension, or pulmonary edema; one of whom died. Four patients with +BCI were in group 2 and had ECG changes at 24 hours; none of these four had any sequelae from their +BCI. None of the ECHOs demonstrated abnormal wall motion. Patients who sustain blunt chest trauma with a normal ECG, normal blood pressure, and no dysrhythmias on admission require no further intervention for BCI. Patients with ST segment changes, dysrhythmias, or hypotension following blunt chest trauma should be monitored for 24 hours, as this subgroup occasionally requires further treatment for complications of BCI. ECHO adds nothing as a screening test.
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PMID:Determining which patients require evaluation for blunt cardiac injury following blunt chest trauma. 1121 49

The study was conducted in 35 cases of acute tubular necrosis of varied aetiology. Cases were divided in 2 groups, Group A--17 cases treated conservatively and Group B--18 cases managed by early haemodialysis. Criteria for early haemodialysis were blood urea < 120 mg% and serum creatinine < 7 mg%. Before starting therapy both the groups had comparable biochemical and renal parameters (p > 0.05). Overall mortality was lower in Group B as compared to Group A (22.2% Vs 29.4). Complication events such as uraemic encephalopathy, pulmonary oedema, haematemesis and malena, thrombophlebitis and vomiting were significantly lower in Group B (p < 0.05). Hospital stay was also significantly lower (p < 0.05) in Group B (18 +/- 2.5 days Vs 28 +/- 3 days), this can reduce the cost of treatment also.
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PMID:Early haemodialysis in acute tubular necrosis. 1122 83

The Hantavirus pulmonary and cardiovascular syndrome (HPCVS) is an emerging disease in Brazil. In this study, eight confirmed cases of HPCVS were studied. All the patients presented fever and dyspnea as well as thrombocytopenia and hypoxemia. Tachycardia, malaise, hypotension and lung rales occurred in 75 to 87.5% of the cases. Hemoconcentration, blood cell count increased and immature neutrophils, and high levels of creatinine were observed in 75 to 87.5%. Intravenous liquid infusion, the use of drugs for increasing systemic vascular resistance and inotropism, and mechanic ventilation were used for the patients. Mechanical ventilation and volume administration should be started precociously, preferable in intensive care units employing recommended universal and respiratory precautions. Careful volume administration should be limited if signs of pulmonary edema develop. Mortality (50%) is high and probably related to the severity of the disease as well as to a delayed attending of the patients for intensive management. It is important to report hantaviruses and HPCVS to the Brazilian medical community considering that many cases could be undiagnosed.
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PMID:[Hantavirus pulmonary and cardiovascular syndrome: epidemiology, clinical presentation, laboratory diagnosis and treatment]. 1134 Apr 92

Patients with atherosclerotic renal artery stenosis may develop hypertension, recurrent pulmonary edema and chronic renal failure, but have a much higher risk of dying from stroke or myocardial infarction than of progressing to end-stage renal disease. Indeed, atherosclerotic renal artery stenosis typically occurs in high risk patients with coexistent vascular disease elsewhere. Recent controlled trials comparing medication to revascularization have shown that only a minority of such patients can expect hypertension cure, whereas the results of trials designed to document the ability of revascularization to prevent progressive renal failure are not yet available. Revascularization should be undertaken in patients with atherosclerotic renal artery stenosis and resistant hypertension or heart failure, and probably in those with rapidly deteriorating renal function or with an increase in plasma creatinine levels during angiotensin-converting enzyme inhibition, especially if their renal resistance--index before revascularization is less than 80. With or without revascularization, medical therapy using antihypertensive agents, statins and aspirin is necessary in almost all cases.
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PMID:[Management of atherosclerotic renal artery stenoses]. 1207 Aug 43

Most recently we have shown that 4-aminotetrahydrobiopterin (4-ABH4), an analogue of tetrahydrobiopterin (cofactor of NO synthase), even administered 2 h after endotoxin challenge, improves survival rate in rats. The following experiment was performed to examine the effects of 4-ABH4 with respect to endotoxin-induced hemodynamic alterations and organ failure. At 2 h after endotoxic challenge (10 mg kg(-1) body weight) animals received 4-ABH4 at a dose of 1, 10, or 100 mg kg(-1) body weight. The controls were treated similarly but received saline at the same volume. Eight hours after endotoxin challenge cardiac index and stroke volume were significantly increased in animals treated with 10 mg 4-ABH4 compared to controls (0.23 +/- 0.06 vs. 0.16 +/- 0.04 mL min(-1) kg(-1) and 0.29 +/- 0.05 vs. 0.22 +/- 0.03 mL beat(-1)) while mean arterial pressure and peripheral vascular resistance index did not significantly differ among the groups. Plasma alanine aminotransferase (ALT) and creatinine levels were significantly increased in endotoxin controls compared with laboratory controls (ALT: 1643 +/- 1436 vs. 74 +/- 17 U L(-1); Creatinine: 91 +/- 29 vs. 42 +/- 3 micromol L(-1)) which was attenuated in animals treated with 10 mg kg(-1) 4-ABH4 (ALT: 417 +/- 318 U L(-1); Creatinine: 78 +/- 26 micromol L(-1)). Moreover, endotoxin-induced lung edema and intestinal necrosis were significantly reduced by 4-ABH4. Our study provides information that tetrahydrobiopterin analogue, 4-ABH4, improves LPS induced hemodynamic conditions and organ injury. This may, at least in part, account for the previously observed protection of rats by 4-ABH4 against endotoxin-induced mortality in the same endotoxic shock model.
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PMID:A 4-amino analogue of tetrahydrobiopterin attenuates endotoxin-induced hemodynamic alterations and organ injury in rats. 1216 80

Severe or complicated malaria is defined by infestation by Plasmodium falciparum into all red blood cells, especially those in the brain, causing coma and repeated convulsions; severe anemia (6 g/dl hemoglobin, 20% hematocrit); renal insufficiency (265 mcmol/l creatinine, 400 ml/day diuresis); pulmonary edema; hypoglycemia (2.2 ml/l or 0.4 g/l); shock; diffuse hemorrhaging; massive hemoglobinuria; and blood acidosis. Other possible symptoms of severe malaria are clouded thinking, changes in behavior, and inability to focus. It is most common in people with no immunity to malaria (children aged 4 and travelers in endemic zones). Pregnancy, splenectomy, corticotherapy, or poorly maintained immunity status favor severe anemia in adults. Sources of chloroquine-resistant P. falciparum have existed since 1960. Resistance has since expanded from Southeast Asia and South America to Africa, posing treatment problems. Malaria usually begins with fever (40 or more degrees Celsius), headaches, muscular pain, digestive troubles (e.g., diarrhea, nausea, or vomiting), and abdominal pain. In suspected cases of malaria, a blood sample or a thick blood smear as well as treatment (even in the absence of parasitological proof) needs to be done as soon as possible. Intravenous quinine diluted in a 5-10% glucose solution should be delivered at a rate of 24 mg/kg/day. In the case of severe jaundice, the dose should be cut in half beginning 8 hours after treatment began. If intravenous delivery is impossible, intramuscular delivery should be done. Corticosteroids, anticoagulants, and aspirin are contraindicated. In 2-4 days, oral administration (chloroquine, halofantrine, or mefloquine) is warranted. 20% of malaria-related deaths among patients who receive treatment are due to complications of the central nervous system. Protection against mosquito bites prevents malaria. Chemoprophylaxis in endemic zones should be limited to short trips to malaria zones or to pregnant women.
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PMID:[Severe malaria]. 1229 Jan 83

Three hundred sixty-seven male Wistar rats were used to compare the efficiency of urea cycle amino acids (arginine, citrulline and ornithine; Group O), furosemide (Group F), and fluid therapy (saline solution; Group FT) to treat ammonia toxicity. Rats were injected ip initially with an ammonium acetate solution at 99.9% of the lethal dose. Three min later the rats were allocated randomly to Group C (control, received 1.2 mL distilled water). Group O (amino acids listed earlier, 2 mmol/kg bw), Group F (furosemide, 2 mg/kg bw), Group FT (7mL saline), or Groups O+F, O+FT, F+FT, or O+F+FT. All treatments were given ip except for Group F given im injections. Plasma ammonia, urea and creatinine, and hematocrit and pulmonary dry matter were determined. The highest survival rates were obtained with O+FT (57%) and O+F+FT (62.5%); only 6% of the controls survived. Plasma ammonia levels were ten-fold lower in rats treated with O+FT and O+F+FT (p<0.0001). Fatally-poisoned rats had higher plasma ammonia, creatinine and hematocrit and exhibited pulmonary edema. Surviving rats had lower plasma urea. Animals given treatments with O, FT and F had (p<0.005) higher urea, lower creatinine and less severe pulmonary edema, respectively, than those untreated.
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PMID:Treatment of ammonia intoxication in rats with urea cycle amino acids, furosemide and fluids. 1267 88

The clinical diagnosis of renal artery stenosis relies on a high index of suspicion and confirmation by noninvasive imaging modalities. There are three distinct clinical syndromes associated with renal artery stenosis: renin-dependent hypertension, essential hypertension, and ischemic nephropathy. Clinical features that should heighten suspicion for renal artery stenosis include abrupt-onset or accelerated hypertension at any age, unexplained acute or chronic azotemia, azotemia induced by angiotensin-converting enzyme (ACE) inhibitors, asymmetric renal dimensions, and congestive heart failure with normal ventricular function. Patients with true renin-dependent (renovascular) hypertension are typically young or middle-age women with renal fibromuscular dysplasia (FMD). Initial therapy for renovascular hypertension associated with FMD is an ACE inhibitor; refractory hypertension responds readily to balloon angioplasty without stenting. Elderly patients with generalized atherosclerosis and hypertension often have atherosclerotic renal artery stenosis (ARAS); hypertension in these patients is usually not renin dependent (ie, essential hypertension). Hypertension alone, even if treated with multiple medications, is not a compelling indication for renal artery revascularization; these patients should be treated aggressively with antihypertensive medical therapy. Renal artery revascularization with stenting may be considered for refractory severe hypertension, and would be expected to improve blood control and modestly reduce medication requirements. Renal revascularization rarely cures hypertension in patients with ARAS. Patients with ARAS, hypertension, and end-organ injury should be considered for renal revascularization. Manifestations of end-organ injury include nonischemic pulmonary edema; hypertensive crisis associated with acute coronary syndrome, aortic dissection, or neurologic impairment; and renal insufficiency. Ischemic nephropathy is best treated before the development of advanced renal failure. The best candidates for revascularization are those with baseline serum creatinine less than 2.0 mg/dL, bilateral renal artery stenosis, normal renal resistive indices, no proteinuria, and one or more manifestations of end-organ injury. In these patients, renal revascularization is best accomplished by stenting, although surgical revascularization may be considered in patients with concomitant severe aortic aneurysmal or occlusive disease.
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PMID:Atherosclerotic Renal Artery Stenosis. 1268 6

Renal artery stenosis (RAS) may cause hypertension, azotemia, episodes of flash pulmonary edema and congestive heart failure. Renal artery angioplasty and stenting was performed in 207 patients from 1991 to 1997. Thirty-nine of these patients (19%) underwent renal artery stenting for the control of recurrent episodes of congestive heart failure and flash pulmonary edema. All patients had angiographic evidence of severe (>70%) bilateral RAS (n = 18) or severe RAS to a solitary functioning kidney (n = 21). Sixteen patients (41%) were male and 23 (59%) were female, mean age 69.9 years (range 50-85 years). Of the 18 patients with bilateral RAS, 12 (66.6%) underwent bilateral stenting. Mean blood pressure decreased from 174/85 +/- 32/23 mmHg to 148/72 +/- 24/14 mmHg (p < 0.001). Mean number of blood pressure medications decreased from 3 +/- 1 to 2.5 +/- 1 (p = 0.006). Twenty-eight patients (71.8%) had improvement in blood pressure control. The mean serum creatinine decreased from 3.16 +/- 1.61 to 2.65 +/- 1.87 (p = 0.06). Six of 39 patients (15.4%) used angiotensin converting enzyme (ACE) inhibitors prior to stenting whereas 19 of 39 patients (48.7%) used ACE inhibitors poststenting (p = 0.004). Twenty of 39 patients (51.4%) demonstrated improvement in serum creatinine, 10 of 39 patients (25.6%) had stabilization of serum creatinine and nine of 39 patients (23%) demonstrated worsening. The number of hospitalizations due to congestive heart failure in the year preceding renal artery stenting was 2.4 +/- 1.4 and poststenting was 0.3 +/- 0.7 (p < 0.001). The New York Heart Association Functional Class decreased from 2.9 +/- 0.9 prestenting to 1.6 +/- 0.9 poststenting (p < 0.001). Thirty of 39 patients (77%) had no hospitalizations for congestive heart failure during a mean follow-up period of 21.3 months. Nine patients expired during the course of follow up; eight of the nine patients died within the first year after renal artery stenting. Renal artery stenting decreased the frequency of congestive heart failure, flash pulmonary edema, and the need for hospitalization in most patients. Blood pressure was markedly improved in the majority of patients with improved or stabilized renal function. Evaluation for RAS is important in hypertensive patients who present with recurrent congestive heart failure or flash pulmonary edema.
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PMID:Clinical benefit of renal artery angioplasty with stenting for the control of recurrent and refractory congestive heart failure. 1271 Aug 43


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