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

The current interest in understanding the role of stress-induced cytokines in heart failure relates to the observation that many of the untoward pathophysiologic responses of the failing circulation might be explained by these compounds. These small molecules appear to cause left ventricular dysfunction, precipitate pulmonary edema, cause cardiomyopathy, reduce peripheral organ perfusion, induce ventricular remodeling, activate the fetal gene program in animal models, and cause anorexia and cachexia. Thus, the elaboration of cytokines, similar to the upregulation of neurohormones, may represent a biochemical mechanism that is responsible for producing symptoms and remodeling in heart failure patients. To better understand how cytokines play a role in heart failure, it is important to delineate the concept of cytokine bioactivity in this setting.
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PMID:Cytokines and heart failure. 1042 71

Unusual clinical and pathological observations in the field in goats and sheep suffering from Strongyloides papillosus infection prompted experimental work on this parasite. Goats were infected percutaneously with either single or multiple, low or high levels of S. papillosus. Young goats up to 12 months of age were found to be the most susceptible. Some animals, however, showed substantial resistance to infective doses. Clinical signs included transient diarrhoea, misshapen, elongated faecal pellets terminally, dehydration, anorexia, cachexia, gnashing of teeth, foaming at the mouth, anaemia and nervous signs such as ataxia, a wide-based stance, stupor and nystagmus. A 'pushing syndrome' was seen in 22% of the animals. The pathological changes are described and included enteritis, status spongiosus in the brain, hepatosis leading to rupture of the liver, nephrosis, pulmonary oedema, interstitial pneumonia and pneumonia. About 6% of the goats died acutely from fatal hepatic rupture. The development of an acquired immunity was determined. The immunity elicited an allergic skin reaction at the application site of larvae or injection sites of larval metabolites. This immunity, however, could be breached by large doses of larvae. The most profound clinicopathological changes induced by the parasites were an anaemia (most pronounced in the young goats) and hypophosphataemia. Trace element analyses provided evidence of Cu, Mn and possibly Se deficiencies in some goats.
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PMID:Experimental studies with Stronglyloides papillosus in goats. 1063 9

From 1994 to 1999, 16 captive African hedgehogs (Atelerix albiventris), from among 42 necropsy cases, were diagnosed with cardiomyopathy. The incidence of cardiomyopathy in this study population was 38%. Fourteen of 16 hedgehogs with cardiomyopathy were males and all hedgehogs were adult (>1 year old). Nine hedgehogs exhibited 1 or more of the following clinical signs before death: heart murmur, lethargy, icterus, moist rales, anorexia, dyspnea, dehydration, and weight loss. The remaining 7 hedgehogs died without premonitory clinical signs. Gross findings were cardiomegaly (6 cases), hepatomegaly (5 cases), pulmonary edema (5 cases), pulmonary congestion (4 cases), hydrothorax (3 cases), pulmonary infarct (1 case), renal infarcts (1 case), ascites (1 case), and 5 cases showed no changes. Histologic lesions were found mainly within the left ventricular myocardium and consisted primarily of myodegeneration, myonecrosis, atrophy, hypertrophy, and disarray of myofibers. All hedgehogs with cardiomyopathy had myocardial fibrosis, myocardial edema, or both. Other common histopathologic findings were acute and chronic passive congestion of the lungs, acute passive congestion of the liver, renal tubular necrosis, vascular thrombosis, splenic extramedullary hematopoiesis, and hepatic lipidosis. This is the first report of cardiomyopathy in African hedgehogs.
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PMID:Cardiomyopathy in captive African hedgehogs (Atelerix albiventris). 1102 39

Adult rats exposed to hyperoxia develop anorexia, weight loss, and a lung injury characterized by pulmonary edema and decreased lung liquid clearance. We hypothesized that maintenance of nutrition during hyperoxia could attenuate hyperoxia-induced pulmonary edema. To test this hypothesis, we enterally fed adult male Sprague-Dawley rats via gastrostomy tubes and exposed them to oxygen (inspired O(2) fraction >0.95) for 64 h. In contrast to controls, enterally fed hyperoxic animals did not lose weight and had smaller pleural effusions and wet-to-dry weight ratios (a measure of lung edema) that were not different from room air controls. Enterally fed rats exposed to hyperoxia had increased levels of mRNA for the Na(+)-K(+)-ATPase alpha(1)- and beta(1)-subunits and glutathione peroxidase. These findings suggest that maintenance of nutrition during an oxidative lung injury reduces lung edema, perhaps by allowing for continued expression and function of protective proteins such as the Na(+)-K(+)-ATPase.
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PMID:Continuous enteral nutrition attenuates pulmonary edema in rats exposed to 100% oxygen. 1105 23

Almost every second trekker or climber develops two to three symptoms of the high altitude illness after a rapid ascent (> 300 m/day) to an altitude above 4000 m. We distinguish two forms of high altitude illness, a cerebral form called acute mountain sickness and a pulmonary form called high altitude pulmonary edema. Essentially, acute mountain sickness is self-limiting and benign. Its symptoms are mild to moderate headache, loss of appetite, nausea, dizziness and insomnia. Nausea rarely progresses to vomiting, but if it does, this may anticipate a progression of the disease into the severe form of acute mountain sickness, called high altitude cerebral edema. Symptoms and signs of high altitude cerebral edema are severe headache, which is not relieved by acetaminophen, loss of movement coordination, ataxia and mental deterioration ending in coma. The mechanisms leading to acute mountain sickness are not very well understood; the loss of cerebral autoregulation and a vasogenic type of cerebral edema are being discussed. High altitude pulmonary edema presents in roughly twenty percent of the cases with mild symptoms of acute mountain sickness or even without any symptoms at all. Symptoms associated with high altitude pulmonary edema are incapacitating fatigue, chest tightness, dyspnoe at the minimal effort that advances to dyspnoe at rest and orthopnoe, and a dry non-productive cough that progresses to cough with pink frothy sputum due to hemoptysis. The hallmark of high altitude pulmonary edema is an exaggerated hypoxic pulmonary vasoconstriction. Successful prophylaxis and treatment of high altitude pulmonary edema using nifedipine, a pulmonary vasodilator, indicates that pulmonary hypertension is crucial for the development of high altitude pulmonary edema. The primary treatment of high altitude illness consists in improving hypoxemia and acclimatization. For prophylaxis a slow ascent at a rate of 300 m/day is recommended, if symptoms persist, acetazolamide at a dose of 500 mg/day is effective. Mild acute mountain sickness may also be treated with the same dose acetazolamide. Glucocorticoids are the first line treatment of the malignant form of acute mountain sickness. Nifedipine is effective only for the prophylaxis and treatment of high altitude pulmonary edema.
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PMID:[Mountaineering and altitude sickness]. 1144 1

A significant portion of the world's geography lies above 10,000 feet elevation, an arbitrary designation that separates moderate and high altitude. Although the number of indigenous people living at these elevations is relatively small, many people travel to high altitude for work or recreation, exposing themselves to chronic or intermittent hypoxia and the associated risk of acute mountain sickness (AMS) and less frequently, high altitude pulmonary edema (HAPE) and high altitude cerebral edema (HACE). The symptoms of AMS (headache, nausea, anorexia, fatigue, lassitude) occur in those who travel too high, too fast. Some investigators have linked the development of these symptoms with the condition of altered blood-brain barrier permeability, possibly related to hypoxia induced free radical formation. The burden of oxidative stress increases during the time spent at altitude and may even persist for some time upon return to sea level. The physiological and medical consequences of increased oxidative stress engendered by altitude is unclear; indeed, hypoxia is believed to be the trigger for the cascade of signaling events that ultimately leads to adaptation to altitude. These signaling events include the generation of reactive oxygen species (ROS) that may elicit important adaptive responses. If produced in excess, however, these ROS may contribute to impaired muscle function and reduced capillary perfusion at altitude or may even play a role in precipitating more serious neurological and pulmonary crisis. Oxidative stress can be observed at altitude without strenuous physical exertion; however, environmental factors other than hypoxia, such as exercise, UV light exposure and cold exposure, can also contribute to the burden. Providing antioxidant nutrients via the diet or supplements to the diet can reduce oxidative stress secondary to altitude exposure. In summary, the significant unanswered question concerning altitude exposure and antioxidant supplementation is when does oxidative stress become potentially damaging enough to merit antioxidant therapy and conversely, what degree of oxidative stress is necessary to foster the adaptive response of altitude exposure?
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PMID:Work at high altitude and oxidative stress: antioxidant nutrients. 1232 88

The authors encountered a case of portal-systemic venous shunt newly diagnosed after initiation of hemodialysis. A 68-year-old Japanese woman began hemodialysis because of symptoms of uremia including loss of appetite and pulmonary edema. Loss of consciousness occurred suddenly after her ninth session of hemodialysis. No hepatic functional abnormality was found other than hyperammonemia (314 microg/dL [184 micromol/L]). Loss of consciousness subsequently occurred often after hemodialysis. Color Doppler ultrasonography and magnetic resonance angiography depicted a large shunt between the left gastric vein and left renal vein resulting in portal flow entering the systemic circulation via the renal vein. Because the shunt was large, ligation of it was performed surgically. Results of histologic examination of a liver biopsy specimen obtained intraoperatively were normal. The patient became well postoperatively. This patient's encephalopathy appeared to be caused by the flow of ammonia-rich portal venous blood into the systemic circulation via the large shunt owing to a decrease in intravenous pressure after rapid hemodialysis. Portal-systemic shunt encephalopathy should be recognized as a "new" neuropsychiatric disorder characteristic of patients undergoing hemodialysis.
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PMID:Hemodialysis-related portal-systemic encephalopathy. 1533 38

Thallotoxicosis is described in an adult Pit Bull Terrier. The dog exhibited anorexia, emesis, weakness, conscious proprioceptive deficits, and a hemorrhagic diarrhea before death. A severe, acute necrotizing enterocolitis was evident upon histological examination, as was a multifocal to coalescing pulmonary edema. Liver and kidney thallium concentrations were 18 and 26 ppm, respectively. The source of the thallium was determined to be thallium sulfate obtained by a person with the intent to harm family members. Although thallium has not been produced in the United States for 20 years, this report demonstrates the need to consider thallium toxicosis as a differential diagnosis for animals presenting with vague and mixed gastrointestinal and neurological signs.
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PMID:Thallium toxicosis in a Pit Bull Terrier. 1656 74

A 10-yr-old male gorilla (Gorilla gorilla gorilla) with a history of conspecific bite wounds was evaluated for acute onset of depression, anorexia, and right hemiparesis. The animal was immobilized for diagnostic examination and treatment for suspected toxic shock from a necrotizing, emphysematous wound infection, but was euthanized due to complications during recovery. Gross and histopathologic examination revealed acute necrotizing myositis, fasciitis, cellulitis, and emphysema in the affected wound area, with large numbers of large Gram-positive rods among necrotic muscle fibers. Severe pulmonary edema with airways containing fibrin, acute hemorrhage in multiple body sites, thrombosis in blood vessels in the skeletal muscle, liver, and lung, and lymph node hyperplasia with lymphoid necrosis and hemorrhage. Immunohistochemical fluorescent antibody staining of muscle from the wound site was positive for
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PMID:Clostridium septicum myositis in a western lowland gorilla (Gorilla gorilla gorilla). 1731 73

Diuretics, especially thiazide-type diuretics, are widely used in the treatment of essential hypertension. The most frequent adverse reactions are hypotension, photosensitivity, hypokalaemia, anorexia and epigastric distress. Life-threatening adverse reactions are rare. We report a case of pulmonary oedema associated with low left ventricular filling pressures and hypotension, occurring in a patient shortly after ingestion of 12.5 mg of hydrochlorothiazide (HCTZ). By reviewing the literature (Medline search) 49 similar cases were found. We compared the findings of all these patients in an attempt to reveal the underlying mechanism of this non-cardiogenic pulmonary oedema and shock. We believe that an allergic type III reaction is most likely the underlying mechanism of this adverse drug reaction to HCTZ. It is important to recognize the causality of the symptoms of this rare but life-threatening side effect of thiazide-type diuretics, in order to stop the drug intake immediately and to prevent any unthoughtful reinitiation of this treatment.
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PMID:Hydrochlorothiazide-associated noncardiogenic pulmonary oedema and shock: a case report and review of the literature. 1753 14


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