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

While cholera is not endemic in Taiwan, the number of imported cases is increasing. We report a 59-year-old Taiwanese male who developed severe diarrhea and vomiting, two days after returning from Bali. The patient admitted drinking a beverage with ice purchased from a street vendor. On admission he was weak and dehydrated. The patient suffered from hypovolemic shock and acute renal failure. Elevated creatine phosphokinase indicated rhabdomyolysis. Fluid replacement with Ringer's lactate solution was instituted. Dyspnea and pulmonary edema developed, and hemodialysis was begun to remove excess fluid due to decreased urinary output. Isolation of Vibrio cholerae O1 from stool confirmed the diagnosis of cholera, and doxycyline was begun. The patient's condition stabilized, with increased urinary output, and resolution of diarrhea, vomiting and dyspnea. Cholera, although rare in Taiwan, can be lethal if left untreated. Rapid intervention with fluid replacement is essential to prevent hypovolemic shock and circulatory collapse in severe cases.
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PMID:Cholera associated with acute renal failure and rhabdomyolysis: a case report. 904 70

Antiarrhythmic treatment (AAT) adjusted to the variety of arrhythmia and risk to develop complications was given to 336 patients with ischemic heart disease associated with paroxysms of supraventricular tachycardia (SVT), atrial fibrillation or atrial flutter. In the presence of risk to develop AAT complications, the method of choice for SVT patients is transesophageal pacing and impulse therapy. In the presence of arrhythmic collapse, cardiac asthma and pulmonary edema it is preferable to correct arrhythmia by electric impulse therapy.
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PMID:[The treatment of paroxysmal supraventricular arrhythmias in IHD patients with a high risk of developing complications from the anti-arrhythmic therapy]. 908 3

Genes of an influenza A (H5N1) virus from a human in Hong Kong isolated in May 1997 were sequenced and found to be all avian-like (K. Subbarao et al., Science 279:393-395, 1998). Gene sequences of this human isolate were compared to those of a highly pathogenic chicken H5N1 influenza virus isolated from Hong Kong in April 1997. Sequence comparisons of all eight RNA segments from the two viruses show greater than 99% sequence identity between them. However, neither isolate's gene sequence was closely (>95% sequence identity) related to any other gene sequences found in the GenBank database. Phylogenetic analysis demonstrated that the nucleotide sequences of at least four of the eight RNA segments clustered with Eurasian origin avian influenza viruses. The hemagglutinin gene phylogenetic analysis also included the sequences from an additional three human and two chicken H5N1 virus isolates from Hong Kong, and the isolates separated into two closely related groups. However, no single amino acid change separated the chicken origin and human origin isolates, but they all contained multiple basic amino acids at the hemagglutinin cleavage site, which is associated with a highly pathogenic phenotype in poultry. In experimental intravenous inoculation studies with chickens, all seven viruses were highly pathogenic, killing most birds within 24 h. All infected chickens had virtually identical pathologic lesions, including moderate to severe diffuse edema and interstitial pneumonitis. Viral nucleoprotein was most frequently demonstrated in vascular endothelium, macrophages, heterophils, and cardiac myocytes. Asphyxiation from pulmonary edema and generalized cardiovascular collapse were the most likely pathogenic mechanisms responsible for illness and death. In summary, a small number of changes in hemagglutinin gene sequences defined two closely related subgroups, with both subgroups having human and chicken members, among the seven viruses examined from Hong Kong, and all seven viruses were highly pathogenic in chickens and caused similar lesions in experimental inoculations.
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PMID:Comparisons of highly virulent H5N1 influenza A viruses isolated from humans and chickens from Hong Kong. 965 15

Malaria remains an overwhelming problem in tropical developing countries, with 300 to 500 million new cases and 1.5 to 3.5 million deaths per year. Malaria is a potentially life-threatening disease for travelers to the tropics. Imported malaria is an important clinical problem in nonendemic areas of the world because of increasing numbers of travelers, overseas workers, and immigrants from endemic areas. According to the World Health Organization's criteria, the recognition of one or more of the following clinical features should raise the suspicion of severe malaria: cerebral malaria (unrousable coma), severe anemia (hemoglobin <5 g/dL), renal failure (serum creatinine >3 mg/dL), pulmonary edema or adult respiratory distress syndrome, hypoglycemia (glucose <40 mg/dL), circulatory collapse or shock, disseminated intravascular coagulation, repeated generalized convulsions, acidosis (pH <7.25), macroscopic hemoglobinuria, hyperparasitemia (>5 percent of the erythrocytes infested by parasites), or jaundice (bilirubin >3 mg/dL). Although only a small proportion of patients with malaria develops severe manifestations, these patients require the most urgent and intensive care. Mortality among patients with cerebral malaria, even when treated in modern intensive care units, exceeds 30%, and when complicated by the adult respiratory distress syndrome, it may approach 80%. Among travelers, mortality remains a serious issue because of failure to obtain and use preventive measures, delay in seeking medical attention, and misdiagnosis.
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PMID:Imported severe falciparum malaria in Israel. 977 25

During an outbreak of hand-foot-mouth disease caused by enterovirus 71 (EV-71) in 1997, 4 children presented with sudden cardiopulmonary collapse and minimal neurologic features. All children received cardiopulmonary resuscitation but died within a few hours of admission. Postmortem studies showed infection by EV-71 with extensive damage to the medulla and pons. We postulate an etiologic link between EV-71 and brainstem encephalomyelitis as the cause of pulmonary edema and death.
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PMID:Fatal enterovirus 71 encephalomyelitis. 984 48

The effects of long-term preoperative administration of low-dose erythromycin (EM) were experimentally examined in relation to the treatment of reperfusion disorders following pulmonary thermal ischemia. EM was administered at a dose of 100 mg/day for 1 month to adult mongrel dogs with an average weight of about 12 kg (EM group). A control group that did not receive EM was also enrolled. Using a pulmonary autograft model, collapse-thermal ischemia of the lungs was performed on each animal for 60 minutes. In the early stage of reperfusion, the following measurements were assessed: gas-exchange potency in the left lung, hemodynamics, water content, adhesion of neutrophils to vascular endothelium, and concentration of blood eicosanoids. The results for the 2 groups were then compared. In the control group, the blood level of leukotriene B4 (LTB4) increased shortly after reperfusion, neutrophils migrated toward the vascular endothelium and adhered to it, and pulmonary edema developed after 1 hour. However in the EM group, the blood level of thromboxane B2 was significantly suppressed before and after hilar stripping, and the increase in the blood LTB4 level and the migration of neutrophils shortly after reperfusion in thermal ischemia were suppressed. Eventually alleviation of pulmonary edema was indicated and significantly improved gas exchange was maintained. In conclusion, pulmonary injury during detachment of the hilum of the lung, as well as warm ischemia-reperfusion pulmonary injury, may be alleviated by preoperative administration of low-dose EM on a long-term basis.
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PMID:[Effects of long-term preoperative administration of low-dose erythromycin on warm ischemia-reperfusion pulmonary injury]. 991 77

Acute respiratory distress syndrome (ARDS) is a life-threatening lung injury that is characterized by arterial hypoxemia and noncardiogenic pulmonary oedema. One feature of ARDS is an alteration of pulmonary surfactant that increases surface tension at the air-liquid interface and results in alveolar collapse and the impairment of gas exchange. Type-II secretory phospholipase A2 (sPLA2-II) plays a major role in the hydrolysis of surfactant phospholipids and its expression is inhibited by surfactant. Here, we discuss the evidence that in pathological situations, such as ARDS, in which surfactant is altered, sPLA2-II production is exacerbated, leading to further surfactant alteration and the establishment of a vicious cycle.
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PMID:A role for phospholipase A2 in ARDS pathogenesis. 1036 19

Pulmonary surfactant is a complex and highly surface active material composed of lipids and proteins which is found in the fluid lining the alveolar surface of the lungs. Surfactant prevents alveolar collapse at low lung volume, and preserves bronchiolar patency during normal and forced respiration (biophysical functions). In addition, it is involved in the protection of the lungs from injuries and infections caused by inhaled particles and micro-organisms (immunological, non-biophysical functions). Pulmonary surfactant can only be harvested by lavage procedures, which may disrupt its pre-existing biophysical and biochemical micro-organization. These limitations must always be considered when interpreting ex vivo studies of pulmonary surfactant. A pathophysiological role for surfactant was first appreciated in premature infants with respiratory distress syndrome and hyaline membrane disease, a condition which is nowadays routinely treated with exogenous surfactant replacement. Biochemical surfactant abnormalities of varying degrees have been described in obstructive lung diseases (asthma, bronchiolitis, chronic obstructive pulmonary disease, and following lung transplantation), infectious and suppurative lung diseases (cystic fibrosis, pneumonia, and human immunodeficiency virus), adult respiratory distress syndrome, pulmonary oedema, other diseases specific to infants (chronic lung disease of prematurity, and surfactant protein-B deficiency), interstitial lung diseases (sarcoidosis, idiopathic pulmonary fibrosis, and hypersensitivity pneumonitis), pulmonary alveolar proteinosis, following cardiopulmonary bypass, and in smokers. For some pulmonary conditions surfactant replacement therapy is on the horizon, but for the majority much more needs to be learnt about the pathophysiological role the observed surfactant abnormalities may have.
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PMID:Pulmonary surfactant in health and human lung diseases: state of the art. 1044 27

Congenital aortic stenosis accounts for about 5% of cardiac malformations recognized in childhood. It belongs to the category of acyanotic congenital heart disease. These lesions produce a load on the heart because of left ventricular outflow tract obstruction. Severe aortic stenosis in the newborn period (critical aortic stenosis) presents with signs of left sided heart failure (pulmonary edema, poor perfusion), right sided heart failure (hepatomegaly, peripheral edema) and may progress rapidly to total circulatory collapse. We present a case of an infant with critical aortic stenosis presenting with cyanosis, who was entirely dependent on ductal patency for systemic output. When oxygen was given, the ductus started to close, with a worsening of the left sided output and subsequent acidosis. With the right to left shunt across the ductus, the baby was cyanotic and dependent on prostaglandin to keep the ductus open. There was minimal flow across the aortic valve because of the stenosis and extremely poor left ventricular function prior to surgery. After relief of the aortic valvular obstruction, there was finally good antegrade flow across the aortic valve, terminating cyanosis.
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PMID:One day old infant with acyanotic congenital heart disease: critical aortic stenosis. 1056 81

An unusual case diagnosed as connective tissue-type mast cell leukemia with marked mastocyte infiltration into visceral organs in a seven-year-old female Curly-Coated retriever is presented. Acute circulatory collapse, emesis, diarrhea, abdominal enlargement, icterus, cyanosis, dyspnea, pulmonary edema, hepatomegary, ascites, and right ventricular enlargement were observed. Hematologic and biochemical examinations revealed mast cell leukemia, mature neutrophilia, monocytosis, thrombocytopenia, hemolytic hyperbilirubinemia, hyperhistaminemia, renal and hepatic injuries. Mast cells were distributed systemically, but predominantly in the diaphragm and liver with a large mass among the serosa of ileum, cecum and colon. Mast cells were stained intensely by both safranin and berberine sulfate.
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PMID:Connective tissue-type mast cell leukemia in a dog. 1072 Jan 89


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