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

Malaria is a major cause of morbidity and mortality amongst adults in sub-Saharan Africa, but descriptions of symptoms and mortality in this group have received little attention in the past. A retrospective study was performed on adults admitted to a tertiary hospital in Tanzania with a primary diagnosis of malaria. Frequency and mortality for the criteria in the WHO definition of severe malaria were recorded. Logistic regression analysis was then used to identify symptoms with the greatest prognostic value. Two hundred and sixty-nine adults (median age 28 years) with a primary diagnosis of malaria were studied, with an overall mortality rate of 15.2%. Logistic regression identified three key prognostic indicators: unconsciousness (odds ratio (OR) 44.44; 95% CI 4.05-488.24), renal failure (OR 7.37; 95% CI 1.70-31.96) and pulmonary oedema (OR 13.83; 95% CI 3.52-54.32). Whilst the WHO criteria predicted all of the 41 adults who died, 37 (90.2%) had at least one of the following symptoms: unconsciousness (n=39, fatality rate 74.4%), renal failure (n=26, fatality rate 66.7%) and pulmonary oedema (n=28, fatality rate 64.3%). These symptoms can therefore identify those at a high risk of death in African adults with malaria.
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PMID:Indicators of mortality in African adults with malaria. 1672 43

Severe malaria is invariably caused by Plasmodium falciparum. In India, both adults and children are affected by severe malaria. However, children are more prone for developing anemia and convulsions as manifestations of severe malaria, while acute renal failure and jaundice are more common among adults. Pregnant women are vulnerable to hypoglycemia, anemia and pulmonary complications. The case-fatality rate due to severe malaria is 10-15% in spite of therapy but it increases in the presence of renal failure or respiratory distress (pulmonary edema or ARDS). Of late, multi-organ failure and high mortality figures are being reported increasingly from different parts of India. Early diagnosis and prompt treatment will reduce the mortality due to malaria. Cerebral malaria should always be suspected in a patient with altered sensorium in a malaria-endemic area. However, other causes of unconsciousness such as encephalitis, meningitis or hepatic coma should also be excluded. Parenteral quinine is the mainstay of therapy. A recent multi-centric study has demonstrated the efficacy of intravenous artesunate in reducing the mortality by 30%. The usefulness of adjunct therapy is still controversial.
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PMID:Management of severe and complicated malaria. 1710 47

Lung involvement in malaria has been recognized for more than 200 hundred years, yet our knowledge of its pathogenesis and management is limited. Pulmonary edema is the most severe form of lung involvement. Increased alveolar capillary permeability leading to intravascular fluid loss into the lungs is the main pathophysiologic mechanism. This defines malaria as another cause of acute lung injury (ALI) and acute respiratory distress syndrome (ARDS).Pulmonary edema has been described most often in non-immune individuals with Plasmodium falciparum infections as part of a severe systemic illness or as the main feature of acute malaria. P.vivax and P.ovale have also rarely caused pulmonary edema.Clinically, patients usually present with acute breathlessness that can rapidly progress to respiratory failure either at disease presentation or, interestingly, after treatment when clinical improvement is taking place and the parasitemia is falling. Pregnant women are particularly prone to developing pulmonary edema. Optimal management of malaria-induced ALI/ARDS includes early recognition and diagnosis. Malaria must always be suspected in a returning traveler or a visitor from a malaria-endemic country with an acute febrile illness. Slide microscopy and/or the use of rapid antigen tests are standard diagnostic tools. Malaria must be treated with effective drugs, but current choices are few: e.g. parenteral artemisinins, intravenous quinine or quinidine (in the US only). A recent trial in adults has shown that intravenous artesunate reduces severe malaria mortality by a third compared with adults treated with intravenous quinine. Respiratory compromise should be managed on its merits and may require mechanical ventilation.Patients should be managed in an intensive care unit and particular attention should be paid to the energetic management of other severe malaria complications, notably coma and acute renal failure. ALI/ARDS may also be related to a coincidental bacterial sepsis that may not be clinically obvious. Clinicians should employ a low threshold for starting broad spectrum antibacterials in such patients, after taking pertinent microbiologic specimens. Despite optimal management, the prognosis of severe malaria with ARDS is poor.ALI/ARDS in pediatric malaria appears to be rare. However, falciparum malaria with severe metabolic acidosis or acute pulmonary edema may present with a clinical picture of pneumonia, i.e. with tachypnea, intercostal recession, wheeze or inspiratory crepitations. This results in diagnostic confusion and suboptimal treatment. Whilst this is increasingly being recognized in malaria-endemic countries, clinicians in temperate zones should be aware that malaria may be a possible cause of 'pneumonia' in a visiting or returning child.
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PMID:Pulmonary manifestations of malaria : recognition and management. 1715 71

The cytoadhesion of Plasmodium falciparum-infected erythrocytes (IEs) to the endothelial cells lining the microvasculature, clogging the microvessels of various organs, is a key event in the pathogenesis of certain severe forms of malaria, such as cerebral malaria and pulmonary edema. Studies aiming to identify possible correlations between the severity of clinical cases and the presence of particular cytoadhesion phenotypes have been largely unsuccessful. One of the possible reasons for this failure is that some of the key receptors and/or mechanisms involved have yet to be identified. By combining IE selection, cell transfection, and adhesion inhibition assays, we identified a new cytoadhesion receptor, neural cell adhesion molecule (NCAM). NCAM is a member of the immunoglobulin superfamily and has nonpolysialylated and polysialylated isoforms, the latter being rare in adults. The nonpolysialylated form is present on the surfaces of endothelial cells in the microvessels of various organs in which IE sequestration occurs. We found that multiphenotypic IEs interacted with nonpolysialylated NCAM and with another, as yet unidentified receptor. These IEs also displayed cytoadhesion in flow conditions, presenting the unique ability to form adherent macroaggregates composed of hundreds of IEs. These features may act as virulence factors, increasing the capacity of IEs to clog microvessels via receptor synergy and macroaggregate formation, thereby facilitating the pathogenesis of severe forms of malaria.
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PMID:Neural cell adhesion molecule, a new cytoadhesion receptor for Plasmodium falciparum-infected erythrocytes capable of aggregation. 1748 55

Reported here is a rare case of babesiosis with pulmonary complications followed by a review of the literature. Babesiosis presents clinically as a malaria-like illness with fever, chills, headache, fatigue with lymphopenia, atypical lymphocytes, mildly or transiently elevated serum transaminases, thrombocytopenia, and increased lactate dehydrogenase (LDH) levels. The diagnosis of babesiosis is based on identification of Babesia spp. on a peripheral blood smear. Babesiosis is usually mild in normal hosts, but it may be severe or even fatal in asplenic patients. Pulmonary manifestations are rare in babesiosis, but non-cardiogenic pulmonary edema (NCPE) is the most frequent manifestation. NCPE in babesiosis does not appear to be related to the degree of parasitemia or splenic function and its onset may be early or late. NCPE usually resolves rapidly with supportive treatment; it is rarely fatal. Clinicians should suspect NCPE in patients with babesiosis who acutely develop shortness of breath and have chest radiograph findings compatible with acute pulmonary edema without cardiomegaly or pleural effusions.
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PMID:Pulmonary complications of babesiosis: case report and literature review. 1755 89

Pulmonary edema is a recognized complication of Plasmodium falciparum malaria but is uncommon with Plasmodium vivax infection. We report the case of a non-immune adult with imported P. vivax malaria who developed pulmonary edema during treatment. The case was further complicated by a recurrent malaria episode after failure of acute quinine and doxycycline treatment followed by terminal primaquine therapy. Prompt recognition and appropriate management of pulmonary edema is needed for optimal outcomes of P. vivax infection, as well as awareness of the potential failure of terminal therapy for liver hypnozoites.
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PMID:Pulmonary edema due to Plasmodium vivax malaria in an American missionary. 1772 40

The cytoadhesion of Plasmodium falciparum-infected erythrocytes (IEs) in organ microvessels is a key event in the pathogenesis of cerebral malaria and pulmonary edema. Identification of the molecules involved in the interaction between IEs and endothelial cells has been a major goal of research into severe forms of malaria. In contrast, the consequences of cytoadhesion for endothelial cells have been largely ignored. By combining phenotypic selection, cytoadhesion assays and flow cytometry, we demonstrated that the cytoadhesion of CSA-binding IEs inhibited the cytoadhesion of CD36-binding IEs. We identified CD44 as a signal receptor for CSA-binding IEs cytoadhesion, and demonstrated that the signal was transduced to CD36 through a pathway involving the Src-kinase family and MEK. CD36-mediated cytoadhesion was modulated independently of changes in CD36 expression. These results provide the first evidence that some IEs can downregulate the cytoadhesion of IEs of another phenotype, by modifying endothelial cells via a signaling pathway relating CD44 to CD36. Mimicking this phenomenon may constitute an interesting therapeutic strategy for inhibiting the adhesion of CD36-binding IEs -- the most abundant phenotype among field isolates -- and promoting their degradation in the spleen.
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PMID:CD44, a signal receptor for the inhibition of the cytoadhesion of CD36-binding Plasmodium falciparum-infected erythrocytes by CSA-binding infected erythrocytes. 1791 42

Fatal complications of Plasmodium falciparum malaria have been reported. However, complicated P. vivax malaria is rare. We observed two unusual cases of P. vivax malaria who presented with clinical pictures of toxic shock. Both showed disseminated intravascular coagulation with marked thrombocytopenia, oliguric renal failure, and pulmonary edema. Examination of initial blood smears showed a P. vivax parasitemia of 2,352/microL and 12,376/microL, respectively. The patients were treated with hydroxychloroquine and primaquine without an antibacterial agent. These cases emphasize the importance of considering the possibility of P. vivax malarial infection in patients with a clinical picture resembling toxic shock if they have a travel history to malaria-endemic areas.
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PMID:Two cases of Plasmodium vivax Malaria with the clinical picture resembling toxic shock. 1797 57

Acute renal failure (ARF) is seen mostly in Plasmodium falciparum infection, but P vivax and P. malariae can occasionally contribute for renal impairment. Malarial ARF is commonly found in non-immune adults and older children with falciparum malaria. Occurance of ARF in severe falciparum malaria is quite common in southeast Asia and Indian subcontinent where intensity of malaria transmission is usually low with occasional microfoci of intense transmission. Since precise mechanism of malarial ARF is not known, several hypotheses including mechanical obstruction by infected erythrocytes, immune mediated glomerular and tubular pathology, fluid loss due to multiple mechanisms and alterations in the renal microcirculation, etc, have been proposed. Increased fluid administration, oxygen toxicity, and yet unidentified factors may contribute to pulmonary edema, acute respiratory distress syndrome (ARDS), multiorgan failure and death. Mainstay of treatment consists of appropriate antimalarial drug therapy, fluid replacement, and renal replacement therapy. Loop diuretics can convert an oliguric renal failure to non-oliguric renal failure without affecting outcome of the disease though the conversion reduces the risk of volume overload. There is little evidence on beneficial effect of vasoactive drugs. Nephrotoxic drugs such as ACE inhibitors, NSAIDs, aminoglycosides, cephalosporins should be avoided. Currently, high quality intensive care, early institution of renal replacement therapy, and avoidance of nephrotoxic drugs are standard practice of the prevention and management of ARF.
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PMID:Renal failure in malaria. 1859 37

Fevers of unknown origin (FUOs) are defined as prolonged fevers of 101 degrees F or greater lasting 3 or more weeks that remain undiagnosed after comprehensive inpatient/outpatient laboratory testing. Tick-borne infections are uncommon causes of FUOs. Any infectious disease accompanied by prolonged fevers can present as an FUO if the diagnosis is not suspected or if specific laboratory testing is not done to confirm the diagnosis. Babesiosis is transmitted by the Ixodes scapularis ticks endemic to areas in the northeastern United States. We present the case of a 73-year-old, non-human immunodeficiency virus, male from Long Island who presented with FUO for 6 weeks. As with malaria, there are usually few or no localizing signs in babesiosis. During the patient's hospitalization, babesiosis was suspected on the basis of nonspecific laboratory findings, that is, relative lymphopenia, thrombocytopenia, thrombocytopenia, and an elevated lactate dehydrogenase. When babesiosis was considered in the differential diagnosis, stained blood smears demonstrated the red blood cell inclusions of babesiosis. In the hospital, the patient developed noncardiac pulmonary edema, which rapidly resolved which has been described as a rare complication of babesiosis. He also had an elevated immunoglobulin-M Lyme titer indicating coinfection with Lyme disease. Although his hemolytic anemia persisted for weeks, he only had 3% parasitemia and intact splenic function. We believe this to be the first case of babesiosis presenting as an FUO in a normal host.
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PMID:Fever of unknown origin (FUO) due to babesiosis in a immunocompetent host. 1899 33


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