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Query: UMLS:C0032285 (pneumonia)
 54,520 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

This communication documents the radiographic appearance of multiple rib infarcts that may develop during the course of patients with sickle cell states. It can be associated with and be the cause of the 'acute chest syndrome' which has traditionally be attributed, on scanty evidence, to lung infarcts and pneumonia. Bony changes take time to develop but extrapleural changes are readily detected in radiographs. The rib lesions repair leaving residual sclerosis. Sequestra do not develop. The pathogenesis may be due to back pressure in the azygos venous system.
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PMID:Rib infarcts in sickling disease. 156 7

In the absence of evidence for pneumonia or pulmonary embolus, primary pulmonary infarction has been assumed to be the cause of the syndrome of chest pain, fever, and pulmonary infiltrate on chest X-ray that commonly complicates sickle cell anaemia. To find out whether the syndrome might be due to rib infarction, 99mTc-diphosphonate bone scans were done. In the eleven episodes thus investigated (10 patients) the scans showed segmental areas of increased radionuclide uptake in ribs, indicative of bone infarction. A possible sequence of events is that the rib infarcts are primary and cause bone pain, followed by soft tissue reaction, pleuritis, and splinting. The resultant hypoventilation leads to atelectasis and subsequent development of the radiographic changes of the acute chest syndrome. Prevention of hypoventilation and treatment of bone pain are important therapeutic goals.
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PMID:Rib infarcts and acute chest syndrome in sickle cell diseases. 167 22

A 6-year-old girl with sickle cell disease was admitted to the hospital with the diagnosis of the acute chest syndrome. The laboratory findings and the radionuclear lung scan supported a diagnosis of pulmonary infarction rather than pneumonia. She improved with intravenous fluids, oxygen, penicillin, and theophylline. The most likely explanation for the rapid resolution of the clinical syndrome, the chest x-ray, and lung scan abnormalities is that masses of sickled cells caused transient pulmonary vascular occlusion leading to perfusion defects and ischemia, and that the sickled cell thrombi were dislodged before the infarction occurred. To our knowledge, this phenomenon has not been described as a cause of the acute chest syndrome in sickle cell disease in children.
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PMID:Acute reversible pulmonary ischemia. A cause of the acute chest syndrome in sickle cell disease. 406 60

The acute chest syndrome (ACS), a pneumonia-like illness in sickle cell patients, is one of the most frequent causes of their morbidity and hospitalizations. Repeated ACS events may predict the development of chronic lung disease. ACS is reported as a frequent cause of death in these patients. We examine here the incidence and risk factors of ACS in 3,751 patients with sickle cell disease who were observed prospectively for at least 2 years (19,867 patient-years [pt-yrs]) as part of a multicenter national study group. The ACS, defined by a new pulmonary infiltrate on x-ray, occurred at least once in 1,085 patients (2,100 events). ACS incidence was higher in patients with homozygous sickle cell disease (SS; 12.8/100 pt-yrs) and in patients with sickle cell-beta(0) -thalassemic (9.4/100 pt-yrs), and lower in patients with hemoglobin (Hb) SC disease (5.2/100 pt-yrs) and patients with sickle cell-beta(+) thalassemia (3.9/100 pt-yrs). alpha-Thalassemia did not affect the rate of ACS incidence in SS patients. Within each Hb type the incidence was strongly but inversely related to age, being highest in children 2 to 4 years of age (25.3/100 pt-yrs in SS) and decreasing gradually to its lowest value in adults (8.8/100 pt-yrs in SS). In SS children (< 10 years of age), we documented an age-related within-person reduction in ACS attack rates. Adults with a higher ACS rate had a higher rate of mortality (from all causes) than those with low ACS rates. This increased rate of mortality might also have contributed to the decline in ACS rate with age. In multivariate analysis, other factors affecting incidence in SS patients were degree of anemia (lower ACS rates in patients with lower steady-state Hb levels) and fetal Hb (lower rates in patients with high fetal Hb). There was also a positive association between ACS rate and steady-state leukocyte count. The relationship of ACS rate to higher steady-state Hb levels in SS patients is unexplained but might be caused by increased blood viscosity.
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PMID:The acute chest syndrome in sickle cell disease: incidence and risk factors. The Cooperative Study of Sickle Cell Disease. 751 23

The acute chest syndrome is a clinical entity appearing in patients suffering from sickle cell anaemia. It presents with pleuritic pain, fever, leucocytosis and pulmonary infiltrates in the thoracic radiology. The etiological diagnosis is difficult, and it is necessary to distinguish between pneumonia and pulmonary infarction. This syndrome is quite frequent among the patients at risk, and can be lethal according to the severity and the etiology of the event. A case of acute chest syndrome due to a S. pneumoniae sepsis is presented. The interest of the case lies in the rareness of this disease in our population and the peculiar evolutive clinical features of this case, with the development of intracranial hypertension and death.
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PMID:[Acute thoracic syndrome]. 798 60

Chlamydia pneumoniae has now been associated with pneumonia, bronchitis, pharyngitis, acute chest syndrome of sickle cell disease, and asthma. Because of the difficulty of primary isolation and tissue-culture adaptation of this organism, we used a previously developed polymerase chain reaction-enzyme immunoassay (PCR-EIA) to screen 132 culture-negative bronchoalveolar lavage (BAL) specimens from 108 immunocompromised patients (34% of whom were positive for human immunodeficiency virus) and 7 healthy volunteers. Thirteen specimens (9.8%) from 12 immunocompromised patients (11.1%) gave a positive result; one patient had two positive specimens obtained 3 days apart. No healthy volunteer had a PCR-EIA-positive BAL specimen. Twelve (11.1%) of the immunocompromised patients also had diagnostic levels of antibody. Four patients had positive results in both PCR-EIA and serological tests. Thus 20 (18.5%) of the 108 patients had laboratory evidence of C. pneumoniae infection. These data indicate that diagnosis of acute infection with C. pneumoniae can be established more rapidly and reliably by PCR-EIA than by culture or serology, particularly among immunocompromised patients, in whom serological changes in response to infection are relatively undependable. With an infection rate of 11.1% according to PCR-EIA, C. pneumoniae should be considered in the evaluation and treatment of pneumonia in immunocompromised patients.
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PMID:Detection of Chlamydia pneumoniae by polymerase chain reaction-enzyme immunoassay in an immunocompromised population. 826 55

Patients with sickle cell disease often develop acute chest syndrome (ACS). Signs of ACS include chest pain, fever, prostration, and pulmonary opacities. Pneumonia and infarction have been implicated in the pathogenesis of this syndrome. Infarction as a result of microvascular occlusion and pneumonia are not easily differentiated with chest radiography or ventilation-perfusion scintigraphy. The authors evaluated the ability of thin section (3-mm) chest computed tomography (CT) to help diagnose microvascular occlusion in ACS and thus help differentiate two of its most likely causes. CT scans of the chest of 10 patients with moderate to severe ACS were retrospectively reviewed by two observers, who listed the number of bronchopulmonary segments showing consolidation; areas of ground-glass attenuation due to early hemorrhagic edema; and paucity or absence of small vessels, arterioles, and venules. In all patients, the degree of hypoxia was out of proportion to the extent of consolidation evident at chest radiography. The CT scans showed microvascular occlusion and areas of ground-glass attenuation in nine patients. Infection was ruled out in eight patients. High-resolution CT may play an important role in the initial evaluation and timely selection of an appropriate treatment regimen aimed at improving tissue perfusion, thus forestalling irreversible organ damage and chronic pulmonary arterial hypertension in patients with sickle cell disease.
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PMID:Acute chest syndrome in sickle cell disease: CT evidence of microvascular occlusion. 845 35

Two hematologic emergencies are reviewed in this article: transfusion reactions and crises in patients who have sickle cell disease. Transfusion reactions may be due to incompatibility, IgA deficiency, allergy or, rarely, bacterial contamination of the blood product. A major hemolytic reaction due to incompatibility may progress to hypotension and shock. To prevent this type of reaction, blood products should be given only when necessary and attention should be given to eliminating clerical errors, which are responsible for many hemolytic reactions. In patients with sickle cell disease, a painful crisis due to vascular occlusion is the most common emergency. Rehydration is essential, and narcotics may be needed to relieve pain. Aplastic crisis is managed by transfusion of packed red blood cells and supportive care. Sickle cell crisis may affect major organ systems. The acute chest syndrome can be complicated by pneumonia; rapid respiratory failure may occur if multiple lobes are involved. Splenic or hepatic sequestration requires aggressive rehydration and transfusion. In patients who have had stroke or subarachnoid hemorrhage, a long-term exchange transfusion program is needed to keep hemoglobin S levels below 30%.
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PMID:Hematologic emergencies. Management of transfusion reactions and crises in sickle cell disease. 846 76

The acute chest syndrome (ACS), characterized by fever, chest pain, leukocytosis and a new infiltrate on chest roentgenogram, is a common complication of sickle hemoglobinopathies. The major differential diagnoses of ACS are pneumonia and pulmonary vaso-occlusive disease, which may occur simultaneously. Bacterial pulmonary infections are documented infrequently in ACS with the exception being in the pediatric population under 5 years of age. Because there are no clinical or laboratory parameters that clearly allow for distinction between pneumonia and vaso-occlusive disease, empiric use of antibiotics directed against S. pneumoniae and other pathogens commonly seen in community-acquired pneumonias remain a mainstay of therapy.
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PMID:The acute chest syndrome of sickle cell disease. 848 94

Acute chest syndrome (ACS) is associated with significant morbidity and is the leading cause of death in patients with sickle cell disease (SCD). Recent reports suggest that bone marrow fat embolism can be detected in many cases of severe ACS. Secretory phospholipase A2 (sPLA2) is an important inflammatory mediator and liberates free fatty acids, which are felt to be responsible for the acute lung injury of the fat embolism syndrome. We measured SPLA2 levels in 35 SCD patients during 20 admissions for ACS, 10 admissions for vaso-occlusive crisis, and during 12 clinic visits when patients were at the steady state. Eleven non-SCD patients with pneumonia were also evaluated. To determine if there was a relationship between sPLA2 and the severity of ACS we correlated SPLA2 levels with the clinical course of the patient. In comparison with normal controls (mean = 3.1 +/- 1.1 ng/mL), the non-SCD patients with pneumonia (mean = 68.6 +/- 82.9 ng/mL) and all three SCD patient groups had an elevation of SPLA2 (steady state mean = 10.0 +/- 8.4 ng/mL; vaso-occlusive crisis mean = 23.7 +/- 40.5 ng/mL; ACS mean = 336 +/- 209 ng/mL). In patients with ACS sPLA2 levels were 100-fold greater than normal control values, 35 times greater than values in SCD patients at baseline, and five times greater than non-SCD patients with pneumonia. The degree of SPLA2 elevation in ACS correlated with three different measures of clinical severity and, in patients followed sequentially, the rise in SPLA2 coincided with the onset of ACS. The dramatic elevation of SPLA2 in patients with ACS but not in patients with vaso-occlusive crisis or non-SCD patients with pneumonia and the correlation between levels of SPLA2 and clinical severity suggest a role for SPLA2 in the diagnosis and, perhaps, in the pathophysiology of patients with ACS.
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PMID:Phospholipase A2 levels in acute chest syndrome of sickle cell disease. 863 Apr 25


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