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

Diffuse pulmonary edema, capable of arising in the absence of hemodynamic disorders is rare in infectious disease. They take on two different clinical appearances: a) acute edema of the lung with the syndrome of asphysia, b) a subacute dyspneic pneumonia with hypoxemia and hypo or normocapnia. These initial disorders can be followed by progressive respiratory failure secondary to the development of diffuse interstitial lesions with fibrosis and intra-alveolar hyaline deposits. The bronchiolo-alveolar lesions which induce a fibrin rich exudate are directly caused by the patogenic agent: myxovirus, essentially influenzae, and more rarely adeno or herpes virus. The role of bacteria and of certain parasites is more debateable.
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PMID:[Pulmonary edemas of infectious origin]. 0 55

Pulmonary parenchymal or pleural reactions to chemotherapeutic agents used in the management of patients with malignant diseases are being recognized with increasing frequency. Alkylating agents, asparaginase, bleomycin, methotrexate and procarbazine have all been implicated. Some of the reactions, such as the rare procarbazine pleuritis and pneumonitis, represent hypersensitivity phenomena. Others, such as alkylating agent pulmonary toxicity, appear to be direct toxic effects of the drugs. The severity of the toxicity is variable. The appearance of these pulmonary changes must be differentiated from tumor progression or a variety of possible infections. The awareness of possible pulmonary toxicity is of great importance since early discontinuation of the agent following the first hint of pulmonary toxicity may allow partial or complete reversal of the process. Continued therapy in the face of drug-related pulmonary toxicity may enhance the likelihood of irreversible pulmonary compromise with respiratory failure and death.
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PMID:Pulmonary toxicity of antineoplastic agents. 7 57

Among the causes of death of 43 scoliotics were 5 directly due to complications of congenital heart disease. Over half (57.9%) of the remaining 38 died of cardiac or respiratory causes. The paralytic scolitoics tended to die of pneumonia or respiratory failure, while the nonparalytic scoliotics died of cardiac failure. Right ventricular hypertrophy was present in 65% of the 17 subjects examined postmortem. Electrocardiographic evidence of right ventricular hypertrophy correlated well with the postmortem findings. The vital capacity was less than 1.75 liters in 84% of the dead subjects. The case records of a further 719 living scoliotics were examined for evidence of congenital heart disease. This was found in: 34 (4.5%) of the whole group of 762, 6.9% of the congenital ; 3.4% of the idiopathic scoliotics; 22.7% of those with Marfan's syndrome.
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PMID:Causes of death, right ventricular hypertrophy, and congenital heart disease in scoliosis. 15 77

Two mortal cases of varicella pneumonitis are described. The patients were respectively 41 and 34 years-old men of good health. They caught the disease from their children. The disease lasted one week, and death was due in both cases to respiratory failure. The autopsy confirmed massive lung involvement with varicella pneumonia, and also showed other organs involvement (liver, spleen, pancreas, lymph nodes, oesophagus). In both cases, human fibroblast cultures infected by material obtained from cutaneous lesions (in the second case also from the spleen) revealed the presence of Herpesvirus varicellae. A review of 41 cases of adult mortal varicella in the literature demonstrates that death is practically always due to pneumonia and consequent respiratory failure. The dissemination of the virus in other organs is constant. Circumstances, such as pregnancy, immunosuppression, etc., which aggravate the prognosis of varicella in adults, are discussed.
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PMID:[Fatal varicella pneumonia in adults. Report of two cases and review of literature (author's transl)]. 22 15

Ten of 70 children (14%) with acute lymphoblastic leukemia developed severe interstitial pneumonitis within three weeks after induction of central nervous system prophylactic therapy. The clinical picture was characterized by fever, cough, progressive dyspnea, and hypoxemia with complete resolution in one to three weeks, except in one patient who died during the acute illness from respiratory failure. P. carinii organisms were found in the lung tissue of only one patient. The etiology of the pneumonitis in the other nine children was probably viral, acquired or activated during a period of lymphopenia and immunosuppression. The morbidity and potential mortality from the pneumonitis warrants early recognition by open lung biopsy and intensive supportive therapy.
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PMID:Acute respiratory illness in children with acute lymphoblastic leukemia. 30 Jul 96

Thirty-two confirmed and 24 highly probable cases of Legionnaires' disease occurred in Vermont between May 1 and Oct 15, 1977. Confirmed cases had positive results for direct fluorescent antibody testing of lung tissue or fourfold rise in antibody titer. Highly probable cases had one elevated titer (greater than or equal to 1:256) and a compatible illness. Forty-eight (86%) had underlying chronic disease, and 22 (39%) were immunocompromised. Prominent early symptoms were fever, cough, chills, and malaise. All but one patient had verified pneumonia. Courses ranged from a pneumonia not requiring hospitalization to respiratory failure necessitating support with mechanical ventilation. Seventeen patients died. Although the clinical presentation was variable, rapid development of high fever and leukocytosis together with negative cultures of lower respiratory tract secretions strongly suggested the diagnosis in an epidemic setting.
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PMID:Legionnaires' disease in Vermont, May to October 1977. 35 Dec 19

Patients aged over 45 admitted to hospital with exacerbations of chronic bronchitis alone or in association with cor pulmonale, pneumonia, or respiratory failure were placed in one of three groups (men with hypoxia, men without hypoxia, and women). Patients within these groups were then randomly allocated to receive either standard drug treatment alone or standard drug treatment plus intermittent positive-pressure ventilation (IPPV). No significant differences occurred between the controls and patients receiving physiotherapy and IPPV in any group. We conclude that when a patient with chronic bronchitis and respiratory failure is deteriorating emphasis should be on correct diagnosis, fluid electrolyte balance, and nutrition together with oxygen treatment when necessary, rather than on additional physiotherapy.
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PMID:Physiotherapy and intermittent positive-pressure ventilation of chronic bronchitis. 36 89

Pneumonia caused by Legionnaires' disease bacterium was recognized in eight patients during a 7-month period. The patients were immunosuppressed by their underlying illness, corticosteroid therapy, and other exogenous immunosuppressive agents. Five of the patients had received immunosuppressive therapy for less than 16 days. Clinical presentation was similar to that of other bacterial pneumonias in compromised patients. Legionnaires' disease progressed to necrotizing pneumonia with abscess formation and respiratory failure in two patients. Diagnosis was made by [1] culture of lung tissue and bronchial washings; [2] direct fluorescent antibody staining of lung tissue, sputum, and bronchial washings; and [3] serologic evidence of infection. Therapy with oral erythromycin was ineffective. Intravenous erythromycin was given to six patients, with a good response. However, two patients showed further clinical improvement after rifampin was added. Because this illness may be more severe in compromised hosts, open lung biopsy and special microbiologic tests should be done when Legionnaires' disease is suspected.
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PMID:The compromised host and Legionnaires' disease. 37 43

Three patients received respectively 190 mg, 175 mg, and 196 mg of methotrexate and developed bilateral pulmonary infiltrates without evidence of peripheral blood eosinophilia. Sputum in the three cases failed to reveal acid-fast bacilli, pathogenic fungi, or opportunistic organisms by cultures and appropriate stains. Despite discontinuance of the drug and/or institution of corticosteroid therapy, progressive respiratory failure led to death. In all three cases, autopsy revealed gross and microscopic features indistinguishable from those seen in the Hamman-Rich syndrome, and methotrexate hepatotoxicity was present in one. Pulmonary eosinophilia or granulomas, classically seen in previously reported cases of methotrexate pneumonitis, were not observed. It is suggested therefore that methotrexate be added to the list of agents capable of inducing diffuse interstitial pulmonary fibrosis. Conversely, diffuse interstitial pulmonary fibrosis should be considered in the differential diagnosis of patients receiving methotrexate who develop bilateral pulmonary infiltrates seen on chest roentgenograms.
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PMID:Methotrexate-induced diffuse interstitial pulmonary fibrosis. 42 24

We describe a patient with sickle cell hemoglobin C(SC) disease in whom severe pneumonia developed complicated by large bilateral pleural effusions and respiratory failure. Mycoplasma infection was not initially suspected but was subsequently proved serologically. The course of the illness was unusually long. A review of the literature showed occurrence of large pleural effusions to be infrequent for pulmonary infection with Mycoplasma in adults, with only eight such cases previously reported. The possibility of Mycoplasma pneumonia should not be dismissed merely because of the severity of the illness or the presence of pleural effusions.
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PMID:Severe mycoplasma pneumonia with pleural effusions in a patient with sickle cell-hemoglobin C(SC) disease. Case report and review of the literature. 43 75


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