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

In an intensive care unit an important role is assigned to respiratory physiotherapy. Its principal task is efficacious toilet of the bronchi by fluidifying the secretions, promoting their ungluing from the respiratory tree and facilitating their evacuation by cough or by aspiration with a catheter or bronchoscope. The technique comprises the inhalation of a secretolytic (e.g. Bisolvon, NaCl 9%) and, in the case of asthma, bronchospasmolytic (e.g. Ventoline) aerosol followed by breathing exercises. The other objectives of physiotherapy are to ensure a better distribution of inspired air, increase failing ventilation, ameliorate disturbed gas exchange, relax the contracted respiratory muscles and prevent bronchiolar collapse in emphysema during expiration. The field of application of respiratory physiotherapy is large; its purpose is prophylactic and therapeutic. The method is prophylactic in all patients confined to bed, where there is a risk of bronchial obstruction or ventilatory failure, especially in those with severe operation, traumatism or consciousness disorder. Physiotherapy has a therapeutic role in several, principally broncho-pulmonary diseases, such as asthma, obstructive emphysema, pneumonia, bronchiectasis, pulmonary abscess, atelectasis, and pulmonary and pleural fibrosis. Myocardial infarction and pulmonary embolism in the acute state, acute pulmonary edema, pneumothorax and pulmonary hemorrhage are contraindications for physiotherapy. If the method is to be effective the intensive care unit should have a specialized physiotherapist attached to it working there on a daily basis.
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PMID:[The role of respiratory physiotherapy in an intensive care unit]. 52 99

The radiologic examination of the chest is an essential part of the evaluation of the pediatric patient presenting to the emergency room with respiratory distress. In many cases the chest radiograph will be diagnostic of a specific cause for the distressful symptom. Opaque foreign bodies are readily visualized in the tracheobronchial tree. The presence of massive atelectasis or severe obstructive emphasema may be visualized. Large pleural fluid collections or tension pneumothoraces can be localized and immediately treated by proper drainage. The presence of pneumonia, acute pulmonary edema, and pulmonary hemorrhage may be identified. Complications associated with bronchial asthma (pneumomediastinum, pneumothorax, and atelectasis) may be manifested radiographically before clinical signs are obvious. Lung compression by large mediastinal tumors and delayed congenital hernias may be readily demonstrated by chest radiography.
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PMID:Radiologic evaluation of the nontraumatized child with respiratory distress. 68 12

The heart and the lung make up an inseparable anatomic and functional unit. The changes in one affect the other and vice versa. In acute myocardial infarction a heart failure syndrome develops. This syndrome is characterized by passive pulmonary congestion, which leads to hypoxemia. This hypoxemia indicate the functional disturbance of the lung, and the hemodinamic evolution of the disease. Arterial gases determination is the best way to assess the sickness progression. A certain paralelism exists among the central venous saturation, cardiac insufficiency and the degree of pulmonary disfunction. Such a procedure is not very appreciable and does not substitute the direct analysis of the arterial PO2. The pulmonary complications in the myocardial infarction shock are directly responsable of death in 50% of the patients. To heart failure and shock, hipperfusion and hypoxia are added. Many vessels close due to the decrease in the pulmonary flow. This brings about the release of substances that are toxic to the vessel causing an inflammatory vascular reaction. The decrease in the flow harms the lung cell and for this reason atelectasia or alveolar colapse occur; besides inducing the formation of shunts. Under these conditions the lung compliance decreases. The areas that are badly ventilated and hypoperfused can easily become infected and pneumonitis and abscesses cause even more harm to the tissue. The decrease in the speed of circulation and hematologic changes of shock, induce a diseminated intravascular coagulation. What was stated before leads to an important reduction of the lung as a depurating organ and makes the shock irreversible. As far as therapy is concerned in the prevention of vascular colaps and the improvement of the oxemia, oxygen is very useful when there is a venous congestion (clinically, X rays, and oxemia). When the concentration of O2 is lower than 50% in the cases with slight cardiac failure; do not use oxygen in higher concentrations unless the hypoxia is associated to acute pulmonary edema and shock. Mechanic ventilators, and intermitent possitive pressure are recommended even though they have a posenous effect on the cardiac output. Always keep the air ways permeable: changing position, breathing exercises, humidifications, aspiration of secretions, intubation, or traqueostomy depending upon the various cases.
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PMID:[Pulmonary complications of acute myocardial infarct. Therapeutic orientation]. 115 8

In a two year period 44 endobronchial resections using the Neodymium-YAG laser have been performed in 28 patients. The majority of cases had either bronchogenic carcinoma (57%) or metastatic carcinoma (18%) involving the bronchial tree. Adenoid cystic carcinoma, benign tumours, lymphoma, tracheal papillomatosis, Wegener's granulomatosis and benign stricture comprised the other cases. Rigid bronchoscopy and general anaesthesia were used in the majority. Symptomatic improvement of dyspnoea when relief of bronchial obstruction occurred was marked in ten of 17 cases, moderate in four and absent in three. Haemoptysis was markedly improved in two of three cases and obstructive pneumonitis resolved in one of two cases. Significant respiratory function improvement was observed in Raw (most sensitive), FEV11, FVC and TLC. Laser treatment restored the lumen to normal calibre in 52% (including all patients with tracheal lesions), to greater than half normal in 28% and to less than half normal in 20% of cases. Re-expansion of a collapsed lung or lobe occurred in seven of eight patients. In six of these patients laser treatment was the initial therapy resulting in immediate re-expansion and symptomatic relief prior to further therapy. In patients with bronchogenic carcinoma the mean time to retreatment or death was 72 days. For metastatic carcinoma this was 60 days. Two early deaths (3 hours, 36 hours) due to respiratory failure occurred in patients with very severe bilateral bronchial obstruction too advanced for effective clearance. Other complications included laryngeal oedema requiring prolonged intubation (1), bronchospasm (1), atrial fibrillation (1), and acute pulmonary oedema (1). Laser treatment provides effective palliation for bronchial obstruction and haemoptysis in selected proximal endobronchial cancers.
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PMID:Endobronchial resection with the Nd-YAG laser--two years experience in an Australian unit. 169 70

A case of Brucella pneumonitis and myocarditis complicated by acute pulmonary edema is presented. The clinical, laboratory and roentgenographic findings are discussed.
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PMID:Acute pulmonary edema in Brucella myocarditis and interstitial pneumonitis. 232 33

One hundred consecutive patients 80 years of age or older consented to and subsequently underwent open-heart operations at our institution between July 1976 and May 1987. Fifty of the patients had aortic valvular disease (28 with coexisting coronary artery disease), and 41 had isolated coronary artery disease. Eight patients had mitral valvular disease, and one had a dissecting aortic aneurysm. Ninety had Class IV disease that was functional, ischemic, or both. The most compelling indications for operation in 85 patients were unstable or postinfarction angina, syncope, acute pulmonary edema, or cardiogenic shock. Twenty-nine patients died soon after operation (within 90 days). New York Heart Association Class IV disease, previous myocardial infarction, cachexia, and emergency operation were preoperative variables associated with early death. Forty-three patients had no complications except for atrial arrhythmias and were discharged from the hospital a mean (+/- SD) of 11.5 +/- 3.7 days after operation. Low cardiac output, acute myocardial infarction, reoperation for bleeding, renal insufficiency, pneumonia, and prolonged endotracheal intubation were the most common serious postoperative complications. Twenty-eight patients who survived postoperative complications were discharged 24.9 +/- 19.6 days after operation. Seventeen patients died 2 to 104 months after discharge from the hospital. Actuarial calculation predicts the survival of 59 percent of patients at three years and 54 percent at five years. Of the 54 patients still alive at this writing, 53 have disease within New York Heart Association and Canadian Cardiovascular Society Classes I or II. For selected octogenarians with unmanageable cardiac symptoms, operation may be an effective therapeutic option.
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PMID:Open-heart surgery in octogenarians. 338 92

This paper describes the release of platelet-activating factor (PAF) into the circulation of rabbits with acute pulmonary injury induced by antibody reacting with pulmonary endothelium. Eight rabbits were injected i.v. with 2 mg/kg of body weight of goat anti-rabbit lung angiotensin-converting enzyme gamma-globulin (GtARbACE). All animals developed acute pneumonitis, characterized by severe endothelial damage, accumulation of polymorphonuclear leukocytes (PMN) and platelets (Plt) in the lumina of alveolar capillaries, and deposits of goat IgG and rabbit C3 along alveolar capillary walls. Six of the rabbits died from acute pulmonary edema. PAF was detected in the plasma of all animals within 5 min after injection of GtARbACE. Five other rabbits were depleted of leukocytes by nitrogen mustard and then injected with 2 mg/kg of body weight of GtARbACE. In three of these rabbits release of PAF was demonstrated, though in amounts smaller than in non-leukocyte-depleted rabbits; all three animals died from pulmonary edema. After injection of 0.03 mg/kg of body weight of GtARbACE in six additional rabbits, three of them leukocyte-depleted, small amounts of PAF were detected in the circulation. None of these six rabbits died of pulmonary edema. PAF release was not observed in ten rabbits injected i.v. with 2 or 0.03 mg/kg of body weight of normal goat gamma-globulin. In separate experiments in vitro, incubation of isolated lung or thoracic aorta with GtARbACE resulted in deposits of goat IgG along endothelia and significant release of PAF. PAF was also released from endothelial cells removed from thoracic aorta by cellulose acetate paper and then incubated with GtARbACE. When segments of thoracic aorta were stripped of endothelium and then incubated with GtARbACE, PAF release could not be shown. The data obtained are consistent with the interpretation that PAF released into the circulation after binding of GtARbACE to the endothelia of lung and aorta originates from leukocytes and from lung and thoracic aorta endothelial cells.
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PMID:Release of platelet activating factor in rabbits with antibody-mediated injury of the lung: the role of leukocytes and of pulmonary endothelial cells. 631 99

Among 369 patients with native valve infective endocarditis observed during a 14-year period, 17 were related to S: pneumoniae. Fourteen of them were observed in the last 7 years. At the time of admission 13 exhibited purulent meningitis, 6 of them being comatose. An apparent portal of entry was present in 13 patients including Pneumonia (n = 11) and otitis media (n = 2). Major alcoholism was present in 6 cases. The mean delay between the onset of fever and the discovery of the cardiac murmur was 15 days (range 1 to 60). Twelve patients exhibited congestive heart failure with acute pulmonary oedema in 9. The aortic valve was involved in 12 and the mitral valve in 7 (in 2 patients both mitral and aortic valves were involved). Myocardial and/or annular abscesses were found in 7 patients. Nine patients underwent surgical procedure (3 died) whereas 6 comatose patients were not operated on and died. The overall mortality was 59%. Although antibiotics are effective, the severity of anatomical lesions leads to prompt surgical treatment. The high mortality is mainly due to purulent meningitis.
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PMID:Pneumococcal endocarditis. 651 90

Twenty one- to two-month-old Holstein, Angus, or Holstein-Angus crossbred calves were given intravenous complete Freund's adjuvant and their lungs were examined at 24 hours to 30 days post-injection. Two calves given intravenous saline served as normal controls. The evolving pulmonary inflammatory response was characterized initially by multifocal vasculitis and acute multifocal exudative pneumonitis which progressed to a granulomatous interstitial pneumonitis by seven days post-injection. Discrete granulomas characterized the lesions in the lungs and lymph nodes at 30 days post-injection, and granulomas also were seen in liver, kidney, and spleen. Clinically, the calves were tachypneic and pyrexic during the first week post-injection. Four calves developed acute pulmonary edema and died during, or shortly after, administration of the adjuvant. This model of experimental pneumonia in calves is similar to complete Freund's adjuvant-induced experimental pneumonia in other species. It is reproducible and predictable in its course of development and resolution, and provides a useful model for studying basic mechanisms of pulmonary inflammatory injury and repair in the bovine lung.
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PMID:The bovine pulmonary inflammatory response: adjuvant pneumonitis in calves. 714 10

The pulmonary complications in 110 consecutive renal transplant recipients on cyclosporin and low-dose steroid immunosuppression were studied retrospectively. The pulmonary complications were: acute pulmonary oedema in 19 patients, pneumonia in 18, tuberculosis in 9, acute pulmonary embolism in 5, and lung abscess in 1. Sixty-nine patients (62.7%) had no pulmonary complications; 69% of the complications occurred in the first 4 months after the transplant. Pulmonary tuberculosis became evident later. The mean age, period of follow-up, human leucocyte antigen (HLA) B/DR mismatches, mean serum urea and serum creatinine concentrations, systolic and diastolic blood pressures, and cyclosporin dosage did not differ between the groups with no complications, infectious complications and non-infectious complications. The number of rejection episodes treated with bolus steroids was significantly higher in the infectious and non-infectious complications groups compared with the group with no complications. The incidence of pulmonary complications after renal transplantation, especially pneumonia and tuberculosis, was still high despite the use of low-dose steroids and cyclosporin. Pulmonary complications were the commonest cause of death in the first 3 years after the transplant. A high index of suspicion for pulmonary tuberculosis and pulmonary embolism in these patients is necessary.
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PMID:Pulmonary complications in 110 consecutive renal transplant recipients. 777 66


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