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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

Their frequency is estimated with difficulty, although on autopsy pulmonary edema is found almost routinely. It is a major complication of overdoses (48 p. 100 of severe intoxications). Their formation can be suspected, when after the first phase of respiratory depressions, with coma, myosis, and a variable latent period, a second attack of respiratory insufficiency occurs with tachypnea, and cyanosis. The chest X-ray shows diffuse alveolar infiltration, sparing the apices. The heart being generally of normal size. Rapid disappearance of this infiltrate (24 to 48 hours) enables the elimination of two diagnoses: pneumonia due to inhalation of gastric fluid, an infectious pneumonia. Their pathogenesis remains very debatable: - in the majority of cases abrupt L.V.F. can be eliminated: -on the other hand it could be an allergic accident of the anaphylactic type, or local liberation of histamine, or a local toxic action on the pulmonary capillaries; - hypoxia, secondary to respiratory depression, could lead to pulmonary edema, by the same mechanism as at altitude; - finally, owing to the central neurological disorders a neurogenic theory can be put forward. Their treatment is essentially a combination of Nalorphine with oxygen therapy (by mask, or if necessary by assisted, controlled ventilation) with prevention of inhalation of gastric fluid (gastric emptying) or curative treatment of possible aspiration by antibiotics, and cortico-steroids. Diuretics can be useful, as well as cardiotonics.
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PMID:[Pulmonary edemas due to acute heroin poisoning]. 0 75

The respiratory pathophysiology of A2 influenza infection was studied in mice treated with small-particle aerosols (SPA) of rimantadine or ribavirin. Untreated infections in mice resulted in survival rates of 15% or less and were characterized by (i) severe hypoventilation (decreased P(O2) and increased P(CO2)), (ii) compensated respiratory acidosis (increased P(CO2) and HCO(3) (-), with normal pH), (iii) pneumonia with increased ratio of wet/dry lung weight, and (iv) hypothermia. Treatment with SPA of rimantadine (21 mg/kg per day for 4 days) beginning 72 h after virus challenge significantly improved survival rate (80%) but failed to alter lung pathology from that found in infected, untreated mice. Rimantadine treatment decreased somewhat the severity of hypoventilation, respiratory acidosis, lung wet weight, hypothermia, and lung virus titers from that observed in infected, untreated mice. SPA of ribavirin (26 mg/kg per day for 4 days) initiated 6 h after SPA exposure of mice to virus significantly improved survival rate (95%) and reduced lung virus titers and lung pathology. Gas exchange and pulmonary edema in ribavirin-treated, infected mice were significantly improved over those of infected, untreated controls. The mechanisms for increased survival rates induced by SPA of rimantadine remain uncertain, since increased survival rates could not be ascribed entirely to improvements in lung functions. In contrast, however, ribavirin treatment appeared to improve survival rates by reducing major lung pathology and pulmonary dysfunction. This was probably mediated through the antiviral effects of ribavirin.
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PMID:Effects of small-particle aerosols of rimantadine and ribavirin on arterial blood pH and gas tensions and lung water content of A2 influenza-infected mice. 1 87

The present paper deals with the findings on examination of the chest and at autopsy in 100 selected surgical patients under intensive care; of these 17% were post-traumatic, 55% had post-operative lung complications and in 28% there had been no trauma or previous operations. The accuracy of the radiological diagnosis was checked against the autopsy findings. Pneumonia and pulmonary oedema were the most common lung complications in all three groups, with an incidence of 59 to 82%, and were diagnosed with an accuracy of 92 to 95%. Other conditions which were looked for were pulmonary congestion, emboli and lung infarcts, pleural effusions, atelectasis, pulmonary haemorrhage or contusion and pneumothorax. The most common mis-diagnosis was in the demonstration of emboli and infarcts, where accuracy was only 64%. The difficulties in differential diagnosis of the radiological appearances due to these pulmonary complications are discussed.
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PMID:[A review of the findings on chest examinations and at autopsy in surgical patients under intensive care (author's transl)]. 13 94

Clinical studies have long suggested the presence of a specific cardiomyopathy in sickle cell anemia secondary to intracoronary thrombosis and subsequent infarction. Fifty-two autopsy patients were studied (48 with SS hemoglobin, 4 with S-C or S-Thal hemoglobin) to ascertain the range of cardiac pathologic abnormalities associated with this disease. The average age was 17 years (range 1 month to 48 years). Renal failure and infection were the most common causes of death; the former was a more common cause in adults than in children. Right and left ventricular hypertrophy and dilatation were the most common abnormal pathologic findings. No evidence of recent or remote myocardial infarction, coronary thrombosis or arteritis was noted in any patient. Eight patients who were studied with postmortem coronary arteriograms exhibited markedly increased coronary arterial caliber with no evidence of atherosclerosis. Seventeen of the 52 patients studied had clinical evidence of congestive heart failure before death. Of these 17 patients, 7 had moderate to severe left ventricular hypertrophy associated with chronic renal failure and hypertension, 2 had right ventricular hypertrophy with organized pulmonary thrombosis, 2 had rheumatic mitral valve disease and 2 died during the second trimester of pregnancy. Two of the 17 patients thought to have pulmonary edema before death in fact had aspiration pneumonia and hemorrhagic pneumonitis, respectively. The data suggest that cardiac dysfunction in sickle cell anemia can usually be explained by the adverse effect of coexisting disease on the diminished cardiac reserve of chronic anemia. The data do not support the concept of a specific "sickle cell cardiomyopathy".
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PMID:Clinicopathologic analysis of cardiac dysfunction in 52 patients with sickle cell anemia. 15 Jul 86

Non cardiogenic pulmonary edema is caused by an increase of alveolocapillary permeability, due to different etiologies: fat embolism, multiple trauma, septic shock, influenza pneumonia, aspiration syndrome... Chest radiographs exhibit interstitial and/or alveolar pattern, severity of injury is assessed by the magnitude of intra-pulmonary shunting. Pulmonary wedge pressure is normal, and increased pulmonary vascular resistance is sometimes evidence in prolonged evolutions, especially in fatal cases. Treatment consists in the suppression of hypervolemia, and ventilation with positive and expiratory pressure (PEEP). Extra-corporeal membrane lung oxygenation remains since now rather unsuccessful.
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PMID:[Non cardiogenic pulmonary edema (author's transl)]. 22 Jul 23

We have recently described a new method for measuring distributions of ventilation-perfusion ratios (VA/Q) based on inert gas elimination. Here we report the initial application of the method in normal dogs and in dogs with pulmonary embolism, pulmonary edema, and pneumonia. Characteristic distributions appropriate to the known effects of each lesion were observed. Comparison with traditional indices of gas exchange revealed that the arterial PO2 calculated from the distributions agreed well with measured values, as did the shunts indicated by the method and by the arterial PO2 while breathing 100 per cent 02. Also the Bohr dead space closely matched the dispersion of ventilation in realtion to VA/Q. Assumptions made in the method were critically evaluated and appear justified. These include the existence of a steady state of gas exchange, an alveolar-end-capillary diffusion equilibration, and the fact that all of the observered VA/Q inequality occurs between gas exchange units in parallel. However, theoretical analysis suggests that the method can detect failure of diffusion equilbration across the blood-gas barrier should it exist. These results suggest that the method is well-suited to clinical investigation of patients with pulmonary disease.
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PMID:Distribution of ventilation-perfusion ratios in dogs with normal and abnormal lungs. 23 70

The acute effects of a triolein infusion in dogs were secondary to the mechanical effects of this neutral fat which was distributed in the pulmonary and systemic vascular tree of all organs without inflammatory change. Hypoxia developed immediately and became progressively worse as the infusion was continued. Pulmonary hypertension developed during the fat infusion without pneumonia, congestive heart failure or pulmonary edema. There was a slow leak of 14C triolein into the systemic circulation rather than a rapid shower, and this radioactive fat was recirculated between the pulmonary and systemic vasculature. Seventy-six per cent of the 14C triolein was retained in the lungs. Terminally, the dogs had a respiratory arrest without cardiac decompensation, cardiac arrest or pulmonary edema; cerebral fat embolism in addition to severe hypoxia appears to be the cause.
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PMID:Effects and distribution of acute fat embolism in spontaneously breathing dogs using radioactive carbon triolein. 24 Feb 11

A teenage girl in bone marrow remission with acute lymphocytic leukemia died suddenly from pulmonary edema. She had taken her first oral dose of methotrexate and cyclophosphamide 10 hours previously when she was feeling well and was asymptomatic. One week previously she had received the last of four intrathecal injections of methotrexate. Autopsy showed marked pulmonary edema as well as chronic lung changes, as previously described in patients with methotrexate pneumonitis. There is usually at least a 12-day interval from the onset of administration of methotrexate to the onset of the lung toxicity. The authors suggest the patient was sensitized by the intrathecal methotrexate and then reacted with angioneurotic edema of the lung when given the first oral dose of methotrexate. Careful examination for infectious agents, including electron microscopy, was negative.
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PMID:Methotrexate-induced sudden fatal pulmonary reaction. 26 2

Hypoxic pulmonary disorders and head injuries associated with increased intracranial pressure (ICP) frequently co-exist. Positive end-expiratory pressure (PEEP) improves hypoxemia but has been reported to impede cerebral venous return, potentially causing a further increase in ICP. This study examined the effects of PEEP on ICP at different levels of brain compliance. continuous ICP recordings were obtained after insertion of Scott cannulas to the lateral ventricles of seven comatose patients. Brain compliance was assessed by calculation of the pressure volume index. Patients were maintained in a 30 degrees head-up position. Maintenance of PEEP to levels of 40 cm H2O pressure for as long as 18 hours did not increase ICP in patients with either normal or low intracranial compliance, and did not increase ICP in the absence of pulmonary disease. Central venous pressure and pulmonary artery wedge pressure increased proportionately as PEEP was increased. No consistent changes were found in blood pressure recordings, nor were there any reductions in cardiac output found during the studies. Abrupt discontinuation of PEEP did not result in increased ICP except for a transient rise on two occasions when respiratory secretions became copious and the patients were inadequately ventilated. Improved oxygenation in two patients as a result of PEEP was concomitant with improved intracranial compliance and neurological status. In patients with brain injuries, PEEP improves arterial oxygenation without increasing ICP as previously supposed. Consequently, PEEP is a valuable form of therapy for the comatose patient with pulmonary disorders such as pneumonia or pulmonary edema.
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PMID:Effects of positive end-expiratory pressure on intracranial pressure and compliance in brain-injured patients. 32 31


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