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

Immaturity and oxygen toxicity have been implicated in the pathogenesis of the neonatal disease bronchopulmonary dysplasia. The present study aimed to investigate the use of magnetic resonance imaging (MRI) to assess hyperoxia-mediated lung injury in the term and premature neonate. Term (gestation, 22 d) and premature (21 d) rat pups were exposed to hyperoxia (>95%) or air for a 6-d period (n = 7) and assessed for lung damage by MRI. Pulmonary signal intensities of T1-weighted images were significantly increased in both hyperoxia-exposed term and premature neonates, relative to air-breathing controls (p < 0.01). T2-weighted MRI signal intensities were also greater in premature and term rat pups exposed to hyperoxia, but failed to reach significance (p > 0.05). Elevated MRI pulmonary signal intensities may have represented an increase in magnetic resonance-detectable free water, possibly indicating an increase in edema. Corresponding histologic evidence of lung injury was detected in both term and premature rat pups exposed to hyperoxia. Histologic samples indicated focal regions of alveolar hemorrhage, immune cell infiltration, edema, and collapse in both term and premature rat neonates exposed to hyperoxia. Alveolar air space was assessed (n = 5) by light microscopy within a 0.5 mm2 region of the superior left and inferior right pulmonary lobes of each treatment group. Alveolar area of the superior left lung lobe of the premature hyperoxia treatment group was significantly smaller than other treatment groups (p < 0.05). Reduced area for respiratory exchange was probably a result of observed focal areas of edema and collapse. MRI-detectable increases in lung signal intensity may have represented an increase in hyperoxia-induced pulmonary edema in the 6-d-old rat neonate. Increases in signal intensity correlated with the appearance of edema in pulmonary histologic samples. Premature delivery had a less defined effect on lung injury but possibly exacerbated hyperoxia-mediated pulmonary damage.
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PMID:Magnetic resonance imaging of pulmonary damage in the term and premature rat neonate exposed to hyperoxia. 1156 94

Mechanical ventilation in premature infants may injure the lungs or exacerbate the pre-existing condition that led to the need for mechanical ventilation. Ventilator-induced lung injury (VILI) may be associated with alveolar structural damage, pulmonary oedema, inflammation, and fibrosis. This injury is not uniform and is associated with surfactant dysfunction. Recovery from VILI includes clearance of pulmonary oedema and alveolar structural repair. Mechanisms of VILI include high airway pressure (barotrauma), large gas volumes (volutrauma), alveolar collapse and re-expansion (atelectotrauma), and increased inflammation (biotrauma). Injury to the lung may lead to other organ dysfunction. The premature lung is more susceptible to VILI, and lung injury may exacerbate the disturbance of lung development that occurs after birth. Therapies targeting specific processes in lung injury, and which complement the protective ventilator management strategies to avoid atelectotrauma and lung overdistension are an area of active research.
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PMID:Mechanisms of ventilator-induced lung injury in premature infants. 1246 97

Enterovirus 71 (EV71) infection can lead to devastating clinical outcomes. An appreciation of the scientific relationship between cytokine response and patient mortality may help limit the risks posed by this deadly illness. We present the results of a study that compared the cerebrospinal fluid (CSF) and serum levels of interleukin-6 (IL-6) and interleukin-1beta (IL-1beta) in 24 patients with EV71 infection. Cases in this study involved diverse manifestations or complications, including encephalitis, poliomyelitis-like syndrome, meningitis, and pulmonary edema. CSF levels of IL-6 in study patients were found to be consistently higher during the first 2 days of central nervous system (CNS) involvement than afterward. Compared with patients who did not have pulmonary edema, patients who experienced pulmonary edema had dramatically varied blood values, including IL-6, white blood cell counts, and glucose levels. Our findings suggest that the combination of CNS and systemic inflammatory response may trigger EV71-related cardiopulmonary collapse.
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PMID:Proinflammatory cytokine reactions in enterovirus 71 infections of the central nervous system. 1253 66

This case report illustrates the presentation and course of reexpansion pulmonary edema (REPE) in a young man with spontaneous pneumothorax. REPE is considered relatively uncommon by most accounts, but in certain clinical circumstances the incidence is much higher. Although supportive therapy is the rule, the condition is far from benign and mortality estimates are as high as 20%. Risk factors, including young age, a large pneumothorax and longer duration of collapse, may help predict which patient will encounter this complication. In patients with these risk factors, the thoracostomy tube should be initially left off suction in an effort to prevent REPE primarily. When REPE is encountered, therapy is supportive.
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PMID:Reexpansion pulmonary edema: a case report and review of the current literature. 1255 36

A 64-yr-old man was admitted to our hospital for the examination of the abnormal shadow in his left lung field, which was diagnosed later as lung cancer. Radical operation was scheduled under combined epidural/general anesthesia. One lung ventilation was performed to facilitate the operative procedure for two hours and fifteen minutes. About two hours after the re-expansion of his left lung, he complained of dyspnea. He was hypoxic and moist rale was audible in his left lung. Cloudy shadow emerged in the left field of his chest X-P. Under bronchofiberoptic observation, excessive serous secretions was seen, but no obstructive lesions were found in his bronchial tree. Re-expansion pulmonary edema was suspected for these findings. It was improved with mechanical ventilation with PEEP. Re-expansion pulmonary edema seldom occurs in one lung anesthesia. Although radical operation of esophageal cancer performed six years before might have induced the development of re-expansion pulmonary edema in our case, complete collapse with quick re-expansion of the lung is clearly a potential risk of re-expansion pulmonary edema. Careful management is necessary after one lung ventilation.
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PMID:[A case of re-expansion pulmonary edema after one lung ventilation for the radical operation of lung cancer]. 1264 71

Non-invasive positive pressure ventilation (NIPPV) has been discussed comprehensively in the last years, but usage of non-invasive ventilation in Intensive Care Units is rare. The reasons may be uncertainty in indications and difficulties in handling the masks and ventilators. In the last years the introduction of full face masks and respiratory helmets has made it possible to ventilate patients with unusual facial forms and to avoid problems of pressure necrosis. Software components designed for NIPPV are available for standard respirators. Indications for NIPPV (neuromuscular diseases, spinal abnormalities, chest wall malformations, COPD, cardiogenic pulmonary edema) have been ensured in clinical trials. No sufficient data are available for the application of NIPPV in weaning and respiratory failure following extubation. Indication for NIPPV becomes apparent when therapy starts in early stage with sufficient ventilation pressure. Compared to standard therapy, no reliable advantage has been seen for NIPPV in hypoxic hypercapnia respiratory failure except for malignant diseases. However, prophylactic use in patients with high risk might be conceivable. For these patients strict criteria of termination are required to avoid missing the time point for intubation. Gas exchange disturbances in advanced lung fibrosis, pneumonia and ARDS are not amenable to NIPPV. Contraindications for NIPPV are non-compliant patients, absence of cough- and pharyngeal reflexes as well as retention of secretions and malignant ventricular arrhythmia. Relative contraindications are catecholamine-dependent circulatory collapse and acute myocardial infarction, since sufficient data for NIPPV are missing.
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PMID:[Noninvasive ventilation in the intensive care unit -- is it still negligible?]. 1267 84

One hundred and one (6%) of 1,678 patient studied had bilateral reexpansion pulmonary oedema(RPO). On the whole, one thousand, seven hundred and seventy nine (1,779) pleural spaces were studied, fifteen pleural spaces (0.8%), with mean age of 23 +/- 4.5 years had RPO. Among these 15 patients with RPO, the mean period of lung collapse before pneumothorax (PThx) was evacuated was 31.8 +/- 21.8 days and for hydrothorax (HThx) was 31.3 +/- 30.1 days; for 15 patients without RPO (controls), matched for age and sex, the mean period of lung collapse before CTTD was 7.5 +/- 4.1 days and 5.4 +/- 1.3 days respectively for PThx and HThx. The differences in the period of lung collapse among patients with RPO and those without, for each pleural disease was statistically significant (P < 0.03). Volume of pleural fluid drained before RPO was noticed was 2196 +/- 1103 mls, for the 15 matched patients without RPO (controls), it was 1060 +/- 115 mls (p < 0.05). Volume of pleural fluid drained among the patients with SR (Severe response), MR (mild to moderate response) and RD (radiological diagnosis) did not correlate with severity of response. We conclude that prevention of RPO is the desired goal in the management of pleural effusion or Pneumothorax. RPO is commonest among young patients who have had lung collapse for 7 or more days. In these circumstances RPO is prevented, its incidence and severity reduced by methods of gradual evacuation of PThx or pleural fluid drainage.
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PMID:Reexpansion pulmonary oedema as a complication of pleural drainage. 1269 Jun 82

Re-expansion pulmonary oedema is a well-recognized rare complication of the treatment of spontaneous pneumothorax. It has been associated with death in 20% of cases. A fit 20-year-old man who had returned from holiday 2 days previously presented with a large left-sided pneumothorax of 10 days' duration. He had exhibited symptoms of chest pain and shortness of breath during the return flight. He showed no signs of respiratory distress at presentation to the Accident and Emergency Department, but after treatment with a chest tube in the ensuing 90 min developed severe unilateral re-expansion pulmonary oedema and circulatory collapse. Factors in the aetiology of the condition and prevention are considered.
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PMID:Re-expansion pulmonary oedema and circulatory shock in a 20-year-old man. 1278 75

Acute respiratory distress syndrome/acute lung injury is characterised by profound hypoxaemia due to a permeability pulmonary oedema. In this setting, recruitment manoeuvres (RMs) can be a useful tool as adjuncts to lung protective ventilatory strategies to prevent cyclic alveolar stress and avoid alveolar collapse. Many experimental and physiological studies have discussed the use of RMs but only a few heterogeneous clinical experiences have demonstrated the beneficial and deleterious effects that can occur using these manoeuvres. Besides, a lot of questions remain to be answered to find the best way to perform optimal RMs. Further experimental and clinical trials are needed to understand the potential beneficial effects of recruitment manoeuvres when using a protective mechanical ventilation strategy. This paper is a general review of experimental works that support application of recruitment manoeuvres emphasising the clinical studies that have been published to date in acute respiratory distress syndrome patients.
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PMID:Recruitment manoeuvres in acute lung injury/acute respiratory distress syndrome. 1294 99

A 33 years old woman was admitted to the hospital after four days with cough, dyspnea, orthopnea and hemoptysis. Blood pressure was 170/90 mmHg, pulse was 112 and temperature was normal. She had cyanosis and a left ventricular gallop, without heart murmurs. A chest radiograph revealed pulmonary edema and echocardiogram showed a global left ventricular systolic disfunction. Oxygen and furosemide were started, but cardiopulmonary collapse ensued. The patient was supported with mechanical ventilation and treated with inotropic drugs. A right sided cardiac catheterization showed pulmonary wedge pressure of 18 mmHg and a cardiac index of 3 l/min/m2. The levels of creatinine and urea nitrogen were elevated and a urine protein was 97 mg/dl. Coagulation tests were normal except by a positive lupic anticoagulant. Markers of connective tissue diseases or vasculitis were negatives. The clinical evolution suggested that a catastrophic antiphospholipid syndrome was ongoing. Intravenous corticoids, gammaglobulin and cyclophosphamide were administered with transient improvement. On her fourth day of treatment, the patient presented sudden pulmonary bleeding and embolism. A plasmapheresis was performed with improvement of renal, cardiac and pulmonary function. After this episode, the patient has been treated with prednisone and oral anticoagulants treatment for the last two years, without further clinical events.
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PMID:[Catastrophic antiphospholipid syndrome and acute heart failure. Report of a case]. 1463 91


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