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

Postpneumonectomy pulmonary oedema (PPO) develops in approximately 5% of patients undergoing pneumonectomy or lobectomy, and has a high associated mortality (>50%). In its extreme form, PPO follows a clinical and histopathological course indistinguishable from acute respiratory distress syndrome. Perioperative fluid overload, impaired lymphatic drainage following node dissection and trauma caused by surgical manipulation have been implicated in the pathogenesis of PPO. However, PPO more probably represents the pulmonary manifestation of a panendothelial injury consequent upon inflammatory processes induced by the surgical procedure, which involves collapse and re-expansion of the operative lung to permit hilar dissection and pulmonary resection. High inspired oxygen concentrations are required to overcome the effects of shunt. Animal studies have shown that pulmonary ischaemia/reperfusion can result in oedema formation, possibly due to the generation of pro-oxidant forces. Moreover, plasma taken from patients undergoing lobectomy or pneumonectomy (but not lesser resections) shows evidence of oxidative damage. Such evidence suggests either that the high inspired oxygen concentrations associated with one-lung ventilation, or ischaemia/reperfusion injury, may modulate post-pneumonectomy pulmonary oedema. Mechanisms by which redox imbalance may result in tissue damage and postpneumonectomy pulmonary oedema are discussed.
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PMID:The pathogenesis of lung injury following pulmonary resection. 1078 Jul 50

Continuous as well as cyclic (with each expiration) lung collapse in acute respiratory failure can be reduced by positive end-expiratory pressure (PEEP) or short expiration times, as in inverse ratio ventilation (IRV). In 20 pigs with oleic acid-induced lung edema, we compared the effects of a PEEP of 20 cm H(2)O with IRV, using an inspiratory-to-expiratory ratio of 3:1 without external PEEP. During IRV, expiration times of 0.5 or 1.0 s were obtained with respiratory rates of 30 breaths/min or 15 breaths/min, respectively. In 15 animals, ventilation-perfusion relationships were studied through the multiple inert gas elimination technique, and lung morphology was studied with computed tomography. In another five pigs, blood flow distribution was studied with perfusion scintigraphy. All three ventilatory modes had similar effects on mean arterial blood pressure, cardiac output, oxygen delivery, and mean airway pressure. PEEP reduced shunt and improved oxygenation to a greater extent than the two modes of IRV, although there was a large variation within each group. The improvement, irrespective of which ventilatory mode was superior in a particular pig, was caused by greater and more even aeration of the lung, whereas the perfusion distribution with PEEP was the same as with IRV. Thus, the strategy of stabilizing the lungs through short expiration times, as in IRV, did not offer any advantages in our lung injury model.
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PMID:Effects of inverse ratio ventilation and positive end-expiratory pressure in oleic acid-induced lung injury. 1080 51

Status epilepticus is common and associated with significant mortality and complications. It affects approximately 50 patients per 100,000 population annually and recurs in >13%. History of epilepsy is the strongest single risk factor for generalized convulsive status epilepticus. More than 15% of patients with epilepsy have at least one episode of status epilepticus and low antiepileptic drug levels are a potentially modifiable risk factor. Other risks include young age, genetic predisposition, and acquired brain insults. Fever is a very common risk in children, as is stroke in adults. Mortality rates are 15% to 20% in adults and 3% to 15% in children. Acute complications result from hyperthermia, pulmonary edema, cardiac arrhythmias, and cardiovascular collapse. Long-term complications include epilepsy (20% to 40%), encephalopathy (6% to 15%), and focal neurologic deficits (9% to 11%). Neuronal injury leading to temporal lobe epilepsy is probably mediated by excess excitation via activation of the N-methyl-D-aspartate (NMDA) subtype of glutamate receptors and consequent elevated intracellular calcium that causes acute necrosis and delayed apoptotic cell death. Some forms of nonconvulsive status epilepticus may also lead to neuronal injury by this mechanism, but others may not. Based on clinical and experimental observations, complex partial status epilepticus is more likely to result in neuronal injury similar to generalized convulsive status epilepticus. Absence status epilepticus is much less likely to result in neuronal injury, and complications because it may be mediated primarily through excess inhibition. Future research strategies to prevent complications of status epilepticus include the study of new drugs (including NMDA antagonists, new drug delivery systems, and drug combinations) to stop seizure activity and prevent acute and delayed neuronal injury that leads to the development of epilepsy.
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PMID:Status epilepticus: risk factors and complications. 1088 37

Asymptomatic cardiomegaly and subsequent fulminant pulmonary edema developed in an AIDS patient with end-stage renal disease who had no prior history of cardiac disease. Intravenous thiamine administration led to dramatic resolution of both obtundation and cardiovascular collapse within 4 hours. Prolonged thiamine administration led to decreased cardiomegaly. These findings are consistent with Shoshin beriberi.
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PMID:Shoshin beriberi in an AIDS patient with end-stage renal disease. 1096 32

Patients with acute cardiogenic pulmonary edema require rapid assessment and therapy to prevent progression to respiratory failure and cardiovascular collapse. The goal of therapy is to decrease the pulmonary capillary wedge pressure by decreasing intravascular volume and shifting the blood volume into peripheral vascular beds. Mainstays of therapy include morphine sulfate (a venodilator and an anxiolytic), furosemide (a venodilator and diuretic), nitroglycerin preparations (venodilators), and, in some cases, aminophylline, nitroprusside, and beta-adrenergic agents or milrinone. Patients who do not respond to more conservative measures may require interventional procedures, including Swan-Ganz catheterization or arterial pressure monitoring, continuous positive airway pressure or mechanical ventilation, intra- aortic balloon counterpulsation, and mechanical removal of fluid. Because the prognosis for patients with acute cardiogenic pulmonary edema depends on identification and correction of the underlying disease process, it is essential to define the cause of the edema during and after stabilization of the patient. Evaluation should include Doppler echocardiography, cardiac catheterization, and coronary angiography.
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PMID:Acute Pulmonary Edema. 1109 92

Ipsilateral pulmonary edema may occur in a lung that has been rapidly reinflated after a period of collapse. The syndrome of re-expansion pulmonary edema is associated with variable degrees of hypotension and hypoxemia. In its extreme form, it may result in cardiac arrest and death. The initial cause of uninflated pulmonary parenchyma described with re-expansion pulmonary edema has typically been either a large undrained pleural effusion or a pneumothorax. The authors describe a patient in whom re-expansion pulmonary edema developed when inadvertent puncture of large emphysematous bullae released previously atelectatic lung.
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PMID:Re-expansion pulmonary edema following puncture of a giant bulla. 1121 67

Physical examination of the pulmonary system includes inspection, auscultation, percussion, and palpation. By integrating these findings, it is often possible to diagnose and differentiate pulmonary edema, pleural effusion, pneumothorax, pulmonary fibrosis, and tracheal collapse. The veterinarian can use the physical examination optimally by initially performing examinations with those who are experienced with the methods and with an understanding of the relatively simple laws of physiology and physics governing transmission of sounds from the patient's lung.
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PMID:Physical examination of the pulmonary system. 1122 76

The aim of this study was to assess the frequency of new abnormalities on routine chest radiographs of ventilated, very low birth weight (VLBW) infants during the acute stage of their illness. Infants were identified who had had at least three daily routine chest radiographs. The appearance of their subsequent radiographs was compared to that obtained on the 1st day of ventilatory support and the timing of new abnormalities (malposition of the endotracheal or nasogastric tube, pulmonary interstitial emphysema, pleural effusion, pulmonary oedema, lobar collapse or consolidation) noted. A total of 100 radiographs were examined from 30 VLBW infants, median gestational age 27 weeks (range 23-32 weeks). New abnormalities were present on the radiographs of 24 infants and on 50% of the radiographs examined. The commonest abnormalities noted were pulmonary interstitial emphysema, collapse and consolidation. Conclusion. Routine daily chest radiographs in mechanically ventilated, very low birth weight infants during the acute stage of their respiratory illness can yield new information important in patient care, new abnormalities being demonstrated in 50% of radiographs examined.
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PMID:Routine daily chest radiographs in ventilated, very low birth weight infants. 1127 73

Acute respiratory failure is caused by many factors and remains one of the most common reasons for admission to the intensive care unit (ICU). In all cases of acute respiratory failure, there is a shortage of surfactant at the alveolar level. This deficit of surfactant leads to an increase in alveolar surface tension that increases the retraction forces of the lung, leading to end-expiratory alveolar collapse, finally resulting in respiratory dysfunction, which includes hypoxemia, low lung compliance, increase of intrapulmonary shunts, low functional residual capacity, atelectasis, and pulmonary edema. The goal of the treatment and prevention of acute respiratory failure is therefore based on the following three main items: re-opening the collapsed alveolar units; preserving the active surfactant component in the remaining functional alveolar units, and preventing end-expiratory collapse. The following strategies can be used to prevent and/or treat acute respiratory failure: counterbalancing the retraction forces of the lung by applying sufficiently high external pressures; and/or decreasing the surface tension at the air-liquid interface by means of exogenous surfactant, and/or eliminating the air-liquid interface by filling the lung with perfluorocarbons. By applying these therapeutic strategies in routine clinical practice, we should achieve a reduction in the mortality rate of patients suffering from acute respiratory failure.
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PMID:Treatment and prevention of acute respiratory failure: physiological basis. 1134 4

Pulmonary edema formation resulting from loss of capillary barrier properties is a prominent finding in lung ischemia/reperfusion (I/R) injury. The role of endogenous nitric oxide (NO) in this process is unresolved. We exposed buffer-perfused rabbit lungs to warm I/R and measured air space NO liberation and intravascular accumulation of NO degradation products. In lungs undergoing 210 min of ischemia with normoxic ventilation, with maintenance of positive intravascular pressure to avoid vascular collapse, NO synthesis was moderately reduced during ischemia but was fully restored upon reperfusion, and a moderate leakage response occurred during reperfusion. Pretreatment with the NO synthase inhibitor N(G)-monomethyl-L-arginine (L-NMMA) suppressed NO synthesis but did not affect the leakage. During ischemia with anoxic ventilation, NO synthesis was fully abrogated, but again promptly reappeared upon reperfusion and entrance of oxygen into the system. It was with this protocol that the most severe vascular leakage was encountered, which was markedly reduced in the presence of L-NMMA or superoxide dismutase. We conclude that endogenous NO does not play a major role in the induction or mitigation of I/R injury under conditions of normoxic ischemia, but that return of endogenous NO synthesis upon reperfusion after anoxic ischemia contributes substantially to the triggering of vascular leakage, possibly via interaction with superoxide.
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PMID:Endogenous nitric oxide synthesis and vascular leakage in ischemic-reperfused rabbit lungs. 1150 Mar 42


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