Unilateral Pulmonary Edema Research Articles

Hemodynamic and Pulmonary Edema Protein Measurements in a Case of Reexpansion Pulmonary Edema

We describe a patient with unilateral reexpansion pulmonary edema following thoracocentesis of a right pleural effusion. The pulmonary edema-serum total protein ratio was 0.85. Right heart catheterization revealed a normal pulmonary wedge pressure. The pulmonary edema cleared quickly. This is the first case to our knowledge in which pulmonary hemodynamics and lung fluid total protein levels have been monitored in reexpansion pulmonary edema.

Hypoglycemia and Unilateral Pulmonary Edema in a Newborn

A case of cardiomegaly with unilateral pulmonary edema is presented. The predisposing etiologies were severe hypoglycemia and a hypertonic glucose infusion into a branch of the left lower lobe pulmonary vein. Resolution resulted following maintenance of adequate glucose levels, vigorous cardiopulmonary support, and repositioning of the catheter tip in the inferior vena cava. The pathophysiologic mechanism was direct endothelial injury with an osmotic diuresis. The role of the release of a vasoactive substance was postulated.

Unilateral pulmonary edema in rabbits after reexpansion of collapsed lung

The effects of the mode of reinflation and of the duration of prior collapse on the development of unilateral pulmonary edema following reexpansion of collapsed lung were studied in a rabbit model simulating the human syndrome of "reexpansion pulmonary edema." The right lungs of rabbits were maintained in an atelectatic state for 0.5 h to 8 days, by injection of air into the pleural space. Reexpansion was achieved in 2 h by application of positive pressure to the airway while a chest tube was connected to underwater seal, or by application of negative pressure (-20 to -100 Torr) to a screened window in the partietal pleura. The lung surface pressures we actually applied by the two methods are not known. Animals were then killed and pulmonary edema was determined by wet-to-dry weight ratios. The incidence of unilateral pulmonary edema increased as the duration of prior collapse was increased (85% after 7--8 days; 17% after 3 days; and 0% after 0,5 h) when reinflated with -100 Torr applied to the pleural window. Although the incidence was less, it also occurred following the use of pleural window pressure less negative than -100 Torr, and after reinflation by positive airway pressure.

Unilateral pulmonary edema following thoracotomy for the spontaneous pneumothorax

Unilateral pulmonary edema following thoracotomy for the spontaneous pneumothorax

Unilateral pulmonary edema.

Unilateral pulmonary edema was found to occur following or in conjunction with 18 different clinical situations. In half of them the edema developed on the same side as the causative factor and was related to conditions altering the delicate balance at the alveolar-capillary interface. In the other situations, pulmonary capillary perfusion was deficient on the opposite side prior to the onset of edema.

Unilateral diffuse lung opacity; Differential diagnosis with emphasis on lymphangitic spread of cancer.

One hundred adults with unilateral diffuse lung opacity have been studied. Seventy cases involve the right lung. Lymphangitic cancer, pneumonia, pulmonary edema, aspiration, and radiation injury account for the majority of cases (90%). Unilateral pulmonary edema is usually right sided, and, frequently, the heart is not enlarged. Unilateral lymphangitic spread of cancer is usually right sided and most often due to a primary lesion in the involved lung. Occasionally a cancer outside the lung may spread unilaterally.

Misplacement of central venous pressure catheters and unilateral pulmonary edema

Misplacement of central venous pressure catheters and unilateral pulmonary edema

Misplacement of Central Venous Pressure Catheters and Unilateral Pulmonary Edema

Two instances of misplacement of a central venous pressure monitoring catheter into a pulmonary artery are presented. In one case, reported in detail, unilateral pulmonary edema developed during administration of 0.5N saline for the treatment of diabetic acidosis via the misplaced catheter, and it reverted following repositioning of the catheter in the superior vena caca. Experiments were carried out in dogs to explore possible causes of this phenomenon. The results of these experiments suggest that the release of vasoactive substances, stimulation of neural reflexes, or both are the pathophysiological mechanisms responsible for the development of the pulmonary edema.

Unilateral Pulmonary Edema with Contralateral Thoracic Sympathectomy in the Adult Respiratory Distress Syndrome

A case is presented of pathologically proved unilateral pulmonary edema due to uremia and blood transfusion. The lung that was spared had been denervated by a thoracic sympathectomy eight years earlier. That this denervation may have been responsible for the unilaterality of the pulmonary edema is suggested by experimental evidence supporting a neurogenic etiology of noncardiac pulmonary edema. The literature is briefly reviewed, and implications for therapy are discussed.

Misplacement of central venous pressure catheters and unilateral pulmonary edema

Two instances of misplacement of a central venous pressure monitoring catheter into a pulmonary artery are presented. In one case, reported in detail, unilateral pulmonary edema developed during administration of 0.5N saline for the treatment of diabetic acidosis via the misplaced catheter, and it reverted following repositioning of the catheter in the superior vena caca. Experiments were carried out in dogs to explore possible causes of this phenomenon. The results of these experiments suggest that the release of vasoactive substances, stimulation of neural reflexes, or both are the pathophysiological mechanisms responsible for the development of the pulmonary edema.

Unilateral pulmonary edema after renal transplantation.

UNILATERAL pulmonary edema has been described after re-expansion of pneumothorax,1 in congenital heart disease,2 after thoracentesis3 and in failure of the left side of the heart.4 The two cases re...

Unilateral Pulmonary Edema—Differential Diagnosis

SUMMARY Our experience with fifteen cases of unilateral pulmonary edema, its roentgen appearance and differential diagnosis is presented. Representative patients with unilateral pulmonary edema caused by rapid re-expansion of pneumothorax, congestive heart failure, blunt chest trauma, aspiration of acid gastric contents and following systemic pulmonary artery shunt procedures in children with cyanotic congenital heart lesions are reported in more detail.

Unilateral pulmonary oedema following re-expansion of pneumothorax.

Unilateral pulmonary oedema is a rare complication in the routine management of spontaneous pneumothorax. Previous reports have emphasized excessive negative intrapleural pressure, rapid re-expansion of the lungs and bronchial obstruction as major factors in the pathogenesis. We have encountered four cases, and at least one of these factors have been absent in each case. Review of the literature, and our own experience suggests that the major factor is chronic and total lung collapse resulting in hypoxia and increased alveolar-capillary membrane permeability. Other factors which may be contributory are discussed.

Unilateral Pulmonary Edema in Swyer-James Syndrome

We report a case of Swyer-James syndrome which showed the unusual feature of unilateral pulmonary edema in the normally perfused lung occurring during periods of cardiac decompensation. This case complements the two reported by Kieffer and co-workers, where the unilateral pulmonary edema occurred in conjunction with the proximal interruption of a pulmonary artery.

Changes in Left Atrial and Systemic Arterial Pressures and Blood Flow Following Graded Aortopulmonary Anastomosis

Aortopulmonary anastomosis can produce cardiac failure, unilateral pulmonary edema, or both if constructed too large. The effects on the heart and systemic circulation of aortopulmonary anastomoses of varying sizes were studied in a series of dogs. The larger the shunt, the greater the changes in left atrial pressure and systolic and diastolic arterial pressures. Shunt flow is related to the diameter of the shunt as well as to the existing pulmonary artery pressure. Unilateral pulmonary edema occurred when left atrial pressure was 18 to 20 mm. Hg.

Unilateral Pulmonary Edema

PULMONARY edema can manifest itself in chronic obstructive lung disease with an atypical pattern. 1 The classic appearance of pulmonary edema as bat wing on chest roentgenogram can occur regardless of the underlying disease. Unilateral pulmonary edema is rare and at times it may present problems in differential diagnosis such as aspiration pneumonitis or an inflammatory process. Report of a Case A 68-year-old white man was admitted to William Beaumont Hospital with increasing shortness of breath. Since the patient had been 17 years of age, he was known to be asthmatic. He also had a long history of schizophrenia. Tedral was given (a mixture of theophylline, ephedrine hydrochloride, and pentobarbital), one tablet three times a day, prednisone, 5 mg/day, and chlorpromazine, 200 mg/day. The patient was also known in the past to adjust medications at his own discretion. On the day of admission, he had wheezing and slight shortness of

Unilateral pulmonary oedema after drainage of spontaneous pneumothorax.

<h3><b>Background</b></h3> Psychologically informed practice emphasizes routine identification of modifiable psychological risk factors being highlighted. <h3><b>Objective</b></h3> The purpose of this study was to test the predictive validity of the STarT Back Screening Tool (SBT) in comparison with single-construct psychological measures for 6-month clinical outcomes. <h3><b>Design</b></h3> This was an observational, prospective cohort study. <h3><b>Methods</b></h3> Patients (n=146) receiving physical therapy for low back pain were administered the SBT and a battery of psychological measures (Fear-Avoidance Beliefs Questionnaire physical activity scale and work scale [FABQ-PA and FABQ-W, respectively], Pain Catastrophizing Scale [PCS], 11-item version of the Tampa Scale of Kinesiophobia [TSK-11], and 9-item Patient Health Questionnaire [PHQ-9]) at initial evaluation and 4 weeks later. Treatment was at the physical therapist9s discretion. Clinical outcomes consisted of pain intensity and self-reported disability. Prediction of 6-month clinical outcomes was assessed for intake SBT and psychological measure scores using multiple regression models while controlling for other prognostic variables. In addition, the predictive capabilities of intake to 4-week changes in SBT and psychological measure scores for 6-month clinical outcomes were assessed. <h3><b>Results</b></h3> Intake pain intensity scores (β=.39 to .45) and disability scores (β=.47 to .60) were the strongest predictors in all final regression models, explaining 22% and 24% and 43% and 48% of the variance for the respective clinical outcome at 6 months. Neither SBT nor psychological measure scores improved prediction of 6-month pain intensity. The SBT overall scores (β=.22) and SBT psychosocial scores (β=.25) added to the prediction of disability at 6 months. Four-week changes in TSK-11 scores (β=−.18) were predictive of pain intensity at 6 months. Four-week changes in FABQ-PA scores (β=−.21), TSK-11 scores (β=−.20) and SBT overall scores (β=−.18) were predictive of disability at 6 months. <h3><b>Limitations</b></h3> Physical therapy treatment was not standardized or accounted for in the analysis. <h3><b>Conclusions</b></h3> Prediction of clinical outcomes by psychology-based measures was dependent upon the clinical outcome domain of interest. Similar to studies from the primary care setting, initial screening with the SBT provided additional prognostic information for 6-month disability and changes in SBT overall scores may provide important clinical decision-making information for treatment monitoring.

Massive unilateral pulmonary oedema as a rapid re-expansion sequel (the post-expansion syndrome). Report of a case and review of the literature.

The unusual complication of unilateral pulmonary oedema following closed thoracotomy drainage for massive spontaneous pneumothorax, which is presented in this communication, occurred in a patient suffering from advanced pulmonary emphysema. The physiopathology of the “Post-expansion syndrome” is discussed and the literature reviewed.Restoration of cardio-respiratory physiology following development of pneumothorax, can be accomplished by closed thoracotomy drainage, a simple and safe procedure leading to air-leakage sealing and subsequently to complete re-expansion of the collapsed lung. However, in spite of the simplicity of the method and its widespread clinical acceptance, such a procedure may be followed by fatal complications in connection with sudden lung expansion and coincide with rapid removal of air into a vacuum system of closed drainage. We became interested in this remarkable pathological condition two years ago when we first encountered a case of 100% spontaneous pneumothorax, in which closed thoracotomy drainage was followed by massive pulmonary oedema on the involved side, leading shortly thereafter to death.

Unilateral pulmonary edema after pneumothorax.

THE typical "batwing" or "butterfly" pattern of pulmonary edema1 2 3 is well known. The relative symmetry of perihilar and basal infiltrates in both lungs is indeed an indicator often used by the radiologist to favor a diagnosis of pulmonary edema as opposed to other possible differential diagnoses (aspiration pneumonia, bacterial pneumonia, etc.). Although it is known that pulmonary edema can sometimes be predominantly unilateral as a result of many possible factors (patient positioning,4 congenital heart disease,5 pre-existing unilateral lung disease,6 etc.), gross asymmetry of involvement in acute pulmonary edema is relatively uncommon. Ipsilateral pulmonary edema has been noted rarely after rapid . . .

Localized Unilateral Pulmonary Edema: An Unusual Presentation of Left Heart Failure

A patient with mitral insufficiency caused by infarction of the anterior papillary muscle, presenting with localized unilateral pulmonary edema, is reported. On the basis of previous reports it appears that unilateral presentation of acute pulmonary edema, although unusual, is not so rare as is generally believed. The exact underlying mechanism is not clear but various hypotheses put forward to explain the unilateral distribution include the effect of gravity and posture, variations in the pulmonary venous pressure and some disturbance of the neurogenic control of capillary size and permeability. We believe that a wider recognition of the unilateral presentation of acute pulmonary edema is important to avoid unnecessary delay in diagnosis and proper management.