The chest roentgenogram in pulmonary edema

It has been shown that the chest roentgenogram is a sensitive and accurate pool for detecting and quantitating cardiogenic pulmonary edema. This can be done at the interstitial stage, when it cannot be detected by physical examination. At the same time the chest film can provide useful information about the circulating blood volume. In patients with the ARDS, a characteristic peripheral and patchy distribution of alveolar edema associated with an absence of peribronchial cuffing, septal lines and effusions has been shown. Enlargement of the right side of the heart and main pulmonary artery may precede actual development of edema in ARDS and provide the opportunity for early diagnosis. Radiographic "scoring" in cases of ARDS correlates well with PO2 (measured with an F1O2 = .21) standardized to a PCO2 of 40 mm Hg. The three main forms of lung edema (that is, cardiogenic, renal or overhydration, and injury edema) appear to have radiographic features that can be used to separate them. The accuracy and objectivity of this approach has been confirmed by taking the radiographic signs as input variables for discriminant analysis. Different hemodynamic conditions and changes of the extravascular protein osmotic forces may be the main factors underlying the radiographic patterns in the various types of pulmonary edema.     

Chest radiographic features of engraftment syndrome

About the time of hematopoietic engraftment, patients undergoing autologous hematopoietic stem cell transplantation in the form of peripheral blood stem cell transplantation (PSCT) may develop an "engraftment syndrome" that includes fever, skin rash, and capillary leak. This condition is usually self-limited, as opposed to other early complications of bone marrow transplantation such as infection and drug reactions. This article describes the chest radiographic manifestations of engraftment syndrome. The medical records and chest radiographs of 50 consecutive breast cancer patients who underwent PSCT were retrospectively reviewed. Engraftment syndrome was diagnosed if the expected clinical findings occurred at the time of engraftment of neutrophils and no other cause was identified. The chest radiographs were correlated with the clinical course. Sixteen patients were found to have engraftment syndrome (32%). Of these, eight had abnormal radiographs. Radiographic findings consisted of pleural effusions and interstitial pulmonary edema. No patient progressed to adult respiratory distress syndrome. Interstitial pulmonary edema and pleural effusions were observed in association with engraftment syndrome from PSCT. Correlation of these findings with clinical history and neutrophil count is important so that engraftment syndrome can be distinguished from other causes of fever.     

Lack of association of pleural effusion with chronic pulmonary arterial and right atrial hypertension

Right atrial hypertension has been considered to have a major physiologic influence on the formation of transudative pleural effusions. Since pleural fluid is thought to be cleared primarily by the parietal pleural lymphatic vessels that empty into the systemic veins, systemic venous hypertension secondary to right atrial hypertension should decrease the lymphatic drainage of the pleural space. We retrospectively studied nine patients and prospectively studied 18 patients with long-term right atrial or pulmonary arterial hypertension (or both). All patients had stable respiratory symptoms, and none had a significantly elevated pulmonary arterial wedge pressure. Our purpose was to determine the relationship of right atrial and pulmonary arterial hypertension to the development of transudative pleural effusions. Posteroanterior and bilateral decubitus chest roentgenograms and ultrasound were used to detect pleural effusions. Pleural effusions were not identified in any of the 27 patients, even in four patients with right atrial pressures greater than 20 mm Hg. We conclude that chronic elevation of right atrial pressure or pulmonary arterial pressure (or both) alone is not a cause of pleural effusion. In contrast, elevation of left atrial and pulmonary arterial wedge pressures is associated with the formation of transudative pleural effusions in man. Thus, if pleural effusions are detected in patients who have cor pulmonale, a search should be made for coexisting left heart failure or a primary cause of pleural inflammation, such as pulmonary emboli or infection.     

Engraftment syndrome after hematopoietic stem cell transplantation: high-resolution computed tomography findings in 2 patients

Engraftment syndrome is a noninfectious pulmonary complication after hematopoietic stem cell transplantation that represents a form of diffuse capillary leak associated with lung injury and pulmonary edema. The high-resolution computed tomography findings are interstitial edema and pleural effusions. A combination of clinical information and high-resolution computed tomography findings may help to confirm the diagnosis.     

Chest roentgenographic abnormalities in IL-2 recipients. Incidence and correlation with clinical parameters.

The chest roentgenograms of 54 patients receiving high dose interleukin-2 with or without lymphokine-activated killer cell therapy for advanced cancer were retrospectively reviewed. Thirty-nine patients (72 percent) developed chest roentgenographic abnormalities consisting of pleural effusions, 28 (52 percent); diffuse infiltrates (pulmonary edema), 22 (41 percent); and focal infiltrates, 12 (22 percent). These abnormalities resolved in 30 of 39 (77 percent) patients by four weeks after therapy. Simple pleural effusions were the only residual roentgenographic abnormalities seen and were present primarily in patients receiving IL-2 by bolus intravenous injection (8 of 28) (29 percent) as compared to continuous intravenous infusion (1 of 24) (4 percent) (p = 0.03). Only roentgenographic evidence of pulmonary edema appeared to correlate with the degree of clinical pulmonary toxicity (p = 0.001). The development of chest roentgenographic abnormalities correlated with the administration of IL-2 solely by bolus intravenous injection (p = 0.04), a pretreatment FEV1 of less than 3 L (p = 0.04), and treatment associated bacteremia (p = 0.09), but not with prior therapy, the presence of pulmonary metastases or the degree of systemic capillary leak as measured by percentage of weight gain during therapy. Although the roentgenographic abnormalities did not relate to the number of LAK cells received, two patients developed sudden onset of dyspnea and chest roentgenographic evidence of pulmonary edema shortly after the first LAK cell administration, implying that a direct cause-and-effect relationship exists in some patients. Possible mechanisms for these IL-2 related chest roentgenographic abnormalities and pulmonary toxicity in general are discussed.     

Pleural effusion associated with pulmonary embolization

Pulmonary embolization should be considered as a possible cause of any pleural effusion of unknown etiology. This disorder may be the one that is most commonly overlooked in the work-up of patients with pleural effusions. Although para-embolic effusions have classically been considered to be bloody exudates with a predominance of polymorphonuclear leukocytes, many such effusions have none of these characteristics. Up to 25 per cent may be transudates and the RBC count exceeds 100,000 per mm3 in fewer than 20 per cent of such effusions. The WBC may range from less than 100 to more than 50,000 cells per mm3. Characteristics of these effusions are so variable that no diagnostic patterns can be said to occur. Paraembolic effusions usually begin to resolve within a few days after institution of anticoagulant therapy, although those that are associated with parenchymal infiltrates may resolve more slowly. Unless complications occur (which are rare), pulmonary embolism with associated pleural effusion is treated no differently than is pulmonary embolism without effusion.     

Is there any treatment other than drugs to alleviate dyspnea in COPD patients?

Patients with chronic obstructive pulmonary disease (COPD) are often limited in their activities by breathlessness. In these patients, exercise training may result in significant improvements in dyspnea, exercise tolerance, and health related quality of life (HRQoL). Further possibilities are to reduce ventilatory demand by decreasing the central respiratory drive or to lessen the perceived breathing effort by increasing respiratory muscle strength through specific respiratory muscle training. Upper limb training may also improve exercise capacity and symptoms in these patients through the modulation of dynamic hyperinflation. Ventilatory assistance during exercise reduces dyspnea and work of breathing and enhances exercise tolerance, although further studies should be required to define their applicability in the routine pulmonary rehabilitation programs. Lung volume resection surgery and lung transplantation in selected patients may control symptoms and improve HRQoL.     

Central sleep apnea syndrome

Central sleep apnea syndrome (CSAS) is a disorder characterized by repeated apneic events during sleep with no associated ventilatory effort. CSAS is classified as either hypercapnic or non-hypercapnic. In the hypercapnic form of CSAS, increases in PaCO(2) generally result from reductions in ventilation or outright apneas due to an underlying depression of respiratory drive. Hypercapnic CSAS is common in central hypoventilation syndromes which may be primary (idiopathic) or secondary to other disorders that cause damage to the respiratory center. Non-hypercapnic CSAS is not associated with either a primary reduction in respiratory drive or respiratory muscle weakness. Non-hypercapnic CSAS can be a primary disorder or can occur secondary to high altitude, other medical illnesses such as congestive heart failure and central nervous system disease.     

Comparison of angiographic findings and demographic variables in patients with coronary artery disease presenting with acute pulmonary edema versus those presenting with chest pain

One hundred nineteen patients admitted to the coronary care unit with pulmonary edema were retrospectively reviewed to identify the demographic characteristics and underlying cardiac disorders of this population. The patients with pulmonary edema were compared with 119 patients admitted to the coronary care unit with chest pain. Cardiac catheterization in 71 patients with pulmonary edema and 93 with chest pain showed left main and 3-vessel coronary artery diseases to be equally common in both groups, although anginal pain was infrequent in patients with pulmonary edema (n = 28, 24%). Left ventricular function was reduced in the patients with pulmonary edema compared with those with chest pain (mean ejection fraction 42 vs 59%; p < 0.001). More patients with pulmonary edema were black, and had diabetes and preexisting hypertension than those with chest pain. The results of cardiac catheterization were the same for black and white patients with pulmonary edema. In conclusion, patients with pulmonary edema have a high incidence of cardiac disease, and pulmonary edema may be 1 manifestation of silent myocardial ischemia. Important demographic differences exist between patients admitted with pulmonary edema and those who present with chest pain.     

Pulmonary edema in cerebral malaria patients in Thailand.

Pulmonary edema is a serious complication of falciparum malaria that usually occurs in association with cerebral malaria, acute renal failure, high parasitemias, or delayed antimalarial treatment. From 1993 to 1996, 120 adult patients admitted to the intensive care unit of the Bangkok Hospital for Tropical Diseases were enrolled in a prospective study to assess the combination of artesunate and mefloquine for the treatment of cerebral malaria. Twenty-five patients (21%) presented with pulmonary edema and a majority developed complications in other organs as well, especially acute renal failure. In most patients (19 of 25), pulmonary edema was noted on the first day of admission and was associated with higher parasitemias and levels of acidemia, than in patients without pulmonary edema. Ten of the 25 patients diagnosed with pulmonary edema developed signs consistent with adult respiratory distress syndrome (ARDS). The mean central venous pressure when pulmonary edema was diagnosed was markedly lower in ARDS than in non-ARDS patients, supporting the argument that fluid imbalance is not essential for malaria-induced lung injury. Seven of 10 patients with ARDS died, 5 within 24 hours of admission, but there were no deaths in the 15 pulmonary edema patients without ARDS. Early diagnosis and prompt treatment remain important principles to reduce the morbidity and mortality associated with complicated falciparum malaria. This report emphasizes that ARDS, when concurrently occurs, is a poor prognostic clinical indicator in cerebral malaria.     

Therapeutic thoracentesis: the role of ultrasound and pleural manometry

PURPOSE OF REVIEW: Therapeutic thoracentesis is one of the most commonly performed medical procedures. The availability of handheld ultrasound machines has greatly enhanced the evaluation and management of patients with pleural effusions, with advantages including the absence of radiation, ease of use, portability and real-time/dynamic imaging. Pleural manometry refers to the measurement of pleural pressure during thoracentesis. Though described more than 122 years ago, most physicians do not measure pleural pressure, or even consider the role pleural pressures plays in the development of pleural effusions. This review summarizes the relevant data behind the use of ultrasound and manometry and explores their use during therapeutic thoracentesis RECENT FINDINGS: The use of ultrasound has been associated with a higher sensitivity for identifying pleural effusions, avoiding 'near misses' and a lower pneumothorax rate for thoracentesis. Pleural manometry can be used to distinguish patients with lung entrapment from those with trapped lung. Manometry is also able to predict the ability to pleurodesis patients with malignant effusions, and possibly minimize the risk of reexpansion pulmonary edema when large volumes of pleural fluid are removed. SUMMARY: The use of ultrasound and pleural manometry enhances the understanding of pleural disease and is associated with clinical benefit that will lead to improved patient care.     

Persistent respiratory insufficiency secondary to diastolic heart failure

This study assessed two 85-year-old patients diagnosed with diastolic heart failure and persistent respiratory insufficiency characterized by severe obstructive ventilatory disorder and gas exchange alterations. The possibility that the respiratory impairment was consequent to primary pulmonary disease was excluded. Radiological signs of mild pulmonary edema had been observed in 1 of the patients during the 4 years preceding the first hospitalization. The respiratory findings were attributed to pulmonary lesions conditioned to the presence of chronic pulmonary edema. The incidence of the disease in very elderly patients may create an illness that can be called congestive pulmonary disease.     

Eosinophilic pleural effusions

Eosinophilic pleural effusions, defined as a pleural effusion that contains at least 10% eosinophils, may be caused by almost every condition that can cause pleural disease. Eosinophilic pleural effusion occurs most commonly during conditions associated with the presence of blood or air in the pleural space, infections, and malignancy. Drug-induced pleural effusions, pleural effusions accompanying pulmonary embolism, and benign asbestos pleural effusions are also among the common causes of eosinophilic pleural effusion. No etiology is found in as many as one third of patients. Because studies evaluating different diagnostic approaches with eosinophilic pleural effusions are lacking, the authors suggest that certain noninvasive and invasive diagnostic tools must be used based on the patient's clinical characteristics.     

Left ventricular cardiac tamponade in the setting of cor pulmonale and circumferential pericardial effusion. Case report and review of the literature

Circumferential pericardial effusion typically results in biventricular tamponade and equalization of intracardiac and pericardial pressure during diastole. However, tamponade may involve the right or left ventricle. While isolated left ventricular cardiac tamponade (LVCT) can occur as a postoperative complication from localized posterior pericardial effusions, circumferential pericardial effusions leading to LVCT are rare. We report a case of a patient with severe pulmonary hypertension, a large nonloculated pericardial effusion, and LVCT, which was probably due to a chronic undifferentiated connective tissue disorder. This case illustrates that when evaluating patients with circumferential pericardial effusions and associated pulmonary hypertension, the typical findings of cardiac tamponade (pulsus paradoxus, right ventricular diastolic compression and hypotension) may be masked. The echocardiogram must be reviewed carefully as it may reveal left ventricular diastolic compression, the hallmark of LVCT, which may significantly compromise left ventricular filling and cardiac output.     

Permeability pulmonary edema following lung resection

The etiology of edema associated with pulmonary resection was investigated in five patients during the immediate postoperative period. Three patients received pneumonectomy while two patients had one lobe resected. All patients suffered from severe respiratory distress and had x-ray evidence of diffuse interstitial pulmonary edema within 12 hours of surgery. Hemodynamic data were obtained with radial and pulmonary artery catheters. Edema fluid was obtained along with blood samples for simultaneous determination of protein and albumin content. All patients studied had normal or high cardiac output, normal cardiac filling pressures, and edema fluid protein to serum protein ratio of 0.6 or greater suggestive of permeability changes contributing to edema fluid accumulation. Calculated shunt fraction exceeded 25 percent in all patients. Pulmonary edema has been noted in patients following pulmonary resection in the early postoperative period. In patients reviewed here, two factors appeared to be significant. First is an increase in pulmonary capillary pressure associated with passage of a normal to high cardiac output in a reduced volume pulmonary vascular bed. The second factor, as demonstrated by protein content in the edema fluid, is injury to the alveolar capillary membrane.     

Radiographic features of pleural effusions in pulmonary embolism

A prospective analysis of 155 patients with pulmonary embolism was undertaken to describe the radiographic characteristics of associated pleural effusions and related abnormalities. Approximately one half of these patients had pleural effusions. Patients with other potential causes of effusion, such as heart failure, pneumonia, or cancer, were eliminated from further analysis. In the remaining 62 patients, radiographic evidence of pulmonary infarction accompanied pleural effusions in one half of the cases. One third of patients with parenchymal consolidation had no evidence of effusion. Atelectasis and other nonspecific radiographic abnormalities occurred in less than one fifth of the cases. Typically, pleural effusions were small and unilateral, appeared soon after symptoms of thromboembolism began, and tended to reach their maximal size very early in the course of the disorder. Pulmonary infarction was associated with larger effusions that cleared more slowly and were more often bloody in appearance on thoracentesis. Chest pain occurred in all but one patient and was a valuable diagnostic clue. Pain and pleural effusions were always ipsilateral and almost always unilateral, but neither correlated well with the presence or time course of infarction. Effusions that were delayed in onset or that enlarged late in the course were associated with recurrent pulmonary embolism or superinfection. These radiographic features may be helpful in the diagnosis and management of pulmonary embolism.     

Non-invasive ventilation

Non-invasive ventilation is a technique to ventilate patients without endotracheal intubation and analgosedation. Pressure tight masks allow the ventilation of patients with severe respiratory or ventilatory insufficiency. Non-invasive ventilation may be used as short-term treatment for patients with acute ventilatory decompensation, as well as for long-term therapy at home for patients with chronic respiratory diseases. The typical indications are hypoxaemic respiratory failure in pneumonia or cardiogenic pulmonary edema, and hypercapnic ventilatory insufficiency in severe chronic obstructive pulmonary disease, neuromuscular disorders, or advanced kyphoscoliosis. The physiological background, technical aspects of performing non-invasive ventilation, and typical indications are discussed.     

Nichtinvasive Beatmung

Non-invasive ventilation is a technique to ventilate patients without endotracheal intubation and analgosedation. Pressure tight masks allow the ventilation of patients with severe respiratory or ventilatory insufficiency. Non-invasive ventilation may be used as short-term treatment for patients with acute ventilatory decompensation, as well as for long-term therapy at home for patients with chronic respiratory diseases. The typical indications are hypoxaemic respiratory failure in pneumonia or cardiogenic pulmonary edema, and hypercapnic ventilatory insufficiency in severe chronic obstructive pulmonary disease, neuromuscular disorders, or advanced kyphoscoliosis. The physiological background, technical aspects of performing non-invasive ventilation, and typical indications are discussed.     

Thoracoscopy talc poudrage : a 15-year experience

OBJECTIVES: To review our experience with thoracoscopy and talc poudrage during the previous 15 years with regards to efficacy, side effects, morbidity, and mortality. METHODS: Six hundred fourteen consecutive patients (58.6% female; mean age, 54.5 years) underwent thoracoscopy with talc poudrage from August 1983 to May 1999. Of these, 457 patients had malignant pleural effusions, 108 patients had benign pleural effusions, and 49 patients had spontaneous pneumothorax. RESULTS: Sixty-four patients were excluded from evaluation for efficacy: 30 patients (4.9%) because the lung did not expand at the time of the procedure and 34 patients (5.5%) because they died within 30 days of the thoracoscopy. All exclusions were in the malignant group. The overall success rate of the 393 patients with malignant pleural effusions was 93.4%, while the overall success for the 108 patients with benign effusions was 97%, although 7 patients (7%) with benign effusions required a second thoracoscopy. The success rate with pneumothorax was 100%. Major morbidity included empyema in 4%, reexpansion pulmonary edema in 2.2%, and respiratory failure 1.3%. CONCLUSION: Thoracoscopy with talc poudrage is effective in producing a pleurodesis in malignant and benign pleural effusion and in spontaneous pneumothorax. However, it should be noted that the insufflation of talc has a systemic distribution associated with a low rate of morbidity and perhaps does induce ARDS, which is sometimes fatal in a small percentage of patients. Because of these side effects, the search for a better agent should be continued.     

Pulmonary complications in the patient with acute head injury: neurogenic pulmonary edema

Neurogenic pulmonary edema (NPE) is a serious complication associated with various central nervous system insults. Experimental and clinical data support the occurrence of pulmonary edema as a result of neurogenic factors. Patients with NPE have increased intracranial pressure and respiratory distress, and their care presents a challenge to critical care nurses. The pathophysiology of this disease is not well understood. We discuss the current theories of NPE, its signs and symptoms, and the nursing management for patients with NPE.