You are in: eMedicine Specialties > Radiology > CHEST Pulmonary Edema, NoncardiogenicArticle Last Updated: May 7, 2008AUTHOR AND EDITOR INFORMATIONSection 1 of 11
  Author: Ali Nawaz Khan, MBBS, FRCS, FRCP, FRCR, LRCP, Chairman of Medical Imaging, Professor of Radiology, NGHA, King Fahad National Guard Hospital, King Abdulaziz Medical City, Riyadh, Saudi Arabia Ali Nawaz Khan is a member of the following medical societies: American Institute of Ultrasound in Medicine, Radiological Society of North America, Royal College of Physicians, Royal College of Physicians and Surgeons of the United States, Royal College of Radiologists, and Royal College of Surgeons of England Coauthor(s): Klaus L Irion, MD, PhD, Consulting Staff, The Cardiothoracic Centre Liverpool NHS Trust, The Royal Liverpool University Hospital, UK; Ram Sundar Kasthuri, MBBS, Specialist Registrar, Department of Radiology, North Manchester General Hospital; Sumaira MacDonald, MBChB, PhD, MRCP, FRCR, Lecturer, Sheffield University Medical School; Endovascular Fellow, Sheffield Vascular Institute Editors: Jeffrey A Miller, MD, Associate Professor of Clinical Radiology, University of Medicine and Dentistry of New Jersey; Associate Chief of Service, Department of Radiology, Veterans Affairs of New Jersey Health Care System; Bernard D Coombs, MB, ChB, PhD, Consulting Staff, Department of Specialist Rehabilitation Services, Hutt Valley District Health Board, New Zealand; John D Newell, Jr, MD, FACR, FCCP, FASER, Co-Director of Thoracic Imaging, UCDHSC; Director of Lung Imaging Center, Professor of Radiology and Professor of Medicine, Department of Radiology, University of Colorado Health Sciences Center, National Jewish Medical and Research Center; Univ. Colorado Hospital; Robert M Krasny, MD, Consulting Staff, Department of Radiology, The Angeles Clinic and Research Institute; Kavita Garg, MD, Professor, Department of Radiology, University of Colorado Health Sciences Center Author and Editor Disclosure Synonyms and related keywords: PE, noncardiogenic PE, NPE, lung edema, neurogenic pulmonary edema, nonhemodynamic pulmonary edema, nonhemodynamic PE, inhalation lung injury, aspiration pulmonary edema, drug-induced pulmonary edema, uremic pulmonary edema, adult respiratory distress syndrome, ARDS, shock lung, stiff lung, adult respiratory distress syndrome, acute respiratory distress syndrome, transfusion-related acute lung injury, TRALI, high-altitude pulmonary edema, HAPE INTRODUCTIONSection 2 of 11
  BackgroundPulmonary edema is differentiated into 2 categories: cardiogenic and noncardiogenic. The latter, noncardiogenic pulmonary edema (NPE), is caused by changes in permeability of the pulmonary capillary membrane as a result of either a direct or an indirect pathologic insult. Many causes of NPE exist, including drowning, acute glomerulonephritis, fluid overload, aspiration, inhalation injury, neurogenic pulmonary edema, allergic reaction, and adult respiratory distress syndrome (ARDS). The correct diagnosis relies on clinical and radiologic findings, despite some overlap in the clinical and imaging findings between the different causes. An initial and rapid increase in pulmonary vascular pressure due to pulmonary vasoconstriction or pulmonary blood flow can lead to pulmonary microvascular injury. An increase in vascular permeability consequently results in edema formation, as suggested by the frequent observation of pulmonary hemorrhage in NPE (ie, the blast theory). Two major components contribute to the pathogenesis of NPE: elevated intravascular pressure and pulmonary capillary leak. Therefore, hemodynamic cardiogenic and noncardiogenic components exist. These components often work in concert, as in pulmonary edema after epileptic convulsions or intracranial pressure elevation. The hemodynamic component is relatively brief and may unmask pure NPE, such as that seen in experimental seizures. Whether the hemodynamic changes produce a pulmonary capillary leak through pressure-induced mechanical injury to the pulmonary capillaries or whether some direct nervous system control over pulmonary capillary permeability exists remains uncertain. The neuro-effector site for nervous system–induced pulmonary edema appears to be relatively well established in regions about the caudal medulla, where nuclei regulating systemic arterial pressure, as well as afferent and efferent pathways to and from the lungs, are located. In order to avoid life-threatening complications, prompt recognition of NPE is important. The use of chest radiography and other tests is key to establishing the diagnosis and to distinguishing between the 2 types of pulmonary edema. PathophysiologyPulmonary edema is a major manifestation of left ventricular heart failure, renal insufficiency, shock, and diffuse alveolar damage and lung hypersensitivity states. Fluid is retained within the lungs. In early stages, the fluid retention is confined to the lower lobes; in advanced edema, however, all lung lobes may be involved, acquiring a rubbery, gelatinous consistency. On pathologic sectioning of the lungs, there is free escape of a mixture of air and fluid in the form of frothy, sanguineous fluid. Histologic examination of lung tissue shows that the edema fluid first accumulates about the septal capillaries, with widening of the septa. With further progression of pulmonary edema, proteinaceous fluid, no longer retained in the histologic section, escapes into the alveolar sacs. The alveolar fluid appears as a granular pink coagulate. Edema fluid, when present for some time, is often complicated by hypostatic pneumonia. Types of NPE or conditions that can result in NPE include the following1:
Adult respiratory distress syndrome ARDS is a syndrome of severe respiratory failure associated with pulmonary infiltrates that is similar to infant hyaline membrane disease. ARDS can occur in children as well as in adults. The condition originates from a number of insults involving damage to the alveolocapillary membrane with subsequent fluid accumulation in the airspaces of the lung. Histologically, these changes have been termed diffuse alveolar damage. NPE results from the loss of integrity of the alveolar-capillary membrane, resulting in increased permeability to plasma. Fluid enters the alveolar space and disrupts the function of pulmonary surfactant, resulting in micro-atelectasis and impaired gas exchange. Ultimately, regional variations in pulmonary perfusion, ventilation/perfusion (V/Q) mismatch with shunting of blood through unventilated alveoli, and an increased alveolar-arterial oxygen gradient occurs. ARDS is defined as the presence of bilateral pulmonary infiltrates on chest radiograph, impaired oxygenation resulting in a PaO2-to–fraction of inspired oxygen (FIO2) ratio of less than 200, and absence of elevated pulmonary arterial occlusion pressure (PAOP) or left atrial pressure. Stated another way, ARDS is the presence of pulmonary edema in the absence of volume overload or depressed left ventricular function. Neurogenic pulmonary edema The pathogenesis of NPE is not completely understood. The most common neurologic event associated with NPE is increased intracranial pressure, which is considered a key etiologic factor. In the central nervous system (CNS), the sites responsible for the development of NPE are not fully established. Animal studies indicate a potential role played by the hypothalamus, the medulla, intracranial hypertension, and activation of the sympathetic system. Hypothalamic lesions and stimulation of the vasomotor centers of medulla can increase output along the sympathetic trunk. The medulla is believed to activate the sympathetic nervous system. Experimental work shows that bilateral lesions of the nuclei in the medulla can produce profound pulmonary and systemic hypertension and pulmonary edema. Alpha-adrenergic blockade (ie, phentolamine) and spinal cord transection at the C7 level prevent the formation of NPE, suggesting an important role for sympathetic activation. An acute neurologic insult, associated with a marked increase in intracranial pressure, may stimulate the hypothalamus and the vasomotor centers of the medulla. This, in turn, initiates a massive autonomic discharge mediated by preganglionic centers within the cervical spine. A CNS lesion can produce a dramatic change in Starling forces, which govern the movement of fluid between capillaries and the interstitium. The hemodynamic (cardiogenic) and nonhemodynamic (noncardiogenic) components contribute toward edema formation. Alterations in pulmonary vascular pressures appear to be the most likely Starling force to influence the formation of NPE, as evidenced by protein-rich edema fluid. Experimental observations suggest 2 mechanisms by which pulmonary capillary hydrostatic pressures can be acutely increased; one of these involves increased left atrial pressure, and the second involves pulmonary venoconstriction. An increase in left atrial pressure may occur due to an increase in sympathetic tone and an increase in venous return. Left ventricular performance may deteriorate secondary to the direct effects of catecholamines and other mediators, as well as secondary to transient systemic hypertension. Pulmonary venoconstriction occurs with sympathetic stimulation, which may increase the capillary hydrostatic pressure and produce pulmonary edema without affecting left atrial or pulmonary capillary wedge pressure. An increase in capillary permeability can result in NPE without the elevation of pulmonary capillary hydrostatic pressure, since causative hemodynamic alteration is inconsistent; however, evidence shows that alpha-adrenergic blockade can protect against NPE. Epinephrine, norepinephrine, and even a release of secondary mediators may directly increase pulmonary vascular permeability. Whether the capillary leak is produced by pressure-induced mechanical injury because of the elevated capillary hydrostatic pressure or results from some direct nervous system control over the pulmonary capillary permeability remains uncertain. Pulmonary edema in renal failure/fluid overload Impaired salt and/or water excretion leads to plasma volume expansion. This, along with decreased plasma oncotic pressure and an increase in capillary permeability, results in pulmonary edema. Secondary left ventricular failure and cardiogenic pulmonary edema can also occur. Negative-pressure pulmonary edema Negative-pressure pulmonary edema is associated with upper airway obstruction. Most described cases are associated with croup or epiglottitis requiring airway intervention in the pediatric population and adults requiring emergent airway intervention for laryngospasm or upper airway tumors. Laryngospasm is life threatening, and rapid identification and resolution of the obstructed glottis is required. Although the incidence of laryngospasm is low, postextubation laryngospasm is possible in any patient. The pathogenesis is multifactorial. Negative intrapleural pressure is the primary pathologic event. This induces pulmonary edema formation by increasing venous return to the right heart and by decreasing the output of the left ventricle, thereby increasing pulmonary blood volume and microvascular pressures. These effects are augmented by the hypoxia and hyperadrenergic state that develop secondary to the airway obstruction, promoting translocation of blood from the systemic to the pulmonary circulation and further increasing pulmonary microvascular pressures.2 Pulmonary edema in marathon runners Hyponatremia, cerebral edema, and NPE can occur in healthy marathon runners. In these persons, NPE is often associated with hyponatremic encephalopathy. The condition may be fatal if undiagnosed. It can be successfully treated with hypertonic saline.3, 4, 5 Decompression sickness NPE is a recognized but uncommon manifestation of type 2 decompression sickness. It typically occurs within 6 hours of a dive. Because ARDS in this setting is believed to be due to microbubbles in the pulmonary vasculature, recompression in a hyperbaric chamber has been recommended as a form of therapy.6 Heroin and naloxone overdose NPE is a known complication of heroin or naloxone overdose.7 The pathogenesis of the pulmonary edema in this setting is unknown. It is usually clinically apparent immediately after or within 2 hours following drug use. Signs include rales; significant hypoxia; pink, frothy sputum; and bilateral, fluffy infiltrates on chest radiography. Most patients require mechanical ventilation because of severe hypoxia and respond in 24-36 hours with supportive care. This syndrome has been characterized as noncardiogenic on the basis of hemodynamic and pulmonary fluid analyses. Drug-Related NPE NPE and acute paraplegia in a 35-year-old woman has been reported following the accidental intra-arterial injection of benzathine penicillin in the gluteal region.8 A magnetic resonance imaging (MRI) scan indicated that syringomyelia and spinal cord ischemia at T9 through T10 were present. Vascular injury from microemboli of the injected crystals of the penicillin salts was implicated. Essential hypertension is commonly treated with diuretics, especially the thiazide type. Hypotension, photosensitivity, hypokalemia, anorexia, and epigastric distress constitute the most frequent adverse reactions. However, the adverse reactions are rarely life threatening. Goetschalckx and colleagues reported on a patient in whom pulmonary edema was associated with low left ventricular filling pressures and hypotension, which developed soon after the person ingested 12.5 mg of hydrochlorothiazide.9 Forty-nine cases of NPE have been reported in the literature following administration of thiazide-type diuretics. The Goetschalckx study postulated an allergic type III reaction as the mechanism behind this reaction.9 A severe, life-threatening NPE has been reported following an idiosyncratic reaction after clopidogrel use.10 Pulmonary complications are said to occur in 20% of patients receiving cytotoxic chemotherapy.11 The following types of drug-induced injury may occur:
The clinical and imaging findings are similar to those of NPE due to other causes. Pulmonary complications of pregnancy NPE can occur in pregnancy. Physiologic changes during pregnancy affect nearly every organ system. In the thoracic cavity, the diaphragm is elevated by as much as 4 cm because of displacement of the abdominal organs by the gravid uterus, decreasing lung volumes. Maternal blood volume and cardiac output increase approximately 45% by midpregnancy. Cardiac output can increase as much as 80% during vaginal delivery and up to 50% with cesarean delivery. These changes result in pulmonary vascular engorgement, progressive left ventricular dilatation, and mild hypertrophy. Drowning In drowning, the extent and severity of the edema depends on the amount of water aspirated and the degree of hypoxia. Pulmonary edema in drowning is due to injury of the alveolar septa, increased permeability of the pulmonary vascular endothelium, pulmonary microvascular platelet aggregation, and intra-alveolar edema. Whether the water is fresh or salt makes no difference on the pulmonary findings. NPE induced by a molecular adsorbent recirculating system NPE is a well-recognized manifestation of acute lung injury that has been related, among others, to blood or blood-product transfusion, intravenous contrast injection, air embolism, and drug ingestion. Doria and colleagues described 2 cases of NPE after use of a molecular adsorbent recirculating system, a cell-free dialysis technique.12 Patients in that series were undergoing evaluation for liver transplantation. Two (6.6%) of 30 patients thus treated for acute-on-chronic liver failure and intractable pruritus had normal chest radiographs before treatment. After treatment, both developed severe pulmonary edema in the absence of cardiogenic causes. For each patient, the investigators reviewed the history of blood or blood-product transfusion, daily chest radiographs, and, as available, echocardiograms, pretreatment and posttreatment blood pressures, central venous pressures, pulmonary arterial pressures, cardiac output, cardiac index, systemic vascular resistance index, and arterial blood gases. Their data suggested that NPE may result from the molecular adsorbent recirculating system, possibly by means of an immune-mediated mechanism. Transfusion-related pulmonary edema between mother and child Transfusion-related acute lung injury (TRALI) is an underdiagnosed and serious complication of blood transfusion characterized by the rapid onset of respiratory distress, hypoxia, and NPE during or soon after blood transfusion.13 The presence of anti–human leukocyte antigen (anti-HLA) and/or antigranulocyte antibodies in the plasma of donors is implicated in the pathogenesis of TRALI. Yang and colleagues reported 2 cases of TRALI that were caused by designated blood transfusion between mothers and daughters.14 One of these occurred in a 4-month-old girl who received designated packed red blood cells (RBCs) donated by her mother; the second occurred in a 78-year-old mother who received blood from her daughter. In both cases, examination of mother's serum revealed panel-reactive, cytotoxic HLA antibodies. The mothers were likely sensitized from earlier pregnancy and produced HLA antibodies against the daughters' paternally derived HLA antigens. Designated blood transfusion between multiparous mothers and their children might add an additional transfusion-related risk owing to the increased likelihood of the HLA antibody-antigen specificity between mother and child. NPE after lung transplantation Lung transplantation has become a well-established treatment for end-stage pulmonary parenchymal and vascular disease. Complications of lung transplantation include the reimplantation response, acute rejection, pleural effusion, lymphoproliferative disorders, bronchiolitis obliterans, infection, and airway stenosis or dehiscence. The reimplantation response is a form of NPE that begins soon after surgery and resolves in days to weeks. Acute rejection occurs in most recipients; a dramatic response to steroid therapy is the most diagnostic clinical feature. Imaging is important in differentiating the various complications. Infections remain the major cause of morbidity and mortality post transplant.15 NPE in children with nonaccidental injury NPE in children may occur after head injury, prolonged seizure, acute airway obstruction, or ingestion or inhalation of toxic drugs or chemicals. Rarely, NPE may be associated with child abuse or maltreatment.16 FrequencyUnited StatesThe precise incidence of NPE is hard to quantify, as this is a clinical syndrome associated with a wide range of associated conditions. Furthermore, most cases occur after hospitalization. A worldwide rate of approximately 70 cases per 100,000 population has been suggested. The incidence of pulmonary edema associated with airway obstruction has been estimated to be 12% and 11% in children and adults (respectively) requiring active airway intervention—that is, intubation or tracheostomy—for acute upper airway obstruction of varying etiology. Drowning is the third highest cause of accidental death in children; this is often associated with NPE. Acute pulmonary edema occurs frequently (57%) after lung transplantation. InternationalNo data suggest that the incidence of NPE internationally varies from that in the US. Mortality/MorbidityPulmonary edema is a serious complication of heart failure and renal insufficiency. Pulmonary edema due to noncardiogenic causes also carries serious risk, although the mortality and morbidity depend on the etiology. The patient's prognosis is determined by the course of underlying neurologic problems, as well as by other factors, such as patient age and any comorbid pathology. Despite years of research, mortality rates related to ARDS remain as high as 40-60%. AgeNo specific epidemiologic data related to NPE are currently available. The distribution depends on that of the underlying pathology resulting in pulmonary edema.16 Clinical DetailsClinical features of NPE The characteristic features of NPE are dyspnea, hypoxemia, and radiographic pulmonary infiltrates developing within a few hours of a neurologic event. Whatever the etiology, pulmonary edema impedes normal ventilatory lung function. Patients are breathless, have difficulty in lying flat, and have tachypnea and varying degrees of tachycardia. Characteristically, major auscultatory findings are coarse rales, particularly at the lung bases. In severe pulmonary edema, the collection of fluid in the bronchial tree gives rise to loud rales, which can be heard at the patient's bedside. Pulmonary edema is often complicated by hypostatic pneumonia. Features of high-altitude pulmonary edema Kobayashi and colleagues examined 27 consecutive patients with high-altitude pulmonary edema.17 The altitude at onset was 2680-3190 m above sea level. Symptoms included marked dyspnea, cough, and stridor. Physical findings included cyanosis, tachycardia, and rales. Neurologic disturbances, seen in 17 patients, included headache, vomiting, memory disturbance, clouding of consciousness, or coma. Chest radiographs revealed patchy infiltrates throughout the pulmonary fields, often in an asymmetrical pattern, and enlargement of the right ventricle. Hemodynamic studies via right cardiac catheterization showed that the high-altitude pulmonary edema was noncardiogenic. In 2 patients, pulmonary edema fluid collected through the endotracheal tube was rich in protein. Computed tomography (CT) scans of the brain showed small ventricles and cisterns, disappearance of sulci, and diffuse hypoattenuation of the cerebrum, indicating cerebral edema in 8 of 9 cases. Retinal hemorrhage and papilledema were observed in 5 patients. Differential diagnosis The differential diagnosis of NPE includes ARDS, cardiogenic pulmonary edema, bacterial pneumonia, and aspiration pneumonia. This last condition is one of the main differential diagnoses of NPE, because it also occurs in the setting of altered consciousness. NPE usually develops more rapidly than does aspiration pneumonia. Fever associated with NPE is unusual, but it may accompany the underlying neurologic insult that causes the NPE. Generally, aspiration pneumonia takes 1-2 weeks to resolve, whereas NPE resolves more quickly (from within hours to after several days). Preferred ExaminationMost patients with NPE are seriously ill and immobile. Conventional chest radiography is readily and universally available, and it has the added advantage of portability; chest radiography is the examination of choice. In conjunction with the clinical presentation, radiographic findings are generally sufficient to arrive at a diagnosis of NPE. Limitations of TechniquesThe specificity of chest radiographs, particularly portable, anteroposterior (AP) images, is low, and it may not be possible to differentiate the various causes of lung parenchymal shadowing on radiographs alone. Most patients with NPE are generally ill, and there may be transportation problems to CT scanning and MRI units. Moreover, because these patients may be restless, sedation may be required to obtain images that are not degraded by motion artifacts. DIFFERENTIALSSection 3 of 11
Aspiration Pneumonia Pneumonia, Atypical Bacterial Pneumonia, Typical Bacterial Pulmonary Edema, Cardiogenic Other Problems to Be ConsideredARDS RADIOGRAPHSection 4 of 11
FindingsThe heart is usually enlarged in cardiogenic pulmonary edema, but it may be normal in lung injury and NPE. However, the heart may also be of normal size in cardiogenic edema after acute myocardial infarction. Pulmonary vascular plethora often occurs with upper lobe blood diversion in cardiogenic cases; vessels of the upper lobe are balanced to cephalic in fluid overload but are normal in lung injury. Pleural effusion may be seen in all 3 causes. Septal lines indicative of interstitial edema are more frequent with cardiogenic causes than with others. The infiltrates of cardiogenic pulmonary edema are usually diffuse, and air bronchograms are rare. Infiltrates in nephrogenic pulmonary edema are classically described as having a bat-wing distribution, whereas those in lung injury tend to be more peripheral. Although the peripheral infiltrate is fairly specific for lung injury, the diffuse variety is seen with equal frequency in lung injury. The presence of air bronchograms is also fairly specific for lung injury. One of 3 patterns is seen: a normal chest, bilateral perihilar pulmonary edema, or generalized pulmonary edema. The early signs of pulmonary edema (interstitial edema) are the septal lines (Kerley B lines), which are horizontal lines seen laterally in the lower zones. The septal lines arise from the pleural surface and are typically 1 mm thick and 10 mm long; unlike blood vessels, these reach the edge of the lung. As the edema progresses, alveolar edema is observed in a butterfly pattern characterized by the central predominance of shadows, with a clear zone at periphery lobes. Another feature that may be seen is cardiac enlargement, in cases of previous cardiac failure. In its initial stages, ARDS may resemble cardiac pulmonary edema. However, over the course of 24-48 hours following the onset of tachypnea, dyspnea, and hypoxia, ARDS becomes more widespread and uniform. A useful characteristic for differentiating cardiac pulmonary edema from NPE, as well as from pneumonia and other widespread exudates, is the amount of time it takes for the edema to develop and to vanish. If substantial improvement occurs within 24 hours, this is virtually diagnostic of cardiac pulmonary edema. NPE is a known complication of lung transplantation. Herman and colleagues reviewed the postoperative chest radiographic and CT scan findings in 13 patients who underwent bilateral lung transplantation.18 Portable chest radiography was performed daily for about 10 days, after which upright posteroanterior studies were performed daily for about 10 days and then as clinically required. CT scanning was performed when a complication was suspected. The reimplantation response (NPE due to ischemia, trauma, denervation, and lymphatic interruption) occurred in 12 patients and usually consisted of bilateral perihilar and basal consolidation. Twelve episodes of acute rejection, an imprecise clinical diagnosis, occurred in 10 patients. Radiographic changes consisted of bibasal (n = 2) and right middle and lower (n = 2) or left basal consolidation (n = 1); no changes were observed in 7 episodes. Following the intravenous administration of steroids, radiographic resolution occurred in 4 cases. Radiographic findings associated with the re-implantation response and rejection were nonspecific and were mimicked by fluid overload and infection. Bronchial dehiscence and/or stricture formation occurred in 7 patients. In general, chest radiography was inaccurate in the assessment of these complications, and CT scanning was accurate in such assessments. The authors found chest radiography helpful but not definitive in distinguishing problems after bilateral lung transplantation. CT scanning was excellent for the demonstration of airway problems. Degree of ConfidenceConventional chest radiographs are universally available. The cause of the pulmonary edema can be determined with a high degree of accuracy by paying careful attention to certain radiographic features. Milne and colleagues conducted an independent, 2-observer study of 216 chest radiographs in 61 patients with cardiac disease, 30 with renal failure or overhydration, and 28 with capillary permeability edema.19 They identified 3 principal and 7 ancillary features; all of these were statistically significant and in a large percentage of cases allowed accurate determination of the cause of edema. The 3 principal features found were the distribution of pulmonary flow, the distribution of pulmonary edema, and the width of the vascular pedicle. The ancillary features were pulmonary blood volume, peribronchial cuffing, septal lines, pleural effusions, air bronchograms, lung volume, and cardiac size. Differing constellations of these features, each characteristic of a specific type of edema, were found. Overall accuracy of diagnosis in the Milne study was in the range of 86-89%. The highest accuracy was obtained in distinguishing capillary permeability edema from all other varieties (91%). The lowest accuracy (81%) was obtained in distinguishing chronic cardiac failure from renal failure. False Positives/NegativesLiebman and co-authors assessed the usefulness of portable chest radiographs in defining the amount of physiologic shunting and the severity of NPE.20, 21 Ten of their 11 patients had acute respiratory failure. Radiographic assessment of the amount of pulmonary edema and the severity of left ventricular failure was compared with the physiologic shunt fraction, tracer-measured lung water, and pulmonary arterial wedge pressure. The radiographic scores for edema were not predictive for the shunt fraction or for the tracer-measured lung water. The radiographic score for congestive heart failure was correlated with the wedge pressure but not well enough to be clinically useful. About 5% of the radiographs were false positive, and 11% were false negative. Radiographic findings lagged behind physiologic derangements. Therefore, the radiographic findings were predictive for the shunt value of the preceding day. The study's results indicate that it is hazardous to accept a portable radiographic diagnosis of congestive heart failure as a cause of pulmonary edema. CT SCANSection 5 of 11
FindingsCT scanning is seldom used in assessing patients with NPE and ARDS, mostly because of problems in transporting and monitoring these severely ill individuals. CT scan findings in NPE are similar to those of ARDS. High-resolution CT (HRCT) scanning demonstrates widespread airspace consolidation, which may have predominant distribution in the dependent lung regions. A reticular pattern with a striking anterior distribution is a frequent finding of follow-up CT scanning in ARDS survivors and is most strongly related to the duration of pressure-controlled, inverse-ratio ventilation. Tagliabue and colleagues reviewed the findings of 74 patients with ARDS who underwent chest CT scanning.22 Lung opacities were bilateral in almost all patients and in most cases (86%) were dependent. The opacities were patchy (42%), homogeneous (23%), ground glass (8%), or mixed (27%). Opacities prevailed in basal regions (68%), in comparison with hilar and apical ones. Air bronchograms were frequently seen in areas of consolidation (89%). Gattinoni and co-authors examined 10 patients with full-blown ARDS who were receiving mechanical ventilation with positive end-expiratory pressure (PEEP) and who underwent lung CT scanning.23 Seven healthy subjects also were included in the study. Three tomographic levels, specifically, apex, hilum, and base, were selected. The most consistent morphologic finding in ARDS was attenuating in the dependent regions of the lung. Assuming that the 3 levels were a representative sample of the whole lung, the authors computed lung weight from the mean CT scan number and lung gas volume. Through analysis of the CT scan number frequency distribution, the authors found the following definite patterns of distribution:
Stark and colleagues described the CT scan features of 28 patients with ARDS.24 Diffuse lung consolidation, lobar or segmental disease, and multifocal, patchy involvement were observed. Large lung cysts and small cysts producing a Swiss-cheese appearance of the parenchyma were detected. These findings were not regularly appreciated on chest radiographs. The overall mortality rate of patients was 72.7%. Patients with lung cysts had a trend toward higher mortality (87.5%. Other unexpected findings were basilar lung abscesses and empyema. In 15 patients, CT scans provided additional information not obvious on bedside chest radiographs and led to a change in care for 5 patients. Degree of ConfidenceThe diagnosis of NPE usually depends on clinical and conventional radiographic findings. CT scanning is seldom used in NPE. False Positives/NegativesCT scanning is usually not helpful in differentiating the various causes of NPE. Cardiogenic edema can also give rise to a similar appearance. MRISection 6 of 11
FindingsMRI has no direct role in the diagnosis of pulmonary edema. ULTRASOUNDSection 7 of 11
FindingsIn general, ultrasonography has a limited role, if any, in the diagnosis of NPE. However, ultrasonography is useful in the characterization of pleural effusions. Echocardiography may also play a role in the differentiation of cardiogenic pulmonary edema from NPE. NUCLEAR MEDICINESection 8 of 11
FindingsGallium-67 (67Ga) scanning Raijmakers and co-investigators studied the effectiveness of a noninvasive, bedside, dual-radionuclide method (67Ga circulating transferrin and technetium-99m [99mTc]–labeled RBCs) of measuring pulmonary microvascular permeability, in differentiating between hydrostatic pulmonary edema and pulmonary edema due to ARDS.25 Patients in the study suffered from respiratory insufficiency and bilateral, alveolar pulmonary edema, as demonstrated on chest radiographs. All but 1 of the patients were mechanically ventilated. The 2 radionuclides were used to calculate the pulmonary leak index. With various definitions, a supranormal pulmonary leak index for ARDS had a sensitivity of 100%, while its specificity ranged from 46-75%. On receiver operating characteristic curves, the pulmonary leak index performed best when ARDS and hydrostatic pulmonary edema were defined only on the basis of risk factors. The index was better than hemodynamic measures, and its performance equaled that of ventilatory variables in discriminating between edema types (if definitions were based primarily on hemodynamic and ventilatory variables, respectively). The investigators concluded that the 67Ga pulmonary leak index can be effectively used in distinguishing ARDS from hydrostatic pulmonary edema. Fluorodeoxyglucose positron emission tomography Chen and Schuster measured neutrophil glucose uptake with fluorodeoxyglucose (FDG)–positron emission tomography (PET) scanning in anesthetized dogs after intravenous, oleic acid–induced, acute lung injury (n = 6) or after low-dose, intravenous endotoxin (which is known to activate neutrophils without causing lung injury) followed by oleic acid (n = 7).26 The authors concluded that the rate of FDG uptake in the lungs during lung injury reflects the state of neutrophil activation. FDG-PET scanning can depict pulmonary sequestration of activated neutrophils, even when alveolar neutrophilia are absent. Therefore, FDG-PET scanning may be useful for studying neutrophil kinetics during oleic acid–induced lung injury. Iodine-123 (123I) meta-iodobenzylguanidine scanning 123I meta-iodobenzylguanidine (MIBG) results can be considered indicators of pulmonary endothelial cell function. Koizumi and colleagues studied serial scintigraphic assessment of 123I MIBG lung uptake in a patient with high-altitude pulmonary edema.27 The initial evaluation was performed 7 days after the patient's admission. The lung-to–upper mediastinum ratios of 123I MIBG uptake were 1.33 for the right lung and 1.12 for the left lung. The second examination, performed 2 months later, showed ratios of 1.39 for the right lung and 1.33 for the left lung. The investigators speculated that the reduction of lung uptake observed in the early recovery stage might be associated with impairment in pulmonary endothelial cell metabolic function in the development of high-altitude pulmonary edema. INTERVENTIONSection 9 of 11
Bedside catheterization of the pulmonary artery in critically ill patients is a more accurate means than is clinical assessment alone for determining the cause of shock (hypovolemic, cardiogenic, or septic) or for assessing the cause of severe pulmonary edema (cardiogenic or noncardiogenic).28 Improvement in the ability to determine the specific cause of any given case of pulmonary edema aids in the provision of more rapid and definitive treatment. Wedge pressures and measurements of cardiac output derived from Swan-Ganz catheterization assist in making this determination, but the procedure is invasive, expensive, associated with complications, and not infrequently inaccurate. Medical/Legal Pitfalls
MULTIMEDIASection 10 of 11
REFERENCESSection 11 of 11
Pulmonary Edema, Noncardiogenic excerpt Article Last Updated: May 7, 2008 | ||||||||||||||||||||||||||||
