Onset Of Pulmonary Edema Research Articles

Breath-by-breath assessment of acute pulmonary edema using electrical impedance tomography, spirometry and volumetric capnography in a sheep (Ovis Aries) model.

The bedside diagnosis of acute pulmonary edema is challenging. This study evaluated the breath-by-breath information from electrical impedance tomography (EIT), respiratory mechanics and volumetric capnography (VCap) to assess acute pulmonary edema induced by xylazine administration in anesthetized sheep. To determine the ability and efficiency of each monitoring modality in detecting changes in lung function associated with onset of pulmonary edema. Twenty healthy ewes were anesthetized, positioned in sternal (prone) recumbency and instrumented. Synchronized recordings of EIT, spirometry and VCap were performed for 60 s prior to start of injection, during xylazine injection over 60 s (0-60 s) and continuously for 1 min (60-120 s) after the end of injection. After visual assessment of the recorded mean variables, statistical analysis was performed using a mixed effect model for repeated measures with Bonferroni's correction for multiple comparisons, to determine at which breath after start of injection the variable was significantly different from baseline. A significant change over time was defined as an adjusted p < 0.05. All statistics were performed using GraphPad Prism 0.1.0. Electrical impedance tomography showed significant changes from baseline in all but two variables. These changes were observed simultaneously during xylazine injection at 48 s and were consistent with development of edema in dependent lung (decreased end-expiratory lung impedance, ventilation in centro-ventral and ventral lung region) and shift of ventilation into non-dependent lung (decreased non-dependent silent spaces and increased center of ventilation ventral to dorsal and increased ventilation in centro-dorsal and dorsal lung region). All changes in lung mechanics also occurred during injection, including decreased dynamic respiratory system compliance and increased peak expiratory flow, peak inspiratory pressure and airway resistance at 48, 54 and 60 s, respectively. Changes in VCap variables were delayed with all occurring after completion of the injection. In this model of pulmonary edema, EIT detected significant and rapid change in all assessed variables of lung function with changes in regional ventilation indicative of pulmonary edema. Volumetric capnography complemented the EIT findings, while respiratory mechanics were not specific to lung edema. Thus, EIT offers the most comprehensive method for pulmonary edema evaluation, including the assessment of ventilation distribution, thereby enhancing diagnostic capabilities.

Pulmonary pathogenesis in a murine model of inhaled arsenical exposure.

Arsenic trioxide (ATO), an inorganic arsenical, is a toxic environmental contaminant. It is also a widely used chemical with industrial and medicinal uses. Significant public health risk exists from its intentional or accidental exposure. The pulmonary pathology of acute high dose exposure is not well defined. We developed and characterized a murine model of a single inhaled exposure to ATO, which was evaluated 24h post-exposure. ATO caused hypoxemia as demonstrated by arterial blood-gas measurements. ATO administration caused disruption of alveolar-capillary membrane as shown by increase in total protein and IgM in the bronchoalveolar lavage fluid (BALF) supernatant and an onset of pulmonary edema. BALF of ATO-exposed mice had increased HMGB1, a damage-associated molecular pattern (DAMP) molecule, and differential cell counts revealed increased neutrophils. BALF supernatant also showed an increase in protein levels of eotaxin/CCL-11 and MCP-3/CCL-7 and a reduction in IL-10, IL-19, IFN-γ, and IL-2. In the lung of ATO-exposed mice, increased protein levels of G-CSF, CXCL-5, and CCL-11 were noted. Increased mRNA levels of TNF-a, and CCL2 in ATO-challenged lungs further supported an inflammatory pathogenesis. Neutrophils were increased in the blood of ATO-exposed animals. Pulmonary function was also evaluated using flexiVent. Consistent with an acute lung injury phenotype, respiratory and lung elastance showed significant increase in ATO-exposed mice. PV loops showed a downward shift and a decrease in inspiratory capacity in the ATO mice. Flow-volume curves showed a decrease in FEV0.1 and FEF50. These results demonstrate that inhaled ATO leads to pulmonary damage and characteristic dysfunctions resembling ARDS in humans.

Subclavian versus femoral arterial cannulations during extracorporeal membrane oxygenation: A propensity-matched comparison.

During peripheral extracorporeal veno-arterial membrane oxygenation (VA-ECMO) support, subclavian arterial cannulation provides, in comparison to femoral arterial cannulation, an anterograde flow which may prevent from left ventricular (LV) distention and improve outcomes. We aimed to compare the effectiveness of subclavian cannulation to femoral cannulation in reducing LV overdistension consequences, hemostatic complications and mortality. This retrospective study conducted in two intensive care units of the Lille academic hospitals from January 2013 to December 2019 included 372 non-moribund adult patients supported by VA-ECMO. The primary endpoint was a new onset of pulmonary edema (PO) or LV unloading. Secondary endpoints were myocardial recovery, serious bleeding (according to Extracorporeal Life Support Organization definition), thrombotic complications (a composite of stroke, cannulated limb or mesenteric ischemia, intracardiac or aortic-root thrombosis) and 28 day mortality. Differences in outcomes were analyzed using propensity score matching (PSM) and inverse probability of treatment weighting adjustment (IPTW). As compared to femoral cannulation (n=320 patients), subclavian cannulation (n=52 patients) did not reduce the occurrence of new onset of PO or LV unloading after PSM [HR 0.99 (95% CI 0.51-1.91)]. There was no other difference in outcomes in PSM cohort. In IPTW adjustment cohort, subclavian cannulation was associated with reduced recovery and increased serious bleeding with four accidental decannulations observed. Subclavian artery cannulation was not associated with reduced LV distension related complications, thrombotic complications and 28 day mortality. Rather, it may increase serious bleeding and accidental decannulations, and reduce recovery. Therefore, subclavian cannulation should be limited to vascular accessibility issues.

Asymmetrical and Late Onset of Pulmonary Edema Post Scorpion Sting: Case Report of Rare Manifestation

Asymmetrical and Late Onset of Pulmonary Edema Post Scorpion Sting: Case Report of Rare Manifestation

A rare cause of dyspnea in emergency medicine: transfusion-related acute lung injury

The earliest definition of transfusion-related acute lung injury (TRALI) included all patients who developed acute respiratory distress, moderate to severe hypoxemia, rapid onset of pulmonary edema, mild to moderate hypotension, and fever within 6 hours of receiving a plasma containing blood transfusion. The definition excluded patients if they had underlying cardiac or respiratory disease. The mechanism is not known exactly but it causes morbidity and mortality. Incidence of TRALI changes between 0.08% and 15% of patients receiving a blood transfusion. A 78 year old female patient with history of myelodysplastic syndrome, coronary artey disease and hypertansion, was admitted to the hospital because of dyspnea after the blood transfusion. She was managed as TRALI after diagnostic workup and transported to the intensive care unit. In the following days her clinical status changed dramatically with complete recovery.

Guidelines on the management of anaemia and red cell transfusion in adult critically ill patients.

Forward This document aims to summarize the current literature guiding the use of red cell transfusion in critically ill patients and provides recommendations to support clinicians in their day-to-day practice. Critically ill patients differ in their age, diagnosis, co-morbidities, and severity of illness. These factors influence their tolerance of anaemia and alter the risk to benefit ratio of transfusion. The optimal management for an individual may not fall clearly within our recommendations and each decision requires a synthesis of the available evidence and the clinical judgment of the treating physician. This guideline relates to the use of red cells to manage anaemia during critical illness when major haemorrhage is not present. A previous British Committee for Standards in Haematology (BCSH) guideline has been published on massive haemorrhage (Stainsby et al, 2006), but this is a rapidly changing field. We recommend readers consult recent guidelines specifically addressing the management of major haemorrhage for evidence-based guidance. A subsequent BCSH guideline will specifically cover the use of plasma components in critically ill patients.

Neurogenic Pulmonary Edema and Acute Respiratory Distress Syndrome in a Healthy Child With Febrile Status Epilepticus

Neurogenic pulmonary edema is a clinical syndrome that manifests as an acute onset of pulmonary edema in the setting of a central nervous system injury, without cardiac dysfunction. Neurogenic pulmonary edema is rare in children, and the mechanism is still not completely understood. The clinical pathology overlaps with acute lung injury and acute respiratory distress syndrome. The authors report a case of a 14-month-old previously healthy child who presented with febrile status epilepticus, fulminant neurogenic pulmonary edema, and acute respiratory distress syndrome. Neurogenic pulmonary edema should be considered in the differential diagnosis for the rapid progression of respiratory failure following an acute neurological injury such as status epilepticus in a child. Prompt respiratory support and treatment of the acute neurological insult can prevent further cerebral hypoxemic injury.

Analysis of edema fluids and histologic features of the lung in reexpansion pulmonary edema during video-assisted thoracoscopic surgery

J Thorac Cardiovasc Surg Takashi Suzuki and Masashi Handa Satoshi Suzuki, Hiromichi Niikawa, Jotaro Shibuya, Tomoko Hosaka, Sumiko Maeda, edema during video-assisted thoracoscopic surgery Analysis of edema fluids and histologic features of the lung in reexpansion pulmonary http://jtcs.ctsnetjournals.org/cgi/content/full/123/2/387 the World Wide Web at: The online version of this article, along with updated information and services, is located on

Pulmonary Edema During Pregnancy. Unilateral Presentation Is Not Rare.

Information regarding pulmonary edema in obstetric patients is limited, especially its natural history as most cases are from tertiary care centers. The incidence, etiology, and course of pulmonary edema in all obstetric patients at a primary-secondary care center was studied prospectively among 29,621 obstetric cases in the past 3.5 years. Pulmonary edema developed in 18 cases (0.06%) of all obstetric patients that were associated with pre-eclampsia-eclampsia and tocolysis with beta-mimetics. The onset of pulmonary edema was 1-8 days postpartum in 12 patients, 1 day antepartum in 3 patients, and 26-32 gestational weeks in 3 patients. The cause was mainly cardiogenic, and the mean time taken for resolution was 2.2 days. Unilateral pulmonary edema occurred in 4 patients and there was delayed resolution compared with bilateral pulmonary edema because of delayed treatment. Pulmonary edema associated with pregnancy developed in 0.06% of cases, mainly during the peripartum, and resolved rapidly. Unilateral pulmonary edema was not uncommon.

Fatal Postoperative Pulmonary Edema: Pathogenesis and Literature Review

Pulmonary edema is a known postoperative complication, but the clinical manifestations and danger levels for fluid administration are not known. We studied (1) 13 postoperative patients (11 adult, 2 pediatric) who developed fatal pulmonary edema, and (2) one contemporaneous year of inpatient operations at two university teaching hospitals to determine the clinical manifestations, causes, epidemiology, and guidelines for fluid administration. Retrospective analysis of 13 patients with fatal postoperative pulmonary edema and one contemporaneous year of major inpatient surgery. Thirteen patients had net fluid retention of at least 67 mL/kg in the initial 24 postoperative hours and developed pulmonary edema. Ten were generally healthy while three had serious associated medical conditions. There was no measurement, laboratory value, or clinical finding predictive of impending pulmonary edema. The most common clinical manifestation following the onset of pulmonary edema was cardiorespiratory arrest (n = 8). Patients had metabolic acidosis (pH = 7.15 +/- .33), hypoxia (PO2 = 45 +/- 18 mm Hg), and normal electrolytes. The diagnosis of pulmonary edema was established by chest radiograph and confirmed by autopsy and pulmonary artery pressure (21 +/- 4 mm Hg). The mean net fluid retention was 7.0 +/- 4.5 L (90 +/- 36 mL/kg/d) and exceeded 67 mL/kg/d in all patients. Autopsy revealed pulmonary edema with no other cause of death. Among 8,195 major operations, 7.6% developed pulmonary edema with a mortality of 11.9%. Extrapolation to the 8.2 million annual major surgeries in the United States yields a projection of 8,000 to 74,000 deaths. Pulmonary edema can occur within the initial 36 postoperative hours when net fluid retention exceeds 67 mL/kg/d. There are no known predictive warning signs and cardiorespiratory arrest is the most frequent clinical presentation. The monitoring systems currently in use neither detect nor predict impending pulmonary edema, and as yet, there are no known panic values for excessive fluid administration or retention.

A profile of amino acid and catecholamine levels during endotoxin-induced acute lung injury in sheep: Searching for potential markers of the acute respiratory distress syndrome

The identification of plasma markers of the course of the acute respiratory distress syndrome (ARDS) is needed to improve its treatment and to further advance the development of new therapeutic agents. The status of markers of lung injury in ARDS is reviewed and some new potential markers are proposed. This study focused on plasma amino acids, related amino compounds, and catecholamine levels during the acute phase of endotoxin-induced lung injury in 8 sheep characterized by the onset of pulmonary edema caused by increased microvascular permeability. A number of significant changes from baseline values were found. During the sixth hour of a 12-hour period of endotoxin infusion, norepinephrine, epinephrine, and alanine levels increased whereas the isoleucine level decreased. During the sixth hour of the immediate postendotoxin period, the taurine level increased while the levels of arginine, citrulline, glycine, isoleucine, methionine, ornithine, serine, threonine, and tryptophan decreased. These findings are compared with prior studies in human subjects detailing the amino acid profile characteristic of advanced sepsis. We conclude that the present profile of catecholamine and amino acid changes during endotoxemia in sheep deserves further study in human subjects to determine its significance as a marker of the early stage of ARDS.

Response of cultured human pulmonary artery endothelial cells to endotoxin

Endotoxemia is the leading cause of the adult respiratory distress syndrome. The effects of endotoxin on pulmonary endothelium, both in vivo and in culture, are diverse and complicated, and vary between species and cellular origin. Species such as sheep and cows are particularly sensitive to endotoxin, whereas rats and mice are more resistant. Studies using cultured pulmonary endothelial cells confirm these findings. Such species variations lead us to question whether human pulmonary artery endothelial cells (HPAEC) are directly affected by endotoxin. The present study examined the effects of endotoxin on HPAEC. Cells were exposed to endotoxin (0.001-10 micrograms/ml) for 24 h and were examined by phase-contrast microscopy, and measurements were made of lactate dehydrogenase, prostacyclin, and prostaglandin E2 release in the cell-free supernatant. In the presence of serum, endotoxin doses as small as 0.01 microgram/ml resulted in endothelial retraction and pyknosis compared with controls (P < 0.05). Exposure to 10 micrograms/ml of endotoxin resulted in a significant increase in the number of pyknotic cells (P < 0.05), and lactate dehydrogenase release paralleled this finding. Endotoxin also resulted in a gradual increase in prostaglandin E2 release, reaching significance at 1 and 10 micrograms/ml of endotoxin (P < 0.05). A similar trend was noted for prostacyclin release. We conclude that the direct cytotoxic effects elicited by endotoxin on HPAEC may contribute to the onset of pulmonary edema in patients with adult respiratory distress syndrome.

Cardiac injury associated with neurogenic pulmonary edema following subarachnoid hemorrhage.

To describe the clinical features of cardiac injury associated with neurogenic pulmonary edema (NPE) in patients with acute subarachnoid hemorrhage (SAH). NPE is generally viewed as a form of noncardiogenic pulmonary edema related to massive sympathetic discharge. Case series. We found echocardiographic evidence of reduced global and segmental left ventricular (LV) systolic function in five women (mean age, 44; range, 36 to 57) with SAH and NPE. None had a history of heart disease. Four patients were Hunt/Hess grade III and one was grade IV. All five patients experienced (1) sudden hypotension (systolic blood pressure < 110 mm Hg) following initially elevated blood pressures, (2) transient lactic acidosis, (3) borderline (2 to 4%) creatine kinase MB elevations, and (4) varied acute (< 24 hours) electrocardiographic changes followed by widespread and persistent T wave inversions. Pulmonary artery wedge pressures were normal in 3/3 patients at the onset of pulmonary edema but reached high levels (> 16 mm Hg) in all four patients studied beyond this period. Reduced cardiac output and LV stroke volume were identified in three patients; the fourth patient demonstrated normal values on high doses of intravenous pressors. Cerebral infarction due to vasospasm occurred in four patients and resulted in two deaths. Follow-up echocardiography performed 2 to 6 weeks after SAH revealed normal LV function in all three survivors. A reversible form of cardiac injury may occur in patients with NPE following SAH and is associated with characteristic clinical findings. Impaired LV hemodynamic performance in this setting may contribute to cardiovascular instability, pulmonary edema formation, and complications from cerebral ischemia.

Indices of Oxidative Stress in Hamster Lung Following Exposure to Cobalt(II) Ions: In Vivo and In Vitro Studies

Cobalt, a metal with numerous industrial applications, has been associated with lung disease, an extreme form of which is an interstitial fibrosis. The biochemical mechanisms underlying this toxicity are not understood. In vitro studies have suggested that cobalt(II) ions are able to generate reactive oxidant species (possibly hydroxyl radical) in a reaction with hydrogen peroxide, and we have hypothesized that the occurrence of such an event in lung tissue, and the subsequent development of oxidative damage, may contribute to this pulmonary toxicity. The intratracheal instillation of CoCl2 into hamster lungs resulted after 3 h in decreased levels of reduced glutathione and increases in levels of oxidized glutathione and in the activity of the pentose phosphate pathway. These changes, which are compatible with the generation of oxidative stress, were reversed by 48 h at low Co2+ doses (1.0 to 1,000 micrograms/kg). Irreversible changes at higher doses coincided with the onset of pulmonary edema. Incubation of lung slices with CoCl2 (0.1 to 10 mM) resulted in time- and Co2+ concentration-dependent increases in levels of oxidized glutathione and protein-mixed disulfides and a decrease in reduced glutathione. A concentration-dependent stimulation of the pentose phosphate pathway was also observed. These changes preceded the detection of overt cell toxicity, as assessed by various biochemical parameters. These data indicate that thiol oxidation constitutes an early event in the pulmonary toxicity of cobalt(II) ions and are compatible with the hypothesis that the generation of oxidative stress may be of significance to the toxic process.

Bronchial artery ligation modifies pulmonary edema after exposure to smoke with acrolein.

Pulmonary edema can follow smoke inhalation and is believed to be due to the multiple chemical toxins in smoke, not the heat. We have developed a synthetic smoke composed of aerosolized charcoal particles to which one toxin at a time can be added to determine whether it produces pulmonary edema. Acrolein, a common component of smoke, when added to the synthetic smoke, produced a delayed-onset pulmonary edema in dogs in which the extravascular lung water (EVLW) as detected by a double-indicator technique began to rise after 42 +/- 2 (SE) min from 148 +/- 16 to 376 +/- 60 ml at 165 min after smoke exposure. The resulting pulmonary edema was widespread macroscopically but appeared focal microscopically with fibrin deposits in alveoli adjacent to small bronchi and bronchioles. Bronchial vessels were markedly dilated and congested. Monastral blue B when injected intravenously leaked into the walls of the bronchial vessels down to the region of the small bronchioles (less than or equal to 0.5 mm ID) of acrolein-smoke-exposed dogs but not into the pulmonary vessels. Furthermore, ligation of the bronchial arteries delayed the onset of pulmonary edema (87 +/- 3 min, P less than 0.05) and lessened the magnitude (232 +/- 30 ml, P less than 0.05) at 166 +/- 3 min after acrolein-smoke exposure.(ABSTRACT TRUNCATED AT 250 WORDS)

Applications of applied potential tomography (APT) in respiratory medicine.

Impedance pneumography, electrical impedance measurements of the lung, is a technique which has been widely used to monitor respiration non-invasively and more recently, the onset of pulmonary oedema. Attempts have been made to try to localise the changes in impedance using electrode arrays and electrode guarding. These techniques allow localisation to a particular hemithorax, but the resolution of the majority of the systems remains poor. To assess the performance and possible clinical applications of APT, measurements have been made following increases in lung volume and pulmonary blood volume. During inspiration an increase in both the area and the magnitude of the impedance changes over the area of the lungs was observed. Numerical analysis of the impedance changes in normal subjects reveals a consistently high correlation between the volume of air inspired and the magnitude of the impedance changes. The resolution of the system is sufficient to monitor differences in ventilation in the right and left lung and to measure variations in these levels with posture. Preliminary clinical work suggests that APT may be used to detect ventilatory defects in certain types of lung disease. APT measurements show a decrease in resistivity over the area of the lungs when the pulmonary blood volume is increased by the intravenous infusion of 1.5 litres of isotonic saline. Similar changes in the volume of fluid in the lungs are known to occur in pulmonary oedema. APT measurements of lung impedance may detect the onset of pulmonary oedema in high risk patients.

Acute respiratory failure induced by bleomycin and hyperoxia: Pulmonary edema, cell kinetics, and morphology

The acute manifestations of experimental bleomycin- and hyperoxia-induced lung damage were examined. Hamsters were treated with 5 U/kg bleomycin intratracheally followed by exposure to 80% oxygen (O 2). As little as 12 hr of O 2 exposure potentiated the bleomycin injury; however, the onset of mortality was 72 hr after treatment. The onset of pulmonary edema, measured by radiolabeled tracers, also occurred 72 hr after treatment. Cell kinetics studies showed that 24 hr exposure to 80% O 2 did not alter early alveolar cell proliferation. Treatment with bleomycin alone did result in an early increase in alveolar macrophage and type II pneumocyte labeling. Animals treated with both bleomycin and hyperoxia had an increase in macrophage labeling, but not in type II pneumocyte labeling. We conclude that increased macrophage numbers associated with suppressed type II pneumocyte proliferation may play key roles in the potentiation and development of lung damage caused by bleomycin and hyperoxia treatment.

Early detection of extravascular lung water in an inhalation injury animal model

A rabbit inhalation injury model, and a dual tracer radioactive isotope technique (Rowland et al., 1986), have been utilized with small- and medium-sized towards normal values some time within 24h if fluid 2 h after smoke inhalation or fluid resuscitation and especially with the combination of inhalation injury and fluid resuscitation. This oedema appears to have decreased by 24 h post-injury. There does not appear to be any difference between the small- and medium-sized tracers in the transit times of tracer in the lung vascular compartment. The increases in extravascular water volume have been confirmed by gravimetric analyses of the lungs. Thus the pulmonary oedema in the rabbit animal model is detectable within 2 h post-injury, with a return towards normal values some time within 24h if fluid challenged for short periods. Fluid resuscitation exacerbates the amount of oedema that developed. The onset of pulmonary oedema may therefore be earlier than previously seen clinically, and fluid resuscitation modifications may be of benefit in smoke inhalation injury.

Alveolar pressure in fluid-filled occluded lung segments during permeability edema.

In a model of increased hydrostatic pressure pulmonary edema Parker et al. (J. Appl. Physiol.: Respirat. Environ. Exercise Physiol. 44: 267-276, 1978) demonstrated that alveolar pressure in occluded fluid-filled lung segments was determined primarily by interstitial fluid pressure. Alveolar pressure was subatmospheric at base line and rose with time as hydrostatic pressure was increased and pulmonary edema developed. To further test the hypothesis that fluid-filled alveolar pressure is determined by interstitial pressure we produced permeability pulmonary edema-constant hydrostatic pressure. After intravenous injection of oleic acid in dogs (0.01 mg/kg) the alveolar pressure rose from -6.85 +/- 0.8 to +4.60 +/- 2.28 Torr (P less than 0.001) after 1 h and +6.68 +/- 2.67 Torr (P less than 0.01) after 3 h. This rise in alveolar fluid pressure coincided with the onset of pulmonary edema. Our experiments demonstrate that during permeability pulmonary edema with constant capillary hydrostatic pressures, as with hemodynamic edema, alveolar pressure of fluid-filled segments seems to be determined by interstitial pressures.

Delayed Onset of Pulmonary Oedema following Accidental Exposure to Ethyl Chloroformate

Delayed Onset of Pulmonary Oedema following Accidental Exposure to Ethyl Chloroformate