Mechanism Of Pulmonary Edema Research Articles

Recent advances in enterovirus A71 pathogenesis: a focus on fatal human enterovirus A71 infection.

Enterovirus A71 (EV-A71) is one of the major pathogens responsible for hand, foot, and mouth disease (HFMD). Many HFMD outbreaks have been reported throughout the world in the past decades. Compared with other viruses, EV-A71 infection is more frequently associated with severe neurological complications and even death in children. EV-A71 can also infect adults and cause severe complications and death, although such cases are very uncommon. Although fatal cases of EV-A71 infection have been reported, the underlying mechanisms of EV-A71 infection, especially the mode of viral spread into the central nervous system (CNS) and mechanisms of pulmonary edema, which is considered to be the direct cause of death, have not yet been fully clarified, and more studies are needed. Here, we first summarize the pathological findings in various systems of patients with fatal EV-A71 infections, focussing in detail on gross changes, histopathological examination, tissue distribution of viral antigens and nucleic acids, systemic inflammatory cell infiltration, and tissue distribution of viral receptors and their co-localization with viral antigens. We then present our conclusions about viral dissemination, neuropathogenesis, and the mechanism of pulmonary edema in EV-A71 infection, based on pathological findings.

Dysregulation of ion transport in the lung epithelium infected with SARS-CoV-2.

Dysregulation of ion transport in the lung epithelium infected with SARS-CoV-2.

The role of the lymphatic system in the homeostasis of the interstitial fluid in the lung and pleural liquid

Accomplishments in the identifcation of lymphatic endothelial cells and the ability to differentiate them from the endothelial cells of blood vessels have contributed to progress in recent decades in studying the role of the lymphatic system in the body. Preclinical and clinical studies of the last decade have shown that changes in the lymphatic vascular network are observed in almost all lung diseases. At the same time, it remains unclear whether the lymphatic vessels and lung nodes are being part of the overall process of lung remodeling or they make a defnite contribution to the pathogenesis of diseases of the respiratory system. This review presents current data on the morphology and physiology of lymphatic vessels and nodes, their role in the regulation of interstitial fluid homeostasis, lipid transportation and immune responses as well as describes the mechanisms of regulation of the transport function of lymphatic vessels. Data on the role of the lymphatic system of the lungs in the exchange of fluid in the interstitial space of the lungs are presented in the review. The results of studies of the last two decades on the formation and reabsorption of pleural fluid and the role of various lymphatic networks in regulating its volume are described. Finally, modern ideas on the mechanisms of pulmonary edema are outlined and important questions of the lymphatic biology of the respiratory system are identifed, still remaining unanswered today.

New insights into the mechanisms of pulmonary edema in acute lung injury.

Appearance of alveolar protein-rich edema is an early event in the development of acute respiratory distress syndrome (ARDS). Alveolar edema in ARDS results from a significant increase in the permeability of the alveolar epithelial barrier, and represents one of the main factors that contribute to the hypoxemia in these patients. Damage of the alveolar epithelium is considered a major mechanism responsible for the increased pulmonary permeability, which results in edema fluid containing high concentrations of extravasated macromolecules in the alveoli. The breakdown of the alveolar-epithelial barrier is a consequence of multiple factors that include dysregulated inflammation, intense leukocyte infiltration, activation of pro-coagulant processes, cell death and mechanical stretch. The disruption of tight junction (TJ) complexes at the lateral contact of epithelial cells, the loss of contact between epithelial cells and extracellular matrix (ECM), and relevant changes in the communication between epithelial and immune cells, are deleterious alterations that mediate the disruption of the alveolar epithelial barrier and thereby the formation of lung edema in ARDS.

Preventing and Treating Complications After Hip Arthroscopy.

Although arthroscopic procedures are less invasive than open surgical techniques, arthroscopy is not without complications. Complications of hip “scopes” may include traction-related nerve injuries, fluid extravasation, infection, osteonecrosis, and heterotopic ossification (HO). How to address and avoid these complications are the topics of this month’s “Case Connections” article. In the August 27, 2014 JBJS Case Connector , Uquillas and Youm report on a fifty-one-year-old man who presented with symptoms consistent with right-sided femoroacetabular impingement (FAI). Radiographs revealed mixed cam and pincer impingement, and MRI showed an acetabular labral tear, spurring of the acetabulum and femoral neck, a loose body, and chondral delamination. Surgeons used hip arthroscopy to address these multiple problems. Six months after the procedure, the patient had developed increasing lateral hip pain and tightness. At the eight-month follow-up, he reported a sharp spike in hip pain and showed mild impingement signs. Radiographs revealed HO near the greater trochanter, a finding validated by CT (Fig. 1). MRI revealed inflammation surrounding the area of heterotopic bone. Fig. 1 Three-dimensional CT reconstruction showing heterotopic ossification near the greater trochanter. After a year of ineffective anti-inflammatory medication and physical therapy, interventional radiologists performed an ultrasound-guided pulse lavage (1% lidocaine followed by saline solution) to irrigate and debride the 1.3 × 0.08 × 1.1-cm calcific deposit that had been observed on a preprocedure ultrasound. Dispersion of the deposition was noted during the procedure, which was followed by a steroid/anesthetic injection to provide immediate pain relief and treat inflammation. The …

Human lung on a chip: innovative approach for understanding disease processes and effective drug testing

Human lung on a chip: innovative approach for understanding disease processes and effective drug testing

Molecular pathology of pulmonary edema after injury in forensic autopsy cases

The lung is vulnerable to trauma; pulmonary edema starts quickly as part of the systemic responses involved in shock. The present study investigated the molecular pathology of posttraumatic alveolar damage and responses involving pulmonary edema in forensic autopsy cases of injury (n = 66) compared with acute cardiac death cases (n = 13). Intrapulmonary mRNA and immunohistochemical expressions of matrix metalloproteinases (MMPs; MMP-2 and MMP-9), intercellular adhesion molecule-1, claudin-5, and aquaporins (AQPs, AQP-1 and AQP-5) were examined. Subacute injury deaths showed an increase in lung weight similar to that in acute cardiac death, but relative mRNA quantification using the Taqman real-time PCR assay demonstrated different findings among the causes of death; higher expressions were detected for all markers, except for AQP-5 in sharp instrument injury, for MMP-2 in blunt brain injury, and for MMP-9 in non-brain blunt injury, but these expression levels were lower in acute cardiac death. In immunostaining, only MMPs showed differences among the causes of death: MMP-2 expression was evident in most subacute deaths due to blunt brain injury and sharp instrument injury, whereas MMP-9 was intensely positive in those of non-brain blunt injury and sharp instrument injury. These findings suggest significant differences in the mechanism of pulmonary edema among fatal injuries and acute cardiac death, especially between blunt and sharp instrument injury. Systematic analysis of gene expressions using real-time PCR in combination with immunohistochemistry may be useful in evaluating pulmonary damage and responses after injury in death investigations, especially in connection with posttraumatic shock.

Pulmonary vascular permeability index should not be called extravascular lung water pulmonary blood volume ratio

In their recent paper, Michelle Chew and colleagues [1] evaluated the performance accuracy of three extra vascular lung water (EVLW) ratios in patients with shock at risk for or with acute lung injury (ALI). Th ey indexed EVLW to actual body weight (ABW), predicted body weight (PBW) and pulmonary blood volume (PBV), and confi rmed that all EVLW ratios were higher in patients with ALI and in non-survivors and correlated with respiratory parameters. Although these fi ndings are interesting, they deserve some comments. First, whereas indexing EVLW to PBW may reduce the number of patients with acute respiratory distress syndrome (ARDS) with normal EVLW, in this population, the EVLW/ABW index performed best [2]. Furthermore, the absence of a link between EVLW and PaO 2 /FiO 2 (calculated r2 of 0.14 to 0.23) could explain that these indices identifi ed only 33% of ALI and 38% of ARDS cases. Second, the EVLW/PBV terminology appears very unusual. Th e transpulmonary thermodilution technique determines cardiac output, intrathoracic thermal volume (ITTV), pulmonary thermal volume (PTV) and global end-diastolic volume (Global end-diastolic volume (GEDV) = ITTV - PTV). Th e estimated blood volume of the chest (Intra thoracic blood volume (ITBV) = GEDV + PBV) permits the calculation of PBV (ITBV = 1.25 × GEDV - 28.4 ml) [3]. Importantly, the PiCCO monitor automatically provides, at each calibration, an estimation of the pulmonary vascular permeability index (PVPI), based on the ratio of EVLW to PBV, which refl ects alveolar-capillary barrier permeability and is of importance for the mechanisms of pulmonary edema [4,5]. Th us, I believe that it would be more pertinent to use the PVPI instead of the EVLW/PBV ratio and that it is time to promote an international consensus on this. Abbreviations ABW, actual body weight; ALI, acute lung injury; ARDS, acute respiratory distress syndrome; EVLW, extravascular lung water; GEDV, global end-diastolic volume; ITBV, intrathoracic blood volume; ITTV, intrathoracic thermal volume; PBV, pulmonary blood volume; PBW, predicted body weight; PVPI, pulmonary vascular permeability index. Competing interests The author declares that they have no competing interests.

Case Scenario: Acute Postoperative Negative Pressure Pulmonary Edema

A 25-yr-old man (weight, 68 kg; height, 183 cm) presentedto the surgery center for excision of back and thigh schwan-nomas on the same day. The patient’s medical history wassignificant only for his history of multiple schwannoma re-sections and a history of smoking one pack of cigarettes perweek for the past 5 yr. He denied previous problems withgeneral anesthesia, and his baseline peripheral oxygen satu-ration was 99% on ambient air.Thepatientwaspremedicatedwith2mgmidazolam,andanesthesia was induced with 250 mg fentanyl, 500 mg thio-pental, and 8 mg vecuronium given for facilitation of tra-cheal intubation. He was atraumatically intubated with a7-mm ID endotracheal tube using a no. 3 Macintosh laryn-goscope (Teleflex Medical, Research Triangle Park, NC) onthe first attempt with direct visualization of the vocal cords.The patient was turned prone, bilateral breath sounds werereconfirmed, and schwannoma excisions were performed ontheleftthighandtheleftflank.Atotalof0.5mghydromor-phone was administered for analgesia. The intraoperativecoursewasunremarkable.Thepatientwashemodynamicallystable with minimal blood loss and was easily ventilated andoxygenated. A total of 500 ml lactated Ringer’s solution wasadministeredduringthe65-minsurgicalprocedure.Thepa-

Acute pulmonary edema progressing from unilateral to bilateral after brief laparoscopic surgery under lateral position in elderly patient - A case report -

Although pulmonary vascular permeability and gravity changes have been known to be the mechanism of pulmonary edema, yet the etiology of pulmonary edema remains speculative. The multiple conditions such as congestive heart failure, fluid overload, hypoalbuminemia, upper air way obstruction, increased pulmonary artery pressure and laparoscopic surgery cause poor pulmonary circulatory condition. Pulmonary edema usually occurs bilaterally, but unilateral pulmonay edema is uncommon entity. Unilateral pulmonary edema was reported to occur in special circumstances such as one lung ventilation, lateral decubitus position and unilateral pulmonary damage. We experienced abruptly onset and rapid healing pulmonary edema from unilateral to bilateral after brief laparoscopic operation under lateral decubitus position. Thus, we report this case as complicated condition of acute pulmonary edema in elderly patient without fluid overload, long operation time.

Progress toward a systems biology approach to acute lung injury

presenting the comroe lecture at the Experimental Biology 2002 conference in New Orleans, Norman Staub, a pioneer of modern research into the mechanisms of pulmonary edema and acute lung injury, decried the disconnection between clinical medicine and molecular biology ([12][1]). He attributed this

Different proinflammatory reactions in fatal and non-fatal enterovirus 71 infections: implications for early recognition and therapy.

The mechanism of pulmonary oedema, a life-threatening manifestation of enterovirus 71 (EV71) encephalitis, is unclear. Our aim was to assess the relationship of proinflammatory cytokines to EV71-related pulmonary oedema. Proinflammatory responses in 33 EV71 patients with various complications and 21 normal healthy children were measured using an enzyme-linked immunosorbent assay. EV71 patients with both encephalitis and pulmonary oedema were found to have much higher levels of blood interleukin-6 (IL-6) (947 +/- 1239 vs 4.9 +/- 3.1 pg/ml, p = 0.0003), tumour necrosis factor-alpha (TNF-alpha) (22.4 +/- 29.5 vs 5.3 +/- 1.0 pg/ml, p = 0.0035), interleukin Ibeta (IL-1beta) (48.4 +/- 85.2 vs 4.9 +/- 10.1 pg/ml, p = 0.01), white blood cell count (28.3 +/- 7.6 vs 15.5 +/- 6.8 10(9)/L, p > or = 0.0001) and blood glucose (501 +/- 186 vs 165 +/- 117 mg/dL, p = 0.0009) than patients with EV71 encephalitis alone. In fact, the cytokine levels in patients with encephalitis only or in those without complications were not significantly different from the levels found in normal children. The sensitivity, specificity, positive and negative predictive values of IL-6 > 70 pg/ml for EV71 encephalitis with pulmonary oedema were all 100%. Patients with EV71-related encephalitis combined with pulmonary oedema were found to have significantly elevated levels of proinflammatory cytokines and the best predictor for this complicated condition was found to be the level of serum IL-6.

Different proinflammatory reactions in fatal and non‐fatal enterovirus 71 infections: implications for early recognition and therapy

Aim: The mechanism of pulmonary oedema, a life‐threatening manifestation of enterovirus 71 (EV71) encephalitis, is unclear. Our aim was to assess the relationship of proinflammatory cytokines to EV71‐related pulmonary oedema. Methods: Proinflammatory responses in 33 EV71 patients with various complications and 21 normal healthy children were measured using an enzyme‐linked immunosorbent assay. Results: EV71 patients with both encephalitis and pulmonary oedema were found to have much higher levels of blood interleukin‐6 (IL‐6) (947 ± 1239 vs 4.9 ± 3.1 pg/ml, p= 0.0003), tumour necrosis factor‐α (TNF‐α) (22.4 ± 29.5 vs 5.3 ± 1.0 pg/ml, p= 0.0035), interleukin 1β (IL‐1β) (48.4 ± 85.2 vs 4.9 ± 10.1 pg/ml, p= 0.01), white blood cell count (28.3 ± 7.6 vs 15.5 ± 6.8 109/L, p± 0.0001) and blood glucose (501 ± 186 vs 165 ± 117 mg/dL, p= 0.0009) than patients with EV71 encephalitis alone. In fact, the cytokine levels in patients with encephalitis only or in those without complications were not significantly different from the levels found in normal children. The sensitivity, specificity, positive and negative predictive values of IL‐6 < 70 pg/ml for EV71 encephalitis with pulmonary oedema were all 100%. Conclusion: Patients with EV71‐related encephalitis combined with pulmonary oedema were found to have significantly elevated levels of proinflammatory cytokines and the best predictor for this complicated condition was found to be the level of serum IL‐6.

Cardiopulmonary manifestations of fulminant enterovirus 71 infection.

The pathogenesis of acute pulmonary edema and cardiac collapse after enterovirus 71 (EV71) infection are not completely understood. To determine the hemodynamic features and the mechanism of pulmonary edema (PE) after EV71 infection by direct intracardiac monitoring. Prospective clinical and laboratory study at a tertiary medical center. Five consecutive infants, ages 2 to 13 months, with EV71 infection-proved by viral isolation in 4 and antibody in 1-with PE were enrolled. The clinical characteristics were systemically assessed. Hemodynamic profiles were determined every 4 hours by simultaneously implanted pulmonary arterial and central venous catheters during the acute stage. Magnetic resonance imaging revealed that all 5 infants had brainstem lesions. All patients had tachycardia and hyperthermia. Transient systolic hypertension was noted in 1 patient, and 1 presented with hypotension. Pulmonary artery pressure in all 5 infants was normal or mildly elevated (26-31 mm Hg), and central venous pressure ranged from 10 to 22 mm Hg. Pulmonary artery occlusion pressures were normal or slightly elevated (13-16 mm Hg). Systemic and pulmonary vascular resistances were transiently increased in only 1 patient. The stroke volume index decreased to 15.3 to 35.7 mL/M2 (normal: 30-60 mL/M2), but because of the elevated heart rate, the cardiac index did not decrease. All hemodynamics normalized within days. Fulminant EV71 infection may lead to severe neurologic complications and acute PE. The acute PE and cardiopulmonary decompensation in EV71 infection are not directly caused by viral myocarditis. The mechanism of PE may be related to increased pulmonary vascular permeability caused by brainstem lesions and/or systemic inflammatory response instead of increased pulmonary capillary hydrostatic pressure.

Evidence for a Hydrostatic Mechanism in Human Neurogenic Pulmonary Edema

To identify the relative contribution of hydrostatic and permeability mechanisms to the development of human neurogenic pulmonary edema. Retrospective review of patients with neurogenic pulmonary edema who had pulmonary edema fluid analysis. University hospital ICU. Twelve patients with neurogenic pulmonary edema in whom the associated neurologic condition was subarachnoid hemorrhage (n = 8, 67%), postcraniotomy (n = 2), and stroke (n = 2). Protein concentration was measured from pulmonary edema fluid and plasma samples obtained shortly after the onset of clinical pulmonary edema. The mechanism of pulmonary edema was classified according to the initial alveolar edema fluid to plasma protein concentration ratio. A hydrostatic mechanism (ratio < or = 0.65) was observed in seven patients, none of whom had cardiac failure or intravascular volume overload. Five patients had evidence for increased permeability (ratio > 0.70). Patients with a hydrostatic mechanism had better initial oxygenation (mean +/- SD PaO2/FIO2 [fraction of inspired oxygen] = 233 +/- 132) compared with patients with increased permeability (PaO2/FIo2 = 80 +/- 42), and oxygenation improved more rapidly in the hydrostatic patients. Overall mortality (58%) was high, but it was related to unresolved neurologic deficits, not to respiratory failure. Many of our patients had a hydrostatic mechanism for neurogenic pulmonary edema. This is a novel observation in humans since prior clinical case reports have emphasized increased permeability as the usual mechanism for neurogenic pulmonary edema. These findings are consistent with pulmonary venoconstriction or transient elevation in left-sided cardiovascular pressures as contributing causes to the development of human neurogenic pulmonary edema.

Noncardiogenic Pulmonary Edema Induced by Sublingual Buprenorphine

A 21-year-old woman developed noncardiogenic pulmonary edema within 90 min after the use of buprenorphine, 0.2 mg, sublingually for severe dysmenorrhea. No organic cardiovascular illness was detected. The pulmonary edema resolved spontaneously with conservative treatment. The mechanism of pulmonary edema may be an allergic reaction to buprenorphine.

Adult respiratory distress syndrome: a consideration with rapid respiratory decompensation in association with preeclampsia

Adult respiratory distress syndrome, presenting as rapid respiratory decompensation in the setting of preeclampsia at 36 weeks of gestation, was managed by early hemodynamic monitoring with pulmonary artery catheterization. With confirmation of the diagnosis of preeclampsia the patient was delivered promptly; improvement of her respiratory failure was observed within 48 hours. Consideration of adult respiratory distress syndrome in the setting of preeclampsia is discussed, with emphasis on early confirmation of the diagnosis and determination of the precise mechanisms of pulmonary edema.

Anaesthetic implications of 32% Dextran-70 (Hyskon) during hysteroscopy: hysteroscopy syndrome.

This review describes the properties and side effects of Hyskon and the implications for the patient and anaesthetist during hysteroscopy. The amount of Hyskon absorbed is dependent on the injection pressure, the extent of tissue trauma, the seal of the hysteroscope around the cervix, and the duration of infusion. The mechanism of pulmonary oedema after absorbtion of Hyskon is fluid overload, and not injury to pulmonary capillary endothelium. The haematological effects are primarily due to haemodilution. However, case reports suggest that Dextran 70 may cause a syndrome resembling disseminated intravascular coagulation. The allergic response to Hyskon consists of both an anaphylactic and an anaphylactoid component. It is recommended that hysteroscopy with Hyskon be limited to 45 min, and that all possible measures be taken to minimize tissue trauma and bleeding. The volume of Hyskon should be limited to less than 500 ml, since pulmonary oedema and coagulopathy have been described with even lesser amounts. The cumulative volume of Hyskon should be monitored frequently and the patient should be closely monitored for signs of impending pulmonary oedema.

Cardiac Dysfunction and Pulmonary Edema following Scorpion Envenomation

Our own experience and published studies on scorpion envenomation do not provide the certitudes of Gueron and Sofer about the mechanisms of pulmonary edema (PE) following scorpion envenomation and the underlying cardiac dysfunction. Cardiac Dysfunction and Pulmonary Edema following Scorpion EnvenomationCHESTVol. 102Issue 4PreviewTo the Editor: Full-Text PDF

What is the Mechanism of Pulmonary EDEMA during High Volume Ventilation?

"What is the Mechanism of Pulmonary EDEMA during High Volume Ventilation?." American Review of Respiratory Disease, 143(5_pt_1), pp. 1198–1199