Academic literature on the topic 'Acute pulmonary oedema'
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Journal articles on the topic "Acute pulmonary oedema"
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Powell, Jessica, David Graham, Sarah O’Reilly, and Gillian Punton. "Acute pulmonary oedema." Nursing Standard 30, no. 23 (February 3, 2016): 51–60. http://dx.doi.org/10.7748/ns.30.23.51.s47.
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Wrigglesworth, Sue. "Acute pulmonary oedema." Nursing Standard 31, no. 38 (May 17, 2017): 72–73. http://dx.doi.org/10.7748/ns.31.38.72.s50.
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Purvey, Megan, and George Allen. "Managing acute pulmonary oedema." Australian Prescriber 40, no. 2 (April 3, 2017): 59–63. http://dx.doi.org/10.18773/austprescr.2017.013.
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KHOO, S. T., and F. G. CHEN. "Acute localised pulmonary oedema." Anaesthesia 43, no. 6 (June 1988): 486–89. http://dx.doi.org/10.1111/j.1365-2044.1988.tb06639.x.
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Pugh, G. "Acute Pulmonary Oedema and Mountaineering." Wilderness & Environmental Medicine 10, no. 4 (December 1999): 252. http://dx.doi.org/10.1580/1080-6032(1999)010[0252:apoam]2.3.co;2.
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Ingrams, Duncan, Martin Burton, Alison Goodwin, and John Graham. "Acute pulmonary oedema complicating laryngospasm." Journal of Laryngology & Otology 111, no. 5 (May 1997): 482–84. http://dx.doi.org/10.1017/s0022215100137703.
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AbstractPulmonary oedema is an uncommon but important complication of laryngeal spasm which in turn occurs more commonly in ENT practice than in most other surgical specialities. A case is reported and the literature reviewed, with particular reference to the proposed pathophysiological mechanism of this phenomenon.
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HSU, Yung-Hsiang, Shang Jyh KAO, Ru-Ping LEE, and Hsing I. CHEN. "Acute pulmonary oedema: rare causes and possible mechanisms." Clinical Science 104, no. 3 (February 14, 2003): 259–64. http://dx.doi.org/10.1042/cs1040259.
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Acute pulmonary oedema usually has a fatal outcome. In this clinical report, we present rare cases of pulmonary oedema that were associated with Japanese B encephalitis, lymphangitis in breast carcinoma, fat embolism due to long-bone fracture, and the rupture of cerebral mycotic aneurysms. A total of 18 patients in the four disease categories were collected in two teaching hospitals in Taipei and Hualien. Upon admission, routine and specific examinations were taken and all patients showed clear lungs by chest X-ray; however, signs of acute pulmonary oedema occurred within 7 days. After resuscitation, all patients died of acute pulmonary oedema. In patients with fat embolism, the levels of non-esterified plasma fatty acids, cGMP, 5-hydroxytryptamine (serotonin) and nitrates/nitrites were increased during pulmonary oedema. Immunohistochemical staining revealed virus infection and neuronal death, predominantly in the medial, ventral and caudal medulla in cases of Japanese B encephalitis. The pulmonary oedema due to central sympathetic activation in Japanese B encephalitis may be related to destruction of depressor mechanisms in the medulla. The rupture of mycotic aneurysms is known to cause cerebral compression that results in acute pulmonary oedema. Blockade of lymphatics, capillaries and venules in breast carcinoma with lymphangitis causes the development of rapid lung oedema. The pathogenesis of pulmonary oedema is much more complicated in fat embolism. Mediators such as cGMP, 5-hydroxytryptamine, nitric oxide and presumably other chemical substances may also be involved.
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Crawley, F., I. Saddeh, S. Barker, and H. Katifi. "Acute pulmonary oedema: presenting symptom of multiple sclerosis." Multiple Sclerosis Journal 7, no. 1 (February 2001): 71–72. http://dx.doi.org/10.1177/135245850100700112.
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Acute pulmonary oedema and headache are both common. The former is usually cardiogenic in origin. Severe headache of sudden onset in a young person may be suggestive of subarachnoid headache. We describe a 24-year-old man who presented with headache and pulmonary oedema, finally ascribed to multiple sclerosis. This is the first report of neurogenic pulmonary oedema as the first symptom of multiple sclerosis. We review the neuroanatomical basis and experimental evidence for neurogenic pulmonary oedema.
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Shrivastava, Savitri, Munesh Tomar, and Sitaraman Radhakrishnan. "Acute pulmonary oedema following percutaneous balloon pulmonary valvoplasty in children." Cardiology in the Young 13, no. 6 (December 2003): 576–78. http://dx.doi.org/10.1017/s1047951103001227.
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Pulmonary oedema complicating balloon dilation of the pulmonary valve is extremely rare. We describe two children who developed acute pulmonary oedema soon after successful dilation of the pulmonary valve. They were treated with diuretics, ionotropes, and ventilatory support. Despite the supportive therapy, the complication proved fatal in one.
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Bonello, M., R. Pullicino, and AJ Larner. "Acute pulmonary oedema: not always cardiogenic." Journal of the Royal College of Physicians of Edinburgh 47, no. 1 (2017): 57–59. http://dx.doi.org/10.4997/jrcpe.2017.112.
Full textDissertations / Theses on the topic "Acute pulmonary oedema"
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Hui, Chi-hoi, and 許志海. "Nurse-led non-invasive mechanical ventilation guideline for acute pulmonary oedema patients in acute medical wards." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2011. http://hub.hku.hk/bib/B4658190X.
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Johansson, Joakim. "Function of granulocytes after burns and trauma, associations with pulmonary vascular permeability, acute respiratory distress syndrome, and immunomodulation." Doctoral thesis, Linköpings universitet, Institutionen för klinisk och experimentell medicin, 2013. http://urn.kb.se/resolve?urn=urn:nbn:se:liu:diva-94513.
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Background: Our innate immunesystem protects us from infections but, since its methods is not all specific for microorganisms, may also induce collateral damage. Severe physical injury often proved deadly throughout evolution. Such injuries may induce massive collateral damage. Nowadays we can initiate advanced critical care for affected patients and save them from imminent trauma-related death. We are therefore faced with the fact that the collateral damage from the immune system may pose a major threat to the patient, the pathophysiology of which is not amenable to direct medical treatment and which leaves us with only passive supportive measures. In this thesis we investigated the role of leucocytes under such circumstances. Our main aim was to understand better the role of leucocytes in the development of increased vascular permeability after burns and trauma. More specifically we investigated the impact of an injury on the function of leucocytes such as the dynamic change of certain cell-surface receptors on the leucocytes and in their numbers and immature forms. We wanted to find out if the increased pulmonary vascular permeability after a burn could be mediated through heparin binding protein (HBP) released from granuloctes, and whether HBP could be used as a biomarker for respiratory failure after trauma. We also wanted to confirm the possible role of histamine as a mediator of the systemic increase in vascular permeability after burns. Methods: The dynamic change of cell-surface receptors was measured by flow-acquired cytometer scanning (FACS) on blood samples taken after burns. The concentrations of HBP after a burn and mechanical trauma were analysed in plasma. Pulmonary vascular permeability after a burn was assessed using transpulmonary thermodilution. The histamine turnover after a burn was assessed with high performance liquid chromatography (HPLC) for concentrations of histamine and methylhistamine in urine. Results: We confirmed earlier investigations showing altered expression of receptors on leucocytes after a burn, receptors intimately associated with leucocyte functions (study I). In a pilot study of 10 patients we measured plasma concentrations of HBP and found them to be increased soon after a burn (study II). This finding was not confirmed in a larger, more extensive and specific study of 20 patients. We did, however, find an association between alterations in the number of leucocytes soon after a burn and pulmonary vascular permeability, indicating that they had a role in this process (study III). In another study of trauma (non burn) we found an association between the concentration of HBP in early plasma-samples after injury and the development of ARDS, indicating that granulocytes and HBP have a role in its aetiology (study IV). We found a small increase in urinary histamine and normal urinary methylhistamine concentrations but had anticipated a distinct increase followed by a decrease after reading the current papers on the subject. This indicates that the role of histamine as a mediator of increased vascular permeability after burns may have been exaggerated (study V). Conclusions: We conclude that leucocytes are affected by burns and trauma, and it is likely that they contribute to the development of respiratory failure and acute respiratory distress syndrome (ARDS). HBP is a candidate biomarker for the early detection of ARDS after trauma, and the white blood count (WBC) is a useful biomarker for the detection of decreased oxygenation soon after a burn.
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Lafargue, Mathieu. "Plasminogen Activator Inhibitor-1 (PAI-1) and Activated Protein C (aPC) Modulation Mechanisms of Pseudomonas aeruginosa Induced Pulmonary Edema." Thesis, Bordeaux 2, 2012. http://www.theses.fr/2012BOR22020/document.
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Une coagulopathie aigue endogène (EAC) est présente chez 25% des patients de traumatologie dès leur arrivée. Des résultats d’études récentes montrent que cette EAC est liée à l’activation de la voie de la protéine C (aPC). Quelques heures après, se développe un état pro-coagulant associant un niveau abaissé d’aPC et un taux plasmatique élevé de l’inhibiteur de l’activateur du plasminogene (PAI-1). Nous trouvons que l’incidence des pneumopathies associées à la ventilation est significativement augmentée chez ces patients sans toutefois connaître le rôle exact de ces anomalies de coagulation. Basé sur cette hypothèse central de susceptibilité augmentée a l’infection et plus particulièrement aux pneumopathie a P.aeruginosa (PA) le but de ce travail est d’identifier les mécanismes par lesquels PAI-1 et aPC peuvent moduler la perméabilité de la barrière alveolo capillaire et ceci a travers 3 objectifs spécifiques1 – Objectif 1 : déterminer les mécanismes par lequel PA augmente la perméabilité endothéliale. 2 – Objectif 2 : déterminer le rôle d’aPC dans la modulation des effets de PA sur l’œdème pulmonaire lésionnel.3 – Objectif 3 : déterminer le rôle de PAI-1 dans la modulation des effets de PA sur l’œdème pulmonaire lésionnel.En utilisant un inhibiteur spécifique des petites GTPases nous démontrons le rôle centrale joué par RhoA dans le développement de l’œdème pulmonaire induit par PA. PAI-1 et aPC sont impliquées dans le mécanisme lésionnel pulmonaire. aPC et l’inhibition de la voie du RhoA attenue le développement de l’œdème pulmonaire et diminue la dissémination systémique bactérienne. Cependant le blocage invivo de la voie de PAI-1 est associé à une surmortalité et à une augmentation de la charge bactérienne suggérant un rôle de PAI-1 dans l’activation de la réponse inflammatoire nécessaire a l’éradication de PAA clinically significant acute endogenous coagulopathy (EAC) is present in 25% of major trauma patients upon arrival in the emergency department, before any fluid resuscitation. Results from recent clinical studies indicate that EAC is primarily caused by the activation of the anticoagulant protein C pathway. Several hours later, there is the development of a systemic procoagulant activity associated with low plasma levels of activated protein C (aPC) and an inhibition of the fibrinolysis caused by elevated plasma levels of plasminogen activator inhibitor 1 (PAI-1). We have found that the incidence of ventilator-associated pneumonia (VAP) is significantly increased in trauma patients with these coagulation abnormalities [6, 9]. However, whether these coagulation abnormalities play a mechanistic role in the increased susceptibility to nosocomial lung infection observed after severe posttraumatic hemorrhage is unknown. Thus, the central hypothesis is that the increased susceptibility to P. aeruginosa (PA) pneumonia following severe trauma with tissue hypoperfusion is mediated in part by these posttraumatic coagulation abnormalities within the airspaces of the lung. Specifically, in this work, we will identify through 3 specific aims the mechanisms by which PAI-1 and aPC modulate PA–mediated increase in alveolar-capillary barrier permeability.1 - Specific Aim 1: To determine the mechanisms by which PA increases lung endothelial permeability.2 - Specific Aim 2 : To determine the Role of aPC in modulating the effect of PA on the lung endothelial barrier function3 - Specific Aim 3 : To determine the Role of PAI-1 in modulating the effect of PA on the lung endothelial barrier functionIn the present work, we demonstrated the central role small GTPases RhoA plays in the increase of permeability induced by pseudomonas infection. PAI-1 and aPC are deeply involved in the control of early lung inflammation. aPC and inhibition of the RhoA pathway attenuates the development of pulmonary edema and decrease in the systemic dissemination of P. aeruginosa. However, in vivo disruption of PAI-1 signalling is associated with higher mortality at 24 h and significant increase in the bacterial burden suggesting that PAI-1 is required for the activation of the innate immune response necessary for the eradication of PA from the distal airspaces of the lung
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Prunet, Bertrand. "Contusion pulmonaire : aspects physiopathologiques et conséquences thérapeutiques." Thesis, Aix-Marseille, 2015. http://www.theses.fr/2015AIXM5001.
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L’association lésionnelle d’une contusion pulmonaire et d’un état de choc hémorragique est fréquente et constitue un réel chalenge thérapeutique. La prise en charge de ce choc va nécessiter une réanimation hémodynamique dans laquelle le remplissage vasculaire tient une place centrale. Mais dans ce contexte de poumon contus, il devra être raisonné car délétère sur le plan pulmonaire, notamment en terme d'oedème et d'altération de la compliance. Ce remplissage devra donc être titré, basé sur des objectifs tensionnels clairs et un monitorage hémodynamique fiable. L'utilisation de solutés à haut pouvoir d'expansion volémique (sérum salé hypertonique, colloïdes) présente un intérêt, de même que l'introduction précoce de vasopresseurs. Le monitorage hémodynamique permettra de conduire cette réanimation sur des objectifs de pression artérielle, sur des indices de précharge dépendance et sur la mesure de l'eau pulmonaire extravasculaire. Notre travail, basé sur des études expérimentales et cliniques, a pour objectif de caractériser les modalités actuelles de prise en charge d’une contusion pulmonaire, sur les plans hémodynamiques et respiratoiresPulmonary contusion is often associated with hemorrhagic shock, constituting a challenge in trauma care. For patients who have sustained lung contusions, fluid resuscitation should be carefully performed, because injured lungs are particularly vulnerable to massive fluid infusions with an increased risk of pulmonary edema and compliance impairment. Fluid administration should be included in an optimized and goal directed resuscitation, based on blood pressure objectives and hemodynamical monitoring. The use of fluids with high volume-expanding capacities (hypertonic saline, colloids) is probably interesting, as well as early introduction of vasopressors. Hemodynamic monitoring will allow to conduct resuscitation on blood pressure objectives, on preload parameters and on extravascular lung water measurement.Our work, based on experimental and clinical studies, objective to characterize the current modalities of ventilatory and hemodynamical aspect of pulmonary contusion care
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Menaouar, Ahmed. "Mécanismes de l'oedème pulmonaire provoqué par le chlore : effets de l'inhalation de monoxyde d'azote." Université Joseph Fourier (Grenoble), 1996. http://www.theses.fr/1996GRE10190.
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L'inhalation de chlore (cl2) provoque des lesions tracheo-bronchiques et un deme pulmonaire de type inflammatoire. Nous avons etabli des modeles experimentaux ex vivo et in vivo pour etudier les mecanismes de cet deme ainsi que l'efficacite therapeutique de l'inhalation de monoxyde d'azote (no). Sur le poumon isole de lapin, nous avons provoque un deme pulmonaire par inhalation de 500 ppm de cl2 pendant 10 minutes. La pression de filtration, la clairance de l'albumine (calb) et le coefficient de filtration (kf = conductivite a l'eau x surface de filtration) ont ete mesures avant et 30 minutes apres administration de cl2. L'inhalation de cl2 a augmente de 200% le kf et la calb, de 100% l'eau extravasculaire (eev), sans modifications de la pression et de la surface de filtration. Ces resultats suggerent que l'deme alveolaire induit par le cl2 est du essentiellement a une augmentation de la permeabilite capillaire et que sa formation est facilitee par la lesion de l'epithelium alveolaire. L'inhalation de 40 ppm de no, 5 minutes apres l'inhalation de cl2, a diminue de 30% l'alteration du kf, de calb et de eev. Le mecanisme d'action du no n'est pas une diminution de la pression de filtration. Il s'agit davantage d'une diminution de l'alteration de la permeabilite capillaire que d'une diminution de la surface de filtration des zones lesees. Chez le chien anesthesie, l'exposition a 250 ppm de cl2 pendant 10 minutes a entraine une augmentation du debit lymphatique pulmonaire par un facteur 2,8, de la clairance des proteines par un facteur 2,5, et de eev par un facteur 1,5. Ce modele in vivo, ou la microcirculation bronchique est fonctionnelle, a montre des differences avec le modele ex vivo, notamment l'importance du spasme bronchique et de l'hypoventilation alveolaire. Le mecanisme de l'deme pulmonaire dans ce modele etait une augmentation a la fois de la permeabilite capillaire et de la pression de filtration
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Jabaudon, Gandet Matthieu. "Approche translationnelle de la voie RAGE au cours du syndrôme de détresse respiratoire aiguë : implications diagnostiques, physiopathologiques et thérapeutiques." Thesis, Clermont-Ferrand 1, 2016. http://www.theses.fr/2016CLF1MM09.
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Le syndrome de détresse respiratoire aiguë (SDRA) est caractérisé par des lésions alvéolaires diffuses menant à un œdème alvéolaire lésionnel et une insuffisance respiratoire aiguë hypoxémique. Malgré les progrès récents dans la prise en charge des patients de réanimation, le SDRA reste un syndrome fréquent et associé à une morbimortalité importante. Deux mécanismes principaux du SDRA semblent associés à une mortalité plus élevée et à des réponses thérapeutiques différentes : la déficience de la clairance liquidienne alvéolaire (AFC, pour alveolar fluid clearance), l’incapacité pour l’épithélium alvéolaire de résorber l’œdème alvéolaire, et la présence d’un phénotype « hyper-inflammatoire ». Les approches pharmacologiques du traitement du SDRA restent limitées et il est nécessaire de poursuivre l’étude des voies biologiques impliquées dans la pathogénie du SDRA et dans sa résolution afin de développer des approches innovantes des prises en charge diagnostique et thérapeutique du SDRA. RAGE, le récepteur des produits de glycation avancée, est un récepteur multi-ligands, exprimé abondamment par les cellules épithéliales alvéolaires du poumon (pneumocytes), qui module de nombreuses voies de signalisation intracellulaire. De nombreuses études récentes suggèrent que sRAGE, la forme soluble principale de RAGE, pourrait servir de marqueur lésionnel du pneumocyte de type I, et que RAGE pourrait jouer un rôle-pivot dans la pathophysiologie du SDRA, en initiant et en entretenant la réponse inflammatoire alvéolaire. Nos objectifs étaient de caractériser les rôles de RAGE au cours du SDRA, grâce à une approche translationnelle combinant études cliniques et précliniques. D’abord, des études cliniques observationnelles et interventionnelles ont été conduites afin de caractériser sRAGE comme un véritable biomarqueur dans le SDRA. Ensuite, des cultures in vitro de cellules épithéliales et de macrophages, ainsi qu’un modèle expérimental in vivo de SDRA murin par instillation trachéale d’acide chlorhydrique ont été utilisés pour décrire les effets de la voie RAGE sur les mécanismes d’AFC et l’inflammation macrophagique médiée par l’inflammasome « Nod-Like Receptor family, Pyrin domain containing 3 » (NLRP3). Enfin, l’effet d’une inhibition de RAGE, par sRAGE recombinant ou par anticorps monoclonal anti-RAGE, était testée en modèle murin. Nos résultats issus des études cliniques suggèrent que sRAGE présente toutes les caractéristiques d’un biomarqueur au cours du SDRA, avec un intérêt dans le diagnostic, le pronostic et la prédiction du risque de développer un SDRA dans une population à risque. Pris ensemble, notre travail suggère que la voie RAGE joue un rôle important dans la régulation de l’atteinte pulmonaire, de l’AFC et de l’activation macrophagique au cours du SDRA. Toutefois, les mécanismes précis de cette régulation restent incertains. La forme soluble de RAGE (sRAGE), lorsqu’elle est dosée dans le plasma, présente toutes les caractéristiques d’un biomarqueur pouvant être utile en pratique clinique, mais son intérêt dans la sélection de sous-groupes (ou « phénotypes ») de patients pouvant bénéficier de traitements ciblés reste à étudier. La voie RAGE pourrait enfin représenter une cible thérapeutique prometteuse. Bien que des études de validation restent nécessaires, ces résultats pourraient ouvrir de nouvelles perspectives dans la prise en charge des patients atteints de SDRAThe acute respiratory distress syndrome (ARDS) is associated with diffuse alveolarinjury leading to increased permeability pulmonary edema and hypoxemic respiratory failure. Despite recent improvements in intensive care, ARDS is still frequent and associated with high mortality and morbidity. Two major features of ARDS may contribute to mortality and response to treatment: impaired alveolar fluid clearance (AFC), i.e. altered capacity of the alveolar epithelium to remove edema fluid from distal lung airspaces, and phenotypes of severe inflammation. Pharmacological approaches of ARDS treatment are limited and further mechanistic explorations are needed to develop innovative diagnostic and therapeutic approaches. The receptor for advanced glycation endproducts (RAGE) is a multiligand pattern recognition receptor that is abundantly expressed by lung alveolar epithelial cells andmodulates several cellular signaling pathways. There is growing evidence supporting sRAGE (the main soluble isoform of RAGE) as a marker of epithelial cell injury, and RAGE may be pivotal in ARDS pathophysiology through the initiation and perpetuation of inflammatory responses. Our objectives were to characterize the roles of RAGE in ARDS through a translational approach combining preclinical and clinical studies. First, observational and interventional clinical studies were conducted to test sRAGE as a biomarker during ARDS.Then, cultures of epithelial cells, macrophages and a mouse model of acidinduced lung injury were used to describe the effects of RAGE pathway on AFC and inflammation, with special emphasis on a macrophage activation through NodLikeReceptor family, Pyrindomain containing 3 (NLRP3) inflammasome. Acidinjured mice were treated with an antiRAGE monoclonal antibody or recombinant sRAGE to test the impact of RAGE inhibition on criteria of experimental ARDS. Results from clinical studies support a role of sRAGE as a biomarker of ARDS, withdiagnostic, prognostic and predictive values. In addition, plasma sRAGE is correlated with a lung imaging phenotype of nonfocal ARDS and could inform on therapeutic response. Herein, we also describe in vivo and in vitro effects of RAGE activation on transepithelial fluid transport and expression levels of epithelial channels (aquaporin 5, αNa,KATPaseandαENaC) and on macrophage activation through NLRP3 inflammasome. Finally, RAGE inhibition improves AFC and decreases lung injury in vivo. Taken together, our findings support a role of RAGE pathway in the regulation of lung injury, AFC and macrophage activation during ARDS, albeit precise regulatory mechanisms remain uncertain. sRAGE has most features of a validated biomarker that could be used in clinical medicine, but whether it may help to identify subgroups (or phenotypes) of patients that would benefit from tailored therapy remains underinvestigated. Modulation ofRAGE pathway may be a promising therapeutic target, and though validation studies are warranted, such findings may ultimately open novel diagnostic and therapeutic perspectivesin patients with ARDS
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Thornton, Charlene. "Benchmarking the hypertensive disorders of pregnancy : improving outcomes for mothers and babies via clinical practice change." Thesis, 2010. http://handle.uws.edu.au:8081/1959.7/500486.
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An average of one hundred and thirty four mothers and 410 babies die every day around the world as a result of the hypertensive disorders of pregnancy (HDP). This figure, whilst staggering, in no way reflects the degree of morbidity which results from these disorders. Randomised controlled data and isolated hospital specific databases can provide us with snapshots at single points in time within obstetric units and populations, but there is no routinely collected or mandatory dataset which accurately reflects the type and severity of complications which occur. Eclampsia, acute renal failure (ARF), acute pulmonary oedema (APO) and growth restriction are well documented complications of the HDPs, yet there is considerable variation in the literature in describing their incidence. There is currently no consensus on treatment modalities which will optimise outcomes. Without accurate data, obstetric care providers and obstetric units are unable to be confident that the care they provide is optimal if they have no standard or benchmark against which to compare. The aim of the study herein, was to establish a database across obstetric units and countries to determine if accurate rates of morbidity could be obtained, and if this data could be the basis for the establishment of ‘best achievable outcomes’. Further, the utility of the audit and feedback process was tested as the means by which clinical practice change could be instituted.
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Chebli, Jasmine. "Le rôle des canaux potassiques dans la résolution des paramètres du syndrome de détresse respiratoire aiguë." Thèse, 2016. http://hdl.handle.net/1866/18897.
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Le syndrome de détresse respiratoire aiguë (SDRA) est caractérisé par des dommages au niveau de la barrière alvéolo-capillaire, résultant en la formation d’un œdème pulmonaire et une réponse inflammatoire exacerbée. Sans résolution rapide de ces paramètres, le syndrome progresse vers le développement de fibrose menant à l’insuffisance respiratoire. Or, il a été établi que la réparation de l’épithélium alvéolaire est une étape cruciale pour la résolution du SDRA. Une meilleure compréhension des mécanismes de réparation de l’épithélium alvéolaire est donc nécessaire afin de proposer de nouvelles thérapies pour le SDRA, pour lequel aucun traitement efficace n’existe. Il a été montré que les mécanismes de réparation sont régulés par des protéines membranaires, non seulement par les récepteurs aux facteurs de croissance et les intégrines, mais également par les canaux ioniques, en particulier les canaux potassiques.
L’objectif principal de cette étude était donc de caractériser l’impact de la modulation des canaux potassiques KCa3.1 et KvLQT1 dans la résolution du SDRA. Dans un premier temps, nos résultats ont montré le rôle coopératif du canal potassique KCa3.1, de la matrice extracellulaire et de l’intégrine-β1 dans les processus de réparation de l’épithélium alvéolaire in vitro. Nous avons montré que la matrice de fibronectine et le KCa3.1 étaient impliqués dans la migration et dans la réparation de monocouches de cellules alvéolaires de cultures primaires de rat.
Dans un deuxième temps, nous avons étudié l’impact de la modulation du canal potassique KvLQT1 dans certains aspects physiopathologiques du SDRA à l’aide de modèles in vivo. Nous avons montré que KvLQT1 n’était pas seulement impliqué dans les mécanismes de réparation de l’épithélium alvéolaire, mais également dans la résorption de l’œdème pulmonaire et la résolution de la réponse inflammatoire.
Nos résultats démontrent que les canaux potassiques, tels que KCa3.1 et KvLQT1, pourraient être identifiés en tant que cibles thérapeutiques potentielles pour le SDRA.Acute respiratory distress syndrome (ARDS) is characterized by alveolar-capillary barrier damage, resulting in the formation of pulmonary oedema and an exacerbated inflammatory response. Without rapid recovery of these parameters, there is a gradual development of fibrosis, leading to respiratory failure. It has been established that alveolar regeneration is a critical step for the resolution of ARDS. A better understanding of alveolar epithelial repair mechanisms is hence necessary to identify new therapies for ARDS, for which no effective treatment exist. It has been shown that repair mechanisms are regulated by membrane proteins, not only by growth factor receptors and integrins, but also by ion channels, in particular potassium channels. Therefore, the main objective of this study was to characterize the impact of KCa3.1 and KvLQT1 potassium channels modulation in the resolution of ARDS. First, our results have shown the cooperative role of the potassium channel KCa3.1, the extracellular matrix and the β1-integrin in alveolar epithelial repair processes in vitro. We have shown that the fibronectin matrix and KCa3.1 are involved in the migration and repair of primary cultures of rat alveolar cell monolayers. Our data also revealed a putative relationship between Kca3.1 and the β1-integrin. Second, we studied the impact of KvLQT1 potassium channel modulation on ARDS pathophysiological aspects with in vivo models. We showed that KvLQT1 was not only involved in alveolar epithelial repair, but also in the resolution of pulmonary oedema and inflammatory response. Taken together, our data demonstrate that potassium channels, such as KCa3.1 and KvLQT1, may be identified as potential therapeutic targets for the resolution of ARDS.
Books on the topic "Acute pulmonary oedema"
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Tanaka, Sébastien, and Jacques Duranteau. Management of acute non-cardiogenic pulmonary oedema. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0165.
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Severe capillary leak is an important factor in the pathogenesis of organ dysfunction following inflammatory syndromes such as sepsis-induced acute lung injury and acute respiratory distress syndrome (ARDS). Various interventions, such as a conservative fluid strategy, albumin, and diuretics are designed to maintain an adequate intravascular colloid osmotic pressure, reduce capillary leak and reduce extravascular water. Of these, only a conservative, rather than liberal fluid strategy is currently recommended. Preclinical studies in ARDS and sepsis suggest that preventing microvascular leak may represent a viable therapeutic approach to prevent or ameliorate organ dysfunction. The challenge is to now go further with carefully designed clinical trials.
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Ware, Lorraine B. Pathophysiology of acute respiratory distress syndrome. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0108.
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The acute respiratory distress syndrome (ARDS) is a syndrome of acute respiratory failure characterized by the acute onset of non-cardiogenic pulmonary oedema due to increased lung endothelial and alveolar epithelial permeability. Common predisposing clinical conditions include sepsis, pneumonia, severe traumatic injury, and aspiration of gastric contents. Environmental factors, such as alcohol abuse and cigarette smoke exposure may increase the risk of developing ARDS in those at risk. Pathologically, ARDS is characterized by diffuse alveolar damage with neutrophilic alveolitis, haemorrhage, hyaline membrane formation, and pulmonary oedema. A variety of cellular and molecular mechanisms contribute to the pathophysiology of ARDS, including exuberant inflammation, neutrophil recruitment and activation, oxidant injury, endothelial activation and injury, lung epithelial injury and/or necrosis, and activation of coagulation in the airspace. Mechanical ventilation can exacerbate lung inflammation and injury, particularly if delivered with high tidal volumes and/or pressures. Resolution of ARDS is complex and requires coordinated activation of multiple resolution pathways that include alveolar epithelial repair, clearance of pulmonary oedema through active ion transport, apoptosis, and clearance of intra-alveolar neutrophils, resolution of inflammation and fibrinolysis of fibrin-rich hyaline membranes. In some patients, activation of profibrotic pathways leads to significant lung fibrosis with resultant prolonged respiratory failure and failure of resolution.
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Rahimi, Kazem. Acute heart failure. Edited by Patrick Davey and David Sprigings. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199568741.003.0091.
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Heart failure is a clinical syndrome characterized by an inadequate cardiac output for the needs of the body in the absence of low filling pressures, and reflects abnormal cardiac structure or function. Although various definitions for acute heart failure (AHF) exist, here AHF is defined as new-onset heart failure or an acute exacerbation of chronic heart failure, requiring urgent therapy. Patients with AHF typically have clinical features of organ hypoperfusion, with or without pulmonary and peripheral oedema.
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Jolly, Elaine, Andrew Fry, and Afzal Chaudhry, eds. Acute medical emergencies and practical procedures. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199230457.003.0001.
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Chapter 1 covers the basic science and clinical topics relating to acute medical emergencies and practical procedures which trainees are required to learn as part of their basic training and demonstrate in the MRCP. It covers cardiorespiratory arrest, shock, acute coronary syndromes, tachycardia, bradycardia, hypertensive emergencies, pulmonary oedema, acute asthma, massive pulmonary embolism, acute upper gastrointestinal haemorrhage, acute kidney injury, coma, traumatic brain injury, status epilepticus, adrenal crisis, thyroid emergencies, acute poisoning, and burns.
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McAuley, Danny F., and Thelma Rose Craig. Measurement of extravascular lung water in the ICU. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0140.
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The accumulation of fluid in the interstitium and alveolar space is known as extravascular lung water (EVLW). EVLW is associated with increased morbidity and mortality in critically ill patients and is elevated in patients with cardiogenic pulmonary oedema, acute lung injury (ALI), and the acute respiratory distress syndrome (ARDS). Pulmonary oedema is a consequence of increased pulmonary capillary hydrostatic pressure and/or an increased capillary permeability. The quantity of pulmonary oedema fluid is dependent on the balance of fluid formation and clearance, and this contributes to the overall dynamic net lung fluid balance. Measurement of EVLW is therefore an indirect surrogate measurement of the alveolar epithelial and endothelial damage in ALI/ARDS. The single indicator transpulmonary thermodilution technique is an available bedside technique to measure EVLW.
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Lee, Jae Myeong, and Michael R. Pinsky. Cardiovascular interactions in respiratory failure. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0087.
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Acute respiratory failure not only impairs gas exchange, but also stresses cardiovascular reserve by increasing the need for increased cardiac output (CO) to sustain O2 delivery in the face of hypoxaemia, increased O2 demand by the increased work of breathing and inefficient gas exchange, and increased right ventricular afterload due to lung collapse via hypoxic pulmonary vasoconstriction. Mechanical ventilation, though often reversing these processes by lung recruitment and improved arterial oxygenation, may also decrease CO by increasing right atrial pressure by either increasing intrathoracic pressure or lung over-distention by excess positive end-expiratory pressure or inadequate expiratory time causing acute cor pulmonale. Finally, spontaneous negative swings in intrathoracic pressure also increase venous return and impede left ventricular ejection thus increasing intrathoracic blood volume and often precipitating or worsening hydrostatic pulmonary oedema. Positive-pressure breathing has the opposite effects.
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Lancellotti, Patrizio, and Bernard Cosyns. Critically Ill Patients. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780198713623.003.0012.
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Echocardiography is one of the most powerful diagnostic and monitoring tools available to the modern emergency/critical care practitioners. It can provide important information throughout the whole patient pathway. This chapter details the role of lung ultrasound and 2D echocardiography and colour Doppler for a variety of critical acute care conditions. These include acute cardiogenic pulmonary oedema, acute dyspnoea, and acute lung injury. More general information on how to perform a lung ultrasound, specific problems in ventilated patients and echocardiographic examination in cardiorespiratory arrest and focused echocardiography protocols are also discussed.
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Martin, Daniel S., and Michael P. W. Grocott. Pathophysiology and management of altitude-related disorders. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0350.
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Acute high-altitude related illnesses include acute mountain sickness (AMS), high altitude pulmonary oedema (HAPO) and high altitude cerebral oedema (HACO). AMS is characterized by headache, lack of appetite, poor sleep, lethargy, and fatigue. AMS is a common, generally benign, self-limiting condition if managed with rest, no ascent, and symptomatic treatment. Descent is indicated in severe cases. HACO and HAPO are rare, but serious conditions that should be considered life-threatening medical emergencies. HACO is characterized by the presence of neurological signs (including confusion) at altitude, commonly in the presence of headache. HAPO is characterized by breathlessness and signs of respiratory distress at altitude, particularly accompanying exercise. Management of HACO and HAPO involves urgent descent, supplemental oxygen (cylinder, concentrator, or portable hyperbaric chamber) if available, and specific treatment with dexamethasone (HACO) or nifedipine (HAPO). Slow controlled ascent (adequate acclimatization) is the best prophylaxis against the acute high-altitude-related illnesses. Acetazolamide is an effective prophylaxis against AMS.
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Farmer, Brenna M., and Neal Flomenbaum. Management of salicylate poisoning. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0317.
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Salicylates are weak acids that work as neurotoxins. The goal of management is to keep salicylates out of the brain and enhance elimination. Acute salicylate toxicity manifests as tinnitus, nausea, vomiting, and hyperventilation in a patient who takes a single large ingestion. Chronic salicylate toxicity is associated with long-term use, has a more insidious onset, and symptoms tend to be less severe, resulting in delayed diagnosis. It is more commonly seen in elderly patients. Therapeutic interventions for toxicity include gastrointestinal decontamination, serum and urine alkalinization, and haemodialysis. Mechanical ventilation may lead to clinical deterioration and death in a salicylate-poisoned patient due to worsening acidosis from respiratory failure. This results in severe acidosis, cerebral oedema, pulmonary oedema, and cardiac arrest.
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Spoletini, Giulia, and Nicholas S. Hill. Non-invasive positive-pressure ventilation. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0090.
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Non-invasive ventilation (NIV) has been increasingly used over the past decades to avoid endotracheal intubation (ETI) in critical care settings. In selected patients with acute respiratory failure, NIV improves the overall clinical status more rapidly than standard oxygen therapy, avoids ETI and its complications, reduces length of hospital stay, and improves survival. NIV is primarily indicated in respiratory failure due to acute exacerbations of chronic obstructive pulmonary disease, cardiogenic pulmonary oedema and associated with immunocompromised states. Weaker evidence supports its use in other forms of acute hypercapnic and hypoxaemic respiratory failure. Candidates for NIV should be carefully selected taking into consideration the risk factors for NIV failure. Patients on NIV who are unstable or have risk factors for NIV failure should be monitored in an intensive or intermediate care units by experienced personnel to avoid delay when intubation is needed. Stable NIV patients can be monitored on regular wards.
Book chapters on the topic "Acute pulmonary oedema"
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Sprigings, David, and John B. Chambers. "Acute pulmonary oedema." In Acute Medicine - A Practical Guide to the Management of Medical Emergencies, 5th Edition, 305–10. Chichester, UK: John Wiley & Sons, Ltd, 2017. http://dx.doi.org/10.1002/9781119389613.ch47.
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Staub, Norman C., Marlys Gee, and Carol Vreim. "Mechanism of Alveolar Flooding in Acute Pulmonary Oedema." In Ciba Foundation Symposium 38 - Lung Liquids, 255–72. Chichester, UK: John Wiley & Sons, Ltd., 2008. http://dx.doi.org/10.1002/9780470720202.ch15.
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Bernardi, P., F. Fontana, C. Ventura, S. Spampinato, M. Cavazza, L. Bastagli, N. Spagnolo, and S. Lenzi. "Relationship between endogenour opioids and the cardiovascular system: dynorphin measurement in the human heart: β-endorphin plasmatic levels assay during acute pulmonary oedema." In Atherosclerosis and Cardiovascular Diseases, 395–98. Dordrecht: Springer Netherlands, 1987. http://dx.doi.org/10.1007/978-94-009-3205-0_52.
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Brown, Anthony F. T. "Acute pulmonary oedema." In Emergency Medicine, 140–46. Elsevier, 2009. http://dx.doi.org/10.1016/b978-0-7295-3876-3.10009-7.
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"Acute cardiogenic pulmonary oedema." In Non-invasive Ventilation and Weaning: Principles and Practice, 311–28. CRC Press, 2010. http://dx.doi.org/10.1201/b13434-42.
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Raman, PG, and LC Gupta. "Acute Pulmonary Oedema (APO)." In Manual of Medical Emergencies, 47. Jaypee Brothers Medical Publishers (P) Ltd., 2001. http://dx.doi.org/10.5005/jp/books/11606_10.
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Verges, Samuel, and Patrick Levy. "High-altitude pulmonary oedema." In ESC CardioMed, 1078–80. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780198784906.003.0261.
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At high altitude, the reduction in arterial oxygenation frequently leads to symptoms of acute mountain sickness. While these symptoms generally resolve spontaneously, high-altitude pulmonary oedema can develop and represents a potentially lethal form of high-altitude disease. High-altitude pulmonary oedema is a non-cardiogenic oedema due to exaggerated pulmonary vasoconstriction and altered alveolar–capillary permeability. In addition to descending to lower altitude, it requires specific emergency cares such as oxygen administration, a hyperbaric bag, and vasodilator drugs.
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Victor, Kelly, Justin Kirk-Bayley, and Nicholas Ioannou. "Acute respiratory distress syndrome." In Focused Intensive Care Ultrasound, edited by Marcus Peck and Peter Macnaughton, 225–34. Oxford University Press, 2019. http://dx.doi.org/10.1093/med/9780198749080.003.0027.
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This chapter will review the targets for ultrasound assessment, including biventricular function, extravascular water, and systemic volume assessment. Importantly, it will discuss how to differentiate cardiogenic from non-cardiogenic pulmonary oedema, how to recognize acute cor pulmonale, and when to look for a patent foramen ovale. The advanced section will introduce Doppler-based methods to evaluate right ventricular systolic function and pulmonary arterial systolic pressure, which can both become compromised in acute respiratory distress syndrome.
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Beltrame, John, and John Horowitz. "The management of acute cardiogenic pulmonary oedema." In Caring for the Heart Failure Patient, 93–101. CRC Press, 2004. http://dx.doi.org/10.3109/9780203640630-8.
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Pistolesi, Massimo, and Mariaelena Occhipinti. "Pulmonary venous hypertension." In ESC CardioMed, edited by Christian Herold, 403–6. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780198784906.003.0078.
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The chest radiograph reflects quite accurately the sequence of lung water accumulation as it may result from conditions of acute and chronic left heart dysfunction leading to pulmonary venous hypertension. Filtration and reabsorption of liquids is a rather dynamic process that occurs in the lung extravascular space, a delicate space working as both a gas and liquid exchanger. Interference of lung liquid accumulation with the gas exchange function is the most relevant clinical consequence of pulmonary venous hypertension. Lymphatics respond slowly to the increased filtration rate secondary to acute pulmonary venous hypertension, whereas the long-standing disequilibrium of liquid exchange in chronic conditions induces several adaptive changes in lung tissue and lymphatics. Thus, there might be lower amounts of lung oedema for the same level of pulmonary venous hypertension in chronic with respect to acute left heart failure conditions. Knowledge of chest radiographic signs of acute and chronic pulmonary venous hypertension allows better understanding of patients’ clinical conditions. Radiographic scoring of pulmonary interstitial oedema and assessment of vascular pedicle width is recommended to determine extravascular lung liquid balance and intravascular volume status in critically ill patients.
Conference papers on the topic "Acute pulmonary oedema"
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Bork, K., and G. Witzke. "LCNG-TEFM SUBSTITUTION WITH Cl-INACTIVATOR IN PATIENTS WITH HEREDITARY AND ACQUIRED Cl-INH DEFICIENCY AND LIFE-THREATENING ANGIOEDEMA." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1644329.
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Patients with hereditary car acquired cl-inactivator (Cl-INH) deficiency suffer frcm repeated episodes of oedema of the skin and internal organs, which often constitute a threat to life (laryngeal, pulmonary and brain oedama). The treatment which is rapidly effective in the other, much more common, forms of angio-oedema (idiopathic, allergic or anaphylactoid, often associated with urticaria) has little or no effect in these cases. This applies particularly to treatment with antihistamin agents and corticosteroids. However, in patients with hereditary angiooedana (HAE) Danazol is effective for long-term prophylaxis and the substitution of Cl-INH for acute treatment. In isolated cases long-term prophylaxis, which is generally reliable, cannot be used because of intolerability reactions. Moreover, it is ineffective in the oedema of acquired Cl-INH deficiency.As other forms of therapy did not achieve the desired response, long-term substitution with a concentrate of Cl-inactivator (Behringwerke AG, Marburg) was carried out in 2 patients (H.W., 47 yrs, male, hereditary angiooedana, 9 siblings died from angiooedana; W.K., 55 yrs, male, professional truipeter, suffering from angiooedana of unknown origin for 5 years, without other underlying disorders). The initial values wereSubstitution was carried out according to the clinical symptoms. Patient H.W. required 500 U Cl-inactivator every 4th day and patient W.K. 1000-1500 U every 5th day until. During substitution therapy (which in pat. H.W. has so far been carried out for 8 months and in pat. W.K. for 6 months) there was a rise in Cl-INH and C4 with an almost total absence of clinical syirptans. No undesirable effects were observed.