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Journal articles on the topic 'Acute pulmonary oedema'

Author: Grafiati
Published: 20 February 2023

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1

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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2

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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3

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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4

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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5

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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6

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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7

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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8

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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9

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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10

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.

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11

Jackson, R. "NIPPV for acute cardiogenic pulmonary oedema." Emergency Medicine Journal 18, no. 6 (November 1, 2001): 464–65. http://dx.doi.org/10.1136/emj.18.6.464.

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12

KURDOWSKA, ANNA K. "Unusual causes of acute pulmonary oedema." Clinical Science 104, no. 3 (March 1, 2003): 265. http://dx.doi.org/10.1042/cs20020331.

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13

Dennis, A. T., and C. B. Solnordal. "Acute pulmonary oedema in pregnant women." Anaesthesia 67, no. 6 (March 15, 2012): 646–59. http://dx.doi.org/10.1111/j.1365-2044.2012.07055.x.

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14

Dennis, A. T., and C. B. Solnordal. "Acute pulmonary oedema in pregnant women." Anaesthesia 67, no. 6 (May 7, 2012): 694. http://dx.doi.org/10.1111/j.1365-2044.2012.07202.x.

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15

Barbisan, J. N. "Scintigraphic diagnosis of acute pulmonary oedema." Heart 91, no. 5 (May 1, 2005): 629. http://dx.doi.org/10.1136/hrt.2004.038562.

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16

KURDOWSKA, ANNA K. "Unusual causes of acute pulmonary oedema." Clinical Science 104, no. 3 (February 14, 2003): 265–66. http://dx.doi.org/10.1042/cs1040265.

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17

Resta, Onofrio, Mariapia Foschino Barbaro, Patrizia Guido, Clelia Tozzi, Maria Damiano, Giovanna Pietrafesa, and Salvatore Talamo. "Noramidopyrine-Induced Acute Pulmonary Permeability Oedema." Clinical Drug Investigation 18, no. 3 (1999): 239–41. http://dx.doi.org/10.2165/00044011-199918030-00009.

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18

Al-Ani, Mohammad, Media Ismael, and David E. Winchester. "Morphine in Acute Pulmonary Oedema Treatment." Current Emergency and Hospital Medicine Reports 5, no. 2 (April 1, 2017): 88–93. http://dx.doi.org/10.1007/s40138-017-0131-8.

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19

O'Mahony, D., G. Hendry, P. Strube, M. Jonas, and D. Sumner. "Acute pulmonary oedema in late pregnancy." Postgraduate Medical Journal 71, no. 839 (September 1, 1995): 571–73. http://dx.doi.org/10.1136/pgmj.71.839.571.

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20

O’Leary, A. M., G. Veall, P. Butler, and G. H. Anderson. "Acute pulmonary oedema after tourniquet release." Canadian Journal of Anaesthesia 37, no. 7 (October 1990): 826–27. http://dx.doi.org/10.1007/bf03006552.

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21

Chioncel, Ovidiu, Sean P. Collins, Andrew P. Ambrosy, Mihai Gheorghiade, and Gerasimos Filippatos. "Pulmonary Oedema—Therapeutic Targets." Cardiac Failure Review 1, no. 1 (2015): 38. http://dx.doi.org/10.15420/cfr.2015.01.01.38.

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Pulmonary oedema (PO) is a common manifestation of acute heart failure (AHF) and is associated with a high-acuity presentation and with poor in-hospital outcomes. The clinical picture of PO is dominated by signs of pulmonary congestion, and its pathogenesis has been attributed predominantly to an imbalance in Starling forces across the alveolar–capillary barrier. However, recent studies have demonstrated that PO formation and resolution is critically regulated by active endothelial and alveolar signalling. PO represents a medical emergency and treatment should be individually tailored to the urgency of the presentation and acute haemodynamic characteristics. Although, the majority of patients admitted with PO rapidly improve as result of conventional intravenous (IV) therapies, treatment of PO remains largely opinion based as there is a general lack of good evidence to guide therapy. Furthermore, none of these therapies showed simultaneous benefit for symptomatic relief, haemodynamic improvement, increased survival and end-organ protection. Future research is required to develop innovative pharmacotherapies capable of relieving congestion while simultaneously preventing end-organ damage.
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22

Luks, Andrew M., Erik R. Swenson, and Peter Bärtsch. "Acute high-altitude sickness." European Respiratory Review 26, no. 143 (January 31, 2017): 160096. http://dx.doi.org/10.1183/16000617.0096-2016.

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At any point 1–5 days following ascent to altitudes ≥2500 m, individuals are at risk of developing one of three forms of acute altitude illness: acute mountain sickness, a syndrome of nonspecific symptoms including headache, lassitude, dizziness and nausea; high-altitude cerebral oedema, a potentially fatal illness characterised by ataxia, decreased consciousness and characteristic changes on magnetic resonance imaging; and high-altitude pulmonary oedema, a noncardiogenic form of pulmonary oedema resulting from excessive hypoxic pulmonary vasoconstriction which can be fatal if not recognised and treated promptly. This review provides detailed information about each of these important clinical entities. After reviewing the clinical features, epidemiology and current understanding of the pathophysiology of each disorder, we describe the current pharmacological and nonpharmacological approaches to the prevention and treatment of these diseases.
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23

Fisher, M. McD, and I. F. Stevenson. "Unexplained Acute Membrane Pulmonary Oedema Related to Anaesthesia." Anaesthesia and Intensive Care 14, no. 1 (February 1986): 29–31. http://dx.doi.org/10.1177/0310057x8601400107.

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Five patients developed severe pulmonary oedema in relationship to elective anaesthesia and surgery. The oedema was due to increased capillary permeability in four patients and probably due to increased capillary permeability in the other. No cause could be found in any patient.
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24

Khwaja, Samir A., Umasuthan Srirangalingam, and William M. Drake. "A rare cause of acute pulmonary oedema." Clinical Medicine 12, no. 6 (December 2012): 535–37. http://dx.doi.org/10.7861/clinmedicine.12-6-535.

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25

McRitchie, Robert, Megan Purvey, and George Allen. "Letter to the Editor: Acute pulmonary oedema." Australian Prescriber 40, no. 4 (August 1, 2017): 126. http://dx.doi.org/10.18773/austprescr.2017.051.

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26

Wakhloo, Renu, Anjana Raina, Juhi Sharma, and Satyadev Gupta. "Acute pulmonary oedema in an antenatal patient." Journal of Anaesthesiology Clinical Pharmacology 26, no. 1 (2010): 120. http://dx.doi.org/10.4103/0970-9185.75149.

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27

Fenner, Peter J., John A. Williamson, Kumar Gunawardane, William Murtha, Joseph W. Burnett, David M. Colquhoun, and Stephen Godfrey. "The “Irukandji syndrome” and acute pulmonary oedema." Medical Journal of Australia 149, no. 3 (August 1988): 150–56. http://dx.doi.org/10.5694/j.1326-5377.1988.tb120544.x.

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28

Chen, Yi-Ting, Wei-Kai Wu, and Yung-Hsiang Hsu. "Acute respiratory distress syndrome or pulmonary oedema?" Thorax 70, no. 5 (March 10, 2015): 511. http://dx.doi.org/10.1136/thoraxjnl-2015-206806.

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29

Wilde, V. De, J. Vandenbogaerde, and W. Buylaert. "Acute Cholinesterase Inhibitor Poisoning Mimicking Pulmonary Oedema." Acta Clinica Belgica 44, no. 2 (January 1989): 133–36. http://dx.doi.org/10.1080/17843286.1989.11718001.

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30

Barin, E. S., I. F. Stevenson, and G. L. Donnelly. "Pulmonary Oedema following Acute Upper Airway Obstruction." Anaesthesia and Intensive Care 14, no. 1 (February 1986): 54–57. http://dx.doi.org/10.1177/0310057x8601400112.

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31

Nestor, ThomasA, WarrenI Tamamoto, TiongH Kam, and Terry Schultz. "ACUTE PULMONARY OEDEMA CAUSED BY CRYSTALLINE METHAMPHETAMINE." Lancet 334, no. 8674 (November 1989): 1277–78. http://dx.doi.org/10.1016/s0140-6736(89)91883-7.

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32

Hall, M. "Is morphine indicated in acute pulmonary oedema." Emergency Medicine Journal 22, no. 5 (May 1, 2005): 391. http://dx.doi.org/10.1136/emj.2003.011460.

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33

Mursell, Ian. "Drug regimes for acute cardiogenic pulmonary oedema." Journal of Paramedic Practice 1, no. 4 (January 2009): 140–44. http://dx.doi.org/10.12968/jpar.2009.1.4.42036.

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34

White, J. "The “Irukandji syndrome” and acute pulmonary oedema." Toxicon 28, no. 5 (January 1990): 588. http://dx.doi.org/10.1016/0041-0101(90)90308-t.

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35

Cleland, John GF, Ashraf S. Yassin, and Kayvan Khadjooi. "Acute heart failure: focusing on acute cardiogenic pulmonary oedema." Clinical Medicine 10, no. 1 (February 2010): 59–64. http://dx.doi.org/10.7861/clinmedicine.10-1-59.

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36

Pahade, A., K. M. J. Green, and J. P. de Carpentier. "Non-cardiogenic pulmonary oedema due to foreign body aspiration." Journal of Laryngology & Otology 113, no. 12 (December 1999): 1119–21. http://dx.doi.org/10.1017/s0022215100158074.

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AbstractA patient who developed non-cardiogenic pulmonary oedema secondary to acute airway obstruction caused by an aspirated foreign body is presented. The literature is reviewed, discussing the theories regarding the formation of non-cardiogenic pulmonary oedema. The case highlights the importance of this rare complication of foreign body aspiration and surgeons and anaesthetists should be alert to continued respiratory symptoms following relief of acute airway obstruction.
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37

Hamza, Shebeen. "Non-Invasive Ventilation in Acute Cardiogenic Pulmonary Oedema." Journal of the Intensive Care Society 10, no. 4 (October 2009): 307–8. http://dx.doi.org/10.1177/175114370901000421.

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38

Wong, A. "Acute pulmonary oedema complicating polyethylene glycol intestinal lavage." Archives of Disease in Childhood 87, no. 6 (December 1, 2002): 537. http://dx.doi.org/10.1136/adc.87.6.537.

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39

Agarwal, R. "Non-invasive ventilation in acute cardiogenic pulmonary oedema." Postgraduate Medical Journal 81, no. 960 (October 1, 2005): 637–43. http://dx.doi.org/10.1136/pgmj.2004.031229.

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40

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 (March 1, 2003): 259. http://dx.doi.org/10.1042/cs20020166.

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41

Crawley, F., I. Saddeh, S. Barker, and H. Katifi. "Acute pulmonary oedema: presenting symptom of multiple sclerosis." Multiple Sclerosis 7, no. 1 (February 1, 2001): 71–72. http://dx.doi.org/10.1191/135245801669565077.

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42

Knutsen, Brostrup, and Ole Jacob Broch. "HAEMODYNAMICS IN ACUTE PULMONARY OEDEMA IN CORONARY PATIENTS." Acta Medica Scandinavica 183, no. 1-6 (April 24, 2009): 531–34. http://dx.doi.org/10.1111/j.0954-6820.1968.tb10518.x.

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43

Naeije, R., and C. Melot. "Acute pulmonary oedema on the Ruwenzori mountain range." Heart 64, no. 6 (December 1, 1990): 400–402. http://dx.doi.org/10.1136/hrt.64.6.400.

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44

Gammage, Michael. "Treatment of acute pulmonary oedema: diuresis or vasodilatation?" Lancet 351, no. 9100 (February 1998): 382–83. http://dx.doi.org/10.1016/s0140-6736(98)22006-x.

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45

Spreng, U. "Negative pressure pulmonary oedema after acute airway obstruction." European Journal of Anaesthesiology 23, Supplement 37 (June 2006): 255. http://dx.doi.org/10.1097/00003643-200606001-00915.

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46

Boykett, M. "Pulmonary oedema after acute asphyxia in a child." BMJ 298, no. 6678 (April 8, 1989): 928. http://dx.doi.org/10.1136/bmj.298.6678.928.

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47

Sobieszek, Anna, Marcin Konopka, Marek Cacko, Marek Kuch, and Wojciech Braksator. "Immersion pulmonary oedema in a triathlete – a diagnostic challenge in sports cardiology." Journal of Ultrasonography 21, no. 86 (August 16, 2021): e252-e257. http://dx.doi.org/10.15557/jou.2021.0041.

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Immersion pulmonary oedema, also referred to as swimming-induced pulmonary oedema, is a form of pulmonary oedema which usually occurs during swimming in cold water. The condition is most common in triathlon athletes; it was first reported in military divers. The main symptoms include acute dyspnoea, cough, and occasionally haemoptysis, which usually subside within approximately 48 hours. The pathomechanism is not fully understood, but oedema is suspected to be due to an increased systemic vascular resistance that overloads the left ventricle. The diagnostic process can be challenging and require multiple stages to rule out a number of other possible conditions. In view of the circumstances in which incidents typically occur, immersion pulmonary oedema poses an immediate life threat to individuals involved in selected forms of physical activity, where survival is often determined by appropriate training of medical services.
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48

Khanduri, Ayesha, Usha Anand, Maged Doss, and Louis Lovett. "Severe acute mitral valve regurgitation in a COVID-19-infected patient." BMJ Case Reports 14, no. 1 (January 2021): e239782. http://dx.doi.org/10.1136/bcr-2020-239782.

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The ongoing SARS-CoV-2 (COVID-19) pandemic has presented many difficult and unique challenges to the medical community. We describe a case of a middle-aged COVID-19-positive man who presented with pulmonary oedema and acute respiratory failure. He was initially diagnosed with acute respiratory distress syndrome. Later in the hospital course, his pulmonary oedema and respiratory failure worsened as result of severe acute mitral valve regurgitation secondary to direct valvular damage from COVID-19 infection. The patient underwent emergent surgical mitral valve replacement. Pathological evaluation of the damaged valve was confirmed to be secondary to COVID-19 infection. The histopathological findings were consistent with prior cardiopulmonary autopsy sections of patients with COVID-19 described in the literature as well as proposed theories regarding ACE2 receptor activity. This case highlights the potential of SARS-CoV-2 causing direct mitral valve damage resulting in severe mitral valve insufficiency with subsequent pulmonary oedema and respiratory failure.
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49

Oldman, James, Sarah Morwood, James Willis, and Daniel Xavier Augustine. "Myocardial oedema in the setting of immersion pulmonary oedema - Cause or effect?" BMJ Case Reports 16, no. 1 (January 2023): e251274. http://dx.doi.org/10.1136/bcr-2022-251274.

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Immersion pulmonary oedema (IPE) is an under-reported and poorly understood phenomenon thought to be related to exercise-induced haemodynamic changes while submersed in water. Previous work has demonstrated reversible myocardial dysfunction during acute episodes. We present a case of IPE with concomitant, transient, left ventricular myocardial oedema characterised via MRI. This is a novel finding and may be evidence of left ventricular strain due to pressure overload or secondary to a subclinical myocarditis.
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50

Mawhinney, E., M. Watt, and GV McDonnell. "Transient cardiomyopathy as the presenting feature of acute disseminated encephalomyelitis." Multiple Sclerosis Journal 15, no. 12 (December 2009): 1534–36. http://dx.doi.org/10.1177/1352458509348518.

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Brainstem lesions are rarely associated with neurogenic pulmonary oedema (NPO) in multiple sclerosis and other disorders. The exact mechanism for this is unknown. We describe a case of a 15-year-old boy who presented with transient cardiomyopathy and severe acute pulmonary oedema. Several days after his initial presentation he developed an ataxic syndrome with limb, truncal and gait ataxia and nystagmus on primary gaze. Investigations confirmed acute disseminated encephalomyelitis (ADEM). For the first time, we describe a case of transient cardiomyopathy and NPO as the initial manifestation of ADEM.
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