Neurogenic pulmonary oedema.

Kerr, GaryW

doi:10.1136/emj.15.4.275

Cited by 8 publications

(3 citation statements)

References 32 publications

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“…However, in those cases the lung injury had occurred before the patients were invasively monitored. In a few cases in which pulmonary vascular pressures were being monitored at the onset of NPO, an acute increase in pulmonary capillary wedge pressure was noticed (58,59). Initial clinical reports attempted to elucidate the mechanism of NPO by measuring the protein concentration in the pulmonary edema fluid.…”

Section: Avlonitis Et Almentioning

confidence: 97%

Pulmonary Transplantation: the role of brain death in donor lung injury

et al. 2003

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The paucity of suitable lung donors and the high early mortality as the result of primary graft failure remain major challenges in pulmonary transplantation. There is evidence that the lung is injured in the donor by the process of brain death and often is made unusable or fails posttransplantation after amplification of the injury by the process of ischemia-reperfusion. An understanding of the mechanism of donor lung injury could lead to the development of new treatment strategies for the donor to reduce lung injury, increase the number of donors with acceptable lungs, and improve the results of transplantation. The pathophysiology of brain death is complex and involves sympathetic, hemodynamic, and inflammatory mechanisms that can injure the lung. The literature is reviewed, and these mechanisms are discussed together with their possible interrelations.

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Section: Avlonitis Et Almentioning

confidence: 97%

Pulmonary Transplantation: the role of brain death in donor lung injury

et al. 2003

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“…NPO usually arises rapidly within the first few hours of presentation, particularly in the setting of traumatic brain injury and acute intracranial haemorrhage, as highlighted in table 1 3 11 12 14. We found one case report of delayed NPO occurring 4 days after the onset of subarachnoid haemorrhage; however, at that time, there was angiographic evidence of significant cerebral arterial spasm which could have triggered the NPO 10.…”

Section: Discussionmentioning

confidence: 87%

“…Severe traumatic brain injury, intracranial haemorrhage and seizures are the commonly reported neurological insults associated with NPO (table 1). 9–17 On the other hand, ischaemic stroke is a relatively rare trigger. The provoking infarction is usually large and clinically significant, often requiring intravenous thrombolysis or neurosurgical intervention 18–20.…”

Section: Discussionmentioning

confidence: 99%

Delayed onset of neurogenic pulmonary oedema following an evolving ischaemic stroke

Liarakos

Tran

2022

BMJ Case Rep

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Any insult to the central nervous system can lead to the rare occurrence of neurogenic pulmonary oedema (NPO). It is usually associated with significant neurological injury (eg, subarachnoid haemorrhage or traumatic brain injury) with a relatively rapid onset. As an exception to this observation, we report a middle-aged woman who developed NPO 72 hours after the onset of a subtle but evolving right middle cerebral artery infarction confirmed on CT. Aggressive use of diuretics and vasodilators, as is normally the case for cardiogenic pulmonary oedema, can compromise cerebral blood flow and the ischaemic penumbra. This case illustrates how the diagnostic and therapeutic challenges were successfully addressed with the aid of bedside ultrasonography and close haemodynamic monitoring to reverse the respiratory failure while protecting the brain.

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Special issues in the management and selection of the donor for lung transplantation

Naik

Angel

2011

Semin Immunopathol

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Lung transplantation is a viable treatment option for select patients with end-stage lung disease. Two issues hamper progress in transplantation: first, donor shortage is a major limitation to increasing the number of transplants performed. Secondly, recipient outcomes remain disappointing when compared with other solid organ transplant results. Outcomes are limited by primary graft dysfunction (PGD), the posttransplant acute lung injury that increases both short-and long-term mortality. Attempts to overcome donor shortage have included aggressively managing solid organ donors to increase the number of donor lungs suitable for transplantation. Yet, the quality of the lung donor is likely to be related to the probability of the recipient experiencing PGD. PGD is the culmination of a series of insults, hemodynamic, metabolic, and inflammatory, that begin with the brain dead donor and result in poor recipient outcomes. Understanding the mechanism of donor lung injury resulting from brain death and the possible treatment strategies for its inhibition could help to increase the number of usable lungs and decrease the rate of PGD in the recipient. Here we present a review of the key pathways which result in donor lung injury, and follow this with a brief review of recent biomarkers that are proving to be instrumental to our ability to predict truly unsuitable lungs, and our ability to predict and hopefully prevent or treat recipients with subsequent lung injury.

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Neurogenic pulmonary oedema.

Cited by 8 publications

References 32 publications

Pulmonary Transplantation: the role of brain death in donor lung injury

Pulmonary Transplantation: the role of brain death in donor lung injury

Delayed onset of neurogenic pulmonary oedema following an evolving ischaemic stroke

Special issues in the management and selection of the donor for lung transplantation

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