Neurogenic pulmonary edema in subarachnoid hemorrhage: relevant clinical concepts
Abstract Background Subarachnoid hemorrhage (SAH) continues to be a condition that carries high rates of morbidity, mortality, and disability around the world. One of its complications is neurogenic pulmonary edema (NPE), which is mainly caused by sympathetic hyperactivity. Due to the complexity of...
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oai:doaj.org-article:c61c0435be8a41fa93c182588796f1692021-11-21T12:30:07ZNeurogenic pulmonary edema in subarachnoid hemorrhage: relevant clinical concepts10.1186/s41984-021-00124-y2520-8225https://doaj.org/article/c61c0435be8a41fa93c182588796f1692021-11-01T00:00:00Zhttps://doi.org/10.1186/s41984-021-00124-yhttps://doaj.org/toc/2520-8225Abstract Background Subarachnoid hemorrhage (SAH) continues to be a condition that carries high rates of morbidity, mortality, and disability around the world. One of its complications is neurogenic pulmonary edema (NPE), which is mainly caused by sympathetic hyperactivity. Due to the complexity of the pathophysiological process and the unspecificity of the clinical presentation, it is little known by general practitioners, medical students and other health care workers not directly related to the neurological part, making the management of this chaotic condition difficult. This review aims to present recent evidence on clinical concepts relevant to the identification and management of NPE secondary to SAH. Main body of the abstract NPE is defined as a syndrome of acute onset following significant central nervous system (CNS) injury. Its etiology has been proposed to stem from the release of catecholamines that produce cardiopulmonary dysfunction, with this syndrome being associated with spinal cord injury, cerebrovascular disorders, traumatic brain injury, status epilepticus, and meningitis. NPE has long been considered a rare event; but it may occur more frequently, mainly in patients with SAH. There are two clinical presentations of NPE: the early form develops in the first hours/minutes after injury, while the late form presents 12–24 h after neurological injury. Clinical manifestations consist of non-specific signs of respiratory distress: dyspnea, tachypnea, hypoxia, pink expectoration, crackles on auscultation, which usually resolve within 24–48 h in 50% of patients. Unfortunately, there are no tools to make the specific diagnosis, so the diagnosis is by exclusion. The therapeutic approach consists of two interventions: treatment of the underlying neurological injury to reduce intracranial pressure and control sympathetic hyperactivity related to the lung injury, and supportive treatment for pulmonary edema. Short conclusion SAH is a severe condition that represents a risk to the life of the affected patient due to the possible complications that may develop. NPE is one of these complications, which due to the common manifestation of a respiratory syndrome, does not allow early and accurate diagnosis, being a diagnosis of exclusion. Therefore, in any case of CNS lesion with pulmonary involvement, NPE should be suspected immediately.Ivan David Lozada-MartínezMaría Manuela Rodríguez-GutiérrezJenny Ospina-RiosMichael Gregorio Ortega-SierraMauro Antonio González-HerazoLina Marcela Ortiz-RoncalloRafael Martínez-ImbettAndrés Elías Llamas-NievesTariq JanjuaLuis Rafael Moscote-SalazarSpringerOpenarticleSubarachnoid hemorrhagePulmonary edemaNeurogenic inflammationLung injuryTreatmentsDiagnosisSurgeryRD1-811Neurosciences. Biological psychiatry. NeuropsychiatryRC321-571ENEgyptian Journal of Neurosurgery, Vol 36, Iss 1, Pp 1-6 (2021) |
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Subarachnoid hemorrhage Pulmonary edema Neurogenic inflammation Lung injury Treatments Diagnosis Surgery RD1-811 Neurosciences. Biological psychiatry. Neuropsychiatry RC321-571 |
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Subarachnoid hemorrhage Pulmonary edema Neurogenic inflammation Lung injury Treatments Diagnosis Surgery RD1-811 Neurosciences. Biological psychiatry. Neuropsychiatry RC321-571 Ivan David Lozada-Martínez María Manuela Rodríguez-Gutiérrez Jenny Ospina-Rios Michael Gregorio Ortega-Sierra Mauro Antonio González-Herazo Lina Marcela Ortiz-Roncallo Rafael Martínez-Imbett Andrés Elías Llamas-Nieves Tariq Janjua Luis Rafael Moscote-Salazar Neurogenic pulmonary edema in subarachnoid hemorrhage: relevant clinical concepts |
description |
Abstract Background Subarachnoid hemorrhage (SAH) continues to be a condition that carries high rates of morbidity, mortality, and disability around the world. One of its complications is neurogenic pulmonary edema (NPE), which is mainly caused by sympathetic hyperactivity. Due to the complexity of the pathophysiological process and the unspecificity of the clinical presentation, it is little known by general practitioners, medical students and other health care workers not directly related to the neurological part, making the management of this chaotic condition difficult. This review aims to present recent evidence on clinical concepts relevant to the identification and management of NPE secondary to SAH. Main body of the abstract NPE is defined as a syndrome of acute onset following significant central nervous system (CNS) injury. Its etiology has been proposed to stem from the release of catecholamines that produce cardiopulmonary dysfunction, with this syndrome being associated with spinal cord injury, cerebrovascular disorders, traumatic brain injury, status epilepticus, and meningitis. NPE has long been considered a rare event; but it may occur more frequently, mainly in patients with SAH. There are two clinical presentations of NPE: the early form develops in the first hours/minutes after injury, while the late form presents 12–24 h after neurological injury. Clinical manifestations consist of non-specific signs of respiratory distress: dyspnea, tachypnea, hypoxia, pink expectoration, crackles on auscultation, which usually resolve within 24–48 h in 50% of patients. Unfortunately, there are no tools to make the specific diagnosis, so the diagnosis is by exclusion. The therapeutic approach consists of two interventions: treatment of the underlying neurological injury to reduce intracranial pressure and control sympathetic hyperactivity related to the lung injury, and supportive treatment for pulmonary edema. Short conclusion SAH is a severe condition that represents a risk to the life of the affected patient due to the possible complications that may develop. NPE is one of these complications, which due to the common manifestation of a respiratory syndrome, does not allow early and accurate diagnosis, being a diagnosis of exclusion. Therefore, in any case of CNS lesion with pulmonary involvement, NPE should be suspected immediately. |
format |
article |
author |
Ivan David Lozada-Martínez María Manuela Rodríguez-Gutiérrez Jenny Ospina-Rios Michael Gregorio Ortega-Sierra Mauro Antonio González-Herazo Lina Marcela Ortiz-Roncallo Rafael Martínez-Imbett Andrés Elías Llamas-Nieves Tariq Janjua Luis Rafael Moscote-Salazar |
author_facet |
Ivan David Lozada-Martínez María Manuela Rodríguez-Gutiérrez Jenny Ospina-Rios Michael Gregorio Ortega-Sierra Mauro Antonio González-Herazo Lina Marcela Ortiz-Roncallo Rafael Martínez-Imbett Andrés Elías Llamas-Nieves Tariq Janjua Luis Rafael Moscote-Salazar |
author_sort |
Ivan David Lozada-Martínez |
title |
Neurogenic pulmonary edema in subarachnoid hemorrhage: relevant clinical concepts |
title_short |
Neurogenic pulmonary edema in subarachnoid hemorrhage: relevant clinical concepts |
title_full |
Neurogenic pulmonary edema in subarachnoid hemorrhage: relevant clinical concepts |
title_fullStr |
Neurogenic pulmonary edema in subarachnoid hemorrhage: relevant clinical concepts |
title_full_unstemmed |
Neurogenic pulmonary edema in subarachnoid hemorrhage: relevant clinical concepts |
title_sort |
neurogenic pulmonary edema in subarachnoid hemorrhage: relevant clinical concepts |
publisher |
SpringerOpen |
publishDate |
2021 |
url |
https://doaj.org/article/c61c0435be8a41fa93c182588796f169 |
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