scholarly journals Neurogenic pulmonary edema in subarachnoid hemorrhage: relevant clinical concepts

2021 ◽  
Vol 36 (1) ◽  
Author(s):  
Ivan David Lozada-Martínez ◽  
María Manuela Rodríguez-Gutiérrez ◽  
Jenny Ospina-Rios ◽  
Michael Gregorio Ortega-Sierra ◽  
Mauro Antonio González-Herazo ◽  
...  

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.

2001 ◽  
Vol 40 (8) ◽  
pp. 826-828 ◽  
Author(s):  
Masafumi TAKAHASHI ◽  
Takeshi MITSUHASHI ◽  
Takaaki KATSUKI ◽  
Uichi IKEDA ◽  
Hidenobu TANAKA ◽  
...  

2012 ◽  
Vol 154 (12) ◽  
pp. 2179-2185 ◽  
Author(s):  
Joji Inamasu ◽  
Keiko Sugimoto ◽  
Yasuhiro Yamada ◽  
Tsukasa Ganaha ◽  
Keisuke Ito ◽  
...  

2017 ◽  
Vol 159 (4) ◽  
pp. 705-712 ◽  
Author(s):  
Tijana Nastasovic ◽  
Branko Milakovic ◽  
Jelena Eric Marinkovic ◽  
Danica Grujicic ◽  
Mila Stosic

2015 ◽  
Vol 59 (4) ◽  
pp. 469-477 ◽  
Author(s):  
Jingyin Chen ◽  
Cong Qian ◽  
Hongyu Duan ◽  
Shenglong Cao ◽  
Xiaobo Yu ◽  
...  

2019 ◽  
Vol 41 (5-6) ◽  
pp. 125-132
Author(s):  
Tijana Nastasović ◽  
Branko Milaković ◽  
Mila Stošić ◽  
Ivana Lazarević ◽  
Miloš Kaluđerović ◽  
...  

2010 ◽  
Vol 68 (3) ◽  
pp. 461-462 ◽  
Author(s):  
Eberval Gadelha Figueiredo ◽  
Arthur Maynart Pereira Oliveira ◽  
Carlos Eduardo Romeu de Almeida ◽  
Manoel Jacobsen Teixeira

2011 ◽  
pp. 975-979 ◽  
Author(s):  
J. ŠEDÝ ◽  
J. KUNEŠ ◽  
J. ZICHA

Neurogenic pulmonary edema (NPE), which is induced by acute spinal cord compression (SCC) under the mild (1.5 %) isoflurane anesthesia, is highly dependent on baroreflex-mediated bradycardia because a deeper (3 %) isoflurane anesthesia or atropine pretreatment completely abolished bradycardia occurrence and NPE development in rats subjected to SCC. The aim of the present study was to evaluate whether hypertension-associated impairment of baroreflex sensitivity might exert some protection against NPE development in hypertensive animals. We therefore studied SCC-induced NPE development in two forms of experimental hypertension – spontaneously hypertensive rats (SHR) and salt hypertensive Dahl rats, which were reported to have reduced baroreflex sensitivity. SCC elicited NPE in both hypertensive models irrespective of their baroreflex sensitivity. It is evident that a moderate impairment of baroreflex sensitivity, which was demonstrated in salt hypertensive Dahl rats, does not exert sufficient protective effects against NPE development.


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