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 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.

Peroxiredoxin 2 Is a Potential Objective Indicator for Severity and the Clinical Status of Subarachnoid Hemorrhage Patients

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Respiratory Patterns in Neurological Injury, Pathophysiology, Ventilation Management, and Future Innovations: A Systematic Review

“…Recognizing NPE is difficult due to its nonspecific presenting symptoms and is currently considered a diagnosis of exclusion. 32 In addition, it has been theorized that an abrupt increase in ICP causes a systemic catecholamine release and vasoconstriction (Cushing effect). Intravascular hydrostatic engorgement induces endothelial injury further increasing pulmonary fluid extravasation.…”

Use of bedside ultrasound in the evaluation of acute dyspnea: a comprehensive review of evidence on diagnostic usefulness

“…In particular, it was observed that there are high-risk events where the impact of this tool on morbidity, costs and survival has not been studied, such as lung injury secondary to traumatic brain injury, ventilation alteration due to metabolic causes or tumors, among others (27)(28)(29). Almost all the studies come from high-income countries, where the conditions of health services and academic preparation are of better quality (30), so it can be deduced that the external validity of the results is not very reliable, especially because a considerable volume of studies use ultrasonography as a gold standard comparator, experienced senior physicians.…”