Ariana Alejandra Chacón-Aponte, Érika Andrea Durán-Vargas, Jaime Adolfo Arévalo-Carrillo, Iván David Lozada-Martínez, Maria Paz Bolaño-Romero, Luis Rafael Moscote-Salazar, Pedro Grille, Tariq Janjua
Acute Crit Care. 2022;37(1):35-44. Published online February 11, 2022
The brain-lung interaction can seriously affect patients with traumatic brain injury, triggering a vicious cycle that worsens patient prognosis. Although the mechanisms of the interaction are not fully elucidated, several hypotheses, notably the “blast injury” theory or “double hit” model, have been proposed and constitute the basis of its development and progression. The brain and lungs strongly interact via complex pathways from the brain to the lungs but also from the lungs to the brain. The main pulmonary disorders that occur after brain injuries are neurogenic pulmonary edema, acute respiratory distress syndrome, and ventilator-associated pneumonia, and the principal brain disorders after lung injuries include brain hypoxia and intracranial hypertension. All of these conditions are key considerations for management therapies after traumatic brain injury and need exceptional case-by-case monitoring to avoid neurological or pulmonary complications. This review aims to describe the history, pathophysiology, risk factors, characteristics, and complications of brain-lung and lung-brain interactions and the impact of different old and recent modalities of treatment in the context of traumatic brain injury.
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The clinical course is described in this article.
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When a rapidly re-expanding lung has been in a state of collapse for more than several days, pulmonary edema sometimes occurs. This is called reexpansion pulmonary edema. In general, it most commonly occurs in patients with a large pneumothorax of long duration. In this case, a 15 year old female patient with a 2.3 cm sized bulla in the right lung developed right pneumothorax after anesthetic induction. Although early drainage by closed thoracostomy was performed, right pulmonary edema eventually occurred. It is unusual that vigorous reexpansion pulmonary edema developed even though early decompression was performed within one hour after development of pneumothorax.
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Hunter syndrome is one of the mucopolysaccharidoses, characterized by abnormal accumulation and deposition of mucopolysaccharides in the tissues of several organs which are known to complicate anaesthetic and airway management.
We experienced a case of pulmonary edema which developed during induction of general anesthesia of Hunter syndrome after several attempts of intubation and airway obstruction.
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We present a case report with review of related articles.
Pulmonary edema that follows upper airway obstruction may occur in a variety of clinical situations. Post anesthetic laryngospasm has been implicated as the most frequent cause of this syndrome. Risk factors for development of post laryngospasm pulmonary edema include difficult intubation; nasal, oral, or pharyngeal surgical site; and obesity with obstructive apnea. We report a case that developed acute bilateral pulmonary edema after laryngospasm induced by failed intubation.