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While the acronyms are similar, reactive airway disease (RAD) and reactive airways dysfunction syndrome (RADS) are not the same. [1]Reactive airways dysfunction syndrome was first identified by Stuart M. Brooks and colleagues in 1985 as an asthma-like syndrome developing after a single exposure to high levels of an irritating vapor, fume, or smoke.
Reactive airways dysfunction syndrome (RADS) is a severe form of irritant induced asthma where respiratory symptoms usually develop in the minutes or hours after a single accidental inhalation of a high concentration of irritant gas, aerosol, vapor, or smoke.
Stuart Merrill Brooks is an American pulmonary doctor who is credited [1] for discovering and researching Reactive Airways Dysfunction Syndrome (RADS) [2] to describe an asthma-like syndrome developing after a single exposure to high levels of an irritating vapor, fume, or smoke. [3] It involves coughing, wheezing, and dyspnea. [4]
The Berlin definition included ALI as a mild form of ARDS. [53] However, the criteria for the diagnosis of ARDS in the Berlin definition excludes many children, and a new definition for children was termed pediatric acute respiratory distress syndrome (PARDS); this is known as the PALICC definition (2015). [54] [55]
RAD Reactive airway disease: RIND Reversible ischemic neurologic deficit: RLF Retrolental fibroplasia: RLS Restless legs syndrome: RMDs Repetitive motion disorders: ROP Retinopathy of prematurity: RS Reye's syndrome: RSD Reflex sympathetic dystrophy: RTI Respiratory tract infection: RVF Rift Valley fever
This page was last edited on 21 April 2009, at 08:15 (UTC).; Text is available under the
Reactive airway disease; Reactive arthritis; Reactive attachment disorder (RAD) Reactive attachment disorder of early childhood; Reactive attachment disorder of infancy; Reactive hypoglycemia; Reardon–Hall–Slaney syndrome; Reardon–Wilson–Cavanagh syndrome; Rectal neoplasm; Rectophobia; Rectosigmoid neoplasm; Recurrent laryngeal papillomas
The pathophysiology of acute respiratory distress syndrome involves fluid accumulation in the lungs not explained by heart failure (noncardiogenic pulmonary edema). It is typically provoked by an acute injury to the lungs that results in flooding of the lungs' microscopic air sacs responsible for the exchange of gases such as oxygen and carbon dioxide with capillaries in the lungs. [1]