...that our understanding of pulmonary edema originates in the 18th century?
Hyppolyti Francisci Albertini was an Italian physician who observed that patients experiencing severe dyspnea prior to death had excessive lung fluid at autopsy. Albertini associated this phenomenon with an "affection of the heart or precordia", and in so doing was the first to describe cardiogenic pulmonary edema . For almost a century pulmonary edema was exclusively attributed to "cardiogenic" origins. However, in the early 19th century the British physician Rene Theophile Hyacinthe Laennec described pulmonary edema arising from non-cardiogenic origins . Laennec noticed that individuals suffering from pneumonia (péripneumonie as he originally portrayed it) experienced three phases throughout the disease course. During the first phase (first degree of péripneumonie), liquid and inflammatory secretions were found in niches targeting the alveolar spaces, giving the lung a distinctive "spongy" texture. Worsening of the first phase of péripneumonie, in some patients, was accompanied by increased lung fluid accumulation and tissue disorganization that caused death. Patients who survived the first phase transitioned to the second phase, which was characterized by a so-called "hepatization" (stiffening of the tissue due to cellular and matrix infiltration into the lung parenchyma). The third phase, although it was not rigorously described, represented resolution of the inflammatory process. Thus, Laennec defined pulmonary edema of non-cardiogenic origin, and described the pathological changes occurring during lung injury.
During the next 150 years, our understanding of the dynamics of fluid balance and vascular permeability contributing to non-cardiogenic pulmonary edema was advanced by seminal contributions of prestigious scientists (Starling, Landis, Pappenheimer, Kedem & Katchalsky, Guyton, Taylor, Staub, Brigham, among others). Yet, in the clinical scenario, the pathogenesis of non-cardiogenic pulmonary edema was unknown. In the late 1960's, Ashbaugh, Bigelow, Petty, and Levine recognized that non-cardiogenic pulmonary edema could systematically occur from multiple etiologies each resulting in a clinical pattern characterized by dyspnea, cyanosis refractory to oxygen supplementation, loss of lung compliance, and bilateral alveolar infiltrates. They defined this constellation of clinical findings as the acute respiratory distress syndrome (ARDS) . By the 1990's mortality secondary to ARDS was estimated to range from 10 to 90%; such variability in the estimated mortality rate was likely due to the lack of a consensus in the definition of the syndrome and by the absence of established therapeutical guidelines. In 1994 a consensus was attained in which ARDS was defined as a syndrome of inflammation and increased permeability associated with clinical, radiologic, and physiological abnormalities that cannot be explained by left atrial or pulmonary capillary hypertension . ARDS was distinguished from its less severe form, acute lung injury (ALI), by the severity of the blood gas abnormalities: PaO2/FIO2 ≤300 vs ≤200 for ALI and ARDS, respectively. Even after 190 years of medical advancement since Laennec's original description of non-cardiogenic pulmonary edema, the high mortality rate, which still exceeds 35%, illustrates our lack of understanding of the mechanisms leading to ALI/ARDS.
This article written by Diego Alvarez, May 2006.
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