Updates in Management of Non Cardiogenic Pulmonary Oedema in Adults

Abstract

Pulmonary oedema is differentiated into 2 categories: cardiogenic and noncardiogenic. In cardiogenic pulmonary oedema, a high pulmonary capillary pressure (as estimated clinically from the pulmonary artery wedge pressure) is responsible for the abnormal fluid movement. In contrast, noncardiogenic pulmonary oedema is caused by various disorders in which factors other than elevated pulmonary capillary pressure are responsible for protein and fluid accumulation in the alveoli. The distinction between cardiogenic and noncardiogenic causes is not always possible, since the clinical syndrome may represent a combination of several different disorders. Many causes of NPE exist, including drowning, acute glomerulonephritis, fluid overload, aspiration, inhalation injury, neurogenic pulmonary oedema, allergic reaction, adult respiratory distress syndrome. The diagnosis is important, however, because treatment varies considerably depending upon the underlying pathophysiologic mechanisms. The correct diagnosis relies on clinical and radiologic findings, despite some overlap in the clinical and imaging findings between the different causes. An initial and rapid increase in pulmonary vascular pressure due to pulmonary vasoconstriction or pulmonary blood flow can lead to pulmonary microvascular injury. An increase in vascular permeability consequently results in oedema formation, as suggested by the frequent observation of pulmonary hemorrhage in NPE (i.e., the blast theory). Two major components contribute to the pathogenesis of NPE: elevated intravascular pressure and pulmonary capillary leak. Therefore, hemodynamic cardiogenic and noncardiogenic components exist. These components often work in concert, as in pulmonary oedema after epileptic convulsions or intracranial pressure elevation. The hemodynamic component is relatively brief and may unmask pure NPE, such as that seen in experimental seizures. Whether the hemodynamic changes produce a pulmonary capillary leak through pressure-induced mechanical injury to the pulmonary capillaries or whether some direct nervous system control over pulmonary capillary permeability exists remains uncertain. The neuro-effector site for nervous system–induced pulmonary oedema appears to be relatively well established in regions about the caudal medulla, where nuclei regulating systemic arterial pressure, as well as afferent and efferent pathways to and from the lungs, are located.