Noncardiogenic Pulmonary Edema

Noncardiogenic pulmonary edema is a disease process that results in acute hypoxia secondary to a rapid deterioration in respiratory status (see Image. Noncardiogenic Pulmonary Edema). The disease process has multiple etiologies, requiring prompt recognition and intervention. Increased capillary permeability and changes in pressure gradients within the pulmonary capillaries and vasculature are mechanisms for noncardiogenic pulmonary edema. To differentiate from cardiogenic pulmonary edema, pulmonary capillary wedge pressure is not elevated and remains less than 18 mmHg. It is important to differentiate as management changes based on this distinction. Other findings during the patient's initial evaluation may include a lack of acute cardiac disease or inappropriate fluid balance, flat neck veins, and the absence of peripheral edema. Chest imaging may reveal a peripheral distribution of bilateral infiltrates with no evidence of excessive pulmonary vasculature congestion or cardiomegaly. An echocardiogram may also be used to confirm a lack of acute systolic or diastolic dysfunction.

These findings suggest a noncardiogenic source. Arguably, the most recognized form of noncardiogenic pulmonary edema is acute respiratory distress syndrome (ARDS), which is a noncardiogenic pulmonary edema that has an acute onset secondary to an underlying inflammatory process such as sepsis, pneumonia, gastric aspiration, blood transfusion, pancreatitis, multisystem trauma or trauma to the chest wall, or drug overdose. Diagnosis of ARDS also requires bilateral infiltrates on chest radiograph with a ratio of the partial pressure of oxygen (PaO₂) to the fraction of inspired oxygen (FiO₂) to be less than 300 mmHg with positive end-expiratory pressure of 5 cmH₂O. Clinical context also necessitates no evidence of acute heart failure or hypervolemia in the setting of ARDS. The scope of noncardiogenic pulmonary edema is much broader than ARDS. It includes other etiologies, including high altitude pulmonary edema (HAPE), neurogenic pulmonary edema, opioid overdose, salicylate toxicity, pulmonary embolism, reexpansion pulmonary edema, reperfusion pulmonary edema, and transfusion-related acute lung injury (TRALI). Treatment is specific to the underlying etiology, and all require prompt recognition as clinical decline can be rapid and severe.