BACKGROUND: Neurogenic pulmonary edema (NPE) as a systemic consequence early after aneurysmal subarachnoid hemorrhage (SAH) sometimes complicates perioperative and postoperative fluid management and increases the risk of a poor outcome. This is the first report to demonstrate the ability of a bedside transpulmonary thermodilution device to trace physiological patterns consistent with current theories regarding the mechanism and course of post-SAH NPE. METHODS: Three SAH patients admitted within 4 hours of ictus and diagnosed as having NPE were studied. Cardiac output, global end-diastolic volume (GEDV), extravascular lung water, and pulmonary vascular permeability index (PVPI) were measured by the transpulmonary thermodilution immediately after the diagnosis. Biochemical makers relating to stress and fluid regulation were also sampled. RESULTS: In all cases, extravascular lung water was abnormally high on initial measurement, in which an elevation of plasma catecholamine and B-type natriuretic peptide was detected. The fluid distribution of each patient was characterized by either (1) high PVPI and low GEDV without cardiac dysfunction (permeability edema); or (2) low cardiac output and high GEDV accompanied by transient cardiac dysfunction without PVPI elevation (hydrostatic edema). Although the volume status of 2 patients normalized by day 4 and was successfully managed with routine fluid therapy, a patient categorized initially with permeability edema complicated with hydrostatic edema due to heart failure and pneumonia showed a poor outcome. CONCLUSIONS: Our clinical experience suggests that the present monitoring system is capable of distinguishing different etiologies for pulmonary edema complicating SAH that may assist with fluid management decisions.
BACKGROUND:Neurogenic pulmonary edema (NPE) as a systemic consequence early after aneurysmal subarachnoid hemorrhage (SAH) sometimes complicates perioperative and postoperative fluid management and increases the risk of a poor outcome. This is the first report to demonstrate the ability of a bedside transpulmonary thermodilution device to trace physiological patterns consistent with current theories regarding the mechanism and course of post-SAH NPE. METHODS: Three SAHpatients admitted within 4 hours of ictus and diagnosed as having NPE were studied. Cardiac output, global end-diastolic volume (GEDV), extravascular lung water, and pulmonary vascular permeability index (PVPI) were measured by the transpulmonary thermodilution immediately after the diagnosis. Biochemical makers relating to stress and fluid regulation were also sampled. RESULTS: In all cases, extravascular lung water was abnormally high on initial measurement, in which an elevation of plasma catecholamine and B-type natriuretic peptide was detected. The fluid distribution of each patient was characterized by either (1) high PVPI and low GEDV without cardiac dysfunction (permeability edema); or (2) low cardiac output and high GEDV accompanied by transient cardiac dysfunction without PVPI elevation (hydrostatic edema). Although the volume status of 2 patients normalized by day 4 and was successfully managed with routine fluid therapy, a patient categorized initially with permeability edema complicated with hydrostatic edema due to heart failure and pneumonia showed a poor outcome. CONCLUSIONS: Our clinical experience suggests that the present monitoring system is capable of distinguishing different etiologies for pulmonary edema complicating SAH that may assist with fluid management decisions.