To investigate whether rapid or slowly infused intravenous fat emulsions affect the ratio of prostaglandin I2/thromboxane A2 in arterial blood, pulmonary hemodynamics, and gas exchange.
Prospective, controlled, randomized, crossover study.
Operative intensive care unit of a university hospital.
Eighteen critically ill patients. Ten patients were stratified with severe sepsis, and eight patients had acute respiratory distress syndrome (ARDS).
Patients were assigned randomly to receive intravenous fat emulsions (0.4 x resting energy expenditure) over 6 hrs (rapid fat infusion) or 24 hrs (slow fat infusion) along with a routine parenteral nutrition regimen, by using a crossover study design.
Systemic and pulmonary hemodynamics as well as gas exchange measurements were recorded via respective indwelling catheters. Arterial thromboxane B2 and 6-keto-prostaglandin-F1alpha plasma concentrations were obtained by radioimmunoassay, and 6-keto-prostaglandin-F1alpha/thromboxane B2 ratios (P/T ratios) were calculated. Data were collected immediately before and 6, 12, 18, and 24 hrs after onset of fat infusion. In the ARDS group, P/T ratio increased by rapid fat infusion. Concomitantly, pulmonary shunt fraction, alveolar-arterial oxygen tension difference [P(a-a)o2]/Pao2, and cardiac index increased as well, whereas pulmonary vascular resistance and Pao2/Fio2 declined. After slow fat infusion, a decreased P/T ratio was revealed. This was accompanied by decreased pulmonary shunt fraction, lowered P(a-a)o2/Pao2, and increased Pao2/Fio2. Correlations between plasma concentrations of 6-keto-prostaglandin-F1alpha or thromboxane B2 and measures of respiratory performance could be shown during rapid and slow fat infusion, respectively. In the sepsis group, the P/T ratio remained unchanged at either infusion rate, but pulmonary shunt fraction and P(a-a)o2/Pao2 decreased after rapid fat infusion, whereas Pao2/Fio2 increased.
Pulmonary hemodynamics and gas exchange are related to changes of arterial prostanoid levels in ARDS patients, depending on the rate of fat infusion. In ARDS but not in sepsis patients clear of pulmonary organ failure, a changing balance of prostaglandin I2 and thromboxane A2 may modulate gas exchange, presumably via interference with hypoxic pulmonary vasoconstriction.
"The risk factors for developing fatal RV dysfunction are poorly understood. Severe adult respiratory distress syndrome (ARDS) or mechanical obstruction to pulmonary artery flow by massive fat embolism (FES) may induce significant pulmonary hypertension and subsequent RV failure [5, 7]. The primary treatment strategy focuses on prevention, early diagnosis, and supportive therapy [4, 6, 8]. "
[Show abstract][Hide abstract] ABSTRACT: Fat embolism syndrome (FES) is a life-threatening condition in which multiorgan dysfunction manifests 48-72 hours after long bone or pelvis fractures. Right ventricular (RV) failure, especially in the setting of pulmonary hypertension, is a frequent feature of FES. We report our experience treating 2 young, previously healthy trauma patients who developed severe hypoxemia in the setting of FES. Neither patient had evidence of RV dysfunction on echocardiogram. The patients were treated with inhaled nitric oxide (NO), and their oxygenation significantly improved over the subsequent few days. Neither patient developed any cardiovascular compromise. Patients with FES that have severe hypoxemia and evidence of adult respiratory distress syndrome (ARDS) are likely at risk for developing RV failure. We recommend that these patients with FES and severe refractory hypoxemia should be treated with inhaled NO therapy prior to the onset of RV dysfunction.
"Use of SO-based lipid emulsions increases availability of free arachidonic acid, the precursor fatty acid of lipid mediators in septic patients . A deterioration of the PaO2/FiO2 ratio has been attributed to fast infusion (6 hours) instead of slow infusion (24 hours) of a SO-based lipid emulsion in patients with acute respiratory distress syndrome due to generation of arachidonic acid-derived prostaglandins and thromboxane . In a simplified model, sepsis may be described as starting with a hyperinflammatory phase followed by a phase of immune suppression. "
[Show abstract][Hide abstract] ABSTRACT: Lipid emulsions based on soybean oil have been an integral part of parenteral nutrition supplying n-6 fatty acids, with possible negative effects in critically ill patients. Newer lipid emulsions supply less n-6 fatty acids. In addition, fish oil-based lipids may be included in the lipid component of parenteral nutrition. While clinical benefits of lipid emulsions with a reduced fraction in n-6 lipids and the addition of fish oil have been described in postoperative patients, data are less clear in critically ill or septic patients. Recent data suggest that beneficial effects may be achieved when used early but clearly more data are needed to come to a definitive conclusion. The present commentary will highlight current data in critically ill and septic patients and the use of fish oil as a part of parenteral nutrition.
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