Eckhard Müller

Predicting Delirium After Vascular Surgery: A Model Based on Pre- and Intraoperative Data

Objective The aim of the study was to determine pre- and intraoperative risk factors for the development of postoperative delirium among patients undergoing aortic, carotid, and peripheral vascular surgery to predict the risk for postoperative delirium. Summary Background Data Although postoperative delirium after vascular surgery is a frequent complication and is associated with the need for more inpatient hospital care and longer length of hospital stay, little is known about risk factors for delirium in patients undergoing vascular surgery. Methods Pre-, intra-, and postoperative data were prospectively collected, including the first 7 postoperative days with daily follow-up by a surgeon and a psychiatrist of 153 patients undergoing elective vascular surgery. Delirium (Diagnostic and statistical Manual of Mental Disorders IV) was diagnosed by the psychiatrist. Multivariate linear logistic regression and a cross validation analysis were performed to find a set of parameters to predict postoperative delirium. Results Sixty patients (39.2%) developed postoperative delirium. The best set of predictors included the absence of supraaortic occlusive disease and hypercholesterinemia, history of a major amputation, age over 65 years, a body size of less than 170 cm, preoperative psychiatric parameters and intraoperative parameters correlated to increased blood loss. The combination of these parameters allows the estimation of an individual patients’ risk for postoperative delirium already at the end of vascular surgery with an overall accuracy of 69.9%. Conclusions Postoperative delirium after vascular surgery is a frequent complication. A model based on pre- and intraoperative somatic and psychiatric risk factors allows prediction of the patients risk for developing postoperative delirium.

Risk factors for postoperative delirium in vascular surgery.

The aim of this study was to identify psychiatric and somatic risk factors associated with the development, severity and duration of postoperative delirium after vascular surgery. Forty-seven patients underwent aortic, carotid artery and peripheral artery surgery. Both, surgeon and psychiatrist, monitored patients preoperatively with daily follow up. Preoperative psychiatric assessment included standardized psychopathological scales for the detection of psychiatric symptoms and cognitive deficits. We diagnosed delirium using DSM IV criteria. Delirium Rating Scale was used to estimate delirium severity. Surgical parameters included patient history, diagnoses, medication and laboratory parameters. A statistical analysis was performed using multivariate regression analyses to find factors significantly associated with delirium development, severity, and duration. Thirty-six percent of the patients developed postoperative delirium after surgery. Comparison of different parameters revealed that especially preoperative depression symptoms and perioperative transfusions/infusions had significant predictive value for the development as well as for the severity of postoperative delirium.

Assessment of microvascular oxygen saturation in gastric mucosa in volunteers breathing continuous positive airway pressure

OBJECTIVE Adequate oxygenation of the gastrointestinal mucosa to preserve its barrier function is a basic objective in the prevention of multiple organ failure. Sustaining a positive airway pressure during the entire respiratory cycle remains a cornerstone in the therapeutic regimen to improve systemic oxygenation. Whereas increased systemic oxygenation during breathing continuous positive airway pressure has been shown, the impact of continuous positive airway pressure on regional oxygenation in the gastrointestinal tract has not yet been evaluated. We hypothesized that continuous positive airway pressure decreases microvascular oxygen saturation in gastric mucosa. DESIGN Prospective, randomized study. SETTING University department of anesthesiology. PARTICIPANTS Twelve healthy volunteers. INTERVENTIONS Incremental increases of continuous positive airway pressure (0, 5, and 10 cm H(2)O) and subsequent release of continuous positive airway pressure. MEASUREMENTS AND MAIN RESULTS We continuously measured microvascular oxygen saturation in gastric mucosa by reflectance spectrophotometry. Systemic oxygen saturation, end-tidal Pco(2), respiratory rate, heart rate, and arterial blood pressure were obtained noninvasively. In every volunteer, microvascular oxygen saturation in gastric mucosa was reduced corresponding to the level of continuous positive airway pressure, although systemic variables, especially systemic oxygen saturation, did not change. Continuous positive airway pressure reduced microvascular oxygen saturation in gastric mucosa from 59 +/- 7% (baseline with 0 cm H(2)O continuous positive airway pressure, mean +/- sd) to 54 +/- 8% (p <.05) during 5 cm H(2)O continuous positive airway pressure and to 50 +/- 9% (p <.05) during 10 cm H(2)O continuous positive airway pressure, returning to 59 +/- 7% during spontaneous breathing with 0 cm H(2)O continuous positive airway pressure. End-tidal Pco(2), respiratory rate, as well as hemodynamic variables, remained stable. CONCLUSIONS Reflectance spectrophotometry meticulously monitored changes in microvascular oxygen saturation in gastric mucosa during breathing continuous positive airway pressure. Microvascular oxygen saturation in gastric mucosa decreased with increasing levels of continuous positive airway pressure despite steady systemic variables. These results suggest that the impact of altering airway pressures on splanchnic oxygenation is not mirrored necessarily by concomitant changes in systemic circulation. Moreover, if these findings also apply to critically ill patients, monitoring microvascular oxygen saturation in gastric mucosa would be useful to further optimize the setting of ventilation variables.

Lethal systemic capillary leak syndrome associated with severe ventilator-induced lung injury: An experimental study

ObjectiveWe report the evolution of severe ventilator-induced lung injury associated with lethal systemic capillary leak syndrome, when sheep were ventilated at a peak inspiratory pressure of 50 cm H2O, at a respiratory rate of 8 breaths·min−1, with an inspiratory time of 2.5 secs. DesignA prospective laboratory animal study. SettingExperimental animal research laboratory. SubjectsMixed breed sheep. InterventionsSheep were anesthetized, paralyzed, and mechanically ventilated. Measurements and Main ResultsThis sheep model was characterized by a rapidly evolving massive anasarca, hemoconcentration, cardiac dysfunction, multiple system organ failure, and severe ventilator-induced lung injury. Cardiovascular changes and profound hemoconcentration developed within 6 hrs from the start of mechanical ventilation, along with a major decline in pulmonary compliance and deterioration in arterial blood gases. When total static lung compliance decreased to 0.15 mL (cm H2O)−1·kg−1 (7–30 hrs), the sheep were randomized to two groups. Group I received high (recruitive) positive end-expiratory pressure (9–20 cm H2O), adjusted as needed; group II received low (supportive) positive end-expiratory pressure (2–6 cm H2O). Sheep in both groups progressively deteriorated and died with cardiocirculatory failure and multiple system organ failure within 12–24 hrs from start of treatment. ConclusionsThis model of lethal systemic capillary leak syndrome with multiple system organ failure differs greatly from our previous sheep model of acute ventilator-induced lung injury in which sheep were ventilated with a peak inspiratory pressure of 50 cm H2O, a respiratory rate of 4 breaths·min−1, and an inspiratory time of 1.35 secs, without inducing capillary leak syndrome. The mere change of respiratory rate from 4 to 8 breaths·min−1, with a near doubling of the inspiratory time to 2.5 secs, although maintaining eucapnia, resulted in lethal systemic capillary leak syndrome and multiple system organ failure with both gross and microscopic pathology of lungs greatly different from our previous model of mechanical ventilation-induced acute respiratory distress syndrome.