Preoperative changes of forced vital capacity due to body position do not correlate with postoperative respiratory function in obese subjects.

BACKGROUND: Obese patients are at risk of developing postoperative pulmonary complications. We hypothesized that preoperative changes in dynamic spirometry due to body posture would correlate with the drop of forced vital capacity (FVC) measured early after surgery. METHODS: Thirty consecutive morbidly obese patients undergoing gastric banding were investigated. All subjects were studied the day before surgery (T0) and on postoperative day one (T1). Forced Vital Capacity (FVC) was measured, together with heart rate, mean arterial pressure and respiratory rate. At T0 measurements were taken in a random fashion with subjects in upright and in supine position. Subjects were then investigated after surgery in the supine position (T1). Postoperative pain was assessed at T1 using visual analogue scale. Intraoperative variables were also collected. RESULTS: Body Mass Index (BMI) of the investigated subjects was 43.9 ± 5.7 Kg/m2 (range 33.8-60); their age was 40 ± 8 years. All dynamic spirometric data decreased significantly from upright to supine position (P<0.05) and after surgery from 3.07 L (2.77-3.71) to 1.50 (1.15-2.12) (FVC T0 supine vs. T1, P<0.05). Changes of FVC due to body position did not correlate with changes of FVC occurring after surgery (R2=0.105, P=0.081). When subjects were stratified by the median postoperative drop of FVC (45.74%), preoperative (anthropometric and spirometric data), intraoperative (ventilatory settings and hemodynamics) and postoperative (FVC and pain) parameters were similar between groups. The duration of pneumoperitoneum was correlated with the drop of FVC (R2=0.551, P<0.05). CONCLUSION: The derangement of FVC that occurs in obese subjects after gastric banding is not predictable before surgery from anthropometric or spirometric data. The duration of pneumoperitoneum significantly contributes to postoperative impairment of respiratory function.

Kidney instant monitoring (K.IN.G): a new analyzer to monitor kidney function.

AIM: The key role of the kidney in the regulation of body fluids and acid-base status is well known. Nonetheless, urine analysis has not received great attention in critically ill patients, likely due to the common practice of only analyzing 24-hour collected specimens. We hypothesized that the kidney may react more rapidly to minimal hemodynamic and acid-base status variations than can be assessed by a 24-hour analysis. Accordingly, we developed and tested a urine analyzer, allowing quasi-continuous urinary analysis. METHODS: A novel analyzer (Kidney INstant monitorinG--K.IN.G) was developed that allows non-invasive, quasi-continuous analysis of urine pH, sodium, chloride, potassium and ammonium levels. Analytic measurement accuracy was calculated for urine samples of patients admitted to ICUs as well as medical staff, using standard techniques as references. For clinical investigation, approximately 200 patients were connected to the analyzer after ICU admission until discharge. Clinically relevant parameters were recorded. Here, three cases are presented. RESULTS: For each analytic parameter, the accuracy of measurements obtained with the K.IN.G analyzer appeared to be acceptable as compared to those of the reference techniques. In case 1, urine analysis revealed increased urinary sodium and chloride excretion strictly in parallel with mean arterial pressure, and increased ammonium excretion which was associated with moderate hypercapnia. Case 2 showed increases in urinary pH and sodium and chloride levels following awakening after sedation suspension. In case 3, urine analysis revealed an impairment of renal concentrative power, which was associated with hypovolemia. CONCLUSION: The K.IN.G analyzer, allowing quasi-continuous monitoring of urinary pH and principal electrolyte levels, may represent a novel tool for clinical and research purposes.

Physical and biological triggers of ventilator-induced lung injury and its prevention.

Ventilator-induced lung injury is a side-effect of mechanical ventilation. Its prevention or attenuation implies knowledge of the sequence of events that lead from mechanical stress to lung inflammation and stress at rupture. A literature review was undertaken which focused on the link between the mechanical forces in the diseased lung and the resulting inflammation/rupture. The distending force of the lung is the transpulmonary pressure. This applied force, in a homogeneous lung, is shared equally by each fibre of the lung's fibrous skeleton. In a nonhomogeneous lung, the collapsed or consolidated regions do not strain, whereas the neighbouring fibres experience excessive strain. Indeed, if the global applied force is excessive, or the fibres near the diseased regions experience excessive stress/strain, biological activation and/or mechanical rupture are observed. Excessive strain activates macrophages and epithelial cells to produce interleukin-8. This cytokine recruits neutrophils, with consequent full-blown inflammation. In order to prevent initiation of ventilator-induced lung injury, transpulmonary pressure must be kept within the physiological range. The prone position may attenuate ventilator-induced lung injury by increasing the homogeneity of transpulmonary pressure distribution. Positive end-expiratory pressure may prevent ventilator-induced lung injury by keeping open the lung, thus reducing the regional stress/strain maldistribution. If the transpulmonary pressure rather than the tidal volume per kilogram of body weight is taken into account, the contradictory results of the randomised trials dealing with different strategies of mechanical ventilation may be better understood.

Sepsis: state of the art.

In recent years, we have considerably widened our knowledge of the pathophysiology of sepsis and some procedures, aiming both to relieve symptoms and control the inflammation/coagulation reaction, have proven to be effective in increasing survival. This improves when mechanical ventilation is applied with low tidal volumes, fluid replacement and the use of cardioactive drugs are titrated on the oxygen saturation of hemoglobin in the central venous system and blood glucose does not exceed certain limits. It is also evident that inflammation and coagulation are closely related to each other. The inhibition of only one pathway, such as the inhibition of inflammation with high dosage steroids or the inhibition of coagulation with antithrombin, does not produce a survival improvement. The only molecule which has proven to be notably effective in reducing mortality is Activated Protein C interacting on coagulation/fibrinolysis, as well as on inflammation processes. Multinodal modulation of several interdependent processes may be the probable reason for the proven effectiveness of this treatment.