Correction to: "Familial venoms": a thallium intoxication cluster.

The original version of this article unfortunately contained a mistake. The presentation of Table 1 was incorrect. The corrected Table 1 is given below.

Relationship between systemic glucose and cerebral glucose is preserved in patients with severe traumatic brain injury, but glucose delivery to the brain may become limited when oxidative metabolism is impaired: implications for glycemic control.

OBJECTIVE: To clarify the dynamics of glucose delivery to the brain and the effects of changes in blood glucose after severe traumatic brain injury. DESIGN: Retrospective analysis of a prospective observational cohort study. SETTING: Neurosurgical intensive care unit of a university hospital. PATIENTS: Seventeen patients with acute traumatic brain injury monitored with cerebral and subcutaneous microdialysis. INTERVENTIONS: None. MEASUREMENTS AND MAIN RESULTS: For continuous, accurate systemic monitoring, glucose was measured in the interstitial space of subcutaneous adipose tissue using microdialysis, and 39 specific episodes of spontaneous rises in glucose were identified. During these episodes, there was a significant positive linear relationship between systemic glucose levels and brain glucose concentrations measured by microdialysis (p < .0001). The basal lactate/pyruvate ratio, with a threshold of 25, was adopted to distinguish between disturbed and presumably preserved cerebral oxidative metabolism. Using normal vs. elevated lactate/pyruvate ratio as variable factor, the relationship between brain and systemic glucose during the episodes could be described by two significantly distinct parallel lines (p = .0001), which indicates a strong additive effect of subcutaneous glucose and lactate/pyruvate ratio in determining brain glucose. The line describing the relationship under disturbed metabolic conditions was lower than in presumably intact metabolic conditions, with a significant difference of 0.648 ± 0.192 mM (p = .002). This let us to accurately predict that in this situation systemic glucose concentrations in the lower range of normality would result in critical brain glucose levels. CONCLUSIONS: The linear relationship between systemic and brain glucose in healthy subjects is preserved in traumatic brain-injured patients. As a consequence, in brain tissue where oxidative metabolism is disturbed, brain glucose concentrations might possibly drop below the critical threshold of 0.8 mM to 1.0 mM when there is a reduction in systemic glucose toward the lower limits of the "normal" range.

Prevalence of endotoxemia after surgery and its association with ICU length of stay.

INTRODUCTION: The aim of this observational study was to investigate the prevalence of endotoxemia after surgery and its association with ICU length of stay. METHODS: 102 patients admitted to a university ICU after surgery were recruited. Within four hours of admission, functional data were collected and APACHE II severity score calculated. Arterial blood samples were taken and endotoxemia was measured by chemiluminescence (Endotoxin Activity (EA)). Patients were stratified according to their endotoxin levels (low, intermediate and high) and according to their surgical procedures. Differences between endotoxin levels were assessed by ANOVA, accepting P < 0.05 as significant. Data are expressed as mean +/- SD. RESULTS: EA levels were low in 68 (66%) patients, intermediate in 17 (17%) and high in 17 (17%). Age (61 +/- 17 years) and APACHE II score 8.3 +/- 3.7 (P = 0.542) were not significantly different in the three EA groups. Functional parameters on admission were similar between EA groups: white blood cells 11093 +/- 4605 cells/mm3 (P = 0.385), heart rate 76 +/- 16 bpm (P = 0.898), mean arterial pressure 88.8 +/- 13.6 mmHg (P = 0.576), lactate 1.18 +/- 0.77 mmol/L (P = 0.370), PaO2/FiO2 383 +/- 109 mmHg (P = 0.474). Patients with high levels of EA were characterized by longer length of stay in the ICU: 1.9 +/- 3.0 days in the low EA group, 1.8 +/- 1.4 days in intermediate and 5.2 +/- 7.8 days in high group (P = 0.038). CONCLUSIONS: 17% of our patients were characterized by high levels of endotoxemia as assessed by EA assay, despite their low level of complexity on admission. High levels of endotoxin were associated with a longer ICU length of stay.

Prone position delays the progression of ventilator-induced lung injury in rats: does lung strain distribution play a role?

OBJECTIVE: To investigate if prone position delays the progression of experimental ventilator-induced lung injury, possibly due to a more homogeneous distribution of strain within lung parenchyma. DESIGN: Prospective, randomized, controlled trial. SETTING: Animal laboratory of a university hospital. SUBJECTS: Thirty-five Sprague Dawley male rats (weight 257 +/- 45 g). INTERVENTIONS: Mechanical ventilation in either supine or prone position and computed tomography scan analysis. MEASUREMENTS: : Animals were ventilated in supine (n = 15) or prone (n = 15) position until a similar ventilator-induced lung injury was reached. To do so, experiments were interrupted when respiratory system elastance was 150% of baseline. Ventilator-induced lung injury was assessed as lung wet-to-dry ratio and histology. Time to reach lung injury was considered as a main outcome measure. In five additional animals, computed tomography scans (GE Light Speed QX/I, thickness 1.25 mm, interval 0.6 mm, 100 MA, 100 Kv) were randomly taken at end-expiration and end-inspiration in both positions, and quantitative analysis was performed. Data are shown as mean +/- sd. MEASUREMENTS AND MAIN RESULTS: Similar ventilator-induced lung injury was reached (respiratory system elastance, wet-to-dry ratio, and histology). The time taken to achieve the target ventilator-induced lung injury was longer with prone position (73 +/- 37 mins vs. 112 +/- 42, supine vs. prone, p = .011). Computed tomography scan analysis performed before lung injury revealed that at end-expiration, the lung was wider in prone position (p = .004) and somewhat shorter (p = .09), despite similar lung volumes (p = .455). Lung density along the vertical axis increased significantly only in supine position (p = .002). Lung strain was greater in supine as opposed to prone position (width strain, 7.8 +/- 1.8% vs. 5.6 +/- 0.9, supine vs. prone, p = .029). CONCLUSIONS: Prone position delays the progression of ventilator-induced lung injury. Computed tomography scan analysis suggests that a more homogeneous distribution of strain may be implicated in the protective role of prone position against ventilator-induced lung injury.

Effects of continuous negative extra-abdominal pressure on cardiorespiratory function during abdominal hypertension: an experimental study.

OBJECTIVE: To investigate whether negative extra-abdominal pressure (NEXAP) improves respiratory function and induces a blood shift from the intrathoracic compartment and to assess whether these effects are influenced by abdominal pressure. DESIGN AND SETTING: Prospective, randomized, controlled trial in the animal laboratory of a university hospital. SUBJECTS: Eight sedated and paralyzed pigs (19.6+/-3.4 kg). INTERVENTIONS: Application of NEXAP (-20 cmH(2)O). MEASUREMENTS AND RESULTS: Airway, esophageal, gastric and central venous pressures were recorded simultaneously. Intrathoracic blood volume was assessed by PiCCO. The effects of NEXAP were assessed with and without abdominal hypertension by intraperitoneal insufflation of helium. NEXAP caused a lasting drop of gastric (1.97+/-2.26 mmHg) and esophageal (1.21+/-0.67 mmHg) pressures, while end-expiratory airway pressure was similar, hence transpulmonary pressure increased. Intrathoracic blood volume dropped from 358+/-47 to 314+/-47 ml. The fall was associated with a decrease in central venous pressure (R(2)=0.820). When peritoneal pressure was raised (24.7+/-5.5 mmHg), the effects were less marked. However, the difference between negative pressure around the abdomen and the pressure inside the abdomen (effective NEXAP) was correlated with the proportional changes in intrathoracic blood volume (R(2)=0.648), being greater with more negative effective NEXAP. NEXAP improved chest wall elastance during abdominal hypertension (from 0.067+/-0.023 to 0.056+/-0.021 cmH(2)O/ml). CONCLUSIONS: NEXAP increases lung volume and causes a shift of blood from the intrathoracic compartment. It needs to be tailored against abdominal pressure to be effective.