05 Oct 08
Posted in Acid-Base disorders, Glycemic control at 13:45 by Laci
By A K Simpson, N Levy and G M Hall
Anaesthesia 2008;63:1043-1045
It is estimated by the International Diabetes Federation that 246 million adults worldwide have diabetes mellitus and the figure is expected to reach 380 million by 2025. Anaesthetists will be involved in the care of more diabetic patients as they present in increasing numbers for surgery as a result of the complications of diabetes. The cornerstone of metabolic control in the peri-operative period, except for Type II diabetics undergoing minor surgery, is the administration of intravenous (iv) glucose with potassium chloride and a variable insulin infusion. Standard anaesthetic and surgical texts recommend the use of 5% or 10% glucose at a rate of 125–83 ml.h−1. This corresponds to practice in nine out of 11 acute hospitals in the East Anglia region as shown by the authors’ recent audit (unpublished results). It is likely, therefore, that this regimen is common nationally.
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Posted in Propofol, Sedation at 13:40 by Laci
By J Fong, L Sylvia, R Ruthazer, G Schumaker, M Kcomt, JW Devlin
Crit Care Med 2008;36:2281-2287
To identify predictors of mortality in patients with suspected propofol infusion syndrome and to develop a simple scoring system to identify patients with suspected propofol infusion syndrome who are most at risk of death.
Design
Retrospective, database analysis.
Setting
MEDWATCH system.
Participants
Reports (1989-2005) where propofol was associated with >=1 of 24 published propofol infusion syndrome clinical manifestations.
Interventions
None
Measurements and Main Results
After comparison of demographic and clinical manifestations between survivors and nonsurvivors, a multivariate logistic regression model was built through a stepwise selection process and then used to develop a simplified mortality scoring system. Of 1139 patients with suspected propofol infusion syndrome, 342 (30%) were fatal. Death was more likely if patients were <=18 yrs (odds ratio [95% confidence interval], 2.3 [1.7-3.2]), male (1.3 [1.1-1.7]), received a vasopressor (1.8 [1.3-2.5)]), or had the following clinical manifestations: cardiac (3.8 [2.88-4.91]), metabolic acidosis (3.7 [2.7-5.0]), renal failure (1.9 [1.4-2.6]), hypotension (1.8 [1.3-2.3]), rhabdomyolysis (1.8 [1.3-2.3]), or dyslipidemia (2.0 [1.2-3.4]). The multivariable modeling process found that cardiac symptoms, rhabdomyolosis, hypotension, metabolic acidosis, renal failure, and age each affected survival, although significant interactions existed between some of these factors. Based on the combination of the presence or absence of the six factors in the multivariate model, a propofol infusion syndrome mortality risk score of 0 to 4 resulted in a predicted %/observed % mortality for each score of 0 (10%/10%), 1 (24%/24%), 2 (47%/44%), 3 (72%/81%), and 4 (89%/83%).
Conclusions
A number of characteristics are independently associated with higher mortality in patients with suspected propofol infusion syndrome, only some of which are currently reflected in the package insert. Further research should focus on prospectively evaluating the mortality scoring system in patients with suspected propofol infusion syndrome.
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Posted in Brain injury, Neuroprotection at 13:39 by Laci
By P Sanchez-Pena, A-R Pereira, N-A Sourour, A Biondi, L Lejean, C Colonne, A-L Boch, M Al Hawari, L Abdennour, L Puybasset
Crit Care Med 2008;36:2267-2273
Studies of new neuroprotective approaches in patients with subarachnoid aneurysmal hemorrhage and better family information would benefit from the development of laboratory markers of brain ischemia. The goal of this study was to evaluate mean 15-day S100B for predicting outcomes after subarachnoid aneurysmal hemorrhage.
Design
Single center prospective cohort with consecutive inclusions.
Setting
Anesthesiology and Critical Care Neurosurgical Unit of a university hospital.
Patients
One hundred nine patients admitted within 48 hrs after subarachnoid aneurysmal hemorrhage onset and treated by surgical clipping or coiling within 48 hrs following admission.
Interventions
We recorded initial World Federation of Neurologic Surgeons and Fisher grades; comorbidities; initial severity; aneurysm location; presence of acute hydrocephalus; presence of intraventricular hemorrhage; initial seizures and neurogenic lung edema; initial troponin values; treatment of aneurysm; and occurrence of vasospasm.
Measurements and main results
S100B was assayed daily over the first 15 days. Glasgow Outcome Scores were recorded at intensive care unit discharge and after 6 and 12 months. The main outcome criterion was the 12-month Glasgow Outcome Scale score dichotomized as poor (Glasgow Outcome Scale 1-3) or good (Glasgow Outcome Scale 4-5). Seventy percent of patients had good 12-month outcome. Poor outcome was associated with higher initial World Federation of Neurologic Surgeons and Fisher scores, neurogenic lung edema, high mean 15-day S100B but not initial, troponin initial value, intraventricular hemorrhage, angiographically documented vasospasm, all in an univariate manner. After multivariate analysis, only mean 15-day S100B value significantly predicted outcome (p < 0.0005). The best cutoff for the mean 15-day S100B value was 0.23 [mu]g/L (specificity 0.90, 95% confidence interval [CI] 0.81-0.95; sensitivity 0.91, 95% CI 0.75-0.98; area under the curve 0.98, 95% CI 0.87-0.99).
Conclusion
S100B elevation over the first 15 days after subarachnoid aneurysmal hemorrhage is associated with poor outcome after subarachnoid aneurysmal hemorrhage. This result supports the use of S100B as a surrogate marker for brain ischemia in patients with subarachnoid aneurysmal hemorrhage.
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03 Oct 08
Posted in BNP, Sepsis at 19:10 by Laci
By R Pirracchio, N Deye, A Lukaszewicz, A Mebazaa, B Cholley, J Mateo et al
Crit Care Med 2008; 36:2542-2546
High B-type natriuretic peptide (BNP) levels are reported in the context of septic shock. We hypothesized that high BNP levels might be related to an alteration in BNP clearance pathway, namely neutral endopeptidase (NEP) 24.11. NEP 24.11 activity was measured in septic shock and in cardiogenic shock patients. We further evaluated whether baseline plasma BNP can predict fluid responsiveness and whether BNP can still be released in plasma despite high initial BNP levels, in response to overloading.
Material and Methods
Prospective observational study. Patients in severe sepsis (S) or in septic shock (SS) needing a fluid challenge were included. Stroke volume (SV) and BNP were measured before (SV1, BNP1) and 45 mins after (SV2, BNP2) a standardized fluid challenge. DeltaBNP was defined as the difference between BNP2 and BNP1. NEP 24.11 activity was determined by fluorometry in 12 SS and 4 S patients before fluid challenge and in 5 cardiogenic shock patients.
Results
Twenty-three patients (61 +/- 18 years old, Simplified Acute Physiology Score II: 54 +/- 21; 19 SS, 4 S; BNP1: 1371 +/- 1434 pg/mL) were studied. BNP1 concentrations were significantly higher in SS than in S (1643 +/- 1437 vs. 80 +/- 35 pg/mL; p = 0.002). There was no correlation between baseline BNP and fluid responsiveness. Nine of the 11 patients with BNP1 >1000 pg/mL were fluid responders. DeltaBNP was greater in fluid nonresponders than in fluid responders (22 +/- 27% vs. 6 +/- 11%, p = 0.028). Plasma BNP was higher in SS than in cardiogenic shock patients (1367 +/- 1438 vs. 750 +/- 346 respectively; p = 0.027). NEP 24.11 activity was lower in SS than in S patients (0.10 +/- 0.06 nmole/mL/min vs. 0.50 +/- 0.22 nmole/mL/min, p <0.0001) cardiogenic shock patients (0.10 +/- 0.06 nmole/mL/min vs. 0.58 +/- 0.19 nmole/mL/min; p = 0.002).
Conclusion
High levels of BNP might be related to an alteration in BNP clearance. During sepsis, high BNP levels are not predictive of fluid nonresponsiveness. Nevertheless, in fluid nonresponders, acute ventricular stretching can result in further BNP release.
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