02 Feb 10

Atomised lidocaine for airway topical anaesthesia in the morbidly obese: 1% compared with 2%

Posted in Anesthesia at 1:00 by Laci

By C Woodruff , P Wieczorek, T Schricker, B Vinet and S Backman

Anaesthesia 2010;65:12-17

Airway anaesthesia using atomised lidocaine for awake oral fibreoptic intubation in morbidly obese patients was evaluated using two doses of local anaesthetic. In this randomised, blinded prospective study, 40 ml of atomised 1% (n = 11) or 2% (n = 10) lidocaine was administered with high oxygen flow as carrier. Outcomes included time for intubation, patient tolerance to airway manipulation, haemodynamic parameters, the bronchoscopist’s overall satisfaction, and serial serum lidocaine concentrations. Patients receiving lidocaine 1% had a longer mean (SD) time from the start of topicalisation to tracheal tube cuff inflation than those receiving lidocaine 2% (8.6 (0.9) min vs 6.9 (0.5) min, respectively; p < 0.05). Patients in the 1% cohort demonstrated increased responses to airway manipulation (p < 0.0001), reflecting lower bronchoscopist’s satisfaction scores (p < 0.03). Haemodynamic responses to topicalisation and airway manipulation were similar in both groups. Peak plasma concentration was lower in the 1% group (mean (SD) 1.4 (0.3) and 3.8 (0.5) μg.ml−1, respectively; p < 0.001). Airway anaesthesia using atomised lidocaine for awake oral fibreoptic intubation in the morbidly obese is efficacious, rapid and safe. Compared with lidocaine 1%, the 2% dose provides superior intubating conditions.

31 Jan 10

Recently published papers: Renal support in acute kidney injury – is low dose the new high dose?

Posted in Acute Kidney Injury/RRT at 0:56 by Laci

By Y Syed J Tomlinson and L Forni

Critical Care 2009, 13:1014

Despite 21st century definitions, the management of acute kidney injury remains steadfastly rooted in the 20th century with treatment being principally supportive. Protection from potential causative agents is an essential part of management and to that end protection against contrast-induced nephropathy has received yet more attention. When optimization of volume status, haemodynamic parameters, electrolyte and acid-base disturbances have failed we turn to renal replacement therapy. The time ‘bought’ on renal support gives a period for renal recovery but although renal replacement therapy is widely employed, many management issues remain unanswered, including the timing, duration and the dose of treatment. In contrast to respiratory support for acute lung injury, for example, there is a paucity of large randomized studies addressing these fundamental issues. We describe some recent studies focusing on these issues with the hope that they may lead to better treatment for our patients.

22 Jan 10

Smoking, smoking cessation and risk for type 2 diabetes mellitus

Posted in Diabetes, Pre-operatie evaluation at 0:32 by Laci

By Y Hsin-Chieh, B Duncan,  M Schmidt, N Wang F Brancati

Ann Int Med 2010;152:10-17

Cigarette smoking is an established predictor of incident type 2 diabetes mellitus, but the effects of smoking cessation on diabetes risk are unknown.

Objective
To test the hypothesis that smoking cessation increases diabetes risk in the short term, possibly owing to cessation-related weight gain.

Design
Prospective cohort study.

Setting
The ARIC (Atherosclerosis Risk in Communities) Study.

Patients
10 892 middle-aged adults who initially did not have diabetes in 1987 to 1989.

Measurements
Smoking was assessed by interview at baseline and at subsequent follow-up. Incident diabetes was ascertained by fasting glucose assays through 1998 and self-report of physician diagnosis or use of diabetes medications through 2004.

Results
During 9 years of follow-up, 1254 adults developed type 2 diabetes. Compared with adults who never smoked, the adjusted hazard ratio of incident diabetes in the highest tertile of pack-years was 1.42 (95% CI, 1.20 to 1.67). In the first 3 years of follow-up, 380 adults quit smoking. After adjustment for age, race, sex, education, adiposity, physical activity, lipid levels, blood pressure, and ARIC Study center, compared with adults who never smoked, the hazard ratios of diabetes among former smokers, new quitters, and continuing smokers were 1.22 (CI, 0.99 to 1.50), 1.73 (CI, 1.19 to 2.53), and 1.31 (CI, 1.04 to 1.65), respectively. Further adjustment for weight change and leukocyte count attenuated these risks substantially. In an analysis of long-term risk after quitting, the highest risk occurred in the first 3 years (hazard ratio, 1.91 [CI, 1.19 to 3.05]), then gradually decreased to 0 at 12 years.

Limitation
Residual confounding is possible even with meticulous adjustment for established diabetes risk factors.

Conclusion
Cigarette smoking predicts incident type 2 diabetes, but smoking cessation leads to higher short-term risk. For smokers at risk for diabetes, smoking cessation should be coupled with strategies for diabetes prevention and early detection.

20 Jan 10

Predicting dead space ventilation in critically ill patients using clinically available data

Posted in Mechanical ventilation at 0:52 by Laci

By D Frankenfield, S Alam, E Bekteshi, R Vender

Crit Care Med 2010;38:288-291

To develop and validate an equation to predict dead space to tidal volume ratio (Vd/Vt) from clinically available data in critically ill mechanically ventilated patients.

Design
Prospective, observational study using a convenience sample of patients whose arterial blood gas and respiratory gas exchange had been measured with indirect calorimetry.

Setting
Medical and surgical critical care units of a university medical center.

Patients
Adult, mechanically ventilated patients at rest with Fio2 ≤0.60 and no air leaks who had recent arterial blood gas recordings and end-tidal carbon dioxide concentration monitoring.

Intervention
Observational only.

Measurements and main results
Indirect calorimetry was used to determine carbon dioxide production and expired minute ventilation in 135 patients. Tidal volume and respiratory rate were recorded from the ventilator. End tidal carbon dioxide concentration, body temperature, arterial carbon dioxide partial pressure (Paco2), and other clinical data were recorded. Vd/Vt was calculated using the Enghoff modification of the Bohr equation (Paco2 − PECO2/Paco2). Regression analysis was then used to construct a predictive equation for Vd/Vt using the clinical data: Vd/Vt = 0.32 + 0.0106 (Paco2 − ETCO2) + 0.003 (RR) + 0.0015 (age) (R2 = 0.67). A second group of 50 patients was measured using the same protocol and their data were used to validate the equations developed from the original 135 patients. The equation was found to be unbiased and precise.

Conclusions
Vd/Vt is predictable from clinically available data. Whether this predicted quantity is valuable clinically must still be determined.

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