Two-thirds of the patients dying after out-of-hospital cardiac arrest died due to neurological injury and this proportion was approximately the same for ventricular fibrillation/ventricular tachycardia and pulseless electrical activity/asystole. Approximately a quarter of the patients dying after in-hospital cardiac arrest died due to neurological injury.

SummaryUsing a retrospective analysis of the Intensive Care National Audit and Research Centre Case Mix Programme Database (ICNARC CMPD), we have summarised the characteristics and outcomes for mechanically ventilated patients admitted to UK intensive care units (ICUs) after cardiac arrest. Descriptive statistics on case mix, physiology, treatment, service delivery, outcome and activity were described separately for community cardiac arrest, in-hospital cardiac arrest (peri-operative) and in-hospital cardiac arrest (not peri-operative). The impact on outcome of several patient characteristics and physiological values were analysed using multivariable logistic regression. Mechanically ventilated survivors of cardiac arrest accounted for 24 132 (5.8%) of all admissions to the 174 ICUs in the ICNARC CMP. Of these, 10 347 (42.9%) survived to leave the ICU and 6778 (28.6%) survived to acute hospital discharge. The ICNARC model gives much better discrimination than APACHE II for predicting hospital mortality after admission to ICU following cardiac arrest: the predicted hospital mortality based on the APACHE II and ICNARC model was 41.9% and 79.7%, respectively.

Summary A telephone survey was carried out on the use of hypothermia as part of the management of unconscious patients following cardiac arrest admitted to United Kingdom (UK) intensive care units (ICUs). All 256 UK ICUs listed in the Critical Care Services Manual 2004 were contacted to determine how many units have implemented therapeutic hypothermia for unconscious patients admitted following cardiac arrest, how it is implemented, and the reasons for non‐implementation. Two hundred and forty‐six (98.4%) ICUs agreed to participate. Sixty‐seven (28.4%) ICUs have cooled patients after cardiac arrest, although the majority of these have treated fewer than 10 patients. The commonest reasons given for not using therapeutic hypothermia in this situation are logistical or resource issues, or the perceived lack of evidence or consensus within individual ICU teams.

Intensive insulin therapy to control blood glucose has been found to reduce mortality among critically ill patients in a surgical intensive care unit, though a simple prescriptive insulin infusion protocol to achieve this has not been published previously. This study documents the development and routine use of a simple prescriptive intravenous insulin infusion protocol for critically ill patients and compares the results with previous practice. During development the protocol was optimized and practical issues of implementation addressed. The optimized protocol was then used for all ICU admissions, and a prospectively defined retrospective chart audit performed for the first month of use. Results were compared with a similar time period the previous year. In September 2002, 27 admissions were started on the protocol. Blood glucose for the time on the protocol had a median value of 6.2 (IQR 5.9-7.1) mmol/l compared with 9. 2 (IQR 8.1-10.2) mmol/l for those on insulin in 2001. Blood glucose for the whole ICU stay for those on the protocol in 2002 had a median value of 6.6 (IQR 6.0-7.4) mmol/l compared with 8.6 (IQR 8.0-9.4) mmol/l in 2001. Blood glucose for all ICU patients in 2002 ) mmol/l in 2001.Three blood glucose recordings were less than 2.2 mmol/l in September 2002. This study provides initial effectiveness and safety data for the Bath Insulin Protocol. Further audits in a larger patient population are now needed.

Critical Care 2017, 21(Suppl 1):P349 Introduction Imbalance in cellular energetics has been suggested to be an important mechanism for organ failure in sepsis and septic shock. We hypothesized that such energy imbalance would either be caused by metabolic changes leading to decreased energy production or by increased energy consumption. Thus, we set out to investigate if mitochondrial dysfunction or decreased energy consumption alters cellular metabolism in muscle tissue in experimental sepsis. Methods We submitted anesthetized piglets to sepsis (n = 12) or placebo (n = 4) and monitored them for 3 hours. Plasma lactate and markers of organ failure were measured hourly, as was muscle metabolism by microdialysis. Energy consumption was intervened locally by infusing ouabain through one microdialysis catheter to block major energy expenditure of the cells, by inhibiting the major energy consuming enzyme, N+/K + -ATPase. Similarly, energy production was blocked infusing sodium cyanide (NaCN), in a different region, to block the cytochrome oxidase in muscle tissue mitochondria. Results All animals submitted to sepsis fulfilled sepsis criteria as defined in Sepsis-3, whereas no animals in the placebo group did. Muscle glucose decreased during sepsis independently of N+/K + -ATPase or cytochrome oxidase blockade. Muscle lactate did not increase during sepsis in naïve metabolism. However, during cytochrome oxidase blockade, there was an increase in muscle lactate that was further accentuated during sepsis. Muscle pyruvate did not decrease during sepsis in naïve metabolism. During cytochrome oxidase blockade, there was a decrease in muscle pyruvate, independently of sepsis. Lactate to pyruvate ratio increased during sepsis and was further accentuated during cytochrome oxidase blockade. Muscle glycerol increased during sepsis and decreased slightly without sepsis regardless of N+/K + -ATPase or cytochrome oxidase blocking. There were no significant changes in muscle glutamate or urea during sepsis in absence/presence of N+/K + -ATPase or cytochrome oxidase blockade. ConclusionsThese results indicate increased metabolism of energy substrates in muscle tissue in experimental sepsis. Our results do not indicate presence of energy depletion or mitochondrial dysfunction in muscle and should similar physiologic situation be present in other tissues, other mechanisms of organ failure must be considered. , and long-term follow up has shown increased fracture risk [2]. It is unclear if these changes are a consequence of acute critical illness, or reduced activity afterwards. Bone health assessment during critical illness is challenging, and direct bone strength measurement is not possible. We used a rodent sepsis model to test the hypothesis that critical illness causes early reduction in bone strength and changes in bone architecture. Methods 20 Sprague-Dawley rats (350 ± 15.8g) were anesthetised and randomised to receive cecal ligation and puncture (CLP) (50% cecum length, 18G needle single pass through anterior and posterior wa...