Model-based insulin-nutrition administration for glycemic control in Malaysian critical care: First pilot trial

© 2018, Springer Science+Business Media Singapore. Stress-induced hyperglycemia is prevalent in critical care, even in patients with no history of diabetes. Control of blood glucose level with tight insulin therapy has been shown to reduce incidences of hyperglycemia leading to reduced mortality and improved clinical outcomes. STAR is a tablet-based glucose control protocol with a specialized user interface into which insulin and nutrition information can be entered and predicted. This research describes the first clinical pilot trial of STAR approach in International Islamic University Hospital, Kuantan, Malaysia. The clinically specified target for blood glucose level is between 4.4 and 8.0 mmol/L. Seven episodes (of 359 h) were recruited based on the need for glucose control. Overall, 43.93% of measurement are in the range of 4.4–8.0 mmol/L band. The blood glucose median is 8.30 [6.32–10.00] mmol/L with only 1 patient having below than 2.22 mmol/L which is the guaranteed minimum risk level. This pilot study shows that STAR protocol is a patient specific approach that provides a good glycemic control in critically ill patients. Nevertheless, its implementation in Malaysian intensive care environments requires modifications and improvements in certain areas

The clinical utility window for acute kidney injury biomarkers in the critically ill

Introduction: Acute Kidney Injury (AKI) biomarker utility depends on sample timing after the onset of renal injury. We compared biomarker performance on arrival in the emergency department (ED) with subsequent performance in the intensive care unit (ICU).Methods: Urinary and plasma Neutrophil Gelatinase-Associated Lipocalin (NGAL), and urinary Cystatin C (CysC), alkaline phosphatase, γ-Glutamyl Transpeptidase (GGT), α- and π-Glutathione S-Transferase (GST), and albumin were measured on ED presentation, and at 0, 4, 8, and 16 hours, and days 2, 4 and 7 in the ICU in patients after cardiac arrest, sustained or profound hypotension or ruptured abdominal aortic aneurysm. AKI was defined as plasma creatinine increase ≥26.5μmol/l within 48 hours or ≥50% within 7 days.Results: In total, 45 of 77 patients developed AKI. Most AKI patients had elevated urinary NGAL, and plasma NGAL and CysC in the period 6 to 24 hours post presentation. Biomarker performance in the ICU was similar or better than when measured earlier in the ED. Plasma NGAL diagnosed AKI at all sampling times, urinary NGAL, plasma and urinary CysC up to 48 hours, GGT 4 to 12 hours, and π-GST 8 to 12 hours post insult. Thirty-one patients died or required dialysis. Peak 24-hour urinary NGAL and albumin independently predicted 30-day mortality and dialysis; odds ratios 2.87 (1.32 to 6.26), and 2.72 (1.14 to 6.48), respectively. Urinary NGAL improved risk prediction by 11% (IDIevent of 0.06 (0.002 to 0.19) and IDInon-event of 0.04 (0.002 to 0.12)).Conclusion: Early measurement in the ED has utility, but not better AKI diagnostic performance than later ICU measurement. Plasma NGAL diagnosed AKI at all time points. Urinary NGAL best predicted mortality or dialysis compared to other biomarkers.Trial registration: Australian and New Zealand Clinical Trials Registry ACTRN12610001012066. Registered 12 February 2010

Model iterative airway pressure reconstruction during mechanical ventilation asynchrony: Shapes and sizes of reconstruction

© 2018, Springer Science+Business Media Singapore. Model-based methods estimating patient-specific respiratory mechanics may help intensive care clinicians in setting optimal ventilation parameters. However, these methods rely heavily on the quality of measured airway pressure and flow profiles for reliable respiratory mechanics estimation. Thus, asynchronous and/or spontaneous breathing cycles that do not follow a typical passive airway profile affect the performance and reliability of model-based methods. In this study, a model iterative airway pressure reconstruction method is presented. It aims to reconstruct a measured airway pressure affected by asynchronous breathing iteratively, trying to match the profile of passive breaths with no asynchrony or spontaneous breathing effort. Thus, reducing the variability of identified respiratory mechanics over short time periods where changes would be due only to asynchrony or spontaneous artefacts. A total of 2000 breathing cycles from mechanically ventilated patients with known asynchronous breathing were analyzed. It was found that this method is capable of reconstructing an airway pressure free from asynchronous or spontaneous breathing effort. This work focuses on several cases, detailing how iterative pressure reconstruction method performs under different cases, as well as its limitation

Acute Kidney Injury Urinary Biomarker Time-Courses

Factors which modify the excretion profiles of acute kidney injury biomarkers are difficult to measure. To facilitate biomarker choice and interpretation we modelled key modifying factors: extent of hyperfiltration or reduced glomerular filtration rate, structural damage, and reduced nephron number. The time-courses of pre-formed, induced (upregulated), and filtered biomarker concentrations were modelled in single nephrons, then combined to construct three multiple-nephron models: a healthy kidney with normal nephron number, a non-diabetic hyperfiltering kidney with reduced nephron number but maintained total glomerular filtration rate, and a chronic kidney disease kidney with reduced nephron number and reduced glomerular filtration rate. Time-courses for each model were derived for acute kidney injury scenarios of structural damage and/or reduced nephron number. The model predicted that pre-formed biomarkers would respond quickest to injury with a brief period of elevation, which would be easily missed in clinical scenarios. Induced biomarker time-courses would be influenced by biomarker-specific physiology and the balance between insult severity (which increased single nephron excretion), the number of remaining nephrons (reduced total excretion), and the extent of glomerular filtration rate reduction (increased concentration). Filtered biomarkers have the longest time-course because plasma levels increased following glomerular filtration rate decrease. Peak concentration and profile depended on the extent of damage to the reabsorption mechanism and recovery rate. Rapid recovery may be detected through a rapid reduction in urinary concentration. For all biomarkers, impaired hyperfiltration substantially increased concentration, especially with chronic kidney disease. For clinical validation of these model-derived predictions the clinical biomarker of choice will depend on timing in relation to renal insult and interpretation will require the pre-insult nephron number (renal mass) and detection of hyperfiltration