Managing Hyperglycemia in Critically Ill Patients: Where are We Now?

Hyperglycemia is common in critically ill patients and is associated with increased morbidity, mortality, rate of infections and length of hospital stay. For decades, hyperglycemia in critically ill population was considered an adaptive response and interventions were only considered if diabetic ketoacidosis (DKA) or severe hyperosmolar states developed. Furnary et al published studies showing lower sternal wound infection rates in cardiac surgical patients with control of glucose (180-220 mg/dl). This led to the dissemination of the “Portland Protocol,” but it was not widely accepted.1, 2 Management of hyperglycemia changed with the publication of Van Den Berghe study.3 This was a prospective, randomized, controlled study involving adults admitted to a surgical intensive care unit (ICU) who were receiving mechanical ventilation (MV). A total of 1548 patients were enrolled with patients randomly assigned to two groups. One group received intensive insulin therapy (IIT) with goal blood glucose of 80-110 mg/dl. The second group received conventional treatment whereby insulin was given only if the blood glucose level exceeded 215 mg/dl with goal glucose level of 180-200 mg/dl. Pages: 20-23

Diagnostic Accuracy of Procalcitonin in Differentiating Sepsis from Noninfectious SIRS in Adult Patients with Subarachnoid Hemorrhage

Background: Subarachnoid hemorrhage (SAH) is a frequent diagnosis in the neuro-intensive care unit (NICU) that can result in the development of systemic inflammatory response syndrome (SIRS) and fever. The differentiation between central fever and infectious fever is paramount in order to prevent superfluous diagnostic testing and overuse of empiric antibiotics. Methods: A prospective chart review study conducted in the NICU between December 2012 and September 2015. Patients with SAH, fever (≥101.0°F) and/or who were SIRS positive and had PCT levels measured were included. The primary outcome was clinical infection defined as any positive culture or infiltrate on chest X-ray within three days of onset of fever. Results: Out of 129 patients, 54 were positive for any culture: 14 with PCT ≤0.2, 12 with PCT \u3e0.2 and ≤0.5, and 28 with PCT \u3e0.5. Using multiple logistic regression, PCT between 0.2-0.5 had an odds ratio of 2.99 (95% CI 1.12-8.00) while PCT \u3e0.5 had an odds ratio of 29.11 (CI 8.49-99.83) and p-value of \u3c0.001. All other predictors were not statistically significant. For procalcitonin \u3e0.5, specificity is 94.7%, sensitivity 51.9%, positive predictive value 87.5%, and negative predictive value 73.2%. ROC Curve area: 79.3%. Conclusion: PCT of 0.5 ng/mL or greater was useful for distinguishing infectious from central fever in SAH patients, with PCT values between 0.2-0.5 as somewhat predictive of infection. The test has high specificity and a reasonably high negative predictive value, so it can be a valuable tool to rule out infectious fever in patients with SAH

Mortality from gastrointestinal congenital anomalies at 264 hospitals in 74 low-income, middle-income, and high-income countries: a multicentre, international, prospective cohort study

Summary Background Congenital anomalies are the fifth leading cause of mortality in children younger than 5 years globally. Many gastrointestinal congenital anomalies are fatal without timely access to neonatal surgical care, but few studies have been done on these conditions in low-income and middle-income countries (LMICs). We compared outcomes of the seven most common gastrointestinal congenital anomalies in low-income, middle-income, and high-income countries globally, and identified factors associated with mortality. Methods We did a multicentre, international prospective cohort study of patients younger than 16 years, presenting to hospital for the first time with oesophageal atresia, congenital diaphragmatic hernia, intestinal atresia, gastroschisis, exomphalos, anorectal malformation, and Hirschsprung’s disease. Recruitment was of consecutive patients for a minimum of 1 month between October, 2018, and April, 2019. We collected data on patient demographics, clinical status, interventions, and outcomes using the REDCap platform. Patients were followed up for 30 days after primary intervention, or 30 days after admission if they did not receive an intervention. The primary outcome was all-cause, in-hospital mortality for all conditions combined and each condition individually, stratified by country income status. We did a complete case analysis. Findings We included 3849 patients with 3975 study conditions (560 with oesophageal atresia, 448 with congenital diaphragmatic hernia, 681 with intestinal atresia, 453 with gastroschisis, 325 with exomphalos, 991 with anorectal malformation, and 517 with Hirschsprung’s disease) from 264 hospitals (89 in high-income countries, 166 in middleincome countries, and nine in low-income countries) in 74 countries. Of the 3849 patients, 2231 (58·0%) were male. Median gestational age at birth was 38 weeks (IQR 36–39) and median bodyweight at presentation was 2·8 kg (2·3–3·3). Mortality among all patients was 37 (39·8%) of 93 in low-income countries, 583 (20·4%) of 2860 in middle-income countries, and 50 (5·6%) of 896 in high-income countries (p<0·0001 between all country income groups). Gastroschisis had the greatest difference in mortality between country income strata (nine [90·0%] of ten in lowincome countries, 97 [31·9%] of 304 in middle-income countries, and two [1·4%] of 139 in high-income countries; p≤0·0001 between all country income groups). Factors significantly associated with higher mortality for all patients combined included country income status (low-income vs high-income countries, risk ratio 2·78 [95% CI 1·88–4·11], p<0·0001; middle-income vs high-income countries, 2·11 [1·59–2·79], p<0·0001), sepsis at presentation (1·20 [1·04–1·40], p=0·016), higher American Society of Anesthesiologists (ASA) score at primary intervention (ASA 4–5 vs ASA 1–2, 1·82 [1·40–2·35], p<0·0001; ASA 3 vs ASA 1–2, 1·58, [1·30–1·92], p<0·0001]), surgical safety checklist not used (1·39 [1·02–1·90], p=0·035), and ventilation or parenteral nutrition unavailable when needed (ventilation 1·96, [1·41–2·71], p=0·0001; parenteral nutrition 1·35, [1·05–1·74], p=0·018). Administration of parenteral nutrition (0·61, [0·47–0·79], p=0·0002) and use of a peripherally inserted central catheter (0·65 [0·50–0·86], p=0·0024) or percutaneous central line (0·69 [0·48–1·00], p=0·049) were associated with lower mortality. Interpretation Unacceptable differences in mortality exist for gastrointestinal congenital anomalies between lowincome, middle-income, and high-income countries. Improving access to quality neonatal surgical care in LMICs will be vital to achieve Sustainable Development Goal 3.2 of ending preventable deaths in neonates and children younger than 5 years by 2030

Utility of Biomarkers in the Evaluation of Fever in the Intensive Care Unit After Brain Injury

Fever is frequent in patients with neurologic injury. Differentiating infectious fever from central fever can be challenging. It is important to diagnose the cause of fever in the neurological intensive care unit because of the detrimental effects of fever on brain injured patients. This is a comprehensive review of the role of the two commonly available biomarkers, C-reactive protein and procalcitonin in differentiating the central fever from infectious fever. INTRODUCTION AND BACKGROUND Fever is frequently seen in the neurologic intensive care unit (NICU). Incidence rates of up to 70% have been reported in various studies.1-5 Fever can help host defenses by local activation of the coagulation cascade, cytokine-mediated T-cell activation, as well as neutrophil and macrophage recruitment to injured tissues. In brain injured patients, after the initial insult, secondary neuronal injury is speculated to be caused by several processes including mitochondrial dysfunction, inflammatory response, free radical generation, and excitatory neurotransmitter release. Fever has been shown to exacerbate secondary neuronal injury and physiologic dysfunction after traumatic brain injury (TBI), subarachnoid hemorrhage (SAH), and major neurosurgery.