Nutritional support and brain tissue glucose metabolism in poor-grade SAH: a retrospective observational study

Abstract

IntroductionWe sought to determine the effect of nutritional support and insulin infusion therapy on serum and brain glucose levels and cerebral metabolic crisis after aneurysmal subarachnoid hemorrhage (SAH).MethodsWe used a retrospective observational cohort study of 50 mechanically ventilated poor-grade (Hunt-Hess 4 or 5) aneurysmal SAH patients who underwent brain microdialysis monitoring for an average of 109 hours. Enteral nutrition was started within 72 hours of admission whenever feasible. Intensive insulin therapy was used to maintain serum glucose levels between 5.5 and 7.8 mmol/l. Serum glucose, insulin and caloric intake from enteral tube feeds, dextrose and propofol were recorded hourly. Cerebral metabolic distress was defined as a lactate to pyruvate ratio (LPR) > 40. Time-series data were analyzed using a general linear model extended by generalized estimation equations (GEE).ResultsDaily mean caloric intake received was 13.8 ± 6.9 cal/kg and mean serum glucose was 7.9 ± 1 mmol/l. A total of 32% of hourly recordings indicated a state of metabolic distress and < 1% indicated a state of critical brain hypoglycemia (< 0.2 mmol/l). Calories received from enteral tube feeds were associated with higher serum glucose concentrations (Wald = 6.07, P = 0.048), more insulin administered (Wald = 108, P < 0.001), higher body mass index (Wald = 213.47, P < 0.001), and lower body temperature (Wald = 4.1, P = 0.043). Enteral feeding (Wald = 1.743, P = 0.418) was not related to brain glucose concentrations after accounting for serum glucose concentrations (Wald = 67.41, P < 0.001). In the presence of metabolic distress, increased insulin administration was associated with a relative reduction of interstitial brain glucose concentrations (Wald = 8.26, P = 0.017), independent of serum glucose levels.ConclusionsIn the presence of metabolic distress, insulin administration is associated with reductions in brain glucose concentration that are independent of serum glucose levels. Further study is needed to understand how nutritional support and insulin administration can be optimized to minimize secondary injury after subarachnoid hemorrhage.

Population Physiology: Leveraging Electronic Health Record Data to Understand Human Endocrine Dynamics

“…The primary target for each patient was (or ) and the primary caloric source was Osmolite. The NICU population does receive insulin; how and why is complex and is discussed in detail in Schmidt et al [27]. We do not attempt to control for insulin because it is difficult to foresee whether it matters; our results will show that the insulin regimen in the NICU population does not affect our results to first order in statistical moment (i.e., the mean).…”

Nutrition Therapy, Glucose Control, and Brain Metabolism in Traumatic Brain Injury: A Multimodal Monitoring Approach

“…Recently, reports on comatose patients with subarachnoid hemorrhage have shown conflicting results. Schmidt et al (2012) failed to demonstrate an association between nutrition therapy and improvement of brain glucose. In parallel, they showed that insulin was associated with reductions in brain glucose independent of serum glucose (Schmidt et al, 2012).…”

“…Schmidt et al (2012) failed to demonstrate an association between nutrition therapy and improvement of brain glucose. In parallel, they showed that insulin was associated with reductions in brain glucose independent of serum glucose (Schmidt et al, 2012). On the other hand, Kofler et al (2018) recently found significant increases in CMD-glucose levels, independent of the baseline brain metabolic profile and insulin administration.…”

“…At the brain level, the usual consequences of neurotrauma related to glucose metabolism include hyperglycolysis, mitochondrial dysfunction, and low or high CMD glucose (Vespa et al, 2003;O'Connell et al, 2005;Hutchinson et al, 2009;Timofeev et al, 2011;Kurtz et al, 2013;Jalloh et al, 2015aJalloh et al, ,b, 2018. Other than neurotrauma itself, medical interventions in the ICU may affect glucose metabolism, such as enteral/parenteral nutrition and insulin therapy (Vespa et al, 2006(Vespa et al, , 2012Schmidt et al, 2012;Badjatia and Vespa, 2014;Kofler et al, 2018). Excess exogenous glucose or total carbohydrate administration, exceeding the patient's glucose oxidation rate (maximum of 5 mg/kg/min, or 0.3 g/kg/h), may lead to hyperglycemia.…”

Nutrition in the neurocritical care unit

“…The requirements increase over time: Throughout this period the HBE underestimates BEE calculations as compared with indirect calorimetry (IC). [52] Recent brain microdialysis studies have shown that after subarachnoid haemorrhage, over time, the interstitial milieu becomes hyperglycolytic and cerebral glucose consumption increases. Enteral nutrition and insulin administration to control plasma glucose levels may increase metabolic stress in these patients by causing brain interstitial hypoglycaemia and increase in lactate and pyruvate levels.…”