Metabolic Response to Critical Illness

2009 ◽  
pp. 234-234
Author(s):  
Usha Nair
Keyword(s):  
Critical Illness ◽  
Metabolic Response

scholarly journals Metabolic response to the stress of critical illness

2014 ◽  
Vol 113 (6) ◽  
pp. 945-954 ◽  
Author(s):  
J.-C. Preiser ◽  
C. Ichai ◽  
J.-C. Orban ◽  
A.B.J. Groeneveld
Keyword(s):  
Critical Illness ◽  
Metabolic Response

The metabolic and nutritional response to critical illness

2016 ◽  
Author(s):  
Linda-Jayne Mottram ◽  
Gavin G. Lavery
Keyword(s):  
Critical Illness ◽  
Care Management ◽  
Metabolic Response ◽  
Body System ◽  
Rehabilitation Process ◽  
Wasting Syndrome ◽  
The Poor ◽  
Prolonged Recovery ◽  
Catabolic Response ◽  
Hypothalamic Pituitary Axis

The metabolic response to critical illness is complex and affects every body system. The first phase of this response is characterized by increased hypothalamic pituitary activity and resistance (decreased response) to effector hormones in many target tissues. Cytokines released in the early stages of such illness may be important as they appear to stimulate the hypothalamic pituitary axis directly as part of this ‘stress response’. This phase is considered ‘adaptive’ (helpful), increasing the availability of glucose, free fatty acids, and amino acids as substrates for vital organs. However, in prolonged illness, the neuroendocrine response is very different with damped hypothalamic responses, leading to a state in which catabolism predominates, leading to what might be termed the critical illness wasting syndrome. The gastrointestinal (GI) failure often associated with prolonged critical illness appears to be due, at least in part, to an altered neuroendocrine environment. The poor nutritional state associated with GI failure exacerbates the catabolic response, prolonging illness and the period of intensive care management required by the patient. The result is increased mortality and, in survivors, a more prolonged recovery/rehabilitation process.

Metabolic Response to Critical Illness - Part 1

2020 ◽  
Author(s):  
Palmer Q. Bessey
Keyword(s):  
Critical Illness ◽  
Glucose Intolerance ◽  
Protein Metabolism ◽  
Muscle Wasting ◽  
Metabolic Response ◽  
Surgical Patient ◽  
Altered Protein ◽  
Hypermetabolic State ◽  
The Central Nervous System

A wide variety of factors and processes are involved in the metabolic response to critical illness; this chapter reviews some of these factors and metabolic responses in the critically ill surgical patient to help the clinician minimize patient debility. The features of critical illness that can cause debility include wounds, pain, inflammation, infection, and iatrogenic factors. The three major features of the metabolic response are discussed: the hyperdynamic or hypermetabolic state, muscle wasting, and glucose intolerance. Other topics considered include altered temperature regulation, the role of the central nervous system, the role of the gut, manipulating the response to critical illness, altered protein metabolism, altered carbohydrate metabolism, and systemic mediators (e.g., hormones and cytokines).  This review contains 3 highly rendered figures, 17 tables, and 59 references Keywords: Critical illness, metabolic response, thermoregulation, muscle wasting, glucose intolerance, burn victim, sepsis

scholarly journals Metabolomic differences between critically Ill women and men

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Sowmya Chary ◽  
Karin Amrein ◽  
Jessica A. Lasky-Su ◽  
Harald Dobnig ◽  
Kenneth B. Christopher
Keyword(s):  
Critical Illness ◽  
Critically Ill ◽  
Graphical Model ◽  
Metabolic Response ◽  
Simplified Acute Physiology Score ◽  
Admission Diagnosis ◽  
High Dose ◽  
Hydroxyvitamin D ◽  
25 Hydroxyvitamin D ◽  
Over Time

AbstractMetabolism differs in women and men at homeostasis. Critically ill patients have profound dysregulation of homeostasis and metabolism. It is not clear if the metabolic response to critical illness differs in women compared to men. Such sex-specific differences in illness response would have consequences for personalized medicine. Our aim was to determine the sex-specific metabolomic response to early critical illness. We performed a post-hoc metabolomics study of the VITdAL-ICU trial where subjects received high dose vitamin D3 or placebo. Using mixed-effects modeling, we studied sex-specific changes in metabolites over time adjusted for age, Simplified Acute Physiology Score II, admission diagnosis, day 0 25-hydroxyvitamin D level, and 25-hydroxyvitamin D response to intervention. In women, multiple members of the sphingomyelin and lysophospholipid metabolite classes had significantly positive Bonferroni corrected associations over time compared to men. Further, multiple representatives of the acylcarnitine, androgenic steroid, bile acid, nucleotide and amino acid metabolite classes had significantly negative Bonferroni corrected associations over time compared to men. Gaussian graphical model analyses revealed sex-specific functional modules. Our findings show that robust and coordinated sex-specific metabolite differences exist early in critical illness.

Metabolic Response to Critical Illness - Part 1

2020 ◽  
Author(s):  
Palmer Q. Bessey
Keyword(s):  
Critical Illness ◽  
Glucose Intolerance ◽  
Protein Metabolism ◽  
Muscle Wasting ◽  
Metabolic Response ◽  
Surgical Patient ◽  
Altered Protein ◽  
Hypermetabolic State ◽  
The Central Nervous System

A wide variety of factors and processes are involved in the metabolic response to critical illness; this chapter reviews some of these factors and metabolic responses in the critically ill surgical patient to help the clinician minimize patient debility. The features of critical illness that can cause debility include wounds, pain, inflammation, infection, and iatrogenic factors. The three major features of the metabolic response are discussed: the hyperdynamic or hypermetabolic state, muscle wasting, and glucose intolerance. Other topics considered include altered temperature regulation, the role of the central nervous system, the role of the gut, manipulating the response to critical illness, altered protein metabolism, altered carbohydrate metabolism, and systemic mediators (e.g., hormones and cytokines).  This review contains 3 highly rendered figures, 17 tables, and 59 references Keywords: Critical illness, metabolic response, thermoregulation, muscle wasting, glucose intolerance, burn victim, sepsis

scholarly journals Cytokines and Metabolic Patterns in Pediatric Patients with Critical Illness

2010 ◽  
Vol 2010 ◽  
pp. 1-11 ◽  
Author(s):  
George Briassoulis ◽  
Shekhar Venkataraman ◽  
Ann Thompson
Keyword(s):  
Critical Illness ◽  
Acute Stress ◽  
Metabolic Response ◽  
Severity Of Illness ◽  
Carbon Dioxide Production ◽  
Multiple Organ ◽  
Critically Ill Children ◽  
Glucose Response ◽  
Organ System Failure ◽  
Response To Stress

It is not known if cytokines, which are cell-derived mediators released during the host immune response to stress, affect metabolic response to stress during critical illness. The aim of this prospective study was to determine whether the metabolic response to stress is related to the inflammatory interleukin-6 (IL-6), 10 (IL-10), and other stress mediators' responses and to assess their relationships with different feeding patterns, nutritional markers, the severity of illness as assessed by the Multiple Organ System Failure (MOSF), the Pediatric Risk of Mortality Score (PRISM), systemic inflammatory response syndrome (SIRS), and mortality in critically ill children. Patients were classified as hypermetabolic, normometabolic, and hypometabolic when the measured resting energy expenditures (REE) were >110%, 90–110% and, <90% of the predicted basal metabolic rate, respectively. The initial predominance of the hypometabolic pattern (48.6%) declined within 1 week of acute stress (20%), and the hypermetabolic patterns dominated only after 2 weeks (60%). Only oxygen consumption () and carbon dioxide production () () but none of the cytokines and nutritional markers, were independently associated with a hypometabolic pattern. REE correlated with the IL-10 but not PRISM. In the presence of SIRS or sepsis, CRP, IL-6, IL-10, Prognostic Inflammatory and Nutritional Index (NI), and triglycerides—but not glucose, , or increased significantly. High IL-10 levels () and low measured REE () were independently associated with mortality (11.7%), which was higher in the hypometabolic compared to other metabolic patterns (). Our results showed that only and , but not IL-6 or IL-10, were associated with a hypometabolic pattern which predominated the acute phase of stress, and was associated with increased mortality. Although in SIRS or sepsis, the cytokine response was reliably reflected by increases in NI and triglycerides, it was different from the metabolic (, ) or glucose response.

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