Metabolic response to the stress of critical illness.

The metabolic response to stress is part of the adaptive response to survive critical illness. Several mechanisms are well preserved during evolution, including the stimulation of the sympathetic nervous system, the release of pituitary hormones, a peripheral resistance to the effects of these and other anabolic factors, triggered to increase the provision of energy substrates to the vital tissues. The pathways of energy production are altered and alternative substrates are used as a result of the loss of control of energy substrate utilization by their availability. The clinical consequences of the metabolic response to stress include sequential changes in energy expenditure, stress hyperglycaemia, changes in body composition, and psychological and behavioural problems. The loss of muscle proteins and function is a major long-term consequence of stress metabolism. Specific therapeutic interventions, including hormone supplementation, enhanced protein intake, and early mobilization, are investigated. This review aims to summarize the pathophysiological mechanisms, the clinical consequences, and therapeutic implications of the metabolic response to stress.

[1]  J. Preiser,et al.  Energy estimation and measurement in critically ill patients. , 2013, JPEN. Journal of parenteral and enteral nutrition.

[2]  P. Marik,et al.  Stress hyperglycemia: an essential survival response! , 2013, Critical care medicine.

[3]  N. Nguyen,et al.  Sucrose Malabsorption and Impaired Mucosal Integrity in Enterally Fed Critically Ill Patients: A Prospective Cohort Observational Study , 2013, Critical care medicine.

[4]  D. Cook,et al.  A randomized trial of glutamine and antioxidants in critically ill patients. , 2013, The New England journal of medicine.

[5]  G. Van den Berghe,et al.  Reduced cortisol metabolism during critical illness. , 2013, The New England journal of medicine.

[6]  A. Kiss,et al.  Diabetic status and the relation of the three domains of glycemic control to mortality in critically ill patients: an international multicenter cohort study , 2013, Critical Care.

[7]  J. Vincent,et al.  When should we add parenteral to enteral nutrition? , 2013, The Lancet.

[8]  C. Pichard,et al.  Optimisation of energy provision with supplemental parenteral nutrition in critically ill patients: a randomised controlled clinical trial , 2013, The Lancet.

[9]  G. Van den Berghe,et al.  Does artificial nutrition improve outcome of critical illness? , 2013, Critical Care.

[10]  L. Langouche,et al.  Endocrine, Metabolic, and Morphologic Alterations of Adipose Tissue During Critical Illness* , 2013, Critical care medicine.

[11]  B. Bistrian,et al.  Why critically ill patients are protein deprived. , 2013, JPEN. Journal of parenteral and enteral nutrition.

[12]  M. Soeters,et al.  The evolutionary benefit of insulin resistance. , 2012, Clinical nutrition.

[13]  M. Singer,et al.  The stress response and critical illness: A review* , 2012, Critical care medicine.

[14]  O. Ljungqvist.  Jonathan E. Rhoads lecture 2011: Insulin resistance and enhanced recovery after surgery. , 2012, JPEN. Journal of parenteral and enteral nutrition.

[15]  R. Schwartz,et al.  Effects of testosterone supplementation on clinical and rehabilitative outcomes in older men undergoing on-pump CABG. , 2012, Contemporary clinical trials.

[16]  M. Singer,et al.  Ghrelin, appetite and critical illness , 2012, Current opinion in critical care.

[17]  U. Knippschild,et al.  Sepsis-Induced Adipokine Change with regard to Insulin Resistance , 2012, International journal of inflammation.

[18]  J. Daly.  Early versus late Parenteral Nutrition in Critically Ill Adults , 2012 .

[19]  John D. Storey,et al.  A genomic storm in critically injured humans , 2011, The Journal of experimental medicine.

[20]  G. Biolo,et al.  Preoperative insulin resistance and the impact of feeding on postoperative protein balance: a stable isotope study. , 2011, The Journal of clinical endocrinology and metabolism.

[21]  J. Kirk-Bayley,et al.  Functional Disability 5 Years after Acute Respiratory Distress Syndrome , 2011 .

[22]  E. Vicaut,et al.  Postresuscitation syndrome: Potential role of hydroxyl radical-induced endothelial cell damage* , 2011, Critical care medicine.

[23]  P. Kalfon,et al.  Glycemic Control in the Intensive Care Unit and during the Postoperative Period , 2011, Anesthesiology.

[24]  M. Horowitz,et al.  Bench-to-bedside review: The gut as an endocrine organ in the critically ill , 2010, Critical care.

[25]  M. Singer,et al.  Survival in critical illness is associated with early activation of mitochondrial biogenesis. , 2010, American journal of respiratory and critical care medicine.

[26]  J. Preiser,et al.  International recommendations for glucose control in adult non diabetic critically ill patients , 2010, Critical care.

[27]  D. Payen,et al.  Bench-to-bedside review: Glucose and stress conditions in the intensive care unit , 2010, Critical care.

[28]  G. Van den Berghe,et al.  Alterations in adipose tissue during critical illness: an adaptive and protective response? , 2010, American journal of respiratory and critical care medicine.

[29]  F. Ovalle.  Hyperglycemia–related mortality in critically ill patients varies with admission diagnosis , 2010 .

[30]  D. Annane,et al.  Bench-to-bedside review: β-Adrenergic modulation in sepsis , 2009, Critical care.

[31]  Christian Trautwein,et al.  Serum resistin levels in critically ill patients are associated with inflammation, organ dysfunction and metabolism and may predict survival of non-septic patients , 2009, Critical care.

[32]  J. Preiser,et al.  Stress hyperglycaemia , 2009, The Lancet.

[33]  M. Laakso,et al.  Effect of fenofibrate on amputation events in people with type 2 diabetes mellitus (FIELD study): a prespecified analysis of a randomised controlled trial , 2009, The Lancet.

[34]  N. Secher,et al.  Blood Lactate is an Important Energy Source for the Human Brain , 2009, Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism.

[35]  G. Fantuzzi.  Adiponectin and inflammation. , 2009, American journal of physiology. Endocrinology and metabolism.

[36]  W. Gormley.  Sodium lactate versus mannitol in the treatment of intracranial hypertensive episodes in severe traumatic brain-injured patients , 2009 .

[37]  G. Biolo,et al.  Treating hyperglycemia improves skeletal muscle protein metabolism in cancer patients after major surgery , 2008, Critical care medicine.

[38]  B. Pedersen,et al.  Effect of short-term intralipid infusion on the immune response during low-dose endotoxemia in humans. , 2008, American journal of physiology. Endocrinology and metabolism.

[39]  S. Brett,et al.  Postprandial ghrelin suppression is exaggerated following major surgery; implications for nutritional recovery , 2007, Nutrition & metabolism.

[40]  B. Ahlman,et al.  Proteasome proteolytic activity in skeletal muscle is increased in patients with sepsis. , 2007, Clinical science.

[41]  P. Pronovost,et al.  Neuromuscular dysfunction acquired during critical illness: a systematic review , 2007, Critical Care.

[42]  J. Pincemail,et al.  [Oxidative stress]. , 2007, Revue medicale de Liege.

[43]  Asli Ozdas,et al.  INSULIN RESISTANCE DESPITE TIGHT GLUCOSE CONTROL IS ASSOCIATED WITH MORTALITY IN CRITICALLY ILL SURGICAL PATIENTS.: 44 , 2006 .

[44]  O. Friedrich.  Critical illness myopathy: what is happening? , 2006, Current opinion in clinical nutrition and metabolic care.

[45]  A. Goldberg,et al.  Protein degradation by the ubiquitin-proteasome pathway in normal and disease states. , 2006, Journal of the American Society of Nephrology : JASN.

[46]  G. Iapichino,et al.  Metabolic treatment of critically ill patients: energy balance and substrate disposal. , 2006, Minerva anestesiologica.

[47]  S. Brett,et al.  Changes in appetite related gut hormones in intensive care unit patients: a pilot cohort study , 2005, Critical care.

[48]  黄亚明,et al.  European Society of Intensive Care Medicine , 2005, Intensive Care Medicine.

[49]  C. Pichard,et al.  Clinical evaluation of hormonal stress state in medical ICU patients: a prospective blinded observational study , 2005, Intensive Care Medicine.

[50]  M. Watford.  Is the small intestine a gluconeogenic organ. , 2005, Nutrition reviews.

[51]  William C Stanley,et al.  Myocardial substrate metabolism in the normal and failing heart. , 2005, Physiological reviews.

[52]  P. Bollaert,et al.  Relation between muscle Na+K+ ATPase activity and raised lactate concentrations in septic shock: a prospective study , 2005, The Lancet.

[53]  H. Woerle,et al.  Paradoxical changes of muscle glutamine release during hyperinsulinemia euglycemia and hypoglycemia in humans: further evidence for the glucose-glutamine cycle. , 2004, Metabolism: clinical and experimental.

[54]  Domenico Vitale,et al.  Multiorgan failure is an adaptive, endocrine-mediated, metabolic response to overwhelming systemic inflammation , 2004, The Lancet.

[55]  C. Pichard,et al.  Nutritional assessment: lean body mass depletion at hospital admission is associated with an increased length of stay. , 2004, The American journal of clinical nutrition.

[56]  V. Mazzaferro,et al.  Nonhepatic glucose production in humans. , 2004, American journal of physiology. Endocrinology and metabolism.

[57]  H. Ogawa,et al.  Possible role of increased oxidant stress in multiple organ failure after systemic inflammatory response syndrome , 2003, Critical care medicine.

[58]  Steven E Wolf,et al.  Hyperglycemia exacerbates muscle protein catabolism in burn-injured patients , 2002, Critical care medicine.

[59]  C. Pichard,et al.  Position paper of the ESICM Working Group on Nutrition and Metabolism , 2002, Intensive Care Medicine.

[60]  S. Brett,et al.  Clinical review: Intensive care follow-up – what has it told us? , 2002, Critical care.

[61]  L. Carbonell,et al.  Oxidative stress in critically ill patients with systemic inflammatory response syndrome , 2002, Critical care medicine.

[62]  John Land,et al.  Association between mitochondrial dysfunction and severity and outcome of septic shock , 2002, The Lancet.

[63]  F. Visser,et al.  Insulin: a wonder drug in the critically ill? , 2002, Critical care.

[64]  J. Ligtenberg,et al.  Hormones in the critically ill patient: to intervene or not to intervene? , 2001, Intensive Care Medicine.

[65]  P. Hasselgren.  Catabolic Response to Stress and Injury: Implications for Regulation , 2000, World Journal of Surgery.

[66]  R. Little,et al.  Insulin resistance and substrate utilization in human endotoxemia. , 2000, The Journal of clinical endocrinology and metabolism.

[67]  D. Wilmore.  Metabolic Response to Severe Surgical Illness: Overview , 2000, World Journal of Surgery.

[68]  G. Hill,et al.  Sequential Metabolic Changes following Induction of Systemic Inflammatory Response in Patients with Severe Sepsis or Major Blunt Trauma , 2000, World Journal of Surgery.

[69]  G. Van den Berghe,et al.  Increased mortality associated with growth hormone treatment in critically ill adults. , 2000, The New England journal of medicine.

[70]  G. Hill,et al.  Components of energy expenditure in patients with severe sepsis and major trauma: a basis for clinical care. , 1999, Critical care medicine.

[71]  X. Leverve.  Energy metabolism in critically ill patients: lactate is a major oxidizable substrate. , 1999, Current opinion in clinical nutrition and metabolic care.

[72]  G. Van den Berghe,et al.  Clinical review 95: Acute and prolonged critical illness as different neuroendocrine paradigms. , 1998, The Journal of clinical endocrinology and metabolism.

[73]  J. Revelly,et al.  Effects of isoenergetic glucose-based or lipid-based parenteral nutrition on glucose metabolism, de novo lipogenesis, and respiratory gas exchanges in critically ill patients. , 1998, Critical care medicine.

[74]  A. Mason,et al.  Effect of ambient temperature on metabolic rate after thermal injury. , 1996, Annals of surgery.

[75]  R. Wolfe,et al.  Pyruvate dehydrogenase inactivity is not responsible for sepsis-induced insulin resistance. , 1996, Critical care medicine.

[76]  S. Matthaei,et al.  Oxygen consumption and resting metabolic rate in sepsis, sepsis syndrome, and septic shock , 1993, Critical care medicine.

[77]  R. S. V. STRACK VAN SCHIJNDEL,et al.  Effects of Recombinant Human Growth Hormone in Patients With Severe Sepsis , 1992, Annals of surgery.

[78]  M. Jeevanandam,et al.  Substrate efficacy in early nutrition support of critically ill multiple trauma victims. , 1992, JPEN. Journal of parenteral and enteral nutrition.

[79]  G. Hill.  Jonathan E. Rhoads Lecture. Body composition research: implications for the practice of clinical nutrition. , 1992, JPEN. Journal of parenteral and enteral nutrition.

[80]  R. Hamill,et al.  Catecholamines predict outcome in traumatic brain injury , 1987, Annals of neurology.

[81]  Marseille,et al.  Société de Réanimation de Langue Française , 1985 .

[82]  H. Bingham,et al.  Physiological and metabolic correlations in human sepsis , 1980 .

[83]  J H Siegel,et al.  Physiological and metabolic correlations in human sepsis. Invited commentary. , 1979, Surgery.