Insulinresistenz: Bedeutung in Anästhesie und Intensivmedizin – Wie viel Kalorien und Insulin braucht der kritisch Kranke?

Zusammenfassung

Metabolismus und Ernährungstherapie des kritisch kranken Patienten sind dynamische Parameter im Verlauf der schweren Erkrankung, die Einfluss auf den Blutzuckerspiegel nehmen. Nachdem zunächst ein Vorteil hinsichtlich des Überlebens einer intensivierten Insulintherapie in einer Studie gezeigt wurde, konnte dies in den folgenden großen Studien nicht mehr bestätigt werden. Es wurde sogar eine erhöhte Sterblichkeit berichtet. Die Hyperglykämie des Intensivpatienten sollte vor dem Hintergrund des Stress-Stoffwechsels betrachtet werden und ist möglicherweise ein adaptiver Prozess. Neben der endogenen Stressantwort verändern auch exogene Maßnahmen, wie die Therapie mit Katecholaminen und Glukokortikoiden, die Wirkung von Insulin und den Glukosemetabolismus. Hypo- und hyperkalorische Ernährung können ebenfalls die Wirksamkeit der Insulintherapie beeinflussen. Ziel der Ernährungstherapie sollte eine an den Zustand des Patienten angepasste Kalorienzufuhr sein und sowohl eine hyperkalorische Versorgung als auch ein Energiedefizit vermeiden. Unter diesen Rahmenbedingungen sollte die Insulintherapie so eingesetzt werden, dass der gewählte Zielkorridor des Blutzuckers erreicht werden kann, ohne zu einer Steigerung des Risikos für Hypoglykämien zu führen.

Abstract

Metabolism and nutrition of the critical ill are dynamic parameters of the severe disease influencing the blood glucose concentration. After the finding of increased survival in an initial study in tight glucose control, further large multicenter trials could not show such a benefit and even an increased mortality has been found. Hyperglycemia may be a feature of the stress metabolism and is possibly an adaptive process. Next to the endogenous response, therapy with catecholamines and glucosteroids impacts the response to insulin and the glucose metabolism. Hypo- and hypercaloric nutrition also interact with the insulin therapy. Nutritional therapy should be adapted to the actual state of the patient avoiding hypercaloric feeding and an energy deficit. Using this framework, therapy with insulin may be used to achieve a targeted range of glucose avoiding an increased risk of hypoglycaemia.

Schlüsselwörter:

Insulin - Ernährung - Kalorienziel - Blutzuckersteuerung

Key words:

insulin - nutrition - caloric goal - glycemic control

Kernaussagen

• Am Beginn der Ernährungstherapie ist die Energiezufuhr hypokalorisch, allerdings sollte das Kaloriendefizit nicht aus den Augen verloren werden.

• Die aktuellen Leitlinien lehnen eine hyperkalorische Ernährung in der akuten Phase ab.

• In experimentellen Studien sind auch negative Wirkungen von hyperkalorischer Ernährung und Hyperinsulinämie beschrieben.

• Das Konzept der enteralen und metabolischen Toleranz beschreibt die Anpassung der Ernährung an den aktuellen Zustand des Patienten.

• Durch Nutzung von Protokollen kann die Qualität der Ernährung gesteigert werden.

• Eine Einstellung des Blutzuckers in den Bereich 80–110 mg/dl führte in Studien zu einer deutlichen Steigerung der Hypoglykämien.

• Eine Hyperglykämie im Stress beruht auf einem Missverhältnis zwischen Glukosefreisetzung und Insulinwirkung und ist möglicherweise ein adaptiver Prozess.

Literatur

• 1 van den Berghe G et al.. Intensive insulin therapy in the critically ill patients.  N Engl J Med. 2001;  345 1359-1367
• 2 Zerr KJ et al.. Glucose control lowers the risk of wound infection in diabetics after open heart operations.  Ann Thorac Surg. 1997;  63 356-361
• 3 Brunkhorst FM et al.. Intensive insulin therapy and pentastarch resuscitation in severe sepsis.  N Engl J Med. 2008;  358 125-139
• 4 Brunkhorst FM et al.. Intensive insulin therapy in patients with severe sepsis and septic shock is associated with an increased rate of hypoglycemia – results from a randomized multicenter study (VISEP).  Infection. 2005;  33 19-20
• 5 Annane D et al.. Corticosteroid treatment and intensive insulin therapy for septic shock in adults: a randomized controlled trial.  JAMA. 2010;  303 341-348
• 6 Griesdale DE et al.. Intensive insulin therapy and mortality among critically ill patients: a meta-analysis including NICE-SUGAR study data.  CMAJ. 2009;  180 821-827
• 7 Marik PE, Preiser JC. Toward understanding tight glycemic control in the ICU: a systematic review and metaanalysis.  Chest. 2010;  137 544-551
• 8 Stoner HB et al.. The effect of sepsis on the oxidation of carbohydrate and fat.  Br J Surg. 1983;  70 32-35
• 9 Gore DC et al.. Lactic acidosis during sepsis is related to increased pyruvate production, not deficits in tissue oxygen availability.  Ann Surg. 1996;  224 97-102
• 10 Revelly JP et al.. Lactate and glucose metabolism in severe sepsis and cardiogenic shock.  Crit Care Med. 2005;  33 2235-2240
• 11 Chambrier C et al.. Insulin sensitivity of glucose and fat metabolism in severe sepsis.  Clin Sci (Lond). 2000;  99 321-328
• 12 Matsuda N et al.. Nuclear factor-kappaB decoy oligodeoxynucleotides ameliorate impaired glucose tolerance and insulin resistance in mice with cecal ligation and puncture-induced sepsis.  Crit Care Med. 2009;  37 2791-2799
• 13 Callahan LA, Supinski GS. Downregulation of diaphragm electron transport chain and glycolytic enzyme gene expression in sepsis.  J Appl Physiol. 2005;  99 1120-1126
• 14 Callahan LA, Supinski GS. Sepsis induces diaphragm electron transport chain dysfunction and protein depletion.  Am J Respir Crit Care Med. 2005;  172 861-868
• 15 Hargrove DM et al.. Epinephrine-induced increase in glucose turnover is diminished during sepsis.  Metabolism. 1989;  38 1070-1076
• 16 Spitzer JJ et al.. Alterations in the metabolic control of carbohydrates in sepsis.  Prog Clin Biol Res. 1989;  308 545-561
• 17 Mizock BA. Alterations in fuel metabolism in critical illness: hyperglycaemia.  Best Pract Res Clin Endocrinol Metab. 2001;  15 533-551
• 18 Mehta VK et al.. Low-dose interleukin 1 and tumor necrosis factor individually stimulate insulin release but in combination cause suppression.  Eur J Endocrinol. 1994;  130 208-214
• 19 Singer P et al.. ESPEN guidelines on parenteral nutrition: intensive care.  Clin Nutr. 2009;  28 387-400
• 20 Villet S et al.. Negative impact of hypocaloric feeding and energy balance on clinical outcome in ICU patients.  Clin Nutr. 2005;  24 502-509
• 21 Faisy C et al.. Impact of energy deficit calculated by a predictive method on outcome in medical patients requiring prolonged acute mechanical ventilation.  Br J Nutr. 2009;  101 1079-1087
• 22 Alberda C et al.. The relationship between nutritional intake and clinical outcomes in critically ill patients: results of an international multicenter observational study.  Intensive Care Med. 2009;  35 1728-1737
• 23 Finfer S et al.. Intensive versus conventional glucose control in critically ill patients.  N Engl J Med. 2009;  360 1283-1297
• 24 Heyland DK et al.. Total parenteral nutrition in the critically ill patient: a meta-analysis.  JAMA. 1998;  280 2013-2019
• 25 Peck MD et al.. Low protein diets improve survival from peritonitis in guinea pigs.  Ann Surg. 1989;  209 448-454
• 26 Alexander JW et al.. A new model for studying nutrition in peritonitis. The adverse effect of overfeeding.  Ann Surg. 1989;  209 334-340
• 27 Kreymann G et al.. DGEM-Leitlinie Enterale Ernährung: Intensivmedizin.  Aktuel Ernaehr Med. 2003;  28
• 28 Soop M et al.. Euglycemic hyperinsulinemia augments the cytokine and endocrine responses to endotoxin in humans.  Am J Physiol Endocrinol Metab. 2002;  282 1276-1285
• 29 Krogh-Madsen R et al.. Effect of hyperglycemia and hyperinsulinemia on the response of IL-6, TNF-alpha, and FFAs to low-dose endotoxemia in humans.  Am J Physiol Endocrinol Metab. 2004;  286 766-772
• 30 Cury MF Boaventura et al.. Toxicity of a Soybean Oil Emulsion on Human Lymphocytes and Neutrophils.  JPEN J Parenter Enteral Nutr. 2006;  30 115-123
• 31 Bi MH et al.. Induction of lymphocyte apoptosis in a murine model of acute lung injury-modulation by lipid emulsions.  Shock. 2010;  33 179-188
• 32 Scheiermann P et al.. Effects of short-term infusion of lipid emulsions on pro-inflammatory cytokines and lymphocyte apoptosis in septic and non-septic rats.  Br J Nutr. 2011;  27 1-6
• 33 Hotchkiss RS, Nicholson DW. Apoptosis and caspases regulate death and inflammation in sepsis.  Nat Rev Immunol. 2006;  6 813-822
• 34 Elke G et al.. Current practice in nutritional support and its association with mortality in septic patients – results from a national, prospective, multicenter study.  Crit Care Med. 2008;  36 1762-1767
• 35 Devos P et al.. Glucose, insulin and myocardial ischaemia.  Curr Opin Clin Nutr Metab Care. 2006;  9 131-139
• 36 Howell NJ et al.. Glucose-insulin-potassium reduces the incidence of low cardiac output episodes after aortic valve replacement for aortic stenosis in patients with left ventricular hypertrophy: results from the Hypertrophy, Insulin, Glucose, and Electrolytes (HINGE) trial.  Circulation. 2011;  123 170-177
• 37 Kreymann KG et al.. [Nutrition of critically ill patients in intensive care].  Internist (Berl). 2007;  48 1084-1092
• 38 Mentec H et al.. Upper digestive intolerance during enteral nutrition in critically ill patients: frequency, risk factors, and complications.  Crit Care Med. 2001;  29 1955-1961
• 39 Reinhart K et al.. [Prevention, diagnosis, treatment, and follow-up care of sepsis. First revision of the S2k Guidelines of the German Sepsis Society (DSG) and the German Interdisciplinary Association for Intensive and Emergency Care Medicine (DIVI)].  Anaesthesist. 2010;  59 347-370
• 40 Moghissi ES et al.. American Association of Clinical Endocrinologists and American Diabetes Association consensus statement on inpatient glycemic control.  Endocr Pract. 2009;  15 353-369
• 41 Hermanides J et al.. Hypoglycemia is associated with intensive care unit mortality.  Crit Care Med. 2010;  38 1430-1434
• 42 Egi M et al.. The interaction of chronic and acute glycemia with mortality in critically ill patients with diabetes.  Crit Care Med. 2011;  39 105-111
• 43 Barr J et al.. Outcomes in critically ill patients before and after the implementation of an evidence-based nutritional management protocol.  Chest. 2004;  125 1446-1457
• 44 Rood E et al.. Use of a computerized guideline for glucose regulation in the intensive care unit improved both guideline adherence and glucose regulation.  J Am Med Inform Assoc. 2005;  12 172-180
• 45 Eslami S et al.. Implementing glucose control in intensive care: a multicenter trial using statistical process control.  Intensive Care Med. 2010;  36 1556-1565
• 46 Damiani G et al.. The effectiveness of computerized clinical guidelines in the process of care: a systematic review.  BMC Health Serv Res. 2010;  10 2
• 47 Chase JG et al.. Impact of human factors on clinical protocol performance: a proposed assessment framework and case examples.  J Diabetes Sci Technol. 2008;  2 409-416
• 48 Meyfroidt G, Keenan al at. Dynamic characteristics of blood glucose time series during the course of critical illness: effects of intensive insulin therapy and relative association with mortality.  Crit Care Med. 2010;  38 1021-1029
• 49 Egi M et al.. Hypoglycemia and outcome in critically ill patients.  Mayo Clin Proc. 2010;  85 217-224
• 50 Eslami S et al.. Glucose variability measures and their effect on mortality: a systematic review.  Intensive Care Med. [Epub ahead of print] 2011; 
• 51 Bagshaw SM et al.. The impact of early hypoglycemia and blood glucose variability on outcome in critical illness.  Crit Care. 2009;  13
• 52 Monnier L et al.. Activation of oxidative stress by acute glucose fluctuations compared with sustained chronic hyperglycemia in patients with type 2 diabetes.  JAMA. 2006;  295 1681-1687