Aktuelle Ernährungsmedizin 2016; 41(02): 113-117
DOI: 10.1055/s-0042-102160
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© Georg Thieme Verlag KG Stuttgart · New York

Die metabolische Selbstzerstörung des kritisch kranken Patienten (Teil II): Die Bedeutung der modernen Medizin und therapeutische Konsequenzen[1] [2]

Metabolic Self-Destruction in Critically Ill Patients (Part II): The Importance of Modern Medical Care and Therapeutic Consequences
W. H. Hartl
Klinik für Allgemeine, Viszeral-, Transplantations-, Gefäß- und Thoraxchirurgie, Campus Großhadern, LMU München
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Further Information

Publication History

Publication Date:
11 April 2016 (online)

Zusammenfassung

Die moderne Medizin (Intensiv- und Notfallmedizin) ermöglicht das akute Überleben eines Patienten auch nach sehr schwerer Homöostasestörung. Dieser Fortschritt hat jedoch die Nützlichkeit von prinzipiell vorteilhaften, adaptativen metabolischen Reaktionen (Hyperglykämie, Muskeleiweißkatabolismus) dahingehend modifiziert, dass diese nun in übersteigertem Ausmaß ausgelöst werden und dadurch selbstzerstörerische Wirkungen entfalten können. Potenziell schädliche Nebenwirkungen der metabolischen Reaktionen resultieren aus deren Quantität, welche durch Intensität und Dauer der Homöostasestörung bestimmt wird. Adjuvante Therapien wie die künstliche Ernährung können metabolischen Extremreaktionen auf keinen Fall verhindern, sondern allerhöchstens helfen, sekundären Schaden zu minimieren. Eine effektive metabolische Therapie ist nur dann möglich, wenn gleichzeitig die Auslösemechanismen (Trauma, Shock, Sepsis) so aggressiv wie möglich bekämpft werden, um dadurch die metabolischen Triggermechanismen bereits an ihrem Ursprung zu unterbrechen.

Abstract

Modern emergency and intensive care medicine allows patients to survive even extreme disturbances of their homeostasis. This progress, however, has modified utility of originally advantageous metabolic reactions (hyperglycemia, muscle protein catabolism) to a point where their activation is exaggerated thereby revealing auto-destructive elements. Potentially detrimental side effects of metabolic reactions result from their quantity which is determined by extent and duration of the disturbance of homeostasis. Self-destructive metabolic responses cannot be prevented by adjuvant therapies such as artificial nutrition which may only help to ameliorate secondary metabolic damage. Effective treatment is only possible by a simultaneous aggressive therapy of underlying pathologies (such as shock, trauma or infection) thereby interrupting secondary metabolic trigger mechanisms at an early stage.

1 Im Original publiziert unter: Hartl WH, Jauch KW. Metabolic self-destruction in critically ill patients: Origins, mechanisms and therapeutic principles. Nutrition 2014 Mar; 30 (3): 261 – 267


2 Nachdruck aus: DIVI Journal 2015; 6: 102 – 107


 
  • Literatur

  • 1 Hartl WH. Die metabolische Selbstzerstörung des kritisch kranken Patienten (Teil I): Evolutionsbiologische Hintergründe, Mechanismen und Sinnhaftigkeit. Aktuel Ernahrungsmed 2016; 41: 40-44
  • 2 Fu CY, Wang YC, Wu SC et al. Higher glucose on admission is associated with need for angioembolization in stable pelvic fracture. Am J Emerg Med 2012; 30: 26-31
  • 3 Heath DF. Glucose, insulin and other plasma metabolites shortly after injury. J Accid Emerg Med 1994; 11: 67-77
  • 4 Pomerantz WJ, Hashkes PJ, Succop PA et al. Relationship between serum glucose and injury severity score in childhood trauma. J Pediatr Surg 1999; 34: 1494-1498
  • 5 Nakamura M, Oda S, Sadahiro T et al. Correlation between high blood IL-6 level, hyperglycemia, and glucose control in septic patients. Crit Care 2012; 16: R58
  • 6 Thorell A, Nygren J, Ljungqvist O. Insulin resistance: a marker of surgical stress. Curr Opin Clin Nutr Metab Care 1999; 2: 69-78
  • 7 Gletsu N, Lin E, Zhu JL et al. Increased plasma interleukin 6 concentrations and exaggerated adipose tissue interleukin 6 content in severely obese patients after operative trauma. Surgery 2006; 140: 50-57
  • 8 Reeds PJ, Jahoor F. The amino acid requirements of disease. Clin Nutr 2001; 20 (Suppl. 01) 15-22
  • 9 Long CL, Schaffel N, Geiger JW et al. Metabolic response to injury and illness: estimating energy and protein needs from indirect calorimetry and nitrogen balance. JPEN 1979; 3: 452-456
  • 10 Elwyn DH. Protein metabolism and requirements in the critically ill patient. Crit Care Clin 1987; 3: 57-69
  • 11 Wilmore DW. Metabolic management of the critically ill. New York: Plenum Press; 1977: 149
  • 12 Cuesta JM, Singer M. The stress response and critical illness: A review. Crit Care Med 2012; 40: 3283-3289
  • 13 Gentile LF, Cuenca AG, Efron PA et al. Persistent inflammation and immunosuppression: a common syndrome and new horizon for surgical intensive care. J Trauma Acute Care Surg 2012; 72: 1491-1501
  • 14 Doig GS, Simpson F, Sweetman EA et al. Early PN Investigators of the ANZICS Clinical Trials Group. Early parenteral nutrition in critically ill patients with short-term relative contraindications to early enteral nutrition: a randomized controlled trial. JAMA 2013; 309: 2130-2138
  • 15 National Heart, Lung, and Blood Institute Acute Respiratory Distress Syndrome (ARDS) Clinical Trials Network. Rice TW, Wheeler AP, Thompson BT et al. Initial trophic vs full enteral feeding in patients with acute lung injury: the EDEN randomized trial. JAMA 2012; 307: 795-803
  • 16 Heyland D, Muscedere J, Wischmeyer PE et al. Canadian Critical Care Trials Group. A randomized trial of glutamine and antioxidants in critically ill patients. N Engl J Med 2013; 368: 1489-1497
  • 17 Van Zanten AR, Sztark F, Kaisers UX et al. High-protein enteral nutrition enriched with immune-modulating nutrients vs standard high-protein enteral nutrition and nosocomial infections in the ICU: a randomized clinical trial. JAMA 2014; 312: 514-524
  • 18 Casaer MP, Mesotten D, Hermans G et al. Early versus late parenteral nutrition in critically ill adults. N Engl J Med 2011; 365: 506-517
  • 19 NICE-SUGAR Study Investigators. Finfer S, Chittock DR, Su SY et al. Intensive versus conventional glucose control in critically ill patients. N Engl J Med 2009; 360: 1283-1297
  • 20 Wolfe RR. Sepsis as a modulator of adaptation to low and high carbohydrate and low and high fat intakes. Eur J Clin Nutr 1999; 53 (Suppl. 01) S136-142
  • 21 Chambrier C, Laville M, Rhzioual Berrada K et al. Insulin sensitivity of glucose and fat metabolism in severe sepsis. Clin Sci (Lond) 2000; 99: 321-328
  • 22 Long CL, Nelson KM. Nutritional requirements based on substrate fluxes in trauma. Nutr Res 1993; 13: 1459-1478
  • 23 Larsson J, Lennmarken C, Mårtensson J et al. Nitrogen requirements in severely injured patients. Br J Surg 1990; 77: 413-416
  • 24 Ishibashi N, Plank LD, Sando K et al. Optimal protein requirements during the first 2 weeks after the onset of critical illness. Crit Care Med 1998; 26: 1529-1535
  • 25 Shaw JH, Wildbore M, Wolfe RR. Whole body protein kinetics in severely septic patients. The response to glucose infusion and total parenteral nutrition. Ann Surg 1987; 205: 288-294
  • 26 Rennie MJ. Anabolic resistance in critically ill patients. Crit Care Med 2009; 37 (Suppl. 10) S398-399
  • 27 Jensen GL, Mirtallo J, Compher C et al. International Consensus Guideline Committee. Adult starvation and disease-related malnutrition: a proposal for etiology-based diagnosis in the clinical practice setting from the International Consensus Guideline Committee. JPEN J Parenter Enteral Nutr 2010; 34: 156-159
  • 28 Schetz M, Casaer MP, Van den Berghe G. Does artificial nutrition improve outcome of critical illness?. Crit Care 2013; 17: 302
  • 29 Stroud M. Protein and the critically ill; do we know what to give?. Proc Nutr Soc 2007; 66: 378-383
  • 30 Heidegger CP, Berger MM, Graf S et al. Optimisation of energy provision with supplemental parenteral nutrition in critically ill patients: a randomised controlled clinical trial. Lancet 2013; 381: 385-393
  • 31 Mirnezami R, Kinross JM, Vorkas PA et al. Implementation of molecular phenotyping approaches in the personalized surgical patient journey. Ann Surg 2012; 255: 881-889
  • 32 Siegelaar SE, Hermanides J, Oudemans-van Straaten HM et al. Mean glucose during ICU admission is related to mortality by a U-shaped curve in surgical and medical patients: a retrospective cohort study. Crit Care 2010; 14: R224
  • 33 Hart DW, Wolf SE, Chinkes DL et al. Effects of early excision and aggressive enteral feeding on hypermetabolism, catabolism, and sepsis after severe burn. J Trauma 2003; 54: 755-761
  • 34 Rüttinger D, Kuppinger D, Hölzwimmer M et al. Acute prognosis of critically ill patients with secondary peritonitis: the impact of the number of surgical revisions, and of the duration of surgical therapy. Am J Surg 2012; 204: 28-36
  • 35 Chaudery M, Clark J, Wilson MH et al. Traumatic intra-abdominal hemorrhage control: has current technology tipped the balance toward a role for prehospital intervention?. J Trauma Acute Care Surg 2015; 78: 153-163
  • 36 Disseldorp LM, Nieuwenhuis MK, Van Baar ME et al. Physical fitness in people after burn injury: a systematic review. Arch Phys Med Rehabil 2011; 92: 1501-1510
  • 37 Carli F. Postoperative metabolic stress: interventional strategies. Minerva Anestesiol 2006; 72: 413-418
  • 38 Deitch EA. Gut-origin sepsis: evolution of a concept. Surgeon 2012; 10: 350-356
  • 39 Nieves E, Tobón LF, Ríos DI et al. Bacterial translocation in abdominal trauma and postoperative infections. J Trauma 2011; 71: 1258-1261
  • 40 Yatsunenko T, Rey FE, Manary MJ et al. Human gut microbiome viewed across age and geography. Nature 2012; 486: 222-227
  • 41 Kamada N, Chen G, Núñez G. A complex microworld in the gut: Harnessing pathogen-commensal relations. Nat Med 2012; 18: 1190-1191
  • 42 Boyer AF, Kollef MH. Probiotics for ventilator-associated pneumonia: the need for a large, multicenter, randomized controlled trial. Chest 2013; 143: 590-592
  • 43 Petrof EO, Dhaliwal R, Manzanares W et al. Probiotics in the critically ill: a systematic review of the randomized trial evidence. Crit Care Med 2012; 40: 3290-3302
  • 44 Van der Meer JWM, Vandenbroucke-Grauls CMJE. Resistance to selective decontamination: the jury is still out. Lancet Infect Dis 2013; 13: 282-283
  • 45 Besselink MG, van Santvoort HC, Buskens E et al. Dutch Acute Pancreatitis Study Group. Probiotic prophylaxis in predicted severe acute pancreatitis: a randomised, double-blind, placebo-controlled trial. Lancet 2008; 371: 651-659
  • 46 Khoruts A, Sadowsky MJ. Therapeutic transplantation of the distal gut microbiota. Mucosal Immunol 2011; 4: 4-7
  • 47 Van Nood E, Vrieze A, Nieuwdorp M et al. Duodenal infusion of donor feces for recurrent Clostridium difficile. N Engl J Med 2013; 368: 407-415
  • 48 Petrof EO, Gloor GB, Vanner SJ et al. Stool substitute transplant therapy for the eradication of Clostridium difficile infection: ‘RePOOPulating’ the gut. Microbiome 2013; 1: 3
  • 49 Bonetto A, Aydogdu T, Jin X et al. JAK/STAT3 pathway inhibition blocks skeletal muscle wasting downstream of IL-6 and in experimental cancer cachexia. Am J Physiol Endocrinol Metab 2012; 303: E410-421
  • 50 Kumar A, Bhatnagar S, Paul PK. TWEAK and TRAF6 regulate skeletal muscle atrophy. Curr Opin Clin Nutr Metab Care 2012; 15: 233-239
  • 51 Bhatnagar S, Kumar A. The TWEAK-Fn14 system: breaking the silence of cytokine-induced skeletal muscle wasting. Curr Mol Med 2012; 12: 3-13