Abstract
Multisystem organ failure remains the predominant cause of death in the surgical intensive care unit. What used to be thought of as isolated organ failure, such as adult respiratory distress syndrome, is now seen as part of the systemic response to injury and of a systemic injury and repair process. Sepsis has become the systemic inflammatory response to invading microorganisms; the same response is now recognized after severe perfusion deficits and in the presence of continuing sources of dead and injured tissue. Once present, the organ failure syndrome continues to have a high mortality rate. From a treatment perspective, it is being recognized that there is probably no “magic bullet”; that regimens will probably be time-dependent and “multiple-drug”; and that the best treatment is prevention. Malnutrition, as a distinct entity from the changes in body composition that occur as a result of disease process, has become a recognized co-factor in patients with persistent hypermetabolism. In addition, the metabolic processes of hypermetabolism have become increasingly well defined and understood. The result of these 2 processes has been the development of metabolic support principles that are distinct from those of nutritional support and are designed to prevent the end-organ changes of malnutrition, prevent the development of substrate-limited metabolism, to support organ structure and function, and to arrest the metabolic processes. The current state of the art has been to learn to do no harm, an outcome reasonably achieved. In addition, several beneficial results have been recognized, including new substrate techniques to better support total body protein synthesis, hepatic protein synthesis, and energy production. Techniques to better support organ structure and function are currently being tested. No techniques are currently available to control proteolysis and the redistribution of skeletal muscle nitrogen. A great deal of research is necessary in this field which is still in its infancy.
Résumé
Le défaillance multiviscérale reste la cause principale des décès dans les unités de soins intensifs. Ce qui dans le passé a été considéré comme là défaillance d'un seul organe, tel le syndrome de détresse respiratoire de l'adulte, n'est en fait qu'une partie de la réponse globale de l'organisme à l'agression et au processus de réparation. L'infection constitue la réponse inflammatoire systémique à l'infestation microbienne. Un mécanisme similaire est observé après insuffisance patente des perfusions et aussi en présence de la persistance de tissue traumatisé et dévitalisé. Quand elle existe la défaillance multiviscérale est grevée d'une haute mortalité. En ce qui concerne les perspectives d'avenir du traitement il est reconnu qu'il n'y a pas de solution magique, que les soins dépendront probablement du facteur temps et de l'emploi de multiples médicaments mais surtout la meilleure thérapeutique répond à la prévention.
La malnutrition en tant qu'entité distincte par rapport aux modifications de l'organisme qui résultent d'un processus pathologique est maintenant un cofacteur reconnu lorsque les malades présentent un hypermétabolisme persistant dont les phénomènes sont de mieux en mieux compris et définis. Le résultat de la malnutrition et de l'hypermétabolisme a été d'aboutir au développement de principes d'un apport métabolique consistant qui sont distincts de l'apport nutritif. Ils ont pour but de prévenir les modifications organiques terminales de la malnutrition et de prévenir le développement de la limitation du métabolisme d'un substrat; de soutenir la structure et la fonction organique et aussi d'arrêter les processus métaboliques. Le but a été d'apprendre à ne pas nuire. On peut considérer qu'il a été atteint. De plus, plusieurs résultats bénéfiques ont été obtenus: nouvelles techniques de préparation de substrats pour soutenir la synthèse protéique organique totale, la synthèse protéique hépatique, la production énergétique. Les techniques pour mieux soutenir la structure et la fonction organique sont en cours d'étude. Actuellement aucune technique permettant le contrôle de la protéolyse et de la redistribution du nitrogène musculaire n'est connue. Une vaste recherche reste à accomplir dans ce champ qui est en cours de défrichement.
Resumen
La falla orgánica multisistémica se mantiene como la causa predominante de muerte en las unidades de cuidado intensivo quirúrgico. Lo que anteriormente habiá sido considerado como falla orgánica aislada, tal como el síndrome de dificultad respiratoria del adulto, es visualizado en la actualidad como parte de la respuesta sistémica a la lesión y como parte de un proceso sistémico de lesión y reparación. La sepsis es considerada como la respuesta inflammatoria sistémica a la presencia de microorganismos invasores; hoy se reconoce el mismo tipo de respuesta después de severos déficits de perfusión, así como en presencia de fuentes continuadas de necrosis y lesión tisular. Una vez establecido, el síndrome de falla orgánica sigue acompañado de una elevada tasa de mortalidad. Desde la perspectiva terapéutica, se acepta que no existe la “bala mágica”; que los regímenes de manejo probablemente son cronodependientes y multifarmacológicos; y por último, que la prevención es la mejor forma de tratamiento.
La desnutrición, como una entidad diferente de los cambios que ocurren en la composición corporal como resultado del proceso patológico, es reconocida como un co-factor en los pacientes con hipermetabolismo persistente. Además, los procesos bioquímicos del hipermetabolismo han logrado ser mejor identificados y comprendidos. El resultado ha sido el desarrollo de principios de soporte metabólico diferentes de los de soporte nutricional, orientados a la prevención de las alteraciones orgánicas de la desnutrición y del desarrollo de estados metabólicos inducidos por limitación de substrato, al soporte de la función y estructura orgánicas y a detener los procesos metabólicos. El estado actual del manejo se fundamenta en aprender a no hacer daño, objetivo que ha sido razonablemente alcanzado. Por lo demás, se han logrado algunos beneficios, incluso nuevas técnicas con el uso de substratos para un mejor soporte de la síntesis proteica corporal total, de la síntesis proteica en el hígado y de la producción de energía. Están en etapa de prueba nuevas técnicas para un mejor soporte de la estructura y función orgánicas. No hay disponibles en la actualidad métodos que puedan controlar la proteolisis y la redistribución del nitrógeno muscular esquelético. Todavía es necesario realizar mucha investigación en este campo que aún se encuentra en su infancia.
Similar content being viewed by others
References
Carrico, C.J., Meakins, J., Marshall, J., Fry, D., Maier, R.: Multiple organ failure syndrome. Arch. Surg.121:196, 1986
Pine, R.W., Wertz, M.J., Lennard, E.S., Dellinger, P., Carrico, C.J.: Determinants of organ malfunction or death in patients with intraabdominal sepsis. Arch. Surg.118:242, 1983
Madoff, R.D., Sharpe, S.M., Fath, J.J., Simmons, R.L., Cerra, F.B.: Prolonged surgical intensive care. Arch. Surg.120:698, 1985
Cerra, F.B., Siegel, J.H., Border, J., Coleman, B.: Correlations between metabolic and cardiopulmonary measurement in patients after trauma, general surgery and sepsis. J. Trauma19:621, 1979
Border, J.H., Chenier, R., McMenamy, R.H.: Multiple systems organ failure: Muscle fuel deficit with visceral protein malnutrition. Surg. Clin. North Am.56:1147, 1976
Wiles, J.B., Cerra, F.B., Siegel, J.H., Border, J.R.: The systemic septic response: Does the organism matter? Crit. Care Med.8:55, 1980
Deutschman, C., Simmons, R.L., Cerra, F.B.: The systemic resonse to cytomegalovirus: Further evidence for a host dependent response. Arch. Surg. (in press)
Tilney, N., Bailey, G., Morgan, A.: Sequential system failure after rupture of abdominal aortic aneurysms. Ann. Surg.118:117, 1973
Cuthbertson, D., Tilstone, W.: Metabolism during the post-injury period. Adv. Clin. Chem.12:1, 1977
Wilmore, D.W., Orlick, L.: Systemic responses to injury and the healing wound. J. Parent. Ent. Nutr.4:147, 1980
Cerra, F.B., Siegel, J.H., Colman, B., Border, J., McMenamy, R.H.: Autocannibalism, a failure of exogenous nutritional support. Ann. Surg.192:570, 1980
Shoemaker, W.: Hemodynamic and oxygen transport patterns in septic shock: Physiologic mechanisms and therapeutic implications. In Prospectives in Sepsis and Septic Shock, W. Sibbald, C. Sprung, editors, Fullerton, California, S.C.C.M., 1985
Powanda, M.: Host metabolic alterations during inflammatory stress as related to nutritional states. Am. J. Vet. Med.41:1905, 1980
Heideman, M., Hugli, T.E.: Anaphylatoxin generation in multisystem organ failure. J. Trauma24:1038, 1984
Alberti, K.G., Batstone, G.F., Foster, K.: Relative role of various hormones in mediating the metabolic response to injury. J. Parent. Ent. Nutr.4:141, 1980
Bessey, P., Waters, J., Soki, T., Wilmore, D.: Combined hormone infusion simulates the metabolic response to injury. Ann. Surg.200:264, 1984
Clowes, G.H.A., Jr., George, B.C., Ville, C.A., Jr., Saravis, C.A.: Muscle proteolysis induced by a circulating peptide in patients with sepsis and trauma. N. Engl. J. Med.308:545, 1983
Lefer, A.: Eicosanoids as mediators of ischemia and shock. Fed. Proc.14:275, 1985
Barracos, V., Rodemann, H.P., Dienarello, C.: Stimulation of muscle protein degradation on PgE2 release by leukocyte pyrogen. N. Engl. J. Med.308:553, 1983
Giovannini, I., Boldrini, G., Castagneto, M., Sganga, G., Nanni, G., Pittiruti, M., Castiglioni, G.: Respiratory quotient and patterns of substrate utilization in human sepsis and trauma. J. Parent. Ent. Nutr.7:226, 1983
Cerra, F.B., Caprioli, J., Siegel, J., Border, J.: Proline metabolism in sepsis, cirrhosis and general surgery: The peripheral energy deficit. Ann. Surg.190:577, 1979
Clowes, G.H.A., O'Donnell, T.F., Blackburn, G.: Energy metabolism and proteolysis in traumatized and septic man. Surg. Clin. North Am.56:1169, 1976
Elwyn, D.H., Kinney, J.M., Juvanandum, M.: Influence of increasing carbohydrate intake on glucose kinetics in injured patients. Ann. Surg.190:117, 1979
Long, C., Kinney, J., Geiger, J.: Nonsuppressability of gluconeogenesis in septic patients. Metabolism25:193, 1976
Rich, A.J., Wright, P.D.: Ketosis and nitrogen excretion in undernourished surgical patients. J. Parent. Ent. Nutr.3:350, 1979
Birkhan, R., Long, C., Fitkin, D.L., Geiger, J., Blakemore, W.: A comparison of the effects of skeletal trauma and surgery on the ketosis of starvation in man. J. Trauma21:513, 1981
Watters, J., Bessey, P., Wilmore, D.: Catabolic hormones suppress adaptation to starvation. Surg. Forum35:82, 1984
Lindholm, M., Rossner, S.: Rate of elimination of the intralipid fat emulsion from the circulation in ICU patients. Crit. Care Med.10:740, 1983
Cerra, F.B., Siegel, J.H., Border, J., Coleman, B.: The hepatic failure of sepsis: Cellular vs. substrate. Surgery86:409, 1979
Robin, A.P., Askanayi, J., Greenwood, M., Elwyn, D., Kenney, J.: Lipoproteinlipase activity in surgical patients: Effects of trauma and sepsis. Surgery90:401, 1981
Birkhan, R., Long, C., Fitkin, D., Geiger, J., Blakemore, W.: Effects of major skeletal trauma on whole body protein turnover in man measured by 1, 14C leucine. Surgery88:294, 1980
Long, C., Birkhan, R., Geiger, J.: Contribution of skeletal muscle protein in elevated rates of whole-body protein catabolism in trauma patients. Am. J. Clin. Nutr.34:1087, 1981
Powell-Tuck, J., Fern, E., Garlich, P., Waterlow, J.: The effect of surgical trauma and insulin on whole body protein turnover in parenterally fed undernourished patients. Hum. Nutr. Clin. Nutr.38:11, 1984
Long, C.L., Jeevanaudan, M., Kinney, J.M.: Whole body protein synthesis and catabolism in septic man. Am. J. Clin. Nutr.30:1340, 1977
Carpentier, Y., Askanazi, J., Elwyn, D., Gump, F., Kinney, J.: The effect of carbohydrate intake on lipolysis rate in depleted patients. Metabolism29:974, 1980
Wolfe, R., Allsop, J., Burke, J.: Glucose metabolism in man: Responses to intravenous glucose infusion. Metabolism28:210, 1979
Imamura, M., Clowes, G.H., Blackburn, G.: Liver metabolism and gluconeogenesis in trauma and sepsis. Surgery77:868, 1975
Burke, J.F., Wolfe, R., Mullaney, J.: Glucose requirements and possible hepatic and respiratory abnormalities following excessive glucose intake. Ann. Surg.190:274, 1979
Nordenstrom, J., Jeevanandam, M., Elwyn, D., Kinney, J.: Increasing glucose intake during total parenteral nutrition increases norepinephrine excretion in trauma and sepsis. Clin. Physiol.1:525, 1981
Askanazi, J., Rosenbaums, H., Hyman, A., Elwyn, D., Kinney, J.: Respiratory changes induced by high glucose loads of total parenteral nutrition. J.A.M.A.243:1444, 1980
Askanazi, J., Carpentier, Y., Elwyn, D., Kenney, J.: Influence of total parenteral nutrition on fuel utilization in injury and sepsis. Ann. Surg.191:40, 1980
Alden, P.B., Svingen, B.A., Johnson, S.B., Konstantinides, F.N., Holman, R.T., Cerra, F.B.: Partial correction by exogenous lipid of abnormal patterns of polyunsaturated fatty acids in plasma phospholipids of stressed and septic surgical patients. Surgery100:671, 1986
Nordenstrom, J., Askanazi, J., Elwyn, D.H., Kenney, J.: Nitrogen balance during total parenteral nutrition: Glucose vs. fat. Ann. Surg.197:27, 1983
Kirkpatrick, J., Dann, M., Haynes, M.: The therapeutic advantages of a balanced nutrition support system. Surgery89:370, 1981
Barke, S., Holm, L.: Nitrogen-sparing effect of fat emulsion compared with glucose in the postoperative period. Acta Chir. Scand.142:423, 1976
Jacobs, D.H., McNamara, D.J., Ahrens, E.: Alterations in dietary fat affect monocyte fatty acid composition, prostaglandin production and natural killer cell function. A.S.P.E.N. Clin. Cong. 1985
Katy, D., Knittle, J.: Effect of medium and long chain triglyceride on human adipose tissue prostaglandin production. A.S.P.E.N. Clin. Cong. 1985
Moyer, F., Border, J.R., McMenamy, R., Cerra, F.B.: Multiple systems organ failure. V. Alterations in plasma protein profile in septic-trauma-effect of intravenous amino acids. J. Trauma21:645, 1981
Clowes, G.H.A., Jr., Heideman, M., Lindberg, B., Randall, H.T., Hirsch, E.F., Cha, C.-J., Martin, H.: Effects of parenteral alimentation on amino acid metabolism in septic patients. Surgery88:531, 1980
McMenamy, R., Birkhan, R., Oswald, R., Cerra, F.B., Border, J. Multiple systems organ failure. II. The effect of infusion of amino acids and glucose. J. Trauma21:228, 1981
Cerra, F.B., Upson, D., Angelico, R., Wiles, C., III, Lyons, J., Paysinger, J.: Branched chains support postoperative protein synthesis. Surgery92:192, 1982
Cerra, F.B., Mazuski, J., Teasley, K., Nuwer, N., Lysne, J., Shronts, E., Konstantinides, F.: Nitrogen retention in critically ill patients is proportional to the branched chain amino acid load. Crit. Care Med.11:775, 1983
Cerra, F.B., Mazuski, J., Chute, E., Teasley, K., Konstantinides, N.: Branched chain metabolic support. Ann. Surg.199:286, 1984
Bower, R.H., Muggin-Sullam, M., Vallgren, S., Fischer, J.: Branched chain amino acid-enriched solutions in the septic patient: A randomized, prospective trial. Ann. Surg.203:13, 1986
Cerra, F.B., Shronts, E.P., Konstantinides, N., Thoele, S., Konstantinides, F., Teasley, K., Lysne, J.: Enteral feeding in sepsis: A prospective, randomized, double-blind trial. Surgery98:632, 1985
Pingleton, S.K., Hadgima, S.K.: Enteral alimentation and gastrointestinal bleeding in mechanically ventilated patients. Crit. Care Med.11:13, 1983
Saito, H., Trocki, O., Alexander, J.: Comparison of immediate postburn enterai vs. parenteral nutrition. A.S.P.E.N. Clin. Cong. 1985
Alverdy, J.C., Chi, H.S.: The effect of route of nutrient administration on the secretory immune system. A.S.P.E.N. Clin. Cong., 1985
Deutschman, C.S., Raup, S., Peterson, M., Cerra, F.: Transient elevations of hepatic enzymes following resumption of gut feedings in ICU patients. Nutr. Intl. (in press)
Chaudry, I.H., Clemens, M., Baue, A.: Cellular and subcellular function in sepsis and septic shock. In Prospective in Sepsis and Septic Shock, W. Sibbald, C. Sprung, editors, Fullerton, California, S.C.C.M., 1985
Author information
Authors and Affiliations
Rights and permissions
About this article
Cite this article
Cerra, F.B. The hypermetabolism organ failure complex. World J. Surg. 11, 173–181 (1987). https://doi.org/10.1007/BF01656400
Issue Date:
DOI: https://doi.org/10.1007/BF01656400