#PAGE_PARAMS# #ADS_HEAD_SCRIPTS# #MICRODATA#

Multiple organ dysfunction syndrome (MODS) – from molecules to the bedside


Authors: Chvojka Jiří;  Raděj Jaroslav;  Karvunidis Thomas;  Kroužecký Aleš;  Novák Ivan;  Matějovič Martin
Authors‘ workplace: I. interní klinika, Jednotka intenzivní péče, Univerzita Karlova v Praze, Lékařská fakulta v Plzni a Fakultní nemocnice Plzeň
Published in: Anest. intenziv. Med., 21, 2010, č. 3, s. 158-164
Category: Intensive Care Medicine - Review Article

Overview

Multiple organ dysfunction syndrome (MODS) is one of the most common causes of death in the intensive care units. This review summarizes recent progress in our understanding of the pathophysiological mechanisms leading to MODS including the concept of mitochondrial dysfunction and apoptosis. The crucial therapeutic measures are early and adequate haemodynamic resuscitation together with elimination of the causative factors. Prevention of iatrogenic insults, potentially worsening MODS, should be an integral part of the therapeutic approach.

Keywords:
multiple organ dysfunction syndrome – sepsis – shock – pathophysiology – therapy – intensive care – organ support


Sources

1. Tilney, N. L. et al. Sequential system failure after rupture of abdominal aortic aneurysms: an unsolved problem in postoperative care. Ann. Surg., 1973, 178, p. 117–122.

2. Baue, A. E. Multiple, progressive, or sequential systems failure. A syndrome of the 1970s. Arch. Surg., 1975, 110, p. 779–781.

3. Fry, D. E. et al. Multiple system organ failure. The role of uncontrolled infection. Arch. Surg., 1980, 115, p. 136–140.

4. Goris, R. J. et al. Multiple-organ failure. Generalized autodestructive inflammation? Arch. Surg., 1985, 120, p. 1109–1115.

5. Bone, R. C. et al. Definitions for sepsis and organ failure and guidelines for the use of innovative therapies in sepsis. The ACCP/SCCM Consensus Conference Committee. American College of Chest Physicians/Society of Critical Care Medicine. Chest, 1992, 101, p. 1644–1655.

6. Angus, D. C. et al. Epidemiology of severe sepsis in the United States: analysis of incidence, outcome, and associated costs of care. Crit. Care Med., 2001, 29, p. 1303–1310.

7. Vincent, J. L. et al. Sepsis in European intensive care units: results of the SOAP study. Crit. Care Med., 2006, 34, p. 344–353.

8. Warren, H. S. Toll-like receptors. Crit. Care Med., 2005, 33, p. S457–S459.

9. Bianchi, M. E. DAMPs, PAMPs and alarmins: all we need to know about danger. J. Leukoc. Biol., 2007, 81, p. 1–5.

10. Tang, A. H. et al. Pivotal advance: endogenous pathway to SIRS, sepsis, and related conditions. J. Leukoc. Biol., 2007, 82, p. 282–285.

11. Condliffe, A. M. et al. Neutrophil priming: pathophysiological consequences and underlying mechanisms. Clin. Sci. (Lond), 1998, 94, p. 461–471.

12. Rittirsch, D. et al. Harmful molecular mechanisms in sepsis. Nat. Rev. Immunol., 2008, 8, p. 776–787.

13. Hauser, B. et al. Nitric oxide synthase inhibition in sepsis? Lessons learned from large-animal studies. Anesth. Analg., 2005, 101, p. 488–498.

14. Vincent, J. L. et al. Microvascular dysfunction as a cause of organ dysfunction in severe sepsis. Crit. Care, 2005, 9 Suppl. 4, p. S9–12.

15. Sakr, Y. et al. Persistent microcirculatory alterations are associated with organ failure and death in patients with septic shock. Crit. Care Med., 2004, 32, p. 1825–1831.

16. Trzeciak, S. et al. Early increases in microcirculatory perfusion during protocol-directed resuscitation are associated with reduced multi-organ failure at 24 h in patients with sepsis. Intensive Care Med., 2008, 34, p. 2210–2217.

17. Jhanji, S. et al. Microvascular flow and tissue oxygenation after major abdominal surgery: association with post-operative complications. Intensive Care Med., 2009, 35, p. 671–677.

18. Singer, M. et al. Multiorgan failure is an adaptive, endocrine-mediated, metabolic response to overwhelming systemic inflammation. Lancet, 2004, 364, p. 545–548.

19. Protti, A. et al. Bench-to-bedside review: potential strategies to protect or reverse mitochondrial dysfunction in sepsis-induced organ failure. Crit. Care, 2006, 10, p. 228.

20. Fischer, U. et al. New approaches and therapeutics targeting apoptosis in disease. Pharmacol. Rev., 2005, 57, p. 187–215.

21. Hotchkiss, R. S. et al. Apoptosis and caspases regulate death and inflammation in sepsis. Nat. Rev. Immunol., 2006, 6, p. 813–822.

22. Clark, J. A. et al. Intestinal crosstalk: a new paradigm for understanding the gut as the “motor” of critical illness. Shock, 2007, 28, p. 384–393.

23. Swank, G. M. et al. Role of the gut in multiple organ failure: bacterial translocation and permeability changes. World J. Surg., 1996, 20, p. 411–417.

24. Rivers, E. et al. Early goal-directed therapy in the treatment of severe sepsis and septic shock. N. Engl. J. Med., 2001, 345, p. 1368–1377.

25. Dellinger, R. P. et al. Surviving Sepsis Campaign: international guidelines for management of severe sepsis and septic shock: 2008. Crit. Care Med., 2008, 36, p. 296–327.

26. Liu, K. D. et al. Advances in critical care for the nephrologist: acute lung injury/ARDS. Clin. J. Am. Soc. Nephrol., 2008, 3, p. 578–586.

27. Ranieri, V. M. et al. Mechanical ventilation as a mediator of multisystem organ failure in acute respiratory distress syndrome. JAMA, 2000, 284, p. 43–44.

28. Malhotra, A. Low-tidal-volume ventilation in the acute respiratory distress syndrome. N. Engl. J. Med., 2007, 357, p. 1113–1120.

29. Brunkhorst, F. M. et al. Intensive insulin therapy and pentastarch resuscitation in severe sepsis. N. Engl. J. Med., 2008, 358, p. 125–139.

30. Bouchard, J. et al. Fluid accumulation and acute kidney injury: consequence or cause. Curr. Opin. Crit Care, 2009, 15, p. 509–513.

31. Abuelo, J. G. Normotensive ischemic acute renal failure. N. Engl. J. Med., 2007, 357, p. 797–805.

32. Patel, B. M. et al. Beneficial effects of short-term vasopressin infusion during severe septic shock. Anesthesiology, 2002, 96, p. 576–582.

33. Mullens, W. et al. Importance of venous congestion for worsening of renal function in advanced decompensated heart failure. J. Am. Coll. Cardiol., 2009, 53, p. 589–596.

34. Chvojka, J. et al. Renal haemodynamic, microcirculatory, metabolic and histopathological responses to peritonitis-induced septic shock in pigs. Crit Care, 2008, 12, p. R164.

35. Sykora, R. et al. Hemopurification in sepsis: current view. Vnitr. Lek., 2008, 54, p. 1000–1005.

36. Coca, S. G. et al. Long-term risk of mortality and other adverse outcomes after acute kidney injury: a systematic review and meta-analysis. Am. J. Kidney Dis., 2009, 53, p. 961–973.

37. Kumar, A. et al. Duration of hypotension before initiation of effective antimicrobial therapy is the critical determinant of survival in human septic shock. Crit. Care Med., 2006, 34, p. 1589–1596.

38. Kumar, A. et al. Initiation of inappropriate antimicrobial therapy results in a fivefold reduction of survival in human septic shock. Chest, 2009, 136, p. 1237–1248.

39. Kreymann, K. G. et al. ESPEN Guidelines on Enteral Nutrition: Intensive care. Clin. Nutr., 2006, 25, p. 210–223.

40. Singer, P. et al. ESPEN Guidelines on Parenteral Nutrition: intensive care. Clin. Nutr., 2009, 28, p. 387–400.

41. Angstwurm, M. W. et al. Selenium in Intensive Care (SIC): results of a prospective randomized, placebo-controlled, multiple-center study in patients with severe systemic inflammatory response syndrome, sepsis, and septic shock. Crit. Care Med., 2007, 35, p. 118–126.

42. Finfer, S. et al. Intensive versus conventional glucose control in critically ill patients. N. Engl. J. Med., 2009, 360, p. 1283–1297.

43. Ronco, C. et al. A wearable artificial kidney: dream or reality? Nat. Clin. Pract. Nephrol., 2008, 4, p. 604–605.

44. Okamoto, E. et al. Development of a miniature motor-driven pulsatile LVAD driven by a fuzzy controller. J. Artif. Organs, 2007, 10, p. 158–164.

45. Cattaneo, G. et al. Compact intra- and extracorporeal oxygenator developments. Perfusion, 2004, 19, p. 251–255.

46. Fissell, W. H. et al. Dialysis and nanotechnology: now, 10 years, or never? Blood Purif., 2007, 25, p. 12–17.

47. Handley, H. H. et al. Slow continuous intravenous plasmapheresis (SCIP): clinical applications and hemostability of extracorporeal ultrafiltration. Contrib. Nephrol., 2005, 149, p. 334–342.

48. Handley, H. H. et al. Artificial in vivo biofiltration: slow continuous intravenous plasmafiltration (SCIP) and artificial organ support. Int. J. Artif. Organs, 2004, 27, p. 186–194.

49. Ding, F. et al. The bioartificial kidney and bioengineered membranes in acute kidney injury. Nephron Exp. Nephrol., 2008, 109, p. e118–e122.

50. McKenzie, T. J. et al. Artificial and bioartificial liver support. Semin. Liver Dis., 2008, 28, p. 210–217.

Labels
Anaesthesiology, Resuscitation and Inten Intensive Care Medicine
Login
Forgotten password

Enter the email address that you registered with. We will send you instructions on how to set a new password.

Login

Don‘t have an account?  Create new account

#ADS_BOTTOM_SCRIPTS#