跳转至: 导航搜索
多重器官衰竭(Multiple organ dysfunction syndrome )
ICD-9 995.92
EMedicine med/3372
MeSH D009102

器官衰竭多重器官衰竭症候群或稱多重器官衰竭Multiple organ dysfunction syndrome, MODS)、多器官衰竭多臟器功能衰竭,是老年人逝世的重要原因之一,大多是70歲以上的長者。例如有氣管心臟肺臟肝臟腎臟等重要身體器官慢性病,是病患的器官機能惡化到相當程度,在沒有外在介入的情形下,體內無法維持稳态的情形。

Although Irwin-Rippe cautions in 2005 that the use of "multiple organ failure" or "multisystem organ failure" should be avoided,[1] both Harrison's (2015) and Cecil's (2012) medical textbooks still use the terms "multi-organ failure" and "multiple organ failure" in several chapters, and do not use "multiple organ dysfunction syndrome" at all.






The condition usually results from infection, injury (accident, surgery), hypoperfusion and hypermetabolism英语hypermetabolism. The primary cause triggers an uncontrolled inflammatory response. Sepsis is the most common cause. Sepsis may result in septic shock. In the absence of infection, a sepsis-like disorder is termed systemic inflammatory response syndrome英语systemic inflammatory response syndrome (SIRS). Both SIRS and sepsis could ultimately progress to multiple organ dysfunction syndrome. However, in one-third of the patients no primary focus can be found.[1] Multiple organ dysfunction syndrome is well established as the final stage of a continuum: SIRS英语systemic inflammatory response syndrome + infection U+2192.svg sepsis U+2192.svg severe sepsis U+2192.svg Multiple organ dysfunction syndrome. Currently, investigators are looking into genetic targets for possible gene therapy to prevent the progression to Multiple organ dysfunction syndrome. Some authors have conjectured that the inactivation of the transcription factors NF-κB and AP-1 would be appropriate targets in preventing sepsis and SIRS英语systemic inflammatory response syndrome.[2] These two genes are pro-inflammatory. However, they are essential components of a normal healthy immune response英语immune response, so there is risk of increasing vulnerability to infection, which can also cause clinical deterioration.

Some have developed a mouse model sepsis via cecal ligation and puncture (CLP).[3] Male Balb/c英语Balb/c mice subjected to CLP were given an IL-10英语Interleukin 10-carrying vector or an empty control vector. Lung, Liver and kidney tissue destruction were measured by assessing myeloperoxidase and malonialdehyde activity; these last two are endogenous oxidizing compounds produced during tissue inflammation. The authors assessed the level neutrophil infiltration in lung and liver tissue. IL-10英语Interleukin 10 protein expression was measured using immunohistochemistry. The expression of Tumor necrosis factor-alpha (TNF-α) mRNA was measured at 3, 8 and 24 hours after CLP using reverse transcription polymerase chain reaction. Their results show significantly reduced organ damage by IL-10英语Interleukin 10 gene transfer, as quantified by reduced myeloperoxidase activity in the lung, liver and kidney. The malonialdehyde level was not affected by the transfer into the liver. The livers of the mice infected with the adenoviral vector showed reduced neutrophil activity. The lung and kidney samples in mice carrying the gene showed lower expression of TNF-α mRNA. The investigators concluded that increased IL-10英语Interleukin 10 expression significantly reduced sepsis-induced Multiple organ injury.




The most popular hypothesis by Deitch to explain MODS in critically ill patients is the gut hypothesis.[4] Due to splanchnic英语splanchnic hypoperfusion and the subsequent mucosal ischaemia there are structural changes and alterations in cellular function. This results in increased gut permeability英语gut permeability, changed immune function of the gut and increased translocation of bacteria. Liver dysfunction leads to toxins escaping into the systemic circulation and activating an immune response. This results in tissue injury and organ dysfunction.[1]


Gram-negative infections in MODS patients are relatively common, hence endotoxins have been advanced as principal mediator in this disorder. It is thought that following the initial event cytokines are produced and released. The pro-inflammatory mediators are: tumor necrosis factor-alpha (TNF-α), interleukin-1, interleukin-6, thromboxane A2, prostacyclin, platelet activating factor, and nitric oxide.[1]


As a result of macro- and microvascular changes insufficient supply of oxygen occurs. Hypoxemia causes cell death and organ dysfunction.[1]


According to findings of Professor Zsolt Balohh and his team at University of Newcastle (Australia), mitochondrial DNA is the leading cause of severe inflammation due to massive amount of Mitochondrial DNA that leaks into the blood stream due to cell death into the blood stream of patients that survived major trauma.

Mitochondrial DNA is very similar-looking like bacterial DNA. And if bacteria is triggering leukocytes, maybe the mitochondrial DNA does the same. When confronted with bacteria, white blood cells, or neutrophil granulocyte, behave like predatory spiders. They spit out a web, or net, to trap the invaders, then hit them with a deadly oxidative blast, forming neutrophil extracellular traps英语neutrophil extracellular traps (NETs).

This result in catastrophic immune response leading to multiple organ dysfunction syndrome.[5][6]


Since in most cases no primary cause is found, the condition could be part of a compromised homeostasis involving the previous mechanisms.[1]


The European Society of Intensive Care organized a consensus meeting in 1994 to create the "Sepsis-Related Organ Failure Assessment (SOFA)" score to describe and quantitate the degree of organ dysfunction in six organ systems. Using similar physiologic variables the Multiple Organ Dysfunction Score was developed.[1]

Four clinical phases have been suggested:


At present there is no agent that can reverse the established organ failure. Therapy therefore is limited to supportive care, i.e. safeguarding hemodynamics, and respiration. Maintaining adequate tissue oxygenation is a principal target. Starting enteral nutrition within 36 hours of admission to an intensive care unit has reduced infectious complications.[1]


Mortality varies from 30% to 100% where the chance of survival is diminished as the number of organs involved increases. Since the 1980s the mortality rate has not changed.[1] In patients with sepsis, septic shock, or multiple organ dysfunction syndrome that is due to major trauma, the rs1800625 polymorphism is a functional single nucleotide polymorphism, a part of the receptor for advanced glycation end products (RAGE) transmembrane receptor英语transmembrane receptor gene (of the immunoglobulin superfamily英语immunoglobulin superfamily) and confers host susceptibility to sepsis and MODS in these patients.[7]


The historical origin of the concept of MODS is as follows. For many years, some patients were loosely classified as having sepsis or the sepsis syndrome. In more recent years, these concepts have been refined – so that there are specific definitions of sepsis – and two new concepts have been developed: the SIRS英语systemic inflammatory response syndrome and MODS.[1]


  1. ^ 1.00 1.01 1.02 1.03 1.04 1.05 1.06 1.07 1.08 1.09 1.10 1.11 Irwin & Rippe. Intensive Care Medicine. (原始内容存档于November 7, 2005). 
  2. ^ Matsuda N, Hattori Y. Systemic inflammatory response syndrome (SIRS): molecular pathophysiology and gene therapy. J. Pharmacol. Sci. 2006, 101 (3): 189–98. PMID 16823257. doi:10.1254/jphs.CRJ06010X. 
  3. ^ Kabay B, Kocaefe C, Baykal A, 等. Interleukin-10 gene transfer: prevention of multiple organ injury in a murine cecal ligation and puncture model of sepsis. World J Surg. 2007, 31 (1): 105–15. PMID 17171483. doi:10.1007/s00268-006-0066-9. 
  4. ^ Deitch EA. Simple intestinal obstruction causes bacterial translocation in man. Arch Surg英语Arch Surg 1989; 124: 699-701. PMID 2730322
  5. ^ McIlroy DJ; 等. Mitochondrial DNA neutrophil extracellular traps are formed after trauma and subsequent surgery. Journal of Critical Care. 2014, 29 (6): 1133. PMID 25128442. doi:10.1016/j.jcrc.2014.07.013. 
  6. ^ MULTIPLE ORGAN FAILURE. ABC Australia. 7 August 2014. 
  7. ^ Zeng, Ling; 等. Rs1800625 in the receptor for advanced glycation end products gene predisposes to sepsis and multiple organ dysfunction syndrome in patients with major trauma. Critical Care. 2015, 19 (6). PMC 4310192. PMID 25572180. doi:10.1186/s13054-014-0727-2.