Multiple organ dysfunction syndrome (MODS) is altered organ function in an acutely ill patient requiring medical intervention to achieve homeostasis.

The Condition results from infection, injury (accident, surgery), hypoperfusion and hypermetabolism. The primary cause triggers an uncontrolled inflammatory response. Sepsis is the most common cause of Multiple Organ Dysfunction Syndrome and may result in septic shock. In the absence of infection, a sepsis-like disorder is termed 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. 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 would be appropriate targets in preventing sepsis and SIRS. These two genes are pro-inflammatory. However, they are essential components of a normal healthy immune response, so there is risk of increasing vulnerability to infection, which can also cause clinical deterioration.

The most popular hypothesis by Deitch to explain MODS in critically ill patients is the gut hypothesis. Due to splanchnic hypoperfusion and the subsequent mucosal ischaemia there are structural changes and alterations in cellular function. This results in increased 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.

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.

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

Mitochondrial DNA resembles bacterial DNA. If bacteria triggers leukocytes, mitochondrial DNA may do the same. When confronted with bacteria, white blood cells, or neutrophil granulocytes, 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 (NETs).

This results in catastrophic immune response leading to multiple organ dysfunction syndrome. At present, there is no drug or device that can reverse organ failure that has been judged by the health care team to be medically and/or surgically irreversible (organ function can recover, at least to a degree, in patients whose organs are very dysfunctional, where the patient has not died; and some organs, like the liver or the skin, can regenerate better than others), with the possible exception of single or multiple organ transplants or the use of artificial organs or organ parts, in certain candidates in specific situations. Therapy therefore, is usually mostly 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.

Journal of Intensive and Critical Care Nursing is a newly launched Open access, Peer-reviewed scientific journal which will be dedicated to promote the scientific community dealing with utmost care of critically ill patients in the area of Critical Care Nursing, Intensive Care Medicine, Emergency and Critical Care. Manuscripts can be uploaded online at Editorial Tracking System https://www.scholarscentral.org/submissions/intensive-critical-care-nursing.html or send an email attachment to nursingcare@emedsci.com

zoe kemp
Journal Manager
Journal of Intensive and Critical Care Nursing
Email: nursing@emedicalsci.org