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April 2016 Study Finds That a Compromised Immune System after Major Surgery can Lead to Post-Surgical Mortality
Study Finds That a Compromised Immune System after Major Surgery can Lead to Post-Surgical Mortality
NUI Galway research study discovers the partial or complete suppression of an individual’s immune system following major surgery can lead to post-surgical mortality
Scientists at NUI Galway completed a research study which has revealed that post-traumatic immunosuppression (PTI) is one of the leading causes of post-surgical mortality and makes patients vulnerable to hospital-acquired infections, multiple organ failure and many other complications. The study was published today (29 April) in the international journal Clinical & Translational Immunology by Nature Publishing Group.
Lead author of the study, Professor Rhodri Ceredig, Director of the National Centre for Biomedical Engineering Science at NUI Galway, said: “An evolutionarily sophisticated and balanced immune system exists in our body whose equilibrium can be altered by different physical, environmental or psychological stresses. Trauma, including major surgery and accidental injury, leads to post-traumatic immunosuppression (PTI) increasing a patient’s vulnerability to hospital-acquired infections. Florence Nightingale initially raised this question during the Crimean War and great efforts were then made to improve hospital hygiene. Although sanitation has been improved in hospitals, an equivalent phenomenon of post-traumatic deaths from systemic infections persists to this day. ”
Professor Ceredig added, “More and more new infections are still threatening major trauma patients. An important question remains, ‘why do wounded patients acquire systemic infections even in a hygienic environment?’ Research over the past two decades suggests that following trauma, a patient’s immune system is imbalanced, thereby increasing their vulnerability to acquired infections. However, the underlying mechanisms of PTI are poorly defined and as yet, there are no universally accepted treatments. Our study, carried out by Dr Md. Nahidul Islam at NUI Galway in collaboration with Professor Benjamin Bradley of the University of Bristol, used total knee replacement surgery as a model of sterile surgical trauma.”
At sites of tissue damage, whether it be following major surgery or accidental injury, many bioactive molecules are produced. These molecules include so-called ‘danger’ signals expressed by damaged cells that in turn stimulate production by local, undamaged, cells of very potent, soluble hormone-like molecules. Some of these molecules dampen, whereas others stimulate inflammation. It is thought the overall purpose of these early local events is to create an environment favourable to tissue healing.
However, some of the molecules produced locally enter the blood stream and have effects on distant organs such as the liver, brain and organs of the immune system. The overall effect of these is to dampen immune responses thereby rendering the patient more susceptible to oportunistic infections. The origin of such infections can be either external or internal, for example from an imbalance of gut bacteria or failure of the body to control low-grade infection.
In some respects, the profile of bioactive molecules circulating in the blood following sterile surgical intervention can resemble that seen in the early stages of serious bacteriological infections. Hospital-acquired infections and their treatments pose a huge economic burden on healthcare services and are a cause of serious morbidity and even mortality. One key finding of this study was that additional research is necessary in order to be able to distinguish immunosuppression following sterile trauma from that seen in the early stages of non-sterile infection, thereby providing guidelines for the initiation of appropriate treatments.
This study was supported by Science Foundation Ireland, the Irish Research Council and North Bristol NHS Trust.
To read the full study in Clinical & Translational Immunology visit: http://www.nature.com/cti/journal/v5/n4/full/cti201613a.html