Anti-Inflammatory properties of Insulin and its Use in Critical Care Patients
Apart from its use in the management of hyperglycemia, insulin has recently been associated with attenuation of systemic inflammatory response owing to its anti-inflammatory properties hence making it an important drug in critical care patients. This discussion explores anti-inflammatory effect of insulin in critical care patients. The discussion details the documented impacts of insulin on critical care populations as well as the beneficial effects of insulin in critical care. Analysis of relevant literature is applied to determine the anti-inflammatory causes of insulin as well as the manner in which insulin therapy could be applied in enhancing the end results for patients in intensive care units experiencing an inflammatory response to illness. From Pender’s Health Promotion Model (HPM), prevention and early detection of inflammatory response is viewed. Pender’s Health promotion Model explores the complex relationship between pathological, sociological, as well as psychological functions that hinder or encourage intensive insulin therapy for patients in need of critical care.
Insulin has long been applied in regulating hyperglycemia as well as in the treatment of diabetes mellitus since its discovery in 1921 by Banting and Best (Dandona, 2011). Hyperglycemia, which refers to high blood sugar, is a frequent impediment that occurs in critical care patient populations leading to a number of health issues. In addition to its ability to lower blood glucose levels, insulin has recently been associated with anti-inflammatory properties (Chaudhuri et al., 2004). The mechanism of action, however, is still unknown and is under investigation (Chaudhuri et al., 2004).
Several patients with critical health problems, principally the septic patients as well as ones with injuries to the myocardium, portrays an inflammatory reaction following an infarct to the myocardial tissue (Chaudhuri et al., 2004). The inflammatory surge in the critical care population is triggered by inflammation, trauma as well as infection. As a result of the inflammatory process, the systemic inflammatory response syndrome (SIRS) develops initiated by internal and external toxins. Interleukin-1 and (IL-1) tissue necrosis factor-a (TNF-a) are initially produced and triggers numerous cascades. IL-1 & TNF-a impacts the endothelial surfaces causing the production of tissue factor, that facilitates coagulation by prompting thrombin formation. Despite it being a coagulatory mediator, tissue factor is a pro-inflammatory mediator and is associated with the development of SIRS in critically injured patients. Systemic inflammatory response syndrome (SIRS) is advanced by the correlation between inflammation and coagulation (Burdette, Parilo, Kaplan, & Bailey, 2010).
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