View clinical trials related to Multiorgan Failure.
Filter by:Tramadol is opioid analgesic widely used to treat moderate to severe pain. It is metabolized by cytochrome CYP2D6 into two major metabolites: pharmacologically active metabolite O-desmethyltramadol (M1) and inactive N-desmethyltramadol (M2), respectively. Tramadol kinetics in a population of patients undergoing major abdominal surgical procedures, and in patients with a greater or lesser degree of organic failure, is still not well researched. The investigators will measure plasma concentrations of tramadol and its metabolites after usual tramadol doses in ICU patients after major abdominal surgery. Also analgesic affect and side effect of tramadol will be recorded.
Assessing the impact of the nursing technique applied at the insertion site of the central venous catheter using hydrophilic methacrylate gel (HMG) and 2% Chlorhexidine (CHG) upon the incidence of inflammatory complications when treating the surrounding of the central venous catheter.
Multiorgan failure (MOF) as a result of any critical condition is a complex set of immunological and biochemical interactions leading to death in patients who are effectively subjected to primary resuscitation (correction of circulatory hypoxia in trauma and blood loss, restoration of blood circulation after operations with artificial circulation. The frequency of MOF varies depending on the primary diagnosis of a critical patient and, according to a number of authors, is 60% for sepsis, and for severe co-occurring trauma up to 40% of all critical patients. However, if one remembers that the MOF is verified only by clinical scales of assessing the severity of the patient's condition, which presupposes the presence of the already existing pathophysiological mechanisms of MOF as multi-organ dysfunction, it is possible to declare a 100% presence of MOF in all critical patients. The data of Graetz et al (2016) show that none of the available three variants of pathophysiological mechanisms (anomaly of microcirculation, persistent inflammation, immune suppression and catabolism, cellular hibernation and staning) have been unambiguously demonstrated, which also reflected the lack of effectiveness of methods therapy, proposed, based on the pathogenesis options for MOF. A so-called danger-model has a special place in the genesis of the persistence of the MOF, which justifies an active search for distress-associated and pathogen-associated molecular patterns for their objectification and probable elimination. The systemic inflammatory response in patients. included in the study, is not a primary infection. It is also important to determine the role of danger-associated molecular patterns (DAMP) in the genesis of immune suppression as the leading immunological phenotype of MOF in later periods and to evaluate the relationship between DAMP expression and immunosuppressive cells of monocyte origin. The study has a mixed (retro- and prospective) character.