Acute and Chronic Systemic Inflammation: Features and Differences in the Pathogenesis, and Integral Criteria for Verification and Differentiation

Abstract

Currently, there is rationale for separating the systemic manifestations of classical inflammation from systemic inflammation (SI) itself as an independent form of the general pathological process underlying the pathogenesis of the most severe acute and chronic diseases. With this aim in view, we used integral scales of acute and chronic SI (ChSI), including the following blood plasma parameters: interleukins 6, 8, 10; tumor necrosis factor alpha; C-reactive protein; D-dimer; cortisol; troponin I; myoglobin. The presence of multiple organ dysfunction according to the SOFA score was also taken into account. The effectiveness of the scales was tested in groups of intensive care patients during different periods of acute trauma, sepsis, and septic shock. The ChSI scale was applicable under systemic autoimmune diseases, chronic purulent infections, chronic limb threatening ischemia, and end-stage renal disease of various genesis. The number of examined patients was 764 in total. The scales allowed us to verify specific phases of acute SI and identify pathogenetic risk factors of lethal outcomes, as well as the most severe variants of the chronic pathologies course. These scales are open adaptable systems (in terms of the nomenclature and choice of indicators). They are primarily intended for scientific research. However, the SI verification methodology presented in this paper may be useful for developing advanced criteria for assessing both the typical links in the pathogenesis of many diseases and the severity of the overall condition of patients for clinical practice.

Shock-Associated Systemic Inflammation in Amniotic Fluid Embolism, Complicated by Clinical Death

“…There is no single generally accepted classification of shock and, in general, shock conditions are classified based on the characteristics of the causative factor, the leading pathogenesis link, and the identification of the most damaged organ system or the most disturbed link of homeostasis [ 27 ]. A priori, SI can be associated with septic shock, but not with all the variants of sepsis, such as the infectious variant of MODS [ 9 , 10 , 13 ]. In acute blood loss, the hypovolemic shock at the initial stages of its development is not associated with SI and can be effectively managed by replacement fluid therapy.…”

“…Usually, when SI occurs as a result of the gradual transformation of classical inflammation into systemic inflammation (the “punching variant of SI”), it takes a long time (days and sometimes weeks) to develop [ 9 , 10 , 11 , 13 ]. In less favorable variants, a primary and, in some cases, secondary phlogogenic stroke develops, and the depressive phase is realized in the form of a tendency or interphase transition.…”

“…In less favorable variants, a primary and, in some cases, secondary phlogogenic stroke develops, and the depressive phase is realized in the form of a tendency or interphase transition. A more telling case is when the depressive phase is observed as a torpid shock or MODS, in prolonged/subacute sepsis (as in tertiary peritonitis) [ 9 , 10 , 13 ]. In this case, the depressive phase extends over time in the form of a “long depressive tail” (up to several weeks), with manifestations of septic shock and, as a rule, with a fatal outcome.…”

“…Microcirculatory disorders are the core of SI pathogenesis, which can clinically manifest themselves as a complex set of resuscitation syndromes, including disseminated intravascular coagulation (DIC), vascular shock, acute respiratory distress syndrome (ARDS), and multiple organ dysfunction syndrome (MODS) [ 9 , 10 , 11 ]. The development of SI is not attributable to local foci of inflammation but is due to the action of damaging factors in the intravascular environment, regardless of their nature and the way they are generalized in the body [ 12 , 13 ]. In general, SI plays an important role in the pathogenesis of many critical conditions, including the pathogenesis of severe COVID-19 variants [ 14 , 15 ].…”

“…To verify and determine the specific phases of SI, we used the SI scale that had been previously tested in a study of acute infectious and aseptic critical states [ 9 , 13 , 20 , 21 ], and its derivative also studied in severe chronic diseases [ 13 , 20 , 22 ]. As the onset of a critical condition in the patients was sudden and required urgent resuscitation measures, the monitoring of the SI signs was performed already in an intensive therapy setting, including artificial lung ventilation (ALV), administration of vasopressors, and infusion therapy.…”