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

Abstract

Background: Amniotic fluid embolism (AFE) is one of the main causes of maternal mortality in developed countries. The most critical AFE variants may be considered from the perspective of systemic inflammation (SI), a general pathological process that includes high levels of systemic inflammatory response, neuroendocrine system distress, microthrombosis, and multiple organ dysfunction syndrome (MODS). This research work aimed to characterize the dynamics of super-acute SI using four clinical case studies of patients with critical AFE. Methods: In all the cases, we examined blood coagulation parameters, plasma levels of cortisol, troponin I, myoglobin, C-reactive protein, IL-6, IL-8, IL-10, and TNF-α, and calculated the integral scores. Results: All four patients revealed the characteristic signs of SI, including increased cytokine, myoglobin, and troponin I levels, changes in blood cortisol, and clinical manifestations of coagulopathy and MODS. At the same time, the cytokine plasma levels can be characterized not only as hypercytokinemia, and not even as a “cytokine storm”, but rather as a “cytokine catastrophe” (an increase of thousands and tens of thousands of times in proinflammatory cytokine levels). AFE pathogenesis involves rapid transition from the hyperergic shock phase, with its high levels of a systemic inflammatory response over to the hypoergic shock phase, characterized by the mismatch between low systemic inflammatory response values and the patient’s critical condition. In contrast to septic shock, in AFE there is a much more rapid succession of SI phases. Conclusion: AFE is one of the most compelling examples for studying the dynamics of super-acute SI.

Exploring the Pathophysiology of Long COVID: The Central Role of Low-Grade Inflammation and Multisystem Involvement

“…This may result from classical inflammation’s systemic inflammatory response dysfunction, impaired barrier function, or severe systemic alterations unrelated to the classical inflammation focus [ 84 , 85 ]. Common manifestations include refractory shock, resuscitation syndromes such as desensitized intravascular coagulation, secondary acute respiratory distress syndrome, and rapidly progressive multi-organ failure [ 85 , 86 , 87 ].…”

“…-Requires markers of systemic response and endotheliosis -CRP levels (3 to 10 mg/L) insufficient alone -Persistent infection and chronic immune activation [117,118] Systemic hyperinflammation, as a special form of general pathological process, is a priori a dysfunctional process, and arises primarily from systemic microcirculatory disorders in response to significant systemic damage [84]. This may result from classical inflammation's systemic inflammatory response dysfunction, impaired barrier function, or severe systemic alterations unrelated to the classical inflammation focus [84,85]. Common manifestations include refractory shock, resuscitation syndromes such as desensitized intravascular coagulation, secondary acute respiratory distress syndrome, and rapidly progressive multi-organ failure [85][86][87].…”

Atherosclerosis and Inflammation: Insights from the Theory of General Pathological Processes

“…To verify SI as a general pathological process, certain levels of hypercytokinemia [547] need to be established and compared to the severity of other SI phenomena [66]. The development of acute SI is also typical for the aseptic refractory shock [548] and severe polytrauma variants [509].…”