Topical issues of clinical symptoms and diagnostics of septic shock

Abstract

Currently, septic shock remains an unresolved public health problem that leads to serious epidemiological, economic and social problems. Septic shock is a common hemodynamic disorder caused by the interaction between pathogenic microbes and host cells, resulting in developing hypoxia, severe metabolic disorders and multiple organ failure. By now, no unified concept for pathophysiology of septic shock are available. However, the aforementioned data prove that one of the key arms in the pathogenesis is endothelial dysfunction and associated ischemic disorders. In the clinical course of septic shock, three stages are distinguished: the stage of compensation, decompensation as well as the stage of irreversible disorders. The initial stage, or the stage of compensation, is characterized by the activated inflammatory response against infectious agents. Clinically, this stage is characterized by the development of warm shock: fever, dermal hyperemia, hyperventilation, increased cardiac output, and tachycardia. The second stage in developing septic shock is characterized by arising cold shock as a consequence of escalating heart and respiratory failure. The final stage is the development of multiple organ failure manifested by emerging shock organs. Multiple organ failure occurs due to microthrombosis and increasing ischemia, which leads to hypoxia and development of mitochondrial dysfunction in immune cells. At this stage patients are characterized by the progressive cyanosis, developing anuria and intestinal obstruction, as well as altered mental status. Laboratory and instrumental diagnostics of septic shock is a promising approach to examine septic shock. The level of serum C-reactive protein, lactate, and proinflammatory cytokines are not highly specific diagnostic parameters of septic shock, because they can be found in any inflammatory process. Today, the promising diagnostic markers are pentraxin-3, high-density lipoproteins, and phosphatidylcholine. The severity of septic shock can be assessed by determining blood schistocytes, central venous pressure, and the ratio of venous-arterial CO2 and arterial-venous O2 pressure. The following diagnostic methods can be used to determine multiple organ failure: level of serum proenkephalin A119159 and heparin-binding protein; echocardiography, troponin I concentration and N-terminal pro-b-type natriuretic peptides; measuring activity of the renin-angiotensin-aldosterone system. Here we discuss the key aspects of pathogenesis, clinical picture and morphological changes of septic shock. The promising methods for diagnosing the disease and its complications have been studied.