MD, Professor, Retired, Renton, WA, USA
Sepsis (S) has become one of the global problems of world health care in recent years, taking a position among the nosologies that are leading in terms of morbidity, mortality and expenditure of physical, moral and financial resources [1,2]. If a few years ago the total number of S cases in the world was 30 million, of which 6 million ended in death [3-5], then by now the total figure has grown to 49.8 million, and the number of deaths to 11 million [1]. In Europe and North America, i.e. in the conditions of the most advanced health care systems, hospital mortality in S was 20% a few years ago [3,5], but recently this figure has grown to 40% [6]. At the same time, in the USA S is the leading cause of hospital mortality [7].
Although there is an initiative to present S as a separate syndrome, this condition does not arise as a spontaneous phenomenon and has its own causes and origins, uniting a variety of diseases under one identical picture. The most common cause of S development over many years has been acute non-specific inflammation of the lung (ANSIL) or acute pneumonia (AP). If several years ago AP accounted for up to 40% of the primary causes of S [8-10], then in recent years this figure has already reached 60% and even exceeds this limit [11,12]. Such dynamics force an in-depth critical analysis of the characteristics of this disease.
The results of modern treatment of the so-called community-acquired pneumonia (CAP) indicate its low efficiency. Thus, 25% of patients hospitalized with CAP in general departments are transferred to intensive care units (ICU) within the first two days due to deterioration of their condition [13]. After hospitalization, in 40% of cases, against the background and despite the treatment, S develops [14]. In most cases, septic shock (SS) can develop despite intensive treatment, although at the time of hospitalization its signs were absent [15]. Such results are shocking in themselves, aren’t they?
The main goals in achieving success in the treatment of AP are determined by the so-called microbial concept of the disease that prevails today. This concept, which originated in the late 19th - first half of the last century [16], has become deeply rooted in the professional worldview over the long period of antibiotic use. According to the prevailing point of view, today the main cause of the development of AP is still considered to be its pathogen, and etiotropic drugs remain the main therapeutic hope. The beneficial potential of etiotropic therapy is determined only by the spectrum of action of the selected drug, which must correspond to the sensitivity of a specific pathogen. At the same time, it is well known that etiotropic drugs are not able to directly influence the mechanisms of inflammatory transformation of body tissues and, moreover, on the functional disorders that arise in this case. In the context of the dominant role of antibiotics, the expected effect of their action can manifest itself only as an indirect effort of the body itself, which initially requires a certain wait-and-see period, right? In the case of aggressive development of the inflammatory process, relying on indirect-acting drugs is an irreparable loss of precious time (See above paragraph no 3).
Igor Klepikov. “The Problem of Sepsis in Acute Inflammation of Lung Tissue”. EC Pulmonology and Respiratory Medicine 14.4 (2025): 01-13.
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