Article Type : Opinion Article
Authors : Igor Klepikov
Modern ideas about the nature of acute inflammatory
processes in the lungs are focused on the leading significance of the etiology
of the disease. The predominance of this concept defines etiotropic therapy as
the basis for providing medical care to this category of patients. In fact, the
causative agent of acute pneumonia in most patients remains unknown or the
accuracy of its diagnosis is questionable. At the same time, the targeted use
of etiotropic drugs is always delayed due to the delay in the results of
microbiological diagnostics. Recently, these difficulties of etiotropic therapy
have been compounded by an increase in the number of patients with viral lung
inflammation and the lack of effective antiviral drugs.
Modern ideas about the
nature of acute inflammatory processes in the lungs are focused on the leading
significance of the etiology of the disease. The predominance of this concept
defines etiotropic therapy as the basis for providing medical care to this
category of patients. In fact, the causative agent of acute pneumonia in most
patients remains unknown or the accuracy of its diagnosis is questionable. At
the same time, the targeted use of etiotropic drugs is always delayed due to
the delay in the results of microbiological diagnostics. Recently, these
difficulties of etiotropic therapy have been compounded by an increase in the
number of patients with viral lung inflammation and the lack of effective
antiviral drugs.
The paradoxical and
illogical nature of the situation is supplemented by a discrepancy between the
intended and actual goals of diagnosis and treatment. Declaring the leading
role of pathogens in the development and severity of AP, the assessment of the
condition of patients and their further observation within the existing concept
of views are based on signs and tests that are due to the pathogenesis of the
disease and do not depend directly on its etiology. For example, a cardinal
diagnostic test such as an x-ray reflects inflammatory changes in the lung
tissue and their dynamics, without having absolute etiological signs. Changes
in the parameters of respiration, gas exchange and hemodynamics are the result
of impaired lung function as a result of inflammation, regardless of its
pathogen.
In other words, the AP
pathogen plays the role of a burning match that ignites the hearth, and then
the fire continues to spread. But the most important mistake arising from the
existing system of views on the nature of the disease is that by focusing on
the fight against infection, we lose sight of the unique features of the lesion
of the lung tissue in contrast to all other localities of inflammation. The
concentration of efforts on the infectious origin does not exclude the use of
General Therapeutic measures instead of strictly specific ones.
It is well known that
the lungs provide not only respiration and gas exchange, but also perform a
number of non-respiratory functions, among which one of the most important is
participation in blood circulation and its regulation. Having an indissoluble
anatomical connection with the system of the great circle of blood circulation,
the vessels of the lungs are functionally their complete opposite. Maintaining
equal volumes of blood entering each circulatory circle, and simultaneously
maintaining the inverse proportions of their blood pressure are the basis of
compensatory and adaptive mechanisms in the case of pathological abnormalities.
Taking into account these features of pulmonary circulation in the dynamics of
AP development is extremely important, especially since it is a scientifically
proven and indisputable fact. Acute inflammation of the lung tissue primarily
affects the blood flow in the vessels of this organ. However, in practice,
correction of circulatory disorders in the body of patients with AP is carried
out on the basis of evaluating the parameters of systemic circulation.
In other words,
therapeutic efforts are directed not at the cause of pathological deviations,
but at their consequence, which has other, directly opposite norms, is a
secondary link in the mechanism of the disease and reflects an extreme
compensatory reaction. The desire to normalize the indicators of peripheral
blood flow without eliminating the root cause (for example, by intravenous
infusions, vasopressors, hormones) contradicts the pathogenesis of AP and is
not just a paradox, but one of the serious misconceptions in the interpretation
of the mechanisms of disease development.
At a time when
bacterial forms of inflammation prevailed, the attention and main efforts of
doctors were focused on etiotropic therapy of AP for a long period. Treatment
of this group of patients was considered impossible without the widespread use
of antibiotics. The decrease in the effectiveness of antibacterial therapy and
the increase in the number of resistant strains during this time had a gradual
development without sharp jumps and changes, which did not require accelerated
solutions. This dynamic is largely stimulated the development of new
antimicrobial drugs than the study of pathogenetic methods of treatment. The
sudden increase in the number of severe patients with viral forms of pneumonia
and the drop from the General medical list of ways to suppress the pathogen
destroyed the usual stereotypes and clearly showed the weaknesses of providing
assistance for AP.
It is necessary to pay
attention to one undoubted, but very important fact of the current pandemic,
which is noted in the modern literature. For example, in the conditions of
large groups isolated from the outside world, it was found that not all were
subjected to viral aggression, and among the infected, the disease in most cases
had an asymptomatic course [1,2]. The authors of these publications are quite
rightly concerned about the large number of carriers of the virus with an
asymptomatic course and, consequently, the risk of spreading infection. There
is no doubt that this data is a serious problem for epidemiologists, but the
statistics presented here allow us to draw another important conclusion.
In bacterial forms of
lung inflammation, the variety of possible pathogens and the difficulty of
determining them allowed us to use these reasons to explain failures in the
etiotropic treatment of AP. At the same time, the microbial factor did not pose
such a threat to the spread of the disease as is observed in coronavirus. Yes,
the current pandemic creates conditions for strict compliance with sanitary and
anti-epidemic measures. Yes, the number of patients with severe lung damage has
increased significantly. But, at the same time, we are talking about
monoinfection, which, despite the identity of the pathogen, differs in an
infinite variety of clinical manifestations and these individual differences
cannot be explained by the features of the etiology, right? These circumstances
clearly indicate a distortion of ideas about the absolute significance of
pathogens in the problem of AP and the need for a detailed study of the
pathogenesis of the disease.
However, the most
serious and at the same time delicate result of long-term use of antibiotics is
their influence on the formation of a stable worldview about the leading role of
pathogens. This didactic feature is crucial for further study of the problem
solution. The very desire to help patients is commendable, but the difficulty
of overcoming existing stereotypes is confirmed by modern analysis of the
features of medical care for patients with coronavirus disease. In the absence
of effective antiviral drugs, contrary to logic and professional prescriptions,
most of these patients receive antibiotics without clear direct indications
[3-5]. In such conditions, the urgent need for a clear understanding of the
classical mechanisms of the development of the inflammatory process in the lung
tissue is the basis for providing adequate and effective medical care.
Therefore, to get a successful result, it is necessary first of all to conduct
a cardinal revision of the pathogenesis of the disease.
This revision does not
require intensive efforts, because to start this process, it is enough to
remember and use the materials of fundamental medical science, which allow us
to understand the unique features of the pathogenesis of AP. Moreover, this
information has already been systematized and brought into the necessary
sequence in accordance with the dynamics of the disease in acute inflammation
of the lung tissue. The new system of views on the essence of the problem
allowed us to justify a specific approach to the treatment of this particular
pathology, and the results of subsequent clinical studies fully confirmed the
correctness and effectiveness of pathogenetic methods of treatment.
At present, in the
context of the current pandemic with a large number of viral pneumonia, the
lack of effective means of suppressing the pathogen and the lack of
pathogenetically based treatment methods, it is very important and promising to
pay attention to the already proven direction of care for this category of
patients. A detailed description of the materials of this work is currently
quite available and is presented in the recently published monograph of Igor
Klepikov “Acute pneumonia. New doctrine and first results of treatment”.
In this case, we are
talking not so much about the publication of a book, but about the results of
the work already done, the direction of which requires continuation, as the
current situation shows. Classic materials of medical science, which cannot be
ignored in the AP, are the basis for a successful solution of the problem, and
our attitude to these biological rules and laws will not change their role and
significance in the pathogenesis of the disease and will not eliminate the need
to develop and apply special methods of treatment.
The first task to be solved today is to
understand the nature and direction of the body's protective and adaptive
responses when an acute inflammatory process occurs in the lungs. This is
exactly the way of research that will allow you to form a specific and
permanent complex of care for such patients, regardless of the etiology of the
disease.