Respiratory distress syndrome

Acute respiratory damages of lung parenchyma are frequent and serious complications in a number of diseases. First of all of it is referred to viral and bacterial pneumonia, which sometimes has a progressing course and is accompanied by  massive, sometimes total, bilateral damages of lung parenchyma with severe, hard correctable respiratory failure, which for several days, sometimes hours, can lead to death. Secondary to this there can develop destructive processes and even gangrene of the lungs.

The next group consists of acute lung damage, combined by the term "shock lung", developing in patients with severe trauma, who underwent surgery, including cardiopulmonary bypass on open heart (postperfusion pulmonary syndrome), hemorrhagic, septic or anaphylactic shock, massive blood transfusions (syndrome of "homologous blood"), leptospirosis and even tropical malaria with 57% letality  [Bhadade R.R. et al., 2011].

Apart fr om that, lungs are affected in various exogenous intoxications and poisonings. In obstetric practice lung damages develop in eclampsia, amniotic fluid embolism, disseminated intravascular coagulation (DIC) syndrome. Many types of endogenous intoxications, especially such as those developing in acute pancreatitis, are also accompanied by lung damage. 
All these types of acute damages of respiratory lung parenchyma are usually combined by one term - respiratory distress syndrome (RDS).

In Western literature it was commonly referred to as "adult respiratory distress syndrome", or ARDS, wh ere the first letter corresponds to the word “adult”, which far not everyone was satisfied with, since a similar complication is characteristic for both adults and children. Therefore in 1994 the Conciliation Commission (Consensus) of scientists of European and American countries dealing with the problem had reviewed the terminology and, leaving the same initials ARDS, introduced a new term more close to the reality - acute respiratory distress syndrome, and the first letter in the abbreviation of the word has become “acute”  [G.R. Bernard et al., 1994].
This book uses the term "respiratory distress syndrome" – RDS, because this syndrome can not be other than acute.

Considering such a large group of diseases associated with RDS, there are practically no compound statistical information about its frequency, although in 1980, in the U.S.A. there were cited the following data – about 150,000 patients with RDS a year. It is interesting that the materials of mentioned Conciliation Commission exactly the same figures are quoted for the United States for 1994. M.A.Matthay and R.L.Zemans (2011) describe approximately 200.000 critically ill patients with ARDS causes 40% mortality annually in the United States.  Given the difficulties in treatment of this complication, accompanied by high mortality (10 to 90% depending on the severity of damage), this problem is extremely urgent.

Since in the solutions of Conciliation Commission, despite recognizing the essential role of endotoxemia in the genesis of this complication, was not mentioned the possibility of efferent therapy and detoxication in RDS, we have to give more detailed justification of such approach to its treatment and prevention.                  
     
Pathogenesis of respiratory distress syndrome
From the above list of diseases and pathological conditions accompanied by RDS, it is possible to make conclusion about polyetiology of this complication, however pathogenetic mechanisms are common for all types of RDS. They lie in the development of toxic interstitial and then alveolar pulmonary edema due to the cell membranes’ permeability failure on the basis of endotoxemia.
To prove this, in the Research Institute of Pulmonology, USSR Ministry of Health, there were conducted toxicity studies of blood in patients with acute pneumonia using the test of "protozoa survival time". As the protozoathere were used tetrahymena. In the blood of healthy people (and animals) the survival time is about 20 minutes and, depending on the severity of condition of patients with acute pneumonia, this time was reduced to 10, 5 and even 2 minutes. However, this increase in toxicity of blood might have been only one of the consequences of acute pneumonia and have no independent significance in the further development of lung damage, which could have occured simply from the progression of the basic pathological process in the same organ.
In clinical conditions the local pathological process and the accompanying intoxication can not be separated from each other, so it is impossible to identify those changes in the lungs, which are the direct consequence of the local pathological process, and those that arise from the impact of circulating toxic products. In one case, the process should be going in the direction of "alveolar epithelium – interstitium – vascular endothelium", in another – in the opposite direction, that is, from the blood. Only studies in the experiment could shed light on this question.

Our first experiments on rabbits with intratracheal administration of pathogenic (isolated from real patients) pneumococci culture gave quite amazing results – after only 5-10 minutes this pathogen was sown from blood and internal organs (liver, kidney, spleen), and the toxicity of blood increased to the same extent as in patients with acute pneumonia [Kostyanets E.Yu., 1992]. In all probability, the same bacteremia occurs in patients, and only the early start of antibiotic therapy does not allow to identify this phenomenon in more than 30% of them.

In histologic lung study of these animals there is revealed a picture of interstitial and alveolar edema against inflammation – expansion of interalveolar septa with infiltration of interstitium with lymphoid cells; in alveoli there was alveolar fluid rich with protein. Weight of the lungs increased by 32%.
When reproducing a similar level of endotoxemia with intravenous infusion of living or killed cultures of pneumococci there were also observed manifestations of pulmonary edema, such as those described above, but somewhat of smaller scale. Weight of the lungs increased by 25%.
It is interesting that both in intratracheal and intravenous insertion of the causative agent there was also observed a pattern of edema and extravascular fluid volume increase in liver, kidney, spleen [V.A.Voinov et al., 1991].

In experiments on dogs there were carried out thoracotomy and intravital contact lung biomicroscopy. Within 15 min after intravenous injection of both living and killed pneumococci cultures, on the surface of lungs there was noted a thickeningof interalveolar septa with accumulation of frothy fluid inside of alveoli. By the 30th minute, changes in the lung had been increasing, and had reached their maximum by the 180th minute.

For another series of experiments on dogs preliminarily there was received blood ultrafiltrate in its hemodiafiltration under pressure through the dialysis membrane from patients with severe lung damages and concomitant renal insufficiency. The liquid received was rich with medium molecular products. The powder resulting after lyophilization was redissolved for intravenous injection to dogs in such a way that the concentration of medium molecules in the blood of dogs corresponded to that of patients from which the ultrafiltrate had been obtained. 

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