The syndrome of sudden death in children is clearly acute, subacute bronchiolitis accompanied peribronhiolitom and partially focal pneumonia, acquires the character of a generalized pathological process, which can lead to death.But even in cases of sudden death syndrome, when there were clear signs of this painful condition, description of the symptoms of the disease histories absent.
the presence of early reactions, such as those we found in the airways of the syndrome of sudden death in children (SVSD) in order to understand the nature of pathophysiological complications, you need to lead a more thorough argument.It is legitimate to do in relation with airway obstruction and subsequent dispersion atelectasis and edema interstitium and alveoli.
Not all mechanisms of obstruction have pathophysiological significance.On the basis of the material found in the lumen of the bronchioles, it is impossible to make definitive conclusions, even when a longitudinal cut allows you to explore large areas of the bro
nchial tree.However, if the clearance of peripheral bronchial tubes filled with mucus, it must be assumed that she was aspirated as in the peripheral regions of the bronchial tree mucilage is not produced.
Mucus produced in the nasopharyngeal area or in the area of the trachea and main bronchi.Its output in the peripheral parts of the bronchial tree is associated with damage to the epithelium, goblet cells which have previously been involved in the formation of mucus.
also possible passive outflow of mucus, often mixed with mucus mucosal epithelial cells of the respiratory tract or mucous glands or their excretory ducts.Closely spaced cells and expressed ability to staining indicate a significant degree of viscosity of mucus, which undoubtedly makes it difficult to actively delete.Expiratory is limited in infants.When the downward spread of infection is not all areas of the bronchial tree peripheral regions are affected simultaneously.Focal nature of its distribution certainly contributes to blockage due to mucus.
In some cases, sudden death syndrome in children, we considered the possibility of terminal respiratory paroxysms, which could cause partial or full re-opening of the lumen of the bronchioles.
Uolsher paid special attention to these curious changes inherent SVSD, and strongly objected to the fact that they are artifacts of fixation or trauma at autopsy.We agree with Uolsherom that these changes can not be purely autolytic phenomenon, hypostatic origin or artifacts of fixation, since in addition to them, there are the effects of obstruction;namely, atelectasis, acute alveolar or interstitial emphysema and a clear aspiration of epithelial cells in the peripheral parts of the bronchial tree.Moreover, these criteria can also confirm picture intravital microscopic demonstration of reactions, namely hypersecretion and associated destruction of the epithelium.
course, taken separately phenomenon in this chain of events can be interpreted in different ways, but they only put together reveal its true meaning.
be followed by a short stop on the changes in the bronchial tubes, as they observed in 1/3 of the cases investigated SVSD, although their localization in the lungs and each was different.In these cases the mucosa bronchioles wavy folds formed along their entire circumference, constricting the lumen of bronchioles, but without closing it.Such changes are known from experiments on animals after fatal bronchospasm.However, the question arises as to whether this type of post mortem changes saved.
We've talked about atelectasis, the called desquamation cell cover, which was observed in 27% of 292 cases of sudden death syndrome in infants.In 6% of the atelectasis, spreading, captured the entire segment of the lung.A possible etiological and pathogenetic factor behind this process was considered an acute viral infection.It is not yet clear why these changes are observed mainly in infancy and early childhood.Unlike Giza authors suggest that giant cells do not arise only from epithelial cells.Riken believed that these cells are formed within a few hours or at least 1-2 days from the beginning of the emergence of viral infection.Janssen and Bartshi observed the formation of giant cells in the lung after prolonged hypoxia.Forever as interpreted morphological changes in the lungs as a consequence of hypoxia.Electron-microscopic investigations have shown that these cells intraalveolar pneumocytes are formed in large quantities or transformed.The question of whether these operate phagocytic cells, such as microaspiration remains open.
Explicit activation of local lymphatic lung tissue was observed in 38% of the cases studied in the first study.It's not much to say to us about the painful process.In infancy disseminated or local swollen lymph open sites fairly common phenomenon.According to Mueller, the pathogen penetrates through the epithelial barrier of the bronchi can cause the development of local lymphadenitis.Shayler also considers the impact of possible hematogenous route.Paige suggested the existence of substances that stimulate the synthesis of proteins that cause inflammation and therefore lead to lymphocyte migration.More recent data on lymphocyte function indicate that the presence of highly significantly increased intrapulmonary lymph node cell may also be due to the influence of the antigen reaching the bronchi, for example, in acute infection.Sometimes gistopagologicheskaya picture reminds bronchiolitis nodularis.However, in the cases we studied SVSD we have never witnessed a significant increase or increased peribronchial lymph follicles.
Typically, when all acute cellular responses in infancy, apparently predominant mononuclear infiltration, particularly in the first months of life.
Analysis The debate around the value of changes in the lungs in SVSD, testifies to the existence of many unresolved issues, on the one hand, and the important achievements, as well as theoretical possibilities offered by scientific research, on the other hand.
Most authors suggest the presence of acute infection in these children before he died.Other researchers can not imagine that the presence of pulmonary edema, emphysema, haemorrhage and "minimum" pulmonary infiltrates enough to explain the death.Based on their data, Mueller and the staff is subject to toxic damage due to viral infection.
clinical practice shows that the infant children suffer acute bronchiolitis is most often in the third and twelfth month of life, and in the winter months.Infectious diseases of the respiratory tract are the most common diseases in infants, young and older, and can lead to serious complications.Viral-bacterial synergy is accompanied by toxicity is the most severe complication.Primary bacterial infections are relatively rare.
predominant infectious diseases caused by viruses, adenoviruses and picornaviruses.However, in the past, the prevailing types of viruses changed frequently.There is a clear seasonal dependence for infections caused by influenza viruses and adenoviruses.
is difficult to expectorate mucous plugs formed in the inflammatory process in the bronchi, even in older children, can lead to critical situations.When clinically confirmed viral infections, ended by death, was able to detect only Bekroft localized paravertebrally seal the lungs and accumulation of mucus, fibrin exudation and disintegrated epithelial cells in the bronchi.Biit with employees in a comparative study of the cases and SVSD alive, sick children of the same age obtained identical results of serological tests.Shnaveys with employees indicate the possibility of pronounced cytopathic effect, especially in the RS-viruses.
necessary to take into account the age characteristics of the child's physiology: usually all children have a higher resistance to air flow in the bronchi than in adults.It may even be twice as high.In addition, children characterized by a high resistance to deformation of the lung tissue and stretching.
researchers that focus exclusively on the "adult pathology", expect to discover expressed or extensive changes since death is usually preceded by a long illness.However, an exception to this is a flu epidemic in which death can occur at the beginning of the disease.Microscopically we see only hemorrhagic tracheobronchitis and massive haemorrhagic pulmonary edema.Microscopically diagnosis "infection" can rarely be based on classical, commonly in the form of cellular responses, signs of infection.
It remains to consider, whether due to dispersion and atelectasis and / or acute alveolar and interstitial pulmonary edema direct exposure to toxins, such as a viral infection, or whether they are accompanying reactions to pathological disorders of all body functions.
Most lung lesions observed in sudden death syndrome in children reflect the changes that occur in the early phases of the shock.In the initial stage of shock interstitial pulmonary edema with concomitant expansion of lymphatic vessels begins to spread from the lung to the gate of the connective tissue of its shares and interlobar septum.It also disrupted the formation of surfactant.The direct consequences of this are: an increase in the surface tension in the alveoli, the occurrence of negative pressure in the alveolar interstitium, the outflow of fluid from the capillaries and limit total lung capacity.These symptoms are detected only after prolonged shock development.Then shock causes damage to the vascular endothelium and the alveolar epithelium.Damaged layers that participate in gas exchange, followed by a necrosis of a resistant granular alveolocytes.Because of this defense mechanism is damaged antiatelektatichesky surfactant and, hence, the regenerative ability of alveoli wall.The continuation of this process leads to the development of "shock lung."
Let's look at the early phase of shock and try to interpret the intermediate pathophysiological mechanism of "shock", as a disorder in the microcirculation system, aimed at the generalization of the process;This, together with the effect of obstructive mechanisms leads to the following chain of events: alveolar hyperventilation, inadequate injection activity of the heart, ischemic hypoxia and metabolic acidosis in the peripheral circulatory system.On this basis, it is easily explained by the occurrence of further damage: direct damage of the respiratory center and the weakening or paralysis of the respiratory muscles.All of this can be seen as a generalized pulmonary insufficiency due.
In this article, we wanted to show how important the syndrome of sudden death in children is comprehensive, detailed study of the respiratory tract.We believe that the important and appropriate pathological changes can be detected in more than 80% of cases SVSD and their pathophysiological consequences are sufficient to explain the onset of death.
If breathing problems emanating from the peripheral parts of the bronchial tree, viewed in the light of a possible predisposition to the disorder of the regulation of the central nervous system, especially of the respiratory center, we come back to additional harmful combinations.
as possible explanations for occurrence of apnea observed in the neonatal period and sometimes in infancy, we consider the following: 1) early brain damage, 2) growth retardation, 3) the phasing out of the central nervous system due to the increasing of the brain edema.
These factors may act alone or synergistically in combination with the subsequent disorders caused by exogenous factors.
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Female magazine www.BlackPantera.ru: Helmut Althoff