J.Jpn. Surg. Soc.. 61(7): 897-914, 1960

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宿題報告

POSTOPERATIVE ACUTE PULMONARY EDEMA: WITH SPECIAL REFERENCE TO THE CENTRAL NERVOUS SYSTEM

The occurrence of the postoperative acute pulmonary edema is very complicated. We can classify our 46 clinical cases into 3 types such as (1) that occurred after brain operation as well as brain trauma, (2) that occurred after the operations of the cases with cardio -pulmonary diseases accompanied by pulmonary circulatory disturbances, and (3) that occurred after the operation of the cases of metabolic disorder such as hypoalbuminemia, anemia and hepatic or renal disturbance. These 3 types were found to show the specific clinical signs and histological figures, respectively.
Namely, in the cases of the pulmonary edema after operation in the diseases of the central nervous system, the congestion of the pulmonary vascular system was remarkable and the floating of red cells in the alveoli was also notable. At the same time, the exsudation of liquid component stained by eosin into alveoli was considerably clearly seen. On the other hand, in the cases of pulmonary edema after operation in the cardiopulmonary diseases, the congestion of pulmonary vascular system and hemorrhage into the alveoli were more remarkable. Especially, in the cases which had the pulmonary hypertension before opertion, fibrosis of the blood vessel wall and hemorrhage were notable. Though the exsudation of the liquid component into the alveoli was also seen, the degree was much slighter than that of postoperative pulmonary edema accompanied by the central nervous diseases. In the cases of pulmonary edema after operation in the diseases with hypoalbuminemia, anemia and hepatic or renal disturbance, the congestion was not remarkable and much liquid components were chiefly seen in the alveoli.
Secondly, we produced experimental pulmonary edema which was closely similar to the above-mentioned clinical types, respectively, and tried to grasp their pathological physiology. Those which corresponded to the postoperative pulmonary edema of nevous disturbances, were produced by the destruction of the bilateral preoptic areas and the stimulation of the vagal or sympathetic nerve, while those corresponded to that of cardio-pulmonary di seases with pulmonary circulatory disorder, were made by the pneumonectomy, low oxygen respiration with inspiratory resistance and massive rapid transfusion. Those corresponded to that of metabolic disturbances were replaced with those caused by ANTU injection. Further, we clarified the innervation of the pulmonary vessels. On the reflex arc which was consisted of the afferent and efferent pathways of the pulmonary vascular innervation, we assumed the higher and lower centers. The higher center of the reflex arc where the afferent fibres ascended the vegal nerve, was situated in the nuclei of the preoptic areas. The efferent pathway started from this center passed through the pons and medulla and entered the efferent sympathetic pathway. On the other hand, the lower center of the reflex arc where the afferent fibres ascended through the sympathetic nerve or sinus nerve, was situated in the medulla and from this turned to the efferent sympathetic pathway. Accordingly, it was able to produce the pulmonary edema by destruction of the any courses of these pulmonary vascular innervations. We noticed that these 3 types of the experimentally produced pulmonary edema were extremely coincident with those of the above-mentioned clinically classified pulmonary edema from the histological viewpoint.
Regarding experimentally produced pulmonary edema, the following examinations were carried out; respiration, oxygen consumption, arterial blood oxygen saturation, several circulatory significances such as peripheral arterial blood pressure, cardiac output, pulmonary arterial pressure, pulmonary vascular resistance, pulmonary circulation time and pulmonary blood volume, the blood properties such as serum protein and colloidal osmotic pressure of the plasma, the changes of water and electrolytes balance, circulating blood volume, extracellular fluid volume, tissue water volume of the lung and other parenchymatous organs and electrolytes in plasma, urine and tissues, the dynamics of the intrapulmonary water shift measured by incorporation of Na²⁴ and P³², the pulmonary lymphatic flow, the behavior of the reticular fiber of the alveolar wall, factors regading with the permeability of the pulmonary vessels such as trypan blue passage through the pulmonary capillaries, VDM (Ferritin) in the blood and liver, fibrinolytic ferment, pulmonary histamine and freed cathecholamine in urine, renal circulation, hepatic circulation and hepatic function, enzymatic metabolism, RNA, lipoid metabolism, polysaccharide metabolism in the lung and other tissues. From these results the pathophysiology and genesis of the respective experimental pulmonary edema were elucidated. Namely, (1) the characteristic of the pulmonary edema caused by the preoptic lesions, was that by the destruction of the bilateral preoptic areas the primary rising of pulmonary arterial pressure, the prolongation of the pulmonary circulation time and the in crease of the permeability of the pulmonary capillaries were occurred making the chief causes of the pulmonary edema. At the same time, the destruction of the bilateral preoptic areas induced primarily the changes of the renal and hepatic circulations and the several endocrine regulations inviting the balance disturbance of the water and electrolyte metabolism. Integrating these results, the pulmonary edema was accelerated and the edema occurred selectively in the lung alone. (2) The characteristic of the pulmonary edema caused by the pneumonectomy and massive rapid transfusion, was that the continuing rise of the pulmonary arterial pressure and the lowering of the colloidal osmotic pressure of the plasma caused the pulmonary edema as the chief factors and once the pulmonary edema was induced, it became a stress, resulting secondarily in the renal circulatory failure, anomaries of the endocrine organs and the increase of the permeability of the pulmonary capillaries and accelerating pulmonary edema. (3) ANTU-pulmonary edema was characterized with the abnormal increase of the permeability of the pulmonary capillaries as a chief cause. Thus, we can precisely assume the pathophysiology and genesis of the clinical postoperative pulmonary edema from the knowledge of the corresponded experimental pulmonary edema.
In the next place, we studied how the nervous factors participated in the development of the postoperative pulmonary edema by investigating our clinical cases of the post-operative pulmonary edema. In nearly all cases which had pulmonary edema after brain operation and brain trauma, the focus of the brain and of the operative attack showed the close relation to the higher or lower center of the pulmonary vascular innervation which we decided experimentally. On the other hand, in the most cases which had the pulmonary edema after thoracic surgery, the operative attack extended to the vagal or sympathetic nerve, and it was assumed that this was concerned in the occurrence of the pulmonary edema. Furthermore, it was clarified that the bleeding and anemia caused by operation did not only become the factor of the occurrence of pulmonary edema by influencing directly the pulmonary vessels, but also brought the changes to the brain and nerves participating in the occurrence of postoperative pulmonary edema.
Finally, in the first stage of the pulmonary edema, both the water transudation from the pulmonary vessels into the tissues and the reabsorption from the tissues into the vessels were vigorously seen and so far as equilibrium of these both mechanisms existed, the pulmorary edema was reversible or recovered though it developed. If the degree of the pulmonary edema was aggravated and this state continued for some period, the reabsorption function decreased or disappeared by the several factors and the movement of the water became one-sided, so that the pulmonary edema developed to the incurable state. Thus, we established the concept of the "irreversible pulmorary edema" and advocated that naming.
(Author's abstract)

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