This section is from the book "Research In Physiopathology As Basis Of Guided Chemotherapy With Special Application To Cancer", by Emanuel Revici. Also available from amazon: Research In Physiopathology
In spite of the progress realized in the last decade, shock remains one of the most challenging problems in medicine. That lipids have a critical role in shock pathogenesis seems clear from a long term study which began with an investigation of the activity of fatty acids in the induction of the abnormally dark color of blood seen in shock. The results of this study will be discussed here not only because of the intrinsic interest of the problem of shock itself but also because shock often represents the terminal phase of cancer as it does of many other diseases. In this presentation, we will try to remain as much as possible within the framework of our direct contribution to an understanding of shock. A portion of these researches was published in 1943. (40)
In studying the very complex phenomenon of shock, one has to consider a series of well defined problems. Shock has been related not only to a large number of causes but also to a series of very varied clinical manifestations. An initial problem was to determine whether there is any common relationship between the different types—between the shock, for instance, which kills a subject within a few minutes after a severe sudden trauma, and the shock that kills in days through profound systemic metabolic impairments. What is common to, and what is different between them, from the point of view of pathogenesis? What constituents intervene and how, in shock? These and many other problems have been approached systematically.
Types of Shock—As a starting point, we attempted to classify the types of shock and found an interesting relationship according to the time of their appearance, that is, the interval between application of the noxious stimulus and onset of manifestations. Three types could be identified with this criterion.
There is an immediate type of shock which appears within a few minutes after the application of the noxious agent. It is induced experimentally in animals by intravenous injection of a noxious substance, by scalding the animal in hot water, or by strong mechanical trauma. It has predominant central nervous system manifestations, including exophthal mia and paralysis of the posterior limbs, followed by clonic convulsive movements, and usually is terminated by death. A similar superacute type of shock is occasionally seen in humans following transfusions of blood with an incompatible group. It also may be seen following very severe trauma. In the case of bullet wounds, for example, large calibre bullets may bring rapid death. Neither immediate hemorrhage nor any organ impairment is sufficient, in itself, to account for the speed of death in many of these cases. However, it can be explained by the rapid and intensive participation of the central nervous system in this superacute type of shock. Sometimes such shock is not lethal in animals or humans and is followed by a period of prostration and ultimate but slow recovery. We called this type of shock the "superacute."
In a second type of shock, more frequently encountered in humans, the manifestations appear after a certain period of time. Such shock often is seen after direct transfusions, when the rate of injection has been too rapid or when the syringe and tubes have not been well coated with oil or paraffin, or when there has been a subgroup incompatibility between donor and receiver. The patient usually experiences a severe chill within 30 minutes. The chill is succeeded by a rise in temperature which usually lasts 15 to 60 minutes or more. The patient next experiences diaphoresis, after which the episode usually is concluded. In some cases the symptomatology is different. At about the same time—30 minutes—after transfusion, for instance, hypotension with hypothermia, cold and clammy perspiration, and intensive dyspnea are noted. In these cases death can follow in a short time. The same reaction is sometimes seen to occur, usually also in about 30 minutes, after the release of a tourniquet. We have employed the term "acute shock" to describe this second type characterized by its appearance at approximately 30 minutes after the noxious intervention.
A third form, the "state of shock," is considerably slower in onset and persists much longer. Characterized by hypotension, impairment of circulation, cold and clammy perspiration and marked enophthalmia, it may lead to death after several days during which the condition progressively increases in severity. It can, however, also end in recovery. This is the form most often encountered in clinical medicine, in cancer and many terminal conditions.
The next problem was: could a common pathogenic mechanism be recognized despite the greatly varied manifestations of these three forms of shock?