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Industry: Email Alert RSS FeedWound Shock: A History of Its Study and Treatment by Military Surgeons
Military Medicine, Apr 2004 by Hardaway, Robert M
World War I
In World War I, in 1917, death was attributed to "wound shock." Hemorrhage was thought to be distinct from "wound shock" but was considered a complicating factor in the development of shock, "Complicating the wounds, there is usually some loss of blood. Under battle conditions especially there may be cold and exposure, lack of food and water and sweating which when combined with injury may bring about promptly the signs of wound shock."9 It was recognized that if a wounded soldier was not in shock, but was anesthetized with ether or chloroform, a calamitous fall in blood pressure might result. Venous pressure was found to be lower. This was an important observation and presaged the measurement and use of central venous pressure in Vietnam. From 1918 until 1964, however, venous pressure was not a serious consideration in treating shock.
A reference to "normal or increased erythrocyte count" was a remnant of the idea that shock and hemorrhage were separate conditions. The idea that wound shock was characterized by a high hematocrit value persisted through the years and played a great part in the emphasis placed on plasma as opposed to blood transfusion when the United States entered World War II.
A reference to "slight cyanotic appearance" presaged the findings of low oxygen tension (p02) in Vietnam casualties in 1964. Previous to this, the extremely precarious state of oxygenation in many instances of shock was not properly appreciated or documented.
Shock was blamed in part on a "toxic factor" arising from damaged and dying tissue and operation, which caused an increased permeability of the capillary walls and consequent reduction in blood volume by escape of plasma.9 Blalock,10 in 1930, "disproved" the toxin theory and blamed traumatic shock on extravasated blood in the tissues. A "toxic factor" was never found. Much later, during the Korean War, a toxin was again implicated in the production of disseminated intravascular coagulation and multiple organ failure.11
In World War I, there was a real appreciation of the time factor between being wounded and receiving adequate shock treatment. Santy12 noted that if the patient was treated within 1 hour, the mortality rate of nontransportable wounded was only 10%. This increased markedly with time, so that after 8 hours, the mortality rate was 75%. The need for fluid administration was well understood in World War I.9 However, the means of administering fluid volume were only partially developed. Although it was appreciated that the wounded were dehydrated and hypovolemic and needed water, it was thought that this water could, in most instances, be given orally or rectally. If the condition was more urgent, a subcutaneous clysis could be used. It was only in the most urgent cases that the intravenous (IV) route was thought necessary.
It was recognized that any fluid introduced intravenously would increase a low blood pressure. It was thought that this was only of temporary value when normal saline solution was used because of the leakage of the saline solution out of the circulatory system. For this reason, attempts were made to manufacture a colloid solution that would stay in the blood longer. The most common such solution was "gum salt," 6% to 7% acacia in 0.19% sodium chloride. Although used by a great many hospitals, the incidence of febrile and other adverse reactions was high, particularly in those with long-lasting shock and severe hemorrhage or infection. Most hospitals were not in favor of its continued use. Normal saline or Ringer's solution were considerably safer, but were thought to be only temporarily effective.
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