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Chapter II




The development of the concept of whole blood transfusion in the management of battle casualties was intimately related to the development of a correct concept of shock. The confused and incorrect concept of this condition held in many quarters at the onset of World War II accounted, in large part, for the delayed development of the whole blood program in the Zone of Interior and for the trial-and-error period of shock therapy overseas.


Attempts to study shock during World War I by the special committee appointed for that purpose, while generally unsuccessful, at least discredited such existing theories as the reflex vasomotor paralysis theory, the theory of exhaustion of the vasomotor center, the acapnea theory, and the theory of adrenal exhaustion (1, 2). Cannon's (3) conclusion that the absorption of toxins from injured tissues was the primary cause of traumatic shock, which was based on his own clinical and experimental studies for the Shock Committee, was supported by other observers. In retrospect, however, it is clear that this theory was not supported by adequate proof and that the attempt to distinguish between shock and hemorrhage was equally fallacious.


Even in an increasingly mechanized age, severe shock associated with trauma is not often encountered in civilian practice in peacetime, nor, with really rare exceptions, such as the Cocoanut Grove disaster (p. 697), is it ever encountered en masse. Isolated clinical observations are possible in peacetime, but the circumstances of war, with its mass casualties and wide variety of wounds, provide the only really propitious material for the clarification of shock and other problems associated with wounding.

It is not surprising, therefore, that after World War I, the problem of shock was transferred to experimental laboratories, in which attempts were made to study it by physiologic and chemical techniques under a wide variety of experimentally induced conditions.

The theory of toxemic shock persisted until the late twenties, when Blalock (4), and a little later Parsons and Phemister (5), demonstrated that shock produced by trauma to the limbs is not the result of toxemia but of a local loss of blood and fluid and of circulating blood volume. Experiments by a number


of other observers also failed to identify toxic substances in the bloodstream of shocked animals and persons.

Between the wars, a number of misconceptions developed concerning shock. For years, some observers continued to insist that the only explanation of so-called true shock was a generalized increase in capillary permeability, a concept introduced with the theory of traumatic toxemia and based on the observation that red blood cell counts from the capillary bed were high, particularly in comparison with counts from the venous blood. In World War II, this phenomenon was found to be both a late and a very infrequent development. Actually, the explanation of the hemoconcentration was fluid shift. The erroneous concept just described, however, was so widely accepted that it was included in the manual on shock prepared under the auspices of the Committee on Surgery, Division of Medical Sciences, NRC (National Research Council) (6).

In 1936, Freeman and his associates (7) were able to show that in shock there is a reduction of the volume flow of blood in the hand from the normal rate of 7 cc. per minute per 100 cc. volume to 1.3 cc. The result is a progressive tissue asphyxia, which goes on to tissue death if the increasing oxygen debt is not repaid. The rate of blood flow decreases much sooner than the blood pressure falls or hemoconcentration occurs. From their observations, Freeman and his group concluded that the blood volume is a more reliable index of shock than the blood pressure. At this time (1936), there was no practical method of determining blood volume under field conditions. The Freeman group suggested that, as an expedient, it might be useful to make a rough calculation of the time necessary to refill the veins of the forearm and hand after they were stripped; normally, they fill immediately.


When the United States entered World War II, the following concepts of shock were generally accepted:

1. The reduction in blood volume present in peripheral circulatory failure is the most important single factor, if not the initiating factor, in the production of the clinical picture seen in shock. It results from the loss of plasma, at first locally and then generally, into the extravascular tissue spaces. Most therapeutic efforts in shock must be directed toward overcoming this loss of blood volume.

2. The reduction in the rate of blood flow is associated with a diminished venous return, which results in a decreased cardiac output, though the heart and the nervous energies that control it are not incapacitated.

3. The vasomotor center remains active.

4. Hemoconcentration is usually present in shock not associated with hemorrhage (burns, crushing injuries) and tends to reflect the amount of plasma lost.


In 1920, Maj. W. Richard Ohler, MC (8), had expressed the firm opinion, based on his World War I experience, that the most important single factor in shock is hemorrhage and that the degree of shock depends upon the amount of blood lost (p. 8). The therapeutic need, he said unequivocally, is therefore for oxygen-carrying corpuscles, and no intravenous solutions can replace them. It would have been desirable, he continued, to have a method of calculating the total hemoglobin and blood volume, but the use of citrated blood, even without this precise knowledge, was both simple and efficacious.

Between this time and the outbreak of World War II, numerous other observers had arrived at the same point of view, but they did not make their voices heard. Most of them did not even try. The rather general belief at the outbreak of the war that plasma alone could compensate for the loss of whole blood in shock simply reflected the prevailing point of view that blood loss was not necessarily the primary cause of shock. It is not easy, in looking back, to understand how these concepts were ever accepted, yet some of the most competent physicians in the country believed that plasma alone could compensate for the massive blood losses which occurred in trauma. It was a belief which did a disservice to the true and important role of plasma in the therapy of shock. Also, as pointed out elsewhere (p. 9), many observers who believed that only whole blood was effective in shock did not believe that it would ever be practical to provide it for forward areas.

Attempts to transfer controlled laboratory studies to combat conditions led to confusion, as might have been expected, for they were based upon faulty premises. As Beecher (1) pointed out, the belief that plasma would be as effective as whole blood in the management of hemorrhagic shock seems to have been derived from laboratory experiments so set up that the number of variables could be strictly limited. There was, of course, no real resemblance between a combat soldier who had suffered a serious wound or wounds and a rabbit lying quietly in its cage after experimental deprivation of 75 percent of its blood volume. The very management of the wounded soldier, including his successive removal rearward from the battlefield through the chain of evacuation, produced additional trauma, which was further increased by physical and roentgenologic examinations, anesthesia, and operation. Transfer of laboratory conclusions to a combat situation with its additional and widely different variables was simply unsound reasoning, which led to therapeutic confusion.


The prewar confusion in the concept of shock was in no wise diminished by the confusing nomenclature employed to designate the condition and the loose use of the term.

In 1918, Mann (9) defined shock as a term used by surgeons to describe a definite clinical condition probably due to a number of causes but always occurring in one or the other of two groups of cases: (1) those in which clinical manifestations followed some time after the occurrence of conditions incidental to shock, or (2) those in which a severe or fatal condition


supervened immediately upon receipt of the active agent. The vagueness of the definition, propounded, as it was, by a physician of Mann's ability and experience, is indicative of the vagueness of the concept of shock at that time.

In 1930, Parsons and Phemister (5) stated that it was more correct to speak of hemorrhage than of shock, or to speak of shock due to hemorrhage when acute loss of blood in wounds, whether closed or open, was the cause of marked circulatory embarrassment or failure. At the same time, these observers cited Blalock's criticism, in 1927, of the current loose use of the term. Shock, in Blalock's opinion, should be considered not as a disease but as a group of symptoms which might be produced by a number of factors, including acute hemorrhage, wounds, and anesthesia. Later, Blalock (4) was to be the first to use the term "peripheral circulatory failure" for shock.

In 1938, Moon (10) defined shock as a circulatory deficiency, of neither cardiac nor vasomotor origin, characterized by decreased blood volume, decreased cardiac output (reduced blood volume flow), and increased hemoconcentration.

In 1941, Janeway (11) described primary shock as a condition of vascular collapse in which the tone of the peripheral vessels was diminished reflexly as a result of psychic stimuli. Primary shock, in his opinion, was difficult to distinguish from secondary shock, another term used very loosely indeed early in World War II. If there was not prompt improvement after such measures as warmth, hot fluids, morphine, and the shock position (considered useful because gravity played such an important part in the pooling of the blood), then true secondary shock was undoubtedly present. In secondary shock, by Janeway's definition, the volume of blood was insufficient to maintain an adequate peripheral circulation, not because of vasodilatation (as a matter of fact, vasoconstriction was usually present) but because of blood loss. In secondary shock, whole blood was a more desirable replacement fluid than plasma because both red cells and plasma had been lost.

It is significant that, in his excellent study on casualties in the Battle of El Alamein, Lt. Col. W. C. Wilson, RAMC, began with a definition (12):

There is so much variation in the use of the term "shock" that some kind of definition is required. The term is sometimes used to describe any form of circulatory failure after injury. * * * This practice is objectionable in that the label of "shock" is given to many varieties of circulatory collapse, including those caused by peritonitis, other forms of bacterial infection, asphyxia, pneumothorax, and other complicated effects of intrathoracic injury. In this report the term "wound shock" is used in a restricted sense. It does not include circulatory failure from peritonitis, bacterial infection, or intrathoracic injury; nor, unless specially stated, does it refer to the shock which follows burns or injury to the central nervous system. It embraces all other forms of circulatory failure which arise within a few hours as a result of wounding. As a matter of convenience, the term shock is used as a synonym for circulatory failure and the cause is added when this is known, e.g., "shock from hemorrhage."

The ETMD (Essential Technical Medical Data) for NATOUSA (North African Theater of Operations, U.S. Army), for March 1944 (13) suggested that the definition of shock should be extended to include the inability of the organism to meet the demands commonly within the normal physiologic range and should not be limited to a descriptive index of abnormal findings.

By the end of the war, the accepted definition of traumatic shock was a situation produced initially by a decrease in the peripheral circulatory blood volume that is followed by a diminished venous return, an inadequate cardiac output, and depleted physiologic functions. The most usual cause of these changes is gross hemorrhage. This is still (1962) an acceptable definition.


As a matter of convenience, the confusion that arose in the Mediterranean theater because of the mistaken concept of shock and the loose use of the term is discussed under another heading (p. 37).


When the Committee on Transfusions, Division of Medical Sciences, NRC, held its first meeting on 31 May 1940 (14) (p. 73), it appointed a Subcommittee on Anesthesia and Shock (hereafter called the Subcommittee on Shock), with Dr. Alfred Blalock, Professor of Surgery, Vanderbilt University School of Medicine, as Chairman, and a distinguished membership of surgeons and anesthesiologists.

During the war, this subcommittee supervised a large number of research studies dealing with special components of shock and certain variations in its treatment, including an investigation of agents other than whole blood and plasma. All of these studies were undoubtedly of some value but most of them were of value from the negative aspect; that is, the investigators tested and eliminated a large number of agents that had to be tried before they could be discarded. Reports of these investigations can be found in the minutes of the subcommittee, 1940-45.

From a practical standpoint and for the purposes of this history, the significant activities of the Subcommittee on Shock are included in the conferences on shock held under its auspices and in certain of its official reports.

First Conference on Shock

The first Conference on Shock (15) was held under the auspices of the Subcommittee on Shock on 28 June 1941, 6 months before the United States entered the war. The announcement of the meeting carried the statement that emphasis would be placed upon measures of immediate use to the Army and Navy Medical Departments. The agenda included a wide range of subjects but did not include specific presentations on the use of blood or plasma in shock.

Shock Report No. 1

At a conference on 28 June 1941, a committee was appointed to make general recommendations concerning shock. It consisted of Drs. Blalock, Henry K. Beecher, Oliver Cope, Robert F. Loeb, and Stafford Warren. Its report (Report No. 1) (16), issued on 16 July 1942, covered the recognition of shock, its prevention, and its control.

Prevention.-The remarks on prevention in this report began with the following statement:

Since the major single cause of the state of shock seems to be a decrease in the circulating medium (whole blood, plasma, or water and electrolytes, or a combination of these), therapy is based upon checking such losses and replacing body fluids by the best means at hand.


Preventive measures were listed as control of hemorrhage; application of a tourniquet; splinting; postural measures; fluid therapy in traumatic shock, burns, and dehydration; the application of heat; treatment of exposure to cold and immersion; and precautions in regard to analgesia and anesthesia.

Therapy.-The important therapeutic recommendations by the ad hoc committee on shock were as follows (it should be remembered that they were made in July 1942):

1. When shock is imminent or present, blood, plasma, or albumin should be injected as promptly as possible. If massive hemorrhage has occurred or signs of serious anemia are present, whole blood is preferable to blood substitutes.

2. In the absence of evidence of blast injuries and pulmonary irritation, blood or blood substitutes can be given intravenously, as rapidly as 1 pint of isotonic fluid in 10-15 minutes.

3. If the blood pressure has fallen below 80 mm. Hg, an effort should be made to restore it to normal as soon as possible.

4. If blood is available, it should be used in initial amounts of 500 to 1,000 cc. The first injection of reconstituted plasma should be two units and of concentrated albumin, one unit (25 gm.). Not more than 10 units of albumin should be given in 48 hours. If albumin is used, severely dehydrated patients require additional water and salt. When sterile physiologic salt solution is available, concentrated albumin can be diluted in the ratio of two units (50 gm.) to one liter of salt solution.

5. If the desired effect on the blood pressure is not obtained in 15-30 minutes, the dose of blood or blood substitute should be repeated.

6. If anemia appears in the course of treatment with large amounts of plasma or albumin, whole blood transfusions are indicated.

7. Salt and glucose solutions are not recommended in shock. The temporary rise in blood pressure and blood volume which they produce is only temporary and gives rise to a sense of complacency. Their only value is to correct dehydration. They are contraindicated in head injuries and pulmonary damage.

8. Within reasonable limits, there is little risk of injecting too large quantities of replacement fluids immediately after wounding. It is important to watch for fresh bleeding when the blood pressure, in the course of therapy, begins to approach normal.

Second Conference on Shock

At the second Conference on Shock (17) on 1 December 1943, the agenda had become more realistic, in the light of military developments. It included field blood volume determinations by the Phillips-Van Slyke copper sulfate method; the comparative therapeutic effects of whole blood, plasma, albumin, saline solutions, and gelatin in clinical shock; and a vigorous discussion of the use and value of blood and blood substitutes. The proceedings were thus in marked contrast to the proceedings of the first conference, which had been held almost 6 months before Pearl Harbor.

On the other hand, the discussion of shock was still not entirely realistic, for it was divided into early and late shock. The discussion of early shock included infection as an initiating agent, possible techniques for early recognition, and prevention and treatment. The discussion of late shock covered intermediate metabolism, visceral damage, acidosis, vitamin-coenzyme systems, and succinate and Pitressin therapy. Acidosis was stated to be a possible


criterion of the severity of shock but was not considered a cause. Neither succinate nor Pitressin therapy was regarded as promising.

In a report at this session by Dr. E. I. Evans on the comparative therapeutic effects of whole blood and blood substitutes in shock, the following points were made:

1. In patients seen soon after wounding, saline solution seemed to have a beneficial effect, even when the blood loss was quite severe. A marked reduction in the incidence of severe shock could be produced by giving saline solution prophylactically. When saline solution was given to a patient already in severe shock, there might be temporary improvement, with elevation of the blood pressure, but it seldom lasted more than 30 minutes.

2. Both plasma and whole blood were effective in moderately severe shock, but studies of the blood volume after the initial treatment usually indicated the need for whole blood. All patients in shock who had not been given whole blood eventually showed moderate or severe anemia.

Quotation at the conference of a recent letter from Maj. (later Lt. Col.) Henry K. Beecher, MC, then in North Africa, brought the discussion down to a realistic level:

One of the chief problems is concerned with supplying blood in forward areas. Somewhere along the planning line somebody seems to have forgotten that plasma lacks oxygen-carrying power. Much too often the following sequence of events takes place: A man receives a bad wound; he bleeds; hours later his "blood" volume and pressure are restored by plasma infusion; the surgeon decides he is now ready for surgery; there is further loss of the too-small quantity of hemoglobin available in his body, as a result of the surgery; the patient's circulatory system collapses and it is impossible to revive him. Plans are now being worked out for supplying whole blood for the forward areas.

At this second Conference on Shock, Dr. Loeb, chairman of the Subcommittee on Blood Substitutes, made the highly significant announcement that it was the conviction of his group that the ideal treatment of shock due to hemorrhage and skeletal trauma was replacement of lost blood with blood and that every means possible should be utilized for increasing the use of blood in the prevention and treatment of these conditions in various theaters of war (p. 53). It was, however, recognized by his committee:

1. That whole blood could not always be made available.

2. That in crushing injuries, burns, and abdominal wounds, plasma was more desirable than blood at certain stages of treatment.

3. That plasma is more desirable than whole blood when dehydration, for one reason or another, is marked.

4. That plasma has the advantage of convenience of transportation to areas to which whole blood cannot be taken but that there are certain situations in which serum albumin is more practical than plasma.1

Shock Report No. 17

Shock Report No. 17 (18), dated 4 March 1944, was a revision of Shock Report No. 1 (16), dated 16 July 1942. Some of the members of the committee

1This statement does not represent the view of those intimately concerned with the blood program or of medical officers with a special interest in, and knowledge of, resuscitation. In their opinion, there were no circumstances in which albumin was more practical than plasma because of the almost universal necessity of supplying additional fluids when albumin was used.


which prepared the second report had also served on the first committee. The current status of the shock problem was set forth as follows:

1. The establishment of a close correspondence of circulatory changes in experimental and clinical shock has given confidence in the clinical application of results obtained in experimental studies, especially on dogs.

2. Reduction in the circulating blood volume is the most important factor in the initiation of shock. The reduction, whether the injury is mechanical or thermal, is due to loss of blood or fluid at the site of injury. Except possibly in very late stages, there is no notable increase in capillary permeability in nontraumatized areas of the body. The reduction in the circulating blood volume makes its restoration to normal the primary consideration of therapy.

3. The most reliable criteria of the degree of circulatory disturbance underlying shock are cardiac output and blood volume. As shock progresses, cardiac output continues to decrease, even if there is no further reduction in circulating blood volume. The level of arterial pressure is not a reliable criterion of the degree of circulatory impairment in early shock, nor does the hematocrit, considered alone, indicate the relative degree of loss of blood or plasma.

4. After a critical point has been reached in diminution of the blood volume, progressive tissue anoxia leads to metabolic changes and to damage to certain organs, such as the brain, and perhaps the heart and liver. The state which then develops is termed "irreversible shock."

The following prophylactic and therapeutic points were stressed:

1. The consequences of inadequate circulatory volume emphasize the very great importance of early, adequate treatment of shock. Treatment should not be delayed until its manifestations appear.

2. Operation should be carried out as promptly as possible after resuscitation, or sometimes before it is completely accomplished, with blood replacement as indicated during the procedure.

3. Fluid therapy is the most important measure in the therapy of shock. It should take the form of whole blood, which may be required in amounts up to 3,000 cc.

4. The first 500 to 1,000 cc. of blood should be given rapidly. Subsequent administration should be at the rate of 500 cc. per hour or less. Prophylactic transfusions should also be given slowly.

The great difference between these recommendations, in March 1944, and those of July 1942 is the unequivocal advice to use whole blood without delay. The altered concept of shock should also be noted. The advice to inject the blood slowly was founded on the old idea that rapid injection of blood might give rise to speed shock. As a matter of fact, early in the war, it was found that the rapid injection of blood was not only harmless but essential and beneficial. It was not unusual to inject 500 cc. of blood in 5 minutes, and occasionally as much as 20 pints of blood were injected into four different veins in a period of 3 hours. Had members of the various committees of the National Research Council been permitted to visit combat zones, as was several times requested (p. 79), their recommendations would have been more closely related to the facts of military medicine.



In the first months of active U.S. participation in World War II, the confusion that attended the condition that came to be appreciated as the most important single complication of wounding seriously affected the management of wounded casualties. Until the concept of shock was clarified, they were treated with skill and devotion, but they were often not treated entirely correctly, even though, by the time North Africa was invaded in November 1942, it was generally accepted that decreased circulating blood volume was the most important deviation from normal physiology seen in shocked casualties.

The necessary clarification of the concept of shock, with the application of the correct concept to shocked casualties, was accomplished in the Mediterranean theater. Until June 1944, this was the only theater in which large numbers of ground troops were in constant contact with the enemy. For nearly 2 years, the battle casualty rates in it were continuously above 50 per thousand per annum, and for nearly 2 months of this period they were above 100 per thousand. With casualties requiring treatment in such numbers, policies of management had to be established, even in the absence of any proved scientific rationale for them.

The situation began to change when Col. Edward D. Churchill, MC, reported for duty in North Africa on 7 March 1943 as Consultant in Surgery to the theater surgeon. Before he left the Zone of Interior he had been well briefed on the British experience in shock and transfusion (p. 55) and had been informed of the research under way in this field at the Army Medical School and elsewhere.

Colonel Churchill's first official report to the theater surgeon, 2 weeks after his arrival and after a period of temporary duty on the southern Tunisian front, was a memorandum on blood transfusion (19). On 16 April, after the collection of additional data, he set forth several conclusions, the most important of which was that a significant number of wounded went into shock from loss of blood and that plasma was not a total treatment for these casualties (p. 55).

In his first report, Colonel Churchill was critical of both the nomenclature and the concept of shock. He found that in field medical records, histories, and autopsy reports, shock was used with vague significance and often with no definition at all (p. 32). The disturbance of the peripheral circulation which the term indicated might range from slight pallor to impending death.

Further confusion was introduced by the use of the term "irreversible shock," a use which amounted to the assumption that at one moment restoration of the blood volume could halt the process of death while at the next, it could not. Even the most carefully controlled laboratory experiments could not identify this precise baseline. If this held true in a controlled experimental


laboratory, identification of the onset of irreversible shock seemed even more impossible when the medical officer was confronted with the results of random trauma sustained by soldiers under combat conditions.

In the records of battle casualties who died in forward areas, shock or irreversible shock was almost invariably found to be recorded as a secondary cause of death, whether the primary condition was a craniocerebral wound, an overwhelming peritonitis, a fulminating gas gangrene infection, or uncontrollable hemorrhage. In Colonel Churchill's opinion, the terms "shock" and "irreversible shock," as they appeared in records and autopsy protocols in NATOUSA, were completely irrelevant. He therefore found it impossible to comment on the occurrence of shock during the Tunisian campaign in terms that would be helpful to those engaged in research on the subject.

An analysis of 1,263 casualties had shown no deaths from so-called wound shock under terms of the restricted definition in which hemorrhage could be excluded as the important causative factor. The same observations were made in the clinical study of large numbers of wounded. Colonel Churchill therefore concluded:

1. That wound shock, if it occurred among surviving casualties, apparently responded to treatment. Irreversible shock therefore did not appear to be a problem of pressing importance.

2. That wound shock could not be identified as a cause of death in conditions prevailing in the management of battle casualties during the period of the survey.

3. That shock as it was observed in the Tunisian campaign could be controlled by the application of accepted methods of treatment, without the need for the development of additional methods.

These conclusions were amply confirmed in the following months by simple, direct observations on battle casualties properly treated by methods already available, including the replacement of blood losses by whole blood. Clinical observations were later confirmed by a number of special studies. The management of shock in the last year of the Italian campaign, when there was a general appreciation of the need for whole blood and when the blood needed was available in ample quantities from a theater blood bank, was very different from the makeshift management and often complete lack of blood in the Tunisian and early Italian campaigns. Appreciation of the need of blood, however, preceded its supply by many months.


Lalich Study

The first planned studies on shock in the Fifth U.S. Army were made by Capt. Joseph J. Lalich, MC, on the Cassino front in December 1943 and on the Anzio beachhead in March 1944 (19, 20). Studies on the hematocrit, on the plasma protein, nonprotein nitrogen, and chlorides of the blood, and


on the carbon dioxide combining power of the blood supported his thesis that blood loss is the chief factor in shock.

On the basis of his clinical observations alone, Captain Lalich had already advocated that battle casualties in shock be divided into three categories, according to the following criteria:

1. The patient has a normal blood pressure and no significant abnormalities of pulse volume or pulse rate, but his wounds are sufficiently numerous and sufficiently severe to make it reasonable to anticipate circulatory failure. Experience showed that unless patients in this group were treated by replacement therapy, usually in the amount of 500 cc. of plasma and 500 cc. of blood, varying degrees of circulatory failure were likely to occur during operation.

2. The blood pressure ranges from 90 mm. Hg down to the lowest level at which it can be measured. Resuscitation requires at least 1,000 to 2,000 cc. of blood.

3. The blood pressure cannot be determined by auscultation. A patient in this state should receive from 500 to 1,500 cc. of blood, the precise amount depending upon how much is required to raise the systolic pressure to about 100 mm. Hg. After this level has been attained, an additional 500 to 1,000 cc. of blood should be given before surgery is undertaken. If the systolic pressure fails to rise to at least 50 mm. Hg after 1,500 cc. of blood has been given over a period of 15-30 minutes, operation should be resorted to without further delay, for factors other than serious blood loss or continuing hemorrhage are probably contributing to the persistence of shock. Among these factors are gross contamination and infection of the pleural or peritoneal cavities, or both, or toxemia from clostridial myositis. Even when these conditions are chiefly responsible for the state of shock, blood loss may also play some part in the patient's status.

There were numerous variations in this classification, but, on the whole, it represented the consensus of the surgeons and shock officers in the Mediterranean theater.

Stewart-Warner Study

The second study on shock was begun in January 1944, by Maj. (later Col.) John D. Stewart, MC, and 1st Lt. (later Capt.) Frank B. Warner, Jr., MC, when Mobile Unit No. 3, 2d Medical General Laboratory, was operating beside the 3d Platoon of the 11th Field Hospital at Cassino (19, 20). The hospital was doing first priority surgery, and the objective of the investigation was the response of seriously wounded men in respect to shock, hemorrhage, and dehydration. Surgeons caring for the patients investigated were kept informed of the results of the laboratory studies and were able to utilize the information in their management.

The final report on 2 January 1945 covered 100 casualties, of whom (the figures are overlapping) 48 had penetrating abdominal wounds, 32 penetrating thoracic wounds, and 55 compound fractures. Seventeen died during the course of the investigation.


Colonel Stewart and Captain Warner, who had been promoted in the interim, were particularly impressed by the variability of both the vasomotor and the cardiovascular response to wounding and also by the fact that reactions to shock and hemorrhage were considerably less stereotyped than they were usually supposed to be. Their other findings were as follows:

1. A reduction in blood volume was characteristic of untreated shock.

2. Hemoconcentration was not encountered, but decreases in plasma protein concentration and hematocrit values were evident shortly after wounding. Later, both components were lowered.

3. Dehydration and azotemia were common in the early recovery period.

4. Urinary reactions were indicative of a rather mild base deficiency.

5. No evidence of the excessive use of plasma or whole blood was detected in any patient.

Beecher-Burnett Study

The third study, by Major Beecher, Consultant in Shock and Anesthesia to the Surgeon, MTOUSA, and Capt. Charles H. Burnett, MC, was made at Cassino and on the Anzio beachhead and chiefly concerned the timing of surgery in relation to resuscitation (19, 21).

Most medical officers who had made special studies of shock or who had a large clinical experience believed that it was wiser to resuscitate the casualty as completely as possible before surgery unless there was some indication, such as continued hemorrhage or peritoneal contamination, for emergency operation. As a result of their own investigations, Major Beecher and Captain Burnett took the position that surgery should be considered a phase of the routine of resuscitation and given an earlier place in it (p. 584). Specifically, when the systolic blood pressure had reached 80 mm. Hg and the patient was warm and had a good color, they believed that operation should be proceeded with. Whatever additional replacement therapy was indicated could be carried out during operation.

While there was no universal acceptance of this concept, comparative figures seem significant (21): In November and December 1943, resuscitation in the field and evacuation hospitals below Venafro and Mignano on the Cassino front often required 6-8 hours after seriously wounded casualties had been admitted. In 1944, on the Anzio beachhead, even extremely bad surgical risks were prepared for operation on an average of 2 hours and 20 minutes after wounding. The readier availability of whole blood in 1944 had much to do with the reduction in the timelag, but the change in concept of the optimum time for operation undoubtedly also played a major role.


In August 1944, the appointment of a board to study the treatment of severely wounded casualties was recommended by the theater surgeon, then Maj. Gen. Morrison C. Stayer, to the Commanding General, NATOUSA, Lt.


Gen. Jacob L. Devers (19). There were two reasons for General Stayer's request: (1) that the concept of blood loss as the etiologic factor in shock must be documented by cold, hard facts; and (2) that similar proof was required for the use of whole blood as an essential element in the management of wounded men and not as an agent which could be replaced by other substances. Without such proof, shock and its associated problems would be left, at the end of World War II, in the same inconclusive state in which they had been left at the end of World War I. On 3 September 1944, General Devers appointed a Medical Board to Study the Treatment of the Severely Wounded (usually known as the Board for the Study of the Severely Wounded) to operate directly under the theater surgeon. Its membership was composed of Major Beecher; Major Burnett; Capt. Seymour L. Shapiro, SnC; Lt. Col. (later Col.) Fiorindo A. Simeone, MC; Capt. Louis D. Smith, SnC; Maj. (later Lt. Col.) Eugene R. Sullivan, MC; and Lt. Col. Tracy B. Mallory, MC.

In view of this action, it is interesting to recall that the minutes of the first meeting of the Committee on Transfusions, NRC, in May 1940 (14), contained the suggestion that "a group of men be allowed to work in the Army, freed from any of the obligations of Army officers, who would study cases of shock as investigators. This would give opportunity to observe shock on a big scale, an opportunity to get an insight into the nature of shock." More than 4 years after this recommendation, upon which no action was taken, it was, in effect, implemented by the appointment of the Board for the Study of the Severely Wounded. Great advances might have been made, and many lives might have been saved, if this or some similar board had been appointed earlier.

Observations and Conclusions

The 186 patients who were studied during the investigation were carefully selected and directly observed by the medical officers who made up the board (19). The experience proved that a mobile laboratory unit could function competently close to the frontlines-indeed, at time, within them-and that it could perform comprehensive, accurate biochemical studies in such situations. The major consideration was at all times, of course, that the studies must not delay or otherwise interfere with the treatment of the casualties under investigation.

From the standpoint of the relation of blood loss to shock, the board made the following observations:

1. A wounded man could recover after the loss of about 75 percent of his circulating blood volume, a considerably larger amount than had generally been supposed. The quantitative relation demonstrated between the degree of clinical shock and the loss of blood volume or hemoglobin lent further support to the theory that the major cause of shock in wounded men is hemorrhage.

2. Certain visceral changes were found in casualties who had been in shock, but they were not evident until a minimum of 18 hours after injury, in which interval many wounded men had already succumbed to loss of blood.


If infection were not a complication, a return to normal could be demonstrated from the fourth day onward. Pulmonary edema was too inconstant and too late a development to be considered an important factor in the initiation of shock. Pulmonary fat embolism was absent or minimal in most cases and of uncertain significance in the remainder.

This investigation and the other studies of shock conducted in the Mediterranean theater did not settle all the problems of shock or all phases of any problem. They did, however, clearly establish that blood loss, with the resultant decrease in blood volume, is the most important cause of death in battle casualties. Thus, at the end of World War II, in contrast to the situation at the end of World War I, there was a clear understanding of why shock occurs and an equally clear understanding of the rationale of resuscitation therapy and of the necessity for whole blood replacement. Two other factors in the reduction of the mortality from shock should also be mentioned:

1. The skill and fine judgment developed by shock officers and others who supervised the resuscitation and preoperative preparation of casualties (the so-called learning curve described by the chest surgeons of the 2d Auxiliary Surgical Group) (22).

2. The planning and organization of the blood bank at Naples (p. 400), which provided a superior type of banked blood in quantities sufficient to meet all Fifth U.S. Army demands.


Materials and Methods

By the time active fighting began in the European theater, two concepts concerning shock were generally accepted: (1) that the pathogenesis of traumatic shock is a reduction in the circulating blood volume, and (2) that an essential feature of shock therapy is the correction of this deficiency by blood replacement.

From the practical standpoint, a major therapeutic problem was still the determination of the degree of blood volume deficiency. Clinical estimations alone were imprecise. Blood volume measurement, with the techniques then available, was obviously impossible as a routine therapeutic control in the field. Transfusion requirements in any given case were still, therefore, based almost exclusively on the clinical symptoms and signs present and on their response to therapy.

Studies to evaluate the relative importance and reliability of these clinical manifestations were undertaken in July 1944, in a First U.S. Army field hospital, by Maj. Richard V. Ebert, MC, and Maj. Charles P. Emerson, MC, 5th General Hospital (23). A preliminary study on 55 nontransportable casualties was limited to serial determinations of hemoglobin concentration and arterial pressure in relation to their clinical condition and course during resuscita-


tion.2 The data, like those collected in the Mediterranean theater (p. 41), indicated that the magnitude of the blood loss sustained by casualties in severe shock was far greater than had been generally appreciated.

A second study was carried out in September 1944, during the campaign on the German border, on 112 casualties with serious abdominal, thoracic, and extremity wounds. About half were in severe shock. The investigation included, in addition to routine physical examination:

1. Serial determinations of either (a) the hemoglobin concentration, by the acid-hematin technique with the Sahli-Hellige hemoglobinometer, or (b) hematocrit determinations, obtained after rapid centrifuging of oxalated samples in 4-cc. tubes.

2. Determinations of plasma volume by the Gibson-Evans dye technique.

3. Plasma protein concentration determinations by the copper sulfate technique of Phillips et al.

Measurements of the plasma volume, plasma protein concentration, and hematocrit were completed in 57 cases. Multiple blood volume determinations were made in 33 cases, either during transfusion or before or after operation.

Observations and Conclusions

The data which these observers had set out to secure and the conclusions derived from them may be summarized as follows:

1. The degree of blood volume deficit in shock and the extent to which clinical signs could be correlated with varying degrees of oligemia.

The arterial blood pressure proved the most reliable clinical index to blood volume deficiency. All casualties with initial systolic pressures below 85 mm. Hg, except those with spinal transections, were found to have significant degrees of oligemia, the deficit averaging 40 percent of the expected normal blood volume.

2. The degree of spontaneous hemodilution following extensive hemorrhage.

Blood volume and plasma protein determinations indicated that some degree, usually small, of spontaneous hemodilution with low plasma protein values occurred in oligemic shock. It was concluded that a normal hematocrit reading or the demonstration of only a mild anemia within a few hours after injury should not be interpreted to mean that severe blood loss had not occurred. Serious anemia could be produced by the administration of plasma to markedly oligemic patients.

3. The relative importance of losses of whole blood and plasma and the total blood loss resulting from various types of wounds.

The majority of the casualties in the series presented no evidence of excessive losses of plasma in proportion to losses of red blood cells. In a few severe

2A First U.S. Army report mentions that this study was carried out during a pressure period, when casualties were heavy, and that the investigating officers frequently found themselves administering blood and plasma rather than making the detached observations they had planned.


abdominal wounds, a disproportionate plasma loss was demonstrated, with resulting mild erythroconcentrations. The average blood loss estimated to have occurred before admission to the hospital was 63 percent per severely shocked casualty. Hemorrhage was most profuse in extremity wounds and least profuse in uncomplicated chest wounds.

4. The relative requirements for whole blood and plasma in shock and the effect of transfusion on blood volume.

Serial blood volume determinations indicated that hemorrhage had occurred during the course of transfusion in 12 of 23 patients studied. This complication was encountered most often in severe wounds of the extremities; the majority of these patients suffered losses averaging 40 percent of the blood and plasma transfused.

5. The causes of therapeutic failure in the treatment of traumatic shock.

Measurements of plasma protein before and after the injection of blood diluted with equal volumes of preservative solution indicated that retention of the solution in the bloodstream was only transient and not sufficient to produce significant hemodilution.

Casualties in whom clinical evidence of shock was not corrected by appropriate therapy, including restoration of the blood volume to normal, included those with severe infection; lesions involving the central nervous system; anoxia associated with pulmonary damage; and a persistent combination of anemia, oligemia, and hypotension, with terminal signs of myocardial insufficiency.

The case fatality rate for all casualties admitted in severe shock was 32 percent. When, however, the arterial pressure on admission exceeded 85 mm. Hg, the case fatality rate was only 10 percent. The majority of deaths occurred in casualties with abdominal wounds.


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