CHAPTER II
Shock
The development of the concept of whole blood transfusion inthe management of battle casualties was intimately related to the development ofa correct concept of shock. The confused and incorrect concept of this conditionheld in many quarters at the onset of World War II accounted, in large part, forthe delayed development of the whole blood program in the Zone of Interior andfor the trial-and-error period of shock therapy overseas.
HISTORICAL NOTE
Attempts to study shock during World War I by the specialcommittee appointed for that purpose, while generally unsuccessful, at leastdiscredited such existing theories as the reflex vasomotor paralysis theory, thetheory of exhaustion of the vasomotor center, the acapnea theory, and the theoryof adrenal exhaustion (1, 2). Cannon's (3) conclusion that theabsorption of toxins from injured tissues was the primary cause of traumaticshock, which was based on his own clinical and experimental studies for theShock Committee, was supported by other observers. In retrospect, however, it isclear that this theory was not supported by adequate proof and that the attemptto distinguish between shock and hemorrhage was equally fallacious.
OBSERVATIONS BETWEEN THE WORLD WARS
Even in an increasingly mechanized age, severe shockassociated with trauma is not often encountered in civilian practice inpeacetime, nor, with really rare exceptions, such as the Cocoanut Grove disaster(p. 697), is it ever encountered en masse. Isolated clinical observations arepossible in peacetime, but the circumstances of war, with its mass casualtiesand wide variety of wounds, provide the only really propitious material for theclarification of shock and other problems associated with wounding.
It is not surprising, therefore, that after World War I, theproblem of shock was transferred to experimental laboratories, in which attemptswere made to study it by physiologic and chemical techniques under a widevariety of experimentally induced conditions.
The theory of toxemic shock persisted until the latetwenties, when Blalock (4), and a little later Parsons and Phemister (5),demonstrated that shock produced by trauma to the limbs is not the result oftoxemia but of a local loss of blood and fluid and of circulating blood volume.Experiments by a number
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of other observers also failed to identify toxic substancesin the bloodstream of shocked animals and persons.
Between the wars, a number of misconceptions developedconcerning shock. For years, some observers continued to insist that the onlyexplanation of so-called true shock was a generalized increase in capillarypermeability, a concept introduced with the theory of traumatic toxemia andbased on the observation that red blood cell counts from the capillary bed werehigh, particularly in comparison with counts from the venous blood. In World WarII, this phenomenon was found to be both a late and a very infrequentdevelopment. Actually, the explanation of the hemoconcentration was fluid shift.The erroneous concept just described, however, was so widely accepted that itwas included in the manual on shock prepared under the auspices of the Committeeon Surgery, Division of Medical Sciences, NRC (National Research Council) (6).
In 1936, Freeman and his associates (7) were able toshow that in shock there is a reduction of the volume flow of blood in the handfrom the normal rate of 7 cc. per minute per 100 cc. volume to 1.3 cc. Theresult is a progressive tissue asphyxia, which goes on to tissue death if theincreasing oxygen debt is not repaid. The rate of blood flow decreases muchsooner than the blood pressure falls or hemoconcentration occurs. From theirobservations, Freeman and his group concluded that the blood volume is a morereliable index of shock than the blood pressure. At this time (1936), there wasno practical method of determining blood volume under field conditions. TheFreeman group suggested that, as an expedient, it might be useful to make arough calculation of the time necessary to refill the veins of the forearm andhand after they were stripped; normally, they fill immediately.
INITIAL CONCEPTS OF SHOCK AND SHOCK THERAPY IN WORLD WAR II
When the United States entered World War II, the followingconcepts of shock were generally accepted:
1. The reduction in blood volume present in peripheralcirculatory failure is the most important single factor, if not the initiatingfactor, in the production of the clinical picture seen in shock. It results fromthe loss of plasma, at first locally and then generally, into the extravasculartissue spaces. Most therapeutic efforts in shock must be directed towardovercoming this loss of blood volume.
2. The reduction in the rate of blood flow is associated witha diminished venous return, which results in a decreased cardiac output, thoughthe heart and the nervous energies that control it are not incapacitated.
3. The vasomotor center remains active.
4. Hemoconcentration is usually present in shock notassociated with hemorrhage (burns, crushing injuries) and tends to reflect theamount of plasma lost.
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In 1920, Maj. W. Richard Ohler, MC (8), had expressedthe firm opinion, based on his World War I experience, that the most importantsingle factor in shock is hemorrhage and that the degree of shock depends uponthe amount of blood lost (p. 8). The therapeutic need, he said unequivocally, istherefore for oxygen-carrying corpuscles, and no intravenous solutions canreplace them. It would have been desirable, he continued, to have a method ofcalculating the total hemoglobin and blood volume, but the use of citratedblood, even without this precise knowledge, was both simple and efficacious.
Between this time and the outbreak of World War II, numerousother observers had arrived at the same point of view, but they did not maketheir voices heard. Most of them did not even try. The rather general belief atthe outbreak of the war that plasma alone could compensate for the loss of wholeblood in shock simply reflected the prevailing point of view that blood loss wasnot necessarily the primary cause of shock. It is not easy, in looking back, tounderstand how these concepts were ever accepted, yet some of the most competentphysicians in the country believed that plasma alone could compensate for themassive blood losses which occurred in trauma. It was a belief which did adisservice 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 onlywhole blood was effective in shock did not believe that it would ever bepractical to provide it for forward areas.
Attempts to transfer controlled laboratory studies to combatconditions led to confusion, as might have been expected, for they were basedupon faulty premises. As Beecher (1) pointed out, the belief that plasmawould be as effective as whole blood in the management of hemorrhagic shockseems to have been derived from laboratory experiments so set up that the numberof variables could be strictly limited. There was, of course, no realresemblance between a combat soldier who had suffered a serious wound or woundsand a rabbit lying quietly in its cage after experimental deprivation of 75percent of its blood volume. The very management of the wounded soldier,including his successive removal rearward from the battlefield through the chainof evacuation, produced additional trauma, which was further increased byphysical and roentgenologic examinations, anesthesia, and operation. Transfer oflaboratory conclusions to a combat situation with its additional and widelydifferent variables was simply unsound reasoning, which led to therapeuticconfusion.
Nomenclature
The prewar confusion in the concept of shock was in no wisediminished by the confusing nomenclature employed to designate the condition andthe loose use of the term.
In 1918, Mann (9) defined shock as a termused by surgeons to describe a definite clinical condition probably due to anumber of causes but always occurring in one or the other of two groups ofcases: (1) those in which clinical manifestations followed some time after theoccurrence of conditions incidental to shock, or (2) those in which a severe orfatal condition
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supervened immediately upon receipt of the activeagent. The vagueness of the definition, propounded, as it was, by a physician ofMann's ability and experience, is indicative of the vagueness of the conceptof shock at that time.
In 1930, Parsons and Phemister (5) statedthat it was more correct to speak of hemorrhage than of shock, or to speak ofshock due to hemorrhage when acute loss of blood in wounds, whether closed oropen, was the cause of marked circulatory embarrassment or failure. At the sametime, these observers cited Blalock's criticism, in 1927, of the current looseuse of the term. Shock, in Blalock's opinion, should be considered not as adisease but as a group of symptoms which might be produced by a number offactors, including acute hemorrhage, wounds, and anesthesia. Later, Blalock (4)was to be the first to use the term "peripheral circulatoryfailure" for shock.
In 1938, Moon (10) defined shock as acirculatory deficiency, of neither cardiac nor vasomotor origin, characterizedby decreased blood volume, decreased cardiac output (reduced blood volume flow),and increased hemoconcentration.
In 1941, Janeway (11) described primaryshock as a condition of vascular collapse in which the tone of the peripheralvessels was diminished reflexly as a result of psychic stimuli. Primary shock,in his opinion, was difficult to distinguish from secondary shock, another termused very loosely indeed early in World War II. If there was not promptimprovement after such measures as warmth, hot fluids, morphine, and the shockposition (considered useful because gravity played such an important part in thepooling of the blood), then true secondary shock was undoubtedly present. Insecondary shock, by Janeway's definition, the volume of blood was insufficientto maintain an adequate peripheral circulation, not because of vasodilatation(as a matter of fact, vasoconstriction was usually present) but because of bloodloss. In secondary shock, whole blood was a more desirable replacement fluidthan plasma because both red cells and plasma had been lost.
It is significant that, in his excellent study on casualtiesin the Battle of El Alamein, Lt. Col. W. C. Wilson, RAMC, began with adefinition (12):
There is so much variation in the use of theterm "shock" that some kind of definition is required. The term issometimes used to describe any form of circulatory failure after injury. * * *This practice is objectionable in that the label of "shock" is givento many varieties of circulatory collapse, including those caused byperitonitis, other forms of bacterial infection, asphyxia, pneumothorax, andother complicated effects of intrathoracic injury. In this report the term"wound shock" is used in a restricted sense. It does not includecirculatory failure from peritonitis, bacterial infection, or intrathoracicinjury; nor, unless specially stated, does it refer to the shock which followsburns or injury to the central nervous system. It embraces all other forms ofcirculatory failure which arise within a few hours as a result of wounding. As amatter of convenience, the term shock is used as a synonym for circulatoryfailure and the cause is added when this is known, e.g., "shock fromhemorrhage."
The ETMD (Essential Technical Medical Data) for NATOUSA(North African Theater of Operations, U.S. Army), for March 1944 (13) suggestedthat the definition of shock should be extended to include the inability of theorganism to meet the demands commonly within the normal physiologic range andshould not be limited to a descriptive index of abnormal findings.
By the end of the war, the accepted definition of traumaticshock was a situation produced initially by a decrease in the peripheralcirculatory blood volume that is followed by a diminished venous return, aninadequate cardiac output, and depleted physiologic functions. The most usualcause of these changes is gross hemorrhage. This is still (1962) an acceptabledefinition.
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As a matter of convenience, the confusion that arose in theMediterranean theater because of the mistaken concept of shock and the loose useof the term is discussed under another heading (p. 37).
STUDIES ON SHOCK, NATIONAL RESEARCH COUNCIL
When the Committee on Transfusions, Division of MedicalSciences, NRC, held its first meeting on 31 May 1940 (14) (p. 73), itappointed a Subcommittee on Anesthesia and Shock (hereafter called theSubcommittee on Shock), with Dr. Alfred Blalock, Professor of Surgery,Vanderbilt University School of Medicine, as Chairman, and a distinguishedmembership of surgeons and anesthesiologists.
During the war, this subcommittee supervised a large numberof research studies dealing with special components of shock and certainvariations in its treatment, including an investigation of agents other thanwhole blood and plasma. All of these studies were undoubtedly of some value butmost of them were of value from the negative aspect; that is, the investigatorstested and eliminated a large number of agents that had to be tried before theycould be discarded. Reports of these investigations can be found in the minutesof the subcommittee, 1940-45.
From a practical standpoint and for the purposes of thishistory, the significant activities of the Subcommittee on Shock are included inthe conferences on shock held under its auspices and in certain of its officialreports.
First Conference on Shock
The first Conference on Shock (15) was held under theauspices of the Subcommittee on Shock on 28 June 1941, 6 months before theUnited States entered the war. The announcement of the meeting carried thestatement that emphasis would be placed upon measures of immediate use to theArmy and Navy Medical Departments. The agenda included a wide range of subjectsbut did not include specific presentations on the use of blood or plasma inshock.
Shock Report No. 1
At a conference on 28 June 1941, a committee was appointed tomake 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 ofshock, its prevention, and its control.
Prevention.-The remarks on prevention in this reportbegan with the following statement:
Since the major single cause of the state ofshock seems to be a decrease in the circulating medium (whole blood, plasma, orwater and electrolytes, or a combination of these), therapy is based uponchecking such losses and replacing body fluids by the best means at hand.
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Preventive measures were listed as control of hemorrhage;application of a tourniquet; splinting; postural measures; fluid therapy intraumatic shock, burns, and dehydration; the application of heat; treatment ofexposure to cold and immersion; and precautions in regard to analgesia andanesthesia.
Therapy.-The important therapeutic recommendationsby the ad hoc committee on shock were as follows (it should be remembered thatthey were made in July 1942):
1. When shock is imminent or present, blood,plasma, or albumin should be injected as promptly as possible. If massivehemorrhage has occurred or signs of serious anemia are present, whole blood ispreferable to blood substitutes.
2. In the absence of evidence of blastinjuries and pulmonary irritation, blood or blood substitutes can be givenintravenously, as rapidly as 1 pint of isotonic fluid in 10-15 minutes.
3. If the blood pressure has fallen below 80mm. Hg, an effort should be made to restore it to normal as soon as possible.
4. If blood is available, it should be used ininitial amounts of 500 to 1,000 cc. The first injection of reconstituted plasmashould be two units and of concentrated albumin, one unit (25 gm.). Not morethan 10 units of albumin should be given in 48 hours. If albumin is used,severely dehydrated patients require additional water and salt. When sterilephysiologic salt solution is available, concentrated albumin can be diluted inthe ratio of two units (50 gm.) to one liter of salt solution.
5. If the desired effect on the blood pressureis not obtained in 15-30 minutes, the dose of blood or blood substitute shouldbe repeated.
6. If anemia appears in the course oftreatment with large amounts of plasma or albumin, whole blood transfusions areindicated.
7. Salt and glucose solutions are notrecommended in shock. The temporary rise in blood pressure and blood volumewhich they produce is only temporary and gives rise to a sense of complacency.Their only value is to correct dehydration. They are contraindicated in headinjuries and pulmonary damage.
8. Within reasonable limits, there is littlerisk of injecting too large quantities of replacement fluids immediately afterwounding. 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 December1943, the agenda had become more realistic, in the light of militarydevelopments. It included field blood volume determinations by the Phillips-VanSlyke copper sulfate method; the comparative therapeutic effects of whole blood,plasma, albumin, saline solutions, and gelatin in clinical shock; and a vigorousdiscussion of the use and value of blood and blood substitutes. The proceedingswere thus in marked contrast to the proceedings of the first conference, whichhad been held almost 6 months before Pearl Harbor.
On the other hand, the discussion of shock was still notentirely realistic, for it was divided into early and late shock. The discussionof early shock included infection as an initiating agent, possible techniquesfor early recognition, and prevention and treatment. The discussion of lateshock covered intermediate metabolism, visceral damage, acidosis,vitamin-coenzyme systems, and succinate and Pitressin therapy. Acidosis wasstated to be a possible
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criterion of the severity of shock but was not considered acause. Neither succinate nor Pitressin therapy was regarded as promising.
In a report at this session by Dr. E. I. Evans on thecomparative 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 wasquite severe. A marked reduction in the incidence of severe shock could beproduced by giving saline solution prophylactically. When saline solution wasgiven to a patient already in severe shock, there might be temporaryimprovement, with elevation of the blood pressure, but it seldom lasted morethan 30 minutes.
2. Both plasma and whole blood were effectivein moderately severe shock, but studies of the blood volume after the initialtreatment usually indicated the need for whole blood. All patients in shock whohad 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 thediscussion down to a realistic level:
One of the chief problems is concerned with supplyingblood in forward areas. Somewhere along the planning line somebody seems tohave forgotten that plasma lacks oxygen-carrying power. Much too often thefollowing sequence of events takes place: A man receives a bad wound; he bleeds;hours later his "blood" volume and pressure are restored by plasmainfusion; the surgeon decides he is now ready for surgery; there is further lossof the too-small quantity of hemoglobin available in his body, as a result ofthe surgery; the patient's circulatory system collapses and it is impossibleto revive him. Plans are now being worked out for supplying whole blood for theforward areas.
At this second Conference on Shock, Dr. Loeb, chairman of theSubcommittee on Blood Substitutes, made the highly significant announcement thatit was the conviction of his group that the ideal treatment of shock due tohemorrhage and skeletal trauma was replacement of lost blood with blood and thatevery means possible should be utilized for increasing the use of blood in theprevention 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 madeavailable.
2. That in crushing injuries, burns, andabdominal wounds, plasma was more desirable than blood at certain stages oftreatment.
3. That plasma is more desirable than wholeblood when dehydration, for one reason or another, is marked.
4. That plasma has the advantage ofconvenience of transportation to areas to which whole blood cannot be taken butthat there are certain situations in which serum albumin is more practical thanplasma.1
Shock Report No. 17
Shock Report No. 17 (18), dated 4 March 1944, was arevision of Shock Report No. 1 (16), dated 16 July 1942. Some of themembers 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.
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which prepared the second report had also served on the firstcommittee. The current status of the shock problem was set forth as follows:
1. The establishment of a close correspondenceof circulatory changes in experimental and clinical shock has given confidencein the clinical application of results obtained in experimental studies,especially on dogs.
2. Reduction in the circulating blood volumeis the most important factor in the initiation of shock. The reduction, whetherthe injury is mechanical or thermal, is due to loss of blood or fluid at thesite of injury. Except possibly in very late stages, there is no notableincrease in capillary permeability in nontraumatized areas of the body. Thereduction in the circulating blood volume makes its restoration to normal theprimary consideration of therapy.
3. The most reliable criteria of the degree ofcirculatory disturbance underlying shock are cardiac output and blood volume. Asshock progresses, cardiac output continues to decrease, even if there is nofurther reduction in circulating blood volume. The level of arterial pressure isnot a reliable criterion of the degree of circulatory impairment in early shock,nor does the hematocrit, considered alone, indicate the relative degree of lossof blood or plasma.
4. After a critical point has been reached indiminution of the blood volume, progressive tissue anoxia leads to metabolicchanges and to damage to certain organs, such as the brain, and perhaps theheart and liver. The state which then develops is termed "irreversibleshock."
The following prophylactic and therapeutic points werestressed:
1. The consequences of inadequate circulatoryvolume emphasize the very great importance of early, adequate treatment ofshock. Treatment should not be delayed until its manifestations appear.
2. Operation should be carried out as promptlyas possible after resuscitation, or sometimes before it is completelyaccomplished, with blood replacement as indicated during the procedure.
3. Fluid therapy is the most important measurein the therapy of shock. It should take the form of whole blood, which may berequired in amounts up to 3,000 cc.
4. The first 500 to 1,000 cc. of blood shouldbe given rapidly. Subsequent administration should be at the rate of 500 cc. perhour or less. Prophylactic transfusions should also be given slowly.
The great difference between these recommendations, in March1944, and those of July 1942 is the unequivocal advice to use whole bloodwithout delay. The altered concept of shock should also be noted. The advice toinject the blood slowly was founded on the old idea that rapid injection ofblood might give rise to speed shock. As a matter of fact, early in the war, itwas found that the rapid injection of blood was not only harmless but essentialand beneficial. It was not unusual to inject 500 cc. of blood in 5 minutes, andoccasionally as much as 20 pints of blood were injected into four differentveins in a period of 3 hours. Had members of the various committees of theNational Research Council been permitted to visit combat zones, as was severaltimes requested (p. 79), their recommendations would have been more closelyrelated to the facts of military medicine.
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EVOLUTION OF THE CONCEPT AND THERAPY OF SHOCK
IN THEMEDITERRANEAN THEATER
In the first months of active U.S. participation in World WarII, the confusion that attended the condition that came to be appreciated as themost important single complication of wounding seriously affected the managementof wounded casualties. Until the concept of shock was clarified, they weretreated with skill and devotion, but they were often not treated entirelycorrectly, even though, by the time North Africa was invaded in November 1942,it was generally accepted that decreased circulating blood volume was the mostimportant deviation from normal physiology seen in shocked casualties.
The necessary clarification of the concept of shock, with theapplication of the correct concept to shocked casualties, was accomplished inthe Mediterranean theater. Until June 1944, this was the only theater in whichlarge numbers of ground troops were in constant contact with the enemy. Fornearly 2 years, the battle casualty rates in it were continuously above 50 perthousand per annum, and for nearly 2 months of this period they were above 100per thousand. With casualties requiring treatment in such numbers, policies ofmanagement had to be established, even in the absence of any proved scientificrationale 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 Surgeryto the theater surgeon. Before he left the Zone of Interior he had been wellbriefed on the British experience in shock and transfusion (p. 55) and had beeninformed of the research under way in this field at the Army Medical School andelsewhere.
Colonel Churchill's first official report to the theatersurgeon, 2? weeks after his arrival and after a period of temporary duty on thesouthern Tunisian front, was a memorandum on blood transfusion (19). On16 April, after the collection of additional data, he set forth severalconclusions, the most important of which was that a significant number ofwounded went into shock from loss of blood and that plasma was not a totaltreatment for these casualties (p. 55).
In his first report, Colonel Churchill was critical of boththe nomenclature and the concept of shock. He found that in field medicalrecords, histories, and autopsy reports, shock was used with vague significanceand often with no definition at all (p. 32). The disturbance of the peripheralcirculation which the term indicated might range from slight pallor to impendingdeath.
Further confusion was introduced by the use of the term"irreversible shock," a use which amounted to the assumption that atone moment restoration of the blood volume could halt the process of death whileat the next, it could not. Even the most carefully controlled laboratoryexperiments could not identify this precise baseline. If this held true in acontrolled experimental
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laboratory, identification of the onset of irreversible shockseemed even more impossible when the medical officer was confronted with theresults of random trauma sustained by soldiers under combat conditions.
In the records of battle casualties who died in forwardareas, shock or irreversible shock was almost invariably found to be recorded asa secondary cause of death, whether the primary condition was a craniocerebralwound, an overwhelming peritonitis, a fulminating gas gangrene infection, oruncontrollable hemorrhage. In Colonel Churchill's opinion, the terms"shock" and "irreversible shock," as they appeared inrecords and autopsy protocols in NATOUSA, were completely irrelevant. Hetherefore found it impossible to comment on the occurrence of shock during theTunisian campaign in terms that would be helpful to those engaged in research onthe subject.
An analysis of 1,263 casualties had shown no deaths fromso-called wound shock under terms of the restricted definition in whichhemorrhage could be excluded as the important causative factor. The sameobservations were made in the clinical study of large numbers of wounded.Colonel Churchill therefore concluded:
1. That wound shock, if it occurred among survivingcasualties, apparently responded to treatment. Irreversible shock therefore didnot appear to be a problem of pressing importance.
2. That wound shock could not be identified as a cause ofdeath in conditions prevailing in the management of battle casualties during theperiod of the survey.
3. That shock as it was observed in the Tunisian campaigncould be controlled by the application of accepted methods of treatment, withoutthe need for the development of additional methods.
These conclusions were amply confirmed in the followingmonths by simple, direct observations on battle casualties properly treated bymethods already available, including the replacement of blood losses by wholeblood. Clinical observations were later confirmed by a number of specialstudies. The management of shock in the last year of the Italian campaign, whenthere was a general appreciation of the need for whole blood and when the bloodneeded was available in ample quantities from a theater blood bank, was verydifferent from the makeshift management and often complete lack of blood in theTunisian and early Italian campaigns. Appreciation of the need of blood,however, preceded its supply by many months.
SPECIAL STUDIES
Lalich Study
The first planned studies on shock in the Fifth U.S. Armywere made by Capt. Joseph J. Lalich, MC, on the Cassino front in December 1943and on the Anzio beachhead in March 1944 (19, 20). Studies on thehematocrit, on the plasma protein, nonprotein nitrogen, and chlorides of theblood, and
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on the carbon dioxide combining power of the blood supportedhis thesis that blood loss is the chief factor in shock.
On the basis of his clinical observations alone, CaptainLalich had already advocated that battle casualties in shock be divided intothree categories, according to the following criteria:
1. The patient has a normal blood pressure and no significantabnormalities of pulse volume or pulse rate, but his wounds are sufficientlynumerous and sufficiently severe to make it reasonable to anticipate circulatoryfailure. Experience showed that unless patients in this group were treated byreplacement therapy, usually in the amount of 500 cc. of plasma and 500 cc. ofblood, varying degrees of circulatory failure were likely to occur duringoperation.
2. The blood pressure ranges from 90 mm. Hg down to thelowest level at which it can be measured. Resuscitation requires at least 1,000to 2,000 cc. of blood.
3. The blood pressure cannot be determined by auscultation. Apatient in this state should receive from 500 to 1,500 cc. of blood, the preciseamount depending upon how much is required to raise the systolic pressure toabout 100 mm. Hg. After this level has been attained, an additional 500 to 1,000cc. of blood should be given before surgery is undertaken. If the systolicpressure fails to rise to at least 50 mm. Hg after 1,500 cc. of blood has beengiven over a period of 15-30 minutes, operation should be resorted to withoutfurther delay, for factors other than serious blood loss or continuinghemorrhage are probably contributing to the persistence of shock. Among thesefactors are gross contamination and infection of the pleural or peritonealcavities, or both, or toxemia from clostridial myositis. Even when theseconditions are chiefly responsible for the state of shock, blood loss may alsoplay 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 inthe 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 operatingbeside the 3d Platoon of the 11th Field Hospital at Cassino (19, 20). Thehospital was doing first priority surgery, and the objective of theinvestigation was the response of seriously wounded men in respect to shock,hemorrhage, and dehydration. Surgeons caring for the patients investigated werekept informed of the results of the laboratory studies and were able to utilizethe information in their management.
The final report on 2 January 1945 covered 100 casualties, ofwhom (the figures are overlapping) 48 had penetrating abdominal wounds, 32penetrating thoracic wounds, and 55 compound fractures. Seventeen died duringthe course of the investigation.
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Colonel Stewart and Captain Warner, who had been promoted inthe interim, were particularly impressed by the variability of both thevasomotor and the cardiovascular response to wounding and also by the fact thatreactions to shock and hemorrhage were considerably less stereotyped than theywere usually supposed to be. Their other findings were as follows:
1. A reduction in blood volume was characteristic ofuntreated shock.
2. Hemoconcentration was not encountered, but decreases inplasma protein concentration and hematocrit values were evident shortly afterwounding. Later, both components were lowered.
3. Dehydration and azotemia were common in the early recoveryperiod.
4. Urinary reactions were indicative of a rather mild basedeficiency.
5. No evidence of the excessive use of plasma or whole bloodwas detected in any patient.
Beecher-Burnett Study
The third study, by Major Beecher, Consultant in Shock andAnesthesia to the Surgeon, MTOUSA, and Capt. Charles H. Burnett, MC, was made atCassino and on the Anzio beachhead and chiefly concerned the timing of surgeryin relation to resuscitation (19, 21).
Most medical officers who had made special studies of shockor who had a large clinical experience believed that it was wiser to resuscitatethe casualty as completely as possible before surgery unless there was someindication, such as continued hemorrhage or peritoneal contamination, foremergency operation. As a result of their own investigations, Major Beecher andCaptain Burnett took the position that surgery should be considered a phase ofthe routine of resuscitation and given an earlier place in it (p. 584).Specifically, when the systolic blood pressure had reached 80 mm. Hg and thepatient was warm and had a good color, they believed that operation should beproceeded with. Whatever additional replacement therapy was indicated could becarried 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 onthe Cassino front often required 6-8 hours after seriously wounded casualtieshad been admitted. In 1944, on the Anzio beachhead, even extremely bad surgicalrisks were prepared for operation on an average of 2 hours and 20 minutes afterwounding. The readier availability of whole blood in 1944 had much to do withthe reduction in the timelag, but the change in concept of the optimum time foroperation undoubtedly also played a major role.
THE BOARD FOR THE STUDY OF THE SEVERELY WOUNDED
In August 1944, the appointment of a board to study thetreatment of severely wounded casualties was recommended by the theater surgeon,then Maj. Gen. Morrison C. Stayer, to the Commanding General, NATOUSA, Lt.
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Gen. Jacob L. Devers (19). There were two reasons forGeneral Stayer's request: (1) that the concept of blood loss as the etiologicfactor in shock must be documented by cold, hard facts; and (2) that similarproof was required for the use of whole blood as an essential element in themanagement of wounded men and not as an agent which could be replaced by othersubstances. 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 hadbeen left at the end of World War I. On 3 September 1944, General Deversappointed a Medical Board to Study the Treatment of the Severely Wounded(usually known as the Board for the Study of the Severely Wounded) to operatedirectly under the theater surgeon. Its membership was composed of MajorBeecher; 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 theminutes 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 theArmy, freed from any of the obligations of Army officers, who would study casesof shock as investigators. This would give opportunity to observe shock on a bigscale, an opportunity to get an insight into the nature of shock." Morethan 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 theSeverely Wounded. Great advances might have been made, and many lives might havebeen saved, if this or some similar board had been appointed earlier.
Observations and Conclusions
The 186 patients who were studied during the investigationwere carefully selected and directly observed by the medical officers who madeup the board (19). The experience proved that a mobile laboratory unitcould function competently close to the frontlines-indeed, at time, withinthem-and that it could perform comprehensive, accurate biochemical studies insuch situations. The major consideration was at all times, of course, that thestudies must not delay or otherwise interfere with the treatment of thecasualties 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 75percent of his circulating blood volume, a considerably larger amount than hadgenerally been supposed. The quantitative relation demonstrated between thedegree of clinical shock and the loss of blood volume or hemoglobin lent furthersupport to the theory that the major cause of shock in wounded men ishemorrhage.
2. Certain visceral changes were found in casualties who hadbeen in shock, but they were not evident until a minimum of 18 hours afterinjury, in which interval many wounded men had already succumbed to loss ofblood.
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If infection were not a complication, a return to normalcould be demonstrated from the fourth day onward. Pulmonary edema was tooinconstant and too late a development to be considered an important factor inthe initiation of shock. Pulmonary fat embolism was absent or minimal in mostcases and of uncertain significance in the remainder.
This investigation and the other studies of shock conductedin the Mediterranean theater did not settle all the problems of shock or allphases of any problem. They did, however, clearly establish that blood loss,with the resultant decrease in blood volume, is the most important cause ofdeath in battle casualties. Thus, at the end of World War II, in contrast to thesituation at the end of World War I, there was a clear understanding of whyshock occurs and an equally clear understanding of the rationale ofresuscitation therapy and of the necessity for whole blood replacement. Twoother factors in the reduction of the mortality from shock should also bementioned:
1. The skill and fine judgment developed by shock officersand others who supervised the resuscitation and preoperative preparation ofcasualties (the so-called learning curve described by the chest surgeons of the2d 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 quantitiessufficient to meet all Fifth U.S. Army demands.
EBERT-EMERSON STUDY
Materials and Methods
By the time active fighting began in the European theater,two concepts concerning shock were generally accepted: (1) that the pathogenesisof traumatic shock is a reduction in the circulating blood volume, and (2) thatan essential feature of shock therapy is the correction of this deficiency byblood replacement.
From the practical standpoint, a major therapeutic problemwas still the determination of the degree of blood volume deficiency. Clinicalestimations alone were imprecise. Blood volume measurement, with the techniquesthen available, was obviously impossible as a routine therapeutic control in thefield. Transfusion requirements in any given case were still, therefore, basedalmost exclusively on the clinical symptoms and signs present and on theirresponse to therapy.
Studies to evaluate the relative importance and reliabilityof 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 nontransportablecasualties was limited to serial determinations of hemoglobin concentration andarterial pressure in relation to their clinical condition and course duringresuscita-
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tion.2 The data, like those collected in theMediterranean theater (p. 41), indicated that the magnitude of the blood losssustained by casualties in severe shock was far greater than had been generallyappreciated.
A second study was carried out in September 1944, during thecampaign on the German border, on 112 casualties with serious abdominal,thoracic, and extremity wounds. About half were in severe shock. Theinvestigation included, in addition to routine physical examination:
1. Serial determinations of either (a) the hemoglobinconcentration, by the acid-hematin technique with the Sahli-Helligehemoglobinometer, or (b) hematocrit determinations, obtained after rapidcentrifuging of oxalated samples in 4-cc. tubes.
2. Determinations of plasma volume by the Gibson-Evans dyetechnique.
3. Plasma protein concentration determinations by the coppersulfate technique of Phillips et al.
Measurements of the plasma volume, plasma proteinconcentration, and hematocrit were completed in 57 cases. Multiple blood volumedeterminations were made in 33 cases, either during transfusion or before orafter operation.
Observations and Conclusions
The data which these observers had set out to secure and theconclusions derived from them may be summarized as follows:
1. The degree of blood volume deficit in shock and the extentto which clinical signs could be correlated with varying degrees of oligemia.
The arterial blood pressure proved the most reliable clinicalindex to blood volume deficiency. All casualties with initial systolic pressuresbelow 85 mm. Hg, except those with spinal transections, were found to havesignificant degrees of oligemia, the deficit averaging 40 percent of theexpected normal blood volume.
2. The degree of spontaneous hemodilution following extensivehemorrhage.
Blood volume and plasma protein determinations indicated thatsome degree, usually small, of spontaneous hemodilution with low plasma proteinvalues occurred in oligemic shock. It was concluded that a normal hematocritreading or the demonstration of only a mild anemia within a few hours afterinjury should not be interpreted to mean that severe blood loss had notoccurred. Serious anemia could be produced by the administration of plasma tomarkedly oligemic patients.
3. The relative importance of losses of whole blood andplasma and the total blood loss resulting from various types of wounds.
The majority of the casualties in the series presented noevidence of excessive losses of plasma in proportion to losses of red bloodcells. In a few severe
2A First U.S. Army report mentions that this study wascarried out during a pressure period, when casualties were heavy, and that theinvestigating officers frequently found themselves administering blood andplasma rather than making the detached observations they had planned.
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abdominal wounds, a disproportionate plasma loss wasdemonstrated, with resulting mild erythroconcentrations. The average blood lossestimated to have occurred before admission to the hospital was 63 percent perseverely shocked casualty. Hemorrhage was most profuse in extremity wounds andleast profuse in uncomplicated chest wounds.
4. The relative requirements for whole blood and plasma inshock and the effect of transfusion on blood volume.
Serial blood volume determinations indicated that hemorrhagehad occurred during the course of transfusion in 12 of 23 patients studied. Thiscomplication was encountered most often in severe wounds of the extremities; themajority of these patients suffered losses averaging 40 percent of the blood andplasma transfused.
5. The causes of therapeutic failure in the treatment oftraumatic shock.
Measurements of plasma protein before and after the injectionof blood diluted with equal volumes of preservative solution indicated thatretention of the solution in the bloodstream was only transient and notsufficient to produce significant hemodilution.
Casualties in whom clinical evidence of shock was notcorrected by appropriate therapy, including restoration of the blood volume tonormal, included those with severe infection; lesions involving the centralnervous system; anoxia associated with pulmonary damage; and a persistentcombination of anemia, oligemia, and hypotension, with terminal signs ofmyocardial insufficiency.
The case fatality rate for all casualties admitted in severeshock was 32 percent. When, however, the arterial pressure on admission exceeded85 mm. Hg, the case fatality rate was only 10 percent. The majority of deathsoccurred in casualties with abdominal wounds.
References
1. Beecher, H. K.: The Physiologic Effects of Wounds. Arch.Surg. 80: 366-373, March 1960.
2. Cannon, W. B.: Wound Shock. In The MedicalDepartment of the United States Army in the World War. Washington: GovernmentPrinting Office, 1927, vol. XI, pt. I, pp. 185-213.
3. Cannon, W. B.: Traumatic Shock. New York and London: D.Appleton and Co., 1923.
4. Blalock, A.: Principles of Surgical Care, Shock and OtherProblems. St. Louis: C. V. Mosby Co., 1940.
5. Parsons, E., and Phemister, D. B.: Haemorrhage and"Shock" in Traumatized Limbs. An Experimental Study. Surg. Gynec.& Obst. 51: 196-207, August 1930.
6. Freeman, N. E., Blalock, A., and Strumia, M. M.: Shock. InBurns, Shock, Wound Healing, and Vascular Injuries. Prepared under theauspices of the Committee on Surgery, Division of Medical Sciences, NRC.Military Surgical Manuals. Philadelphia and London: W. B. Saunders & Co., 1943.
7. Freeman, N. E., Shaw, J. L. and Snyder, J. C.: TheReduction in Circulation Through the Hand Resulting From Pain, Fear, Cold, andAsphyxia, With Quantitative Measurements of the Volume Flow of Blood in ClinicalCases of Surgical Shock. J. Clin. Invest. 15: 651-664, November 1936.
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8. Ohler, W. R.: Treatment of Surgical Shock in the Zone of the Advance. Am.J. M. Sc. 159: 843-853, June 1920.
9. Mann, F. C.: Further Experimental Study of Surgical Shock. J.A.M.A. 71:1184-1188, 12 Oct. 1918.
10. Moon, V. H.: Shock and Related Capillary Phenomena. New York and London: Oxford University Press, 1938.
11. Janeway, C. A.: War Medicine, With Special Emphasis on the Use of BloodSubstitutes (Medical Progress). New England J. Med. 225: 371-381, 4 Sept.1941.
12. Report, Consultant in Surgery to the Surgeon, NATOUSA, 2 July 1943.
13. ETMD, NATOUSA, for March 1944.
14. Minutes, meeting of Committee on Transfusions, Division of MedicalSciences, NRC, 31 May 1940.
15. Minutes, Conference on Shock, under the auspices of the Subcommittee onShock, Division of Medical Sciences, NRC, 28 June 1941.
16. Shock Report No. 1, General Recommendations Concerning Shock, Subcommitteeon Shock, Division of Medical Sciences, NRC, 16 July 1942.
17. Minutes, Conference on Shock, Subcommittee on Shock, Division of MedicalSciences, NRC, 1 Dec. 1943.
18. Shock Report No. 17, General Recommendations Concerning Shock (Revisionby Subcommittee on Shock of Report No. 1, issued 16 July 1942), Division ofMedical Sciences, NRC, 4 Mar. 1944.
19. Medical Department, United States Army. Surgery in World War II. ThePhysiologic Effects of Wounds. Washington: U.S. Government Printing Office,1952.
20. Snyder, H. E.: Fifth U.S. Army. In Medical Department, UnitedStates Army. Surgery in World War II. Activities of Surgical Consultants. VolumeI. Washington: U.S. Government Printing Office, 1962.
21. Beecher, H. K.: Resuscitation, Control of Pain, and Anesthesia. In MedicalDepartment, United States Army. Surgery in World War II. Vol. II, GeneralSurgery. Washington: U.S. Government Printing Office, 1955.
22. Burford, T. H.: Evolution of Clinical Policies in the MediterraneanTheater of Operations. In Medical Department, United States Army. Surgeryin World War II. Thoracic Surgery, Volume I. Washington: U.S. GovernmentPrinting Office, 1963.
23. Emerson, C. P., and Ebert, R. V.: A Study of Shock in Battle Casualties.Measurements of the Blood Volume Changes Occurring in Response to Therapy. Ann.Surg. 122: 745-772, November 1945.
